Archive for the ‘Female Genetics’ Category

Christine Roden, a postdoctoral researcher at UNC-Chapel Hill, wasone of five women honored this month for the work in STEM fields by L'Oral USA,as part of the cosmetics companys For Women in Science Fellowship program.

L'Oralrecognized the 2019 fellows at a November 7awards ceremony hosted by CBS Evening Newsanchor Norah O'Donnell at the Carnegie Institution for Science in Washington, D.C.

Now in its sixteenth year, the fellowship program, which includes a $60,000 cash award, is administered by the American Association for the Advancement of Science. The program has recognized eighty female postdocstudents with over $4 million since 2003, according to a news release on Tuesday.

Roden is a thirty-two-year-old RNA biologist and Pennsylvania native. She earned a Ph.D.in genetics at Yale University and an undergraduate degree in biology from the University of Pittsburgh.

The fellowship will enable her to spend time learning new techniques for RNA profiling. She can also use the funding to hire an undergraduate to assist her with experiments and data collection.

Her research in RNA biology at the University of North Carolina, Chapel Hill seeks to understand how disrupted RNA structures can result in diseases like ALS or cancer, with the potential to improve treatments for these types of diseases, a L'Oral USA spokeswoman, told the INDY in an email.

The press releasesays the programs funding and support for women scientists comes at a critical time in their careers.

The For Women in Science Fellowship program is rooted in LOrals core belief that the world needs science and science needs women because women in science have the power to change the world, the release states. Although the number of women in science is increasing, there remains a leaky pipeline,with significant career drop-off happening during the years between postdoc and tenure track. In addition to grant funding, fellows receive mentorship, media training, career coaching, and recognition.

The fellowship candidates were evaluated based on their intellectual merit, research potential, scientific excellence, and commitment to supporting women and girls in science. The fellowship winners are required to serveas role models for younger generations, according to the release.

Roden and the four other fellowship recipientsare being honored for their important research across a wide range of fields, from neuroscience to paleoceanography.

Women interested in applying for the fellowship can learn more here.

Contact staff writer Thomasi McDonald at tmcdonald@indyweek.com.

Support independent local journalism.Join the INDY Press Clubto help us keep fearless watchdog reporting and essential arts and culture coverage viable in the Triangle.

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UNC Biology Researcher Honored With National Women in Science Fellowship - INDY Week

If youre the type of person who snoozes your alarm every morning or cant function before (or even after) yourmorning coffee, there might be a genetic reason for that.

New research by DNA testing company,23andMe, has discovered that genetic programming plays a part in our wake up time.

The research studied over 1,500 British people to determine that 7.55am was the UKs average genetic wake up time.

This means that the average Brit willwake upnaturally just before 8am each day.

READ MORE: Drinking tea or coffee has no impact on sleep, according to study

Many people set their alarms for much earlier than that, hence our feelings of tiredness and lack of productivity.

Interrupting your bodys circadian rhythm (which is the official term for our body clock) can leave us feeling out of sorts at the beginning of the day.

If you dont feel tired first thing, it doesnt mean youre immune to these feelings. Many people have tiredness slumps at different points in the day.

READ MORE: Parents can buy children anti-nightmare mist

TheNHShas found that one in five of us get unusually tired and have suggested some good ways to wake yourself up when the slump sets in.

Exerciseis cited as one of the key ways to bolster your energy reserve. Aside from the psychological benefits of exercise, it alsolowers your risk of early death by 30%.

Cutting down oncaffeineis another recommended way to beat the tiredness. As a nation of tea drinkers, we are all at risk of being over-stimulated by the affects of caffeine. Switching to decaffeinated tea and coffee could make all the difference.

Getting into a routine of having daytime naps may also interrupt your bodys circadian rhythm. If you go to sleep every time you feel a bout of tiredness, you may struggle to get to sleep at night, so says the NHS.

Excerpt from:
Scientists reveal why we feel so tired in the morning - Yahoo Lifestyle

While the rate of death from cancer has been declining since the 1990s, an estimated 9.6 million people died from cancer in 2018, making it the second-leading cause of death worldwide [1]. According to the NCI Cancer Trends Progress Report, in the United States, the incidence and death rates of some cancer types have also been increasing. Together, these facts indicate that despite tremendous recent progress, the research community unfortunately still has a long list of tasks to complete to end global suffering from cancer.

The clinical management of cancer has long been rooted in morphological and histopathological analyses for diagnosis, and the triad of surgery, chemotherapy, and radiation for treatment. However, we are quickly moving towards a pervasive reliance on high resolution, high throughput, molecular marker-based diagnostic as well as precision-targeted therapeutic modalities. The progressive development of the paradigm that defined molecular drivers of cancer has exposed therapeutic vulnerabilities; for example, the BCR-ABL1 gene fusion in chronic myeloid leukemia, KIT mutations in gastrointestinal stromal tumors, ERBB2 amplification in a subset of breast cancers, or EGFR mutations and ALK/ ROS/ RET gene fusions in lung cancers to name a few. Fueled by advances in high-throughput sequencing, it is increasingly practical (and arguably affordable) to systematically pursue Targeted Anticancer Therapies and Precision Medicine in Cancer.

PLOS ONE, together with PLOS Computational Biology, launched a Call for Papers earlier this year to increase understanding of this clinically important area. The scope of this call encompassed four areas: identification and classification of driver genes and somatic alterations; target and drug discovery; mechanisms of drug resistance; and early detection and screening.

Today, we are very happy to announce the launch of the resulting Collection. Featuring an initial set of nearly two dozen papers, with more to be added as they are published, these articles represent diverse facets of ongoing efforts in this area, where general knowledge of cancers serves to inform individual patients care, and at the same time particulars from individual cancer cases contribute to improved resolution of our general knowledge pool.

Somatic aberrations that are critical to the development, growth and progression of cancer are defined as drivers that are typically accompanied by large numbers of incidental aberrations referred to as passengers, acquired in the tumors due to the general chromosomal instability characteristic of advanced cancers. Distinguishing driver aberrations from passengers in individual tumors represents an active area of research that involves development of smarter analytical algorithms, as well as definitive functional characterization of candidate aberrations.

Emilie A. Chapeau et al. developed a conditional inducible transgenic JAK2V617F mouse model that recapitulates aspects of human myeloproliferative neoplasms, including splenomegaly, erythroid expansion and hyperproliferation of bone marrow, with some intriguing differences seen between male and female mice. Importantly, the disease phenotype was reversible when transgene expression was switched off. This work underscores the key role for JAK2V617F in the initiation and maintenance of myeloproliferative neoplasms, and suggests that inhibitors specific to this JAK2 mutation might be efficacious in this disease [2].

Using targeted exon sequencing and array comparative genomic hybridization (CGH), Gayle Pageau Pouliot et al. identified monoallelic mutations in Fanconi-BRCA pathway genes in samples collected from children with T cell acute lymphoblastic leukemia (T-ALL). These mutations appeared to arise in early stages of tumorigenesis, suggesting a potential role for Fanconi-BRCA pathway insufficiency in the initiation of T-ALL. Although PARP inhibitors did not affect viability of isolated T-ALL cells with monoallelic Fanconi-BRCA mutations, these cells were hypersensitive to UV irradiation in vitro or ATR inhibition in vivo, suggesting that ATR inhibitors might have therapeutic value in T-ALL [3].

Three papers in this Collection examine links between genetic alterations and prognosis. Sumadi Lukman Anwar et al. report that LINE-1 hypomethylation in human hepatocellular carcinoma samples correlates with malignant transformation, decreased overall survival and increased tumor size [4]. Investigating HER2-positive breast cancer specimens, Arsalan Amirfallah et al. found that high levels of vacuole membrane protein 1 (VMP1) could potentially contribute to cancer progression and might be a marker of poor prognosis [5]. Finally, in their systematic review and meta-analysis, Chia Ching Lee et al. identified low discordance rates in EGFR mutations between primary lung tumors and distant metastases, although they note some differences depending on metastatic site. Notably, discordance rates appear to be higher in bone metastases compared to central nervous system or lung metastases [6]. These studies provide much-needed leads for the potential development of new diagnostic tests or targeted therapies.

Precision therapy of cancers is premised on the identification of tumor-specific driver aberrations that are necessary for tumor growth and survival. These aberrations represent potential therapeutic targets. While matching therapeutics have been developed for some of the tumor-specific targets, particularly many oncogenic kinases, a large number of defined driver aberrations remain in search of effective therapies. Drug discovery efforts to match defined targets represent a vigorous area of ongoing research with implications for survival and quality of lives of cancer patients worldwide. The development of drugs to treat cancers driven by transcription factors, chromatin modifiers, and epigenetic modulators has proved particularly challenging. On the other hand, recent development of novel immunotherapeutic approaches has spurred research to identify potential targets and matching drug discovery efforts.

This Collection highlights several interesting new strategies to identify potential lead compounds for cancer treatment. Thomas W. Miller et al. describe the development of a biochemical quantitative high-throughput screen for small molecules that disrupt the interaction between CD47 and SIRP. Preclinical studies have shown that disrupting this interaction may provide a new approach for cancer immunotherapy. Small molecular inhibitors that specifically target the interaction between CD47 and SIRP are potentially advantageous over biologics that target CD47, because they might have less on target toxicologic issues and greater tissue penetrance [7].

Work from Gabrielle Choonoo, Aurora S. Blucher et al. examines the feasibility of repurposing existing cancer drugs for new indications. The authors compiled information about somatic mutations and copy-number alterations in over 500 cases of head and neck squamous cell carcinoma (HNSCC) and mapped these data to potential drugs listed in the Cancer Targetome [8]. This approach uncovered pathways that are routinely dysregulated in HNSCC and for which potential anti-cancer therapies are already available, as well as those for which no therapies exist. The work opens new therapeutic avenues in the treatment of this disease and also illuminates which pathways could be prioritized for the development of therapies [9].

Another important approach in extending the clinical utility of existing anti-cancer drugs is to determine whether they are effective in other settings. Indeed, Kirti Kandhwal Chahal et al. have demonstrated that the multi-tyrosine kinase inhibitor nilotinib, which is approved for use in chronic myeloid leukemia, binds the Smoothened receptor and inhibits Hedgehog pathway signaling. Nilotinib decreased viability of hedgehog-dependent medulloblastoma cell lines in vitro and in patient-derived xenografts in vivo, suggesting that nilotinib might be an effective therapy in Hedgehog-dependent cancer [10]. (Check out the authors preprint of this article on bioRxiv.) Darcy Welch, Elliot Kahen et al. took a different approach to identify new tricks for old drugs. By testing two-drug combinations of five established (doxorubicin, cyclophosphamide, vincristine, etoposide, irinotecan) and two experimental chemotherapeutics (the lysine-specific demethylase 1 (LSD1) inhibitor SP2509 and the HDAC inhibitor romidepsin), they found that combining SP2509 with topoisomerase inhibitors or romidepsin synergistically decreased the viability of Ewing sarcoma cell lines in vitro [11].

Two papers in this collection describe potential new therapeutic approaches in cancer. Vagisha Ravi et al. developed a liposome-based delivery mechanism for a small interfering RNA targeting ferritin heavy chain 1 (FTH1) and showed that this increased radiosensitivity and decreased viability in a subpopulation of glioma initiating cells (GICs) [12]. Yongli Li et al. identified 2-pyridinealdehyde hydrazone dithiocarbamate S-propionate podophyllotoxin ester, a podophyllotoxin derivative that inhibits matrix metalloproteinases and Topoisomerase II. Treatment with this compound decreased the migration and invasion of human liver cancer cell lines in vitro, as well as growth of HepG2-derived tumors in mouse xenografts [13].

The success of precision cancer therapy targeting defined somatic aberrations is hampered by an almost inevitable, eventual treatment failure due to the emergence of drug resistance. Resistance often involves new mutations in the therapeutic target itself, or it may result due to activation of alternative pathways. Identification and therapeutic targeting of drug resistant clones represents an ongoing research problem with important practical implications for the clinical management of cancer.

Afatinib is a pan-human epidermal growth factor receptor (HER) inhibitor under investigation as a potential therapeutic option for people with gastric cancer; however, preclinical studies have found that some gastric cancer cell lines are resistant to afatinib treatment. Karolin Ebert et al. identify a potential mechanism behind this lack of response, demonstrating that siRNA-mediated knockdown of the receptor tyrosine kinase MET increases afatinib sensitivity of a gastric cancer cell line containing a MET amplification. As upregulation of MET has been linked to resistance to anti-HER therapies in other cancers, these findings support a role for MET in afatinib resistance in gastric cancer and suggest that combined afatinib and anti-MET therapy might be clinically beneficial for gastric cancer patients [14].

Identifying mechanisms to circumvent drug resistance is critically important to improve response and extend survival, but it is equally important to identify individuals who could be at risk of not responding to anti-cancer therapeutics. Lucas Maahs, Bertha E. Sanchez et al. report progress towards this end, showing that high expression of class III -tubulin in metastatic castration-resistant prostate cancer (CRPC) correlated with decreased overall survival and worse response rate (as measured by changes in prostate-specific antigen (PSA) levels) in CRPC patients who received docetaxel therapy. The development of a biomarker indicating potential treatment resistance to docetaxel could help develop treatment plans with the best chance of success [15].

The converse approach identifying biomarkers that correlate with drug sensitivity could help distinguish subsets of patients who would benefit most from a certain anti-cancer therapy. Kevin Shee et al. mined publicly available datasets to identify genes whose expression correlate with sensitivity and response to chemotherapeutics and found that expression of Schlafen Family Member 11 (SLFN11) correlates with better response to a variety of DNA-damaging chemotherapeutics in several types of solid tumors [16]. Separately, Jason C. Poole et al. validated the use of the Target Selector ctDNA assay, a technology developed by their group that allows the specific amplification of very low frequency mutant alleles in circulating tumor DNA (ctDNA). Testing for EGFR, BRAF and KRAS mutations yielded a very high, >99% analytical sensitivity and specificity with the capability of single mutant copy detection, indicating that accurate molecular disease management over time is possible with this minimally invasive method [17].

Work from Georgios Kaissis, Sebastian Ziegelmayer, Fabian Lohfe et al. uses a machine learning algorithm to differentiate subtypes of pancreatic ductal adenocarcinoma based on 1,606 different radiomic features. Intriguingly, the subtypes identified in their analysis correlated with response to chemotherapeutic regimens and overall survival [18]. An imaging approach taken by Seo Young Kang et al. demonstrates the potential power of fluorodeoxyglucose (FDG) PET/CT scans in determining the response of people with metastatic differentiated thyroid cancer to radioactive iodine treatment [19].

Since cancer growth and development accrues progressive accumulation of somatic aberrations, early detection holds the promise of more effective interventions. Similarly, screening of at risk demographics has been found effective in preventing or better managing cancer care, as exemplified by the significant reduction in cases of cervical cancer after the introduction of the Pap smear as well as human papillomavirus (HPV) testing.

Biomarker development is also critically important for the early detection of cancer and metastatic disease; moreover, biomarkers are being identified that can provide insight into patient prognosis. Several papers in this Collection report interesting findings in the area of biomarker development. A report from Lingyun Xu et al. describes a magneto-nanosensor-based multiplex assay that measures circulating levels of PSA and four proteins associated with prostate cancer. This approach segregates people with prostate cancer from those with benign prostate hyperplasia with high sensitivity and specificity [20].

Two articles provide new insight into markers of disease progression and survival. Vidya Balagopal et al. report the development of a 22-gene hybrid-capture next generation sequencing panel to identify measurable residual disease in patients with acute myeloid leukemia (AML). In their retrospective study, the panel was effective at detecting evidence for residual disease. Importantly, it correctly identified patients who had never relapsed in that no evidence of residual disease was detected in any of these respective samples. Once validated, this approach could potentially be useful in monitoring patients with AML to ensure that recurrence or relapse is identified as soon as possible [21]. Separately, Yoon-Sim Yap et al. use a label-free microfluidic platform to capture circulating tumor cells (CTCs) from people with breast cancer and show that absolute numbers of CTCs predict progression-free survival with higher levels of CTCs correlating with a worse prognosis [22].

Finally, Lucia Suzuki et al. report findings into a potential role for the intestinal stem cell marker olfactomedin 4 (OLFM4) as a biomarker for metastasis in esophageal adenocarcinoma. The authors found that OLFM4 expression was not significantly associated with disease-free or overall survival; however, low OLFM4 expression was detected in poorly differentiated early and advanced-stage esophageal adenocarcinoma and was an independent prognostic variable for lymph node metastasis [23].

This collection of studies encompassing the range of research topics under the banner of targeted anticancer therapies highlights the diversity, complexity and inter-disciplinary nature of research efforts actively contributing to our collective knowledge base with the hope to positively impact the lives of all cancer patients.

We would like to thank all Academic Editors and reviewers for their expert evaluation of the articles in this Collection as well as the authors for their contributions to this field. Special thanks to Senior Editor, Team Manager Emily Chenette for her invaluable help and guidance in publishing this Collection.

Andrew Cherniack

Andrew Cherniack is a group leader in the Cancer Program at the Broad Institute of MIT and Harvard and in the Department of Medical Oncology at the Dana Farber Cancer Institute. He led the Broad Institutes effort to analyze somatic DNA copy number alterations for The Cancer Genome Atlas (TCGA) and is now co-principal investigator of the Broad Institutes copy number Genome Data Analysis Center for the National Cancer Institutes Genomic Data Analysis Network (GDAN). He also leads the oncoming effort to identify new cancer therapeutic targets for the partnership with Bayer. Prior to joining the Broad Institute in 2010, Dr. Cherniack worked in both academia and industry, with a 9-year tenure at the Abbott Bioresearch Center following a similar time period in the Program in Molecular Medicine at UMass Medical School, where he was a postdoctoral researcher and a research assistant professor. Dr. Cherniack holds a Ph.D. in molecular genetics from Ohio State University and a B.A. in biology from the University of Pennsylvania.

Anette Duensing

Anette Duensing is an Assistant Professor of Pathology at the University of Pittsburgh School of Medicine and a Member of the Cancer Therapeutics Program at the University of Pittsburgh Medical Center (UPMC) Hillman Cancer Center. Dr. Duensings research focuses on bone and soft tissue sarcomas with the goal of identifying novel therapeutic approaches that target the underlying molecular biology of these malignancies. Her special interest and expertise are in gastrointestinal stromal tumors (GISTs), a sarcoma characterized by mutations in the KIT or PDGFRA receptor tyrosine kinases and the first solid tumor entity that was successfully treated with small molecule kinase inhibitors. Dr. Duensing holds an M.D. degree from the University of Hannover School of Medicine, Germany, and was a research scholar of the Dr. Mildred Scheel Stiftung fr Krebsforschung (German Cancer Aid/Deutsche Krebshilfe) at Brigham and Womens Hospital, Harvard Medical School. She is the recipient of an AACR Scholar-in-Training Award (AACR-AstraZeneca), a Young Investigator Award from The Liddy Shriver Sarcoma Initiative, a UPCI Junior Scholar Award, a Jeroen Pit Science Award, a Research Award from the GIST Group Switzerland and was named Hillman Fellow for Innovative Cancer Research. Dr. Duensing is co-founder and leader of the Pittsburgh Sarcoma Research Collaborative (PSaRC), a highly translational, interdisciplinary sarcoma research program. She is also affiliated with the Department of Urology at the University of Heidelberg, Germany. Dr. Duensing is an Academic Editor for PLOS ONE and author of nearly 70 original articles, reviews and book chapters.

Steven G. Gray

Steven Gray graduated from Trinity College Dublin in 1992. He joined the laboratory of Tomas J. Ekstrm at the Karolinska Institute (Sweden) in 1996 and received his PhD in 2000. He moved to the Van Andel Research Institute in Michigan, USA where he continued his studies on the therapeutic potential of histone deacetylase inhibitors in the treatment of cancer. He also spent time as a visiting fellow at Harvard Medical School, Boston working on epigenetic therapies for neurodegenerative disease. Returning to Europe, Dr. Gray spent some time at the German Cancer Research Centre (DKFZ Heidelberg), and subsequently moved to Copenhagen to work for Novo Nordisk as part of the research team of Prof Pierre De Meyts at the Hagedorn Research Institute working on epigenetic mechanisms underpinning diabetes pathogenesis. Dr. Gray is currently a senior clinical scientist at St Jamess Hospital at the Thoracic Oncology Research Group at St. Jamess Hospital. He holds adjunct positions at both Trinity College Dublin (senior clinical lecturer with the Dept. of Clinical Medicine), and at Technical University Dublin (adjunct senior lecturer, School of Biology DIT). Dr. Gray has published over 100 peer-reviewed articles, 15 book chapters and has edited 1 book. Research in Dr Grays laboratory focuses on Receptor Tyrosine Kinases as potential therapeutic targets for the treatment of mesothelioma; epigenetic mechanisms underpinning drug resistance in lung cancer; targeting epigenetic readers, writers and erasers for the treatment of mesothelioma and thoracic malignancy; circulating tumour cells; and non-coding RNA repertoires in mesothelioma and thoracic malignancy.

Sunil Krishnan

Sunil Krishnan is the Director of the Center for Radiation Oncology Research and the John E. and Dorothy J. Harris Professor of Gastrointestinal Cancer in the department of Radiation Oncology at MD Anderson Cancer Center. He received his medical degree from Christian Medical College, Vellore, India and completed a radiation oncology residency at Mayo Clinic, Rochester, Minnesota. In the clinic, he treats patients with hepatobiliary, pancreatic and rectal tumors with radiation therapy. His laboratory has developed new strategies and tools to define the roles and mechanisms of radiation sensitization with gold nanoparticles, chemotherapeutics, biologics and botanicals. Dr. Krishnan serves as the co-chair of the gastrointestinal scientific program committee of ASTRO, co-chair of the gastrointestinal translational research program of RTOG, consultant to the IAEA for rectal and liver cancers, chair of the NCI pancreatic cancer radiotherapy working group, and Fellow of the American College of Physicians. He has co-authored over 200 peer-reviewed scientific publications, co-authored 17 book chapters, and co-edited 3 books.

