Archive for the ‘Male Genetics’ Category

An elderly woman wears a mask as a precautionary measure against covid-19, as people take their ... [+] daily exercise in Battersea Park in London on March 28, 2020, as life in Britain continues during the nationwide lockdown to combat the novel coronavirus pandemic. - The two men leading Britain's fight against the coronavirus -- Prime Minister Boris Johnson and his Health Secretary Matt Hancock -- both announced Friday they had tested positive for COVID-19, as infection rates accelerated and daily death rate rose sharply. (Photo by Tolga AKMEN / AFP) (Photo by TOLGA AKMEN/AFP via Getty Images)

According to a recent Reuters/Ipsos poll, 54% of women said they were very concerned about Coronavirus. For men, this number was only 45%.

And thats just the beginning. The poll also reported men to be less likely to wash their hands and use hand sanitizers frequently, less committed to avoiding public gatherings, less supportive of the closing of public schools, and more likely to believe people were unnecessarily panicked about COVID-19.

Clearly, men are more cavalier in their assessment of the risk posed by COVID-19. But is this reflective of some underlying wisdom or calculated cost-benefit analysis, or is it another case of male stubbornness? Research in gender psychology suggests that there may be truth to both of these ideas. They are discussed below.

Stereotypes abound regarding the stubbornness of men. Men are less likely to stop and ask for directions when they are lost. They are less likely to take the advice of others. They are more likely to engage in risky behaviors.

And, where theres smoke, theres fire. Research has found men to be significantly less likely to seek out professional help to address mental or physical health problems. Mens reluctance to visit a doctor may be one of the reasons why they tend to die younger than women and why they have a higher mortality rate for 14 out of the 15 most common causes of death.

Even more damning is the finding that men are more likely to refer others to seek out health-related help; they just tend not to take their own advice.

Why is this the case? Part of it has to do with societal expectations. In cultures around the world, men are expected to be strong, dominant, confident, and unemotional. This begins early in their socialization, when boys are taught that real men dont show emotion or ask for help. Over time, this leads to the development of behaviors that negatively impact their health for example, increased substance use, fighting, and risky sexual behaviors.

It may also have to do with underlying male personality traits. Research has found men to be less agreeable than women, and less extroverted. Women also tend to be more cooperative in social and economic situations. Whether or not these trait differences are due to socialization pressures or genetics is an open debate. The most likely answer is that both factors are at play.

In the case of COVID-19, these traits may explain why men are generally less concerned about the disease. In the face of threat, they are expected to exhibit an air of invincibility; it is a trait promoted by culture and society as much as it may be hardwired into their personality.

Theres also evidence to suggest that men are better than women at tapping into their rational mind. For instance, a recent study published in the Journal of Behavioral and Experimental Economics examined gender differences on three brain teasers used to measure a persons ability to engage in reflective, systematic, and non-intuitive thinking. In case you are curious, the questions are listed below and the answers can be found at the end of the article.

If youve reviewed the answers, youll see how these questions assess a persons ability to forgo intuitive yet incorrect responses in favor of correct answers that require a deeper level of thinking.

The researchers examined over 44,000 responses to these questions from 21 different countries. They found clear evidence of a male advantage. They write, We find that: (i) males perform better in every single question, (ii) females are more likely to answer none of the questions correctly, and (iii) males are more likely to answer all three questions correctly. Importantly, gender differences persist even when we control for test characteristics (for example, monetary incentives, computerized, student samples, positioning of the experiment, etc.).

Again, whether there is a genetic component to this difference, or whether it is based solely on environmental factors, is an open debate (and a controversial one). It does, however, suggest that men might be better equipped to size up the COVID-19 risk for what it is: a threat that, in most cases, is still exceptionally remote.

There is a third factor at play, and that has to do with the finding that men might be less equipped to fight off the disease in the event they are exposed to it. This was discussed in a recent New York Times opinion piece, written by Dr. Sharon Moelem. He states, The disproportionate toll this virus is taking on males isnt an anomaly. When it comes to survival, men are the weaker sex. If true, perhaps this tips the scale in favor of the stubbornness hypothesis.

Brain teaser answers:

Excerpt from:
Men Are Less Concerned About COVID-19 Than Women. Is This Due To Reason Or Stubbornness? - Forbes

As citizens of developed nations continue to live longer and longer, dementia cases will begin to appear more frequently.

One in 14 Americans over the age of 65 will experience cognitive decline, and nearly one in six will endure the same at some point in their eighties. Despite the prevalence of the disease, there is a lot we still dont know about its pathology.

Advanced stages of dementia typically follow a series of muted symptoms patients might mistake for less serious conditions, like stress or sleep deprivation. In fact, according to a new study conducted by researchers from Duke University, many of us evidence one of the premiere red flags associated with the illness almost every day.

There has been a misperception that financial difficulty may occur only in the late stages of dementia, but this can happen early, and the changes can be subtle, explained senior author P. Murali Doraiswamy, MBBS, a professor of psychiatry and geriatrics at Duke University, in a media release.

The new paper, published in The Journal of Prevention of Alzheimers Disease, examines the cross-sectional relationship between dementia and financial management skills in the elderly. The strength of the reports findings highlights how limited the diagnostic scope has been up until very recently.

The researchers began with a longitudinal study of 243 adults between the ages 55 and 90 from the Alzheimers Disease Neuroimaging Initiative.

The study pool contained a heterogeneous mix of cognitively healthy adults, adults with mild memory impairment and adults who had been previously diagnosed with Alzheimers disease before recruitment.

After coupling financial literacy tests with brain scans that measured levels of protein buildup of beta-amyloid plaque, the researchers were able to establish a punitive correlation between the two.

On balance, even healthy adults showcased a drop in financial skills as they age, but after controlling for relevant variables the data yielded a direct relationship between increased amyloid plaques (a common predictor of degenerative disease) and a decreased ability to comprehend basic financial concepts, successfully calculated values and effectively balance an account.

Using a multicenter study sample, we document that financial capacity is impaired in the prodromal and mild stages of AD and that such impairments are, in part, associated with the extent of cortical -amyloid deposition. In normal aging, -amyloid deposition is associated with slowing of financial tasks. These data confirm and extend prior research highlighting the utility of financial capacity assessments in at-risk samples, the authors wrote in the report.

These outcomes were consistent among male and female participants.

As covered in a previously published Ladders article, the protein-plaque buildup is a biological inevitability that is not in and of itself instructive of onset cognitive decline. This rule also applies to many of the symptoms mentioned above. Any and each warrant concern when genetics and severity are applied.

Plaque buildup in adults who go on to develop dementia occurs aggressively, as do the pathological substrates associated with it. The problem is diagnosis is more often than not informed by reduced memory capabilityan important feature of cognitive illness but by no means the only reliable one.

Older adults hold a disproportionate share of wealth in most countries and an estimated $18 trillion in the U.S. alone, Doraiswamy continues. Little is known about which brain circuits underlie the loss of financial skills in dementia. Given the rise in dementia cases over the coming decades and their vulnerability to financial scams, this is an area of high priority for research.

Link:
This very common issue could be an early sign of dementia - Ladders

Helen PilcherBloomsbury Sigma2020384 pp.Purchase this item now

Hailing from rare wild mutants, the golden gnu, an uncharacteristically fawn-colored wildebeest, was for the past decade at the center of a speculation bubble in the African trophy-hunting business. Owners of wildlife preserves banked on hunters being willing to part with large sums for the privilege of shooting these beasts, and breeding stock changed hands for up to US$500,000 per animal. The speculators were wrong. The price people were prepared to pay was nowhere near what ranchers had hoped. Prices plummeted and reserve owners were left with herds of worthless mutant wildlife.

This is one of many tales Helen Pilcher tells in Life Changing, the central theme of which is how humans are, more deeply and pervasively than ever before, changing nature. She interprets her brief broadly, loosely weaving together intentional as well as accidental changes, (self-)domestication, conventional breeding, genetic modification (including CRISPR-Cas9), cloning, de-extinction, sterile male and kamikaze-gene techniques, hybridization, contemporary evolution, assisted evolution, conservation genetics, and rewilding.

Pilcher presents these stories in a pleasant, chatty style, garnished with funny asides. Part of the book consists of retellings of stories from other recent books on this topic (13). Still, it covers some new ground and makes for exciting reading, especially when Pilcher gives firsthand accounts of, for example, a captive breeding program for the endangered kkp parrot in New Zealand or an assisted evolution facility for coral at Londons Horniman Museum.

Pilcher tends to skirt around the more challenging parts of her subjects, such as the evolutionary biology of how species have adapted, and continue to adapt, to humans. When her examples involve her own academic field (cellular biology), however, she is on more secure footing. Her tale of the world of horse-cloning techniques and their implications, for instance, is fascinating.

Around 10 years ago, Argentinian polo champion Adolfo Cambiaso produced no fewer than six copies of his favorite mare, Cuartetera. In polo, players can change to fresh horses throughout the game, meaning that Cambiaso can ride multiple clones in a single match.

Toward the end of the book, Pilcher surveys her portfolio of human-induced changes in the worlds species and ponders what their impact will be on ecosystems of the future. She reminds readers of Darwins words that natural selection is immeasurably superior to mans feeble efforts and that there is hubris in thinking that we can fix the environment using technology.

Her chapter on rewilding shows how new ecosystems will appear, as if by magic, if we stop interfering with nature. The Knepp estate in England, for example, where feral pigs play their original role as a keystone species, is now a mosaic of habitats where rare species, once characteristic of the English half-open forest landscape, abound.

Pilcher waxes lyrical about successful attempts to save biodiversity by micromanaging species genetic makeup, as has been done to prevent inbreeding in the precariously small Kkp population. Unfortunately, the vertebrate component of biodiversity is negligible compared with the huge numbers of nonvertebrate organisms that make up the bulk of the food web. To this point, when the remaining wild Kkps entered the captive breeding program, they were dewormed, which probably drove to extinction Stringopotaenia psittacea, the kkps unique tapeworm species. For all its technological prowess, the net biodiversity benefit of the Kkp Recovery Program is probably exactly zero.

While the ultimate impact of intentional modification of species should not be oversold, the unintentional impact of our actions on the worlds ecosystems might be even vaster than Pilcher dares imagine. Forecasting these changes will be impossible, and only time will tell how those ecosystems will look and function.

References and notes1. L. A. Dugatkin, L. Trut, How to Tame a Fox (and Build a Dog) (Univ. of Chicago Press, 2017).2. T. Kornfeldt, The Re-Origin of Species (Scribe, 2018).3. K. van Grouw, Unnatural Selection (Princeton Univ. Press, 2018).

The reviewer is at the Naturalis Biodiversity Center, Darwinweg 2, 2333 CR Leiden, Netherlands.

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Through actions big and small, intentional and unintentional, we are reshaping life on Earth - Science Magazine

Fukami M, Shozu M, Ogata T. Molecular bases and phenotypic determinants of aromatase excess syndrome. Int J Endocrinol. 2012;2012:584807. doi: 10.1155/2012/584807. Epub 2012 Jan 26.

Fukami M, Shozu M, Soneda S, Kato F, Inagaki A, Takagi H, Hanaki K, Kanzaki S, Ohyama K, Sano T, Nishigaki T, Yokoya S, Binder G, Horikawa R, Ogata T. Aromatase excess syndrome: identification of cryptic duplications and deletions leading to gain of function of CYP19A1 and assessment of phenotypic determinants. J Clin Endocrinol Metab. 2011 Jun;96(6):E1035-43. doi: 10.1210/jc.2011-0145. Epub 2011 Apr 6.

Fukami M, Tsuchiya T, Vollbach H, Brown KA, Abe S, Ohtsu S, Wabitsch M, Burger H, Simpson ER, Umezawa A, Shihara D, Nakabayashi K, Bulun SE, Shozu M, Ogata T. Genomic basis of aromatase excess syndrome: recombination- and replication-mediated rearrangements leading to CYP19A1 overexpression. J Clin Endocrinol Metab. 2013 Dec;98(12):E2013-21. doi: 10.1210/jc.2013-2520. Epub 2013 Sep 24.

Shihara D, Miyado M, Nakabayashi K, Shozu M, Ogata T, Nagasaki K, Fukami M. Aromatase excess syndrome in a family with upstream deletion of CYP19A1. Clin Endocrinol (Oxf). 2014 Aug;81(2):314-6. doi: 10.1111/cen.12329. Epub 2013 Oct 18.

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Aromatase excess syndrome - Genetics Home Reference - NIH

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In being released into a South Taranaki river, whio Tipunakore, Trev and Tui made history.

It was a low key event for three juvenile whio blue ducks released to the Kapuni Stream recently - the first release of whio ona South Taranaki river in Egmont National Park.

A previous event with Te Korowai o Ngruahine, Supporting Today's At Risk Teenagers (START) Taranaki, and whio support groupswas cancelled due to Covid-19 risk.

Two male and one female whio were bred at Ng Manu Nature Reserve in Waikanae and taken to a 'hardening' facility at the Tongariro Trout Centre where thebirds provided new genetics to the current population.

The birds join a record number of whio ducklings found by Department of Conservation rangers on eight regularly surveyed rivers.

READ MORE:Whio population boosted by release of three more ducks on Mt Taranaki

The upcoming five yearly whio census scheduled in 2020would determine if overall numbers have increased since 2015.

There are now estimated to be more than 80 whio in the national park.

The released whio - Tipunakore, Trev and Tui - are named after two Taranaki START students now working with the Taranaki Mounga Project, and a supporter of the programme.

Taranaki Mounga project manager Sean Zieltjes saidTrev, one of the students, hadworked with the project for nearly a year.

He wasstokeda whio is named after him, Zieltjes said.

"Trev worked incredibly hard to help protect these taonga.

"Hebuilt over 300 DOC200 stoat traps in his neighbour's carport, and also helped to cut the tracks were these traps are all active on the southern side of the maunga.

"Thanks to Trevhe's protecting whio and giving them the best chance to thrive."

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Juvenile whio ducks take to the water for first time on a South Taranaki river - Stuff.co.nz

Newswise Women undergoing radiotherapy for many cancers are more likely than men to be cured, but the side effects are more brutal, according to one of Australias most experienced radiation oncology medical physicists.

University of South Australia (UniSA) Professor of Medical Radiation, Eva Bezak, says women are generally more sensitive to radiation than men, but this is not considered in international guidelines for radiation dosages.

Current guidelines are generally based on a persons height, weight or BMI, and radiobiological responses of the general population.

In a paper published in Critical Reviews in Oncology/Hematology, Professor Bezak and her colleagues Louis de Courcy from University College Dublin and Professor Loredana Marcu from the University of Oradea in Romania highlight the need for gender to be taken into account when administering radiation.

It is clear that gender plays a role in the occurrence and response to therapy of many diseases, Professor Bezak says.

For example, it is already well established that men are more susceptible to head, neck and blood cancers and women are more prone to auto immune diseases as well as developing osteoporosis.

Scientists also know that individual responses to radiotherapy are up to 80 per cent determined by genetics.

So, where do we start with gendered medicine?

