Archive for September, 2019

AMR has a newly done and published professional market study and research titled CRISPR Cas9 Market 2019-2025 with focusing industry Top key manufactures and Regions to help and make wise decisions to the client on their business strategies with it can be most useful to consultants, researchers, investors, business executive along with students, people.

With 152 number of study pages included in this market report, it provides or gives proper information which is written and composed to understand market terminologies.

It has multiple versions of licenses to purchase for Global and Regional.

In this report, we analyze the CRISPR/Cas9 industry from two aspects. One part is about its production and the other part is about its consumption. In terms of its production, we analyze the production, revenue, gross margin of its main manufacturers and the unit price that they offer in different regions from 2014 to 2019. In terms of its consumption, we analyze the consumption volume, consumption value, sale price, import and export in different regions from 2014 to 2019. We also make a prediction of its production and consumption in coming 2019-2024.

At the same time, we classify different CRISPR/Cas9 based on their definitions. Upstream raw materials, equipment and downstream consumers analysis is also carried out. What is more, the CRISPR/Cas9 industry development trends and marketing channels are analyzed.

Get to know more about The CRISPR Cas9 market at https://www.amplemarketreports.com/report/global-crispr-cas9-industry-874374.html

The research methodology used for CRISPR Cas9 market as n number of face-to-face or telephone interviews with the representative companies and leading players with small companies. The upstream operators, suppliers, distributors, importers, installers, wholesalers and consumers are all included in the interviews.

For the Quality of market research study, there are a number of Data validation done that provides Quantitative data such as market estimates, production and capacity of manufacturer, market forecasts and investment feasibility.

CRISPR Cas9 market report offers definite information about the principal business-giants challenging with several other in the global CRISPR Cas9 in terms of trade, demand, sales, revenue production, authentic products development, providing most excellent services, and also post-sale methods at the global level.

Key business-giants focused and analysis done in this report:

Caribou Biosciences, Integrated DNA Technologies (IDT), CRISPR Therapeutics, Merck, Mirus Bio, Editas Medicine, Takara Bio, Thermo Fisher Scientific, Horizon Discovery Group, Intellia Therapeutics, Agilent Technologies, Cellecta, GenScript, GeneCopoeia, Synthego

Without delay get the Sample report pages for The CRISPR Cas9 market in your email : https://www.amplemarketreports.com/sample-request/global-crispr-cas9-industry-874374.html

Key Regions focused and analysis done in this report:

This market study provides in-depth extensive analysis for regional segments that focuses on Global Outlook, Manufacturing processes, Classifications, Market definitions, Cost structures, Development policies, and plans. The data and facts being well manifested in this report utilizing number of charts, graphs, diagrams, and more by Current Trends, Dynamics, and Business Statistics with Extent Scope.

North America, Europe, Asia Pacific, Middle East & Africa, Latin America

Market size by Product

Biotechnology Companies, Pharmaceutical Companies, Academic Institutes, Research and Development Institutes

Market size by End User

Genome Editing, Genetic engineering, gRNA Database/Gene Librar, CRISPR Plasmid, Human Stem Cells, Genetically Modified Organisms/Crops, Cell Line Engineering

Key Questions and Answers for CRISPR Cas9 market

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CRISPR Cas9 Market Outlook -Industry Growth Factors, Market Revenue and More - Stock Market Pioneer

The hubris of some scientists knows no bounds. Less than a year after He Jiankui, a Chinese biophysicist, drew scorn and censure for creating gene-edited twins, Denis Rebrikov, a Russian molecular biologist, boldly announced his plan to follow in Hes genome editing footsteps. Rebrikovs initial stated goal for his proposed research was to prevent the transmission of HIV from infected women to their offspring, though he later suggested other targets, including dwarfism, deafness, and blindness.

In 1998, Nobel laureate Mario Capecchi suggested that resistance to HIV infection was a genetic enhancement that might appeal to potential parents. Twenty years later, in November 2018, He revealed his use of CRISPR-Cas9 genome editing technology to disable a gene called CCR5 in an attempt to create children with resistance to HIV.

Hes research activities were known to a number of senior American scientists, all of whom elected to remain silent about his work. It was only after the twins birth that the world learned of this secret science. Matthew Porteus, one of the scientists who was complicit in the silence, summarized his promise of confidentiality to He this way:

Youre a scientist talking to a scientist. Our culture is that you respect confidentiality and that when people reveal things in confidence to you, you respect that confidence. And I said, well, Im not going to publicly discuss what you just told me because that is for you to publicly discuss.

Read more: He Jiankui tried to protect CRISPR babies against HIV. But his attempted fix shortens lives, study shows

A groundswell of condemnation followed Hes public announcement of the twins birth. There was pointed criticism from Feng Zhang, one of the co-discoverers of the CRISPR-Cas9 genome editing technology, and from David Baltimore, who co-chaired international summits of human genome editing in 2015 and 2018. Quoting from the first International Summit Statement, Zhang and Baltimore independently affirmed that the experiment was irresponsible given the lack of data confirming the safety and effectiveness of using CRISPR in humans, as well as the absence of broad societal consensus.

Members of the organizing committee for the 2018 International Summit on Human Genome Editing where He first presented some of the details of his research described the experiment as irresponsible and said it failed to meet international norms. The committee did not, however, reaffirm the position outlined in the 2015 Summit Statement that [i]t would be irresponsible to proceed with any clinical use of germline editing unless and until: (i) the relevant safety and efficacy issues have been resolved, based on an appropriate understanding and balancing of risks, potential benefits, and alternatives, and (ii) there is broad societal consensus about the appropriateness of the proposed application. Instead, the committee concluded that heritable genome editing could be acceptable in the future and suggested that it was time to define a rigorous responsible translational pathway toward such trials.

Story continues

This shift in orientation is particularly noteworthy when considering the following. In 2015, a researcher performed genome editing on non-viable human embryos that did not involve the transfer of edited embryos to a woman for reproduction. The first summit organizing committee determined that heritable genome editing research was irresponsible unless and until In 2018, He performed genome editing on viable human embryos and transferred these edited embryos to a woman who gave birth to gene-edited children, yet the second summit organizing committee asserted the need for a responsible pathway forward.

Several authors of the 2015 Summit Statement, myself included, disagreed with the position taken by the authors of the 2018 Summit Statement. Along with others, including two of the three CRISPR pioneers Emmanuelle Charpentier and Feng Zhang we issued a call in March 2019 to adopt a moratorium on heritable genome editing. Jennifer Doudna, the other CRISPR pioneer, expressly declined to participate in this initiative.

Read more: The CRISPR shocker: How genome-editing scientist He Jiankui rose from obscurity to stun the world

We reiterated the importance of dialogue within and across nations, and the need for broad societal consensus on the appropriateness of altering the human genome for a particular purpose before any such research could proceed. The purpose of the proposed global moratorium was to provide time for careful study of the relevant technical and ethical issues to determine whether to pursue heritable human genome editing and, if that question were answered in the affirmative, to then determine how to proceed with making modifications to the human genome.

The whether of heritable human genome editing has not been resolved, and yet some scientists continue to race ahead with the how of it, essentially ignoring the myriad calls for public consultation. To be sure, other scientists are willing to heed the call, but would prefer to limit public consultation to public education.

I dont agree with this position. As I write in a new book, Altered Inheritance, we need to move the dial from public education (which typically is limited to talking at the public), to public engagement (which necessarily involves listening to the public), and then on to public empowerment (which is about shared decision-making).

To this end, we need slow science. Science needs time to think and to digest. Time is also needed to promote ethics literacy and to facilitate broad societal consensus where the goal is unity, not unanimity. Decision-making by consensus is about engaged, respectful dialogue and deliberation, where all participants recognize at the outset that knowledge is value laden; that we can and should learn from each other; and that no one should impose his or her will on others.

Read more: Could editing the DNA of embryos with CRISPR help save people who are already alive?

Metaphorically speaking, the human genome belongs to all of us. So we should all have a say in whether to proceed with making heritable changes to our shared genome. Decision-making by consensus, which begins with outreach and openness, is a means to this end. The goal is to create an environment in which all positions (not all persons) can be heard and understood, and in which there are reasonable opportunities for integrity-preserving compromises in pursuit of the common good. The underlying values are inclusivity, responsibility, self-discipline, respect, co-operation, struggle, and benevolence.

Scientists can meaningfully contribute to consensus building around genome editing. As individuals and as committee members, for example, they can effectively serve the common good by helping policymakers, legislators, and members of the public better align scientific information and opportunities with discrete values and interests.

I wrote Altered Inheritance as a call to action. It is a call for scientists to slow down, to reflect deeply on their science and their priorities, and to find meaningful ways to contribute to science policy in pursuit of the common good. It is also a call for all of us to take collective responsibility for the biological and social future of humankind as we think carefully about what kind of world we want to live in, and how genome editing technology might help us build that world.

Franoise Baylis is University Research Professor at Dalhousie University in Halifax, Nova Scotia, and author of Altered Inheritance: CRISPR and the Ethics of Human Genome Editing (Harvard University Press, September 2019).

Read more:
Opinion: Before heritable genome editing, we need slow science and dialogue within and across nations - Yahoo News

The Global CRISPR and Cas Genes Market Research Report Forecast 2019-2028: The research study has been prepared with the use of in-depth qualitative and quantitative analyses of the global CRISPR and Cas Genes Market. The report offers a complete and intelligent analysis of the competition, segmentation, dynamics, and geographical advancement of the Global CRISPR and Cas Genes Market. It takes into account the CAGR, value, volume, revenue, production, consumption, sales, Manufacturing cost, prices, and other key factors related to the global CRISPR and Cas Genes Market.

The report helps the companies to better understand the CRISPR and Cas Genesmarket trends and to grasp opportunities and articulate critical business strategies. Also includes company profiles of market top companies like (contact information, product details, gross capacity, price, cost and more) are covered. this study of top companies in the market have been identified through secondary research, and their shares have been determined through primary and secondary research. and All percentage shares split, and breakdowns have been determined using secondary sources and verified primary sources.

For Better Understanding Go With this Free Sample ReportEnabled with Respective Tables and Figureshttps://marketresearch.biz/report/crispr-and-cas-genes-market/request-sample

Key Players of the Global CRISPR and Cas Genes Market:

Addgene Inc, AstraZeneca Plc., Bio-Rad Laboratories Inc, Caribou Biosciences Inc, Cellectis S.A., Cibus Global Ltd, CRISPR Therapeutics AG, Editas Medicine Inc, eGenesis Bio, GE Healthcare, GenScript Corporation

Market Segmentation:

Segmentation on the basis of product:

Vector-based CasDNA-free CasSegmentation on the basis of application:

Genome EngineeringDisease ModelsFunctional GenomicsKnockdown/ActivationSegmentation on the basis of end user:

Biotechnology & Pharmaceutical CompaniesAcademic & Government Research InstitutesContract Research Organizations

Market Segment by Regions, regional analysis covers 2019-2028:

United States, Canada, and Mexico: North America

Germany, France, UK, Russia, and Italy: Europe

China, Japan, Korea, India, and Southeast Asia: Asia-Pacific

Brazil, Argentina, Colombia, etc.: South America

Saudi Arabia, UAE, Egypt, Nigeria, and South Africa: Middle East and Africa

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Table of Content:

Market Overview: The report begins with this section where product overview and highlights of product and application segments of the global CRISPR and Cas Genes Market are provided. Highlights of the segmentation study include price, revenue, sales, sales growth rate, and market share by product.

Competition by Company: Here, the competition in the Worldwide CRISPR and Cas Genes Market is analyzed, By price, revenue, sales, and market share by company, market rate, competitive situations Landscape, and latest trends, merger, expansion, acquisition, and market shares of top companies.

Company Profiles and Sales Data: As the name suggests, this section gives the sales data of key players of the global CRISPR and Cas Genes Market as well as some useful information on their business. It talks about the gross margin, price, revenue, products, and their specifications, type, applications, competitors, manufacturing base, and the main business of key players operating in the global CRISPR and Cas Genes Market.

Market Status and Outlook by Region: In this section, the report discusses about gross margin, sales, revenue, production, market share, CAGR, and market size by region. Here, the global CRISPR and Cas Genes Market is deeply analyzed on the basis of regions and countries such as North America, Europe, China, India, Japan, and the MEA.

Application or End User: This section of the research study shows how different end-user/application segments contribute to the global CRISPR and Cas Genes Market.

Market Forecast: Here, the report offers a complete forecast of the global CRISPR and Cas Genes Market by product, application, and region. It also offers global sales and revenue forecast for all years of the forecast period.

Research Findings and Conclusion: This is one of the last sections of the report where the findings of the analysts and the conclusion of the research study are provided.

Appendix: Here, we have provided a disclaimer, our data sources, data triangulation, research programs, market breakdown and design, and our research approach.

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Global CRISPR and Cas Genes Market 2019 | Detailed Overview of the Market with Current and Future Industry Challenges and Opportunities - Stock Market...

DARPA Safe Genes concept

WASHINGTON: If you talk with senior defense officials there is one threat they will acknowledge is at the top of their list but they rarely discuss in public biological weapons. NowDARPA wants to develop defenses against biologically engineered threats before they are ever unleashed, the agencys director made clear this morning. That includes proactively editing troops DNA to produce a wide array of antibodies and biochemically blocking hostile attempts to edit DNA.

Our focus is about the protection aspect and the restoration, versus enhancement, Steven Walker said when I asked him about human augmentation during a CSIS conference. All these technologies, theyre dual use. You can use them for good; you can use them for evil and DARPA is about using them for good, to protect our warfighters.

Steven Walker

Super Immunity

That doesnt mean the US military has forsworn the genetic editing of human beings. To the contrary, Walker is very interested in ways to enhance the immune system, effectively turning the body into its own pharmaceutical factory.

Can you actually protect a soldier on the battlefield from chemical weapons and biological weapons by controlling their genome, [by] having the genome produce proteins that would protect the soldier from the inside out? he asked.

Well, why not just brew the necessary vaccines, anti-viral treatments, and anti-toxins in a normal factory and issue them as needed to the troops? Thats how weve dealt with naturally occurring diseases. And DARPA is working on that too, Walker said, with a program to build a vaccine in 60 days or less for 20,000 people for a virus youve never seen before.

The problem is that developing, producing, stockpiling, and dispensing one treatment at a time even in just 60 days may not work fast enough against future bioweapons. As soon as you develop a defense against one form of artificial plague, the enemy can use gene-editing tools to create a different version, one whose biochemical structure is just different enough that the old antibodies dont recognize it anymore.

Many diseases naturally mutate this way all the time. Thats why you can get a series of shots in childhood that protect you against measles or chicken pox for the rest of your life, but you need a new flu shot every year to stop the latest strain and no ones figured out how to stop the common cold. The so-called Spanish Flu of 1918-19 killed more people than World War I; imagine that as a weapon.

To have a shot available for every case that might be out there is becoming more and more intractable, because [of] synthetic biology and the ability of folks anywhere in the world to make something thats slightly different, Walker said. You cant stockpile enough of the vaccine or the antivirus capability to protect the population against that in the future.

Schematic of how CASPR Cas9 gene editing works

Undoing the Edit

DARPA is also looking at neutralizing or even reversing the effects of CRISPR Cas9 itself, the enzyme that made todays breakthroughs in gene-editing possible in the first place. (Its worth noting that China is now a leading country in gene editing science and its technology.)

How do we reverse it [genetic editing] if it gets out into the wild and gets out of control? Thats what the Safe Genes program is all about, Walker said. Weve actually made a lot of progress there in being able to control gene edits.

Walker didnt go into specifics, but theres plenty of non-military work in this area as well. Its even led by some of the pioneers of gene editing themselves, who understandably would like a way to undo the effects if one of their experiments goes wrong.

The irony of gene editing is that the crucial tool wasnt invented from scratch in the lab: It was found in nature. Many bacteria use CRISPR a whole complex of DNA sequences as a natural defense against invading viruses, allowing them to recognize the viral DNA as a foreign body and then use the Cas9 protein to cut it apart, killing the virus. (Though technically viruses arent living things in the first place). Scientists repurposed CRISPR Cas9 to snip apart and reorganize genes.

It turns out that, over millions of years of evolution, some viruses have developed an immunity to CRISP Cas9. They use so-called Anti-CRSPR proteins that shut down the enzyme so it cant start slicing DNA which would stop gene editing dead.

Lisa Porter

Benign Biotech

There are many more benign applications for biotechnology, said Walkers boss, Lisa Porter, the deputy under secretary of defense for research & engineering.

When we think biotech in DoD, we think chem/bio defense, and thats an element of the problem but theres also a lot of opportunity space that people dont necessarily realize unless they talk to the biologists, Porter told the CSIS conference. [So] we will be focusing, not just on the traditional tenets of biotech that we always do, but well be expanding into, what are the opportunities for new materials, new applications?

One biotech project she offered as an example is developing new materials to rapidly lay down new runways. Thats a matter of intense interest to the Air Force, which is increasingly worried its big central bases are easy targets for long-range missiles and wants new ways to either repair them or create alternative sites in a hurry.

What about human augmentation (boosted humans)? That gets a lot of concern and media attention, Porter said and quite rightly: You read about what China is doing and we should be concerned, because they dont have the same set of moral and ethical norms that we have in our country. (DARPA is careful to note in many of the web pages outlining genetic and related work that they work closely with recognized ethicists to ensure they are not crossing lines that should not be crossed.)

Porter, like Walker, did not mention any American plans to biologically enhance our own troops. But there are DARPA efforts that could, in the fast-changing world of biotech, lead to smarter, faster healing and stronger humans. Or try to stop what other countries have done to their troops.