Chandan Kumar-Sinha

Chandan Kumar-Sinha is a Research Associate Scientist in the Department of Pathology at the University of Michigan. He obtained Masters in Biotechnology from Madurai Kamraj University, and PhD in Plant Molecular Biology from Indian Institute of Science. He completed a Postdoctoral Fellowship at the Department of Pathology, University of Michigan, where he worked on genomic profiling of cancers. Thereafter, he joined the Advanced Center for Treatment, Research and Education in Cancer in India as a faculty member. After establishing a cancer genomics group there, he moved back to the University of Michigan to pursue translational cancer research. Dr. Kumar-Sinhas current research involves integrative clinical sequencing using high-throughput genome and transcriptome analyses to inform precision oncology. He has authored over 50 peer-reviewed publications, two book chapters, and is named co-inventor on a patent on prostate cancer biomarkers.

Gayle E. Woloschak

Gayle Woloschak is Professor of Radiation Oncology, Radiology, and Cell and Molecular Biology in the Feinberg School of Medicine, Northwestern University. Dr. Woloschak received her Ph.D. in Medical Sciences from the University of Toledo (Medical College of Ohio). She did her postdoctoral training at the Mayo Clinic, and then moved to Argonne National Laboratory until 2001. Her scientific interests are predominantly in the areas of molecular biology, radiation biology, and nanotechnology studies, and she has authored over 200 papers. She is a member of the National Council on Radiation Protection, the International Commission on Radiation Protection and numerous other committees and also serves on the US delegation to the United National Scientific Committee on the Effects of Atomic Radiation.

Read more from the original source:
Introducing the Targeted Anticancer Therapies and Precision Medicine in Cancer Collection - PLoS Blogs

SOMETIME NEXT year, if all goes to plan, a gay male couple in California will have a child. The child in question will have been conceived by in vitro fertilisation. In this case a group of eggs from a female donor are now being fertilised by sperm from both fathers (half from one, half from the other). Of the resulting embryos, the couple will choose one to be implanted in a surrogate mother. An uplifting tale of the times, then, but hardly a newsworthy event. Except that it is.

Where the story becomes newsworthy is around the word choose. For the parents, in conjunction with a firm called Genomic Prediction, will pick the lucky embryo based on a genetically estimated risk of disease. Such pre-implantation testing is already used in some places, in cases where there is a chance of parents passing on a condition, such as Tay-Sachs disease, that is caused by a single faulty gene. Genomic Prediction is, however, offering something more wide-ranging. It is screening embryos for almost 1m single-nucleotide polymorphisms (SNPs). These are places where individual genomes routinely differ from one another at the level of an individual genetic letter. Individual SNP differences between people rarely have much effect. But add them up and they can raise or lower by quite a lot the likelihood of someone suffering a particular disease. Generate several embryos and SNP-test them, then, and you can pick out those that you think will grow up to be the healthiest.

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Much fuss was made last year about a researcher in China, He Jiankui, who edited the genomes of two human embryos in order to try, he claimed, to make them immune to infection by HIV, the virus that causes AIDS. What Genomic Prediction proposes is different. No editing is involved. There is thus no risk of harming a child by putting it through a risky experimental procedure. Whether Genomic Predictions particular technique will actually deliver super-healthy children remains to be seen. The principle seems plausible, though. History may therefore look back on this moment as the true beginning of designer babies. And the tool that has made that possible is called GWAS.

GWAS stands for genome-wide association study. It is the endpoint of a historical process that began in the mid-19th century with Gregor Mendel, a Moravian abbot and amateur botanist. Mendel worked out the first set of rules of heredity. This led to the idea of a gene. And that, when allied with the discovery that the material of heredity is a chemical called DNA, which encodes genetic information in the order of its component units, known as nucleotides, led to the idea of a gene being a particular piece of DNA that carries in its nucleotides the blueprint of a particular protein. This protein goes on to contribute, in combination with environmental effects such as nutrition, to a particular bodily or behavioural characteristic, known as a phenotypic trait.

Since the 1950s, researchers have tried to quantify the relative contributions of genes and the environment to such traits. Mostly, this is in the context of disease. But behavioural characteristics, personality and cognitive ability have also been matters of interest. GWAs expands this process by looking not just at the effects of individual genes, but across the whole genomefor protein-coding genes make up only about 2% of a persons DNA.

Comparisons, over several generations of a family, of the prevalence of a particular trait yield estimates of its heritabilitya measure of how well individual genetic differences account for variations in that trait in a given population. A heritability of 100% indicates that any differences in a trait between individuals in that population are accounted for solely by genetic factors, while 0% suggests the environment alone is responsible. The phrase given population is important. Some populations may be exposed to relevant environmental variables unknown to others. Conversely, genetic factors present in one group (better response to oxygen scarcity in those evolved to live at high altitude, for example) may be absent in another.

An analysis published in 2015 of more than 2,700 studies of heritability shows that its average value, for all traits looked into in those studies, is about 50%. That includes physical traits like susceptibility to heart disease (44%) and eye disorders (71%), and mental ones, including higher-level cognitive functions (47%) such as problem-solving and abstract thought.

Other, less obvious traits are heritable, too. The amount of time a child spends watching television was assumed for many years to have a heritability close to zero. In 1990, however, a study led by Robert Plomin, now at Kings College, London, compared the habits of adopted children with those of their birth mothers. It found television-watching has a heritability of about 45%. Similar surprisingly heritable traits include a childs tendency to be bullied at school (more than 70%) or to be accident-prone (51%). Even someones likelihood of being religious (30-40%) or of getting divorced (13%) is heritable.

In 1989 James Watson, the first head of the Human Genome Project, summarised the mood of many by declaring that We used to think our fate was in our stars. Now we know, in large measure, our fate is in our genes. There was hope then that the genome project would locate those genes. No one was naive enough to think that there existed, say, such a thing as a gene for television-watching. But it was reasonable to believe that there might be a handful of genes which combined to encourage television-watching indirectly. More important, there was an expectation that the heritable causes of things like heart disease might be pinned down to such genetic handfuls. These might then be investigated as drug targets. To everyones frustration, though, few such genes revealed themselves. And in most cases the contributions they made to a conditions heritability were small. Where, then, was the missing heritability?

With hindsight, the answer was obvious. The number of variants that play a role in disease risk is far higher than Mendel-blinded researchers had imagined. Though human beings are genetically more than 99.9% alike, they have 6bn genetic letters in their genomes. This is where the SNPs are hidden, for a diversity of less than 0.1% still leaves room for millions of them. And when SNPs contributions are combined, their effects can be significant. For height, for example, the number of relevant SNPs is reckoned to be about 100,000each adding or subtracting, on average, 0.14mm to or from a persons adult stature. Furthermore, most of these SNPs are in parts of the genome that do not encode proteins at all. Rather, they regulate the activities of other genes and often have no obvious connection to the trait in question.

To be fair, it was mainly human geneticists who were captivated by the simple Mendelian model of single genes with big effects. According to Peter Visscher of the University of Queensland, Australia, many plant and animal scientists knew of traits genetic complexity long before the Human Genome Project started. But they were more interested in breeding better crops or livestock than in understanding the biology behind such complexity.

Dr Visscher was one of the first to realise that human studies would need to recruit more participants and screen for many thousands more SNPs if they were to capture in full the genetic components of most traits. In 2007 he and his colleagues used models to show that for a condition with a prevalence of 10% in the general population, approximately 10,000 volunteers are required to identify the SNPs marking the 5% of those at highest risk of developing that condition. Earlier studies, often with just a few hundred participants, had simply not been powerful enough to see what was going on. And thus was GWAS born.

Ideally, a GWAS would obtain a full sequence of the genome of every participating individual. However, even though the cost of such sequences has fallen dramatically since the completion of the genome project, to about $1,000 a shot, this would still be prohibitively expensive. Instead, researchers use devices called SNP arrays. These detect hundreds of thousands of the most common SNPs for a price of $50 or so.

A combination of SNP arrays, larger samples of volunteers and better computing methods means it is now possible to find millions of variants that contribute to a trait. An individuals score from these variants, known as his polygenic score, can then be calculated by adding up their contributions to give, for example, his risk of developing a particular disease in later life.

Another advance has been a change in the way volunteers are recruited. Institutions called biobanks have come into existence. These hold both tissue samples from, and a range of medical and other data about, large numbers of people who have agreed to make those data available to researchers who meet the criteria employed by the bank in question.

Among the largest of these repositories is the UK Biobank, in Britain. This has 500,000 depositors. One study that drew on it, published in 2018 by Sekar Kathiresan of the Massachusetts General Hospital in Boston and his colleagues, worked out polygenic risk scores for five diseases, including coronary heart disease and type 2 diabetes. By totting up scores from over 6m genetic variants, they were able to elucidate SNP patterns that identify those who are at a threefold higher risk or worse than the general British population of developing one of these diseases. For heart disease, 8% of the population are at such risk. For type 2 diabetes, 3.5%.

Nasim Mavaddat of the University of Cambridge and her colleagues have similarly calculated polygenic risk scores for breast cancer. These showed that a British womans average ten-year risk of developing breast cancer at the age of 47 (the earliest that Englands National Health Service begins screening for the disease) is 2.6%. The study also found that the 19% of women who had the highest risk scores reached this level of risk by the age of 40. Conversely, the 10% at lowest risk did not cross the threshold until they were 80.

Using these and similar studies, it is possible to draw up lifetime risk profiles for various medical conditions. A British firm called Genomics has done that for 16 diseases (see chart). This will help screening programmes to triage who they screen, by offering their services earlier to those at high risk of developing a condition early in their lives. It will also permit the dispensing of risk-appropriate advice about diet and exercise to those who need it most, and the early offering to those who might benefit from them of things like statins and antihypertensive drugs. In light of all this Englands National Health Service announced in July that 5m healthy Britons would be offered free gene tests.

A third study that drew on the UK Biobank is rather different. It was published in October and demonstrated the power of GWAS to reach beyond non-medical matters. It examined patterns of internal migration in Britain, and showed that there has been an outward migration from former coalmining areas of people with SNP patterns associated with high educational attainmentprecisely the sorts of individuals economically deprived places can least afford to lose.

Educational attainment also demonstrates how heritability varies with environment. In Norway, for example, heritability of educational attainment increased after the second world war as access to education widened. Since all children now had more or less the same opportunities at school, environmental variation was largely ironed out and the effects of genetic differences consequently exaggerated.

Both of these examples foreshadow how the sort of genetics made possible by GWAS can have political consequences. The implication of the internal-migration study is that the geographically left-behind are dimmer, on average, than the leavers. The implication of the Norwegian study might likewise be seen by some as suggesting that those who have done well at school and thus snagged the best (and best-paid) jobs are part of a genetic elite that deserves its success, rather than being the lucky winners of a genetic lottery.

And that is just within a country. Start comparing people from different parts of the world and you enter a real minefield. Because most of the genetic data now available come from populations of European ancestry, their predictive power is poorer for people from elsewhere. Alicia Martin of the Broad Institute in Massachusetts and her colleagues scored West Africans for height based on SNPs drawn from studies on European or European-derived populations. The scores predicted that West Africans should be shorter than Europeans. Actually, they are not.

As more people of non-European ancestry are sequenced, these problems may abate. But if group-based differences emerge or persist in the face of better data, that would be cause for concern. Differences between groups in things like height are rarely cause for prejudice beyond a jocular level. For something like educational attainment, by contrast, there is a risk that politically motivated groups would try to exploit any differences found to support dubious theories of racial superiority.

To some historians, this looks horribly familiar. They fear that the old spectre of eugenics risks rising in a new guise. As Nathaniel Comfort of Johns Hopkins University, in Baltimore, observes, The IQ test was invented in order to identify students who needed extra help in school. But within about a decade, it was being used as a tool to weed out the so-called feebleminded, not just from school but from the gene pool. Such fears of genetic stratification would become particularly acute if polygenic scores were applied to embryos for the purpose of selecting which to implant during IVFas Genomic Prediction is just about to do.

Genomic Prediction and a second firm, MyOme (which is not yet accepting customers), claim to be able to build up an accurate picture of an embryos genome. That is tricky because the sequencing has to be carried out using the tiny quantities of DNA in a few cells taken from that embryo. A sequence so obtained would normally be full of errors. The two companies say they can deal with this by comparing embryonic sequences with those of the biological parents. All of the DNA in the embryo has come from one or other parent, so blocks of embryonic DNA can be matched to well-established sequences from their parental progenitors and an accurate embryonic sequence established. That makes working out the embryos SNP pattern possible.

Genomic Prediction thus says it is able to offer couples undergoing IVF a polygenic risk score for each embryo for a variety of diseases including type 1 diabetes, type 2 diabetes, breast cancer, testicular cancer, prostate cancer, basal-cell carcinoma, malignant melanoma, heart attack, atrial fibrillation, coronary artery disease, hypertension and high cholesterol. At the moment it does not offer scores for non-medical traits like height or educational attainment. But there is nothing to prevent it from doing so should it so wish.

Even for medically relevant scores, however, some worry about this approach. One concern is pleiotropythe phenomenon of the same piece of DNA influencing several apparently unrelated traits. Choosing an embryo with a low risk of heart disease might accidentally give it, say, a higher chance of developing epilepsy. Single-mindedly maximising scores for positive traits like intelligence or height may therefore increase the risk of genetic disorders.

Stephen Hsu of Michigan State University, one of Genomic Predictions founders, acknowledges the theoretical risk of this, but argues that serious pleiotropic effects are unlikely. If you looked at a bunch of kids with IQs of, say, 160 or 170, he says, I doubt youd find much seriously wrong with them. Theyd just be a bunch of geeks. Dr Hsu, who in 2014 predicted that reproductive technologies would soon be used to select for more intelligent offspring, estimates that an IQ gain of between 10 and 15 points would be possible if couples were allowed to choose between ten embryos. He also thinks that further gains would probably accumulate if people selected in this way went on to select their own offspring on the basis of intelligence.

This is plausible. Before 2008, when the first SNP chips for cattle became available, the annual milk yield of dairy cows in America had been increasing at about 50kg per year. After six years of chip-based polygenic selection, the rate of increase had doubled to more than 100kg per year. This suggests the technique is powerfulin cattle at least. Despite Dr Hsus optimism, however, pleiotropism has reared its head in these animals. They have become less fertile and have weaker immune systems.

In the end, then, it is generally a good idea to remember that human beings have already been optimised by a powerful agent called natural selection. Trade-offs between different pieces of physiology, even in domestic animals, will have been forged in the crucible of evolution and will generally be optimal, or close to it. Genetic tinkering may sometimes improve things. But by no means always.

Read more:
Modern genetics will improve health and usher in designer children - The Economist

Although hair loss may seem like a more prominent problem in men, women are nearly as likely to lose or have thinning hair. Most women notice it in their 50s or 60s, but it can happen at any age and for a variety of reasons.

Hair grows in three different cycles: anagen, catagen, and telogen. About 90% of the hair on the head is in the anagen, or growth phase, which lasts anywhere from 2 to 8 years. The catagen, or transition phase, typically lasts 2-3 weeks, during which the hair follicle shrinks. During the telogen cycle, which lasts around 2 to 4 months, the hair rests. An overwhelming majority of the time, the hair is on the scalp; it is growing. Only about 10% of the strands are in transition or resting at any one time. Hair grows about 6 inches a year for most people.

The most common cause of hair loss is a hereditary condition called male-pattern hair loss or female-pattern hair loss. It usually occurs gradually with aging and in predictable patterns a receding hairline and bald spots in men and thinning hair in women. For women, hair loss is most common around ages 45 to 55 but can commence as early as a woman in her 20s. Over half of women will find their hair is thinning by the age of 50. For men, it can happen as early as their teens, and it starts with the hairline receding. Women may notice their part widening or the volume decreasing in the middle of their scalp. When it comes to seeking treatment, women will usually take action far more quickly than men.

Most people lose anywhere from 50 to 100 strands of hair each day, according to the American Academy of Dermatology. On the days when hair is washed, people can lose up to 250 strands. But dont avoid washing in an attempt to keep the hair, as it will fall out eventually, anyway.

For those who dont plan on counting their hair every day, there are ways to know when hair is thinning or being lost at a higher rate. When waking up in the morning, there may be an usually large amount on your pillow. Or, when you comb your hair (especially without tugging, which can pull the hair out), more than normal will be left in the comb. Another way to diagnose whether a woman is experiencing excessive hair loss is through family history. What did your mother, aunts, or grandmothers look like at similar ages? If they had similar amounts of hair loss at such ages, it could be a telltale sign of female pattern hair loss. Typically, each time a normal hair follicle is shed, it is replaced by hair that is equal in size. But in women with female pattern hair loss, the new hair is finer and thinner -a more miniaturized version of itself. The hair follicles are shrinking, and eventually, they quit growing altogether.

If hair loss is sudden or excessive, it is likely to be caused by something other than heredity, like a medical condition. There is a wide range of conditions that can bring on hair loss, with some of the most common being pregnancy, thyroid disorders, and anemia. Others include autoimmune diseases, polycystic ovary syndrome (PCOS), and skin conditions such as psoriasis and seborrheic dermatitis. There also may be a link between menopause and hair loss.

Menopause is also a pretty common culprit in female hair loss and is one of the many symptoms that come about due to the major hormonal fluctuations that occur at this time in a womans life. Menopausal hair loss usually manifests as a general thinning all over the scalp, instead of hugely noticeable bald spots.

Other reasons for hair loss include extreme stress, physical trauma like surgery or intense illness, dramatic weight loss over a short period of time; and taking too much or too little of certain vitamins. And hair loss can occur a couple of weeks to six months after any of these experiences.

Regular, garden variety female pattern baldness is age-related and the most common cause of female hair loss and can occur even in non-menopausal women. This is a genetic condition that is also known as androgenetic alopecia. It is quite normal not that that is of much comfort and is usually confined to overall thinning rather than patchy losses.

One other way to thin hair is self-inflicted -hairstyles like cornrows or too-tight braids can cause hair loss called traction alopecia. All of the things women do to manipulate their hair dyes, chemical treatments, bad brushes, blow dryers, and flat irons can result in damage and breakage. This includes brushing too much and towel drying aggressively when the hair is wet. Luckily, for most of these issues, the hair grows back, or the loss can be reversed with medical treatments. But it is important to see a dermatologist if there seems to be something wrong, because the sooner treatment is started, the better the chances are for improving your growing season. Another thing to keep in mind is that wearing your hair in a tight hairstyle such as a heavy ponytail or bun or tight braids can cause hair loss too.

Well, it mostly depends on the reason for it in the first place. A dietary deficiency can often be corrected with supplements or an improvement in what you eat. Life-stage issues such as pregnancy and menopause are going to take their toll, and quite often, the level of hair loss will even out once the stage is complete. In the case of menopause, that full, lustrous head of hair probably wont return to what it once was, but the hair fall will usually slow dramatically. Hormone replacement therapy can help, although if hair loss is the only symptom worrying you and not too traumatically you may want to forgo the HRT and muddle through.

Just as everybody responds differently to their hair loss, everybody responds differently to treatments for it. Its critical to find out the cause first, so that could mean a visit to your doctor. Once you know what youre dealing with, start there. Maybe you need treatment for stress, for a hormonal imbalance, or for PCOS or another medical condition. But if you find out you have female pattern hair loss, there are certainly treatments that can help manage it. What are some of the most effective treatments/strategies for women with hair loss? Again, the solution for you will depend on your situation, but here are some strategies you might want to look into. It depends on the cause and on the individual, but some of the strategies include:

Minoxidil. Initially developed as a treatment for high blood pressure, it became known as a drug that could grow hair in places where it was lost. Some women not all experience great results. Its important to keep in mind that one must stay on Minoxidil for at least six months to cover the full hair growth cycle. One favorite is Hair Restoration Laboratories Ultra Strength Hair Regrowth Treatment which not only contains FDA-approved 5% minoxidil but also a number of powerful DHT-blocking ingredients that, when combined with 5% minoxidil, significantly improve the quality of hair and scalp.

Platelet Rich Plasma Therapy (PRP). Known as the Vampire treatment, the patients blood is drawn, naturally enhanced to boost the number of platelets and key growth factors, then reinjected back into the scalp. This can revive dying follicles and hair.

Iron supplements Iron deficiency is thought to be a hair loss cause in a lot of women. If women are experiencing hair loss, shedding or thinning, it is highly recommended that they see their doctor for a blood test to check levels, particularly if theyre vegan/vegetarian, have a history of anemia or experience heavy menstrual bleeding. The doctor may prescribe an iron supplement, which could help to remediate the hair loss.

Hair Restoration Laboratories Hair Restore Shampoo and Conditioner Set. This shampoo and conditioner set helps keep hair healthy and protects against the effects that cause hair loss. Combined, the Hair Restore Shampoo and Conditioner Set contains over 30 potent ingredients formulated to fight DHT (the primary factor the causes female pattern hair loss), prevent hair loss and thinning, and stimulate thicker, fuller and healthier hair regrowth.

If you are suffering from hair loss or thinning, the most likely culprit is genetics. While you cannot fight your genetics, there are numerous treatments available to effectively prevent any further loss or thinning and restore the hair that you have already lost. Time is not on your side with hair loss. So, the sooner you consult with a physician to identify the causes, the sooner you will be able to give your hair what it needs to grow strong, thick, and healthy.

Excerpt from:
Female Hair Loss And What To Do About It - Explosion

Projected Lifetime Healthcare Costs of High-Risk Patients on Conventional Medical Therapy, such as Statins, Were Compared with and without the Cardiovascular Risk Reduction Demonstrated with Icosapent Ethyl in the REDUCE IT Study

Analysis Accounted Patient Treatment Outcomes as Well as U.S. Private Insurance and Medicare Costs

DUBLIN, Ireland and BRIDGEWATER, N.J., Nov. 11, 2019 (GLOBE NEWSWIRE) -- Amarin Corporation plc (NASDAQ: AMRN) announced today a summary of results from a patient-level, cost-effectiveness analysis of icosapent ethyl (Vascepa).1 This comprehensive analysis evaluated the cost-effectiveness of icosapent ethyl in reducing cardiovascular (CV) risk among high-risk patients as demonstrated in the landmark REDUCE-IT2cardiovascular outcomes study. In this newly reported analysis, use of icosapent ethyl was projected to not only be cost-effective but also to reduce long-term health care costs in a majority of the scenarios analyzed.