The next step is to ensure that we use both male and female mice even in our pre-clinical testing so we can get a better understanding of how gender influences treatment outcomes.

It is also important to collect data retrospectively so we can compare the radiotherapy outcomes for men and women who were prescribed radiotherapy for the same cancer.

It is a double-edged coin for men, too. Because they are more radio-resistant than women, their healthy tissues are better protected when receiving radiotherapy with fewer side effects, but their long-term survival rates are shorter.

The differences in radiation responses are highlighted by two major events in history: the Chernobyl nuclear reaction disaster in 1986 and the atomic bombings of Hiroshima and Nagasaki in 1945.

Professor Bezak says following Hiroshima and Nagasaki, the incidence of cancer in Japan was much higher in women (58 per cent) compared to men (35 per cent).

Likewise, after the Chernobyl nuclear accident, millions fewer girls were born to irradiated men and women were at greater risk of endocrine imbalance, thyroid cancer and brain tumours.

The one area that does appear to give women some protection against radiation is the female hormone oestrogen, which has a neuroprotective effect during head irradiation.

As healthcare becomes progressively more tailored to the individual, gender is a factor that can no longer be disregarded. It needs to be taken into account as an independent prognostic factor, Prof Bezak says.

A video explaining the differences in radiation outcomes between men and women can be viewed at https://youtu.be/BtDniRA7DMs

Notes for editors

Gender-dependent radiotherapy: the next step in personalised medicine? is published in Critical Reviews in Oncology/Hematology. The other contributing authors are Louis de Courcy from University College, Dublin, and Professor Loredana G. Marcu from the University of Oradea.

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The pros and cons of radiotherapy: will it work for you? - Newswise

TORONTO , March 31, 2020 /CNW/ - The Gairdner Foundation is pleased to announce the 2020 Canada Gairdner Award laureates, recognizing some of the world's most significant biomedical research and discoveries. During these challenging times, we believe it is important to celebrate scientists and innovators from around the world and commend them for their tireless efforts to conduct research that impacts human health.

2020 Canada Gairdner International AwardThe five 2020 Canada Gairdner International Award laureates are recognized for seminal discoveries or contributions to biomedical science:

Dr. Masatoshi Takeichi Senior Visiting Scientist, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan ; Professor Emeritus, Kyoto University , Kyoto, Japan

Dr. Rolf Kemler Emeritus Member and Director, Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany

Awarded "For their discovery, characterization and biology of cadherins and associated proteins in animal cell adhesion and signalling."

Dr. Takeichi

The Work: The animal body is made up of numerous cells. Dr. Takeichi was investigatinghow animal cells stick together to form tissues and organs, and identified a key protein which he named 'cadherin'.Cadherin is present on the surface of a cell and binds to the same cadherin protein on the surface of another cell through like-like interaction, thereby binding the cells together. Without cadherin, cell to cell adhesion becomes weakened and leads to the disorganization of tissues. Dr. Takeichi found that there are multiple kinds of cadherin within the body, each of which are made by different cell types, such as epithelial and neuronal cells. Cells with the same cadherins tend to cluster together, explaining the mechanism of how different cells are sorted out and organized to form functional organs.

Further studies by Dr. Takeichi's group showed that cadherin function is supported by a number of cytoplasmic proteins, includingcatenins, and their cooperation is essential for shaping of tissues. His studies also revealed that the cadherin-dependent adhesion mechanism is involved in synaptic connections between neurons, which are important for brain wiring.

Dr. Kemler

The Work: Dr. Kemler, using an immunological approach, developed antibodies directed against surface antigens of early mouse embryos. These antibodies were shown to prevent compaction of the mouse embryo and interfered with subsequent development. Both Dr. Kemler and Dr. Takeichi went on to clone and sequence the gene encoding E-cadherin and demonstrate that it was governing homophilic cell adhesion.

Dr. Kemler also discovered the other proteins that interact with the cadherins, especially the catenins, to generate the machinery involved in animal cell-to-cell adhesion. This provided the first evidence of their importance in normal development and diseases such as cancer. It has been discovered that cadherins and catenins are correlated to the formation and growth of some cancers and how tumors continue to grow. Beta catenin is linked to cell adhesion through interaction with cadherins but is also a key component of the Wnt signalling pathway that is involved in normal development and cancer. There are approximately 100 types of cadherins, known as the cadherin superfamily.

Dr. Takeichi

The Impact: The discovery of cadherins, which are found in all multicellular animalspecies, has allowed us to interpret how multicellular systems are generated and regulated. Loss of cadherin function has been implicated as the cause of certain cancers, as well as in invasiveness of many cancers. Mutations in special types of cadherin result in neurological disorders, such as epilepsy and hearing loss. The knowledge of cadherin function is expected to contribute to the development of effective treatments against such diseases.

Dr. Kemler

The Impact: Human tumors are often of epithelial origin. Given the role of E-cadherin for the integrity of an epithelial cell layer, the protein can be considered as a suppressor of tumor growth. The research on the cadherin superfamily has had great impact on fields as diverse as developmental biology, cell biology, oncology, immunology and neuroscience. Mutations in cadherins/catenins are frequently found in tumors. Various screens are being used to identify small molecules that might restore cell adhesion as a potential cancer therapy.

Dr. Roel Nusse Professor & Chair, Department of Developmental Biology; Member, Institute for StemCell Biology andRegenerativeMedicine, Stanford University , School of Medicine. Virginia and Daniel K. Ludwig Professor of Cancer Research. Investigator, Howard Hughes Medical Institute

Awarded"For pioneering work on the Wnt signaling pathway and its importance in development, cancer and stem cells"

The Work: Dr. Nusse's research has elucidated the mechanism and role of Wnt signaling, one of the most important signaling systems in development. There is now abundant evidence that Wnt signaling is active in cancer and in control of proliferation versus differentiation of adult stem cells, making the Wnt pathway one of the paradigms for the fundamental connections between normal development and cancer.

Among Dr. Nusse's contributions is the original discovery of the first Wnt gene (together with Harold Varmus) as an oncogene in mouse breast cancer. Afterwards Dr. Nusse identified the Drosophila Wnt homolog as a key developmental gene, Wingless. This led to the general realization of the remarkable links between normal development and cancer, now one of the main themes in cancer research. Using Drosophila genetics, he established the function of beta-catenin as a mediator of Wnt signaling and the Frizzleds as Wnt receptors (with Jeremy Nathans ), thereby establishing core elements of what is now called the Wnt pathway. A major later accomplishment of his group was the first successful purification of active Wnt proteins, showing that they are lipid-modified and act as stem cell growth factors.

The Impact: Wnt signaling is implicated in the growth of human embryos and the maintenance of tissues. Consequently, elucidating the Wnt pathway is leading to deeper insights into degenerative diseases and the development of new therapeutics. The widespread role of Wnt signaling in cancer is significant for the treatment of the disease as well. Isolating active Wnt proteins has led to the use of Wnts by researchers world-wide as stem cell growth factors and the expansion of stem cells into organ-like structures (organoids).

Dr. Mina J. Bissell Distinguished Senior Scientist, Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory; Faculty; Graduate Groups in Comparative Biochemistry, Endocrinology, Molecular Toxicology and Bioengineering, University of California Berkeley , Berkeley, CA , USA

Awarded "For characterizing "Dynamic Reciprocity" and the significant role that extracellular matrix (ECM) signaling and microenvironment play in gene regulation in normal and malignant cells, revolutionizing the fields of oncology and tissue homeostasis."

The Work: Dr. Mina Bissell's career has been driven by challenging established paradigms in cellular and developmental biology. Through her research, Dr. Bissell showed that tissue architecture plays a dominant role in determining cell and tissue phenotype and proposed the model of 'dynamic reciprocity' (DR) between the extracellular matrix (ECM) and chromatin within the cell nucleus. Dynamic reciprocity refers to the ongoing, bidirectional interaction between cells and their microenvironment. She demonstrated that the ECM could regulate gene expression just as gene expression could regulate ECM, and that these two phenomena could occur concurrently in normal or diseased tissue.

She also developed 3D culture systems to study the interaction of the microenvironment and tissue organization and growth, using the mammary gland as a model.

The Impact:Dr. Bissell's model of dynamic reciprocity has been proven and thoroughly established since its proposal three decades ago and the implications have permeated every area of cell and cancer biology, with significant implications for current and future therapies. Dr. Bissell's work has generated a fundamental and translationally crucial paradigm shift in our understanding of both normal and malignant tissues.

Her findings have had profound implications for cancer therapy by demonstrating that tumor cells can be influenced by their environment and are not just the product of their genetic mutations. For example, cells from the mammary glands grown in two-dimensional tissue cultures rapidly lose their identity, but once placed in proper three-dimensional microenvironments, they regain mammary form and function. This work presages the current excitement about generation of 3D tissue organoids and demonstrates Dr. Bissell's creative and innovative approach to science.

Dr. Elaine Fuchs Howard Hughes Medical Institute Investigator and Rebecca C. Lancefield Professor and Head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Cell Biology; The Rockefeller University , New York, NY , USA

Awarded"For her studies elucidating the role of tissue stem cells in homeostasis, wound repair, inflammation and cancer."

The Work: Dr. Fuchs has used skin to study how the tissues of our body are able to replace dying cells and repair wounds. The skin must replenish itself constantly to protect against dehydration and harmful microbes. In her research, Fuchs showed that this is accomplished by a resident population of adult stem cells that continually generates a shell of indestructible cells that cover our body surface.

In her early research, Fuchs identified the proteins---keratinsthat produce the iron framework of the skin's building blocks, and showed that mutations in keratins are responsible for a group of blistering diseases in humans. In her later work, Fuchs identified the signals that prompt skin stem cells to make tissue and when to stop. In studying these processes, Fuchs learned that cancers hijack the fundamental mechanisms that tissue stem cells use to repair wounds. Her team pursued this parallel and isolated and characterized the malignant stem cells that are responsible for propagating a type of cancer called "squamous cell carcinoma." In her most recent work, she showed that these cells can be resistant to chemotherapies and immunotherapies and lead to tumor relapse.

The Impact: All tissues of our body must be able to replace dying cells and repair local wounds. Skin is particularly adept at performing these tasks. The identification and characterization of the resident skin stem cells that make and replenish the epidermis, sweat glands and hair provide important insights into this fountain of youth process and hold promise for regenerative medicine and aging. In normal tissues, the self-renewing ability of stem cells to proliferate is held in check by local inhibitory signals coming from the stem cells' neighbours. In injury, stimulatory signals mobilize the stem cells to proliferate and repair the wound. In aging, these normal balancing cues are tipped in favour of quiescence. In inflammatory disorders, stem cells become hyperactivated. In cancers, the wound mechanisms to mobilize stem cells are hijacked, leading to uncontrolled tissue growth. Understanding the basic mechanisms controlling stem cells in their native tissue is providing new strategies for searching out refractory tumor cells in cancer and for restoring normalcy in inflammatory conditions.

2020 John Dirks Canada Gairdner Global Health AwardThe 2020 John Dirks Canada Gairdner Global Health Award laureate is recognized for outstanding achievements in global health research:

Professor Salim S. Abdool Karim Director of CAPRISA (Centre for the AIDS Program of Research in South Africa), the CAPRISA Professor in Global Health at Columbia University , New York and Pro Vice-Chancellor (Research) at the University of KwaZulu-Natal, Durban, South Africa

Professor Quarraisha Abdool KarimAssociate Scientific Director of CAPRISA, Professor in Clinical Epidemiology, Columbia University , New York and Professor in Public Health at the Nelson Mandela Medical School and Pro Vice-Chancellor (African Health) at the University of KwaZulu-Natal, Durban, South Africa

Awarded"For their discovery that antiretrovirals prevent sexual transmission of HIV, which laid the foundations for pre-exposure prophylaxis (PrEP), the HIV prevention strategy that is contributing to the reduction of HIV infection in Africa and around the world."

The Work: UNAIDS estimates that 37 million people were living with HIV and 1.8 million people acquired HIV in 2017. In Africa, which has over two thirds of all people with HIV, adolescent girls and young women have the highest rates of new HIV infections. ABC (Abstinence, Be faithful, and use Condoms) prevention messages have had little impact - due to gender power imbalances, young women are often unable to successfully negotiate condom use, insist on mutual monogamy, or convince their male partners to have an HIV test.

In responding to this crisis, Salim and Quarraisha Abdool Karim started investigating new HIV prevention technologies for women about 30 years ago. After two unsuccessful decades, their perseverance paid off when they provided proof-of-concept that antiretrovirals prevent sexually acquired HIV infection in women. Their ground-breaking CAPRISA 004 trial showed that tenofovir gel prevents both HIV infection and genital herpes. The finding was ranked inthe "Top 10 Scientific Breakthroughs of 2010" by the journal, Science. The finding was heralded by UNAIDS and the World Health Organization (WHO) as one of the most significant scientific breakthroughs in AIDS and provided the first evidence for what is today known as HIV pre-exposure prophylaxis (PrEP).

The Abdool Karims have also elucidated the evolving nature of the HIV epidemic in Africa , characterising the key social, behavioural and biological risk factors responsible for the disproportionately high HIV burden in young women. Their identification of the "Cycle of HIV Transmission", where teenage girls acquire HIV from men about 10 years older on average, has shaped UNAIDS policies on HIV prevention in Africa .

The impact: CAPRISA 004 and several clinical trials of oral tenofovir led tothe WHO recommending a daily tenofovir-containing pill for PrEP as a standard HIV prevention tool for all those at high risk a few years later. Several African countries are among the 68 countries across all continents that are currently making PrEP available for HIV prevention. The research undertaken in Africa by this South African couple has played a key role in shaping the local and global response to the HIV epidemic.

2020 Canada Gairdner Wightman AwardThe 2020 Canada Gairdner Wightman Award laureate is a Canadian scientist recognized for outstanding leadership in medicine and medical science throughout their career:

Dr. Guy Rouleau Director of the Montreal Neurological Institute-Hospital (The Neuro); Professor & Chair of the Department of Neurology and Neurosurgery, McGill University ; Director of the Department of Neuroscience, McGill University Health Center

Awarded "For identifying and elucidating the genetic architecture of neurological and psychiatric diseases, including ALS, autism and schizophrenia, and his leadership in the field of Open Science."

The Work: Dr. Rouleau has identified over 20 genetic risk factors predisposing to a range of brain disorders, both neurological and psychiatric, involving either neurodevelopmental processes or degenerative events. He has defined a novel disease mechanism for diseases related to repeat expansions that are at play in some of the most severe neurodegenerative conditions. He has significantly contributed to the understanding of the role of de novo variants in autism and schizophrenia. In addition, he has made important advances for various neuropathies, in particular for amyotrophic lateral sclerosis (ALS) where he was involved in the identification of the most prevalent genetic risk factors -which in turn are now the core of innumerable ALS studies worldwide.

Dr. Rouleau has also played a pioneering role in the practice of Open Science (OS), transforming the Montreal Neurological Institute-Hospital (The Neuro) into the first OS institution in the world. The Neuro now uses OS principles to transform research and careand accelerate the development of new treatments for patients through Open Access, Open Data, Open Biobanking, Open Early Drug Discovery and non-restrictive intellectual property.