Originally posted here:
DoD On Biotech: Build Sound Defenses First Breaking Defense - Defense industry news, analysis and commentary - Breaking Defense

Dear Doctor,

My period usually lasts longer than a week, however, this month, it has gone beyond that. I have had it for over two weeks now and the bleeding is heavier than usual. This is accompanied by dizziness and nausea. Is this something I should worry about?

Lyna

Dear Lyna,

What is your age currently? A woman having normal regular menstrual cycles previously can have irregular cycles around menopause. This happens because the balance of hormones governing the menstrual cycles changes at this age. Actual cessation of menses occurs some time later around 50 years of age, some years sooner or later. But the changes start from around 40 years or so. This is manifested in the form of irregular periods with scanty or prolonged and heavy bleeding.

Though this change in menstrual cycles is normal, if recurrent or persistent, it is a cause for concern.

Excess bleeding due to menopause is diagnosed clinically and by investigations to exclude other causes of prolonged bleeding. Treatment is by hormonal therapy. But at this age, it is necessary to weigh the advantage of hormonal therapy, versus the potential harm caused due to its side effects like clotting, hypertension, heart problems, and et cetera. Iron supplements are given if anaemia occurs. In severe cases, the uterus is removed surgically.

Heavy and or prolonged bleeding can be due to uterine fibroids. Fibroid is benign tumour that develops in the inner lining of uterus and can be small or big in size, single or multiple in number. Apart from heavy and or prolonged menstrual bleeding, they can cause lower abdominal pain, discomfort and backache. Fibroids are easily diagnosed by ultrasound. Treatment is by hormones or surgery.

Excess and or prolonged bleeding during menses can be due to other hormonal disorders. Hyperthyroidism, i.e. excess amount of hormones released by thyroid gland is one of them. This can occur at any age. Other manifestations of hyperthyroidism like excess sweating, tremulousness of hands, increased appetite, altered bowel movements, to mention a few, may be present or absent, along with excess menstrual bleeding. Hyperthyroidism is easily diagnosed by a simple blood test and is treatable. Hypopituitarism, adrenal gland disorders are other endocrine ailments, which can cause prolonged menstrual bleeding. These disorders are also easily diagnosed and are treatable.

Excess menstrual bleeding can be a side effect of anti-clotting drugs like aspirin and clopidrogel. Some women may develop it as a manifestation of inherent bleeding disorders.

Heavy and or prolonged bleeding mostly results in chronic anaemia, i.e., deficiency of necessary amount of haemoglobin (component of blood that carries oxygen to the body cells). This manifests as early fatigue, joint pain, palpitations and breathlessness on exertion. Over time, chronic anaemia puts strain over the heart resulting in heart failure. This is prevented by treating heavy bleeding during periods. Treatment depends on the cause.

Dr. Rachna Pande is a specialist in internal medicine.

More here:
What causes prolonged menstrual bleeding? - The New Times

ROCKLAND, MA and NEW YORK, US, September 20, 2019 /PRNewswire/ -- EMD Serono, the biopharmaceutical business of Merck KGaA, Darmstadt, Germany in the US and Canada, and Pfizer Inc. (NYSE: PFE) today announced that the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) adopted a positive opinion recommending approval of BAVENCIO (avelumab) in combination with axitinib for the first-line treatment of adult patients with advanced renal cell carcinoma (RCC). The opinion was based on positive findings from the Phase III JAVELIN Renal 101 study, which demonstrated a significant extension in median progression-free survival (PFS) and a clinically meaningful improvement in objective response rate (ORR) for the combination across all prognostic risk groups compared with sunitinib.1 The CHMP positive opinion will be reviewed by the European Commission (EC), with a decision anticipated in the fourth quarter of this year. EMD Serono and Pfizer have a global strategic alliance to jointly develop and commercialize BAVENCIO.

"Today's positive CHMP opinion is a significant step toward potentially transforming the treatment landscape and bringing much needed options to people living with advanced renal cell carcinoma in Europe. We believe that the combination of BAVENCIO plus axitinib has the potential to help address a significant need for patients with advanced renal cell carcinoma for first-line treatments with a benefit across all prognostic risk groups, and we look forward to a decision from the European Commission," said Luciano Rossetti, Head of Global R&D for EMD Serono.

In 2018, an estimated 136,500 new cases of kidney cancer were diagnosed in Europe, and approximately 54,700 people died from the disease.2 RCC is the most common form of kidney cancer, accounting for about 3% of all cancers in adults.2 Approximately 20% to 30% of patients are first diagnosed with RCC at the advanced stage, and 30% of patients treated for an earlier stage go on to develop metastases.3,4 About half of patients living with advanced RCC do not go on to receive additional treatment after first-line therapy,5,6for reasons that may include poor performance status oradverse events from their initial treatment.5,7,8The five-year survival rate for patients with metastatic RCC is approximately 12%.9

"Kidney cancer represents a significant burden in Europe, where incidence rates are among the highest in the world," said Chris Boshoff, M.D., Ph.D., Chief Development Officer, Oncology, Pfizer Global Product Development. "Pfizer has been a leader in the development of kidney cancer treatments for more than a decade, and it is a privilege to continue our efforts to bring a new treatment option to this community."

The U.S. Food and Drug Administration (FDA) approved BAVENCIO in combination with axitinib for the first-line treatment of patients with advanced RCC in May 2019.10 Asupplemental application for BAVENCIO in combination with axitinib in unresectable or metastatic RCC was submitted inJapanin January 2019.

About the JAVELIN Renal 101 Study

The Phase III JAVELIN Renal 101 study is a randomized, multicenter, open-label study of BAVENCIO in combination with axitinib in 886 patients with untreated advanced or metastatic RCC. The major efficacy outcome measures were PFSas assessed by a Blinded Independent Central Review (BICR) using RECIST v1.1 and overall survival (OS) in the first-line treatment of patients with advanced RCC who have PD-L1-positive tumors (PDL1 expression level 1%). If PFS was statistically significant in patients with PD-L1-positive tumors, it was then tested in all patients irrespective of PD-L1 expression. PFS based on BICR assessment per RECIST v1.1 and OS irrespective of PDL1 expression, objective response, time to response (TTR), duration of response (DOR) and safety are included as secondary endpoints. The study is continuing for OS.

About the JAVELIN Clinical Development Program

The clinical development program for avelumab, known as JAVELIN, involves at least 30 clinical programs and more than 10,000 patients evaluated across more than 15 different tumor types. In addition to RCC, these tumor types include gastric/gastro-esophageal junction cancer, head and neck cancer, Merkel cell carcinoma, non-small cell lung cancer and urothelial carcinoma.

About BAVENCIO (avelumab)

BAVENCIO is a human anti-programmed death ligand-1 (PD-L1) antibody. BAVENCIO has been shown in preclinical models to engage both the adaptive and innate immune functions. By blocking the interaction of PD-L1 with PD-1 receptors, BAVENCIO has been shown to release the suppression of the T cell-mediated antitumor immune response in preclinical models.11-13 BAVENCIO has also been shown to induce NK cell-mediated direct tumor cell lysis via antibody-dependent cell-mediated cytotoxicity (ADCC) in vitro.13-15 In November 2014, EMD Serono and Pfizer announced a strategic alliance to co-develop and co-commercialize BAVENCIO.

BAVENCIO Approved Indication in the US

BAVENCIO (avelumab) in combination with axitinib is indicated in the US for the first-line treatment of patients with advanced renal cell carcinoma (RCC).

BAVENCIO Important Safety Information from the US FDA-Approved Label

BAVENCIO can cause immune-mediated pneumonitis, including fatal cases. Monitor patients for signs and symptoms of pneumonitis, and evaluate suspected cases with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold BAVENCIO for moderate (Grade 2) and permanently discontinue for severe (Grade 3), life-threatening (Grade 4), or recurrent moderate (Grade 2) pneumonitis. Pneumonitis occurred in 1.2% of patients, including one (0.1%) patient with Grade 5, one (0.1%) with Grade 4, and five (0.3%) with Grade 3.

BAVENCIO can cause hepatotoxicity and immune-mediated hepatitis, including fatal cases. Monitor patients for abnormal liver tests prior to and periodically during treatment. Administer corticosteroids for Grade 2 or greater hepatitis. Withhold BAVENCIO for moderate (Grade 2) immune-mediated hepatitis until resolution and permanently discontinue for severe (Grade 3) or life-threatening (Grade 4) immune-mediated hepatitis. Immune-mediated hepatitis occurred with BAVENCIO as a single agent in 0.9% of patients, including two (0.1%) patients with Grade 5, and 11 (0.6%) with Grade 3.

BAVENCIO in combination with axitinib can cause hepatotoxicity with higher than expected frequencies of Grade 3 and 4 alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation. Consider more frequent monitoring of liver enzymes as compared to when the drugs are used as monotherapy. Withhold BAVENCIO and axitinib for moderate (Grade 2) hepatotoxicity and permanently discontinue the combination for severe or life-threatening (Grade 3 or 4) hepatotoxicity. Administer corticosteroids as needed. In patients treated with BAVENCIO in combination with axitinib, Grades3 and 4 increased ALT and AST occurred in 9% and 7% of patients, respectively, and immune-mediated hepatitis occurred in 7% of patients, including 4.9% with Grade3 or 4.

BAVENCIO can cause immune-mediated colitis. Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold BAVENCIO until resolution for moderate or severe (Grade 2 or 3) colitis until resolution. Permanently discontinue for life-threatening (Grade 4) or recurrent (Grade 3) colitis upon reinitiation of BAVENCIO. Immune-mediated colitis occurred in 1.5% of patients, including seven (0.4%) with Grade 3.

BAVENCIO can cause immune-mediated endocrinopathies, including adrenal insufficiency, thyroid disorders, and type 1 diabetes mellitus.

Monitor patients for signs and symptoms of adrenal insufficiency during and after treatment, and administer corticosteroids as appropriate. Withhold BAVENCIO for severe (Grade 3) or life-threatening (Grade 4) adrenal insufficiency. Adrenal insufficiency was reported in 0.5% of patients, including one (0.1%) with Grade 3.

Thyroid disorders can occur at any time during treatment. Monitor patients for changes in thyroid function at the start of treatment, periodically during treatment, and as indicated based on clinical evaluation. Manage hypothyroidism with hormone replacement therapy and hyperthyroidism with medical management. Withhold BAVENCIO for severe (Grade 3) or life-threatening (Grade 4) thyroid disorders. Thyroid disorders, including hypothyroidism, hyperthyroidism, and thyroiditis, were reported in 6% of patients, including three (0.2%) with Grade 3.

Type 1 diabetes mellitus including diabetic ketoacidosis: Monitor patients for hyperglycemia or other signs and symptoms of diabetes. Withhold BAVENCIO and administer antihyperglycemics or insulin in patients with severe or life-threatening (Grade 3) hyperglycemia, and resume treatment when metabolic control is achieved. Type 1 diabetes mellitus without an alternative etiology occurred in 0.1% of patients, including two cases of Grade 3 hyperglycemia.

BAVENCIO can cause immune-mediated nephritis and renal dysfunction. Monitor patients for elevated serum creatinine prior to and periodically during treatment. Administer corticosteroids for Grade 2 or greater nephritis. Withhold BAVENCIO for moderate (Grade 2) or severe (Grade 3) nephritis until resolution to Grade 1 or lower. Permanently discontinue BAVENCIO for life-threatening (Grade 4) nephritis. Immune-mediated nephritis occurred in 0.1% of patients.

BAVENCIO can result in other severe and fatal immune-mediated adverse reactions involving any organ system during treatment or after treatment discontinuation. For suspected immune-mediated adverse reactions, evaluate to confirm or rule out an immune-mediated adverse reaction and to exclude other causes. Depending on the severity of the adverse reaction, withhold or permanently discontinue BAVENCIO, administer high-dose corticosteroids, and initiate hormone replacement therapy, if appropriate. Resume BAVENCIO when the immune-mediated adverse reaction remains at Grade 1 or lower following a corticosteroid taper. Permanently discontinue BAVENCIO for any severe (Grade 3) immune-mediated adverse reaction that recurs and for any life-threatening (Grade 4) immune-mediated adverse reaction. The following clinically significant immune-mediated adverse reactions occurred in less than 1% of 1738 patients treated with BAVENCIO as a single agent or in 489 patients who received BAVENCIO in combination with axitinib: myocarditis including fatal cases, pancreatitis including fatal cases, myositis, psoriasis, arthritis, exfoliative dermatitis, erythema multiforme, pemphigoid, hypopituitarism, uveitis, Guillain-Barr syndrome, and systemic inflammatory response.

BAVENCIO can cause severe or life-threatening infusion-related reactions. Premedicate patients with an antihistamine and acetaminophen prior to the first 4 infusions and for subsequent infusions based upon clinical judgment and presence/severity of prior infusion reactions. Monitor patients for signs and symptoms of infusion-related reactions, including pyrexia, chills, flushing, hypotension, dyspnea, wheezing, back pain, abdominal pain, and urticaria. Interrupt or slow the rate of infusion for mild (Grade 1) or moderate (Grade 2) infusion-related reactions. Permanently discontinue BAVENCIO for severe (Grade 3) or life-threatening (Grade 4) infusion-related reactions. Infusion-related reactions occurred in 25% of patients, including three (0.2%) patients with Grade 4 and nine (0.5%) with Grade 3.

BAVENCIO in combination with axitinib can cause major adverse cardiovascular events (MACE) including severe and fatal events. Consider baseline and periodic evaluations of left ventricular ejection fraction. Monitor for signs and symptoms of cardiovascular events. Optimize management of cardiovascular risk factors, such as hypertension, diabetes, or dyslipidemia. Discontinue BAVENCIO and axitinib for Grade 3-4 cardiovascular events. MACEoccurred in 7% of patients with advanced RCC treated with BAVENCIO in combination with axitinib compared to 3.4% treated with sunitinib. These events included death due to cardiac events (1.4%), Grade 3-4 myocardial infarction (2.8%), and Grade 3-4 congestive heart failure (1.8%).

BAVENCIO can cause fetal harm when administered to a pregnant woman. Advise patients of the potential risk to a fetus including the risk of fetal death. Advise females of childbearing potential to use effective contraception during treatment with BAVENCIO and for at least 1 month after the last dose of BAVENCIO. It is not known whether BAVENCIO is excreted in human milk. Advise a lactating woman not to breastfeed during treatment and for at least 1 month after the last dose of BAVENCIO due to the potential for serious adverse reactions in breastfed infants.

Please see full US Prescribing Information and Medication Guide available at http://www.BAVENCIO.com.

Axitinib Important Safety Information from the US FDA-Approved Label

Hypertension including hypertensive crisis has been observed with axitinib. Blood pressure should be well controlled prior to initiating axitinib. Monitor for hypertension and treat as needed. For persistent hypertension, despite use of antihypertensive medications, reduce the dose. Discontinue axitinib if hypertension is severe and persistent despite use of antihypertensive therapy and dose reduction of axitinib, and discontinuation should be considered if there is evidence of hypertensive crisis.

Arterial and venous thrombotic events have been observed with axitinib and can be fatal. Use with caution in patients who are at increased risk or who have a history of these events.

Hemorrhagic events, including fatal events, have been reported with axitinib. Axitinib has not been studied in patients with evidence of untreated brain metastasis or recent active gastrointestinal bleeding and should not be used in those patients. If any bleeding requires medical intervention, temporarily interrupt the axitinib dose.

Cardiac failure has been observed with axitinib and can be fatal. Monitor for signs or symptoms of cardiac failure throughout treatment with axitinib. Management of cardiac failure may require permanent discontinuation of axitinib.

Gastrointestinal perforation and fistula, including death, have occurred with axitinib. Use with caution in patients at risk for gastrointestinal perforation or fistula. Monitor for symptoms of gastrointestinal perforation or fistula periodically throughout treatment.

Hypothyroidism requiring thyroid hormone replacement has been reported with axitinib. Monitor thyroid function before initiation of, and periodically throughout, treatment.

No formal studies of the effect of axitinib on wound healing have been conducted. Stop axitinib at least 24 hours prior to scheduled surgery.

Reversible Posterior Leukoencephalopathy Syndrome (RPLS) has been observed with axitinib. If signs or symptoms occur, permanently discontinue treatment.

Proteinuria has been observed with axitinib. Monitor for proteinuria before initiation of, and periodically throughout, treatment with axitinib. For moderate to severe proteinuria, reduce the dose or temporarily interrupt treatment.

Liver enzyme elevation has been observed during treatment with axitinib. Monitor ALT, AST, and bilirubin before initiation of, and periodically throughout, treatment.

For patients with moderate hepatic impairment, the starting dose should be decreased. Axitinib has not been studied in patients with severe hepatic impairment.

Axitinib can cause fetal harm. Advise patients of the potential risk to the fetus and to use effective contraception during treatment.

Avoid strong CYP3A4/5 inhibitors. If unavoidable, reduce the dose. Grapefruit or grapefruit juice may also increase axitinib plasma concentrations and should be avoided.

Avoid strong CYP3A4/5 inducers and, if possible, avoid moderate CYP3A4/5 inducers.

Please see full Prescribing Information for axitinib.

ADVERSE REACTIONS (BAVENCIO + AXITINIB)

Fatal adverse reactionsoccurred in 1.8% of patients with advanced renal cell carcinoma (RCC) receiving BAVENCIO in combination with axitinib. These included sudden cardiac death (1.2%), stroke (0.2%), myocarditis (0.2%), and necrotizing pancreatitis (0.2%).

The most common adverse reactions(all grades, 20%) in patients with advanced RCC receiving BAVENCIO in combination with axitinib(vs sunitinib) were diarrhea (62% vs 48%), fatigue (53% vs 54%), hypertension (50% vs 36%), musculoskeletal pain (40% vs 33%), nausea (34% vs 39%), mucositis (34% vs 35%), palmar-plantar erythrodysesthesia (33% vs 34%), dysphonia (31% vs 3.2%), decreased appetite (26% vs 29%), hypothyroidism (25% vs 14%), rash (25% vs 16%), hepatotoxicity (24% vs 18%), cough (23% vs 19%), dyspnea (23% vs 16%), abdominal pain (22% vs 19%), and headache (21% vs 16%).