The findings were disclosed in an abstract titled, Cost-Effectiveness of Icosapent Ethyl in REDUCE-IT, in connection with the 2019 Scientific Sessions of the American Heart Association (AHA), scheduled for November 16 18 in Philadelphia, PA. William S. Weintraub, M.D., director of Outcomes Research with MedStar Cardiovascular Research Network, and lead author of the analysis, is scheduled to present the results in more detail at AHA on Saturday, November 16, at 7:30 a.m.

Dr. Weintraub and the MedStar Cardiovascular Research Network, known for conducting thoughtful pharmacoeconomic analysis, used available data for cost information for treatment and rehabilitation of patients from stroke, myocardial infarction, revascularization, hospitalization and cardiovascular death and assessed how such costs decline relative to the cost of patient treatment with icosapent ethyl based on the results of the REDUCE-IT study.

Background: Despite statin therapy and well-controlled LDL-C, many high CV risk patients continue to experience CV events. This persistent CV risk was evaluated via REDUCE-IT, which enrolled statin-treated patients with controlled LDL-C (>40 - 100 mg/dL) and elevated triglycerides (135 - <500 mg/dL), with established CV disease or diabetes combined with other CV risk factors. Over 4.9 years median follow-up, REDUCE-IT showed that icosapent ethyl lowered risk of first and total CV events by 25% and 30%, respectively.

In REDUCE-IT, adverse events occurring with icosapent ethyl use at greater than 5% and greater than placebo were: peripheral edema (6.5% Vascepa versus 5.0%), although there was no increase in the rate of heart failure in Vascepa patients; constipation (5.4% Vascepa versus 3.6%), although mineral oil, as used as placebo, is known to lower constipation; and atrial fibrillation (5.3% Vascepa versus 3.9%), although there were reductions in rates of cardiac arrest, sudden death and myocardial infarctions observed in Vascepa patients. More information on safety data associated with REDUCE-IT is provided further below.

Methods: The analysis applied treatment effects from REDUCE-IT, health care costs from national sources, including private insurance and Medicare, and conducted a combination cost-effectiveness analysis utilizing both patient-level in-trial cost and clinical outcomes and long-term costs, events and life expectancy derived from Markov simulation models. The model projected lifetime healthcare costs, CV events, survival and quality-adjusted life-years (QALYs) for icosapent ethyl versus placebo in REDUCE-IT eligible patients.

Results: Icosapent ethyl was a dominant strategy (i.e., cost saving) in 70% of simulations, offering the rare finding of better outcomes at lower healthcare costs. In probabilistic sensitivity analysis, >85% of simulations indicated that icosapent ethyl would be cost-effective (i.e., below $50,000 per QALY gained) compared with placebo.

Conclusion: In this combined patient-level and simulation cost-effectiveness analysis, icosapent ethyl in high CV risk patients shows exceptional benefit with CV event reduction as well as cost-savings in-trial and over patients lifetime in the majority of simulations.

John Thero, president and chief executive officer of Amarin, developer of Vascepa, commented, This analysis helps to validate something weve long believed, and that is central to our mission. It is possible to deliver significant innovation that meaningfully addresses our nations most prevalent and costly health epidemic, reduces impacts on patients and families, and drives down costs longer term in the health system. We are working to make this therapy broadly available for improved patient care in high risk patients subject to appropriate regulatory review.

Other Considerations:MedStar Cardiovascular Research Network (MedStar), which conducted this cost-effectiveness analysis, led by its director of Outcomes Research, Dr. Weintraub, is an organization dedicated to fighting heart disease, stroke and other conditions affecting the heart and blood vessels and is affiliated with MedStar Health Research Institute and Medstar Health. Amarin funded this analysis.

The patient cost and actuarial information used by MedStar in this cost-effective analysis were derived from sources independent of Amarin. Data regarding cardiovascular risk reduction demonstrated by Vascepa was sourced from previously published information from the total cohort of the REDUCE-IT study (not from the REDUCE-IT USA cohort published today in Circulation3 which showed even more pronounced results albeit subject to the limitations of subset analysis) with support provided by Amarin in making the data available to MedStar for analysis. Included in this data was outcomes results pertaining to first occurrences of cardiovascular events and recurrent events. As disclosed in the publication of the recurrent events analysis in the Journal of the American College of Cardiology4, the analyses addressed tertiary or exploratory endpoints using a series of statistical models, most of which were prespecified and one of which was post hoc. Each recurrent event statistical model has inherent strengths and weaknesses, with no single model considered definitive or outperforming the other models, as this is an evolving field of science. Nonetheless, results from the total primary and total key secondary endpoint events analyses are consistent across the various recurrent event statistical models and are also consistent with the original primary and secondary endpoint results.

Furthermore, the cost-effectiveness analysis conducted by MedStar, as is typical of cost-effectiveness analyses, was not prespecified. Amarin funded MedStar because of its expertise to conduct this analysis, as opposed to Amarin conducting it on its own, to mitigate perceptions of potential bias inherent in post hoc analyses.

This press release is timed today pursuant to AHAs release of an abstract for this presentation. It is Amarins understanding that AHA plans to release abstracts for some but not all (e.g. not any presentation deemed a late breaker, such as the presentation regarding EVAPORATE) of the seven scientific presentations Amarin listed in its press release dated November 4, 2019. Without potentially jeopardizing presentation at AHA, Amarin looks forward to communications regarding all of these presentations pursuant to their presentation at AHA.

About AmarinAmarin Corporation plc. is a rapidly growing, innovative pharmaceutical company focused on developing therapeutics to improve cardiovascular health. Amarins product development program leverages its extensive experience in polyunsaturated fatty acids and lipid science. Vascepa (icosapent ethyl) is Amarin's first FDA-approved drug and is available by prescription in the United States, Lebanon and the United Arab Emirates. Amarins commercial partners are pursuing additional regulatory approvals for Vascepa in Canada, China and the Middle East. For more information about Amarin, visit http://www.amarincorp.com.

About REDUCE-IT REDUCE-IT, an 8,179-patient cardiovascular outcomes study, was completed in 2018. REDUCE-IT was the first multinational cardiovascular outcomes study that evaluated the effect of prescription pure EPA therapy as an add-on to statins in patients with high cardiovascular risk who, despite stable statin therapy, had elevated triglyceride levels (at least 135 mg/dL). A large proportion of the male and female patients enrolled in this outcomes study were diagnosed with type 2 diabetes.

More information on the REDUCE-IT study results can be found at http://www.amarincorp.com.

About Cardiovascular DiseaseWorldwide, cardiovascular disease (CVD) remains the #1 killer of men and women. In the United States CVD leads to one in every three deaths one death approximately every 38 seconds with annual treatment cost in excess of $500 billion.5,6

Multipleprimary and secondary preventiontrials have shown a significant reduction of 25% to 35% in the risk ofcardiovascular eventswithstatintherapy, leaving significant persistent residual risk despite the achievement of target LDL-C levels.7

Beyond the cardiovascular risk associated with LDL-C, genetic, epidemiologic, clinical and real-world data suggest that patients with elevated triglycerides (TG) (fats in the blood), and TG-rich lipoproteins, are at increased risk for cardiovascular disease.8,9,10,11

About Vascepa (icosapent ethyl) CapsulesVascepa (icosapent ethyl) capsules are a single-molecule prescription product consisting of the omega-3 acid commonly known as EPA in ethyl-ester form. Vascepa is not fish oil, but is derived from fish through a stringent and complex FDA-regulated manufacturing process designed to effectively eliminate impurities and isolate and protect the single molecule active ingredient from degradation. Vascepa, known in scientific literature as AMR101, has been designated a new chemical entity by the FDA. Amarin has been issued multiple patents internationally based on the unique clinical profile of Vascepa, including the drugs ability to lower triglyceride levels in relevant patient populations without raising LDL-cholesterol levels.

The FDA has not completed its review and made a final determination on a supplemental new drug application related to REDUCE IT. FDA has not reviewed the information herein or determined whether to approve Vascepa for use to reduce the risk of major adverse cardiovascular events in the REDUCE-IT patient population.

Indication and Usage Based on Current FDA-Approved Label (not including REDUCE-IT results)

Important Safety Information for Vascepa Based on Current FDA-Approved Label (not including REDUCE-IT results) (Includes Data from Two 12-Week Studies (n=622) (MARINE and ANCHOR) of Patients with Triglycerides Values of 200 to 2000 mg/dL)

FULL VASCEPA PRESCRIBING INFORMATION CAN BE FOUND AT http://WWW.VASCEPA.COM.

Important Safety Information for Vascepa based on REDUCE-IT, as previously reported in The New England Journal of Medicine publication of the primary results of the REDUCE-IT study:

Important Cautionary Information About These DataFurther REDUCE-IT data assessment and data release are expected to yield additional useful information to inform greater understanding of the trial outcome. For example, detailed data assessment by regulatory authorities, such as the FDA and Health Canada, will continue and take time to complete and announce. The FDA advisory committee process and the final evaluation by regulatory authorities of the totality of efficacy and safety data from REDUCE-IT is anticipated to include some or all of the following, as well as other considerations: new information or analyses affecting the degree of treatment benefit on studied endpoints; study conduct and data robustness, quality, integrity and consistency; additional safety data considerations and risk/benefit considerations; and consideration of REDUCE-IT results in the context of other clinical studies. More detailed presentation of such considerations is set forth in the risk factors section of Amarins Quarterly Report on Form 10-Q filed with the U.S. Securities and Exchange Commission. Because regulatory reviews are typically fluid and not definitive interactions between sponsor and agency on individual elements of an application and related information, Amarin does not plan to update investors further on ongoing communications with regulatory authorities. Amarin plans to announce the final outcome of such regulatory reviews when appropriate.

Forward-Looking StatementsThis press release contains forward-looking statements, including statements regarding the use of Vascepa to potentially help millions of patients and projections related to the cost-effectiveness of Vascepa. These forward-looking statements are not promises or guarantees and involve substantial risks and uncertainties. Among the factors that could cause actual results to differ materially from those described or projected herein include the following: uncertainties associated generally with research and development, clinical trials and related regulatory reviews and approvals; the risk that data interpretations or other information from third parties, the regulatory review process, regulatory authorities and in connection with an advisory committee could be made public that are negative or may delay approval or limit Vascepas marketability; the risk that special protocol assessment (SPA) agreements with the FDA are not a guarantee that FDA will approve a product candidate; the risk associated with the FDA's rescinding the REDUCE-IT SPA agreement; the risk related to FDA advisory committee meetings; and the risk that the FDA may not complete its review of the REDUCE-IT sNDA within the timing expected. A further list and description of these risks, uncertainties and other risks associated with an investment in Amarin can be found in Amarin's filings with the U.S. Securities and Exchange Commission, including its most recent Quarterly Report on Form 10-Q. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. Amarin undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise.

Availability of Other Information About AmarinInvestors and others should note that Amarin communicates with its investors and the public using the company website (www.amarincorp.com), the investor relations website (investor.amarincorp.com), including but not limited to investor presentations and investor FAQs, Securities and Exchange Commission filings, press releases, public conference calls and webcasts. The information that Amarin posts on these channels and websites could be deemed to be material information. As a result, Amarin encourages investors, the media, and others interested in Amarin to review the information that is posted on these channels, including the investor relations website, on a regular basis. This list of channels may be updated from time to time on Amarins investor relations website and may include social media channels. The contents of Amarins website or these channels, or any other website that may be accessed from its website or these channels, shall not be deemed incorporated by reference in any filing under the Securities Act of 1933.Amarin Contact Information

Investor Inquiries:Elisabeth SchwartzInvestor RelationsAmarin Corporation plcIn U.S.: +1 (908) 719-1315 investor.relations@amarincorp.com

Lee M. SternSolebury TroutIn U.S.: +1 (646) 378-2992 lstern@soleburytrout.com

Media Inquiries:Gwen FisherCorporate Communications Amarin Corporation plcIn U.S.: +1 (908) 325-0735 pr@amarincorp.com

References_______________1 William S Weintraub, MedStar Washington Hosp Ctr, Washington, DC; Deepak L Bhatt, Brigham and Women's Hosp, Boston, MA; Zugui Zhang, Christiana Care Health System, Newark, DE et al., Cost-Effectiveness of Icosapent Ethyl in REDUCE-IT.2 Bhatt DL, Steg PG, Miller M, et al. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N Engl J Med 2019;380:11-223 Bhatt DL, Miller M, Brinton EA, et al. REDUCE-IT USA: Results from the 3,146 Patients Randomized in the United States. Circulation 2019. DOI: 10.1161/CIRCULATIONAHA.119.044440.4 Bhatt DL, Steg PG, Miller M, et al. Effects of Icosapent Ethyl on Total Ischemic Events: From REDUCE-IT. J Am Coll Cardiol 2019; 73:2791-28025 American Heart Association. 2018. Disease and Stroke Statistics-2018 Update.6 American Heart Association. 2017. Cardiovascular Disease: A Costly Burden for America Projections Through 2035.7 Ganda OP, Bhatt DL, Mason RP, et al. Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management. J Am Coll Cardiol. 2018;72(3):330-343.8 Budoff M. Triglycerides and triglyceride-rich lipoproteins in the causal pathway of cardiovascular disease. Am J Cardiol. 2016;118:138-145.9 Toth PP, Granowitz C, Hull M, et al. High triglycerides are associated with increased cardiovascular events, medical costs, and resource use: A real-world administrative claims analysis of statin-treated patients with high residual cardiovascular risk. J Am Heart Assoc. 2018;7(15):e008740.10 Nordestgaard BG. Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease - New insights from epidemiology, genetics, and biology. Circ Res. 2016;118:547-563.11 Nordestgaard BG, Varbo A. Triglycerides and cardiovascular disease. Lancet. 2014;384:626635.

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New Analysis Shows Icosapent Ethyl (Vascepa) Is Cost Effective and Offers Rare Finding of Better Outcomes at Lower Healthcare Costs When Used to Treat...

Prespecified Analysis of 3,146 Patients in the USA Enrolled in REDUCE-IT Showed 31% Relative Risk Reductions for First Occurrence of Both 5-Point MACE and 3-Point MACE

Significant Reductions Shown in All Predefined Composite and Individual Cardiovascular Endpoints, Including Cardiovascular Death and All-Cause Mortality

Tolerability and Safety Findings Consistent with Full Study

Results Published Today in Circulation and Scheduled for Presentation at American Heart Association 2019 Scientific Sessions on November 17

DUBLIN, Ireland and BRIDGEWATER, N.J., Nov. 11, 2019 (GLOBE NEWSWIRE) -- Amarin Corporation plc (NASDAQ: AMRN) announced today the results from the subgroup of 3,146 patients randomized in the United States within the global Vascepa (icosapent ethyl) cardiovascular (CV) outcomes trial, REDUCE-IT. This prespecified REDUCE-IT subgroup analysis showed robust risk reductions in the USA patients treated with icosapent ethyl 4 g/day versus placebo across all prespecified composite and individual primary and secondary endpoints, including 31% relative risk reduction and 6.5% absolute risk reduction in first occurrence of 5-point major adverse cardiovascular events (MACE), corresponding to a number needed to treat of 15 (NNT=15), and a significant 30% relative and 2.6% absolute risk reduction (NNT=38) in all-cause mortality in the USA subgroup.

Additional prespecified cardiovascular endpoints in which the REDUCE-IT USA subgroup showed significant relative risk reduction included myocardial infarction, cardiovascular death, and stroke, similar to the full cohort in the overall REDUCE-IT global results.1 These results were incremental to the cardiovascular risk reduction achieved by conventional therapy administered to the high-risk patients studied, including incremental to statin therapy.

In the REDUCE-IT USA subgroup, 3,146 patients (38.5% of the full trial cohort) were randomized and followed for a median of 4.9 years; 32.3% were women, 9.7% Hispanic. USA placebo patients had a higher primary endpoint event rate compared with the full cohort (67.4 versus 57.4 per 1,000 patient-years, respectively). The primary endpoint (5-point MACE) occurred in 24.7% of placebo versus 18.2% of icosapent ethyl patients (HR 0.69, 95% CI 0.59-0.80, p=0.000001); the key secondary endpoint (3-point MACE) occurred in 16.6% of placebo versus 12.1% of icosapent ethyl patients (HR 0.69, 95% CI 0.57-0.83, p=0.00008). All prespecified hierarchical primary and secondary endpoints were significantly reduced in the USA subgroup, including myocardial infarction (8.8% to 6.7%, HR 0.72, 95% CI 0.56-0.93, p=0.01), cardiovascular death (6.7% to 4.7%, HR 0.66, 95% CI 0.49-0.90, p=0.007), stroke (4.1% to 2.6%, HR 0.63, 95% CI 0.43-0.93, p=0.02), and all-cause mortality (9.8% to 7.2%, HR 0.70, 95% CI 0.55-0.90, p=0.004). In the full study cohort, there was a trend towards a reduction in all-cause mortality, with each of these other primary and secondary endpoints also achieving statistical significance in the full study cohort. Safety and tolerability findings in the USA subgroup were consistent with the full study cohort.

REDUCE-IT was not specifically powered to examine individual subgroups. P-values presented for the USA subgroup are nominal and exploratory with no adjustment for multiple comparisons. Differences in efficacy outcomes for the USA patients are best viewed as qualitative and not quantitative; nevertheless, the data are useful and provide reassurance that the results in the USA are at least as strong as the results seen outside the USA and in the trial overall.

The REDUCE-IT USA results are scheduled to be presented on Sunday, November 17 at the 2019 Scientific Sessions of the American Heart Association (AHA) in Philadelphia, PA. The REDUCE-IT USA study results were published today in Circulation, AHAs official scientific journal.2 The global results of REDUCE-IT from the full cohort of the study were previously published in The New England Journal of Medicine for the first occurrence of the studys primary and secondary endpoints and results of the studys full cohort with respect to total events were previously published in The Journal of American College of Cardiology.1,3This newly published data in Circulation is the first publication of detailed results from the REDUCE-IT USA cohort.

Scientific presentation: The presentation of the REDUCE-IT USA results at AHA will be delivered by the Global Principal Investigator and Steering Committee Chair of the study, Deepak L. Bhatt, M.D., M.P.H., executive director of Interventional Cardiovascular Programs at Brigham and Womens Hospital Heart and Vascular Center, and professor of medicine at Harvard Medical School. Dr. Bhatts featured presentation, titled REDUCE-IT USA: Results from the 3,146 Patients Randomized in the United States, will be delivered on November 17, 4:20 - 4:25 p.m.

Dr. Bhatt stated: The REDUCE-IT USA results confirm the findings of the global REDUCE-IT trial and further highlight the importance of the prevention of residual, or persistent, risk of cardiovascular events in statin-treated patients with only moderately increased triglycerides. The USA subgroup, which had more risk factors than the overall REDUCE-IT population, experienced particularly robust risk reduction from the use of icosapent ethyl in preventive cardiovascular care, including a statistically significant 30% reduction in death. These findings are also remarkable when you consider that in some multinational cardiovascular trials, patients in the United States experience less benefit.

Amarin perspective The results of the REDUCE-IT USA subgroup are further evidence of the robust and consistent nature of this landmark study and its applicability to typical clinical practice in the United States, stated Steven Ketchum, Ph.D., president of research and development and chief scientific officer of Amarin. We believe that these very impressive results further validate that persistent cardiovascular risk beyond cholesterol management can be significantly reduced with Vascepa in the high-risk patient population studied in REDUCE-IT.

The REDUCE-IT USA subgroup analysis was funded by Amarin. Dr. Bhatt receives research funding from Amarin that goes to Brigham and Womens Hospital.

About AmarinAmarin Corporation plc. is a rapidly growing, innovative pharmaceutical company focused on developing therapeutics to improve cardiovascular health. Amarins product development program leverages its extensive experience in polyunsaturated fatty acids and lipid science. Vascepa (icosapent ethyl) is Amarin's first FDA-approved drug and is available by prescription in the United States, Lebanon and the United Arab Emirates. Amarins commercial partners are pursuing additional regulatory approvals for Vascepa in Canada, China and the Middle East. For more information about Amarin, visit http://www.amarincorp.com.

About REDUCE-IT REDUCE-IT, an 8,179-patient cardiovascular outcomes study, was completed in 2018. REDUCE-IT was the first multinational cardiovascular outcomes study that evaluated the effect of prescription icosapent ethyl (IPE) as an add-on to statins in patients with high cardiovascular risk who, despite stable statin therapy, had elevated triglyceride levels (at least 135 mg/dL). A large proportion of the male and female patients enrolled in this outcomes study were diagnosed, prior to study enrollment, with type 2 diabetes.

More information on the REDUCE-IT study results can be found at http://www.amarincorp.com.

About Cardiovascular DiseaseWorldwide, cardiovascular disease (CVD) remains the #1 killer of men and women. In the United States CVD leads to one in every three deaths one death approximately every 38 seconds with annual treatment costs in excess of $500 billion.4,5

Multipleprimary and secondary preventiontrials have shown a significant reduction in the risk ofcardiovascular eventswithstatintherapy, leaving significant persistent residual risk despite the achievement of target LDL-C levels.6

Beyond the cardiovascular risk associated with LDL-C, genetic, epidemiologic, clinical and real-world data suggest that patients with elevated triglycerides (TG) (fats in the blood), and TG-rich lipoproteins, are at increased risk for cardiovascular disease.7,8,9,10

About Vascepa (icosapent ethyl) CapsulesVascepa (icosapent ethyl) capsules are a single-molecule prescription product consisting of the omega-3 acid commonly known as EPA in ethyl-ester form. Vascepa is not fish oil, but is derived from fish through a stringent and complex FDA-regulated manufacturing process designed to effectively eliminate impurities and isolate and protect the single molecule active ingredient from degradation. Vascepa, known in scientific literature as AMR101, has been designated a new chemical entity by the FDA. Amarin has been issued multiple patents internationally based on the unique clinical profile of Vascepa, including the drugs ability to lower triglyceride levels in relevant patient populations without raising LDL-cholesterol levels.

The FDA has not completed its review and made a final determination on a supplemental new drug application related to REDUCE-IT. FDA has not reviewed the information herein or determined whether to approve Vascepa for use to reduce the risk of major adverse cardiovascular events in the REDUCE-IT patient population.