The Impact: The identification of genetic risk factors has a number of significant consequences. First, allowing for more accurate genetic counselling, which reduces the burden of disease to affected individuals, parents and society. A revealing case is Andermann syndrome, a severe neurodevelopmental and neurodegenerative condition that was once relatively common in the Saguenay-Lac-St-Jean region of Quebec . Now this disease has almost disappeared from that population. Second, identifying the causative gene allows the development of treatments. For instance, his earlier work on a form of ALS linked to the superoxide dismutase-1 gene (SOD1) opened up studies which are now the focal point of phase 2 clinical studies showing great promise.

Byactingasalivinglabforthelast coupleofyears,TheNeuroisspearheading the practice of OpenScience (OS).TheNeurois alsoengagingstakeholdersacross Canadawiththegoal of formalizinganational OSallianceforthe neurosciences.Dr.Rouleau'sworkinOScontributesfundamentallytothetransformationoftheveryecosystemofsciencebystimulatingnewthinkingandfosteringcommunitiesofsharing.InspiredbyTheNeuro'svision,theglobalsciencecommunityisreflecting oncurrentresearchconventionsandcollaborativeprojects,andthemomentumforOSisgainingafootholdinorganizationsandinstitutionsinallcornersoftheearth.

About the Gairdner Foundation:

The Gairdner Foundation was established in 1957 by Toronto stockbroker, James Gairdner to award annual prizes to scientists whose discoveries have had major impact on scientific progress and on human health. Since 1959 when the first awards were granted, 387scientists have received a Canada Gairdner Award and 92 to date have gone on to receive the Nobel Prize.The Canada Gairdner Awards promote a stronger culture of research and innovation across the country through our Outreach Programs including lectures and research symposia. The programs bring current and past laureates to a minimum of 15 universities across Canada to speak with faculty, trainees and high school students to inspire the next generation of researchers. Annual research symposia and public lectures are organized across Canada to provide Canadians access to leading science through Gairdner's convening power.

http://www.gairdner.org

SOURCE Gairdner Foundation

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2020 Canada Gairdner Awards Recognize World-renowned Scientists for Transformative Contributions to Research That Impact Human Health - Yahoo Finance

When it comes to squids, you just can't keep them down.

Not just because they're slippery, but also because they have an incredible genetic editing ability - it lets them tweak their own RNA long after it's left the nucleus.

Here's what that means. Genes, in humans at least, mostly stay unchanging until they're recombined and passed onto the next generation.

This is the same for our messenger RNA (mRNA). Helpful molecules read our DNA, create short little RNA messages, and send them outside the nucleus to tell the rest of the cell which proteins need to be built.

Once that mRNA has exited the nucleus, it's thought the genetic information it carries can't be messed with much - but new research has shown that in squid nerves, this isn't the case.

"We are showing that squid can modify the RNAs out in the periphery of the cell," says Marine Biological Laboratory (MBL), Woods Hole geneticist Joshua Rosenthal.

"It works by this massive tweaking of its nervous system," Rosenthal told Wired. "Which is a really novel way of going through life."

The team took nerves from specimens of adult male longfin inshore squid (Doryteuthis pealeii), and analysed the protein expression, as well as the squids' transcriptome, which is similar to a genome, but for mRNA.

They found that in squid nerves (or neurons), the mRNA was being edited outside of the nucleus, in a part of the cell called the axon.

This mRNA editing allows the squids to finely tune the proteins they produce at local sites (see diagram below). With this finding, squids have become the only creatures we know of that can do this.

(Vallecillo-Viejo et al., Nucleic Acids Research, 2020)

This isn't the first time squids have shown off their genetic editing prowess, though. Back in 2015, a similar team at MBL discovered that squids edit their mRNA inside their nucleus to an incredibly large degree orders of magnitude more than what happens in humans.

"We thought all the RNA editing happened in the nucleus, and then the modified messenger RNAs are exported out to the cell," Rosenthal explains.

But the team showed that although editing is happening in both, it occurs significantly more outside the nucleus in the axon, rather than inside the nucleus.

So, why do squids bother? Why do they need to change their mRNA so much?Well, we don't yet know, but the research team has some ideas.

Octopus, cuttlefish and squids all use mRNA editing to diversify the proteins produced in the nervous system. This could be one of the reasons why these creatures are so much smarter than other invertebrates.

"The idea that genetic information can be differentially edited within a cell is novel and extends our ideas about how a single blueprint of genetic information can give rise to spatial complexity,"the team writes in their new paper.

"Such a process could fine-tune protein function to help meet the specific physiological demands of different cellular regions."

Although right now this is just an interesting genetics study into squids, the researchers think that eventually, this type of system might be able to help treat neurological disorders that include axon dysfunction.

CRISPR has completely changed the game when it comes to editing the DNA inside our cells, and RNA is significantly less permanent and therefore editing it could be less dangerous.

"RNA editing is a hell of a lot safer than DNA editing," Rosenthal told Wired.

"If you make a mistake, the RNA just turns over and goes away."

The research has been published in Nucleic Acids Research.

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Squids Can Edit Their RNA in an Unprecedented Way, Scientists Discover - ScienceAlert

Scientists at the Lewis Katz School of Medicine at Temple University (LKSOM) and Fox Chase Cancer Center show that EGR4, known mainly for its role in male fertility, serves as a critical brake on immune activation. The new study Suppression of Ca2+signals by EGR4 controls Th1 differentiation and anticancer immunityin vivo,published online inEMBO Reports, demonstrates that taking EGR4 away, thus effectively releasing the brake, promotes the activation of killer T cells, which infiltrate and attack tumors and thereby boost anticancer immunity.

While the zinc finger transcription factors EGR1, EGR2, and EGR3 are recognized as critical for Tcell function, the role of EGR4 remains unstudied. Here, we show that EGR4 is rapidly upregulated upon TCR engagement, serving as a critical brake on Tcell activation. Hence, TCR engagement of EGR4/T cells leads to enhanced Ca2+responses, driving sustained NFAT activation and hyperproliferation. This causes profound increases in IFN production under resting and diverse polarizing conditions that could be reversed by pharmacological attenuation of Ca2+ entry, wrote the investigators.

Finally, aninvivomelanoma lung colonization assay reveals enhanced antitumor immunity in EGR4/mice, attributable to Th1 bias, Treg loss, and increased CTL generation in the tumor microenvironment. Overall, these observations reveal for the first time that EGR4 is a key regulator of Tcell differentiation and function.

Other early growth response proteins, or EGRs, are important to T cell activity, but whether EGR4 also has a role in immunity has been largely overlooked, explained Jonathan Soboloff, Ph.D., professor of Medical Genetics and Molecular Biochemistry at the Fels Institute for Cancer Research and Molecular Biology at LKSOM. Our study reveals a new side to the importance of EGR4.

Soboloffs team examined the influence of EGR4 expression in immune cells in collaboration with Dietmar J. Kappes, Ph.D., professor of Blood Cell Development and Cancer at Fox Chase Cancer Center. In initial experiments, the researchers found that T cell activation is associated with EGR4 upregulation. They then showed that knocking-out, or eliminating, EGR4 from immune cells results in a dramatic increase in calcium signaling and expansion of T helper type 1 (Th1) cell populations. Th1 cells, in response to the presence of foreign entities, including tumor cells, activate cytotoxic, or killer, T cells, which then wipe out the invader.

We know from our previous work that T cells control calcium signaling and that when intracellular calcium levels are elevated, calcium signaling can drive T cell activation, Soboloff said.

The Soboloff and Kappes labs next studied the functional importance of EGR4 in cancer immunity by utilizing an adoptive mouse model of melanoma in which some host animals lacked EGR4 expression. Compared to mice with typical EGR4 levels, EGR4 knockout animals showed evidence of expanded populations of Th1 cells and enhanced anticancer immunity. In particular, EGR4 knockout mice had reduced lung tumor burden and fewer metastases than mice with normal EGR4 expression.

In future work, the Soboloff and Kappes groups plan to further explore strategies for EGR4 targeting. The development of an agent to target EGR4 specifically may be difficult, due to the diverse actions of EGR pathways. But eliminating EGR4 specifically from a patients T cells, and then putting those cells back into the patient, may be a viable immunotherapeutic approach, Kappes said.

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Removing EGR4 "Brake" on Immune Activation May Be Viable I/O Therapeutic Approach - Clinical OMICs News

When people talk about Californias legendary cannabis, they frequently mention growing ganja grown deep in the Emerald Triangle and weed sparked up on the bustling streets of Los Angeles and San Francisco. But theres another region in the Golden State that is now demanding attention. Since Californias adult-use cannabis market came online in 2018, Sacramento has exploded onto the scene as a hub of top-shelf indoor cultivation.

Few people in town perhaps only Gov. Gavin Newsom have helped push Sacramento to the top of the cannabis stratosphere more than its cultivators, who are growing some of the best cannabis in the world. But in recent years, one local cultivator has pushed the envelope so far that everyone else in town (and across the state) is now growing the genetics hes helped curate and breed.

As half ofSymbiotic Genetics,The Villagefinds himself among a small group of cultivators giving Sacramentos cannabis a global reach. At one point, there was so much of his Mimosa strain being grown in town, you could have mistaken Sacramento for the brunch capital of the world.

Today, The Village and his breeding partner Budologist are at the top of Hype Mountain. Here is the full story of how he went from budtender to championship breeder leading the City of Trees into the future.

The Village got his start working in 2010 at a medical marijuana dispensary called South Sacramento Care Center for about a year and a half, back in the looser days of Californias medical marijuana market.

I budtended, I vended, it kind of helped me know what was good and what was bad on quality standards, he told Cannabis Now.

When SSCC started their cultivation project in 2011, he knew that was exactly where he wanted to focus his passion for cannabis. He spent a year at the bottom of the ladder as the grunt worker.

I actually lived at the warehouse for four years and I think that really helped me learn a lot as well. Just being there all the time, he said.

The Village spent the first year following orders. Leaf picking and changing reservoirs were common activities. Eventually, as he spent more and more time caring for the plants, he picked up on what he believed to be some flaws in the cultivation process.

I was reading like crazy on all the online forums, just trying to figure out everything, he said. I lived there and I didnt have a life. The Village guessed he would go into the grow room about 20 times a day back then.

Not long after, he took over the whole cultivation facility. Speaking to how he got his nickname, he said that the SSCC workers started calling the facility The Village.

It was just a code word, he said. Instead of saying Hey, were going to the grow, wed say we were going to the village.

A big part of The Villages program in the early years was being the caregiver for numerous patients and growing them a monthly supply of marijuana. He helped supply about a pound of cannabis a month for free to over 15 patients selected to be a part of their compassion program.

We wanted to have them testify if anything ended up in court, but if it were in federal court it wouldnt even matter, The Village said. I thought it was really cool when we started pushing CBD for them once I got a hold of a couple of cuts.

The Village noted that well before he started going public with his brand, he was working with solventless hash enthusiast and medical producer Matt Rize. When Rize would post hash he washed from cannabis provided by The Village, he would list him as a private grower, allowing him to stay anonymous despite the good reputation the product earned.

Me and him had a year or two where we were dropping insane ice wax, The Village said.

Strains like Tangie and Sour Diesel were a hit with everyone lucky enough to score some.

In LA we dropped Tangie for $200 a gram, and it sold out. We only dropped 10 or 20 grams, but the hype was real, and it was crazy, he said.

At this point, The Village still hadnt even started breeding, he was just networking and growing like crazy. He met ET Extracts around that time. ET connected him withBudologist, The Villages eventual partner in crime at their award-winning breeding collaboration, Symbiotic Genetics. Budologist had a Pennywise cut he received from Geek Mike that The Village was keen to add to his stable.

We eventually met up and I got the cut, and we became friends at that point, The Village said. Three or four months later, he went ahead and asked [the breeder behind] Supernova Gardens if he could give me thePurple Punchcut.

A couple of years after they met in 2013, Budologist approached The Village about starting the breeding project that would become the renowned Symbiotic Genetics. Budologist planned to find a Purple Punch male that shared as many traits as possible with the prized Purple Punch female phenos and go from there. After another round of blessings from Supernova, the two built out a two-light breeding room.

It was in the seeds from the original batch that [Supernova] found the clone-only cut, Budologist said. Basically as soon as he gave me the seeds, it gave me the idea I wanted to do breeding. I knew I should pop the seeds and find a male to cross with the female Purple Punch.

Before going on to stabilize Purple Punch in the room and provide seeds to the masses, the first breeding projects featured a Cookies and Cream male Budologist selected. The first crosses in the room which, dont worry, would eventually pump out champions were Cookies and Cream x Forum Cookies and Cookies and Cream x Animal Cookies.

Those didnt work out because we had a lot of [hermaphrodites], and then we started the Punch project right after that, The Village said. We stayed in that two-light room for a while. Then once the Punch took off, when we dropped it, we were like Dang, we dont make enough seeds.

It would end up being roughly two years to get the seeds of the Purple Punch ready after the initial wave of excitement caused by the flower.

They dusted the original elite Purple Punch clone with a male, and then popped 150 seeds. In the process of the Punch propagation, about half of them were males. From the remainder, they narrowed the larger pack down to three of their favorites.

We flowered them out completely. Males, when theyre really towards the end of flower, theyll start putting off resin. You can actually rub that resin. The smell is like what a female would smell like, Budologist said. He also noted that resin will smell just as strong as the resin from a female plant. You can get that sense of what the terps are.

To get down to the three males, they selected phenotypes based on the quality of the bud structure and by picking the ones that had the strongest flavor reminiscent of the female Purple Punch. The seeds from that exceptionally bred Purple Punch hit the wider market in 2017.

The Symbiotic team also crossed the best male with five females, including LA Confidential, Clementine and Tangie.

On one fateful day in 2017, The Village and Budologist named the Purple Punch x Clementine cross Mimosa. In the years since it was released, Mimosa has been seen on podiums and winners lists across the country.

It just feels really good, Budologist said. Its a great thing to see your creation doing well all over the place. Its definitely something that even if people havent heard of Symbiotic Genetics, theyve heard of Mimosa.

The Village says its the teams most famous strain to this day.

Looking towards the future, the Symbiotic Genetics team is building out a new state-of-the-art breeding facility in Sacramento. They also want to get Budologist up to the capitol city full time, so he doesnt have to continue his two-hour commute to participate in the collaboration. Budologist has been working in the corporate world for 12 years as hes simultaneously pursued his plant passion, but he says it is a dream come true to transition full-time to cannabis breeding.

The plan is to get him here, and build an amazing breeding space with multiple rooms, The Village said. Then, well have a pheno-hunting room and a testing room so we can fully test our genetics and not have to send them out to people.

We asked The Village how many times the best phenotype of any given strain had been found by one of the testers he gifted the strain to. He could only think of two occasions where the genetics made their way back to him.