Selected laboratory abnormalities(all grades, 20%) worsening from baseline in patients with advanced RCC receiving BAVENCIO in combination with axitinib(vs sunitinib) were blood triglycerides increased (71% vs 48%), blood creatinine increased (62% vs 68%), blood cholesterol increased (57% vs 22%), alanine aminotransferase increased (ALT) (50% vs 46%), aspartate aminotransferase increased (AST) (47% vs 57%), blood sodium decreased (38% vs 37%), lipase increased (37% vs 25%), blood potassium increased (35% vs 28%), platelet count decreased (27% vs 80%), blood bilirubin increased (21% vs 23%), and hemoglobin decreased (21% vs 65%).

The most common adverse reactions (all grades, 20%)in patients with advanced RCC receiving BAVENCIO in combination with axitinib(vs sunitinib) were diarrhea (62% vs 48%), fatigue (53% vs 54%), hypertension (50% vs 36%), musculoskeletal pain (40% vs 33%), nausea (34% vs 39%), mucositis (34% vs 35%), palmar-plantar erythrodysesthesia (33% vs 34%), dysphonia (31% vs 3.2%), decreased appetite (26% vs 29%), hypothyroidism (25% vs 14%), rash (25% vs 16%), hepatotoxicity (24% vs 18%), cough (23% vs 19%), dyspnea (23% vs 16%), abdominal pain (22% vs 19%), and headache (21% vs 16%).

Selected laboratory abnormalities (all grades,20%)worsening from baselinein patients with advanced RCC receiving BAVENCIO in combination with axitinib(vs sunitinib) were blood triglycerides increased (71% vs 48%), blood creatinine increased (62% vs 68%), blood cholesterol increased (57% vs 22%), alanine aminotransferase increased (ALT) (50% vs 46%), aspartate aminotransferase increased (AST) (47% vs 57%), blood sodium decreased (38% vs 37%), lipase increased (37% vs 25%), blood potassium increased (35% vs 28%), platelet count decreased (27% vs 80%), blood bilirubin increased (21% vs 23%), and hemoglobin decreased (21% vs 65%).

About Merck KGaA, Darmstadt, Germany-Pfizer Alliance

Immuno-oncology is a top priority for Merck KGaA, Darmstadt, Germanyand Pfizer. The global strategic alliance between Merck KGaA, Darmstadt, Germanyand Pfizer enables the companies to benefit from each other's strengths and capabilities and further explore the therapeutic potential of BAVENCIO, an anti-PD-L1 antibody initially discovered and developed by Merck KGaA, Darmstadt, Germany. The immuno-oncology alliance is jointly developing and commercializing BAVENCIO. The alliance is focused on developing high-priority international clinical programs to investigate BAVENCIO as a monotherapy as well as combination regimens, and is striving to find new ways to treat cancer.

All Merck KGaA, Darmstadt, Germany, press releases are distributed by e-mail at the same time they become available on the EMD Group Website. In case you are a resident of the USA or Canada please go to http://www.emdgroup.com/subscribe to register again for your online subscription of this service as our newly introduced geo-targeting requires new links in the email. You may later change your selection or discontinue this service.

About EMD Serono, Inc.

EMD Serono - the biopharmaceutical business of Merck KGaA, Darmstadt,Germany, in the U.S. andCanada- is engaged in the discovery, research and development of medicines for patients with difficult to treat diseases. The business is committed to transforming lives by developing and delivering meaningful solutions that help address the therapeutic and support needs of individual patients. Building on a proven legacy and deep expertise in neurology, fertility and endocrinology, EMD Serono is developing potential new oncology and immuno-oncology medicines while continuing to explore potential therapeutic options for diseases such as psoriasis, lupus and MS. Today, the business has approximately 1,500 employees around the country with commercial, clinical and research operations based in the company's home state ofMassachusetts.www.emdserono.com.

About Merck KGaA, Darmstadt, Germany

Merck KGaA, Darmstadt, Germany, a leading science and technology company, operates across healthcare, life science and performance materials. Around 52,000 employees work to make a positive difference to millions of people's lives every day by creating more joyful and sustainable ways to live. From advancing gene editing technologies and discovering unique ways to treat the most challenging diseases to enabling the intelligence of devices the company is everywhere. In 2018, Merck KGaA, Darmstadt, Germany, generated sales of 14.8 billion in 66 countries.

The company holds the global rights to the name and trademark "Merck" internationally. The only exceptions are the United States and Canada, where the business sectors of Merck KGaA, Darmstadt, Germany operate as EMD Serono in healthcare, MilliporeSigma in life science, and EMD Performance Materials. Since its founding 1668, scientific exploration and responsible entrepreneurship have been key to the company's technological and scientific advances. To this day, the founding family remains the majority owner of the publicly listed company.

Pfizer Inc.: Breakthroughs that change patients' lives

At Pfizer, we apply science and our global resources to bring therapies to people that extend and significantly improve their lives. We strive to set the standard for quality, safety and value in the discovery, development and manufacture of health care products, including innovative medicines and vaccines. Every day, Pfizer colleagues work across developed and emerging markets to advance wellness, prevention, treatments and cures that challenge the most feared diseases of our time. Consistent with our responsibility as one of the world's premier innovative biopharmaceutical companies, we collaborate with health care providers, governments and local communities to support and expand access to reliable, affordable health care around the world. For more than 150 years, we have worked to make a difference for all who rely on us. We routinely post information that may be important to investors on our website at http://www.pfizer.com.In addition, to learn more, please visit us on http://www.pfizer.com and follow us on Twitter at @Pfizer and @Pfizer_News, LinkedIn, YouTube and like us on Facebook at Facebook.com/Pfizer.

Pfizer Disclosure Notice

The information contained in this release is as of September 20, 2019. Pfizer assumes no obligation to update forward-looking statementscontained in this release as the result of new information or future events or developments.

This release contains forward-looking information about BAVENCIO (avelumab), including a potential new indication in the European Union for BAVENCIO in combination with axitinib for the treatment of patients with advanced renal cell carcinoma, the alliance between MerckKGaA, Darmstadt, Germany, and Pfizer involving BAVENCIO and clinical development plans, including their potential benefits, that involves substantial risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. Risks and uncertainties include, among other things, uncertainties regarding the commercial success of BAVENCIO and axitinib; the uncertainties inherent in research and development, including the ability to meet anticipated clinical endpoints, commencement and/or completion dates for our clinical trials, regulatory submission dates, regulatory approval dates and/or launch dates, as well as the possibility of unfavorable new clinical data and further analyses of existing clinical data and uncertainties regarding whether the other primary endpoint of JAVELIN Renal 101 will be met; risks associated with interim data; the risk that clinical trial data are subject to differing interpretations and assessments by regulatory authorities; whether regulatory authorities will be satisfied with the design of and results from our clinical studies; whether and whenany drug applications may be filed for BAVENCIO in combination with axitinib in any other jurisdictions or in any jurisdictions for any other potential indications for BAVENCIO or combination therapies; whether and when the pending applications in the European Union and Japan for BAVENCIO in combination with axitinib may be approved and whether and when regulatory authorities in any jurisdictions where any other applications are pending or may be submitted for BAVENCIO or combination therapies, including BAVENCIO in combination with axitinib may approve any such applications, which will depend on myriad factors, including making a determination as to whether the product's benefits outweigh its known risks and determination of the product's efficacy, and, if approved, whether they will be commercially successful; decisions by regulatory authorities impacting labeling, manufacturing processes, safety and/or other matters that could affect the availability or commercial potential of BAVENCIO or combination therapies, including BAVENCIO in combination with axitinib; and competitive developments.

A further description of risks and uncertainties can be found in Pfizer's Annual Report on Form 10-K for the fiscal year ended December 31, 2018, and in its subsequent reports on Form 10-Q, including in the sections thereof captioned "Risk Factors" and "Forward-Looking Information and Factors That May Affect Future Results", as well as in its subsequent reports on Form 8-K, all of which are filed with the U.S. Securities and Exchange Commission and available at http://www.sec.gov and http://www.pfizer.com.

References

Your Contacts EMD Serono Inc. Media Gangolf Schrimpf +49 6151 72 9591 Investor Relations +49 6151 72 3321

Pfizer Inc., New York, USA Media Jessica Smith +1 212 733 6213 Investor Relations Ryan Crowe +1 212 733 8160

SOURCE EMD Serono

Excerpt from:
CHMP Adopts Positive Opinion for BAVENCIO (avelumab) Plus Axitinib for First-Line Treatment of Patients with Advanced Renal Cell Carcinoma -...

Presentations of interest include a late-breaking abstract on expanded Phase 3 data in BRAF-mutant metastatic colorectal cancer

Pfizer Inc. (NYSE:PFE) is presenting data across its industry-leading oncology portfolio, including company-sponsored and collaborative research studies, spanning 11 therapies in 22 types of cancer, at the European Society for Medical Oncology (ESMO) Congress to be held in Barcelona, Spain, September 27 - October 1, 2019. Data from nearly 50 abstracts involving Pfizer cancer medicines will illustrate the diversity of the portfolio and the companys cutting-edge scientific approach. For the first time, this will include data presentations on compounds from the acquisition of Array Biopharma Inc.

At this years ESMO Congress, were looking forward to showcasing how were embodying ESMOs theme of translating science into better patient care, said Chris Boshoff, M.D., Ph.D., Chief Development Officer, Oncology, Pfizer Global Product Development. Whether its studying patient populations such as those affected by BRAF-mutant metastatic colorectal cancer who are in need of new treatment options, utilizing new techniques like real-world evidence to understand further the impact of our medicines in the non-clinical trial setting, or studying a different way to administer a treatment that may be more convenient for patients, Pfizer is leading the way in taking innovative approaches to meeting the needs of people living with cancer.

Clinical data can be complex and often difficult to understand if a person is not a scientist. To help interested non-scientists better understand the latest research, Pfizer developed summaries in non-technical language for research results being presented at this years ESMO Congress. These informational materials, called abstract plain language summaries (APLS), will be made available for non-scientists to learn more about Pfizers latest scientific developments.

Key Pfizer-sponsored abstracts leveraging the depth of Pfizers scientific advances include:

Details for key Pfizer-sponsored oral presentations, poster discussions and poster presentations are below:

In Europe, BAVENCIO (avelumab)is indicated as monotherapy for the treatment of adult patients with metastatic Merkel cell carcinoma (MCC).

BAVENCIO Important Safety Information from the U.S. FDA-Approved Label

BAVENCIO can cause immune-mediated pneumonitis, including fatal cases. Monitor patients for signs and symptoms of pneumonitis, and evaluate suspected cases with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold BAVENCIO for moderate (Grade 2) and permanently discontinue for severe (Grade 3), life-threatening (Grade 4), or recurrent moderate (Grade 2) pneumonitis. Pneumonitis occurred in 1.2% of patients, including one (0.1%) patient with Grade 5, one (0.1%) with Grade 4, and five (0.3%) with Grade 3.

BAVENCIO can cause hepatotoxicity and immune-mediated hepatitis, including fatal cases. Monitor patients for abnormal liver tests prior to and periodically during treatment. Administer corticosteroids for Grade 2 or greater hepatitis. Withhold BAVENCIO for moderate (Grade 2) immune-mediated hepatitis until resolution and permanently discontinue for severe (Grade 3) or life-threatening (Grade 4) immune-mediated hepatitis. Immune-mediated hepatitis occurred with BAVENCIO as a single agent in 0.9% of patients, including two (0.1%) patients with Grade 5, and 11 (0.6%) with Grade 3.

BAVENCIO in combination with axitinib can cause hepatotoxicity with higher than expected frequencies of Grade 3 and 4 alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation. Consider more frequent monitoring of liver enzymes as compared to when the drugs are used as monotherapy. Withhold BAVENCIO and axitinib for moderate (Grade 2) hepatotoxicity and permanently discontinue the combination for severe or life-threatening (Grade 3 or 4) hepatotoxicity. Administer corticosteroids as needed. In patients treated with BAVENCIO in combination with axitinib, Grades 3 and 4 increased ALT and AST occurred in 9% and 7% of patients, respectively, and immune-mediated hepatitis occurred in 7% of patients, including 4.9% with Grade 3 or 4.

BAVENCIO can cause immune-mediated colitis. Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold BAVENCIO until resolution for moderate or severe (Grade 2 or 3) colitis until resolution. Permanently discontinue for life-threatening (Grade 4) or recurrent (Grade 3) colitis upon reinitiation of BAVENCIO. Immune-mediated colitis occurred in 1.5% of patients, including seven (0.4%) with Grade 3.

BAVENCIO can cause immune-mediated endocrinopathies, including adrenal insufficiency, thyroid disorders, and type 1 diabetes mellitus.

Monitor patients for signs and symptoms of adrenal insufficiency during and after treatment, and administer corticosteroids as appropriate. Withhold BAVENCIO for severe (Grade 3) or life-threatening (Grade 4) adrenal insufficiency. Adrenal insufficiency was reported in 0.5% of patients, including one (0.1%) with Grade 3.

Thyroid disorders can occur at any time during treatment. Monitor patients for changes in thyroid function at the start of treatment, periodically during treatment, and as indicated based on clinical evaluation. Manage hypothyroidism with hormone replacement therapy and hyperthyroidism with medical management. Withhold BAVENCIO for severe (Grade 3) or life-threatening (Grade 4) thyroid disorders. Thyroid disorders, including hypothyroidism, hyperthyroidism, and thyroiditis, were reported in 6% of patients, including three (0.2%) with Grade 3.

Type 1 diabetes mellitus including diabetic ketoacidosis: Monitor patients for hyperglycemia or other signs and symptoms of diabetes. Withhold BAVENCIO and administer antihyperglycemics or insulin in patients with severe or life-threatening (Grade 3) hyperglycemia, and resume treatment when metabolic control is achieved. Type 1 diabetes mellitus without an alternative etiology occurred in 0.1% of patients, including two cases of Grade 3 hyperglycemia.

BAVENCIO can cause immune-mediated nephritis and renal dysfunction. Monitor patients for elevated serum creatinine prior to and periodically during treatment. Administer corticosteroids for Grade 2 or greater nephritis. Withhold BAVENCIO for moderate (Grade 2) or severe (Grade 3) nephritis until resolution to Grade 1 or lower. Permanently discontinue BAVENCIO for life-threatening (Grade 4) nephritis. Immune-mediated nephritis occurred in 0.1% of patients.

BAVENCIO can result in other severe and fatal immune-mediated adverse reactions involving any organ system during treatment or after treatment discontinuation. For suspected immune-mediated adverse reactions, evaluate to confirm or rule out an immune-mediated adverse reaction and to exclude other causes. Depending on the severity of the adverse reaction, withhold or permanently discontinue BAVENCIO, administer high-dose corticosteroids, and initiate hormone replacement therapy, if appropriate. Resume BAVENCIO when the immune-mediated adverse reaction remains at Grade 1 or lower following a corticosteroid taper. Permanently discontinue BAVENCIO for any severe (Grade 3) immune-mediated adverse reaction that recurs and for any life-threatening (Grade 4) immune-mediated adverse reaction. The following clinically significant immune-mediated adverse reactions occurred in less than 1% of 1738 patients treated with BAVENCIO as a single agent or in 489 patients who received BAVENCIO in combination with axitinib: myocarditis including fatal cases, pancreatitis including fatal cases, myositis, psoriasis, arthritis, exfoliative dermatitis, erythema multiforme, pemphigoid, hypopituitarism, uveitis, Guillain-Barr syndrome, and systemic inflammatory response.

BAVENCIO can cause severe or life-threatening infusion-related reactions. Premedicate patients with an antihistamine and acetaminophen prior to the first 4 infusions and for subsequent infusions based upon clinical judgment and presence/severity of prior infusion reactions. Monitor patients for signs and symptoms of infusion-related reactions, including pyrexia, chills, flushing, hypotension, dyspnea, wheezing, back pain, abdominal pain, and urticaria. Interrupt or slow the rate of infusion for mild (Grade 1) or moderate (Grade 2) infusion-related reactions. Permanently discontinue BAVENCIO for severe (Grade 3) or life-threatening (Grade 4) infusion-related reactions. Infusion-related reactions occurred in 25% of patients, including three (0.2%) patients with Grade 4 and nine (0.5%) with Grade 3.

BAVENCIO in combination with axitinib can cause major adverse cardiovascular events (MACE) including severe and fatal events. Consider baseline and periodic evaluations of left ventricular ejection fraction. Monitor for signs and symptoms of cardiovascular events. Optimize management of cardiovascular risk factors, such as hypertension, diabetes, or dyslipidemia. Discontinue BAVENCIO and axitinib for Grade 3-4 cardiovascular events. MACE occurred in 7% of patients with advanced RCC treated with BAVENCIO in combination with axitinib compared to 3.4% treated with sunitinib. These events included death due to cardiac events (1.4%), Grade 3-4 myocardial infarction (2.8%), and Grade 3-4 congestive heart failure (1.8%).

BAVENCIO can cause fetal harm when administered to a pregnant woman. Advise patients of the potential risk to a fetus including the risk of fetal death. Advise females of childbearing potential to use effective contraception during treatment with BAVENCIO and for at least 1 month after the last dose of BAVENCIO. It is not known whether BAVENCIO is excreted in human milk. Advise a lactating woman not to breastfeed during treatment and for at least 1 month after the last dose of BAVENCIO due to the potential for serious adverse reactions in breastfed infants.