Indication and Usage Based on Current FDA-Approved Label (not including REDUCE-IT results)

Important Safety Information for Vascepa Based on Current FDA-Approved Label (not including REDUCE-IT results) (Includes Data from Two 12-Week Studies (n=622) (MARINE and ANCHOR) of Patients with Triglycerides Values of 200 to 2000 mg/dL)

FULL VASCEPA PRESCRIBING INFORMATION CAN BE FOUND AT http://WWW.VASCEPA.COM.

Important Safety Information for Vascepa based on REDUCE-IT, as previously reported in The New England Journal of Medicine publication of the primary results of the REDUCE-IT study:

Important Cautionary Information About These DataFurther REDUCE-IT data assessment and data release are expected to yield additional useful information to inform greater understanding of the trial outcome. For example, detailed data assessment by regulatory authorities, such as the FDA and Health Canada, will continue and take time to complete and announce. The FDA advisory committee process and the final evaluation by regulatory authorities of the totality of efficacy and safety data from REDUCE-IT is anticipated to include some or all of the following, as well as other considerations: new information or analyses affecting the degree of treatment benefit on studied endpoints; study conduct and data robustness, quality, integrity and consistency; additional safety data considerations and risk/benefit considerations; and consideration of REDUCE-IT results in the context of other clinical studies. More detailed presentation of such considerations is set forth in the risk factors section of Amarins Quarterly Report on Form 10-Q filed with the U.S. Securities and Exchange Commission. Because regulatory reviews are typically fluid and not definitive interactions between sponsor and agency on individual elements of an application and related information, Amarin does not plan to update investors further on ongoing communications with regulatory authorities. Amarin plans to announce the final outcome of such regulatory reviews when appropriate.

Forward-Looking StatementsThis press release contains forward-looking statements, including statements regarding the use of Vascepa to potentially help millions of patients. These forward-looking statements are not promises or guarantees and involve substantial risks and uncertainties. Among the factors that could cause actual results to differ materially from those described or projected herein include the following: uncertainties associated generally with research and development, clinical trials and related regulatory reviews and approvals; the risk that data interpretations or other information from third parties, the regulatory review process, regulatory authorities and in connection with an advisory committee could be made public that are negative or may delay approval or limit Vascepas marketability; the risk that special protocol assessment (SPA) agreements with the FDA are not a guarantee that FDA will approve a product candidate; the risk associated with the FDA's rescinding the REDUCE-IT SPA agreement; the risk related to FDA advisory committee meetings; and the risk that the FDA may not complete its review of the REDUCE-IT sNDA within the timing expected. A further list and description of these risks, uncertainties and other risks associated with an investment in Amarin can be found in Amarin's filings with the U.S. Securities and Exchange Commission, including its most recent Quarterly Report on Form 10-Q. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. Amarin undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise.

Availability of Other Information About AmarinInvestors and others should note that Amarin communicates with its investors and the public using the company website (www.amarincorp.com), the investor relations website (investor.amarincorp.com), including but not limited to investor presentations and investor FAQs, Securities and Exchange Commission filings, press releases, public conference calls and webcasts. The information that Amarin posts on these channels and websites could be deemed to be material information. As a result, Amarin encourages investors, the media, and others interested in Amarin to review the information that is posted on these channels, including the investor relations website, on a regular basis. This list of channels may be updated from time to time on Amarins investor relations website and may include social media channels. The contents of Amarins website or these channels, or any other website that may be accessed from its website or these channels, shall not be deemed incorporated by reference in any filing under the Securities Act of 1933.Amarin Contact Information

Investor Inquiries:Elisabeth SchwartzInvestor RelationsAmarin Corporation plcIn U.S.: +1 (908) 719-1315 investor.relations@amarincorp.com

Lee M. SternSolebury TroutIn U.S.: +1 (646) 378-2992 lstern@soleburytrout.com

Media Inquiries:Gwen FisherCorporate Communications Amarin Corporation plcIn U.S.: +1 (908) 325-0735 pr@amarincorp.com

References

1 Bhatt DL, Steg PG, Miller M, et al. Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N Engl J Med 2019; 380:11-22.2 Bhatt DL, Miller M, Brinton EA, et al. REDUCE-IT USA: Results from the 3,146 Patients Randomized in the United States. Circulation 2019. DOI: 10.1161/CIRCULATIONAHA.119.044440.3 Bhatt DL, Steg PG, Miller M, et al. Effects of Icosapent Ethyl on Total Ischemic Events: From REDUCE-IT. J Am Coll Cardio. 2019; 73:2791-2802.4 American Heart Association. 2018. Disease and Stroke Statistics-2018 Update.5 American Heart Association. 2017. Cardiovascular Disease: A Costly Burden for America Projections Through 2035.6 Ganda OP, Bhatt DL, Mason RP, et al. Unmet need for adjunctive dyslipidemia therapy in hypertriglyceridemia management. J Am Coll Cardiol. 2018;72(3):330-343.7 Budoff M, Triglycerides and triglyceride-rich lipoproteins in the causal pathway of cardiovascular disease. Am J Cardiol. 2016;118:138-145.8 Toth PP, Granowitz C, Hull M, et al. High triglycerides are associated with increased cardiovascular events, medical costs, and resource use: A real-world administrative claims analysis of statin-treated patients with high residual cardiovascular risk. J Am Heart Assoc. 2018;7(15):e008740.9 Nordestgaard BG, Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease - New insights from epidemiology, genetics, and biology. Circ Res. 2016;118:547-563.10 Nordestgaard BG, Varbo A. Triglycerides and cardiovascular disease. Lancet. 2014;384:626635.

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REDUCE-IT USA Results, in Prespecified Subgroup Analyses of Landmark REDUCE-IT Global Study, Showed Robust Cardiovascular Risk Reductions Across a...

In the early 18th century, Joseph Priestley, an English preacher, was intrigued by the peculiar smells that came from the brewery near his residence and started studying them. He noted that the gas could put out glowing embers, dissolve in water and give it a tangy taste. He had discovered carbon dioxide.

In Eureka! Greatest Scientists who Changed the World, science writer S. Ananthanarayanan tells us such stories behind famous discoveries and in the process offers short accounts of the lives of 60 scientists.

Eureka moments

Though the books preface notes that the list is incomplete and that the choice can always be questioned, the author has done justice by highlighting the main torchbearers across different fields ranging from astronomy, mathematics, and physics to medicine and genetics.

The book starts with Greek mathematician Euclid who lived around 300 BCE, takes us through the tales of big names such as Galileo, Newton, Darwin and concludes with the story of 1968's Nobel Prize winners for Physiology or Medicine.

Each chapter, just two to three pages, contains a story of the challenges faced, sudden Eureka moments and how secrets of science were unravelled. The book is an easy read and a perfect gift for anyone interested in science. The book can give you a whole range of conversation starters that you can use in daily life. Over a cup of coffee, ask your colleague, Hey, did you know that a physicist invented the drip-pot coffee percolator which gives you filter coffee?, or over a drink tell friends the story of how rum was used during surgeries. My personal favourites Leeuwenhoek who called microbes animalcules, cleanliness freak Joseph Lister, Robert Hooke and his insect anatomy book Micrographia have all made it to this curated list.

The chosen four

In 2004, the author had published Icons from the World of Science in which he highlighted the works of 10 Indian scientists. But unfortunately only four of them entered the new book of 60 scientists S.N. Bose, Nobel Prize winners C.V. Raman, and the India-born Americans, S. Chandrasekhar and Har Gobind Khorana.

Published in 2019, one would expect the book to stretch to the lives of a few 21st century scientists too, but it fails to do so. The final chapter set in the 1960s is on Marshall W. Nirenberg, Robert W. Holley and Indian biochemist Khorana and tells their journey to uncover the genetic sequence or code leading to the sensational outburst in the field of genetics.

Also, the book talks about only two female scientists, astronomer Henrietta Swan Leavitt and two-time Nobel winner Marie Curie. With WikiProject Women Scientists running strong and Indias The Life of Science project working hard to bring women scientists to the limelight, the author could have, or rather should have, included a few more women scientists.

Unfortunately, the bright orange cover also carries a manel clearly showcasing the lack of diversity. The book is, however, a good place to start for anyone wanting to know the history behind famous scientific discoveries.

Eureka! Greatest Scientists who Changed the World; S. Ananthanarayanan, Rupa, 295.

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Eureka! Greatest Scientists who Changed the World review: Recreating great discoveries - The Hindu

Every child is different in just about every wayheight included. But did you know different things can affect height? Different ethnicities have different average heights. Certain disorders, such as down syndrome, can also have an effect on height. Different genders can also change the height of an average 10 year old.

With more and more moms and dads entering the world of parenting, there are more and more questions arising. One question asked by many parents is, Is my child a good average height? Or is he or she above or below? Well, we have the answers for you!

Many things can affect the average height of any 10 year old child:

The Average Height Based on Gender

On average, boys are taller than girls. We all know this, and there is nothing wrong with it. However, at 10 years old, the average height of a boy and a girl is close to the same.

Typically, the average 10 year old boy is about 54.5 inches tall while the average height of a 10 year old girl is 56.3 inches. At this age, it is very normal for girls to be a little taller than boys, as girls hit puberty earlier. This will be discussed later on.

However, the range for normal height for a 10 year old boy is between 50 inches and 58.8 inches. Some young boys will be taller than the average 54.5 inches and others will be shorter. So, dont worry if you think your son is too short or tallhe isnt! The normal range for a girl is roughly the same.

The Average Height Based on Genetics and Ethnicity

Genetics is the main factor in determining height. Roughly 60-80 percent of anything that determines height is genetics. The remaining percentages are things like nutrition and environmental factors.

How tall the mother is and how tall the father is can help you get an idea of how tall your child will be at any age. If both parents are tall, chances are your child will be on the taller side too. If both parents are short, your child will more than likely end up shorter. But you need to look beyond just parents.

Look at other biological relatives. If the mother is short like the grandmother, her child can still end up tall if her father was tall. This goes the same way for the father of the child, too. Looking at patterns of the heights of siblings (the aunts and uncles of the child) can also give you an idea of how tall your child might be.

Different ethnicities and/or races will also help to determine the height of your growing child. However, ethnicity will hardly affect the height of a 10 year old girl or boy. At that age, it is rather standard on the height. However, you can guess how tall your child might be when they are older based on your ethnicity.

For men, on average, the height of an adult African American male is 69.5 inches. The average height of an Asian man is 67 inches and then the average height of a Hispanic man is 67.4 inches.

For women, he average height of an African American female is a out 64.2 inches. The average height of an Asian female is 62.8 inches. Finally, the average height of a Hispanic female is about 62 inches.

However, looking at the genetics and ethnicity combined can give you a good idea of how tall your 10 year old might be.

Nutrition

Nutrition plays a huge factor in how tall your child might end up being by the time they are 10 years old. In many poor or third world countries, you might notice children are shorter than children in first world countries. This is often due to the fact that they get poorer nutrition than our children.

Even in poor parts of first world countries if a child is not getting proper nutrition they might be shorter. Once the child starts to get decent nutrition, he or she will probably have a growth spurt depending on age and how much they needed to grow.

Genetic Disorders and Chronic Illness

Genetic disorders and chronic illnesses can definitely affect the height of your child at any age. It is good to go talk to your child pediatrician if you are worried about any sort of disorder or illness affecting them in any way.

If your child has cancer, he or she might be shorter than they would have been if they were healthy. This is because the illness attacks his or her body and takes away extra nutrients that their bodies need to grow. Plus, chemo and radiation can halt a childs growth because it works by killing off cells.

Arthritis can also impact height. While it is rare for a child as young as 10 to have severe arthritis, it can happen. Depending on the severity, arthritis can damage the joints and cause growth plates to form over and stop the child from growing.

Celiac disease is another than can stunt growth because nutrition might be less. Celiac disease is when you are truly allergic to gluten. You get incredibly sick and sometimes even need hospitalized. Those with celiac disease have a hard time finding enough foods that are 100% gluten free that are affordable, thus the lack of nutrition.

Turner syndrome only affects females. It is a chromosomal condition and while it rarely affect intelligence, it will affect outward appearances as well as a few internal complications. The most common feature in women with turner syndrome will be shorter. You can start to notice the height problem around age five, so by the time the child reaches 10, she will be much shorter than her classmates.

Down syndrome is the most common chromosomal condition in humans. Children with down syndrome have a slower rate of growth. They also tend to be shorter than their other children their age, even as young as 10 years old.

Puberty and Height

Generally, around age 10 girls are a little taller than boys. This is because a girls enters puberty at a younger age. While boys start to show physical signs of puberty such as height as early as 10 years old, girls start around 8 years old.

In a young girl, the average for a girls growth rate to peak is around 12. After she begins menstruating, she will usually grow another 1-2 inches and then reach their final height around 14 or 15. This can vary depending on what age their cycle started.

In a young boy, their major growth spurt is about two years later than girls. So, while they might be shorter than their female peers, that will change once they hit puberty. Boys tend to grow fastest around ages 12 and 15 and slow down or completely stop around age 16.

Other Factors Affecting Height

There are other smaller factors that we forget to think about when it we think about height. Did you know that a premature birth can change how tall your child can be? A smaller baby needs to catch up on growth at a young age and might continue to be catching up throughout his or her life.

Being around cigarette smoke can also cause a child to be a little shorter. The toxic chemicals in the smoke and damage cells when breathed in and therefore affect the childs health. Also, having certain hormones or lacking certain hormones can cause a change in average height.

If a child has to be on certain medications for varying medical reasons, it can also change how they grow. Some will stunt growth more than realized, but height is nothing compared to the overall health of your child.

If you are concerned about where your child is on the growth charts, talk to his or her doctor about it. Your doctor will be able to answer any questions better than any information you will be able to find online.

Source: https://www.familylifeshare.com/average-height-of-a-10-year-old/

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What is the Average Height of a 10 Year Old? - Modern Ghana

Researchers at the University of Utah determined that they have found a link between a brain cell imbalance and the levels of anxiety and Obsessive-Compulsive Disorders. The study revealed a new lineage of specialized brain cells called Hoxb8-lineage microglia.

The research concluded that imbalance or fluctuation in the levels of certain brain cells led to a change in the intensity of anxiety and OCD in mice. The female mice were found more reactive towards anxiety issues but the symptoms were also visible in male mice as well.

"It opens up a new avenue for thinking about anxiety,"Dimitri Trnkner, lead author of the research and assistant professor of biology at Utah University, said. "Since we have this model, we have a way to test new drugs to help these mice and hopefully, at some point, this will help people."

The research suggested that the biological sex hormones (estrogen and progesterone) and genetics, the two major risk factors for anxiety-related disorders in humans, were interlinked. The Hoxb8-lineage microglia which was earlier known only for its crucial role in brain development in the womb was found to be the reason for anxiety in mice.

"We didnt really know what to make of the fact that mice without Hoxb8 appear so normal, until we noticed that they groom significantly more and longer than that would be considered healthy," Mario Capecchi, a distinguished professor of human genetics and a Nobel Laureate, who was also involved in the research, said.

To test the feasibility of their claim, Trnkner, along with his co-workers, tested the mice at different levels of progesterone and estrogen. It was found that at male levels of hormones, the OCD and anxiety behavior in female mice resembled that of the male; whereas, at female levels, the OCD behaviors in male mice resembled that of the female.

"We have a good understanding of how anxiety is produced in people," Trnkner said. "Of all models, I have great faith that mice are one of the best models, as they are so similar to people."

Trnkner also said that the new findings put everyone a little closer to forming a new, effective drug for anxiety particularly. "Scientists want to help these people to get their lives back," he added.

Dozens of countries have had cases of the antibiotic-resistant STI, which means the bacteria responsible for the infection continues to reproduce. Photo: Pixabay

Link:
Brain Cell Imbalance May Lead To Anxiety, OCD: Study - International Business Times

Womens colleges provided essential opportunities for women as both professors and students. But, as Leff points out, womens colleges were colleges, so they didnt support the same type of sophisticated research that Geiringer had been doing in universities. Any research she did would be outside of her college duties and typically unpaid.

Geiringer never found in a US university a position equal to what she had in Germany and Turkey.

After accepting her post at Wheaton, Geiringer wrote to von Mises, I hope there will be better conditions for the next generations of women. In the meantime, one has to go on as well as possible.

And Geiringer did go on. She stayed at Wheaton, which granted her an honorary doctorate in mathematics, until her retirement in 1959, that same year, she was elected a fellow of the American Academy of Arts and Sciences. She still did research when she found the time, but her most significant project post-immigration was compiling, editing, and publishing von Mises unfinished book in two editions after his death in 1953: Probably, Statistics, and Truth in 1964 and Mathematical Theory of Probability and Statistics in 1957.

Even if Geiringer didnt get exactly what she wanted, she never gave up on chasing that deepest need in her life.

Missed Genius

Ask people to imagine a scientist, and many of us will picture the same thing a heterosexual white male. Historically, a number of challenges have made it much more difficult for those who dont fit that stereotype to enter fields like science, math or engineering.

There are, however, many individuals from diverse backgrounds who have shaped our understanding of life and the Universe, but whose stories have gone untold until now. With our new BBC Future column, we are celebrating the missed geniuses who made the world what it is today.

--

Portrait of Hilda Geiringer by Emmanuel Lafont.

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The woman who reshaped maths - BBC News

Evolution is generally thought of as a linear process: Species split off from one another over time, move to different places, and adapt different traits. But species like those in the Heliconius genus make patterns of evolution more interesting.

We need to take into account in our evolutionary models that we can get gene flow between species, Edelman says.

Heliconius made sense to study because of its hybrid-making tendencies. Its also just a cool really insect. The adult Heliconius eats pollen, which no other butterfly does. And Heliconius is smart, Edelman says. It has a home range, meaning it will go to visit the same flower every day, a habit more commonly associated with mammals.

The findings have potential implications for conservation and preserving pollinator populations. Studies show that species variation is key to protecting those populations in a changing climate.

One good thing about genetic diversity is if you have a really variable and diverse population, when environmental conditions change, you have a better chance of responding to them, Edelman says.

So how does hybridization factor in? Researchers dont all agree on whether its likely to contribute to genetic diversity. But it very well might.

Its at least somewhat likely that youre going to increase your variation rather than decrease it, Edelman says.

Conservation can involve protecting species by keeping out its close relatives, to avoid hybridization or a species takeover, but for species like these butterflies, that strategy may not work as well.

Hybridization is pretty common in nature, Edelman says. In some cases it might be good to bring in other species and increase genetic diversity for conservation purposes.

See original here:
Weird butterfly genetics counter popular theory of evolution - Inverse

A chirping, robotic voice welcomes you, spilling from one of six speakers that swivel overhead: Welcome to the sperm bank!

French artist Anne Le Troters site-specific sound installation, which debuted at the Nasher Sculpture Center last Saturday and will run through February 2, 2020 as part of the Sightings series, presents a 17-minute piece that centers on language, like much of her work, confronting the slipperiness of the identity politics inherent in its materiality, in this case in the domain of eugenics.

In a room paneled with rose-colored carpet, six speakers rotate on circular turntables above our heads, black audio cables swung between them, drooping, being pulled up, like fishing lines or netsfor language, perhaps, or for answers.

Curator Leigh Arnold met Le Troter at the Salon de Montrouge in 2016, where Le Troters piece LApptance (Desire) stood out to her: molded blue plastic seats of the kind youd see in a Mtro station, with speakers mounted under them that emitted whisperings. Le Troter had worked with ASMR artists for the recordings. Arnold was struck by these words that appeared public in context, but heard with a hushed intimacy akin to eavesdroppingthe tension of public and private and words showcased as a site of slippage. For her Sightings piece, her first U.S. commission, Le Troters seed notion came from a flight to the U.S., when a woman seated next to her explained her work at a sperm bank. Le Troter later signed onto the website, baffled by this world. The Nasher recording, using sourced words, borrowed language from 400 donor interviews, is, similarly, an exercise in voyeurism, an intrusion on genetics.

In the gallery, the wash of words gathered and remixed is both chilling and lulling, its childlike nursery-rhyme cadence broken by artificial, scientific intrusions. He is very sweetincredibly sweetis your typical sweetheartlike a big teddy bear male and female voices drone, enumerating a litany of positive qualities and attributes that reflect our values back at us. The breakdown begins immediately. Le Troter has arranged clusters of disjointed phrases around adjectives: a very active personvery intelligent, or has his work published in several journals, or again adventurous, outdoorsy, practical, loves his dogs. I came from, a donor voice begins, while robotic voices break in with numbers, Donor 5165, 5155, a small cascade that washes and eddies in the repeated And, um, a refrain that Le Troter sees like a beating heart.

And while the soft, carpeted walls and soothing voices create a cocoon of intimacy, I feel the twinge of danger, the threat in a piece that frames desire and exchange. If the room is a womb, then a womb for what?

The pink carpet on the walls has been swabbed and color-drained with bleach: the erasure of individuality imprinted on the space. Its whiteness bleeds as pigment-absence down to the off-white carpet, which is cellophane-wrapped, asepticized. The adjective clusters remove individuality, Le Troter says: a word is more saleable than a person.

Windows that look out onto Flora Street with its slow-moving traffic and burbling fountain add to the disquieting, womb-like effect. We are looking out at the world from inside what is, quite literally, a bubble. We sit on benches, also strung with audio cable, solid as the genetics encoded in DNA. That is, solid and also not solid. Unsettling and also human. Everything about the piece both holds and destabilizes.

What, really, do we know about what we want? What would it mean to engineer a calculated linguistic expression of desire? What would it entail, ethically, to sculpt a human future? And, underlying this, are the questions of privilege.

This concludesinterviews with400 sperm donorsThank you, and goodbye, the voice intones.

Le Troter herself, wearing a soft pink sweater the color of the walls, on the Friday before the opening, discussed the crafting of the piece, the real voices taken, borrowed, not as identifiable as faces, though dots on the wall represent photographs of the donors as children. The piece is a body with organs, a machine-body made of words and the audio cables the sinews of her work. She remembered the fountain and the view of the outside world, its slow rhythm.

And this space, sequestered from other galleries, may be the best exhibiting conditions shes ever experienced, she says. At the Palais de Tokyo in Paris, another piece of hers is currently part of a group exhibition that explores the idea of a current, contemporary French scene in the art world. The fragility of a sound installation is challenging in a group show with images. Here, we have a cocoon with an aperture on language and thought and sculpture as sound.

The piece is on view at the Nasher through February 2, 2020.