PureMelt gave me his Mimosa pheno. He gave me the Mimosa pheno Exotic Genetix used in their Strawberry line, said The Village. It says Strawberry and Cookies and Cream, but actually, its Mimosa and Cookies and Cream. Its a strawberry-dominant pheno of Mimosa. PureMelt won fourth place at the 2017 Emerald Cup with that one.

Strains from Symbiotic Genetics also took two spots in the top 10 of the personal sungrown cannabis category at theEmerald Cup, the premier competition for Northern California cannabis where many cultivators sell their seeds, in 2018. Their Cherry Punch genetics placed third and Mimosa placed fourth. Now the plan is to produce a lot more seeds. The plan for the new facility is to be able to work with four to five different males at any given time, instead of just the one they previously had the room for.

Well have multiple things going. It will kind of be like the Seed Junky approach where youre just dropping tons of new genetics all the time, The Village said. Were still going to do the whole approach of testing before we release anything. So thats going to slow us down, but once we get stuff stacking, its going to be releasing fast. Im hoping every six months well have a new line.

The essential shift now occurring within Symbiotic Genetics is that its two leaders are no longer thinking about cannabis breeding as a hobby.

We feel like the skys the limit once we have the financial backing, once we have the space to work the types of things we can do, said The Village. We created Mimosa and all these strains with two lights in a small-*ss room.

The potential was more evident than ever at last years Emerald Cup. People traveled from places like Argentina, Spain and Brazil just to get their hands on Symbiotics prized seeds.

Currently, The Village is sitting on over 70 cuts for when things go into full gear, including some of his own phenos and some of the GMO andWiFi Mintsother people have given him. He said hed most like to add to his collection those old OGs you kind of dont see theyre hard to get verified.

Over the years, The Village said he has gotten his hands on things he thought were old school OG cuts, but they never were what was claimed.

I have the Legend, Paris, the Lemon Fuel fromAlien Labs, he said. I mean I could be totally wrong, but they all seem like theres not a big difference between those three.

His theory is that OG is so finicky that it needs a much different environment compared to other strains in order to express its full character.

I think OGs express themselves more if you keep it a little warmer, he said. If you dont, it stays in a state where its unexpressed. So they kind of look the same, but theyre not fully able to push out the characteristics of what they are. So thats my kind of thing.

Other targets for the collection include Chem 91 and Super Silver Haze.

Theres a lot of new stuff I think is amazing, but Id like to go back to the roots, The Village said. He added that this emphasis on old-school cannabis is why Symbiotic Genetics recently pollinated an bunch of different females with a Kombucha male (a cross of Sour Diesel and a Purple Punch F2) featuring the old-school diesel flavor. Thats why we did the Kombucha line, to bring the Sour Diesel back in a new kind of way, he said. Our male we selected was very diesel-dominant.

Like many other cultivators who have been growing cannabis in California since before the 2018 adult-use regulations came down, The Village has been struggling to adapt to the new Golden State. In early 2019, The Villages old facility was shut down right before he was preparing to do a giant Banana Punch propagation because he hit a licensing snafu around the old building.

I mean, it sucks, The Village said. There are a lot of people that are being held back because of licensing. Its just so new to everyone. Were all learning and some of the cities are easier than others.

The Village says a lot of people already had grows that were dialed in to fit the states tight restrictions. But permitting a space youve already been using is hard. Most of the time you give [the states cannabis regulators] plans and they approve it. Well, now youre giving them plans that are already built, so if they dont approve it, then you essentially have to shut down to make those changes, he said.

The Village and Budologist knew they didnt want to do a patchwork job and decided they were just going to do a complete rebuild of the facility instead of a smaller remodel. Theyre now on the hunt for a partner to help fund the effort.

We could have done it ourselves, but it would have been cutting corners because we dont have the capital that you need to build one of these facilities, The Village said.

The Village recognizes certain challenges of the legal market, but were not living in the shadows. When I lived at the warehouse I was very fearful of getting raided. It was scary. But now I guess the only thing you have to worry about is thieves.

And those plotting against the Sacramento cannabis industry have been a major concern as of late. Due to the cannabis industrys lack of banking access, dispensaries are forced to horde large piles of cash to pay taxes. All this money has proven too tempting, and with Sacramentos rise to cannabis prominence, it became an even bigger target.

The Village says its particularly bad at the moment. At the end of the summer in 2019, one of the dispensaries he works with got hit by thieves, and numerous farms have been targeted, too. One night, two different facilities were hit. One dispensary lost $37,000 in four minutes.

Despite the rough nights, things are generally going well for Sacramentos cannabis scene. Its cultivators continue to travel up and down the states highways, returning with every trophy in the game. And when the Cannabis Cup visited Sacramento for the first time as a legal event in 2018, locals stole the show.

Sacramento is awesome, Budologist said. I think there is a lot of competition, which I think is the best thing because competition makes you work harder.

He believes Sacramentos population is open enough not to look down on the industry. Its definitely something people arent as embarrassed about, you know? he said.

While the short term has a bit of mystique to it, The Village, Budologist and their work at Symbiotic Genetics are not going anywhere. We look forward to continue watching them push the bar when it comes to exciting new cannabis genetics.

TELL US, have you tried the Mimosa strain?

Originally published in Issue 40 of Cannabis Now.LEARN MORE

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It Takes The Village - Cannabis Now

An older male influence in your family might have something to do with your sexuality, a study suggests.

According to a study published in journal Proceedings of the Royal Society B, research has revealed that having an older brother increases mens chances of being homosexual.

The studys researchers analyzed 10 separate sexual orientation studies that involved 5,400 men with info regarding their birth order.

The study revealed that men with older brothers have a 38% higher likelihood of being gay compared to men who dont have an older brother.

(Older) brothers increase the probability of homosexuality in later-born males, the study noted.

The information presented also showed that the more older brothers a man had, the higher chance that he would be homosexual. The study stated having three older brothers doubled a mans chances of being gay.

The study also found that mothers of homosexual males bear more children compared to mothers of heterosexual males.

David Spiegelhalter, a statistician and professor at the University of Cambridge, told the Daily Mail that the fascinating study estimates that having an older brother increases the odds of being gay by 38%, supporting the idea that a mothers immune response to having a male child influences subsequent boys.

People have endlessly argued about the possible roles of genetics and upbringing, but this clear result fits in neither category, he said.

The researchers failed to find a connection between sexuality and birth order for women, noting theres no pattern of siblings, their gender or age that would help determine whether a female would be a lesbian.

Much prior research has shown that females do not influence the sexual orientation of their younger siblings, and females sexual orientation is not affected by their numbers of older siblings, study author Dr. Ray Blanchard stated in an interview with the Daily Mail.

The studys authors state they arent sure why their findings are the case, stating they believe it may be attributed to a theory known as maternal immune hypothesis which believes women who give birth to male babies develop antibodies that impact brain development of future male children they have.

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Boys with older brother more likely to be gay: Study - The London Free Press

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One morning in 2005, Shelley Beverley woke up to find that she had gone deaf. She was 21, and living in Johannesburg with her older brother Neil. I was very scared, she says. It was just so sudden. She struggled through the rest of the day, hoping that her hearing would come back, but it didnt. In one sense, her hearing loss wasnt entirely a surprise: Beverleys grandmother had been deaf, Neil had lost his hearing when he was 13, and her mum, Mary, had lost hers when she was 32. We knew it ran in the family, she says, but I thought Id been lucky and not inherited it.

Beverley, 35, lives in Margate, a semi-rural district south of Hobart, with her husband James. The couple migrated to Australia from South Africa in 2010, looking for space, buying 2 hectares of lush green grass at the foot of a forested ridge near the mouth of the Derwent River. We love the wildlife here, says James, looking out the living room window. Weve seen pademelons, echidnas, quolls, blue-tongue lizards, even a Tassie devil. At dusk, hundreds of kangaroos emerge from the forest to gorge on the grass. Its very peaceful, says James. Its really helped us after everything thats happened.

Apart from their deafness, Beverleys family had largely enjoyed good health. Then, in September 2015, her mother, Mary, then 62, started experiencing fatigue and stomach pain. Doctors in Durban ordered a colonoscopy, but the procedure made her worse. Her feet became swollen and purple. Because of their hearing problems, Shelley and Mary had communicated mainly in text messages. But soon I began noticing that her wording got a bit funny, says Beverley. It didnt always make sense.

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Beverley flew to Durban in February 2016, but by that time her mother could no longer talk or walk. She was so weak that she couldnt move her hands or lift her neck. Two days after Beverley arrived in Durban, her mother caught a virus that caused fluid to build up on her lungs. The doctors tried unsuccessfully to drain it. Shortly afterwards, she died. She weighed just 36 kilograms. It was so fast, Beverley says. And we were still in the dark about what she had.

Shortly before Marys death, Neil had also fallen ill. He developed a number of mysterious symptoms, including facial twitches and seizures. He kept falling over and tripping, and experienced vomiting and headaches so severe he lost his vision for weeks at a time. His behaviour became strange showering with his clothes on, and hallucinating.

One day, Dad was driving him around and Neil started talking to all these little people he thought were around his feet, says Beverley. Doctors in Durban had trouble diagnosing him, so they sent a biopsy to London, where he was found to have a type of mitochondrial cytopathy one of a large family of chronic and progressive diseases that affect the muscles, brain and nervous system. As the family soon learnt, the condition has no cure and no effective therapies. One of the common early symptoms is hearing loss.

Neil died in June 2017, aged 34, by which time Beverley had discovered she also had the condition. It was fear, so much fear, she says. She began experiencing symptoms, including migraines and vision loss. She has since developed diabetes, hypertension, gastro-paresis (when your stomach muscles dont work), and pharyngeal dysphagia (difficulty swallowing). Every time I get sick now, the flu or something, I think, When am I going to need a wheelchair or a feeding tube? When will my legs stop working?

Mito has taken everything from me, she says. If I die, at least James will still have a part of me.

Beverley has bright blue eyes and long, straight, ash-brown hair. Shes got a lazy left eye and uncommonly pale skin, which she attributes to her condition. Oh, and I had bunions out in 2010, she says, laughing wryly.

She doesnt know how long shes got left, but she is determined to make it count. She has joined mito awareness groups, and is an active member of the Mito Foundation, which supports sufferers, and funds research. She has exhaustively researched the condition and takes every opportunity to educate doctors. Youd be surprised by how little they know about it, she says.

But her overriding focus has been on a cutting-edge, and currently illegal, procedure called mitochondrial donation, a form of IVF which would allow those with the condition to have children, safe in the knowledge they would not be passing it on. Mito has taken everything from me, she says. If I die, at least James will still have a part of me. I would like him to look at our child, and say, You have your mums smile or your mums eyes.

An IVF treatment known as mitochondrial donation could potentially save up to 60 Australian children a year from being born with the condition. Credit:

Mitochondrial donation has been labelled immoral and unethical, a slippery slope to designer babies, not to mention potentially unsafe. The only country in the world to have legalised it is the UK. A report by medical experts into the technologys potential application in Australia is due to be delivered to Health Minister Greg Hunt this month.

This fight is really personal to me, Beverley says. Short of a cure, people with mito should at least have the option of having healthy children.

Mitochondria are microscopic structures in human cells that provide the body with energy. For this reason, they are often described as the cells powerhouse. They are crucially important: if your mitochondria fail or mutate, your body will be starved of energy, causing multiple organ failure and premature death.

A stylised representation of a mitochondrion, which provides the body with energy. Malfunction can lead to organ failure and death.Credit:Josh Robenstone

Mito, which is maternally inherited, usually affects the muscles and major organs such as the brain, heart, liver, inner ears, and eyes. But it can cause any symptom in any organ, at any age. Indeed, the term mito includes more than 200 disorders, the symptoms of which are maddeningly varied and seemingly unrelated, leading to delayed diagnoses or incorrect diagnoses or, indeed, no diagnosis.

Many of these people have been fobbed off by doctors or laughed off by people who think they are hypochondriacs, says Dr David Thorburn, a mitochondrial researcher at the Murdoch Childrens Research Institute, in Melbourne, who has diagnosed some 700 cases over the past 28 years. Most people are relieved to finally know what it is, because that is the end of that part of their journey.

Its sometimes said babies produced as a result of mitochondrial donation would have three parents the mother, the father, and the donor.

Up to two million people worldwide have some form of mito. - Others, like Beverley, who have a less severe type of the disease, will get adult onset, and can expect to become ill in their 30s, 40s or 50s.

According to Thorburn, One of the things that most dismays families with mito is the lack of control they have over passing the condition down to future generations of their family.

Remaining childless is one way to stop the condition from being passed down, as is adopting, but as Thorburn acknowledges, There is an innate desire in many individuals to have their own children. For these people, mito donation offers the very real prospect that the condition is eliminated from future generations.

Mitochondrial replacement is a highly specialised procedure, requiring a level of manual dexterity sufficient to manipulate a womans egg, which is roughly the width of a human hair. Within that egg is a nucleus, where a persons genes are located, and the cytoplasm, the jelly-like substance that surrounds it. Mitochondria are found in the cytoplasm.

Mitochondrial replacement involves taking a donor females healthy egg, removing its nucleus and replacing it with the nucleus of the woman affected by mitochondrial disease, but whose nucleus is healthy. The egg is then fertilised using her partners sperm. (Another option is to fertilise the egg first, and then swap the nucleus.) The resulting embryo is then implanted into the mother.

Researcher David Thorburn: "Mito donation offers the very real prospect that the condition is eliminated from future generations."Credit:Josh Robenstone

Since more than 99.9 per cent of our genes are found in the eggs nucleus, which remains unaffected, the procedure will have no impact on the childs height, hair colour or mannerisms. Despite that, its sometimes said that babies produced as a result of mitochondrial donation would have three parents the mother, the father, and the donor.

The technology has been tested in mice for more than 30 years, but only since 2009 has research been done on human embryos, mainly in the UK. Almost from the start, the research was subject to sensational headlines about scientists playing God, and the possibility of genetic engineering, with much of the hysteria being fuelled by anti-abortion groups. The Catholic Church described it as a further step in commodification of the human embryo and a failure to respect new individual human lives.

In 2012, the Human Genetics Alert, an independent watchdog group in London, wrote a paper comparing any baby produced with mitochondrial replacement to Frankensteins creation, since they would be produced by sticking together bits from many different bodies. According to the Conservative British MP Jacob Rees-Mogg, the procedure was not a cure for disease, it is the creating of a different person.

Regulators subjected the technology to four separate scientific reviews, together with rounds of ethical debate and community consultation. In 2015, the UK Parliament voted to legalise the technology for use in humans, on the proviso that it only be available to those women at high risk of passing on the disease. Since then, 13 couples in the UK have received the go-ahead to undergo the procedure.

Its unclear how many children, if any, have been born: the parents have asked that details not be published. Meanwhile, scientists like Thorburn wait eagerly for news of any developments. I know the UK researchers well and have asked several of them, and they are keeping completely quiet about it in respecting the families wishes, he says.

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If there have been babies born in the UK using the procedure, they arent the first. In April 2016, a child was born using the technique in Mexico, to a Jordanian mother who carried a fatal mitochondrial condition known as Leigh syndrome. The doctor in charge, an American fertility specialist called Dr John Zhang, later admitted that he had gone to Mexico because the procedure is illegal in America. In Mexico, he admitted, There are no rules.