Please see full U.S. Prescribing Information and Medication Guide for BAVENCIO available at http://www.Bavencio.com.

About INLYTA (axitinib)

In Europe, INLYTA (axitinib) is indicated for the treatment of adult patients with advanced renal-cell carcinoma (RCC) after failure of prior treatment with sunitinib or a cytokine.

In the U.S., INLYTA is indicated for the treatment of advanced RCC after failure of one prior systemic therapy.

INLYTA Important Safety Information from the U.S. FDA-Approved Label

Hypertension including hypertensive crisis has been observed with axitinib. Blood pressure should be well controlled prior to initiating axitinib. Monitor for hypertension and treat as needed. For persistent hypertension, despite use of antihypertensive medications, reduce the dose. Discontinue axitinib if hypertension is severe and persistent despite use of antihypertensive therapy and dose reduction of axitinib, and discontinuation should be considered if there is evidence of hypertensive crisis.

Arterial and venous thrombotic events have been observed with axitinib and can be fatal. Use with caution in patients who are at increased risk or who have a history of these events.

Hemorrhagic events, including fatal events, have been reported with axitinib. Axitinib has not been studied in patients with evidence of untreated brain metastasis or recent active gastrointestinal bleeding and should not be used in those patients. If any bleeding requires medical intervention, temporarily interrupt the axitinib dose.

Cardiac failure has been observed with axitinib and can be fatal. Monitor for signs or symptoms of cardiac failure throughout treatment with axitinib. Management of cardiac failure may require permanent discontinuation of axitinib.

Gastrointestinal perforation and fistula, including death, have occurred with axitinib. Use with caution in patients at risk for gastrointestinal perforation or fistula. Monitor for symptoms of gastrointestinal perforation or fistula periodically throughout treatment.

Hypothyroidism requiring thyroid hormone replacement has been reported with axitinib. Monitor thyroid function before initiation of, and periodically throughout, treatment.

No formal studies of the effect of axitinib on wound healing have been conducted. Stop axitinib at least 24 hours prior to scheduled surgery.

Reversible Posterior Leukoencephalopathy Syndrome (RPLS) has been observed with axitinib. If signs or symptoms occur, permanently discontinue treatment.

Proteinuria has been observed with axitinib. Monitor for proteinuria before initiation of, and periodically throughout, treatment with axitinib. For moderate to severe proteinuria, reduce the dose or temporarily interrupt treatment.

Liver enzyme elevation has been observed during treatment with axitinib. Monitor ALT, AST, and bilirubin before initiation of, and periodically throughout, treatment.

For patients with moderate hepatic impairment, the starting dose should be decreased. axitinib has not been studied in patients with severe hepatic impairment.

Axitinib can cause fetal harm. Advise patients of the potential risk to the fetus and to use effective contraception during treatment.

Avoid strong CYP3A4/5 inhibitors. If unavoidable, reduce the dose. Grapefruit or grapefruit juice may also increase axitinib plasma concentrations and should be avoided.

Avoid strong CYP3A4/5 inducers and, if possible, avoid moderate CYP3A4/5 inducers.

Please see full U.S. Prescribing Information for INLYTA at http://www.Inlyta.com.

About IBRANCE (palbociclib)

In Europe, IBRANCE (palbociclib) is indicated for the treatment of hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative locally advanced or metastatic breast cancer in combination with an aromatase inhibitor; in combination with fulvestrant in women who have received prior endocrine therapy. In pre- or perimenopausal women, the endocrine therapy should be combined with a luteinizing hormone releasing hormone agonist.

In the U.S., IBRANCE (palbociclib) 125 mg capsules is indicated for the treatment of adult patients with HR+/HER2- advanced or metastatic breast cancer in combination with an aromatase inhibitor as initial endocrine-based therapy in postmenopausal women or in men; or fulvestrant in patients with disease progression following endocrine therapy.

IBRANCE Important Safety Information from the U.S. FDA-Approved Label

Neutropenia was the most frequently reported adverse reaction in PALOMA-2 (80%) and PALOMA-3 (83%). In PALOMA-2, Grade 3 (56%) or 4 (10%) decreased neutrophil counts were reported in patients receiving IBRANCE plus letrozole. In PALOMA-3, Grade 3 (55%) or Grade 4 (11%) decreased neutrophil counts were reported in patients receiving IBRANCE plus fulvestrant. Febrile neutropenia has been reported in 1.8% of patients exposed to IBRANCE across PALOMA-2 and PALOMA-3. One death due to neutropenic sepsis was observed in PALOMA-3. Inform patients to promptly report any fever.

Monitor complete blood count prior to starting IBRANCE, at the beginning of each cycle, on Day 15 of first 2 cycles and as clinically indicated. Dose interruption, dose reduction, or delay in starting treatment cycles is recommended for patients who develop Grade 3 or 4 neutropenia.

Severe, life-threatening, or fatal interstitial lung disease (ILD) and/or pneumonitis can occur in patients treated with CDK4/6 inhibitors, including IBRANCE when taken in combination with endocrine therapy. Across clinical trials (PALOMA-1, PALOMA-2, PALOMA-3), 1.0% of IBRANCE-treated patients had ILD/pneumonitis of any grade, 0.1% had Grade 3 or 4, and no fatal cases were reported. Additional cases of ILD/pneumonitis have been observed in the post-marketing setting, with fatalities reported.

Monitor patients for pulmonary symptoms indicative of ILD/pneumonitis (e.g. hypoxia, cough, dyspnea). In patients who have new or worsening respiratory symptoms and are suspected to have developed pneumonitis, interrupt IBRANCE immediately and evaluate the patient. Permanently discontinue IBRANCE in patients with severe ILD or pneumonitis.

Based on the mechanism of action, IBRANCE can cause fetal harm. Advise females of reproductive potential to use effective contraception during IBRANCE treatment and for at least 3 weeks after the last dose. IBRANCE may impair fertility in males and has the potential to cause genotoxicity. Advise male patients to consider sperm preservation before taking IBRANCE. Advise male patients with female partners of reproductive potential to use effective contraception during IBRANCE treatment and for 3 months after the last dose. Advise females to inform their healthcare provider of a known or suspected pregnancy. Advise women not to breastfeed during IBRANCE treatment and for 3 weeks after the last dose because of the potential for serious adverse reactions in nursing infants.

The most common adverse reactions (10%) of any grade reported in PALOMA-2 for IBRANCE plus letrozole vs placebo plus letrozole were neutropenia (80% vs 6%), infections (60% vs 42%), leukopenia (39% vs 2%), fatigue (37% vs 28%), nausea (35% vs 26%), alopecia (33% vs 16%), stomatitis (30% vs 14%), diarrhea (26% vs 19%), anemia (24% vs 9%), rash (18% vs 12%), asthenia (17% vs 12%), thrombocytopenia (16% vs 1%), vomiting (16% vs 17%), decreased appetite (15% vs 9%), dry skin (12% vs 6%), pyrexia (12% vs 9%), and dysgeusia (10% vs 5%).

The most frequently reported Grade 3 adverse reactions (5%) in PALOMA-2 for IBRANCE plus letrozole vs placebo plus letrozole were neutropenia (66% vs 2%), leukopenia (25% vs 0%), infections (7% vs 3%), and anemia (5% vs 2%).

Lab abnormalities of any grade occurring in PALOMA-2 for IBRANCE plus letrozole vs placebo plus letrozole were decreased WBC (97% vs 25%), decreased neutrophils (95% vs 20%), anemia (78% vs 42%), decreased platelets (63% vs 14%), increased aspartate aminotransferase (52% vs 34%), and increased alanine aminotransferase (43% vs 30%).

The most common adverse reactions (10%) of any grade reported in PALOMA-3 for IBRANCE plus fulvestrant vs placebo plus fulvestrant were neutropenia (83% vs 4%), leukopenia (53% vs 5%), infections (47% vs 31%), fatigue (41% vs 29%), nausea (34% vs 28%), anemia (30% vs 13%), stomatitis (28% vs 13%), diarrhea (24% vs 19%), thrombocytopenia (23% vs 0%), vomiting (19% vs 15%), alopecia (18% vs 6%), rash (17% vs 6%), decreased appetite (16% vs 8%), and pyrexia (13% vs 5%).

The most frequently reported Grade 3 adverse reactions (5%) in PALOMA-3 for IBRANCE plus fulvestrant vs placebo plus fulvestrant were neutropenia (66% vs 1%) and leukopenia (31% vs 2%).

Lab abnormalities of any grade occurring in PALOMA-3 for IBRANCE plus fulvestrant vs placebo plus fulvestrant were decreased WBC (99% vs 26%), decreased neutrophils (96% vs 14%), anemia (78% vs 40%), decreased platelets (62% vs 10%), increased aspartate aminotransferase (43% vs 48%), and increased alanine aminotransferase (36% vs 34%).

Avoid concurrent use of strong CYP3A inhibitors. If patients must be administered a strong CYP3A inhibitor, reduce the IBRANCE dose to 75 mg. If the strong inhibitor is discontinued, increase the IBRANCE dose (after 3-5 half-lives of the inhibitor) to the dose used prior to the initiation of the strong CYP3A inhibitor. Grapefruit or grapefruit juice may increase plasma concentrations of IBRANCE and should be avoided. Avoid concomitant use of strong CYP3A inducers. The dose of sensitive CYP3A substrates with a narrow therapeutic index may need to be reduced as IBRANCE may increase their exposure.

For patients with severe hepatic impairment (Child-Pugh class C), the recommended dose of IBRANCE is 75 mg. The pharmacokinetics of IBRANCE have not been studied in patients requiring hemodialysis.

Please see full U.S. Prescribing Information for IBRANCE at http://www.Ibrance.com.

About XTANDI (enzalutamide)

In Europe, XTANDI (enzalutamide) is indicated for the treatment of adult men with high-risk non-metastatic castration-resistant prostate cancer (CRPC); the treatment of adult men with metastatic CRPC who are asymptomatic or mildly symptomatic after failure of androgen deprivation therapy in whom chemotherapy is not yet clinically indicated; the treatment of adult men with metastatic CRPC whose disease has progressed on or after docetaxel therapy.

In the U.S., XTANDI is indicated for the treatment of patients with CRPC.

XTANDI Important Safety Information from the U.S. FDA-Approved Label

Warnings and Precautions

Seizure occurred in 0.4% of patients receiving XTANDI in clinical studies. In a study of patients with predisposing factors for seizure, 2.2% of XTANDI-treated patients experienced a seizure. Patients in the study had one or more of the following pre-disposing factors: use of medications that may lower the seizure threshold; history of traumatic brain or head injury, cerebrovascular accident or transient ischemic attack, Alzheimer's disease, meningioma, or leptomeningeal disease from prostate cancer, unexplained loss of consciousness within the last 12 months, history of seizure, presence of a space occupying lesion of the brain, history of arteriovenous malformation, or history of brain infection. It is unknown whether anti-epileptic medications will prevent seizures with XTANDI. Advise patients of the risk of developing a seizure while taking XTANDI and of engaging in any activity where sudden loss of consciousness could cause serious harm to themselves or others. Permanently discontinue XTANDI in patients who develop a seizure during treatment.

Posterior Reversible Encephalopathy Syndrome (PRES) In post-approval use, there have been reports of PRES in patients receiving XTANDI. PRES is a neurological disorder which can present with rapidly evolving symptoms including seizure, headache, lethargy, confusion, blindness, and other visual and neurological disturbances, with or without associated hypertension. A diagnosis of PRES requires confirmation by brain imaging, preferably MRI. Discontinue XTANDI in patients who develop PRES.

Hypersensitivity reactions, including edema of the face (0.5%), tongue (0.1%), or lip (0.1%) have been observed with XTANDI in clinical trials. Pharyngeal edema has been reported in post-marketing cases. Advise patients who experience any symptoms of hypersensitivity to temporarily discontinue XTANDI and promptly seek medical care. Permanently discontinue XTANDI for serious hypersensitivity reactions.

Ischemic Heart Disease In the placebo-controlled clinical studies, ischemic heart disease occurred more commonly in patients on the XTANDI arm compared to patients on the placebo arm (2.7% vs 1.2%). Grade 3-4 ischemic events occurred in 1.2% of patients on XTANDI versus 0.5% on placebo. Ischemic events led to death in 0.4% of patients on XTANDI compared to 0.1% on placebo. Monitor for signs and symptoms of ischemic heart disease. Optimize management of cardiovascular risk factors, such as hypertension, diabetes, or dyslipidemia. Discontinue XTANDI for Grade 3-4 ischemic heart disease.

Falls and Fractures In the placebo-controlled clinical studies, falls occurred in 10% of patients treated with XTANDI compared to 4% of patients treated with placebo. Fractures occurred in 8% of patients treated with XTANDI and in 3% of patients treated with placebo. Evaluate patients for fracture and fall risk. Monitor and manage patients at risk for fractures according to established treatment guidelines and consider use of bone-targeted agents.

Embryo-Fetal Toxicity Safety and efficacy of XTANDI have not been established in females. XTANDI can cause fetal harm and loss of pregnancy when administered to a pregnant female. Advise males with female partners of reproductive potential to use effective contraception during treatment with XTANDI and for 3 months after the last dose of XTANDI. XTANDI should not be handled by females who are or may become pregnant.

Adverse Reactions

The most common adverse reactions ( 10%) that occurred more frequently ( 2% over placebo) in the XTANDI patients from the randomized placebo-controlled trials were asthenia/fatigue, decreased appetite, hot flush, arthralgia, dizziness/vertigo, hypertension, headache and weight decreased. In the bicalutamide-controlled study, the most common adverse reactions ( 10%) reported in XTANDI patients were asthenia/fatigue, back pain, musculoskeletal pain, hot flush, hypertension, nausea, constipation, diarrhea, upper respiratory tract infection, and weight loss.

In the placebo-controlled study of metastatic CRPC (mCRPC) patients taking XTANDI who previously received docetaxel, Grade 3 and higher adverse reactions were reported among 47% of XTANDI patients and 53% of placebo patients. Discontinuations due to adverse events were reported for 16% of XTANDI patients and 18% of placebo patients. In the placebo-controlled study of chemotherapy-nave mCRPC patients, Grade 3-4 adverse reactions were reported in 44% of XTANDI patients and 37% of placebo patients. Discontinuations due to adverse events were reported for 6% of both study groups. In the placebo-controlled study of non-metastatic CRPC (nmCRPC) patients, Grade 3 or higher adverse reactions were reported in 31% of XTANDI patients and 23% of placebo patients. Discontinuations with an adverse event as the primary reason were reported for 9% of XTANDI patients and 6% of placebo patients. In the bicalutamide-controlled study of chemotherapy-nave mCRPC patients, Grade 3-4 adverse reactions were reported in 39% of XTANDI patients and 38% of bicalutamide patients. Discontinuations with an AE as the primary reason were reported for 8% of XTANDI patients and 6% of bicalutamide patients.

Lab Abnormalities: In the two placebo-controlled trials in patients with mCRPC, Grade 1-4 neutropenia occurred in 15% of XTANDI patients (1% Grade 3-4) and 6% of placebo patients (0.5% Grade 3-4). In the placebo-controlled trial in patients with nmCRPC, Grade 1-4 neutropenia occurred in 8% of patients receiving XTANDI (0.5% Grade 3-4) and in 5% of patients receiving placebo (0.2% Grade 3-4).

Hypertension: In the two placebo-controlled trials in patients with mCRPC, hypertension was reported in 11% of XTANDI patients and 4% of placebo patients. Hypertension led to study discontinuation in <1% of patients in each arm. In the placebo-controlled trial in patients with nmCRPC, hypertension was reported in 12% of patients receiving XTANDI and 5% of patients receiving placebo.

Drug Interactions

Effect of Other Drugs on XTANDI Avoid strong CYP2C8 inhibitors, as they can increase the plasma exposure to XTANDI. If co-administration is necessary, reduce the dose of XTANDI. Avoid strong CYP3A4 inducers as they can decrease the plasma exposure to XTANDI. If co-administration is necessary, increase the dose of XTANDI.

Effect of XTANDI on Other Drugs Avoid CYP3A4, CYP2C9, and CYP2C19 substrates with a narrow therapeutic index, as XTANDI may decrease the plasma exposures of these drugs. If XTANDI is co-administered with warfarin (CYP2C9 substrate), conduct additional INR monitoring.

Please see full U.S. Prescribing Information for XTANDI at http://www.Xtandi.com.

About LORBRENA (lorlatinib)

In Europe, LORBRENA (lorlatinib) is marketed as LORVIQUA and is indicated as monotherapy for the treatment of adult patients with ALK-positive advanced non-small cell lung cancer (NSCLC) whose disease has progressed after alectinib or ceritinib as the first ALK tyrosine kinase inhibitor (TKI) therapy, or crizotinib and at least one other ALK TKI.

In the U.S., LORBRENA is indicated for the treatment of patients with ALK-positive metastatic NSCLC whose disease has progressed on crizotinib and at least one other ALK inhibitor for metastatic disease; or whose disease has progressed on alectinib or ceritinib as the first ALK inhibitor therapy for metastatic disease.

This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial.

LORBRENA Important Safety Information from the U.S. FDA-Approved Label

Contraindications: LORBRENA is contraindicated in patients taking strong CYP3A inducers, due to the potential for serious hepatotoxicity.

Risk of Serious Hepatotoxicity with Concomitant Use of Strong CYP3A Inducers: Severe hepatotoxicity occurred in 10 of 12 healthy subjects receiving a single dose of LORBRENA with multiple daily doses of rifampin, a strong CYP3A inducer. Grade 4 ALT or AST elevations occurred in 50% of subjects, Grade 3 in 33% of subjects, and Grade 2 in 8% of subjects. Discontinue strong CYP3A inducers for 3 plasma half-lives of the strong CYP3A inducer prior to initiating LORBRENA. Avoid concomitant use of LORBRENA with moderate CYP3A inducers. If concomitant use of moderate CYP3A inducers cannot be avoided, monitor AST, ALT, and bilirubin 48 hours after initiating LORBRENA and at least 3 times during the first week after initiating LORBRENA. Depending upon the relative importance of each drug, discontinue LORBRENA or the CYP3A inducer for persistent Grade 2 or higher hepatotoxicity.