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Anne Le Troter's Sound Installation Stirs Up the Politics of Language - D Magazine

In October 1994 in the journal Science, scientists published a strong candidate underlying heritable breast cancer. Their evidence led them to mutations in the BRCA1 gene, located on a stretch of chromosome 17. A bit more than a year later, researchers traced a second suspect, BRCA2, to chromosome 13, reporting their find in Nature. Together, the transformative discoveries set off a firestorm of oncology research, andjust as significantinjected hope for the future into the lives of millions who may carry mutations in one or both genes.

Twenty-five years later, the Basser Center for BRCA within Penn Medicines Abramson Cancer Center relentlessly continues to offer up this hope, fostering advancements in science and translating them to improve lives by emphasizing outreach, prevention, early detection, treatment, and survivorship of BRCA-mutation related cancers.

The Basser Center is focused entirely on BRCA1 and BRCA2, but within that we have this broad scope of everything from basic science to clinical care to increasing awareness, says Susan Domchek, the Basser Centers executive director. So at the same time that were hoping to figure out the basic biology of why a BRCA1 mutation leads to breast cancerand theres a lot about that that we dont know yetsimultaneously we want to use the information that we already have to help people in real time.

These parallel approaches arose from the vision of Mindy and Jon Gray, Penn alums whose initial $30million gift established the Basser Center in 2012. The Centers name honors Mindy Grays sister, Faith Basser, who died from BRCA-related ovarian cancer at age 44. Including subsequent donations, the Grays have committed a total of $55 million in support of the Centers work.

True to their vision of a multi-faceted operation, in the ensuing seven years the Center has facilitated a steady clip of scientific discovery, encouraged community building around the issue of BRCA awareness, and established support systems to aid people who are considering getting tested or weighing challenging decisions about how to proceed after finding out their status.

When we talk about the lifesaving research and innovation that is happening on campus, the Basser Center is one of Penns most important initiatives, says Penn President Amy Gutmann. Its because of Mindy and Jon Grays visionary philanthropy that we can say this so proudly today.

BRCA1 and BRCA2 are named for their association with breast cancer, but mutations also increase risks of ovarian, pancreatic, and prostate cancer, among others. Everyone possesses copies of BRCA1 and BRCA2 genes; the risks arise when their sequence is altered through a genetic mutation, which can be passed from generation to generation.

In their normal form, both genes serve a protective function, creating proteins that work within complex molecular machines to repair damage to DNA. When a mutated gene gives rise to an altered version of one of these proteins, DNA damage builds up within cells, greatly increasing the risk of cancer. Women with a mutation in BRCA1 or BRCA2, for example, have up to a 75 percent chance of developing breast cancer in their lifetime, compared to a 12 percent risk in the general population; similarly, the risk of a carrier developing ovarian cancer is up to 50 percent, compared to a risk under 2 percent in the general population.

When we talk about the lifesaving research and innovation that is happening on campus, the Basser Center is one of Penns most important initiatives. Penn President Amy Gutmann

As the scientific community marks the 25th anniversary of the discovery of the BRCA genes, Basser Center scientists are notching new breakthroughs in understanding the science of heritable cancers. Roger Greenberg, director of basic science for the Basser Center, says support for fundamental laboratory science has already paid off in a number of ways.

There has been so much exchange, so many more interactions on campus because of being here, he says. This had led to grants and papers, clinical trials and philanthropy and publications. Its such an incredible impact, and theres a lot more to come.

Greenberg is a leader in studying how DNA damage repair mechanisms are affected by mutations in BRCA1 and BRCA2, and how this impaired function affects the way people respond to therapy. In recent work, his lab has begun to focus on a relatively new category of drugs called PARP inhibitors. A heartening development in the BRCA field, these agents take advantage of a vulnerability in cells with BRCA mutations, building up so much DNA damage that the cells ultimately die.

Its a very exciting field that continues to grow, says Greenberg.

His labs work has also helped unravel mysteries of how DNA damage influencesthe immune system'sresponse to cancer cells, and how PARP inhibitors themselves create immune responses.

These kinds of insights can absolutely contribute to more personalized care, Greenberg says.

An expert on cancer genetics, Katherine Nathanson, director of genetics for the Basser Center, has also seen the growing role of immunology in cancer science during her years at Penn. Nathanson, who is also deputy director of Penn Medicines Abramson Cancer Center, has contributed extensively to the fields knowledge base around cancer risks associated with particular genetic variants. In recent years, shes also brought her genetics expertise to bear in the context of new breakthroughs in understanding the role of the immune system in controlling cancer.

One thing is clear, says Nathanson. It used to be that cancer immunology and cancer genetics were very far apart. Now there is a lot of intersection and collaboration.

Nathanson was recently awarded a $3 million grant from the Gray Foundation, which is led by Mindy and Jon Gray, to probe more deeply into immune system function in BRCA mutation carriers and in those with related cancers. Those studies have the potential not only to shed more light on BRCA cancers, but on the function of the immune system in general.

Ronny Drapkin, Bassers director of gynecologic research, conducts research that straddles the lab and clinic. A dozen years ago, when Drapkin was completing his postdoctoral training and starting his own lab, he studied the tissues from women who were having prophylactic surgerymastectomies and oophorectomiesafter finding out they possessed a BRCA1 or BRCA2 mutation. His investigations revealed that many cases of ovarian cancer may in fact originate in the fallopian tubes.

That scientific observation has the potential for profound implications for patient care. In addition to be a paradigm shift in science, its also caused a shift in treatment, he says. And that was very much ushered in by the discovery of the BRCA genes 25 years ago.

The current standard of care for women with BRCA1 and BRCA2 mutations is to have their ovaries removed to reduce their cancer risk at approximately age 40. Thus, women experience what is known as surgical menopause, compressing what is normally a 5 to 7 year process into the space of a few hours. This includes experiencing all the menopause-related morbidities of heart and bone disease. Today, two multi-center clinical trials, including one enrolling patients at Penn, are investigating an alternative practice, in which a womans fallopian tubes are removed at a younger age, after child-bearing, and her ovaries are preserveduntil her 50s. These studies are extremely important to evaluate whether this approach is safe and effective.

For this disease, we dont have early detection, we dont have mammography or colonoscopy, Drapkin says. For me its been personally gratifying to see this concept progress into the clinic.

Efforts by Domchek and others in the Basser Center have led to new paradigms for treatment of BRCA-related cancers. These Penn-led studies have helped usher in three FDA approvals related to PARP inhibitor drugs: olaparib for BRCA1- and BRCA2-associated ovarian cancer and metastatic breast cancer, and rucaparib for BRCA1- and BRCA2-associated ovarian cancer. These approvals have transformed care for ovarian cancer, for which there are few other options available. And olaparib represented the first FDA-approved therapy specifically for BRCA-related breast cancer.

More recent findings spearheaded by Basser Center investigators have also suggested PARP inhibitors hold promise for treating pancreatic cancer in patients with specific genetic mutations, including in BRCA1 and BRCA2.

A major priority of the Basser Center is to take concepts not only from the lab to the clinic, but also from the clinic to the public. Since 2012, through more than 50 patient- and public-facing events, the Center has spread lifesaving messages about the importance of genetic testing to targeted communities. The Center holds an annual scientific symposium, attracting the worlds experts on inherited cancers to Penn, and a monthly seminar series to enhance the profile of this type of research more locally. The Basser Global Prize, endowed by Mindy Grays sister, Shari Potter and her husband Len Potter, awards $100,000 annually to a visionary researcher working on BRCA1 and BRCA2, while smaller grants support the work of earlier-career researchers pursuing investigations on the topic.

Thats helped nucleate expertise here at Penn, says Greenberg.

The Centers Basser Leadership Councila group of roughly 20 of the Centers strongest advocates and supportersand Young Leadership Councilwith more than 100 members across the U.S. and beyondamplify these messages so they reverberate out from Penn into communities worldwide.

The Young Leadership Council, for example, enables peer support and discussions of the issues that young people face, such as when confronting a decision about prophylactic surgeriesto reduce cancer risk.

Many of our YLC members have undergone prophylactic surgeries or are thinking about them, and they discuss the challenges of this, what that means for dating,intimacy, and family planningfor example, says Laura Ferraiolo, seniordirector of development forthe Basser Center whose team helps oversees the councils' efforts.

The group has its own, monthlye-newsletter and holds frequent events, such as a cycling fundraiser in three cities earlier this month.

Similarly, the Basser Leadership Council supports the Centers mission in a number of ways. Many of them are either affected by a mutation or have someone in their family who is, and are incredibly engaged in this work, says Beth Stearman, administrative director for the Basser Center. They are lay leaders who support us in promoting outreach events and utilize their personal and professional connections to extend our mission to people in different communities across the country.

Emphasizing the value of knowing ones BRCA status has been a through line of the Centers outreach. An emerging priority, therefore, has been to offer education on genetic testing to primary care physicians, many of whom, Domchek explains, are uncertain of when to recommend testing, and for which patients.

My last name is Domchek, its ethnically ambiguous, she explains. Ive not been asked if Im of Ashkenazi Jewish ancestry and that is a known risk factor for BRCA mutations. Why is that? Were trying to do a lot more provider outreach so physicians are educated and comfortable with these issues.

Roughly one out of 40 people with Ashkenazi Jewish ancestry have a mutation in BRCA1 or BRCA2. The Basser Center has accordingly devoted significant energy into reaching that community. A poster campaign to promote the importance of genetic testing reached 1,500 synagogues in the Centers early years, and efforts through the Basser Leadership Council and Young Leadership Counciland an emerging Parents Leadership Community aimed at issues involved in raising families as a carriercontinue those and related efforts.

Meanwhile, efforts are ramping up in the Center to continue spreading access to genetic counseling and testing across other at-risk populations.

In a New York Times op-ed published earlier this month, attorney and writer Erika Stallings noted that Mathew Knowles, Beyoncs father, had been diagnosed with breast cancer and possessed a genetic mutation in the BRCA2 gene that dramatically increased his cancer risk. Domchek is serving as Knowless oncologist, and recently appeared with him on The Dr. Oz Show, calling attention to the risk that menshare from inherited mutations.

Several years ago, Stallings, a founding co-chair of the Basser Centers Young Leadership Council, discovered that she, too, had a BRCA2 mutation, and took action to lower her risk by undergoing a double mastectomy.

While BRCA mutations are more common in people with Ashkenazi Jewish heritage, its also true that BRCA1 and BRCA2 mutations occur in people of any background, male or female, at a rate of roughly 1 in 300. Black men and women like Knowles and Stallings are no exception. And neither are Latinx individuals, like former White House aide and founder of the Well Woman Coalition Alejandra Campoverdi, a BRCA2 mutation carrier who has partnered with the Basser Center to launch LATINX & BRCA, a campaign to connect the Latinx community with resources related to BRCA-related disease.

Making its official launch at next months BasserJean Bash, a major biennial fundraising event for the Center, LATINX & BRCA has already enabled the translation of many of Bassers educational materials into Spanish, including a list of Spanish-speaking genetic counselors. The Center is planning to spin off a similar effort focusing on the African-American community next year, also working through the Penn Center for Community Health Workers to better connect with people in the Philadelphia area and across the nation.

As momentum around the importance of genetic testing builds, the Basser Center is working to meet the need for responsible genetic counseling to contextualize the testsand supporting people in their decisions of how to act on the results. The Basser Center itself has six genetic counselors on staff, but is also trialing non-traditional ways of getting appropriate counseling to patients.

Everybody working in this space is looking for alternatives to traditional genetic counseling, says Stearman.

In one effort, the Penn Telegenetics Program, launched in 2012 by Angela Bradbury, an associate professor of medicine, medical ethics, and health policy, is using a research-based approach to allowing individuals to access genetic counselors over the phone or through two-way video conferencing. Bradbury and colleagues work has shown that offering such remote cancer genetic counseling sessions can dramatically boost patient participation in counseling. Last year Abramson Cancer Center launched a pilot effort to broadly provide telegenetic counseling services to patients and providers.

Along these lines, Domchek is helping lead the BFOR study (BRCA Founder Outreach Study) that connects at-risk individuals in the Ashkenazi Jewish community with a digital health platform that takes users through disclosures and informed consent procedures through a sophisticated interactive display. Participants can be linked with their primary care providers to receive their results.

This is different from a direct-to-consumer model where people are doing this outside the medical system, Domchek explains. Were trying to create a hybrid model where its still embedded in the medical system.

At the same time that were hoping to figure out the basic biology of why a BRCA1 mutation leads to breast cancerand theres a lot about that that we dont know yetsimultaneously we want to use the information that we already have to help people in real time. Susan Domchek, the Basser Centers executive director

Another study called Point of Care has offered genetic testing to patients already being treated for metastatic prostate and pancreatic cancer, using an 8-minute video to deliver a streamlined counseling session to this specialized population who are already all-too-familiar with the possible risks of a mutation. Yet possessing that information could guide critical treatment decisions tailored to the patients cancers genetic profiles. Testing among this population rose nine-fold after the intervention.

Were still not testing all the people who should get tested, says Domchek.

Basser leaders all stress that the Centers unique efforts wouldnt be possible without its donor-supported model.

I think people dont realize that the kind of infrastructure we have built is really hard to fund out of grants, says Nathanson. And by infrastructure, she means in large part human capacity, for recruiting patients, consenting patients, biobanking samples, getting the clinical data, putting that data in a database, maintaining the database, doing longitudinal follow-up. We cant fund our outreach, our patient awareness off of grants. Philanthropy is critical to supporting these efforts.

And theyre not lowering their sights as they look ahead.

We are continuing to grow the Center, bringing in people who have the expertise we dont currently have, says Drapkin. With our vision for the future, I see us as the epicenter for this kind of research in the world. There are few places that have the basic science, the translational and clinical science that we have. Its rare that you find expertise across the spectrum that can be applied in a way that gets to the patient. We have that here.

Susan Domchek is the Basser Professor in Oncology and executive director of the Basser Center for BRCA at the University of Pennsylvania Perelman School of Medicine.

Roger Greenberg is the J. Samuel Staub, MD Professor, director of the Penn Center for Genome Integrity, and director of basic science for the Basser Center for BRCA at Penn Medicine.

Katherine Nathanson is deputy director of the Abramson Cancer Center, the inaugural Pearl Basser Professor for BRCA-Related Research, and director of genetics for the Basser Center for BRCA at Penn Medicine.

Ronny Drapkin is the Franklin Payne Associate Professor of Pathology in Obstetrics and Gynecology, director of the Penn Ovarian Cancer Research Center, and director of gynecologic cancer research for the Basser Center for BRCA at Penn Medicine.

Beth Stearman is administrative director for the Basser Center for BRCA at Penn Medicine.

Laura Ferraiolo is senior director of development for the Basser Center for BRCA atPenn Medicine.

Homepage photo: Tianpeng Zhang, a postdoctoral researcher in Roger Greenbergs lab, takes fluorescence microscopy images to investigate how the genome is faithfully maintained as it is replicated, and how damage can arise. Zhang and other members of the lab contribute to the basic science research that supports translational discoveries in the Basser Center.

Read more from the original source:
Basser Center takes aim at BRCA - Penn: Office of University Communications

Lump-Sum Options present questions that deserve careful consideration.

Recent changes by the IRS have perked up interest in companies offering lump-sums to recipients of monthly defined benefit pensions. Most recently, General Electric (GE) announced was freezing its defined benefit plan and would be offering lump-sum options to 100,000 retirees. Lumps-sums are not new: AT&T, Ford and GM (Salaried only), and Allstate are among a myriad of companies offering lump-sums to retirees.

GE retirees will now face a complex decision about whether to remain in a monthly pension or take a lump-sum. The mathematical calculation for a lump-sum is prescribed by IRS rules. The interest rate is a blend of three treasury rates, and the life expectancy table is also governed by IRS rules. The math is essentially similar to the calculation of a mortgage: the lump-sum is effectively the value of the mortgage, the period is the life expectancy of the retiree, and the rate is the blended rate. By way of example, a 61-year old retiree with a $6,420 monthly pension would use a 3.11% blended rate to have their lump-sum computed at about $1.3 million.

Each decision is unique and personal in nature. Retirees may share similar lump-sum offers, but have different considerations in marital status, gender, investment expertise, flexibility demands and health situations. To that end, here are some general ideas about when a lump-sum is a good idea, and when it isnt.

When a Lump-sum is likely better:

Residual Value: A lump-sum can create a residual value. Therefore, when the retiree wants to leave assets to a non-spouse beneficiary, the lump-sum can provide that durability, if invested properly.

Withdrawal Flexibility: When a retire desires withdrawal flexibility, the lump-sum provides a wide degree of flexibility. Retirees who will have other jobs, a spouse with employment, or other assets, may enjoy the flexibility of a rollover IRA. Note that IRAs are subject to Required Minimum Distribution (RMD rules).

Investment Control: With a lump-sum, the retiree assumes investment responsibility. If the retiree can manage funds or delegate responsibility and make more than the discounted return (e.g. 3.11% for the 61-year old in the above example), the lump-sum can grow. In the example above, the retiree could get a $1.3 million lump-sum versus a $6,420 monthly pension. If the retiree creates a blended portfolio and earns 6% return, and then continued to withdraw the same monthly pension, her IRA would have more than they started with by ages of 80 and 85 (note RMD rules start to apply at 70.5).

Shorter life expectancy. Lump-sums are calculated on a unisex life expectancy. For example, a 61-year-old (irrespective of sex) is calculated to have about a 24.4-year life expectancy. Obviously, a shorter life expectancy, due to terminal illness, or bad genetics, make the lump-sum more attractive. Our 61-year old with health issues that passes at age 72, who makes 6% and withdraws her same $6,420, would have an IRA balance of about $1.35 million to leave to heirs or charity.

Higher inflation and interest assumptions. Monthly pensions usually do not index to inflation. If a retiree believes inflation or interest rates may rise, the lump-sum makes more sense. A lump-sum may be managed for inflation, and higher future interest rates allow the retiree to re-invest at a rate higher than the blended rate (like the 3.11% in the 61-year-old example).

Other Assets. Retirees with significant other assets or other income sources may want to take a lump-sum to create residual value. For example, if the retiree mentioned earlier had received an inheritance that generated ample income to support her life style, she might choose the lump-sum to delay distribution until RMD date (which may change to age 72 if the SECURE Act passes), and possibly engage in a Roth conversion strategy.

When a monthly pension is likely preferable:

Safety of income stream. When a retiree desires a safe income stream, the monthly pension is a safe alternative. Defined benefit pensions are partially to fully funded and are insured by the Pension Benefit Guaranty Corporation (PBGC). The PBGC insures monthly pensions up to $5,607.95 per month at age 65. The pension is effectively a very safe annuity. Many retirees are offered commercial annuities as alternatives to the lump-sum which seems counter-intuitive: selling an annuity to buy another annuity. Given the costs of a commercial annuity, it would seem very unlikely to find a full-replacement annuity on a commercial level. Current comparison quotes on an immediate Single Premium Immediate Annuity (SPIA) for a 61-year-old female show a slightly lower monthly benefit. It should also be noted that commercial annuities are not fully insured.

Invasion of principal. This is a behavioral issue, but many recipients of lump-sums or immediate wealth tend to make bad decisions. Spending money on family, losing it to bad investments, and even outright fraud can diminish or eradicate a lump-sum. According to the National Endowment of Financial Education, 70% of lotto winners declare bankruptcy within 5 years. Similar statistics apply to NFL players. Managing a lump-sum is a disciplined task. If a retiree has a lot of credit card debt and is undisciplined with money, a lump-sum wont help the situation.

Long life expectancy. A monthly pension is for life (or joint lives); a lump sum is based on a life expectancy table. Life expectancy tables are computed on a 50% probability of being alive at a certain age. This means that half of the people will live longer, and half will live less. A very healthy individual with good genetics may collect a monthly pension for a very substantial period of time. The very first Social Security recipient, Ida Mae Fuller, lived to age 100, paid in a total of $24.75 of taxes and collected $22,888.92 in benefits. Longer life expectancy (of the collective couple) make the monthly payment more attractive.

Investment risk. With a monthly pension, the pension plan assumes all investment risk. Retirees who are risk-averse to market fluctuations will find the monthly pension more attractive.

Other assets. Retirees who have other assets, like a 401(k) plan, to counter the effects of inflation and other prospective issues, may take the monthly pension to secure the cash flow and allow the other asset to grow. Retiree could consider the monthly pension to be the equivalent of a safe bond and they can accordingly take more risk with other assets and retain the monthly pension.

Bottom Line: This is a complex decision. Its personal in nature, depends on many variables of individual circumstance, and warrants careful consideration. If a reader has a question, or wants a second opinion, feel free to contact us with your questions.

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Six Reasons A Lump-Sum Can Look Good And Five Reasons It Might Not - Forbes

Around noon one August day in 2011, a familiar dorsal fin rose from the sea off the coast of Massachusetts. Flecked with tiny white scars, it belonged to Salt, a female humpback whale who scientists had been studying since the 1970s and who was named for those distinctive markings.

Aboard the research vessel Shearwater, Jooke Robbins director of humpback whale research at the Center for Coastal Studies in Provincetown, Massachusetts loaded a crossbow with a dart, modified with a specialized tip and yellow float, and took aim. The bolt went flying. It hit its target but, by design, bounced harmlessly off the whales bulk, taking with it only a few cubic millimeters of flesh almost like a mosquito bite, relative to the whales size.

Robbins and her team collected the sample, preserved it in liquid nitrogen, then sent it away to be analyzed. Now, eight years later, a team supported by the Arizona Cancer Evolution Center (ACE) at Arizona State University has discovered that Salt and other cetaceans the group of mammals that includes whales, dolphins, and porpoises evolved clever ways of dealing with cancer, including an array of tumor-suppressing genes. The team published its findings in May in the journal Molecular Biology and Evolution.

The findings, along with similar work on elephants, suggest that somewhere, hiding in the genetic code and evolutionary history of large mammals, there could be a new cancer treatment for humans. But if the researchers are correct, their window to study these megafauna may be closing as humans continue to threaten the animals populations and the biodiversity of their habitats.

That whales like Salt had value was never in doubt for Robbins. There are many valid reasons to conserve large mammals, from ethical to ecological. But the idea that their genes could be useful for cancer research was a new one for her.