Even those who want mitochondrial donation legalised in Australia concede that much remains unknown about the procedure. Its long-term risks can only be understood through lifelong health check-ups, but this is impossible until any children conceived via this procedure become adults. Implications for subsequent generations also remain unclear.

No medical procedure is 100 per cent safe, says Sean Murray, CEO of the Mito Foundation. But we think we are at the stage now where the benefits of the technology are greater than the risks.

One of the issues around safety concerns the compatibility of the donors mitochondria with the recipients nuclear genes. A 2016 study in mice suggested that mismatched mitochondria affected their metabolism and shortened their lives. Another concern is known as carryover, whereby a tiny amount of mutant mitochondria is inevitably transferred from the affected mothers egg into the donor egg during the procedure.

Instead of it being wiped out, the mutation might then reappear in the descendants of any girls born as a result. For this reason, some people have proposed that the procedure be restricted to male embryos only, but this raises all kinds of ethical issues around selective breeding and sex selection.

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Indeed, it often seems as if the term ethical minefield was coined especially with mitochondrial donation in mind.

My primary ethical concern has to do with the sanctity of human life, says Father Kevin McGovern, a Catholic priest and member of the National Health and Medical Research Councils Mitochondrial Donation Expert Working Committee.

If mitochondrial donation is permitted here, the technique most likely to be used is pronuclear transfer, which requires that both the donors egg and the affected mothers egg be fertilised. [This is to ensure that both eggs are at the same developmental stage.] But once the nucleus is removed from the donors fertilised egg, it is discarded. For people who believe that life begins at conception, this is akin to murder. You are creating two lives and destroying one for spare parts.

The Catholic Church has consistently opposed mitochondrial donation. In a Senate inquiry into the technology in 2018, Dr Bernadette Tobin, director of the Plunkett Centre for Ethics at the Australian Catholic University, suggested the process was intrinsically evil.

The inquiry also heard from Father Anthony Fisher, Catholic Archbishop of Sydney, who raised concerns about the moral right of the child to know how he or she was conceived the problem of what he called genealogical bewilderment and the donors right to remain anonymous. He also worried that women might effectively become egg vending machines: The availability of human ova is often assumed when people talk about reproductive technology as if they were somehow there in a cupboard to be used. In fact, it means women have to be used to obtain these eggs. They are extracted by invasive procedures that do carry some risk.

A report by medical experts into mitochondrial donation and its potential application in Australia is due to be delivered to Health Minister Greg Hunt this month. Credit:Alex Ellinghausen

Equally troubling for the Australian Catholic Bishops Conference, the peak national body for the churchs bishops, was the fact that mitochondrial donation involved conceiving babies not by marital intercourse [but by] a technical procedure.

Most of these concerns are redundant, argues the Mito Foundations Sean Murray. We already have a well defined regulatory framework for dealing with all this, he says. As far as the donors right to remain anonymous, we would defer to the appropriate federal or state and territory regulations that apply for sperm or egg donations. In regard to a kids right to know they had a mitochondrial donor, societally there seems to be a preference to inform kids. Its important for them to understand their genetic lineage.

Then theres the matter of consent. The parents can wrestle with the ethical issues and weigh up all the risks, but the only person who cant consent to the procedure is the unborn child. Well, says Murray, they cant consent to being born with mito, either.

The Mito Foundations Sean Murray: "In regard to a kids right to know they had a mitochondrial donor, societally there seems to be a preference to inform kids."Credit:Joshua Morris

Murray, 47, is one of the founding directors of the Mito Foundation, which was established in Sydney in 2009. Mito runs in my family, he says. My older brother, Peter, died of it in 2009 at 45, and my mum passed away in 2011, at 70. What people often dont understand is that even in families that have mito, each member can have different mutational loads basically, different amounts of bad mitochondria. Peter got a high load, but I didnt. Thats why Im still here.

A computer scientist by training, Murray now works full-time on the foundation. Much of his job involves travelling around the country, explaining mito to politicians, journalists and philanthropists, raising funds for research and, most crucially, advocating for a change to the laws.

Mitochondrial donation falls foul of two pieces of legislation: the Research Involving Human Embryos Act 2002, and the Prohibition of Human Cloning for Reproduction Act 2002. The laws prohibit the implantation of a human embryo that contains more than two peoples genetic material. The laws were subject to a mandatory review in 2010, but the then Labor government recommended they remain the same.

In 2013, the Mito Foundation urged the government to revisit its decision. Two years later, it began lobbying in earnest. What we tried to get across was that the science around mito donation has come a long way since 2010, says Murray. Also, the process that the UK went through to legalise it really reassured us that the procedure is safe and effective.

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In the past five years, Murray and his colleagues have consulted with more than 100 MPs and senators. Only one of them, according to Murray, said I dont like this. They have also talked to dozens of industry experts, including academics and medical and research bodies, about the benefits of mitochondrial donation. Most of them get it straight away, he says. We are talking about a technique that will prevent the chance of having a morbidly ill child.

Now, a breakthrough appears imminent. In February 2019, Health Minister Greg Hunt asked the National Health and Medical Research Council to look into the matter, review the science and conduct public consultation. The NHMRC is due to hand its report to Hunt this month. The expectation among the mito community is that he will recommend the laws be changed. Any proposals would then need to be debated in Parliament, where issues around reproductive medicine have, in the past, been hotly contested.

Murray expects some opposition from more conservative MPs, but nothing like the rancour seen in the NSW Parliament during last years debate over legalising abortion. Shadow health minister Chris Bowen has, for his part, said that Labor will support changing the laws.

Mitochondrial sufferer Shelley Beverley at home in Tasmania. This fight is really personal to me. Credit:Peter Mathew

Whether this will help people like Shelley Beverley is unclear. If Hunt gives it the green light, it will take two years at least for mitochondrial donation to become available to prospective parents, given the time involved in drafting and passing legislation, establishing a regulatory regime and getting doctors up to speed with the technology.

This will probably be too late for Beverley. I really only have about a year left to give it a go, she tells me. After that, my symptoms may progress and biologically things get worse after 35. She says she would consider going to the UK for the treatment, but that at present they are not accepting international patients.

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In the meantime, she watches TV, and reads a little, but not too much. (It puts me to sleep.) She gardens: she has a bed of huge white and pink roses out the back of her house, as a memorial to her mother and brother. And she eats. James cooks for me. He lets me choose the best meat and potatoes! Ive put on weight since I met him. She describes James as something close to an angel. He will listen to every problem I have or feeling I experience. He will always put me first.

Beverley started going out with James when she was 21, right around the time she first went deaf. I was so scared that he wouldnt like me as much. I remember calling him and saying I was scared he would leave me. But James is still here. Im very lucky to have him, she says. If I go, I want him to have a part of me.

To read more from Good Weekend magazine, visit our page at The Sydney Morning Herald, The Age and Brisbane Times.

Tim Elliott is a senior writer with Good Weekend.

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How far should genetic engineering go to allow this couple to have a healthy baby? - Brisbane Times

Elise Robinsons newest office mates are a ficus tree, its broad variegated leaves enjoying the light from a narrow window, and a pair of small succulents perched one above the other at the edges of bookshelves. And these are just a fraction of what Robinson has in her home in Wellesley, where an expansive sunroom mullioned windows on three sides, skylights above hosts a grove of citrus at one end (plus the worlds smallest olive tree on the windowsill) and a table with pots of everything from paperwhite narcissus bulbs to a Norfolk Island pine tree at the other.

This was Robinsons childhood ambition to have a house full of trees. The other was to understand how people make sense of the world, a question that has informed much of her autism research.

Growing up, I was very interested in the way people think and the way they relate to numbers and numeric logic, says Robinson, an institute member at the Broad and assistant professor of epidemiology at Harvard University. At the time, she did not know the technical term to describe this: causal inference. But even so, her work like her habitat still reflects an adult version of who I was at 8.

Robinson also brings the expansive gaze and imagination she exhibited early on to her pursuit of science. Whereas many autism researchers are experts in their own arenas studying genes exclusively, for example, or deeply characterizing autistic peoples traits Robinson is a geneticist with a deep understanding of the conditions clinical presentation.

Elise recognized both sides of the equation as being important, says Mark Daly, Robinsons postdoctoral advisor and director of the Institute for Molecular Medicine Finland at the University of Helsinki. She has really managed, I think in ways that havent been done very effectively before, to bring expertise on both sides together.

This ability led Robinson to explore the interplay between the different types of genetic variants that contribute to autism and to lead a study that aims to bring African populations into autism research on a scale no one has attempted before. This study, with scientists across three continents, is one of my favorite things about my job, she says. It was this beautiful blending of really nice, constructive, productive working relationships with people who are approaching it with different skills.

Robinson is among the few autism researchers who could pull off this cross-disciplinary project. Over the course of her career, she has switched fields multiple times, ranging from anthropology to epidemiology and digging into genetics only when she was already well into her postdoctoral work. Her generous and calm work style, as well as her shrewd experimental designs, have made her a sought-after collaborator. Somer Bishop, one frequent collaborator, told Robinson she wanted to talk on the phone at least once a month. I dont care what we talk about, says Bishop, associate professor of psychiatry at the University of California, San Francisco. Every time I have a conversation with her, I feel like, We can do this we can figure this out together.

Robinson grew up in Kensington, Maryland, a suburb of Washington, D.C. Her mother was an elementary school teacher and her father a lawyer. Her younger sister is also a lawyer, as is Robinsons husband, Tom Byron. Robinson, too, has a way of choosing words carefully when she speaks that could be described as lawyerly precise and persuasive.

As a child, though, her favorite subject was mathematics. When she entered college at Dartmouth University in Hanover, New Hampshire, in 2001, she assumed she would major in mathematics or science, but she struggled to succeed in the formal, lecture-based classes. The things that made grade school and high school unpleasant for me just made college really, really difficult, she says.

She discovered anthropology by luck during her second year and loved it: The discipline played to her strength at working independently. Plus, I just liked it, she says, in a conspiratorial half-whisper. She immersed herself in trying to understand how people make sense of numbers and facts to develop beliefs about causation, questions she had pondered since childhood.

By the time she graduated from Dartmouth, she was ready to do what she describes as more activist research. She enrolled in a masters program in public health at Emory University in Atlanta, Georgia, where she investigated ways to minimize geographic disparities in access to services for people with developmental conditions. Through those two years, she says, I figured out that what I really like is statistics.

She specifically became interested in analyzing the heritability of social skills and autism traits. So she pivoted again, this time to a program in psychiatric epidemiology at Harvard. Her advisor there, epidemiologist Karestan Koenen, connected Robinson to other researchers including Angelica Ronald of Birkbeck University of London in the United Kingdom who had access to data from twin registries and long-term studies of child development.

Robinson immediately showed initiative and leadership that Koenen says is rare in someone at such an early stage of their career.

She showed the independence, and ability to initiate, and ability to lead these collaborations in a way that was Im not sure Ive seen it, Koenen says. Robinson finished the degree in three years instead of the more typical four or five. (Koenen is now another of Robinsons office mates, sharing space with the ficus and succulents.)

After finishing her degree, Robinson stayed at Harvard. Officially, she was a postdoctoral researcher mentored by Susan Santangelo, though she also continued to work closely with Ronald using data from those British studies. In 2013, one of Robinsons analyses yielded some of the strongest evidence then available to support the female protective effect, a leading hypothesis to explain the skewed sex ratio in autism.

No one had really looked at [the female protective effect] as a quantitative trait, in spite of knowing thats a more powerful method, says Stephan Sanders, associate professor of psychiatry at the University of California, San Francisco, and one of Robinsons collaborators. The study was emblematic of Robinsons ability, he says, to distill big questions down to a testable hypothesis and then do a really good study about it.

There was one more turn to come in Robinsons path. One day in 2011, she got drawn into a scientific debate with a postdoctoral researcher in Dalys lab, psychiatric geneticist Benjamin Neale. No one remembers what the debate was about, but it got so heated that at some point they called Daly in to referee. Daly and Robinson got to talking and realized they were both interested in the idea of autism as one end of a continuum of typical traits. She joined his lab as a postdoctoral researcher not long after.

Robinson knew she was entering one of the top labs in the highly competitive, male-dominated field of psychiatric genetics, and with no prior training in genetics. But she was unflappable, Daly says. He attributes Robinsons ease in the situation to the fact that she was not driven by her ego or to score intellectual points: She just wanted to learn at her own pace and pursue questions that interested her.

For the statistically minded Robinson, dealing with genetic variants was not a huge scientific shift. Its really just a different kind of x variable, she says. Plus, as she sees it, genetics provides the cleanest, most powerful approach to her long-time interest in establishing cause and effect.

As her familiarity with genetics ramped up, Robinson contributed to a massive analysis showing that genetic variants linked to autism affect social and communication skills in the general population. She also mined data from existing studies to tackle one of the thorniest problems in autism genetics: the relative contributions to autism of rare and harmful spontaneous mutations versus common and mild inherited variants.

Soon after joining Dalys lab, Robinson began working with him on a grant application that enabled her to set up her own lab in 2013. The following April, she had her first child, a daughter; three years after that, she was named assistant professor of epidemiology and had a second daughter. Her other achievement of 2017 was the debut of a statistical method she had developed called the polygenic transmission disequilibrium test. Neale remembers Robinson leaping up in excitement when she realized the method could be a better way to investigate common variants linked to autism.

In the study, Robinson and her colleagues analyzed genetic data from more than 6,000 families to show that children with autism inherit more common variants associated with the condition than would be expected by chance. Robinson had been skeptical this would be the result. But as someone more interested in finding the correct answer than in proving she had been right all along, she welcomed the experience. That was a productive exercise, she recalls, laughing. I had a nice time figuring out that I was wrong.

For the first time in her career, she has also embarked on collecting genetic and clinical data, from more than 5,000 people in Kenya and South Africa1. Robinsons involvement expanded the projects scope and ambition, says its research director, Victoria de Menil. Before she was leading, the study was going to be much more opportunistic, de Menil says, and the researchers planned to collect brief, categorial data on a few variables. When [Robinson] came on board, she had this conviction that we needed to be doing very deep phenotyping.

That meant taking several months to identify detailed questionnaires that would yield reliable results, hiring additional staff members to administer the surveys and asking participating families for more of their time. Since late 2018, the team has collected data from about 1,000 participants.

Back in Boston, Robinson is also developing a lab that falls in line with her sensibilities. She tends to attract people who have backgrounds as unconventional and diverse as her own and gives them plenty of independence.

If you saw all of us present our research, it would seem very disparate and all over the place, but then Elise can put it all together and show how we are all working for a common goal, says Caitlin Carey, a postdoctoral researcher in Robinsons lab.

Robinson also encourages her lab members to maintain hobbies; her interest in horticulture leads by example: A bunch of people in the lab like plants, so were thinking more about what we as a group can grow.