Central Nervous System (CNS) Effects: A broad spectrum of CNS effects can occur. These include seizures, hallucinations, and changes in cognitive function, mood (including suicidal ideation), speech, mental status, and sleep. Withhold and resume at the same or reduced dose or permanently discontinue based on severity.

Hyperlipidemia: Increases in serum cholesterol and triglycerides can occur. Grade 3 or 4 elevations in total cholesterol occurred in 17% and Grade 3 or 4 elevations in triglycerides occurred in 17% of the 332 patients who received LORBRENA. Eighty percent of patients required initiation of lipid-lowering medications, with a median time to onset of start of such medications of 21 days. Initiate or increase the dose of lipid-lowering agents in patients with hyperlipidemia. Monitor serum cholesterol and triglycerides before initiating LORBRENA, 1 and 2 months after initiating LORBRENA, and periodically thereafter. Withhold and resume at same dose for the first occurrence; resume at same or reduced dose of LORBRENA for recurrence based on severity.

Atrioventricular (AV) Block: PR interval prolongation and AV block can occur. In 295 patients who received LORBRENA at a dose of 100 mg orally once daily and who had a baseline electrocardiography (ECG), 1% experienced AV block and 0.3% experienced Grade 3 AV block and underwent pacemaker placement. Monitor ECG prior to initiating LORBRENA and periodically thereafter. Withhold and resume at reduced or same dose in patients who undergo pacemaker placement. Permanently discontinue for recurrence in patients without a pacemaker.

Interstitial Lung Disease (ILD)/Pneumonitis: Severe or life-threatening pulmonary adverse reactions consistent with ILD/pneumonitis can occur. ILD/pneumonitis occurred in 1.5% of patients, including Grade 3 or 4 ILD/pneumonitis in 1.2% of patients. Promptly investigate for ILD/pneumonitis in any patient who presents with worsening of respiratory symptoms indicative of ILD/pneumonitis. Immediately withhold LORBRENA in patients with suspected ILD/pneumonitis. Permanently discontinue LORBRENA for treatment-related ILD/pneumonitis of any severity.

Embryo-fetal Toxicity: LORBRENA can cause fetal harm. Advise pregnant women of the potential risk to a fetus. Advise females of reproductive potential to use an effective non-hormonal method of contraception, since LORBRENA can render hormonal contraceptives ineffective, during treatment with LORBRENA and for at least 6 months after the final dose. Advise males with female partners of reproductive potential to use effective contraception during treatment with LORBRENA and for 3 months after the final dose.

Adverse Reactions: Serious adverse reactions occurred in 32% of the 295 patients; the most frequently reported serious adverse reactions were pneumonia (3.4%), dyspnea (2.7%), pyrexia (2%), mental status changes (1.4%), and respiratory failure (1.4%). Fatal adverse reactions occurred in 2.7% of patients and included pneumonia (0.7%), myocardial infarction (0.7%), acute pulmonary edema (0.3%), embolism (0.3%), peripheral artery occlusion (0.3%), and respiratory distress (0.3%). The most common (20%) adverse reactions were edema, peripheral neuropathy, cognitive effects, dyspnea, fatigue, weight gain, arthralgia, mood effects, and diarrhea; the most common (20%) laboratory abnormalities were hypercholesterolemia, hypertriglyceridemia, anemia, hyperglycemia, increased AST, hypoalbuminemia, increased ALT, increased lipase, and increased alkaline phosphatase.

Drug Interactions: LORBRENA is contraindicated in patients taking strong CYP3A inducers. Avoid concomitant use with moderate CYP3A inducers and strong CYP3A inhibitors. If concomitant use of moderate CYP3A inducers cannot be avoided, monitor ALT, AST, and bilirubin as recommended. If concomitant use with a strong CYP3A inhibitor cannot be avoided, reduce the LORBRENA dose as recommended. Concomitant use of LORBRENA decreases the concentration of CYP3A substrates.

Lactation: Because of the potential for serious adverse reactions in breastfed infants, instruct women not to breastfeed during treatment with LORBRENA and for 7 days after the final dose.

Hepatic Impairment: No dose adjustment is recommended for patients with mild hepatic impairment. The recommended dose of LORBRENA has not been established for patients with moderate or severe hepatic impairment.

Renal Impairment: No dose adjustment is recommended for patients with mild or moderate renal impairment. The recommended dose of LORBRENA has not been established for patients with severe renal impairment.

Please see full U.S. Prescribing Information for LORBRENA at http://www.Lorbrena.com.

About BRAFTOVI (encorafenib) and MEKTOVI (binimetinib)

In Europe, BRAFTOVI (encorafenib) and MEKTOVI (binimetinib) are indicated for the treatment of adult patients with unresectable or metastatic melanoma with a BRAFV600 mutation.

In the U.S., BRAFTOVI and MEKTOVI are indicated for the treatment of patients with unresectable or metastatic melanoma with a BRAF V600E or V600K mutation, as detected by an FDA-approved test.

Read more from the original source:
Pfizer Presents Scientific Advancements in Cancer Care at the ESMO Congress 2019 Highlighting Expanded Portfolio - Yahoo Finance

Events

n Crosskeys Human Resources Inc. is offering flu shots 10:30-11:30 a.m. Sept. 23 at the Brownsville seniors center, 302 Shaffner Ave., and 11 a.m. to noon Oct. 2 at the Republic facility, 36 Fairgarden St., Republic. A professional from Rite Aid in Grindstone will administer the shots. Participants must bring Medicare/other insurance cards for payment.

n Monongahela Valley Hospital will host a prostate cancer screening and education program at 5 p.m. Sept. 25 in the education conference center. The event is free. At the screening, men will be offered a digital rectal exam (DRE), the standard test for prostate cancer; a hemocult test and a Prostate Specific Antigen (PSA) blood test. The screening and education program will be conducted by MVH staff. Registration: 724-258-1333.

n Monongahela Valley Hospital will host a multiphasic blood analysis 7-10 a.m. Sept. 28 in the education conference center. This 36-function screening costs only $30 and is open to the public. Additional tests available include: Immunochemical Fecal Occult Blood, 3-D mammogram, Hemoglobin A1C, Thyroid Stimulating Hormone, Prostatic Specific Antigen, and Vitamin D. Participants are asked to provide the full name and complete address of the physician to whom their test results will be sent afterwards. Testing is by appointment only. The deadline to register is Sept. 25, and registrations must be made Monday through Friday from 8:30 a.m. to 2:30 p.m. by calling 724-258-1282.

n Medicares annual open enrollment period runs Oct. 15 through Dec. 7. For a list of enrollment centers and their dates and times open for enrollment, call Southwestern Pennsylvania Human Services, Inc. at 724-489-8080.

Courses

n Exercise classes, Tuesdays and Thursdays, Center in the Woods, 130 Woodland Court, Brownsville. Classes include chair dancing at 9:30 a.m. followed by healthy steps at 11 a.m. Information: 724-938-3554.

n Monongahela Valley Hospital will host a free talk about Gastrointestinal Reflux Disease (GERD) on Thursday, Oct. 3, at 6 p.m. in the Anthony M. Lombardi Education Conference Center at Monongahela Valley Hospital. Dr. Arshad Bachelani will discuss GERD, a digestive disorder in which the contents of the stomach flow back into the esophagus, leading to heartburn, difficulty swallowing, regurgitation of food and cough, to name a few. Long term GERD can lead to complications in the esophagus that can make swallowing difficult, cause an ulcer or the cause development of precancerous cells. Dr. Bachelani will talk about treatment options available that include medications as well as surgery. Registration: monvalleyhospital.com or 724-258-1333.

n Monongahela Valley Hospital will host a free talk about Cervical Disc Replacement at 6 p.m. Oct. 15, in the Anthony M. Lombardi Education Conference Center. Dr. Eric Nabors will discuss diseases that affect cervical discs, causing chronic neck and/or arm pain and treatment options. He will thoroughly cover surgical treatment option of cervical disc replacement by describing the procedure, when it is a viable option and who is a good candidate for the surgery. Registration: monvalleyhospital.com or call 724-258-1333.

n The four-week Smoke Free For Life program, sponsored by BREATHE Pennsylvania will be hosted by the Monongahela Valley Hospital 9-11 a.m. every Monday in September. Program participants will learn how to overcome barriers that keep them from quitting, develop a customized quit-plan that will lead to success, learn the art of positive self-talk, practice sound techniques to manage stress, develop strategies that will prevent relapse and receive support in a positive and comfortable environment. The session is broken down into four, two-hour courses. Space is limited and pre-registration is required. Registration: 724-258-1462.

n Monongahela Valley Hospital will host a Weight Control and Wellness Support Group at 6 p.m. Sept. 23 in the education conference center. The bariatric support group activities are designed to reinforce key principles of success and help participants learn concepts that are sometimes difficult to grasp after bariatric surgery. Professionals such as dietitians, psychologists and fitness instructors may be invited to speak. Other presenters may discuss topics such as grooming, dating and cooking. The ultimate purpose of the support group is to help participants achieve and maintain their goal weights in a way that is as physically and mentally healthy as possible. Registration: 724-258-1333.

n Monongahela Valley Hospital will host the course Advanced Carbohydrate Counting from 9 to 11 a.m. Sept. 26 in the education conference center. This program is a diabetes self-management class designed to educate you on how to count carbohydrate content in food to improve blood sugar control. Topics include how to track effects of carbohydrates and blood sugar, glycemic index and how to read food nutrition labels. Registration is required at least one week prior to the start of class by calling 724-258-1483.

n Monongahela Valley Hospital through the Community Care Network is offering a Smoke Free for Life program from 11 a.m. to 1 p.m. Sept. 23 and 30 in the education conference center. The four-week program is broken down into four, two-hour courses and is designed to help participants develop strategies to quit smoking, prevent relapse as well as receive support in a positive and comfortable environment. Registration: 724-258-1462.

Support groups

n Breaking Addiction, HEAL Group for Men. This small group meeting for men is designed to help those who have a desire to overcome addictions and find a new direction in life. All sessions give instruction for practical life skills through Biblical Principles found in Gods Word. Discussion and interaction are encouraged at each group meeting. They are scheduled at 7 p.m. the first, second and fourth Thursdays of the month at Eagle Ranch Ministries Inc., 1579 Pleasant Valley Road, Mount Pleasant. Registration: 724-542-7243.

n Breaking Addiction, HEAL Group for Women. This small group meeting for women is designed to help those who have a desire to overcome addictions and find a new direction in life. All sessions give instruction for practical life skills through Biblical Principles found in Gods Word. Discussion and interaction are encouraged at each group meeting. The meetings are scheduled for 7 p.m. every Tuesday at Eagle Ranch Ministries Inc., 1579 Pleasant Valley Road, Mount Pleasant. Registration: 724-244-5261 or 412-969-8520.

n Caregiver support group, 6:30-8:30 p.m., the fourth Wednesday of the month at Lafayette Manor. Classes meet in the new physical therapy department. Light refreshments are provided. Open for family and friends who have lost a loved one to cancer. Registration: http://www.excelahealth.org or 877-771-1234.

n Mon Valley Hospital will host a Suicide Bereavement Support Group 12:30 p.m. Sept. 23 in the education conference center. This support group is a four-month program that meets the second and fourth Mondays of each month. This program is led by a licensed psychologist and is free and open to all those touched by suicide. Required registration: 724-678-3601.

n Grief support group, 6-8 p.m. first Tuesday of every month, at the St. John the Evangelist Church on West Crawford Avenue in Connellsville. The group is a collaborative effort for those facing grief due to the loss of a loved one from addiction. Information: 724-628-6840.

n Al-Anon Family Groups, 8 p.m. Wednesdays, Trinity Church parlor, Fayette and Morgantown streets, Uniontown. Please enter at the handicapped ramp entrance. A second is scheduled for 7:30 p.m. Fridays, Christian Church, Pittsburgh Street, Connellsville. These meetings are for anyone who has been affected by or is having problems from someone elses drinking. Information: al-anon.alateen.org or pa-al-anon.org.

n Survivors of Incest Anonymous group, 6:30-8 p.m. the first and third Mondays of the month, excluding holidays. This 12-step recovery program is meant for men and women aged 18 or older who were sexually abused by a trusted person as a child. The group meets at the Mount Macrina Retreat Center. A similar group, Healing Friends, is from 6:30-7:30 p.m., East Liberty Presbyterian Church in Pittsburgh, on the second and fourth Tuesdays of the month. Information: peopleofcourage@gmail.com siawso.org, or healingfriends8@gmail.com.

n Missing Piece of My Heart support group, 6-8 p.m. the last Thursday of each month at the Crime Victims Center conference room in the Oliver Square Plaza. The group is for families who have lost a child to a violent crime. Information: 724-438-1470.

n Silver Generation Support Program, 10 a.m. to noon Wednesdays, East End United Community Center, Uniontown. The program is for ages 55 and older. Information: 724-437-1660.

More here:
Health briefs 09-23-19 | Healthy Living - Uniontown Herald Standard

Sleep problems are one of the most common ME/CFS symptoms. Sleep dysfunction is a critical piece of the complex puzzle that is chronic fatigue syndrome, and ME/CFS (myalgic encephalomyelitis / chronic fatigue syndrome) patients are eager for treatments that will help to improve and normalize their sleep. When I was diagnosed with ME/CFS by my primary care physician, she said, The first thing to do is to correct your sleep problems. That will make all of your other chronic fatigue syndrome symptoms improve. She was right! Here are ways to help you fall asleep faster, sleep better, and wake up feeling refreshed.

In order to treat ME/CFS sleep dysfunction, it helps to understand what healthy sleep looks like. A night of refreshing sleep consists of sleep cycles, moving through various stages in a predictable pattern:

Those deep Stages 3 and 4 are especially important for immune health, endocrine (hormone) function, and energy; its when our bodies recover and rebuild.

A healthy endocrine system, which produces hormones at the right times and in the right amounts, helps regulate sleep (and everything else).

Why do ME/CFS patients feel like we are half-awake all night and still exhausted in the morning? Traditional sleep studies comparing ME/CFS patients to healthy controls often find no measurable differences in our sleep cycles, though some show reduced total sleep time and sleep efficiency. Newer studies, using entirely different ways of measuring sleep, though, are finding that ME/CFS patients have more disruptions in REM sleep and deep stage (3 & 4) sleep. Our brains will sometimes jump right from REM or even deep stage sleep into being awake or in light Stage 1 sleep, instead of cycling through each stage as is normal. These REM disruptions in the studies correlated with worse symptoms the next day.

The hormone side is also not entirely clear. The few studies of serotonin levels in ME/CFS patients have shown contradictory results, though some do show abnormal serotonin function, indicating our bodies arent controlling serotonin the way a healthy body should. This matters because sleep deprivation causes a multitude of serious health problems, worsening every aspect of ME/CFS.

When an ME/CFS patient mentions sleep problems, doctors usually send him/her for a sleep study. The problem is, as noted above, that even carefully controlled scientific studies often fail to show abnormalities in our sleep using standard measures. Sleep studies do have an important function, though. They are designed to diagnose primary sleep disorders, like sleep apnea, restless legs syndrome, and narcolepsy. Plenty of ME/CFS patients also have a sleep disorder (some studies indicate we have a greater risk of primary sleep disorders), and its important to diagnose and treat those. Consider a sleep study to diagnose or rule out a primary sleep disorder, but dont expect it to find much with respect to your ME/CFS sleep dysfunction.

The key to correcting our sleep problem at its source is to target those hormones that are responsible for good quality sleep. This is different than taking sedatives to knock you out; it means actually correcting the problem so that your sleep feels normal and natural, and you wake up feeling refreshed. There are different ME/CFS treatment approaches to try, and it often takes some trial and error, sometimes combining treatments, to find what works best for you. Work with a doctor to find the right combination and to prevent increasing serotonin too much.

My son and I both have ME/CFS, plus tick infections, but I listened to my doctor all those years ago and treated sleep dysfunction first. Once my son got sick, we did the same for him, and we have both been sleeping a solid 9-11 hours of good quality, normal-feeling sleep every night for over twelve yearsand waking up feeling refreshed most mornings.

I first tried amitriptyline at its lowest dose, but it left me groggy in the morning. Next, I tried nortriptyline liquid in tiny doses (we started with that for my son) and gradually increased the dose as needed, until we each leveled out at an effective dose; then we switched to more convenient capsules. After a year or two, the nortriptyline wasnt working quite as well, so we added trazodone, again starting low, at just 25 mg. We both ended up (hes an adult now) at a combination of 50 mg nortriptyline and 100 mg trazodone (low doses compared to what is used for depression). We both also take melatonin supplements (5 mg for me and 8 mg for him), and I have a prescription for low-dose Ambien that I only use rarely, when I travel. We both also take plenty of magnesium, B6, and the other nutrients listed above.

Although the sleep dysfunction of ME/CFS cant be corrected just with standard guidelines for sleep hygiene, you do need to promote better sleep, in addition to whatever treatments you try. As one sleep expert explains, getting a good nights sleep requires an intricate coordination of many different elements, including some of the basics:

Myalgic encephalomyelitis and chronic fatigue syndrome are a complex web of intricate causes and effects, involving every system in the body. When sleep is disrupted, problems in the endocrine, immune, and nervous systems occur, worsening all ME/CFS symptoms. Similarly, when you treat sleep problems in ME/CFS, there will be improvements in all of these systems, leading to improved symptoms. Best of all, improving those systems will lead to even better quality sleep, in a positive domino effect. The best treatment approaches not only help you fall asleep and stay asleep but improve the quality of your sleep so that you wake up feeling refreshed and ready for a new day.