I did not think years ago that one of the things we would be studying with this population would be cancer, in general, let alone any kinds of cancer implications for humans, she said. Its unexpected, and very valuable, but I never would have planned it.

In theory, large, long-lived creatures like Salt should have high cancer rates. At its core, cancer begins when a cell splits it divides incorrectly, the potentially fatal mutation spreads to neighboring cells, and, if left unchecked, throughout the body.

Compared to humans, whales and elephants can have hundreds of times the number of cells and have similarly long natural lifespans but their cells mutate, become cancerous, and kill them less frequently. This quirk of nature, which the ACE team is studying, is called Petos Paradox, named for Richard Peto, a British epidemiologist. In the late 1970s, he proposed that there must be some kind of natural selection for cancer suppression, because humans live longer and are much larger than mice, but the species have similar rates of the disease.

In 2011, ACE researchers, along with scientists at 11 other institutions worldwide, first started looking at how Petos Paradox manifests itself in the genomes of humpback whales by comparing the information in Salts genes to those of other cetaceans. According to the results reported this year, the parts of a whales genome that determine how and when a cell splits evolved quickly and coincided with when the animals grew to their enormous size. Marc Tollis a biologist at Northern Arizona Universitys School of Informatics, Computing, and Cyber Systems who joined and began leading the ACE study in 2015 hopes that taking one of the amped up, cancer-fighting whale genes and putting it in the body of a smaller creature will help the latter fight off these cellular mutations: a mouse as a test, a human as a hopeful end result.

Other scientists are also studying Petos Paradox in a different group of huge animals: elephants. In 2012, Joshua Schiffman, a pediatric oncologist at the University of Utah, began investigating cancer defenses in the animals after learning that they had extra copies of a gene responsible for fighting off tumors. It was this same gene that his patients with Li-Fraumeni syndrome, a rare hereditary disorder that predisposes sufferers to cancer development, lacked.

Collaborating with ACEs Carlo Maley, Schiffman and his team worked with local zoos and the Ringling Bros. and Barnum & Bailey Circus before the circus ceased using elephants in its acts and its Center for Elephant Conservation to gather blood samples during regular checkups with veterinarians. In their 2015 paper in the Journal of the American Medical Association, they reported that the elephants extra copies of this tumor-squashing gene triggers a type of programmed cell death and a defense against cancer called apoptosis. When a cell splits and experiences some kind of DNA damage from chemical agents, for example the cell will either try to fix itself, or self destruct to prevent the mutations from spreading to other cells. Both whale and elephant cells are also likely to undergo apoptosis more often compared to humans.

People are smart, but nature is much smarter, said Schiffman. Nature has figured out the solutions to some of our health problems over hundreds of millions of years of evolution.

Its clear elephants and whales have managed to find their resistance to cancer over countless generations, Schiffman added. His team is also looking for other cancer defenses in elephant genetics and trying to transfer this phenomenon to humans.

Whats even more exciting than that [these animals] found the cure, he added, is that, through nature, they evolved ways to prevent cancer in the first place.

So far, 22 of the 90 or so existing cetacean species have had their genomes sequenced and added to the National Center for Biotechnology Information database, with more being added all the time. When Tollis began working on Salts genome in 2015, there were only five. The field moves quickly, he said, with new technologies making the process cheaper and easier.

Scientists have also sequenced the genomes of all three elephant species alive today. While its a start, scientists may not have enough data to get a full picture of how the animals thwart cancer. As human activity eats away at these populations through ecosystem destruction, climate change, and more researchers get fewer and fewer chances to collect samples. The creatures become harder to find and the regulations protecting them grow tighter, delaying research by years.

Considering the rate these species are in decline, Tollis also hopes the research will also make people consider the importance for both cancer research and the environment.

Generally, since were living in a mass-extinction event right now, he said, we need every reason for conservation we can get.

The conservation status of these large mammals is a mixed bag, according to data from the International Union for Conservation of Nature (IUCN), which, among other projects, tracks population health of the worlds animals. Some whale species, like the humpback, have recovered from centuries of hunting while others, like the North Atlantic right whale and Sei whale, are still endangered. African and Asian elephants are listed as vulnerable and endangered, respectively.

Recently, Botswana lifted its five-year ban on elephant hunting and Japan resumed commercial whaling in July. However, conservation experts are even more concerned with habitat loss and other less violent, but thoroughly insidious dangers to the species.

Elephants suffer as their former stomping grounds are turned into industrial areas or farmland, which also leads to human-elephant conflicts, said Chris Thouless, strategic advisor with Save the Elephants, a research and conservation organization based out of Kenya.

In the ocean, whales are increasingly put at risk by marine microplastics and noise from shipping, said Hal Whitehead, a cetacean specialist with the IUCN. Cetaceans use sound to hunt for food and form social bonds, as neither sight nor smell work particularly well under water, and the noise stresses out the creatures.

The species which have been hit the worst are those with the closest contact with humans, Whitehead added.

Even if these species populations recover, there are other challenges for collecting genetic data from a wealth of species. A sample from only one animal isnt necessarily representative of an entire species, said David Baillie, a molecular biologist at Simon Fraser University in Burnaby, British Columbia.

While having an accurate, representative genome of a species gleaned from many samples is valuable, so too are some of the oddities that can arise in the genomes of individuals. Genetic diversity and large population numbers leave a good deal of wiggle room for mutations that could benefit both the creature and further down the line and with the right understanding humans.

The more genomes we have, the better we come to understand the residual diversity that underlies the population structure, Baillie wrote in an email to Undark. He added that rare mutations can be very important when trying to understand disease resistance, for example.

Theres evidence that points to robust genetic variation between regional groups within the same species, and more effort is needed to catalog the genes of an animals distant cousins, Tollis said. Similarly, according to Schiffman, poaching, habitat loss, and inbreeding have caused a bottleneck that has stifled genetic diversity in many species and among the worlds largest creatures in particular.

According to Cristiana Paca Palmer, executive secretary at the UNs Convention on Biological Diversity, the impact of habitat and species loss on medical research more broadly is still unknown.

The loss of large species like elephants and whales is just a microcosm of the cataclysmic species diversity loss happening in ecosystems the world over, she wrote in an email. Really, when we act to preserve biodiversity, we are acting to preserve ourselves.

Its also unknown how, over generations, human activities are changing these animals genomes, and the potentially useful data they hold. Research out of the University of Southampton in the U.K. suggests the median size of mammals will shrink by a quarter as humans continue to pave over untamed habitats, for example. As the genetics of the worlds animals adjust to humanitys tightening grasp on the planet, the genes a species use to defeat any number of diseases and other valuable mutations could be, effectively and inadvertently, bred out of existence.

If we lost the opportunity to study these animals in the wild, and if we dont protect them, Schiffman said, we could be losing cures for many different diseases to come.

Doug Johnson is a Canadian writer, editor, and journalist

A version of this article was originally published on Undarks website as As Elephants and Whales Disappear, They Take Valuable Cancer Clues With Them and has been republished here with permission.

Link:
If we aren't careful, we could miss the chance to learn cancer-fighting secrets from threatened whales and elephants - Genetic Literacy Project

A group of researchers say they have pinpointed the ancestral homeland of all humans alive today: modern-day Botswana.

In a new study published in the journal Nature, scientists analysed mitochondrial DNA genetic information that gets passed down the female line from more than 1,200 people across myriad populations in Africa.

By examining which genes were preserved in people's DNA over time, the anthropologists determined that anatomically modern humans emerged in what was once a lush wetland in Botswana, south of the Zambezi River.

Though scientists agree that modern humans (Homo sapiens sapiens) arose in Africa around 200,000 years ago, they have remained uncertain about exactly where on the continent that evolutionary milestone occurred.

The new study offers an answer to that question and also undermines the idea that our ancestors emerged in East Africa, as limited fossil evidence suggests.

The anthropologist Vanessa Hayes, the senior author of the new paper, said in a press conference that the findings suggested "everyone walking around today" could trace their mitochondrial DNA back to this "human homeland."

To trace the geographic origin of our ancestors, Hayes and her colleagues examined mitochondrial DNA (mtDNA) from people living in southern Africa, such as the Khoisan.

mtDNA, which is passed down the maternal line, is often used to trace human ancestry because it isn't mixed with paternal DNA. That means it changes less over time and leaves a clearer link to distant relatives.

When it comes to mtDNA, modern humans all share a group of genes called the L macro-haplogroup.

This L-branch is split into two subgroups: L1-6 and L0. The latter can be found in the peoples of southern Africa, and that's what Hayes' team analysed. Eva Chan, a coauthor of the study, said this was the "by far the largest L0 study to date."

By pulling on that genetic string, the researchers were able to figure out that every person alive today descended from a woman who lived in modern-day Botswana about 200,000 years ago.

The region this ancestor came from, called the Makgadikgadi-Okavango paleo-wetland, was near the modern Okavango Delta and peppered with lakes and greenery.

The team's analysis, which also included reconstructions of what the area's climate was like at the time, revealed that Homo sapiens sapiens lived in this homeland for about 70,000 years.

Then, as the climate changed, our ancestors dispersed in two waves: First, a group spread northeast 130,000 years ago, then others left in a second migration to the southwest 110,000 years ago.

According to Hayes, these migrating groups likely followed herds of animals out of the region.

This timeline runs counter to the one some scientists have created based on fossil evidence, however.

The oldest-ever specimens of anatomically modern humans skulls and other fossils dating back 195,000 years were found in Ethiopia, which led many anthropologists to think of eastern Africa (rather than southern Africa, as the new study suggests) as the birthplace of our modern ancestors.

The new genetic analysis also offers credence to the idea that all modern humans evolved in one place in Africa before migrating to current-day Europe, Asia, and Australia what's known as the "Out of Africa" hypothesis rather than evolving separately in multiple places around the world at the same time.

According to the study authors, the two-wave migration out of Botswana "paved the way for modern humans to later migrate out of Africa, and ultimately across the world."

But the anthropologist Ryan Raaum, who researches African population genetics at Lehman College, thinks the new study has a significant flaw. According to Raaum, the researchers didn't go back far back enough on the genetic timeline.

Though Hayes' research pinpointed where the L0 haplogroup originated, he said, the mitochondrial DNA of most people in the world can be traced back to the L1-6 subgroup of the L-branch, not L0.

So to find a "single origin" for our species, Raaum said, researchers should find a genetic predecessor who lived before the genetic split between L0 and L1-6 occurred.

"Where I get a little lost in the weeds is when they expand out to argue that these data indicate a southern African origin for anatomically modern humans," he told Business Insider. "The data do not."

Raaum added that he didn't like the phrase "ancestral homeland" in general, since modern humans likely had multiple homelands scattered around the African continent.

"I increasingly think that there probably wasn't a single population in which modern humans evolved. If that is the case, there is no 'homeland'," he said.

Another issue with Hayes' team's findings is that an mtDNA analysis examines only maternal DNA.

Two parts of the cell carry DNA: the nucleus, where most of our genetic material resides, and the mitochondria.

Nuclear DNA (nDNA) is inherited from both parents and is what passes along the Y chromosome; mitochondrial DNA, on the other hand, is passed down from only the mother.

nDNA is rare in the fossil record, which is why studies like Hayes' often don't examine it. But that means such research can't examine the entire genome of our ancestral populations.

In 2014, anthropologists pinpointed the oldest known modern-human lineage based on Y chromosome data. This population was at most 160,000 years old and in central western Africa.

So every person alive today likely descended from a man who lived in a different part of the continent than the homeland Hayes and her colleagues suggest.

Hayes noted that a full genome analysis could yield different results: "There could be other origins and other lineages it's a possibility," she said during the press conference.

But whether or not Botswana was the cradle of life for everyone alive today, the new research certainly suggests this part of Africa was an oasis for our ancestors a significant addition to our understanding of human evolution.

"People want know where they came from," Hayes said.

This article was originally published by Business Insider.

More from Business Insider:

See the original post here:
New Study Pinpoints The Ancestral Homeland of All Humans Alive Today - ScienceAlert

It is society that needs fixing, not intersex bodies activists at the Voices4 London demo talk candidly on Intersex Awareness Day

I look forward to a time when parents arent made to feel the need to hide from their child that they are intersex. I look forward to a day when intersex variations are not treated as disorders that need fixing,Rachelle Newman, anintersex activist, said at the London rally onIntersex Awareness Day 2019.

This day was established in 2003 by US intersex activists Emi Koyama and Betsy Driver to commemorate the first public intersex demonstration in 1996. 23 years on, the fight is still ongoing. Intersex is an umbrella term used to describe people born with biological variations in their sex characteristics that dont fit male or female categories. These variations may be present in peoples chromosomes, hormones, genitals and/or internal sex organs, like testes or ovaries. Intersex traits can also be linked to genetic mosaicism, where some cells in the body have XX chromosomes and others XY.

Medicine has traditionally viewed intersex people as needing to be fixed with involuntary medical intervention, also known as Intersex Genital Mutilation (IGM), simply to make their bodies conform to traditional notions of male or female. Many cases of IGM change the appearance or sexual function of a childs genitals and are carried out at a very young age, without consent and often with no transparency regarding the details.

On Saturday October 26, peaceful direct action groupVoices 4 Londonresponded to an international call by theIntersex Justice Projectto organise events in support of The End Intersex Surgery Campaign. Members of the LGBTQIA+ community gathered in Soho Square Gardens in London to offer support and attention to the intersex activists leading the rally. Through the pouring rain, the crowd listened asNewman was joined by Martin Di Maggio and Valentino Vecchietti to call for an end to non-consensual forced surgery, brandishing hand-painted signs with slogans such as Your Body, Your Choice, Your Rights, Delay is Okay, and Intersex Stories Not Surgeries.

This was followed by a short impromptu march, accompanied by shouts of Your Body, Your Choice. The group gathered in front of the sexual health clinic, 56 Dean Street, to celebrate that the intersex flag was flying there for the first time ever in recognition of Intersex Awareness Day. The services are also currently amending their equalities policy to include intersex people.

Here, we spoke with four intersex activists who were present at the rally about what intersex justice looks like.

What one pervasive myth or misunderstanding around the lived experiences of intersex people do you most wish you could address widely?

Rachelle Newman:That we dont exist. There are many activists doing amazing work to improve intersex visibility yet sadly many people still do not know what the word intersex means. I want intersex people to be able to say Im intersex and receive a response not much more than ah okay, cool!.

Whats something about your experience as an intersex person, that you wish people were aware of and understood?

Rachelle Newman:In regards to my personal experience, I wish society as a whole was more aware of and understood the mental health impacts that resulted from my treatment. Being told I was infertile at age 11 was the worst day of my life but I wish people would also understand the impacts of the events that followed. For example, the dread I would feel thinking about my biannual appointments, having to expose my chest to a doctor without knowing why, the daily reminder of taking tablets I did not understand the purpose of and the internal dialogue with myself as I discovered and wondered why my body was different, why I had scars. I wish people would understand the shame imposed on myself and many other intersex individuals from a young age and the negative repercussions of this.

If you could say something to your younger self, what would you say?

Rachelle Newman:You are not alone. One day it will all make sense. You will become strong and when you share the part of yourself that you have been ashamed of for so long you will receive more acceptance than you can imagine. You will learn to love the things you thought you couldnt.

Whats something about your experience as an intersex person, either generally or specifically within the UK, that you wish people were aware of and understood?

Martin Di Maggio: That we have no protection against molestation and sexual abuse, doctors do and have legally gotten away with sexual abuse because they claim they are only doing medical testing. Yet many of us have experienced intrusive examinations that had a doctor done them on an endosex (non-intersex) woman theyd be imprisoned, yet with us, the law doesnt even protect us and doctors go free. Look up the case of Aivar Bracka.

What are your thoughts on the Gender Recognition Actwithin the context of how it might impact intersex people and, especially, children?

MartinDi Maggio:I think that parents being able to put an X marker on a childs birth certificate means nothing for intersex children as long as we dont have protection against IGM. Having X as an intersex child would perhaps just make us more vulnerable to unwanted medical attention.

What is one misunderstanding around the lived experiences of intersex people that you most wish you could address widely?

Izzy MacCallum: One misunderstanding/assumption that Ive noticed a lot of people have is that they think being intersex is necessarily referring to someones genitalia. In reality, there are a wide variety of traits and sex characteristics that can mean someones biology doesnt fit the typical definitions of male or female. Maybe someone has XY chromosomes and testes but a vagina and no uterus. Or someone has an extra chromosome, like XXY, or they could have mosaic genetics. People can have no ovaries or testes or one of each you see what Im getting at.

Whats something about your experience as an intersex person, either generally or specifically within the UK, that you wish people were aware of and understood?

Izzy MacCallum: The argument that these non-consensual surgeries are done to ease the social discomfort of intersex people not only denies the individual bodily autonomy, but it actually perpetuates social discomfort. Intersex people challenge the social norms and understandings of sex and gender as a binary, and by keeping sex and gender within a binary frame it can be used to enforce and maintain social and historical forms of oppression. It is society that needs fixing, not intersex bodies.

If you had to pinpoint it and youre comfortable sharing it, whats the one external or personal thing that has most positively impacted your life so far?

Valentino Vecchietti:I grew up feeling so alone and scared, and filled with shame. But as an adult, finding connection with other intersex people, and finding acceptance and love amongst my friends, has been an amazing and moving journey for me.

How do you think the Gender Recognition Act could betterprotect intersex people and, especially, children?

Valentino Vecchietti:Current medical protocols for intersex kids dont support our human right to bodily integrity and bodily autonomy.We need ethical, patient-centred, healthcare and medical treatment, which must include the option of correcting birth certificates.

If you could say something to your younger self, what would you say?

Valentino Vecchietti:You will find love, you will find friends, you can belong.

Read more:
Intersex people on how they want to be treated and accepted - Dazed

People with a genetic risk for being overweight or obese are more likely to have an incisional hernia or hernia thats a complication of a surgery and, if obese, a post-surgical infection as well, a study suggests.

Association of Genetic Risk of Obesity with Postoperative Complications Using Mendelian Randomization was published in theWorld Journal of Surgery.

Obesity is thought to be a risk factor for complications after surgery, but most previous studies have been limited in the scope of surgeries assessed, and little attention has been paid to the role of genetics.

Researchers at Vanderbilt University Medical Center (VUMC) addressed these gaps by analyzing two large datasets. The first, from VUMCs patient health records, covered 736,726 individuals, 68,266 of whom who had undergone an abdominal surgery.

The second dataset, from 12 institutions within the eMERGE Network, covered 65,174 people, with 15,355 having undergone abdominal surgery and a known genetic profile. This enabled the team to determine a genetic risk score associated with body mass index (BMI), a ratio of weight to height, and its correlation with surgical complications.

Both groups were predominantly female and white, and about two-thirds of people in each were classified as overweight (BMI of 25 to 29 kg/m2) or obese (BMI of 30 kg/m2 or greater). Median age was 49 in the first group and 67 in the second.

Incisional hernias develop due to a weakening of muscles caused by an incision made in a surgery, and are most commonly a complication of abdominal surgery.

Results from the first group showed that being obese or overweight was associated with a significantly higher likelihood of developing hernia or infection after surgery. This association was strongest in people with the highest BMI (40 kg/m2or more), who had an over five times greater risk of a hernia and were twice as likely to have a post-surgery infection than people with a normal BMI.

In the second group, a genetic score predicting a higher likelihood for obesity was also significantly associated with a greater risk for both of these complications. A subsequent analysis revealed that this increased risk in people genetically predicted to be obese was driven mostly by the change in BMI itself.

In both groups, the link between obesity and post-operative complications was maintained when limiting the analysis to people who had undergone general, urologic, or gynecologic abdominal surgery.

Findings also revealed that overweight or obese individuals in the first group had a lower risk of intestinal obstruction but greater risk of mortality within 90 days after surgery, in comparison with patients with a normal BMI.

This study found that obesity as measured by both BMI and genetic risk is associated with postoperative infections and incisional hernias, the researchers wrote.

Marisa holds an MS in Cellular and Molecular Pathology from the University of Pittsburgh, where she studied novel genetic drivers of ovarian cancer. She specializes in cancer biology, immunology, and genetics. Marisa began working with BioNews in 2018, and has written about science and health for SelfHacked and the Genetics Society of America. She also writes/composes musicals and coaches the University of Pittsburgh fencing club.

Go here to see the original:
Genetic Risk and Obesity Linked to Likelihood of Post-Surgical Hernia and Infection, Study Finds - Genetic Obesity News

When Kathryn Hahn first moved to LA to become an actor, she started auditioning but quickly became disillusioned.

"When I started to see the roles that were available to me, what I was being seen for, I definitely thought ... 'This is just such a small part of me that's being seen. I wish somebody could see more of what I can offer,'" Hahn says.

It wasn't until Hahn was in her late 30s and 40s that she finally began landing the roles she craved, playing complex women in TV series like Transparent and Parks and Recreation, and movies like Bad Moms and Private Life. Hahn notes that most of these roles have been with female directors and producers.

"The most complicated and messy roles I've been able to get have been offered through women," she says. "I'm just so buoyed and galvanized that the juiciest part of [my career] has been post-kids. ... I never anticipated that. So that's terribly exciting."

Hahn is currently starring in the HBO series Mrs. Fletcher. The show, which is based Tom Perrotta's bestselling novel, centers on a divorced woman who has a confusing sexual reawakening after her son leaves home for college.

"We were surrounded by an incredible group of women directors and writers and we had this amazing intimacy coordinator," Hahn says of her work on Mrs. Fletcher. "That was what made it attractive to me. It was finding a woman in her complete privacy of finding pleasure for just herself."

On working with an intimacy coordinator ahead of the sex scenes in Mrs. Fletcher

I'd never worked with [an intimacy coordinator] before, and I was a little hesitant at first, to be frank, because I thought it was going to be [another] voice in the way, in between the director and the actor ... and it was not that at all. Our intimacy coordinator, Claire Warden, what she did was she would take all of us anyone that was performing in the scene and the director she would have conversations with us ... would make sure that we were aware of what was on the page.

This is above and beyond the nudity riders or whatever that would have already been signed, but she would take us all and make sure that we were aware of what was on the page to be filmed, make sure that we were all OK with that, walk us through the steps, make sure that our boundaries our personal boundaries were in place for what we were comfortable with ... so that when we walked in together, we all knew that each other's needs and requests and concerns were heard. And then you could just get to the business of the scene so much quicker.