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Elise Robinson: Untangling the roots of cause and effect - Spectrum

A new statistical study found that men with older brothers are 38% more likely to be gay than men who are their mothers oldest son.

In a paper published in Proceedings of the Royal Society B this week, the researchers explain that they wanted to examine the fraternal birth order effect hypothesis of male homosexuality, the idea that having older brothers increases a mans chance of being gay.

Related: Here are the craziest theories experts have to explain why some people are LGBTQ

The researchers used data from ten other studies and narrowed their dataset down to families with exactly two sons (no matter how many daughters there were) who were either gay or straight. They ended up with a sample of 5390 gay and straight men.

They then calculated the odds of each child being gay, and it turned out that the second child was 38% more likely to be gay than the first.

Fraternal birth order has been studied in relation to male homosexuality since the 1990s. Studies published in the last several decades have found that having older brothers consistently increases the chances that a man will be gay.

One of the theories about why this happens has been called that the mothers immune system reacts to the Neuroligin 4 Y-linked protein, a protein important for brain development in male fetuses. After being exposed to the protein once, the theory states, the mothers immune system attacks it when it sees it again, like when they are pregnant with another male fetus.

The fascinating study estimates that having an older brother increases the odds of being gay by 38 percent, supporting the idea that a mothers immune response to having a male child influences subsequent boys, University of Cambridge statistician David Spiegelhalter told the Daily Mail.

People have endlessly argued about the possible roles of genetics and upbringing, but this clear result fits in neither category.

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Having an older brother makes a man 38% more likely to be gay - LGBTQ Nation

Hair often plays a critical role in forming a womans identity, so it should come as no surprise that female hair loss can have a major effect on self esteem, mood and confidence. It can even result in increased stress, anxiety and clinical depression, according to board certified dermatologist Anna Drosou of DermSurgery Associates in Houston, Texas.

Discussion around female hair loss pales in comparison to talk about male baldness, so we spoke with several experts who explained to us the most common causes of female hair loss and how to treat them.

As always, consult with your doctor before diagnosing yourself with any of the following causes or conditions.

First, Get To Understand Your Hair Cycle

Everyones healthy hair cycle follows a similar pattern: The active growth phase of hair (anagen) lasts 3-5 years, followed by a 10-day transitional period (catagen), and finally the telogen phase, in which the hair sheds and follicles fall out. The follicle is then inactive for three months before the whole cycle is repeated.

Some people experience hair loss at a pace thats more rapid than usual (telogen effluvium), which is a prolonged (and usually sudden) period of hair loss. Telogen effluvium is a reactive type of hair loss, caused by some sort of internal disruption, i.e. nutritional inadequacies, illness, surgery or hypo/hyperthyroid, Anabel Kingsley, a trichologist, associate member of The Institute of Trichologists and brand president at Philip Kingsley, told HuffPost.

SCIENCE PHOTO LIBRARY via Getty Images

Hair loss, thinning and similar issues occur when the normal hair cycle is disrupted, Kingsley explained. This can be due to a variety of reasons, some common for both women and men, others focused specifically on women. The American Academy of Dermatology defines normal hair loss as 50 to 100 strands a day, so anything more than your usual amount could be reason to see a doctor.

Drosou said that hair loss due to hormones, stress, iron and diet-related causes is generally reversible. Its harder to reverse hair loss connected with hereditary causes or rare inflammatory cases. Upon first seeing a patient, Kingsley first conducts blood tests to look at potential hormonal or nutritional deficiencies.

Hormones

Hormones can wreak havoc on our skin, and unfortunately that applies to our hair, too.

A balance of estrogen, progesterone and testosterone is necessary for healthy hair growth, according to Roy Stoller, a board certified surgeon and founder of Hair Transplant NYC.

Although estrogen usually promotes hair growth, when in excess, it can tip the balance and actually increase testosterone, causing a testosterone-related hair loss, Stoller told to HuffPost. In that case, there may be a genetic predisposition to dihydrotestosterone (DHT), which attacks the hair follicle, diminishing and eventually resulting in total loss of the follicle.

Stoller provides a solution to this situation to block the conversion of testosterone to DHT and prolong the life of the hair follicle: The one most prescribed drug is Finasteride. Although only approved for men, women have also had success with it. This is a prescription-only drug, so speak to your doctor if you think it might be a good fit and ensure you know all the contra-indications, which include loss of libido among others.

Pregnancy Hormones

Its not uncommon for a pregnant woman to receive compliments on her hair, which appears fuller, shinier and overall more healthy during pregnancy. Though not every woman experiences this, for those who do its due to a prolonged anagen phase thanks to higher estrogen and progesterone hormones during pregnancy.

However, Stoller noted that 40% of women will experience excessive shedding (telogen effluvium) post-birth. This is due to the physical stress of the labor, and its self-resolving without treatment, Drosou said. Stoller added the effects are temporary, lasting around three to four months, and starting at three months post-birth. Being diligent with the intake of all necessary vitamins and minerals is helpful in dealing with this type of hair loss, and its completely reversible.

Menopause Hormones

Both before and during menopause, hormonal changes affect hair growth, particularly due to a decrease in estrogen and progesterone. Stoller said that female pattern hair loss is more common during that period, and could even relate to hair loss from androgens (male hormones) depending on the womans genetics. The decrease in the female hormones leave the hair cells unprotected from circulating androgens. Over time, the hair shafts will thin, miniaturize and eventually die, Stoller said.

Estrogens are hair friendly and help to keep strands in their growth phase, Kingsley explained. They also offer a sort of buffer against androgens, which are not very good for your scalp hair. The extent to which a woman will experience changes to hair diameter is down to genes, she added.

Studies have shown that Finasteride can be successful against hair loss in pre- and post-menopausal women who do not intend to be pregnant. There are suggestions that anti-androgen hormones can help, as well as iron supplements. Hormone Replacement Therapy (HRT) can be beneficial in hair loss too, by slowing it down or stopping it completely, studies show. Another topical treatment that is proven to work in menopausal women is Minoxidil.

Thyroid Irregularities

The thyroid gland is responsible for regulating our metabolism, and its usually the first thing a doctor will look at if you have issues with weight changes or hair loss.

Thyroid hormones are released in the body at a steady steam, Stoller said, regulating everything from breathing to temperature, body weight and hair growth. Nutrition and thyroid disease can affect the release of those hormones, and Drosou notes that low thyroid hormones, also known as hypothyroidism, can cause reversible alopecia and even lateral eyebrow thinning. With proper medication to support the thyroid, the hair loss can be completely reversed.

Anemia

Anemia, or iron deficiency, is one of the most common causes of hair loss in women, apart from hormones.

Low iron stores can force hair into a chronic rest phase, resulting in increased shedding and reduced density, Stoller said. Drosou adds that iron deficiency is quite common if youve experienced sudden weight loss, and is often the result of going on a vegan diet.

Iron is used both for hair production and red blood cell production, Drosou said. The body wisely prioritizes the red blood cell production, so if it has a limited amount of iron intake, the first thing to be affected is the hair. Speak to your doctor, who will be able to give you a suitable iron/ferritin supplement depending on your needs.

Eating Disorders

These affect the body in various ways, creating physical stress for the body and often resulting in hair loss.

Stoller notes that the protein in hair (keratin) is not essential for the body, and at periods of malnourishment, hair growth will stop. The body prioritizes nutrients going to vital organs (brain, heart, lungs) over hair, so shedding occurs, Stoller said. Depending on a persons age, genetic makeup and health status, regular hair growth usually returns in about six months after the malnourished state is resolved, Stoller said.

Heredity

The hereditary form of alopecia is female pattern hair loss, or androgenetic alopecia, Drosou said. This is usually seen as diffused thinning, not bald spots.

She notes that this form of hair loss can happen at any point during adult life, and is more common in connection to menopause as its connected with androgen levels. Women with conditions like polycystic ovary syndrome, which is connected with androgen levels, could see hair thinning earlier.

Pongsak Tawansaeng / EyeEm via Getty Images

Medications that block androgens, like spironolactone, are somewhat effective at reducing hair loss and preventing worsening of the condition, Drosou said.

Frontal Fibrosing Alopecia

This is a type of hair loss that leaves scars at the front of a womans hairline, and its becoming more common, particularly in post-menopausal women. Kingsley said its now seen even in younger women, but the exact triggers arent known.

It is thought to be caused by a faulty immune response, whereby your body attacks and destroys hair follicles at the front of your hairline, leaving scar tissue behind, Kingsley said. Unfortunately, you cannot regrow hair from a scarring alopecia. However, at [hair] clinics we endeavor to stop it from progressing and reoccurring.

This is not to be confused with traction alopecia, a type of hair loss thats a result of wearing tight hairstyles, like ponytails or tight braids worn repeatedly that pull out the hair follicles. Kingsley said these hair styles should be avoided as they can cause traction breakage, which could pull out hairs from the follicle and then lead to traction alopecia over time. If treated early, the hair can grow back normally after six months. Otherwise, it could cause non-reversible scarring alopecia, which is often seen in women who use weaves, hair extensions, braids and chemical relaxation.

Insulin Imbalance

Insulin is a hormone that regulates energy. Its obtained from the food we eat, and then released into the body to help store energy for future use. Since insulin can affect hair growth, its important to take note of the glycemic index (GI) a ranking of how foods affect your blood glucose levels of foods you eat.

Eating high-glycemic foods in excess, often in combination with a sedentary lifestyle, can cause an overload of insulin in the body, Stoller said. Too much insulin disrupts ovulation and signals the ovaries to make more testosterone, Stoller said. A change in diet and lifestyle can help insulin levels and restore hair growth.

Stress

We know stress can be catastrophic for the body and the mind, so its no surprise that stress plays a major role when it comes to hair loss.

Kingsley notes that anything that affects your physical well-being impacts your hair to an even greater degree. Hair is non-essential to physical survival and so it will always be the first part of you to suffer when something is off-kilter, he said.

Stress is connected to our cortisol levels, which are increased, Stoller said, when insulin levels rise, in turn triggering a testosterone increase. After a particularly stressful event, and 2-4 months after the event, women may experience hair loss, but after 6-plus months hair returns to normal, Stoller added.

Drosou notes that stress-related hair loss is also seen after events like childbirth, hospitalization, divorce and the death of a significant other. The reason is that stress induces a larger percentage of follicles to enter the telogen phase, resulting in increased shedding of hair. The hair follicles remain intact, so complete recovery is expected after 6-12 months, Drosou said.

The Takeaway

No matter what the underlying cause of hair loss might be, as with many health issues, a balanced diet with the necessary nutrients and vitamins is essential.

Hair is the first point of damage when something is out of balance in our bodies, as its a non-essential tissue or a vital organ. But as hair cells are the second-fastest growing cells our body makes (the fastest-growing are the cells lining the gastrointestinal tract), their nutritional requirements are high, Kingsley said. Supplements can be helpful in the support of good hair health, in conjunction with a healthy balanced diet. Looking after the scalp and cleaning it properly is also important to support healthy hair growth, as well.

As soon as you notice an increase in hair loss, its important to take action and see a dermatologist, trichologist or specialist. Every situation is very different, so seeing an expert is essential.

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The Most Common Causes Of Hair Loss In Women And How To Treat Them - HuffPost

An older male influence in your family might have something to do with your sexuality, a study suggests.

According to a study published in journal Proceedings of the Royal Society B, research has revealed that having an older brother increases mens chances of being homosexual.

The studys researchers analyzed 10 separate sexual orientation studies that involved 5,400 men with info regarding their birth order.

The study revealed that men with older brothers have a 38% higher likelihood of being gay compared to men who dont have an older brother.

(Older) brothers increase the probability of homosexuality in later-born males, the study noted.

The information presented also showed that the more older brothers a man had, the higher chance that he would be homosexual. The study stated having three older brothers doubled a mans chances of being gay.

The study also found that mothers of homosexual males bear more children compared to mothers of heterosexual males.

David Spiegelhalter, a statistician and professor at the University of Cambridge, told the Daily Mail that the fascinating study estimates that having an older brother increases the odds of being gay by 38%, supporting the idea that a mothers immune response to having a male child influences subsequent boys.

People have endlessly argued about the possible roles of genetics and upbringing, but this clear result fits in neither category, he said.

The researchers failed to find a connection between sexuality and birth order for women, noting theres no pattern of siblings, their gender or age that would help determine whether a female would be a lesbian.

Much prior research has shown that females do not influence the sexual orientation of their younger siblings, and females sexual orientation is not affected by their numbers of older siblings, study author Dr. Ray Blanchard stated in an interview with the Daily Mail.

The studys authors state they arent sure why their findings are the case, stating they believe it may be attributed to a theory known as maternal immune hypothesis which believes women who give birth to male babies develop antibodies that impact brain development of future male children they have.

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Boys with older brother more likely to be gay: Study - CANOE

First, I want to say this: Im glad youre here. Hair loss is something that most guys will experience in their lives, and if more of us talked about it instead of joking about it, maybe wed all have better information. According to the American Hair Loss Association, two-thirds of American men will experience some degree of appreciable hair loss, with 85 percent of men significantly thinning by the age of 50. About 25 percent of men who experience hair loss begin the process before they reach the age of 21. In other words, this is a nearly universal experiencewhich makes the stigma surrounding hair loss all the more confusing.

Odds are, if youre reading this, you are quite literally already balding or thinningeven if you dont think you can see it. But dont panic! First, its possible to look great bald. But secondly, theres a lot you can do.

There are so many triggers that can create balding, so its important to have a clear understanding of what actually impacts the process, says Palm Beach trichologist Bridgette Hill. (A trichologist is a hair and scalp specialist who is not a doctor.) There is no reason that balding has to be a reality in the 21st century.

But before we get ahead of ourselves, lets start at the root of hair loss.

What causes balding?

Balding is primarily genetic. But contrary to all those fun factoids youve heard about it being your mothers father (or was it your fathers mother?) who caused your current situation, there's no strict rule to determine who is going to lose it.

What science can confirm is that the exact trigger for male-pattern hair loss is a hormone called dihydrotestosterone, otherwise known as DHT. This comes from testosterone thats naturally in your body, but if you have male-pattern hair loss, what youve inherited is a sensitivity to DHT in your hair follicles, says Dr. Alan Bauman, a full-time, board-certified hair restoration physician. Basically, he explains, this sensitivity to DHT causes a miniaturization of the hair follicle, which leads to the overall weakening of hair growth. This manifests itself as that all-too-common receding hairline and thinning in the crown of your head (the bald spot).

But trichologists and doctors alike also assume that, beyond genetics, lifestyle factors also contribute to hair loss. Something men dont really talk about is emotional health and wellbeing, but thats a trigger, Hill says. So is your dieta lot of times, men have high-protein diets without lots of greens or folic acids, which are essential in making hair follicles and protein. Dr. Bauman also adds that poor sleep, some medications, and smoking may worsen things, too.