Suzan Jackson, a frequent ProHealth contributor, is a freelance writer who has had ME/CFS since 2002 and also has Lyme disease. Both of her sons also got ME/CFS, in 2004, but one is now fully recovered after 10 years of mild illness and the other just graduated from college, with ME/CFS plus three tick-borne infections. She writes two blogs, Living with ME/CFS at http://livewithcfs.blogspot.com and Book By Book at http://bookbybook.blogspot.com, and wrote an upcoming book being released in fall 2019, Finding a New Normal: Living with Chronic Illness. You can follow her on Twitter at @livewithmecfs.

Resources:

Trazodone (Desyrel) Is. Phoenix Rising website.

Alban, D, Alban P. Use Tryptophan to Boost Serotonin for Better Mental Health. Be Brain Fit website (April 3, 2019).

Bell, D. Sleep in CFS. Lyndonville News (January 2005) 2(1).

Castro-Marrero, J, SezFrancs, N, et al. Treatment and Management of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: All Roads Lead to Rome. British Journal of Pharmacology (March 2017) 174(5), pp. 345-369.

Cleare, A. The Neuroendocrinology of Chronic Fatigue Syndrome. Endocrine Reviews (April 1, 2003) 24(2), pp. 236-252.

Field, T, Hernandez-Reif, M. et al. Cortisol Decreases and Serotonin and Dopamine Increase Following Massage Therapy. International Journal of Neuroscience (July 7, 2009), pp. 1397-1413.

Jackson, ML, Bruck, D. Sleep Abnormalities in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: A Review. Journal of Clinical Sleep Medicine (December 15, 2012) 8(6), pp. 719-28.

Kishi, A. Presentation: Sleep Disturbances in ME/CFS. The National Academies of Science, Engineering & Medicine Health and Medicine Division. May 5, 2014.

Kishi, A., Natelson, BH., et al. Sleep-stage Dynamics in Patients with Chronic Fatigue Syndrome with or without Fibromyalgia. Sleep (November 1, 2011) 34(11), pp. 1551-60.

Lapp, C. Using Antidepressants to Treat Chronic Fatigue Syndrome. CFIDS Chronicle (Summer 2001).

Morillas-Arques, P,Rodriguez-Lopez, CM,et al. Trazodonefor the treatment offibromyalgia: an open-label, 12-week study. BMC Musculoskeletal Disorders(Sep 10, 2010) 11, p. 204.

Rowe, PC, Underhill, RA, et al. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Diagnosis and Management in Young People: a Primer. Frontiers in Pediatrics (June 19, 2017).

Yamamoto, S, Ouchi, Y, et al. Reduction of Serotonin Transporters of Patients with Chronic Fatigue Syndrome. NeuroReport (December 3, 2004) 15(17), pp. 2571-4.

Go here to read the rest:
Treating Sleep Problems in Chronic Fatigue Syndrome - ProHealth

Bathrooms are one of the only places where we can expect to have complete privacy. In todays world, we bring technology with us everywhere we go. The bathroom is the last sacred place where some of us leave technology behind and completely disconnect. Not for long...

For a while, determined Japanese companies have been bringing innovation to a niche market; the smart toilet market. They have been up to selling high-tech toilets at exorbitant prices since the 1980s. Meanwhile, on the other end of the globe, the Western world has been ignoring a much-needed toilet upgrade. Some of the earliest innovations in the Japanese toilet industry include heated seats to make you as comfortable as possible, remote controls that let you flush the toilet and close the lid with the press of a button and the use of ultraviolet rays to clean the toilet bowl and get rid of bacteria.

How could AI possibly contribute to improving your toilet? Toilets will now be equipped with Amazons Alexa so you can finally order you it to play music, close the lid, flush etc with voice commands, completely hands-free. These toilets are sold, randing from 1000 up to TOTOs 10000 toilet. TOTO was the first company to create smart toilets and they have mastered this market space. An American based company called Kohler has started making their own range of smart toilets which are becoming increasingly popular in the western world, shifting more people away from using traditional toilets.

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AI in smart toilets- could identify signs of diseases - AI Daily

If youre preparing for the United States Medical Licensing Examination (USMLE) Step 1 exam, you might want to know which questions are most often missed by test-prep takers. Check out this example from Kaplan Medical, and read an expert explanation of the answer. Also check outall posts in this series.

A 32-year-old woman comes to the physician because of amenorrhea for the past 15 months after delivering a baby. She says that she has also had fatigue, facial swelling, cold intolerance and has gained an additional 4.5 kg (10 lb) since her baby was born. A review of her records shows that the delivery was complicated by severe hemorrhage. Laboratory studies of serum show:

LH <1 IU/L

Estradiol 5 pg/mL (normal 20100 pg/mL)

TSH 0.1 U/mL

Injection of 500 g of TRH fails to produce an increase in either serum TSH or prolactin. Assay of other hormones is most likely to show normal levels of which of the following hormones?

A. Aldosterone

B. Cortisol

C. Follicle-stimulating hormone (FSH)

D. Gonadotropin-releasing hormone (GnRH)

E. Growth hormone

The correct answer is A.

Sheehan syndrome is hypopituitarism caused by ischemic damage to the pituitary resulting from excessive hemorrhage during parturition. The pituitary is enlarged during pregnancy; it is more metabolically active and more susceptible to hypoxemia. The blood vessels in the pituitary may be more susceptible to vasospasm because of high estrogen levels. In about 30 percent of women who have excessive hemorrhage during parturition, some degree of hypopituitarism eventually manifests.

The symptoms depend on how much of the pituitary is damaged and what cell types are destroyed. Although some pituitary hormones may be unaffected, even in severe hypopituitarism, pituitary hormones and the hormones controlled by them are more likely to be reduced than hormones that are not primarily controlled by anterior pituitary function. Our patient has amenorrhea (decreased LH) and symptoms of hypothryoidism (decreased TSH). Aldosterone secretion is relatively independent of adrenocorticotropic hormone; it is controlled mainly by angiotensin II and plasma potassium concentration. Aldosterone is least likely to be reduced by hypopituitarism. Treatment is replacement of thyroid hormone and cortisol.

Read these explanations to understand the important rationale for each answer to help you prepare with future studying.

Choice B: Cortisol is controlled by pituitary production of ACTH; because ACTH is often impaired in Sheehan syndrome, reduced secretion of cortisol is likely.

Choice C: The pituitary necrosis that is the root cause of Sheehan syndrome is highly likely to reduce secretion of follicle-stimulating hormone (FSH). The observation of reduced estradiol in this patient strongly suggests that FSH is low because estradiol increases as follicular development occurs.

Choice D: The presence of the depressed levels of estradiol and leuteinizing hormone (LH) in this patient releases hypothalamic secretion of GnRH from its normal feedback control. GnRH levels are likely to increase above normal.

Choice E: Growth hormone is very likely to be reduced by the pituitary necrosis.

For more prep questions on USMLE Steps 1, 2 and 3, viewother posts in this series.

The AMA selected Kaplan as a preferred provider to support you in reaching your goal of passing the USMLE or COMLEX-USA.AMA members can save 30% on access to additional study resources, such as Kaplans Qbank and High-yield courses. Learn more.

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Kaplan USMLE Step 1 prep: Woman has amenorrhea after birth of baby - American Medical Association

Monday, September 23 marks the next equinox and the start of Autumn season in the Northern Hemisphere, where days will begin to get shorter, nights get dark earlier, and the temperatures will drop.

Monday marks Autumnal Equinox, one of two days when the sun is located exactly above the Earths equator and day and night are roughly equal.

Fall is an easy season to love. One thing you might not realize, though, is that the change in temperature has some effects on your health.

Here are 19 surprising ways fall weather affects your wellbeing, according to msn.

1. Your risk of heart attack increases

Your heart definitely isnt a fan of that chill in the air. "In colder weather, we typically see rates of heart attacks go up," says New York City-based internist and cardiologist Edo Paz, MD, a doctor with K Health. "There are various reasons for this, including increased blood pressure and increased risk of blood clots. The best way to mitigate this risk is to dress warm."

2. Your eyes get dry

The cold, dry air of the fall has a tendency to dry your eyes out and leave a burning sensation in its wake. "Seasonal changes like dryer air make dry eye worse," according to the experts at Piedmont Eye Care in Charlotte, North Carolina. Thats because they either "cannot produce enough tears or they produce low-quality tears."

When your eyes are begging for moisture, you can get some relief by using artificial tears or getting some eye drops from your doctor. The optometrists at Piedmont also suggest getting a humidifier, protecting your eyes outside with either a hat or sunglasses, staying hydrated, taking breaks from screen time, and trading in your contacts for glasses.

3. Your skin becomes cracked and dry

Cold weather doesnt just bring on eye dryness. It also dries out your skin, says Paz. To combat the problemand make sure youre not itchy and cracked all season longuse plenty of lotion, load up on sunscreen, and skip the long, hot showers and baths, which only dry your skin out even more.

4. You experience more aches and pains

Always feel more achy in the colder months? Youre not alone. Research has shown there may be an association between colder temperatures and an increase in aches and pains, particularly in the back and neck areas.

There are multiple theories behind this, but one prominent one, according to University of Chicago Medicine rheumatologist Anisha Dua, MD, MPH, is because of the "drops in barometric pressure, which causes tendons, muscles, and the surrounding tissues to expand." According to Dua, "because of the confined space within the body, this can cause pain, especially in joints affected by arthritis."

5. Your vitamin D levels plummet

In the summertime, all that sunshine you absorb gives you more than enough vitamin D. However, once the season shifts, thats not quite the case anymore.

"In the fall, our vitamin D levels fall rapidly," says Kristine Blanche, PhD, RPA-C, owner of the New York-based Integrative Healing Center. According to Blanche, as your vitamin D levels fall, youre not only more susceptible to colds and the flu, but this can also affect your hormone levels.

6. You feel depressed

Fall should bring on joy in the form of fun family-centric holidays and cozy movie nights by the fire. However, its also known to bring on the seasonal affective disorder (SAD), which "can cause depression symptoms typically due to less exposure to sunlight, says Paz. His advice? "Stick to a regular workout routine" to keep your endorphin levels up.

7. And you lack energy, too!

SAD doesnt just affect your mood. It also affects your energy levels. Along with making you depressed, the seasonal disorder can also cause you to feel sluggish and agitated come fall, according to the Mayo Clinic. If this is the case for you, chat with your doctor about treatment options so the changing seasons dont dampen your spirits.

8. You have trouble breathing

Once the air gets cold, you might have a harder time breathing. According to the American Lung Association, cold, dry air can irritate the airways of those who are already dealing with breathing issues from asthma or chronic obstructive pulmonary disease (COPD). If you know you have airway issues, always make sure youre bundling up and avoid exercising outdoors when the air is especially dry.

9. Youre at a higher risk of getting sick

When the temperature drops and youre spending more time indoors, youre at a higher risk of coming down with a cold or the flu. According to Berkeley Wellness at the University of California, people pick up viruses in the fall not from the weather itself, but from the subsequent time spent indoors in close proximity to others. Of course, sitting within close range of someone whos sick increases your chances of picking up their germs.

10. Your allergies take a turn

Your allergies are inevitably going to be impacted by the fall weather. However, whether thats for the better or for the worse depends on what exactly youre allergic to.

"The arrival of fall weather will bring relief for some, and a worsening of symptoms for others," says California-based physician Alexandra Stockwell, MD. "Anyone who suffers from an allergy to pollen will start to feel some relief when temperatures drop, humidity improves, and pollen is no longer in the air. And for anyone allergic to mold, the fall weather can exacerbate symptoms. Mold thrives in leaf piles, compost piles, and anywhere organic matter is decomposing. Because its airborne, you can be negatively impacted by mold from surrounding areas."

11. You get more headaches

Its not uncommon for cold weather to cause headaches. Thats because, according to the Mayo Clinic, the fall season is full of migraine triggers, ranging from dry air to barometric pressure changes.

12. You sleep better

When you get enough sleep every night, your mood improves, your energy levels increase, and you have fewer junk food cravings. And the transition from summer to fall could be the key to finally helping you get on a solid sleep schedule.

"Going to bed earlier as it gets dark earlier results in better quality sleep, better insulin control, and feeling rested enough to work out the next day," says Monica Auslander Moreno, MS, RD, LD/N, nutrition consultant for RSP Nutrition in Miami Gardens, Florida. Its a win in the bedroom that translates to more success in the kitchen, at the gym, and pretty much everywhere else.

13. You experience hair loss

According to The Choe Center For Hair Restoration in Virginia Beach, Virginia, people typically lose between 50 and 100 strands of hair a day. However, in the fall monthstypically in October and Novemberthis number tends to be closer to 100. If you notice some extra shedding in the shower or when youre brushing your hair in the fall, its likely nothing to worry about.

14. Your diet could get better

During the summer months, its fun to get out and enjoy the warm weather at outdoor bars and restaurants. In the fall, however, youre much more inclined to make the most of your kitchen, which is great news for both your wellbeing and your waistline.

"The cooler temperatures make fall a great time to hit up the farmers markets and add some local and seasonal foods into your diet," says Sheli Msall, RDN, the dietitian behind Nutritionist Abroad. "Its also a fun season to cook and bake in, as you dont mind warming up the kitchen now that its getting cooler outside."

15. Or you might pack on the pounds

While fall can bring on healthy eating habits, the change in season can also have the opposite effect. "When the weather turns colder, we generally adjust our eating styles to warm comfort foods associated with family events and holidays," says Brenda Rea, MD, DrPH, PT, RD, family and preventive medicine physician at Loma Linda University Health in Loma Linda, California. "This often can result in more hot and sugary drinks, hot soups laden with saturated fat and salt, and, of course fruit pies with sugar, saturated fat, and refined flour."

Luckily, Rea says that these comfort foods can easily be replaced with similarand much healthier!alternatives that are just as satisfying. "Hot sugary drinks can be replaced with hot green tea or lemon water; soups can have less salt and no added fats while still maintaining a fabulous taste, and fruit can be consumed fresh and made into a fruit compote with dates for sweetening," she suggests.

16. You could inadvertently be warding off inflammation

Chronic inflammation can lead to a long list of health problems, from heart disease to autoimmune disorders. The good news? Having the urge to sip on some tea during the chilly fall months could help fight it off. "Fall teas and spices are anti-inflammatory," says Moreno. Sip on green tea, turmeric tea, and ginger tea for the best results.

17. You might become more active

During the summer, the sun is strongoften too strong to allow for a run or any other type of outdoor workout. Once fall hits, though, the weather cools down a little, making it a great time to up your activity levels before winter hibernation hits.

"As the weather cools, its a perfect opportunity to bike, walk, or run outside in the crisp fall weatherespecially in the mornings before work and on weekends," says Moreno. "Who doesnt like to ogle the beautiful foliage?"

18. But you could also become more sedentary

Though for some people the tepid temperatures of fall are ideal for outdoor activities, for others, its quite the opposite. The cooler weather could send you straight into hibernation-mode, causing you to abandon your exercising habits in favor of lounging on the couch.

If youre avoiding the outdoors, make sure youre at least incorporating some at-home exercises into your routine. There are plenty of different apps, online workout programs, and free videos on YouTube to take advantage of.

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It's officially autumn..see how autumn weather may affect your health! - Roya News English

Denisovans are a mysterious group of our ancient relatives, unknown until a decade ago, who lived alongside Neanderthals and Homo sapiens. The hominin species is thought to have ranged from Siberia to Indonesia, and many places in between (although some researchers believe the Denisovans could actually be multiple species or groups). When these curious human cousins vanished, they left behind surviving bits of their DNA in living Melanesian and East Asian people, but not much else. So far, the only known Denisovan fossils include just a few teeth, a finger bone and a small fragment from a Russian cave, and a partial jaw found on the Tibetan Plateau.

Yet today its possible to stare into a Denisovan face for the first time thanks to a striking reconstruction created by some genetic detective work. Scientists used patterns of gene expression mined from ancient Denisovan DNA, which was extracted from a 100,000-year-old pinkie finger, to reconstruct the physical characteristics of a Denisovan face and skulleven though such a fossil has never been found.

Geneticist Liran Carmel of the Hebrew University of Jerusalem said other groups have worked to map anatomical features from the information hidden in our DNA. But his team took a different approach, outlined in a study published today in Cell.

We didnt rely on the DNA sequence per se, Carmel says. But from the sequence we used a technique which allows you to reconstruct gene activity patterns in these ancient individuals so we can compare the way the genes work in the different human groups.

The addition of methyl groups to DNA, or molecules derived from methane, impacts the ways genes activate and express themselves, in turn determining what physiological traits those genes produce. Carmels group mapped these methylation patterns to recreate the likeness of a young female Denisovan, which the pinky bone belonged to. Evolutionarily speaking, its well known that many anatomical or physiological differences between closely related groups are attributed to changes in gene activity patterns. This is exactly what we can find using our technique, Carmel says.

Chris Stringer, a paleoanthropologist at the Natural History Museum, London, who was unaffiliated with the study said via email that the reconstruction of Denisovan anatomy is a pioneering piece of research, which at first glance seems almost like science fiction. This is exciting work, pushing the boundaries of what can be gleaned from ancient genomes.

The techniquemapping methylation patterns in DNA to determine gene expression and anatomyis still fairly new. The research relies on a complex chain of extrapolations, Stringer says. It cannot show us with perfect accuracy what a Denisovan looked like, but earlier research of Neanderthal and Denisovan DNA suggested methylation changes could be used to explain anatomical differences. For the new study, when Carmel and colleagues tested their technique against known Neanderthal and chimpanzee anatomy, they found a close match.