On wanting to be an actor from an early age

I loved the ensemble. I loved the feeling after. I loved the feeling right before as awful as it was. ... I loved the feeling of being on stage ... in communion with the audience, I just loved that feeling. ... Even at very young age, I loved the feeling of something, like, heightened and holy that's what it felt like.

On bad auditions earlier in her career

In my last semester at Yale, I would take the train in to 30 Rock. There was a Banana Republic at the base of 30 Rock. I would go into the Banana Republic. I would buy a suit, go up, audition for a pilot, go down, return the suit at Banana Republic ... and promptly get on the train and never get the gigs. ...

I had a really bad Woody Allen audition that was just awful, horrible for a play ... and I remember someone telling me that he wasn't going to look up and laugh. ... [It] was a long time ago, but I remember auditioning and it was true: He did not laugh at all. And not only did he not laugh, but he looked up when I just botched a joke so badly. It was awful. ...

The Coen Brothers. That was a heartbreaker. ... It was for A Serious Man ... and I was way gung-ho. ... I brought in a bag of props. It was too much. It was just way too much for the space and they were very polite and very kind. And I did not get the part.

On having kids in her mid 30s and being nervous about how it would affect her career

I'll never forget when I found out I got pregnant, I was on my way to work and I was, of course, thrilled, but I went to a Starbucks and I got a latte and I said, "Oh, I guess you better make a decaf," and I burst [out] in hysterical tears. ... I was on my way to a night shoot for a television show. ... I felt so young and old at the same time. You're never ready. I was so grateful, but ... as an actor, you're like, is this really gonna change [my career]? It was all so much. ...

We had had so much time solo. We'd lived in New York forever in our little studio. There was so much history behind us. ... Neither of us were anywhere near where we wanted to be creatively. ... I wish I could have looked back and told that 35-year-old crying in Starbucks, "You have no idea how exciting it's going to be on the other side!"

On the roles that she hopes to land when she's in her 50s

I hope that we keep exploring whatever these chapters are. I just hope that we keep lifting whatever invisibility shield is on all these chapters of just being a woman, like lifting the shame ... and just keep exploring it, because clearly there's so many, so many, so many more stories to be told and looked at with hopefully this degree of nuance, and clarity, and humanity, and complication and all of it. There are so many more stories to be told.

Ann Marie Baldonado and Mooj Zadie produced and edited the audio of this interview. Bridget Bentz, Molly Seavy-Nesper and Patrick Jarenwattananon adapted it for the Web.

TERRY GROSS, HOST:

This is FRESH AIR. I'm Terry Gross. My guest, Kathryn Hahn, stars in the new HBO series "Mrs. Fletcher," which is adapted from the bestselling novel by Tom Perrotta, who created the series. Hahn is known for her roles in the TV series "Transparent" as Rabbi Raquel and in "Parks And Recreation" as Jennifer Barkley, an aggressive political operative. Hahn starred in the films "Bad Moms" and "Private Life."

In "Mrs. Fletcher," Hahn plays Eve Fletcher, a divorced mother of a teenage son. In the first episode, she drives him to college and becomes an empty nester. Just before the trip, after gassing up the car, she goes to his bedroom where he's been sleeping off a hangover - and a shock to hear from behind the closed door that he's having sex with a girl, and he's giving her crude, derogatory sexual commands and calling her the B-word and a slut. On the drive to college, she tries to talk with him about how not to treat women.

(SOUNDBITE OF TV SHOW, "MRS. FLETCHER")

KATHRYN HAHN: (As Eve Fletcher) I guess what I'm trying to say is I think - there are things that you might say to a girl that could scare her without you even realizing it. I mean, look. I know you're not a virgin, right? You know, and I know there's porn in movies and, you know, all these songs about hos and b******. And, you know, that's - you know, that's what it is. So I guess that what I'm trying to say is I think one of the most important things for you to always remember, especially now, you know, in this day and age and in life, really, is that - you have to be nice to women. Do you understand what I'm saying?

JACKSON WHITE: (As Brendan Fletcher) Yeah.

HAHN: (As Eve Fletcher) All right.

GROSS: After dropping off her son, Eve returns alone to a big empty house. Kind of by accident, she finds porn on the Internet, including lesbian porn, and is surprised by how arousing it is. The series alternates between her story and her son's story. He's unprepared for social life in college, where women students he's meeting demand respect and are serious about consent and no meaning no.

Kathryn Hahn, welcome to FRESH AIR. Did you spend a lot of time thinking about how a woman like Eve would raise - could end up having a teenage son who's such a bro, beer-drinking, ogling girls kind of guy, treating them as sex objects. You know, just try to think, like, how does that happen when she's - when the mother is like nothing like that?

HAHN: Yes. I mean, I think it's despite her best, deepest intentions. I mean, I - you know, there's - not to put it all on this divorce that she went through - but he didn't have the greatest examples - male examples. And I think that in a time in which he could have had a lot more attention in terms of, like, his sexual development, he went right to the Internet. And I think she kind of lost him or lost that connection along the way, despite her best intention. I think the harder she went towards him, the more it pushed him away. And that was heartbreaking to me.

I think a lot of people can find that, unfortunately, really relatable. I mean, she really - that's like her worst nightmare. Of course, she doesn't think he's a horrible person. But she can also kind of see it. It's just, like, layers of denial.

GROSS: So Eve Fletcher, your character, is having a very exciting solo sex life (laughter) - her and the Internet.

HAHN: Finally.

GROSS: And she isn't really sure if and how she should extend that solo sexual life with Internet porn into the real world, and if she does - because she's finding this porn, and especially this lesbian porn, very arousing.

HAHN: Mmm hmm.

GROSS: And how did you prepare for that part of the role? Did you feel like, well, it was your responsibility to watch a lot of porn...

HAHN: (Laughter) Terry...

GROSS: ...To get into character?

HAHN: I didn't feel like I had to watch a lot of porn. The porn, for her, was almost kind of like this Gandalf (laughter) for her kind of discovery. It's the most private, taboo thing - the most reckless kind of leap that she could possibly take and also, the most deeply, deeply private. And the avenues that she was - what she was able to see in that, you know, the glow of that computer screen.

So it wasn't about anything salacious or to show anything for anyone else's pleasure. It was for her own. And so that was a beautiful thing and a challenge to try to find is this woman in her completely private bubble. And we were surrounded by an incredible group of women directors and writers. And we had this amazing intimacy coordinator. That was what made it attractive to me. It was finding a woman in her complete privacy.

GROSS: What does an intimacy coordinator do on set?

HAHN: Well, that's interesting, Terry, because I'd never worked with one before. And I was a little hesitant at first, to be frank, because I thought it was going to be a voice in the way, in between the director and the actor, like another voice. And it was not that at all.

Our intimacy coordinator Claire Warden - what she did was she would take all of us - anyone that was performing in the scene and the director - she would have conversations with us on the eve of - no pun intended - but on the eve of whatever the scene was - and would make sure that we were aware of the - what was on the page. This is above and beyond, like, the nudity writers or whatever that we - that would have already been signed.

But she would take us all and make sure that we were aware of what was on the page to be filmed, make sure that we were all OK with that, walk us through the steps, make sure that our boundaries - our personal boundaries were in place for what we were comfortable with. And then she would be able to - so that when we walked in together, that we all knew that each other's needs and requests and concerns were heard. And then you could just get to the business of the scene so much quicker.

GROSS: Is the crew in on this discussion too or just the actors?

HAHN: What she - they're not in on those discussions, but what she will do is she will just make sure that the monitors are closed, that it's the fewest amount of people in the. Or she will ask us what - who we want in the room and make sure that it's just that amount of people, depending on what the scene is.

GROSS: So I don't know, it seems to me - and I don't know if you'd agree with this - that you're kind of part of the first generation of women who came of age with women screenwriters and directors - and, I mean, more than one or two, that you had a cohort. And you've worked with some of them. I mean, you've worked with Nicole Holofcener, Tamara Jenkins, to name a few. And I'm wondering if you agree with that, that you're part of the generation - one of the first...

HAHN: God...

GROSS: ...Or maybe the first that had a cohort of women writers and directors.

HAHN: Oh, God. I mean, that sounds terribly thrilling. I think I do feel like the most - that the most satisfying work I've done has been with women for sure, that the most complicated and messy roles I've been able to get have been offered through women. And it's not lost on me that it's, like, the most fertile chapter of my life has been with these women.

And it also is terribly exciting to me that it's older women - you know what I mean? - that it's not just women that are - you know, when I was a young actor, I thought that having kids would be - I was terrified to have kids. And it's...

GROSS: You thought it would end your career?

HAHN: Or - yeah, yes. Or change it, or I'd be stopped being seen or whatever. That - I'm just so buoyed and galvanized that the juiciest part of it has been post-kids. And not that that is even a choice for everybody. No one even has to have children. But it's just - it's - I think it's more of an age thing, that it can - it's the most satisfying. It's like, post-40 is just - I never anticipated that. So that's terribly exciting.

GROSS: So you're 46 now.

HAHN: Yeah.

GROSS: And some of the roles you've been getting in your 40s are about women dealing with fertility issues.

HAHN: Yes.

GROSS: So I want to play an example of one of those films. And this is "Private Life," which was written and directed by Tamara Jenkins. And you play - you and Paul Giamatti play a married couple who've been trying for years to conceive. And you've tried, like, every kind of fertility treatment. And finally, your doctor says to you you should try an egg donor because none of these fertility treatments are really working for you.

And so in this scene, you've just left the office after getting that message from the doctor. And that is about the last thing that you want to hear. You do not want to use an egg donor. And you and your husband, played by Paul Giamatti, are having a quarrel about that. You speak first.

(SOUNDBITE OF FILM, "PRIVATE LIFE")

HAHN: (As Rachel) We talked about this. We swore we would never do it.

PAUL GIAMATTI: (As Richard) No. You swore that you would never do it. I - (laughter) I kept my mouth shut because I didn't want to pressure you into something that you were going to have to live with for the rest of your life.

HAHN: (As Rachel) Wait. So all this time that I'm assuming that we feel the same way about this, you've been having secret fantasies about egg donation?

GIAMATTI: (As Richard) It's not a secret fantasy.

HAHN: (As Rachel) It is to me. I didn't know about it. I thought that we had decided together as a couple that we would definitely draw the line at science fiction.

GIAMATTI: (As Richard) It's not science fiction, Rach (ph). It's pretty primitive, actually. They do it with farm animals all the time.

HAHN: (As Rachel) Well, I'm not a goat, OK?

GIAMATTI: (As Richard) Bad example. I'm sorry.

HAHN: (As Rachel) Oh, my God. You're, like, so gung-ho right now. It's like - it's freaking me out.

GIAMATTI: (As Richard) I am not gung-ho. I'm just pragmatic. Look, if we do another IVF with your eggs, we've got - what? - a 4% chance of getting pregnant? With a donor egg, we'd be going from four to, like, 65%. So I'm - the gambler in me just wants to put my money on the better odds.

HAHN: (As Rachel) Oh, my God. You're Guy Woodhouse.

GIAMATTI: (As Richard) What?

HAHN: (As Rachel) The husband in "Rosemary's Baby," John Cassavetes. That's you.

GIAMATTI: (As Richard) Yeah, right. That - that's me, standing by while you're raped by a satanic demon. I am just suggesting that we listen to our doctor and look into all the options. We're already signed up for adoption. What is the big deal?

HAHN: (As Rachel) Well, for one, I'm not putting someone else's body parts into my uterus. Excuse me.

UNIDENTIFIED ACTOR: (As character) Excuse me. Sorry.

GIAMATTI: (As Richard) I know it's more complicated for you.

HAHN: (As Rachel) Is it more complicated for you too?

GIAMATTI: (As Richard) Yes, of course it is. Yes. Yes. But you heard him. There's a lot of positives. You would get to carry the baby.

HAHN: (As Rachel) Oh, whoop-de-do. What does that make me, the bellhop?

GROSS: That's Kathryn Hahn...

HAHN: (Laughter).

GROSS: ...And Paul Giamatti in a scene from "Private Life." So when you were in your 20s and wanting to act, did you think that when you were in your 40s, there would be roles like this of - you know, of women in their 30s or early 40s dealing with fertility issues in a way that so many women could relate to?

HAHN: No.

GROSS: Because so many actresses have thought, like, once you reach your 30s, or certainly by 40, your good roles are behind you.

HAHN: Exactly. No, I did not. I had no - you know, Terry, like, I - it's funny because I never thought of myself doing anything else with my life. I had no idea of what it would look like or how it would unfold, of course. Like, I never had any kind of grandiose, like, dreams of success or - yeah, I just knew - there was, like, never a question that I wasn't going to be an actor.

When I got to LA, when I started to see the roles that were available to me on what I was being seen for, I definitely thought - I knew that there was something, which I'm sure it - all actors have, is, like, you think, oh, I wish - this is just such a small part of me that's being seen. I wish somebody could see more of what I can offer. Like, no one is giving me this opportunity. Like, I just - it's, like, genetics or whatever. Like, no one is seeing the all of me.

And so I really didn't - I thought that it would have to take me to get back to the theater. I just wanted to get back to New York. Like, I just didn't feel at home out here, like - or in LA. Like, I just never thought that those roles would start to happen. So again, it has been a real crazy turn of events for me that this has even been able to happen.

GROSS: How old were you when you had your first child? And I'm wondering if, in your mind, there was an age that you thought would be, like, the right age, the best age, to have a child.

HAHN: I was, I think, 35, 30 - almost I think, like, 30 - maybe 35 when I got pregnant, I think, maybe 36 when I had him. And it took a second for us to get pregnant. It was definitely not as easy as we thought. And we - I was called a geriatric mother. I'll never forget that.

GROSS: By your doctor.

HAHN: Yes (laughter).

GROSS: Because you were considered at risk.

HAHN: Yeah, yeah, because I was over 35 and because I was a - yeah, over 35. And I'll never forget, when I found out I got pregnant, though, I was on my way to work. And I was, of course, thrilled. And I - but I was - I went to a Starbucks, and I got a latte. And I said, oh, I guess you better make it decaf. And I burst in hysterical tears.

GROSS: Why were you crying?

HAHN: (Laughter) Because it was just - I was on my way to, like, a night shoot for a show, a television show I was on. Like, it's all - my whole world, like - also, you just never - it was all just - I was - I felt so young and old at the same time. It - I - you know, you're never ready. I - it was like I was so grateful, but I was also, like, you know, an actor. And you're like, is this really going to change? Like, what's - it was all so much.

I'm so glad that we did it when we did. We have now two kids, and they're 10 and 13. And I just want to sob thinking about how fast it's going, Terry. I can't handle it. It's just too much. I mean, I cried when his umbilical cord fell off. I don't know what I'm going to do when he goes away to college.

But we were definitely ready when we - we had been together a really long time. And we were ready when we had him. But still, we were the youngest of our friends. Like, we were the first ones of any of our group, which is interesting, and we were, like, 35.

GROSS: Was part of your ambivalence when you finally got pregnant based on the fact that your body is part of your equipment when you're acting?

See more here:
Actor Kathryn Hahn Says The Best Part Of Her Career Came Post-Kids - WJCT NEWS

Prime Minister Benjamin Netanyahus Twitter account blew up in July in the wake of an extraordinary tweet: A new study of DNA recovered from an ancient Philistine site in the Israeli city of Ashkelon confirms what we know from the Bible that the origin of the Philistines is in southern Europe. ... The Palestinians connection to the Land of Israel is nothing compared to the 4,000 year connection that the Jewish people have with the land.

Netanyahu, like the hundreds of people who replied to the tweet, interpreted the study as overwhelming proof of Jewish ownership of the Land of Israel and proof that the Philistines who share an etymological history with the Palestinians were new immigrants, having arrived here just 3,000 years ago. Officials from the Palestinian Authority were quick to say that Palestinians are the descendants not of the Philistines but rather of the Canaanite Jebusites, who were ostensibly the original inhabitants of the land.

Netanyahus tweet came a few days after the publication in the magazine Science advances of a study by researchers from Germanys Max Planck Institute for the Science of Human History and the Leon Levy Expedition. The researchers sampled DNA from 10 skeletons found in Ashkelon and concluded that their gene pool came from southern Europe. The finding supports the accepted theory that the Philistines migrated from the area of Greece and settled along what is today Israels southern Mediterranean coast.

The studys authors, however, were infuriated by the prime ministers tweets. They considered responding but decided it might give the tweets more exposure. Netanyahus political spin on the research upset many scholars, who saw it as an example of the danger inherent in bringing genetics into the study of human history. Critics fear that used incautiously, genetic research not only has the potential to distort history but also can become a tool for racist propaganda in the hands of extremist politicians and groups.

The ability to extract and sequence DNA from samples that are thousands and even hundreds of thousands of years old has led to significant breakthroughs in the study of evolution. By sequencing Neanderthal genomes, scientists have learned about the health, physical appearance and settlement patterns of Neanderthals. Even more important, DNA research led to the discovery of formerly unknown hominids. The most famous being the Denisovans, which was discovered only thanks to a single finger bone found in a cave in Siberia, from which its owners genome was sequenced. The researchers were also able to determine that most modern human beings carry genes from Neanderthals, Denisovans and additional, as-yet unidentified hominids.

Broad brush

These successes led researches to apply genetic tools to later periods, and according to some critics that is where the danger lies. A study published last week in Science Magazine of 4,000-year-old graves in southern Germany determined, using DNA and as well as the objects with which their occupants were buried that the wealthiest men were locals. Poor men, servants and most of the women came from elsewhere, and most of the high-status women were apparently sent to other communities. One can only manage the political conclusions that could be drawn from the study.

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The problem isnt with the research itself, says Raphael Greenberg, a professor of archaeology at Tel Aviv University. Say I want to know about the connection between the Levant and the Greek region. I have various ways to examine it: pottery, inscriptions, symbols, language, and now something new has been added to my arsenal. Thats great, no one will deny that its useful. The problem is that DNA research has an element of magic to it. Only a few laboratories carry out these tests, at very high cost, and no one can argue with them, Greenberg says. He adds that their operators dont make do with presenting their findings; they go on to interpret the results. He believes that DNA researchers should leave conjectures about population migrations to the relevant experts.

The disagreement surrounding Who We Are and How We Got Here: Ancient DNA and the New Science of the Human Past, by Harvard geneticist David Reich, illustrates Greenbergs argument. Reich is considered the most important researcher in the area of ancient DNA, but his critics attack him for reducing complex historical process into simplified sound bites. He has lost some of the soul of what archaeology and sociology are, wrote Anna Linderholm of Texas A&M University in a review published in Current Anthropology. With his investigations he is painting with large brushstrokes a picture of our past, and in doing so, he might be missing some of the finer points. Who we are is much more than the genetics.

Critics argue that genetics alone cannot tell the complex story of the exchange of genetic material between two population groups, which involves not only migrations but also trade, war and the taking of male and female prisoners.

Gene sequencing, says Prof. Assaf Yasur-Landau of the University of Haifa, is a completely new tool whose potential we dont yet understand.... The danger is in making the connection between genetics and cultural. Its absolutely forbidden and borders on racism.

My granny was a Philistine

The dispute over the archaeological use of DNA is part of a broader discussion. Last year Reich published an opinion piece in The New York Times in which he argued that scientists should stop denying the existence of genetic differences between human population groups, rather than viewing race as entirely a social construct with no biological basis.

It is important to face whatever science will reveal without prejudging the outcome and with the confidence that we can be mature enough to handle any findings. Arguing that no substantial differences among human populations are possible will only invite the racist misuse of genetics that we wish to avoid, Reich wrote.

In an open letter produced by a group of 67 scientists and researchers and published on BuzzFeed, they attacked Reichs approach and warned against returning to a racial-genetic understanding of humanity.

Human beings are 99.5% genetically identical.... [Y]ou could genotype all Red Sox fans and all Yankees fans and find that one group has a statistically significant higher frequency of a number of particular genetic variants than the other group.... This does not mean that Red Sox fans and Yankees fans are genetically distinct races, they wrote.

Michal Feldman, an Israeli geneticist who works at the Max Planck Institute, was the lead author on the article on the skeletons from Ashkelon. Were trying to be cautious in our research and also in our press releases, and to explain exactly what we found, she says. We said we saw a genetic component that came from southern Europe, but that it disappeared after 200 years despite the fact that culturally they were still Philistines. Feldman agrees that the genetics must be separated from culture. Theres no such thing as a pure population or separate groups. Only a tiny part of the genome, 0.01 percent, attests to the origin, and most of the genes within that part are of no importance.

Nimrod Marom, an archaeo-zoologist at the University of Haifa, says the danger is of reducing the discussion to the question, Where did your mother come from?. He says that DNA research is more interested in the origin of the Philistines grandmother than in the way he lived here. In the end it doesnt say much about me and doesnt say much about anyone, he says. We get annoyed today when thats done to us, when we are categorized according to where we came from, so theres no reason not to be annoyed when its done to people from other periods.

Greenberg also believes that the danger of reductionism in genetic studies is much greater than getting an inaccurate picture of the past. We object to these classifications in our daily lives, we dont want to be defined by something that we dont see and have no control over. We want to say who we are by what we think and what we identify with. This method expropriates our identify from us. It says your identity isnt your religion and it isnt the food that you like, its what we tell you it is. Theres not really any such thing as the original inhabitants of this land.

View original post here:
DNA research holds the keys to human history but it's being weaponized by politicians - Haaretz

This will be a challenging budget. It willnot be easy, said Kenney, adding the exact reduction figure is 2.8 per cent.

These are necessary decisions. In fact, I would argue that they are long overdue. We must embrace transformative change to get a smarter government. Thats not going to happen overnight.

The budget is the first one by Kenneys United Conservative government since it defeated the NDP in the spring election.

Kenneyhas promisedthe budget will be alandmark spending document that will balance the books in four years andreorient Albertas economy long after that.

He has pledged to get it done bygetting more value for public money while reducing overall spendingand endinga recent run of multibillion-dollar deficits he says threaten to cripple future generations with unsustainable debt.

Also this

A judge in southwestern Nova Scotia is expected to deliver a decision today in the case against aformer police chief accused of sexually assaulting a 17-year-old girl.

John Collyer was the chief of police in Bridgewater, N.S.