Another interesting cause of balding may very well be in your protein shake. When Dr. Bauman assesses a patients risk factors, he looks for the typical things: inflammation of the scalp, sleep schedule, diet, and mental health. Now, he also asks about a patients intake of excess testosterone, which could come from supplements. Ive been doing this for 25 years and have treated about 30,000 patients, he says. We noticed a common thread of hair loss among guys in their 20s or younger who are in their workout regimen, taking bodybuilding supplements. Some clinical research has shown that creatine supplementation, for example, increases the level of DHT in the bloodstreamwhich means it can exacerbate hair loss in anyone with a genetic sensitivity.

It all starts with the scalp.

Theres also the mechanical element of hair loss, which really lies in how we take care of our scalp. If you want to ensure that you hold onto the hair you have for as long as possible, you have to start getting just as serious with your head as you are about your face. Look at it this way: Your face shows signs of aging through wrinkles, dark spots, and sagging. Your scalp shows signs of aging through thinning and balding.

Continue reading here:
How to Prevent Hair Lossand When to Give Up - GQ

The mammals of New Zealand have long posed a threat to native species. The Predator Free 2050program is an effort to rid the island of these invaders including using the tools of CRISPR-based genome editing to create a gene drive to jumpstart extinctions.

Its a very bad idea.

In the 1993 film Jurassic Park, mathematician Ian Malcolmlistens to arrogant dinosaur daddy John Hammond describe the islands supposedly all-female populations of the giant reptiles:

John, the kind of control youre attempting simply is its not possible. If there is one thing the history of evolution has taught us its that life will not be contained. Life breaks free, it expands to new territories and crashes through barriers, painfully, maybe even dangerously, but, there it is Im simply saying that life, uh finds a way.

The wise Dr. Malcolm may prove prescient when it comes to using gene drive technology to get rid of pesky species.

Today reptiles, albeit smaller ones than dinosaurs, are among the threatened natives of New Zealand. Prior to the arrival of people, only bats and marine species represented class Mammalia, except for a few archaic types a few million years ago. Then the Mori people introduced Polynesian rats and dogs in about 1250 CE, and Europeans five centuries later contributed mice, pigs, more rats (ship stowaways), possums, weasels, stoats, and ferrets. Native birds, reptiles, invertebrates, snails, insects, and even the forest canopies began to lose out in the competition for natural resources and to predation.

The New Zealand government painted the newcomers as pests, interlopers, invaders. Introduced predators: the bad guys, states one pamphlet.

In a simpler and perhaps more violent time, pests might have been shot, drowned, or poisoned. But a 2003 paper fromAustin Burt, a selfish gene proponent from Imperial College, London, proposed the concept of a gene drive.

A gene drive harnesses one of the ways that cells repair DNA, called homing, that snips out one copy of a gene and replaces it with a copy of whatever corresponding gene variant (allele) is on the paired chromosome. It would be like cutting out a word in this sentence and replacing it with a copy of the word below it. If done to a gene that affects fertility in a fertilized ovum aka the germline the intervention can lead, within a few generations, to mass sterility and a plummeting population a gene drive towards extinction.

A gene drive skews Mendelian inheritance. Instead of one of a pair of genes coming from the father and one from the mother, both copies are from one parent. In the language of genetics, the intervention can turn a heterozygote (2 different copies of a gene) into a homozygote (2 identical copies). Nature does this in several ways, but the tools of CRISPR-Cas9, first described in 2012,offer a faster route to a gene drive, and can target several genes at once.

Visions of vanquishing the mosquitoes that carry the malaria parasite or zika virus dampened initial scrutiny of gene drives. In 2016, the National Academies of Sciences, Engineering, and Medicine (NASEM) released a 200+ page reportthat discussed reasons to proceed with caution, but endorsed continued laboratory experimentation as well as limited field trials of gene drives.

In 2017, a short paper in Science responded to the NASEM report with Guiding principles for the sponsors and supporters of gene drive research. Ill return to the new recommendations after a trip down biotech memory lane what distinguishes this blog from the clonal regurgitations of aggregated science news.

I was in graduate school in 1976 when recombinant DNA technology was under heated debate. My mentor dubbed the rising public fear of genetics and biotech the triple-headed purple monster mindset.

In February 1975, a whos who of molecular biologists had convened at Asilomar, on Californias Monterey peninsula, to explore the implications of combining genes of two species, starting with insertion of a bacterial gene into a cancer-causing virus.

The 150 scientists discussed fail-safe measures to control recombinant organisms. The Asilomar conference begat guidelines for physical containment via specialized hoods and airflow systems and biological containment to weaken organisms so that they couldnt survive outside the lab.

Despite initial concerns, recombinant DNA technology turned out to be safer than expected, and it spread to industry fast and in diverse ways. A handful of important drugs, starting with human insulin, became safer and more abundant thanks to recombinant DNA techniques. In the agricultural arena, weve been eating GMO foods for decades, although the containment hasnt exactly worked, as the example of canolagrowing along the roadways of North Dakota illustrates.

In 1985geneticists met again to assess the safety, feasibility, and value of another huge project: sequencing the human genome. I doubt any of them could have foreseen a time when we would carry our genome sequences on our smartphones.

Back then, researchers packed a room at the Cold Spring Harbor Laboratory on New Yorks Long Island. At first those against outnumbered those for 5:1, ticking off their fears: shifting research from inquiry-based experimentation to data dumps, comparing the sequencing effort to climbing Mt. Everest just because its there, and diverting funds to fight HIV/AIDs. Finally, the National Academy of Sciences jumped in to debate both sides, and in 1988, Congress authorized the National Institutes of Health (NIH) and the Department of Energy to start sequencing. Foreshadowing of gene drives?

On the reproductive front, the first test-tube baby, Louise Joy Brown, was discussed as if she were a space alien until her ordinariness became apparent, and today more than 5 million folkshave been born beginning with in vitro fertilization. Similarly, one of the first families to speak to the media about their use of preimplantation genetic diagnosis (PGD) to select an embryo who would one day provide stem cells to save his sister was vilified PGD is now a common adjunctto IVF to select the healthiest embryos.

But a gene drive doesnt provide information, drugs, improved cabbages, or babies. It has the potential to tilt the biosphere.

When the inventors of a new biotechnology pull a 180 on applications of their brainchild, its time to take notice. Thats what Kevin Esvelt from MIT and Neil Gemmell from the University of Otago, Dunedin, New Zealand, did in their Perspective in the November 16, 2017 issue of PLOS Biology,Conservation demands safe gene drive. They shout out a warning.

Back in 2014, Esvelt and his colleagues suggested using self-propagating CRISPR-based drive systems for conservation.They also discussed variations on the theme, including a daisy drive systemthat sets up a series of interventions, like a series of locks on a bank vault, and the trojan femaletechnique that sneaks male infertility mutations into mitochondrial DNA.

Second thoughts about deploying gene drives were perhaps already lurking in the minds of people familiar with the nature of DNA, as Jurassic Parks mathematician intuited. DNA changes! Thats why its the genetic materialand why the idea that we arent still evolving is absurd.

A gene swapped into a rat or a possums genome to squelch fertility can change. Such spontaneous mutation happens because of the nature of the DNA molecule. Each of the 4 types of DNA bases exists, when unlinked, fleetingly, in a slightly alternate form. If a DNA replication fork should happen down the old double helix and catch a clinging base in its rare form, a base pair can be replaced with a different one creating a new allele. Its simply the chemistry of life.

A gene drive also assumes that one allele is predominant in a population, and that isnt necessarily the case. What if the harnessed repair mechanism lassos another variant of that gene, a rarer one? Different outcome.

The inherent changeability of DNA alerted the scientists at Asilomar and Cold Spring Harbor. We can never predict all risks, about anything, and surprises have consequences. Who would have thought wed all have to haul off our boots when checking in at the airport thanks to a lone shoe bomber?

DNA also flits from cell to cell, aboard elements called transposons or, more colorfully, jumping genes. Thats how bacteria share sets of antibiotic resistance genes. What if a CRISPR gene drive harpoons something other than its intended target? Goodbye beloved kiwi birds rather than the weasels that eat their eggs? What if a targeted species hitches a ride to other islands and continents before it eliminates the local population and extinguishes itself? Drs. Esvelt and Gemmell write.

The bottom line: gene drives may create the equivalent of the very thing they are being deployed to fight: invasive species. Write Drs. Esvelt and Gemmell of their former approval of gene drives for conservation, We now believe that inclusion was a mistake: such drive systems lack control mechanisms and are consequently highly invasive.

And so also in November of 2017, Dr. Esvelt, with Charleston Noble, Ben Adlam, George Church, and Martin Nowak from Harvard, published Current CRISPR gene drive systems are likely to be highly invasive in wild populations in bioRxiv. Their paper warns against even limited field tests because of mitigating factors, including scenarios as yet unimagined. They did a mathematical analysis to counter recent reports that downplayed the potential ecological danger of a gene drive by claiming that natural resistances will emerge to block the spread to untargeted wild populations. Sound familiar? Contrary to the National Academy report on gene drive, our results suggest that standard drive systems should not be developed nor field-tested in regions harboring the host organism, they conclude.

The guiding principles for the sponsors and supporters of gene drive research published in todays Science, from Claudia Emerson, Stephanie James, Katherine Littler, and Filippo Randazzo, are dj vu all over again for those of us who recall Asilomar circa 1975. Perhaps the principles are attempting to prevent the public outcry at town hall meetings and destruction of some GM crops (most notablyice minus bacteria on plants)that accompanied the entry and acceptance of recombinant organisms.

According to the principles, gene drive experiments should

have goals of social value and the public good take biosafety measures, comply with regulations, and conduct ecological risk assessment have transparency and accountability, with sharing of data engage the public

Dr. Emerson and her colleagues make a good case for the need to find new ways to limit the spread of vector-borne infectious diseases like malaria and zika. Lets hope that gene drive technology goes the successful way of recombinant DNA technology and not the way of GMO escapees in agriculture or in the hands of bioterrorists.

Lets listen to Dr. Malcolm.

[Editors note: Kevin Esvelt of MIT commented on this article on PLOS Blogs. He wrote:

Respectfully, this somewhat mischaracterizes our point.

We think it unwise to build gene drive systems capable of spreading indefinitely beyond the target population.

Because standard self-propagating gene drive systems can spread indefinitely, we think they should only be developed and used for a handful of applications such as malaria eradication, for which the target population includes every Anopheles gambiae s.l. mosquito in Africa.

In contrast, we feel that self-propagating gene drive should not be used for invasive species control because there is always a native population that could be affected.

Instead, we should focus on developing locally-confined drive systems that cannot spread indefinitely. Local drive systems could enable each community to make decisions about its own environment without necessarily affecting people far away. There are several forms that have been modeled or are under development, including Trojan female, killer-rescue, daisy drive, and threshold drive, and hopefully still better ones will be invented.

A final note: there is essentially no risk that transposons, a natural and nearly ubiquitous form of gene drive, will cause a CRISPR-based drive system to spread in another species. The reason is that CRISPR is highly specific and the target DNA sequences would not be present in the genome, so the system would not function exactly the same way that laboratory genome editing fails when there is a strain-specific mutation in the CRISPR-targeted sequence.

Life usually does find a way eventually; the question is how long it will take. We have a remarkable opportunity to address many serious ecological problems using natures own language. With care, humility, and collective scrutiny as obtained through open research and broadly inclusive societal discussions we have a chance to do so wisely. Sometimes, that means walking away from an exciting idea.]

Ricki Lewis is the GLPs senior contributing writer focusing on gene therapy and gene editing. She has a PhD in genetics and is a genetic counselor, science writer and author of The Forever Fix: Gene Therapy and the Boy Who Saved It, the only popular book about gene therapy. BIO. Follow her at her website or Twitter @rickilewis

A version of this article previously appeared on the GLP on December 7, 2017and was originally published on PLOS Blogs website as An Argument Against Gene Drives to Extinguish New Zealand Mammals: Life Finds a Way.

Read more:
The risks of using gene drives to get rid of 'pesky species' - Genetic Literacy Project

Xiaoyu Xia,1,* Li Wang,1,* Xiao Yang,2 Yanqin Hu,1 Qiang Liu1

1Shanghai Key Laboratory of Reproductive Medicine, Department of Histoembryology, Genetics and Developmental Biology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, Peoples Republic of China; 2Shanghai Key Laboratory of Orthopedic Implants, Department of Orthopedics, Ninth Peoples Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, Peoples Republic of China

*These authors contributed equally to this work

Correspondence: Qiang LiuDepartment of Histoembryology, Genetics and Developmental Biology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, Peoples Republic of ChinaTel +86 21 63846590 Ext. 776761Email qliu0122@shsmu.edu.cn

Background: Curcumin has shown many pharmacological activities in both preclinical and clinical studies. Many technologies have been developed and applied to improve the solubility and bioavailability of curcumin, especially the nanotechnology-based delivery systems. However, there has been evidence that certain nanoparticles have potential reproductive toxicity in practice.Methods: Curcumin-poly (lactic-co-glycolic acid) (PLGA)-PEG nanoparticles (Cur-PLGA-NPs for short) were prepared. The Cur-PLGA-NPs were evaluated with its effect on the proliferation of mouse testicular cell lines in vitro and spermatogenesis in vivo, while PLGA-NPs were used as control. For animal experiments, male BALB/c mice were treated with 20 mg/kg of Cur-PLGA-NPs for continuous 10 days via tail vein injection.Results: We found the curcumin nanoparticles suppressed the proliferation of testicular cell lines in vitro. Furthermore, a short-term intravenous delivery of curcumin-loaded nanoparticles could be harmful to the differentiation of spermatogonia, the elongation of spermatids, as well as the motility of mature sperms.Conclusion: In the present study, we disclosed the acute damage on mouse spermatogenesis and sperm parameters by curcumin-loaded nanoparticles. Our results suggested that the reproductive toxicity of nanoformulated curcumin needs to be prudently evaluated before its application.

Keywords: nano-curcumin, reproductive toxicity, Sertoli cell, sperm motility, spermatogenesis

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Acute Damage to the Sperm Quality and Spermatogenesis in Male Mice Exp | IJN - Dove Medical Press

Males that face tougher competition for females risk having offspring with a greater number of harmful mutations in their genome than males without rivals. Researchers at Uppsala University have discovered this correlation in the beetle species Callosobruchus maculatus.

Many researchers working in the fields of human reproductive biology and more general evolutionary theory have taken an interest in this. The hypothesis is not new in itself but there have been few experiments conducted to test it. This is where we hope our study can contribute an important piece of the puzzle, says David Berger of Uppsala Universitys Department of Ecology and Genetics.

Just as with fish, birds and mammals, in the insect world several males often mate with the same female. This leads to a form of sexual selection in which the males sperm compete to fertilise the females eggs. Males that produce more numerous or more competitive sperm often win the competition and become fathers.

Research conducted at the Department of Ecology and Genetics at Uppsala University has succeeded in demonstrating that increased competition between males can lead to a higher rate of harmful mutations in offspring.

Genomic DNA is damaged with every cell division but this damage is usually prevented or repaired by an effective, but costly, cellular surveillance system. The new study shows that sperm production in competing males of the species Callosobruchus maculatus, or cowpea weevil, comes at the expense of this cellular surveillance.