Using these types of epigenetic techniques to predict the traits of living humans is still difficult, so applying it to the ancient DNA of an extinct hominin species has its limitations. Denisovans, a little-known hominin group that may be comprised of at least three different lineages, were uncovered a decade ago with a bare handful of tooth and bone fragments found in a cave called Denisova in Siberias Altai Mountains. They were the first human group to be named by DNA evidence, as only genetics revealed that the fossil fragments were from people distinct from Neanderthals. Like Neanderthals, they likely descended from an ancestral population that branched off from our own modern human family tree between 520,000 and 630,000 years ago.

But the branches of that tree continued to intertwine for many thousands of years. DNA reveals that modern humans, Neanderthals and Denisovans interbredperhaps more frequently than we might imagine. These ancient interspecies liaisons made headlines last year when a 90,000-year-old female found in a Siberian cave turned out to be the first generation hybrid offspring of a Neanderthal mother and Denisovan dad.

Carmel and colleagues mapped out Denisovan, Neanderthal and human DNA to find regions where methylation patterns differed. They then looked at modern disorders that impact the function of those same genes to try to find out what kinds of anatomical changes the ancient pattern variations might have caused. For this they employed the Human Phenotype Ontology database, which charts the genetic underlies of some 4,000 human disorders, and has produced a catalog of more than 100,000 gene-phenotype associations.

Basically, from the DNA sequence, we infer which genes have changed their activity level across the human groups and from this we make inferences about changes in anatomy, Carmel says.

By this method the team was able to reconstruct what a complete Denisovan skull and face might have looked like. They then put the method and its reconstruction predictions to the test, despite the lack of a Denisovan skull that could show how accurately the DNA evidence predicted various features of its anatomy in their reconstruction.

We tested the approach by pretending that we dont know what a Neanderthal or a chimpanzee looks like. So we reconstructed their anatomy and then compared the results to what is known.

As it turned out, real-world Neanderthal and chimpanzee fossils showed that 85 percent of the trait reconstructions accurately predicted anatomical features, like a shorter or longer section of jawbone.

While the completed study was under peer review, an incredible opportunity arosethe discovery of an actual Denisovan jaw. The 160,000-year-old jawbone was found high on the Tibetan Plateau and identified as Denisovan through the analysis of proteins preserved in the teeth. Carmel and colleagues had a chance to check their work against an actual Denisovan fossil.

This was very exciting for us, Carmel says. When we submitted the paper to Cell we only had a few teeth and a finger bone to compare to our predictions. We immediately went to check how it compared to our predictions. And we find a beautiful match, so this was very reassuring for us.

Stringer agreed that the method has produced some intriguing matches with the fossil record, though it didnt always hit the mark. The results suggest that Denisovans should have features such as a low braincase, a wide pelvis and large joint surfaces and ribcage. Of course, our knowledge of real Denisovan anatomy is very limited, but features such as a long and robust jaw (from the Xiahe mandible), and a flattened and broad braincase (from the only known skull fragment) do seem to match the methods predictions, he says via email. Stringer noted that other characteristics, like thicker enamel and broader fingertips compared with modern humans, didnt match as well.

More Denisovan fossils could not only flesh out what the skulls and faces looked like, but further refine the predictive abilities of DNA methylation patterns.

There are skulls and partial skeletons from Chinese sites such as Jinniushan, Dali, Harbin and Xuchang that might also represent Denisovans, although we dont yet have their DNA or ancient proteins to test this, Stringer says.

If the skulls found in China are Denisovan, they would support the predictions in features like strong brows, wide skulls and a wide pelvis, but their faces would not project Neanderthal-style as the methylation prediction would suggest. Further muddying the waters is growing evidence from both modern and ancient DNA suggesting that the hominins currently dubbed Denisovan may well be a very diverse group that stretched across Asia.

In reality, their anatomy is likely to have shown substantial variation through space and time, Stringer says.

As genetic reconstructions improve, and additional fossils are found to check the predictions, this research could reveal what many early humans looked like. Scientists might even be able to produce an entire gallery of ancient faces, painting a family portrait of long-vanished relatives we could previously only imagine.

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Scientists Recreate the Face of a Denisovan Using DNA - Smithsonian

I'm a man and I will beat up anybody who tries to tell me I'm not a man just because my hair is thinning.

Actor Bruce Willis

Like me, many of you have seen TV ads for regrowth systems and treatments for thinning hair. I'm not talking about those who go through cancer treatments and lose their hair. These ads target people who lose hair or get thin on top due to aging or genetics or both.

These ads feature glowing reports from men about how much more masculine they feel after using the system. Or they feature the "before" guys who sadly say things like, "I didn't want my wife to leave me." Men have been made to feel less manly if they don't sport a thick head of hair.

It's often called male pattern hair loss but I've also heard male pattern baldness. According to the U.S. National Library of Medicine, it's the most common type of hair loss in men and is related to genes and the male sex hormone. It usually follows a pattern of receding hair and thinning on the crown.

Each strand of hair emerges from a tiny hole or cavity in the skin called a follicle. Baldness occurs when the hair follicle shrinks over time, resulting in shorter and finer hair. Eventually the follicle does not grow new hair.

But on the flip side, many women struggle with thinning hair, too. I reached out with questions to the University of Arkansas for Medical Science and got answers from Dr. Lauren Gibson, the chief resident who works in the department of family and preventative medicine.

Gibson says that, yes, there is also female pattern hair loss. While men tend to lose hair in a widow's peak receding pattern, women tend to lose in the front, center part of the scalp close to the forehead, the area known as "the bald spot."

Female hair loss can occur any time after puberty, but more often it happens after menopause. Because it's not as common as in men, there is not a significant amount of research or a consensus about what causes it.

There are many potential causes of hair thinning and loss aside from menopause.

The most common cause is telogen effluvium. It can be caused by diabetes, thyroid disorders, auto-immune diseases, nutritional deficiencies in calories, proteins, vitamins or minerals, smoking tobacco, excessive alcohol, illicit drug use and some medications.

Gibson says telogen effluvium can also be caused by acute or chronic major illness, major surgery, childbirth, rapid weight loss, severe emotional stress, skin infections of the scalp and inflammatory conditions of the scalp.

But this is not an exhaustive list, there are many other causes. I get the impression that this type of hair loss can possibly go away or slow down.

According to The North American Menopause Society, thinning hair happens to about half of all women by age 50, while up to 15% of women begin to experience hair growth on their chins, upper lips or cheeks after menopause.

Hair changes are common during the menopause transition and post menopause. Many factors, including hormonal changes, genetic predisposition and stress, can contribute to midlife hair changes. Along with telogen effluvium, there is also something known as androgenetic alopecia. "Alopecia" means baldness, but it does not have to be complete hair loss. It is seen as hair thinning predominantly over the top and front of the head, affects approximately one-third of all susceptible women and is most commonly seen after menopause.

It has been said that the increased ratio of androgen to estrogen during the midlife transition can influence hair changes.

There are treatments. Topical minoxidil is an FDA-approved, once-daily treatment found in most over-the-counter hair regrowth shampoos.

For those whose hair loss may be caused by underlying illness or other problems, treatment of the problem is the first line of defense.

The bottom line, Gibson says, is that if a woman is concerned by hair loss, she should talk to her doctor first. Together they can evaluate the pattern, gather a history and perform a physical exam, and if needed, evaluate for any underlying causes.

Email me at:

rboggs@arkansasonline.com

Style on 09/23/2019

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PRACTICALLY ACTIVE: Failing follicles? That's a hairy subject - Arkansas Democrat-Gazette

Four wolves were released at Isle Royale National Park in September/NPS, Phyllis Green

Four wolves were moved to Isle Royale National Park in September to bolster the island's predator population, but one died shortly thereafter.

The wolves were moved to the park on September 13 fromMichigans Upper Peninsula. One of the wolve's collars issued a mortality signal last weekend, and biologists located the animal's carcass on Tuesday. The body was to be sent to the USGS National Wildlife Health Center in Madison, Wisconsin, for necropsy.

The surviving wolves included two males and a female. Theybolstered the island wolf population to 17, which now includes nine males and eight females.

Capture, anesthesia, and translocation are stressful events for wolves and the impact of that stress on each individual wolf is unknown, Isle Royale Park Superintendent Phyllis Green said of the dead wolf. There is a field examination, however, underlying health conditions of wolves prior to their capture are difficult to determine. The analysis of the samples collected during the examination and the necropsy may reveal more information about the cause of death, which will inform future transfers.

The National Park Service worked closely with the Michigan Department of Natural Resources, U.S. Department of Agriculture APHIS Wildlife Services (APHIS Wildlife Services), and the State University of New York-College of Environmental Sciences and Forestry on the project.

Three of the four wolves released at Isle Royale National Park in September survived/NPS, Phyllis Green

From September 5 13, seven wolves were captured; three of those not meeting translocation criteria were immediately released. The four adults were examined, documented, tagged, and fitted with tracking collars before being flown to the park on a U.S. Fish and Wildlife Service airplane.

Adding genetics from Michigan wolves was a key piece of the puzzle to provide the best opportunity for genetic diversity that supports the sustainability of the introduced population. The Michigan DNR, APHIS - Wildlife Services, and SUNY-ESF did an outstanding job, given the weather, Green said. Our focus now will be on broad population goals and the opportunity these Michigan wolves represent. We will continue to learn what we can and track how the wolves integrate into the island landscape.

The three to five year effort to establish 20-30 wolves on Isle Royale is being completed in order to restore predation as a key part of the island ecosystem. Researchers involved in the planning effort recommended this number of wolves from the Great Lakes region. Additionally, they recommended an equal number of males and females in order to establish genetic variability in the new population. The NPS and its partners will monitor the wolf population to determine evidence of social organization, reproduction and predation.

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Four More Wolves Moved To Isle Royale, One Dies Shortly Thereafter - National Parks Traveler

HOUGHTON, Mich. (WLUC) - The Isle Royale fall wolf translocation project concluded on September 13 after successfully moving three wolves from Michigans Upper Peninsula to the park.

The new wolves, two males and one female, bolstered the total island wolf population to 17, which now includes nine males and eight females.

A fourth wolf was moved to the park on September 13, but its collar sent out a mortality signal over the weekend. Biologists from the National Park Service (NPS) and State University of New York College of Environmental Sciences and Forestry (SUNY-ESF) located the wolf and confirmed the mortality late on Tuesday afternoon. The carcass of the wolf will be sent to the USGS National Wildlife Health Center in Madison, Wisconsin, for necropsy.

Capture, anesthesia, and translocation are stressful events for wolves and the impact of that stress on each individual wolf is unknown, Isle Royale Park Superintendent Phyllis Green noted. There is a field examination, however underlying health conditions of wolves prior to their capture are difficult to determine. The analysis of the samples collected during the examination and the necropsy may reveal more information about the cause of death, which will inform future transfers.

The NPS worked closely with the Michigan Department of Natural Resources (DNR), US Department of Agriculture APHIS Wildlife Services (APHIS Wildlife Services), and SUNY-ESF on the project. From September 513, seven wolves were captured; three of those not meeting translocation criteria were immediately released.

The four adults were examined, documented, tagged and fitted with tracking collars before being flown to the park on a US Fish and Wildlife Service airplane.

Adding genetics from Michigan wolves was a key piece of the puzzle to provide the best opportunity for genetic diversity that supports the sustainability of the introduced population. The Michigan DNR, APHIS-Wildlife Services, and SUNY-ESF did an outstanding job, given the weather, Green said. Our focus now will be on broad population goals and the opportunity these Michigan wolves represent. We will continue to learn what we can and track how the wolves integrate into the island landscape.

The three to five year effort to establish 20 -30 wolves on Isle Royale is being completed in order to restore predation as a key part of the island ecosystem.

Researchers involved in the planning effort recommended this number of wolves from the Great Lakes region. Additionally, they recommended an equal number of males and females in order to establish genetic variability in the new population. The NPS and its partners will monitor the wolf population to determine evidence of social organization, reproduction and predation.

See the rest here:
3 wolves added to Isle Royale population during fall 2019 wolf project - UpperMichigansSource.com

In 1969, Margaret Rossiter, then 24 years old, was one of the few women enrolled in a graduate program at Yale devoted to the history of science. Every Friday, Rossiter made a point of attending a regular informal gathering of her departments professors and fellow students. Usually, at those late afternoon meetings, there was beer-drinking, which Rossiter did not mind, but also pipe-smoking, which she did, and joke-making, which she might have enjoyed except that the brand of humor generally escaped her. Even so, she kept showing up, fighting to feel accepted in a mostly male enclave, fearful of being written off in absentia.

During a lull in the conversation at one of those sessions, Rossiter threw out a question to the gathered professors. Were there ever women scientists? she asked. The answer she received was absolute: No. Never. None. It was delivered quite authoritatively, said Rossiter, now a professor emerita at Cornell University. Someone did mention at least one well-known female scientist, Marie Curie, two-time winner of the Nobel Prize. But the professors dismissed even Curie as merely the helper to her husband, casting him as the real genius behind their breakthroughs. Instead of arguing, though, Rossiter said nothing: I realized this was not an acceptable subject.

Acceptable or not, the history of women in science would become Rossiters lifework, a topic she almost single-handedly made relevant. Her study, Women Scientists in America, which reflected more than a decade of toil in the archives and thousands of miles of dogged travel, broke new ground and brought hundreds of buried and forgotten contributions to light. The subtitleStruggles and Strategies to 1940announced its deeper project: an investigation into the systematic way that the field of science deterred women, and a chronicling of the ingenious methods that enterprising women nonetheless found to pursue the knowledge of nature. She would go on to document the stunted, slow, but intrepid progress of women in science in two subsequent volumes, following the field into the 21st century.

It is important to note early that womens historically subordinate place, in science (and thus their invisibility to even experienced historians of science) was not a coincidence and was not due to any lack of merit on their part, Rossiter wrote at the outset in the first volume. It was due to the camouflage intentionally placed over their presence in science.

Rossiters research has been revolutionary, said Anne Fausto-Sterling, a Brown University professor emerita and an expert on developmental genetics, who was astonished by the first volume when it came out. It meant that I should never believe anything anybody tells me about what women did or didnt do in the past, nor should I take that as any measure of what they could do in the future.

Academic historians typically dont have an immediate impact on everyday life. Rossiter is the exception. In excavating the lives of forgotten women astronomers, physicists, chemists, entomologists and botanists, Rossiter helped clear the way for women scientists in the future. Her work showed that there were women in science, and that we could increase those numbers, because women are quite capable of it, said Londa Schiebinger, a historian of science at Stanford University. In addition, Rossiters work illustrated that administrators needed to reform academic institutions to make them more hospitable to women. She showed that very talented women faced barriersand so that sparks something.

Rossiters findings were impressive to key figures at the National Science Foundation, which funded her research over many yearsand which, starting in the 1980s, also began funding efforts to increase the representation and advancement of women in engineering and academic science degrees. Schiebinger said, All of Margaret Rossiters well-documented work gives an intellectual foundation for these things.

Today, Rossiter, 75, has scaled back her research efforts and carries a light teaching load at Cornell. But her work remains deeply important, in large part because she knew how to make a point stick. Back in 1993, Rossiter coined a phrase that captures an increasingly well-recognized phenomenon: the Matilda Effect, named after a suffragist, Matilda Gage, whose own work was overlooked by historians, and who also wrote about the way women scientists, in particular, had been erased by history. Rossiters 1993 paper decried the troubling recent history of male scientists receiving credit for work done by female scientists. The phrasethe Matilda Effecttook off, and has been cited in hundreds of subsequent studies. A 2013 paper, The Matilda Effect in Science Communication, reported that both men and women judged research papers by men to be stronger than those by women, and both men and women showed preference for the male authors as possible future collaborators. In the past year alone, dozens of papers on gender discrimination in science have cited the Matilda Effect. In naming the phenomenon, Rossiter identified the issue of misplaced credit as a problem that institutions would have to fight to rectify, and that equality-minded scholars are monitoring with even more rigor.

Both Margaret Rossiter and Matilda Gage made substantial original contributions to American scholarship that were, for too long, not recognized as significant; and, interestingly, both tried to bring to light the work of other women who suffered the same fate. Their births separated by more than a century, the two nonetheless have almost a symbiotic relationship, with the work of one giving new life to that of the other in a collaboration across time to advance the role of women in the sciences, a fight ongoing in laboratories and the halls of academia.

* * *

The Matilda Joslyn Gage Center, in Fayetteville, New York, is a gracious cream-colored Greek Revival building, renovated and restored to something close to the state it was in when Gage was working furiously to secure women the right to vote. A small desk in the bay window of the back parlor is the same one where she likely wrote dozens of editorials for her newspaper, the National Citizen and Ballot Box, the official publication of the National Woman Suffrage Association; upstairs was the guest bedroom where the suffragist Susan B. Anthony, with whom she frequently collaborated, often stayed.

On the day I agreed to meet Rossiter there (she lives in Ithaca, 60 miles to the south), Colleen Pilcher, then the museums deputy director, was waiting to greet her. She had prepared tea and set aside time for a tour. The museums founder, a historian named Sally Roesch Wagner, who has devoted much of her career to uncovering Gages achievements, left a note saying she was sorry not to be there to see Rossiter, to whom we are so grateful for creating the concept of the Matilda Effect, which we refer to regularly.

Rossiter looked around, taking in a framed photo of Gage propped on a side table: Gage, her curly hair by then gray, stared out in profile, intent and focused. Think what they were up against, Rossiter said, speaking of the suffragists. Men controlled everythingthe press, the church, every local and national political office. They had all the power, everywhere.