He was placed on administrative leave from the Bridgewater Police Service in August 2016 after the provinces Serious Incident Response Team confirmed it was investigating the alleged assault.

The 26-year veteran of the force was suspended in May 2017 after the independent police watchdog charged him with one count of sexual assault and two counts of sexual exploitation.

Thecomplainanttestified thatCollyer asked her an inappropriate question while the two were driving in May 2016before puttinghis hand between her legs and assaulting her.

Collyer has denied the accusations.

ICYMI (In case you missed it)

Scientists have written the family tree for the tree of life.

Years of analysis, released in the journal Nature, has allowed researchersto pinpoint a billion years of evolutionary relationships between plants as different as cannabisand cucumbers, orchids and oaks.

Everything isinterrelated,says the University of Albertas Gane Wong, one of the papers dozens of co-authors.

Science has known for a long time that species with significant differences can be related through a common evolutionary ancestor. In plants, those relationships have been studied mostly through how they look or behave. Do they have trunks? Flowers? How do their seeds form?

Wong and his colleagues nearly 200 of them have been looking at how the links are expressed through genetics.

The team couldnt resolve everything. They couldnt find branches in the tree for about five per cent of species, either because there wasnt enough data or because it dated from so long ago it couldnt be read accurately.

But the work is already yielding concrete benefits. Proteins taken from an obscure algae species studied by the researchers were found to turn certain brain neurons on and off. Those proteins are now being used in clinical trials to treat blindness.

What we are watching in the U.S.

Albertas oilsands are at the centre of acourt battle in New York this week that legal experts say could affect future climate lawsuits in Canada.

The evidence thats coming out through this case is absolutely relevant to other lawsuits, said Martin Olszynski, a University of Calgary professor who teaches environmental law.

New Yorksattorney general is accusingExxon Mobil of misrepresenting the risks oilsands operations face as governments move to fight climate change.

Inthe case filed a year ago, the state claims Exxon told investors that it was evaluating projects based on a carbon price that was much higher than the oneused in calculations. That led investors to believe they faced a lower risk and alsoinflated evaluations of Exxons oil reserves.

Exxonhas tried twice to block the case. The companys lawyer, calling the accusations bizarre and twisted,arguedTuesday that Exxon did nothing wrong.

Although the lawsuit deals with a wide array of the multinationals operations, the oilsands feature prominently as Exxon is a major player through its subsidiary Imperial Oil.

In these parts of its business, Exxon often applied a much lower price per ton to a small percentage of its (greenhouse gas) emissions and held those lower costs flat far into the future, court documents say.

What we are watching in the rest of the world

Authorities found 39 people dead in a truck in an industrial park in England and arrested the driver on suspicion of murder in one of Britains worst human-smuggling tragedies.

Police were reconstructing the final journey of the victims as they tried to piece together where they were from and how they came to be in England.

To put 39 people into a locked metal container shows a contempt for human life that is evil, said Jackie Doyle-Price, a member of Parliament who represents the area where the truck was found. The best thing we can do in memory of those victims is to find the perpetrators and bring them to justice.

The truck and the trailer with the people inside apparently took separate circuitous journeys before ending up on the grounds of the Waterglade Industrial Park in Grays, 25 miles (40 kilometres) east of London on the River Thames.

British police said they believe the container went from the port of Zeebrugge in Belgium to Purfleet, England, where it arrived early Wednesday. Police believe the tractor travelled from Northern Ireland to Dublin, where it took a ferry to Holyhead in Wales before picking up the trailer at the dockside in England.

The trucks driver a 25-year-old man from Northern Ireland was arrested on suspicion of murder. He has not been charged and his name has not been released.

On this day in1990

The RCMP announced it would allowIndigenousofficers to wear their hair in braids while in uniform.

Weird and wild

ST. JOHNS, N.L. Animallovers in Newfoundland and Labrador are seeking help for dozens of feral cats facing an uncertain futureas the humansinthe small town where they prowl prepare to relocate.

Residents of Little Bay Islands have voted to resettle the community, andthey have until the end of the year to move before services are withdrawn.

Little Bay Islands, off Newfoundlands northern coast,is one of manyruralcommunities in the province faced with a dwindling population. The 2016 census recorded just 71 people living in the town.

Asresidents grapple with theprospect ofleaving their homes behind, the question of what will happen to theferal felines remains.

Resident Carol Hull estimates there are between 35 and 40 semi-feral catsliving in the community.

Animal welfare groups in other parts of Newfoundland have become involved in the campaign to domesticate and find homes for some of the animals.

Hullis hoping for abump in funding for animal welfare groups willing to take them in.

Your health

TORONTOAnew report from Young Adult Cancer Canada sheds light on such uniqueissues faced by the 22 young adult Canadians, ages 15-39, who are diagnosed with cancer each day.

The study surveyed 622 diagnosed young adults across Canada to explore the physical, social, financial, and emotional challenges they face as compared to their peers without cancer.

It found cancer in young adulthood can disrupt an important period of development and identity formation, which tends to have a cascading impact on all areas of life.

Yet there arefew support programs geared tohelping these patients throughdiagnosis and recovery, the report says.

It also found one of the main issues facing young adults with cancer is financial strain. Treatment and recovery affect their ability to work, and not all treatment costs are covered by public health care in Canada.

The games we play

When softball player and Olympic 2022 hopeful Natalie Wideman was handed a$6,000cheque and told the money came from women she did not know, she was speechless.

I instantly broke down crying, says the 27-year-oldcatcherfrom Mississauga, Ont. In our generation, theres so much stuff being put on women, comparing each other to each other and judging each others choices.

Women helping women is just really, really, special to me.

The money came from Canadian Athletes Now, or Canfund, via a campaign of professional women supporting female athletes.

The 150 Women campaign named for the minimum donation of $150 has cut $6,000 chequesto 109 female athletes in two years. Eight of them have won Olympic gold.

Donors range in age from 18 to 82 with $50,000 the highest single donation so far.

This report by The Canadian Press was first published Oct. 24, 2019.

The Canadian Press

Excerpt from:
The family tree for the tree of life and feral cats; In-The-News for Oct. 24 - CFJC Today Kamloops

This October, focus and awareness are being placed on a health crisis that affects one in every eight women in the United States.

Breast cancer is the second most common cause of death among women in the U.S. For Black women, its even more severe. With a 31% mortality rate, Black women have the highest risk out of all races in the country.

Its not hard to see why talking about breast cancer, telling stories of survival and learning about how it's treated can be life-saving for women. However, women are not the only ones whose lives are turned upside down by breast cancer.

Earlier this month, music executive Matthew Knowlesrevealed he was diagnosed with breast cancer this past July, which he immediately had a mastectomy to treat. Knowles told Michael Strahan in an exclusive interview with Good Morning Americathat he has the BRCA2 mutation gene, which triggers breast, prostate and pancreatic cancer as well as melanoma.

The rest of my life, I have to be very much aware and conscious and do all of the early detection - constant mammograms, constant prostate exams, constant MRIs, for the rest of my life, he said, impassioned by his new awareness and outlook.

Beyonce and Solanges father isnt the first Black male celebrity to be diagnosed with breast cancer: '90s talk show hostMontell Williamsand legendary actor Richard Roundtree were also diagnosed with breast cancer and had mastectomies as a result.

Breast cancer is widely known as a womens disease but still affects over 2,600 men a year, killing around 500 annually, according to data reported by the American Cancer Society. The data also states that much like Black women, Black men are at a higher risk than white men.

American Cancer Society researchers found that young Black men are 76% more likely to die from breast cancer than white men, again, generally because screenings are overlooked.

Once again, being Black at the doctors office proves to be a dangerous game. With our historically damaged trust of the medical community and gaping disparities for preventable and treatable diseases, Black men have to be as diligently aware of their health status as Black women, even for a disease that seems unlikely.

Along with Black men, and men in general, another often-overlooked affected demographic istransgender women. As more transgender women opt to forgo surgery and instead take gender-confirming hormone therapies, their chance of breast cancer increases as well. Based on a case study of 2,260 transgender women, the rate of breast cancer compared to cisgender men was almost 50% higher.

Not only does breast cancer generally fall below the radar of most men, but it also carries a stigma that could deter them. The pink ribbons and female-focused language could be a barrier when it comes to bringing these difficult topics up. Pulling more men into the conversation is another step in the right direction for our entire community.

Despite the rarity in occurrence, breast cancer should absolutely be added to the list of illnesses that Black men remain diligently aware of, not just for their own health but for the health of the children they have or may one day have.

In his public plea for awareness, Matthew Knowles also said his diagnosis prompted his family members to be screened for the BRCA2 gene mutation that caused his breast cancer.

This is genetics, it also means that my kids have a higher chance, a higher risk. Even my grandkids have a higher risk, Matthew told Strahan during his interview, And they handled it like they should, they went and got the test.

According to the Mayo Clinic, genetic testing can be done to screen for the three leading gene mutations that cause breast cancer, BRCA1, BRCA2 and PALB2.

These tests are covered by most insurance companies and even several state Medicaid programs. But the catch is men have to ask the right questions.

Even young Black men should ask their family members about medical history and check with their doctor about risk factors and whether they need to be screened for gene mutations.

Knowing that our symptoms and pain are often overlooked by color-blind doctors, our first line of defense in surviving breast cancer -- no matter what gender, no matter what age -- is to ask questions and stay informed.

Continue reading here:
Everything You Need To Know About Male Breast Cancer In Black Men - BET

The specimens held in natural history collections around the world represent the wealth, beauty and diversity of our planet. But rather than being an objective picture of life on Earth, these collections have long been the result of curatorial bias.

An example of this bias is that there is often an overrepresentation of mammals and birds in collections, despite the far more numerous and diverse invertebrates and plants. What's more, even within these groups there are certain biases in how they were collected.

By looking at the bird and mammal specimens held by five major natural history collections, including those at the Natural History Museum, researchers have been delving into whether there is an underlying sex bias - in others words, whether there were more male specimens in the collections than female ones.

Natural history galleries are often filled with male specimens that have big, showy characteristics The Trustees of the Natural History Museum, London

Dr Natalie Cooper, a researcher at the Museum, led the study which has been published in the journal Proceedings of the Royal Society B.

'We looked at over two million specimen records from the American Museum of Natural History, the Field Museum, Musum National d'Histoire Naturelle, the Smithsonian and the Natural History Museum London,' says Natalie.

'From that we found - perhaps unsurprisingly - that there was a bias towards male specimens. It is worse in birds than in mammals, with only about 40% of bird specimens being females, but around 48% female in mammals.'

Groups which show a particularly pronounced bias towards males are those which the males have ornamentations such as the birds of paradise, hummingbirds, carnivores andartiodactyls, like deer, antelope and cattle.

The disparity between the number of male and female specimens in the collections is not wholly unsurprising - it is often the males that have big, showy characteristics - but it might be expected that more recent scientific collections would try and redress this balance. The data, however, shows that this has not been the case.

This means that, for studies which have used natural history collections in everything - for example, biogeography, morphology, taxonomy, genetics and even parasitology - there is likely to be an underlying male bias in the data.

Females are often under represented in groups such as antelopes The Trustees of the Natural History Museum, London

Showing that there is a skew in natural history collections is one thing, but figuring out where it comes from is just as important.

'We were then interested in trying to work out why there is this bias, because obviously curators don't just throw away the female specimens,' explains Natalie. 'It must be something to do with how they were collected.

'That could be either passive, so something to do with how male and female animals behave in the field, or it could be active whereby collectors are deliberately choosing to target males.'

Male and female animals can and do behave differently in the wild. In some species, for example, males may range more widely and so could be more likely to fall into traps, or maybe their more conspicuous nature means that males are more likely to be spotted.

'It is really hard to collate data on the passive explanations,' says Natalie. 'Although from what we can tell there are not more males in most natural populations. In fact, even though many wild populations are female-skewed, we still find lots more males in the collections, so it does seem like there is some active choice going on.'

If uncorrected, then sex biases can lead to skews in data further down the line The Trustees of the Natural History Museum, London

The data showed that among mammals, collectors were more likely to select large individuals with some form or ornamentation or weaponry such as horns, antlers, mains or tusks. In birds, size was not as important as colouration, as it was the more brightly feathered individuals that were more likely to be collected.

Where you have birds in which the female is more colourful and bigger than the males, however, there are more females than males in the collections.

On the surface, a slight bias towards males in museum collections might not seem like much of an issue. But there are many aspects of a species' biology and behaviour that are affected by an animal's biological sex.

At a basic level, if a study is looking at the taxonomy of a species and there are significant differences between males and females in their morphology, any bias towards the males could result in it being difficult to identify females down to species levels, as females are underrepresented in collections.

These biases can go even deeper. For example, males can be more susceptible to parasites as testosterone inhibits the immune system. Where collections are sex-biased, research looking into infection and immunity within a species could be skewed.

In groups such as the birds of paradise, males frequently have more colourful, elobrate and conspicuous plumage The Trustees of the Natural History Museum, London

As research is advancing into more technical analyses, these biases can cause significant differences. Stable isotope ecology can use the chemicals found in tissue to figure out where an animal may have been living or migrating based on what they were eating during their lifetime. But some species may have sex-segregated diets, meaning that you cannot draw inferences about a species in general if the underlying data is overrepresented by one sex.

'You'd like to hope that visiting researchers would come to the Museum and are selecting specimens with a mind to getting an equal number of males and females,' says Natalie.

'But often when people are doing big studies, they might not even consider the sex. They are more interested in getting as many species represented as possible, or in some cases they might not have a choice due to a limited number of specimens for some species that are available in the first place.'

In the past, hunters often selected those animals with the biggest antlers and horns The Trustees of the Natural History Museum, London

In these situations, researchers simply need to be aware of the skews and build them into their analyses. This is something that is being seen more and more in science, from how crash test dummies have typically been based on the male body to how bulletproof jackets have been designed for men.

One of the most striking biases is seen when looking at type specimens. These are the individual specimens on which a species description is made, and so seen as a typical example of that particular species.

Of these, only 25% of bird and 39% of mammal type specimens were found to be female.

'This bias was found to be way more extreme,' says Natalie, 'but it is also funny because there is a way of fixing it and people don't seem to have bothered to take that option.

'You can have these things called paratypes, which are specimens collected at the same time as the type but will represent other parts of the species diversity. It would seem obvious to me to take an opposite-sex paratype, but people don't seem to be doing that.'

In groups such as hummingbirds, there is a higher porportion of males than females in collections The Trustees of the Natural History Museum, London

Natalie and her colleagues expected that there would be significant sex biases in the early 1800s as trophy hunters went out and selected the biggest and fiercest males, but the team assumed that it would get better over time. It didn't.

'It's exactly the same,' says Natalie. 'It's the most beautiful flat correlation that I've ever seen. It's glorious.'

Museums as whole, it turns out, are simply really bad at recording the sex of specimens in their collections. Of the two million that were looked at for this study almost half were unsexed, even in species where the sex is obvious. So one of the most basic things that could be done is to actually record the sex of an individual in the first place.

Continued here:
There are more male than female specimens in natural history collections - The Natural History Museum

In-The-News is a roundup of stories from The Canadian Press designed to kickstart your day. Here is what's onthe radar of our editorsfor themorning of Oct. 24.

What we are watching in Canada ...

The Alberta government is to table a budget today that will cut program spending by nearly three per cent.

But Premier Jason Kenney, in a TV addresslast night, reiterated that health and education funding will not bereduced and maintaining front-line services is a priority.

"This will be a challenging budget. It willnot be easy," said Kenney, adding the exact reduction figure is 2.8 per cent.

"These are necessary decisions. In fact, I would argue that they are long overdue. We must embrace transformative change to get a smarter government. That's not going to happen overnight."

The budget is the first one by Kenney's United Conservative government since it defeated the NDP in the spring election.

Kenneyhas promisedthe budget will be alandmark spending document that will balance the books in four years andreorient Alberta's economy long after that.

He has pledged to get it done bygetting more value for public money while reducing overall spendingand endinga recent run of multibillion-dollar deficits he says threaten to cripple future generations with unsustainable debt.

Also this ...

A judge in southwestern Nova Scotia is expected to deliver a decision today in the case against aformer police chief accused of sexually assaulting a 17-year-old girl.

John Collyer was the chief of police in Bridgewater, N.S.

He was placed on administrative leave from the Bridgewater Police Service in August 2016 after the province's Serious Incident Response Team confirmed it was investigating the alleged assault.

The 26-year veteran of the force was suspended in May 2017 after the independent police watchdog charged him with one count of sexual assault and two counts of sexual exploitation.

Thecomplainanttestified thatCollyer asked her an inappropriate question while the two were driving in May 2016before puttinghis hand between her legs and assaulting her.

Collyer has denied the accusations.

---

ICYMI (In case you missed it) ...

Scientists have written the family tree for the tree of life.

Years of analysis, released in the journal Nature, has allowed researchersto pinpoint a billion years of evolutionary relationships between plants as different as cannabisand cucumbers, orchids and oaks.

"Everything isinterrelated,"says the University of Alberta's Gane Wong, one of the paper's dozens of co-authors.

Science has known for a long time that species with significant differences can be related through a common evolutionary ancestor. In plants, those relationships have been studied mostly through how they look or behave. Do they have trunks? Flowers? How do their seeds form?

Wong and his colleagues nearly 200 of them have been looking at how the links are expressed through genetics.

The team couldn't resolve everything. They couldn't find branches in the tree for about five per cent of species, either because there wasn't enough data or because it dated from so long ago it couldn't be read accurately.

But the work is already yielding concrete benefits. Proteins taken from an obscure algae species studied by the researchers were found to turn certain brain neurons on and off. Those proteins are now being used in clinical trials to treat blindness.

---

What we are watching in the U.S. ...

Alberta's oilsands are at the centre of acourt battle in New York this week that legal experts say could affect future climate lawsuits in Canada.

"The evidence that's coming out through this case is absolutely relevant to other lawsuits," said Martin Olszynski, a University of Calgary professor who teaches environmental law.

New York'sattorney general is accusingExxon Mobil of misrepresenting the risks oilsands operations face as governments move to fight climate change.

Inthe case filed a year ago, the state claims Exxon told investors that it was evaluating projects based on a carbon price that was much higher than the oneused in calculations. That led investors to believe they faced a lower risk and alsoinflated evaluations of Exxon's oil reserves.

Exxonhas tried twice to block the case. The company's lawyer, calling the accusations bizarre and twisted,arguedTuesday that Exxon did nothing wrong.

Although the lawsuit deals with a wide array of the multinational's operations, the oilsands feature prominently as Exxon is a major player through its subsidiary Imperial Oil.

"In these parts of its business, Exxon often applied a much lower price per ton to a small percentage of its (greenhouse gas) emissions ... and held those lower costs flat far into the future," court documents say.

---

What we are watching in the rest of the world ...

Authorities found 39 people dead in a truck in an industrial park in England and arrested the driver on suspicion of murder in one of Britain's worst human-smuggling tragedies.

Police were reconstructing the final journey of the victims as they tried to piece together where they were from and how they came to be in England.

"To put 39 people into a locked metal container shows a contempt for human life that is evil," said Jackie Doyle-Price, a member of Parliament who represents the area where the truck was found. "The best thing we can do in memory of those victims is to find the perpetrators and bring them to justice."

The truck and the trailer with the people inside apparently took separate circuitous journeys before ending up on the grounds of the Waterglade Industrial Park in Grays, 25 miles (40 kilometres) east of London on the River Thames.

British police said they believe the container went from the port of Zeebrugge in Belgium to Purfleet, England, where it arrived early Wednesday. Police believe the tractor travelled from Northern Ireland to Dublin, where it took a ferry to Holyhead in Wales before picking up the trailer at the dockside in England.

The truck's driver a 25-year-old man from Northern Ireland was arrested on suspicion of murder. He has not been charged and his name has not been released.

---

On this day in1990

The RCMP announced it would allowIndigenousofficers to wear their hair in braids while in uniform.

---

Weird and wild ...

ST. JOHN'S, N.L. Animallovers in Newfoundland and Labrador are seeking help for dozens of feral cats facing an uncertain futureas the humansinthe small town where they prowl prepare to relocate.

Residents of Little Bay Islands have voted to resettle the community, andthey have until the end of the year to move before services are withdrawn.

Little Bay Islands, off Newfoundland's northern coast,is one of manyruralcommunities in the province faced with a dwindling population. The 2016 census recorded just 71 people living in the town.

Asresidents grapple with theprospect ofleaving their homes behind, the question of what will happen to theferal felines remains.

Resident Carol Hull estimates there are between 35 and 40 "semi-feral" catsliving in the community.

Animal welfare groups in other parts of Newfoundland have become involved in the campaign to domesticate and find homes for some of the animals.

Hullis hoping for abump in funding for animal welfare groups willing to take them in.

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Your health ...

TORONTOAnew report from Young Adult Cancer Canada sheds light on such uniqueissues faced by the 22 young adult Canadians, ages 15-39, who are diagnosed with cancer each day.

The study surveyed 622 diagnosed young adults across Canada to explore the physical, social, financial, and emotional challenges they face as compared to their peers without cancer.

It found cancer in young adulthood can "disrupt an important period of development and identity formation, which tends to have a cascading impact on all areas of life."

Yet there arefew support programs geared tohelping these patients throughdiagnosis and recovery, the report says.

It also found one of the main issues facing young adults with cancer is financial strain. Treatment and recovery affect their ability to work, and not all treatment costs are covered by public health care in Canada.

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The games we play ...

When softball player and Olympic 2022 hopeful Natalie Wideman was handed a$6,000cheque and told the money came from women she did not know, she was speechless.

"I instantly broke down crying," says the 27-year-oldcatcherfrom Mississauga, Ont. "In our generation, there's so much stuff being put on women, comparing each other to each other and judging each other's choices.

"Women helping women is just really, really, special to me."

The money came from Canadian Athletes Now, or Canfund, via a campaign of professional women supporting female athletes.

The 150 Women campaign named for the minimum donation of $150 has cut $6,000 chequesto 109 female athletes in two years. Eight of them have won Olympic gold.

Donors range in age from 18 to 82 with $50,000 the highest single donation so far.

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This report by The Canadian Press was first published Oct. 24, 2019.

The Canadian Press

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The family tree for the tree of life and feral cats; In-The-News for Oct. 24 - Airdrie Today