In experiments, male beetles were exposed to radiation in order to damage their genome. After a period of recuperation, the males were allowed to mate with females and become fathers. The researchers then followed their offspring to measure the varying quality of subsequent generations and discovered that males kept in groups, with the concomitant risk of sperm competition, had offspring with a greater number of harmful new mutations than those that lived alone.

The researchers behind the study do however point out that competition between males need not lead to deteriorating gene health in the long term. This is because, as the study also shows, males from populations with high sperm competition over many generations adapt to the new conditions by producing more sperm and more viable offspring compared to males adapted to a life of monogamy.

Even if the direct effect of sperm competition is to increase the number of mutations in offspring, the paradoxical long-term effect of sexual selection may be a lower rate of mutation, explains David Berger.

The researchers behind the study explain that both of these mechanisms play important roles in how genetic variation arises and is maintained in species where males compete to mate. This in turn can affect the potential for evolutionary adaptation, which depends on genetic variation.

The study is published in the scientific journal Nature Ecology & Evolution. J. Baur, D. Berger, (2020), Experimental evidence for effects of sexual selection on condition-dependent mutation rates. Nature Ecology & Evolution. DOI: 10.1038/s41559-020-1140-7

More:
Male rivals risk having offspring with a greater number of harmful mutations - Mirage News

Women have two X chromosomes (homogametic sex), while men have an X and a Y (heterogametic sex). The unguarded X hypothesis suggests that as our chromosomes age, men dont have a backup plan when their X begins to falter, having a Y leaves that X unprotected. Alternatively, there is the toxic Y hypothesis, where the Y acts as a bit of a rogue adversely altering gene expressions and mutations. A group of researchers considered the life-span across all the species where two genes created homogametic or heterogametic genders. Their data set included 229 species, 99 families, 38 orders and eight classes [1]

Across a wide range of species including us mammals, insects, reptiles, and ray-finned fish (fish whose fins are supported by a bony infrastructure), the homogametic gender on average lives 17.6% longer. As it turns out, in birds, moths, and butterflies, the male is homogametic (noted as ZZ), and the female is heterogametic (ZW). Again, the homogametic gender lives longer. So it seems that the unguarded X hypothesis contains some truth.

The second finding by the researchers suggests a limit to the effect of an unguarded X.

that when males are heterogametic sex they die 20.9% earlier than their female counterparts, but when females are the heterogametic sex, they die only 7.1% earlier than their male counterparts.

Why might that be? The researchers suggest that those lonely Ys, and for the birds, their W genes are more degraded than those lusty Xs and Zs. Or that estrogen is protective of telomere length, or that the higher mortality in males [is a] side effects of sexual selection wooing and mating takes a lot out of us. In any case, an unguarded X fails to explain everything.

While we are tossing candidate theories into the ring, might I suggest that the 13.8% higher mortality for heterogametic males than heterogametic females has to do with estrogen, testosterone, and their effect on lifestyle? Men are less risk-averse; they take more chances, and perhaps that is fueled, in part by the testosterone milieu that baths their brains. Women, and yes, I recognize the generalization, maybe a little more risk-sensitive. Women are less likely to smoke than men, less likely to be overweight (although they are more likely to be obese), men tend to drive faster and are involved in many more high-speed car accidents.

Once again, it is not a question of nature or nurture, but how much do genetics and lifestyle contribute and interact in our life-span. It seems that in reality, at least for us mammals, men are the weaker sex.

[1] A refresher, the classifications are, Domain, Kingdom, Phyla, Class, Order, Family, Genus, Species

Source: The sex with the reduced sex chromosome dies earlier: a comparison across the tree of life

Biology Letters DOI: 10.1098/rsbl.2019.0867

Read the rest here:
Men, The Truly Weaker Sex - American Council on Science and Health

As sweeping efforts to contain theCOVID-19 pandemic go into effect around the globe, researchers are starting toget hints of just when patients are most contagious.

People infected with the SARS-CoV-2virus, which causes the disease, may test positive for the virus both beforeand after they have symptoms. But a new study of nine people who contracted thevirus in Germany suggests that people are mainly contagious before they havesymptoms and in the first week of the disease.

Infectious viruses were isolated fromabout 17 percent of nose and throat swabs and more than 83 percent of phlegmsamples during that first week, researchers report March 8 in a study posted atmedRxiv.org.

Patients produced thousands to millionsof viruses in their noses and throats, about 1,000 times as much virus as producedin SARS patients, Clemens Wendtner, director of infectious disease and tropicalmedicine at Munich Clinic Schwabing, a teaching hospital, and his colleaguesfound. That heavy load of viruses may help explain why the new coronavirus isso infectious.

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Scientists identified these nine peoplesome time after they had been exposed to the coronavirus, so researchers dontknow for sure when exactly people begin giving off virus. After the eighth dayof symptoms, however, the researchers could still detect the viruss geneticmaterial, RNA, but they could no longer find infectious viruses. Thats anindication that antibodies that the bodys immune system makes against SARS-CoV-2are killing viruses that get out of cells, Wendtner says.

The study brings an important point tolight; finding RNA or pieces of a virus in a swab or sample is no guaranteethat the virus is live, or infectious, says Ali Khan, dean of the College ofPublic Health at the University of Nebraska Medical Center in Omaha. Some ofit is discouraging news because when you are mildly [ill] or just [getting]sick, youre putting out a whole lot of virus, which explains why were seeingso much transmission within our communities, says Kahn, was not involved in thestudy.

But theres encouraging news, too.Plummeting numbers of infectious virus after antibody production turns onmeans that after about 10 days or so, youre not likely to be infecting otherpeople, Khan says. Other studies also suggest that people with very mild orasymptomatic infections dont shed as much virus and arent as likely to infectother people as people with more severe cases, he says.

Wendtner and colleagues put the nine patientsthrough tests every morning during their hospital stay, collecting blood,urine, stool, nasal and throat swabs and asking the people to cough up sputum,or phlegm. We were learning with the patients because we did not know whenwould be the best and safest time to discharge them, Wendtner says.

The high levels of virus shedding fromthe nose and throat happened very early in infection by the time of testing,most patients upper airway virus production had already peaked. As theinfection progresses, the virus moves deeper into the lungs, the findingssuggest.

The team never found evidence of thevirus in blood or urine and has stopped collecting those samples from a secondwave of 23 COVID-19 patients now being treated at the hospital. Researchersdid detect viral RNA in feces, but no infectious virus there. That suggeststhat the virus isnt spread through stool, an unknown until now.

All nine patients are employees ofWebasto, an auto supplier in Stockdorf. They caught the virus from a malecoworker, who became known as Patient 1. He originally got the virus from abusiness colleague from Shanghai who came to Germany in January for aseries of meetings (SN: 1/31/20). BothPatient 1 and his Shanghai colleague transmitted the virus before developingsymptoms, the first documented cases of asymptomatic spread.

As health officials tested otheremployees of the company, they found the study participants and placed them inisolation at the Munich clinic. In one case, Patient 1 sneezed during a meetingwith one person, Wendtner says. That was enough for infection. In othercases, they had simple business meetings, sitting together for 60 minutes, 90minutes [at a table or] in front of a computer, with no physical contact justone handshake, thats all, Wendtner says. The infectivity is quite high.

Most had coughs, but only two developeda fever, the most common symptom reported in other studies. Most symptoms were mild and one person neverdeveloped any at all. One patient developed severe pneumonia.

Two of the nine had runny noses,previously reported as a rare symptom of COVID-19. Another four had stuffynoses and reported that they couldnt smell or taste anything. In all of ourpatients, it cleared up, but it was a little bit annoying for two weeks or so,Wendtner says. They could order anything they wanted [to eat], but [if] youcant taste it, it doesnt matter.

A temporary lack of smell or taste also affectedsome SARS patients in 2003, he says. That symptom may indicate that in additionto causing swelling in the nose, the virus may infect nerve cells responsiblefor identifying odors, he says.

Patients in the study started makingantibodies against the virus about six to 12 days after symptoms started. Onceantibody production kicked in, researchers still found high levels of viral RNAin phlegm and in nose and throat swabs, but patients were no longer giving offinfectious virus.

The early and extreme contagiousness of the virus tell us that gatherings of people should be avoided, Wendtner says. But the results also may suggest that isolation periods could be shorter for people who have RNA but no virus. Researchers thought that because tests could still detect RNA for up to weeks after symptoms had cleared (SN: 2/28/20), patients were infectious for that long. Most patients are not released from the hospital until two separate tests within 24 hours come back negative, Wendtner says.

But Wendtner isnt suggesting letting people out of quarantine before their two weeks are up. Fourteen days is safe, and you have to keep it simple, Wendtner says. Maybe its safe 10 days after symptoms start, but you have to prove they have those neutralizing antibodies. Tests for the antibodies, however, are not widely available.

The reliable science journalism you count on is expensive. It takes professional reporters, editors, fact checkers, designers and digital producers to make sureScience Newsreflects the depth and breadth of science.We need your financial support to make it happen every contribution makes a difference.

Originally posted here:
Coronavirus is most contagious before and during the first week of symptoms - Science News

Coconut oil comes from the copra the kernel or meat of coconuts.

It contains a high percentage of saturated fats, particularly from medium-chain triglycerides (MCTs).

Coconut oil has various applications in cooking, beauty, skin care, and health.

Along with these applications, it has been suggested that coconut oil increases testosterone levels and improves sexual function, but research on the topic is scarce.

This article discusses everything you need to know about coconut oils effect on testosterone levels in men.

Testosterone is a powerful hormone.

While both men and women produce it, men produce 20 times more than women (1).

In men, testosterone plays an important role in muscle and body hair growth, bone health, and sexual function, among other areas (2).

Testosterone levels peak in men around the age of 19 and decline by approximately 16% by age 40, on average (3).

Most of the testosterone in your blood is bound to two proteins albumin and sex hormone-binding globulin (SHBG).

SHBG is strongly bound to testosterone, making the hormone unavailable for use by your body, whereas albumin is weakly bound and can be used by your body with some effort.

The remaining testosterone, which is known as free testosterone, is not bound to proteins and can be readily used by your body.

Free testosterone and albumin-bound testosterone make up your bioavailable or usable testosterone (4).

The sum of your bioavailable and SHBG-bound testosterone make up your total testosterone.

Testosterone is the predominant male hormone that increases muscle mass, maintains bone strength, and regulates sexual function.

While testosterone levels are influenced by a number of lifestyle factors, such as diet and exercise, coconut oils effects on testosterone levels in humans remain largely unknown (5).

Still, coconut oil contains a high percentage of fat from MCTs about 54% in the form of lauric acid (42%), caprylic acid (7%), and capric acid (5%). These MCTs have been shown to affect a hormone similar to testosterone called dihydrotestosterone (DHT) (6, 7).

Your body uses an enzyme called 5-alpha reductase to convert about 5% of free testosterone to DHT (8, 9).

DHT performs many of the same functions as testosterone but is thought to contribute to male pattern hair loss (10).

Interestingly, MCTs especially lauric acid have been shown to block the enzyme that converts testosterone to dihydrotestosterone (DHT) in test-tube and animal studies (11, 12, 13).

Medications called 5-alpha reductase inhibitors, which are prescribed for the treatment of male pattern hair loss, work in the same way by blocking the 5-alpha reductase enzyme.

Still, studies in humans are needed to determine whether consuming MCTs from coconut oil helps prevent or treat male pattern hair loss, as the condition is also influenced by genetics (14).

Animal and test-tube studies have demonstrated that MCTs inhibit the enzyme that converts testosterone to DHT, a hormone linked to male pattern hair loss.

Low testosterone has been linked to erectile dysfunction (ED), the inability to get or maintain an erection (15).

The condition can be debilitating for men, cause embarrassment and low self-esteem, and lead to an unsatisfactory sex life.

The global prevalence of ED ranges from 377% and tends to become more common with age (16).

Specific foods, including coconut oil, have been suggested to increase testosterone and improve sexual function (17, 18).

Still, there is no evidence to suggest that coconut oil can directly increase testosterone or alleviate ED.

ED is common among people with diseases or conditions that affect the blood vessels, such as diabetes, high blood pressure, high cholesterol, and overweight or obesity (19).

If any of these are present, you may be able to reduce or improve ED with lifestyle changes, such as engaging in regular physical activity, consuming a diet rich in fruits and vegetables, maintaining a healthy weight, and not smoking (20).

There is no evidence to suggest that coconut oil increases testosterone or alleviates ED. Exercising regularly, consuming a healthy diet, and maintaining a healthy weight are lifestyle factors that may improve ED.

Coconut oil is an oil thats extracted from the copra or meat of coconuts.

It contains a high percentage of MCTs, which animal and test-tube studies have shown can block the enzyme that converts testosterone to DHT the hormone linked to male pattern baldness.

Still, evidence that coconut oil can help treat this condition is lacking.

While coconut oil has been suggested to alleviate ED and improve sexual function by increasing testosterone, there is no research to support this theory.

See original here:
Coconut Oil and Testosterone: Is There a Connection? - Healthline

Male Breast Cancer Treatment Market Analysis 2020

Garner insights has published an analytical study titled as global Male Breast Cancer Treatment Market 2020. This statistical data focuses on the performance of both historical records along with the recent trends. It includes a complete analysis of different attributes such as manufacturing base, type, and size. This report evaluates the market segmentation along with the competitive landscape at global as well as domestic level.

Male breast cancer (male breast neoplasm) is a rare cancer in males that originates from the breast. Many males with breast cancer have inherited a BRCA mutation, but there are other causes, including alcohol abuse and exposure to certain hormones and ionizing radiation.

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Male Breast Cancer Treatment Market trends and Future demand as well as Top Players Pfizer, Roche, GlaxoSmithKline, Sanofi, Novartis etc. - Galus...

Updated March 11, 2020 09:35:21

Two incredibly rare white giraffes have been killed by poachers in Kenya, a spokesperson for the local conservancy has confirmed, leaving only one remaining in the world.

The Ishaqbini Hirola Community Conservancy said the country's only female white giraffe and her calf were found in a "skeletal state after being killed by armed poachers".

The giraffes gained global attention in 2017 when they were first captured on film. After the deaths, only one young male white giraffe remains at the Hirola Conservancy.

"This is a very sad day for the community of Ijara and Kenya as a whole," the conservancy's Mohammed Ahmednoor said.

"We are the only community in the world who are custodians of the white giraffe. Its killing is a blow to tremendous steps taken by the community to conserve rare and unique species, and a wake-up call for continued support to conservation efforts."

Experts believe the giraffes have a rare genetic mutation known as leucism, which causes a partial loss of pigmentation.

"This is a long-term loss given that genetics studies and research, which were significant investment into the area by researchers, has now gone down the drain," Mr Ahmednoor said.

"Further to this the white giraffe was a big boost to tourism in the area."

The African Wildlife Foundation estimates that 40 per cent of the overall giraffe population has been lost in the past 30 years.

Topics:animals,human-interest,kenya

First posted March 11, 2020 09:26:08

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Two rare white giraffes killed by poachers, Kenyan conservancy says, leaving only one left on Earth - ABC News