Gage was the daughter of an exceptionally forward-thinking father, an abolitionist and doctor who raised his daughter to practice medicine. No medical school in her area would accept a woman, so instead, while the mother of five children, she channeled her intellect into abolitionist activism (her home was a stop on the Underground Railroad), as well as the burgeoning suffragist movement. She spoke at the third National Womans Rights Convention in Syracuse, in 1852, and was a founding member of (and frequent officeholder in) the National Woman Suffrage Association.

A freethinker who championed the separation of church and state, Gage was also the first known American woman to publish a study of American women in scienceanticipating Rossiter by a century. In Woman as an Inventor, published as a tract in 1870 and in the North American Review in 1883, she wrote, The inventions of a nation are closely connected with the freedom of its people. Given more liberty, she argued, women would only help the countrys technological progress. To support her argument, she listed many of the inventions women had initiated (the baby carriage, a volcanic furnace for smelting ore, the gimlet-point screw, to name a few). Gage also asserteda contention some historians considerthat Eli Whitney merely manufactured the cotton gin after being given very specific directions by its actual inventor, Catharine Littlefield Greene, widow of Revolutionary War general Nathanael Greene, who had settled in Georgia. Every part of the world felt the influence of this womans idea, wrote Gage. If Greene did not take out a patent for the invention, Gage said, it was because to have done so would have exposed her to the ridicule and contumely of her friends and a loss of position in society, which frowned upon any attempt at outside industry for woman.

Rossiter first learned about Gage in the early 1990s, while reading a relatively obscure book about overlooked women intellectuals. Soon after that, in 1993, Rossiter attended a conference at which researchers presented several papers on women scientists whose work had wrongly been credited to men. It was a phenomenon, Rossiter recalled thinking. You need to name it. It will stand larger in the world of knowledge than if you just say it happened. She decided on the Matilda Effect, after Matilda Gage, and wrote an essay in the journal Social Studies of Science that she called The Matthew Matilda Effect in Science. (The Matthew Effect was a term coined previously by two sociologists, to describe the practice of more powerful scientists being given credit for the work of those with less recognition.) Gage, Rossiter wrote in that essay, noticed that the more woman worked the more the men around her profited and the less credit she got.

The purpose of naming the phenomenon, Rossiter asserted in her essay, was to help current and future scholars to write a more equitable and comprehensive history and sociology of science that not only does not leave all the Matildas out, but calls attention to still more of them.

Rossiters historical research has spotlighted hundreds of women scientists in america. here are a few of the most notable who persevered to expand our understanding of the universe, from black holes to genes to computers

The cytogeneticist was the first woman to receive an unshared Nobel Prize in Physiology or Medicine, awarded in 1983. She traveled extensively for two decades to collect maize samples in South and Central America. Her research demonstrated the existence of mobile genetic elements, also known as genetic transposition, the capacity of genes to change position on a chromosome.

Rossiter cited one victim of the Matilda Effect who dated back to the 11th century, but also included more recent examples such as Jocelyn Bell Burnell, a doctoral student in radio astronomy at Cambridge University in the late 1960s. Bell Burnell was the first in her lab to discover the astronomical object that would lead to the identification of pulsars. Despite her obvious contributions, she was not included in the all-male citation when her team won the physics Nobel Prize for this work in 1974. Last year, 25 years after Rossiter acknowledged Bell Burnells accomplishments, and 44 years after she was robbed of the Nobel, Burnell won the Special Breakthrough Prize. The award comes with $3 million, all of which she donated to Englands Institute of Physics, to fund underrepresented figureswomen, refugees and ethnic minorities. I have this hunch that minority folk bring a fresh angle on things, Burnell told the BBC.

* * *

Rossiter thought that her first visit to the Gage museum would be a pleasant excursion to a historical site of personal interest to her. Instead, it turned out to be something of a revelation. It was not, in fact, the patriarchy that wrote Matilda Gage out of history, Pilcher explained, citing decades of research by her colleague Wagner. The powerful figures who marginalized Gage were her two fellow suffragist collaborators, after a falling out over the role of religion in the movement.

Gage felt that Christianity was the root of womens problems, Pilcher said. Elizabeth Cady Stantons writings, Pilcher explained, would later reveal how strongly Stanton concurred; but in the desperate pursuit of an expanding constituency to support the vote for women, Stanton and Susan B. Anthony made what they must have perceived as necessary compromises. They collaborated with religious womens groups, including the Temperance Union run by Frances Willard, which wanted to establish Jesus as the titular head of the United States government. The move alienated Gage, who split from Stanton and Anthony to found her own, competing suffragist group. When Stanton and Anthony revised a work on which Gage had originally collaborated, the History of Woman Suffrage, Gage was no longer listed as an author.

Hmm! Rossiter exclaimed, clearly fascinated. You would have thought theyd have been more sisterly. It was fortunate, she added, that the house still stood. It was here that Wagner had discovered a trove of letters that shed so much light on this hidden figure of history. If the house had burned down, Rossiter said, that would have been the end of it.

It is an odd wrinkle of feminist history that one of the most powerful terms used to identify overlooked female scientists has been named after a woman diminished not by male credit-grabbers but arguably the two most influential feminists in American history. In their effort to win the vote, Stanton and Anthony made choices that bowed to traditional power structuressome of them racist, some of them based in the church, and all of them controlled by men. In that regard, perhaps, it could be said that it was the male establishment that coerced Stanton and Anthony to erase Gage. But in the end, patriarchy eliminated even Susan B. Anthony and Elizabeth Cady Stanton, Rossiter later wrote in an email. Because in my day (undergrad and grad in the 1960s) all womens history had been forgotten or obliterated and was not taught at much of any colleges. When the founders of womens history began to start research and writing (1970s), they all had to bone up and read Eleanor Flexners Century of Struggle, the only survey of the subject and for which the author had had a hard time finding a publisher.

* * *

Fifth generation of Malden, Mass., Rossiter likes to say of her birth, as if that New England pedigree reveals much about her essence. Malden may be little known, but its history of resistance is rich: It was the first town to petition the colonial government to secede from British rule. The first same-sex couple to get legally married in the United States was from Malden (they were married in nearby Cambridge). Rossiters father was a Harvard graduate and high school history teacher; and her mother, who graduated from Radcliffe, raised her children, only working outside the home later in life, after receiving a masters degree. By high school, Margaret Rossiter, a bookish girl in a bookish home, had developed a fascination with the history of science. Margaret, who plans to study math at Radcliffe this Fall, lists biographies of the 17th century as her favorite reading matter, the Boston Globe reported in 1962, in an article that celebrated Rossiter as one of several National Merit Scholarship winners from the area. That was before Newton developed the calculus, 17-year-old Rossiter was quoted saying. She went on to Radcliffe, and would graduate in 1966. Even in her first year she remembers poring over Isis, the history of science journal, in a top bunk in her dorm room.

Following an unsatisfying grad-school stint at the University of Wisconsin, Rossiter transferred to Yale, which is where she found herself, on Friday afternoons, surrounded by pipe smoke, beer and history of science professors and students, nearly all male. From 4:30 to 6, Rossiter said, you endured this for self-preservation. Mary Ellen Bowden, also a history of science graduate student at the time, would become a senior research fellow at the Science History Institute. She recalls Rossiter, as a graduate student, as someone who seemed like a quiet sort, but once you got her one on one, talked on and onshe was very perceptive and critical of the things going on around her. Some scholars just hit the books, but Margaret had other interests in humanity. Rossiter completed her PhD at Yale, in 1971, a rare woman in a small, backward-looking field, and took a fellowship at Harvard, where she happened, one afternoon, to peruse American Men of Science, a kind of encyclopedic history. Despite the certainty of her mentors at Yale about the nonexistence of women scientists, and despite the very title of the volume, she was surprised to see entries about womenbotanists trained at Wellesley, geologists from Vermont. There were names, and patterns she could trace from one to the other. (Rossiter also would conduct research on women in science at Smithsonian Institution archives and libraries in Washington, D.C.)

In Malden she picked up the family Volkswagen, then drove around to womens colleges, delving into boxes of archives. She identified what she called protg chains of women educated by professors who then went on to replace those professors, some tracing their lineage back several generations. Scouring indexes for obituaries, she discovered women scientistsbut they were segregated, cloistered at womens colleges (she defined this as territorial segregation); or they were undervalued, underpaid, kept in assistant jobs where they did mountains of tedious work, never promoted like their male counterparts (hierarchical segregation). She also discovered, reading letters of recommendation, a way of thinking she called restrictive logic, in which male scientists relied on nonsensical rationales to explain why a particular female scientist could not be promoted (a classic example: because there was no precedent). She found, in short, that many men of science were incapable of reason when it came to women. Womens credentials, she wrote, were dismissed as irrelevant in favor of stereotypes, fears, and long-cherished views. Examining, for example, the collective efforts of male professors to halt the likely appointment to a full professorship of the famous German physicist Hertha Sponer, at Duke, Rossiter vented that Sponer was evidently up against not only all the other applicants for a job at Duke in 1936 but also certain physicists collective views and misconceptions about all of womankind.

Rossiter herself, more than a decade out of graduate school, still had failed to secure a tenured position, and was a visiting scholar at Cornell. Margaret knew she deserved to be on a tenure track, Fausto-Sterling recalls, and something was wrong that she was notit wasnt like, Oh, Im so lucky to have any job. It was, This is not right.

Then, in late 1982, Rossiter published the first volume of Women Scientists in America, with Johns Hopkins University Press. To her surprise and her publishers, the New York Times gave the historical tome a rave review. The rich detail she discovered about the history of American women scientists is placed in the context of social change in the 19th and 20th centuries, and the result is a splendid book, wrote the reviewer, Alice Kimball Smith, a historian.

Rossiter was a visiting scholar at Cornell when she was awarded a MacArthur Fellowship (or the so-called genius grant) in 1989. The following spring of 1990, a tenure-track offer arrived from the University of Georgia. Even so, Cornell seemed ready to let her depart. She thinks a female member of the Cornell board of trustees intervened, because, suddenly, Cornell offered to create a new department aligned with Rossiters intereststhe Graduate Program in the History and Philosophy of Science and Technology. Tenure followed in 1991. I remember being so relievednow I could get back to my next book, instead of apartment hunting, said Rossiter. After many years of identifying with the struggles of those whom she was studying, at last she found the kind of institutional support to document the obstacles faced by those who did not have such support but deserved it.

It is not only women in science who have much to learn from Rossiters research, said M. Susan Lindee, a historian of science at the University of Pennsylvania. We have to look at her past work carefully, said Lindee, and re-examine all those brilliant strategies that women used to contest institutional power, which was oriented around preventing them from succeeding.

In 2013, Fausto-Sterling, whose own work has challenged sexist presumptions in evolutionary science, stepped forward to make sure that Rossiters contributions would be widely accessible. Fausto-Sterling joined forces with a former student of hers, Maia Weinstock, who had led a series of Wikipedia edit-a-thons, events where volunteers amplified entries about the lives and achievements of female scientists published in the free, crowd-sourced online encyclopedia. Fausto-Sterling found that Rossiter, at that point, merited only whats known as a stuba few lines. I was shocked that she had this skeleton entry, said Fausto-Sterling, who went on, during that editing session, to contribute a fleshed-out entry about Rossiter.

Rossiter was one of the first to map out a problem in science that its practitioners are only now struggling to address with peak urgency: Earlier this year, the prestigious medical journal the Lancet devoted an entire issue to the underrepresentation of women in science, announcing, among other things, that less than 30 percent of the worlds researchers in science are women. The Lancet studies took up many of the questions that Rossiter first posed in 1982. What biases are holding women back? Where are their numbers lowest, and why? Why do they receive less funding than men? But the mistreatment of women in science and other professions had already caught fire in the public imagination with the rise of the #MeToo movement.

* * *

The University of California, Berkeley found in 2015 that the prominent astronomer Geoffrey Marcy had violated its sexual harassment policy. A 2018 report from the University of Texas system found that about 20 percent of female science students, more than 25 percent of female engineering students and more than 40 percent of female medical students had experienced sexual harassment from faculty or staff. This year, Dartmouth reached a settlement of $14 million with nine women who alleged that three tenured professors in the Psychological and Brain Sciences department had been allowed to cultivate an environment of sexual harassment and discrimination.

It is fascinating, then, that Rossiter could have written no fewer than 1,200 pages about women in sciencewho had even less power and fewer rights during the period she covered than they do nowwithout so much as a hint that sexual harassment and, quite likely much worse, drove some women away from the sciences. Until recently, Rossiter said, she had not considered just how powerful a role harassment or assault must have played in the history of women in science. It explains the dropout rate, she said.

Rossiter said she never experienced any sexual harassment herself; and never knew, for example, that more than one of her professors at Yale shocked her fellow student Mary Ellen Bowden by making sexual overtures. I remember feeling like it was my fault, Oh, I must have led him on, said Bowden, who realized only with the advent of the #MeToo movement that she was not to blameand that she should have been protected from harassment.

If Rossiters fellow student and friend was not revealing her secrets in real time, neither were the scores of women, long dead, whom Rossiter was studying through their letters, reviews, prizes and pay stubs. She coaxed, from those dusty papers in cardboard boxes, administrative workings and ventings about pay and overt biases and self-justifying rationales; she cross-referenced job trends with hiring patterns, the professionalization of a field with college graduation rates. But it is clear only now how much more those archives hid than they disclosed.

Nobody ever mentioned anything, said Rossiter. Those women likely just disappeared from the field. M. Susan Lindee, the science historian from the University of Pennsylvania, said she is not surprised that those issues did not surface in the documents. There was no infrastructure, no way for it to show up in administrative records, said Lindee, who nonetheless believes that harassment must have been everywhere.

Perhaps a future scholar, were she or he to sift through the same thousands of documents that Rossiter examined, might read between the lines of those letters and administrative files. There must have been incidents of harassment and violence, but also genuine office love affairs, complicating resentments that male colleagues felt about women in the workplace; there would have been ambition punished with shame, and compromise mixed with resignation.

When Rossiter started her research, the Xerox was fresh technology; she worked with paper trails, but of a certain discreet kind. Archivists were discouraged from acquiring papers that were too personal. I never saw a love letter, any financial materials, nothing on health, hardly anything about children, she wrote in an email. What I did was a kind of preliminary mapping.

Rossiter frequently goes to her office at Cornell, stacked with boxes overflowing with paper, but she cannot get into the basements and attics where families tended to stash their great-grandmothers letters. She is not terribly interested in digital research; for her, nothing is more satisfying than a manila envelope full of long-ignored documents.

In one of those many cartons in Rossiters office is a letter, from a woman scientist, that was particularly meaningful to Rossiter, mailed not long after the publication of her first volume of Women Scientists. I greatly enjoyed your work, Rossiter recalled the letter as saying. The woman went on, I have spent a lot of money on psychotherapy because people kept telling me I was maladjusted.

Rossiter, with one well-constructed sentenceAs scientists they were atypical women; as women they were unusual scientistshad made it clear to this particular woman that she was not the problem. Societys restrictions were the problem.

Rossiters book, the woman said, had done more to help her than therapy.

This was revelatory. It had never occurred to Rossiter, she said, that a clear rendering of history could be so useful.

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Women Scientists Were Written Out of History. It's Margaret Rossiter's Lifelong Mission to Fix That - Smithsonian.com

Name: Susan Alberts

Title: Robert F. Durden Professor of Biology and Chair of Dukes Department of Evolutionary Anthropology

Years at Duke: 21

What she does: Susan Alberts spends most of her work hours looking at or thinking about baboons.

Since the late 1980s, Alberts has worked with the Amboseli Baboon Research Project to gather data on hundreds of baboons in Kenyas Amboseli National Park. She studies how the social and physical environments of the baboons determine their life outcomes.

She has published more than 100 peer-reviewed articles in the fields of anthropology, genetics, endocrinology, biologyand primatology.

Her research has led to a number of findings. Her team discovered that female baboons that integrated into their social groups have higher offspring survival rates. Meanwhile, baboons who experience adversity early in life droughts, death of a parent or a mother that is socially isolated die younger than other baboons.

Were not just understanding baboons but uncovering general principals about how social life affects opportunities and health, Alberts said. Theres a lot of coincidence in how social issues affect baboons and humans.

Alberts teaches The Life and Work of Darwin, Behavioral Ecology and the Evolution of Animal Behavior, Concepts in Evolutionary Anthropology and other courses in the biology and evolutionary anthropology departments at Duke.

She also takes graduate and undergraduate students with her to Kenya for field research.

Were staying in our research camp for weeks with not a lot of modern convenience, she said. Its always exciting to watch the students adjust and thrive in a completely new environment.

What she loves about Duke: Alberts cant think of another university that would allow her the opportunity to focus on research as much as the leadership at Trinity College of Arts & Sciences.

Duke is one of the few places I have the freedom to do to my kind of research, Alberts said. It takes a lot of infrastructure to do this abroad. It takes good grant support. It takes good administrative support. Duke has worked really hard to make all this possible.

Memorable day at work: The U.S. National Academy of Sciences, a nonprofit organization of the countrys leading scientific researchers, elected Alberts as a member in May. The recognition is considered one of the highest honors a scientist can receive.

I was thrilled and honored, Alberts said. Its my job now to pay it forward and make the most of the opportunity.

Special object in her office: When the National Academy of Sciences named Alberts a member, she popped a bottle of champagne and placed the cork among a collection of eight others on a bookshelf in her office. Other corks represent each Ph.D. student Alberts has advised.

We always celebrate with a glass of champagne when they defend their thesis, Alberts said. I collect the corks because each of those moments is a huge event. I feel so much admiration to my students.

Best advice received: As as postdoctoral researcher, Alberts received a Fellowship at Harvard Universitys Society of Fellows, a group of scholars recognized for their academic potential, after completing her Ph.D. at the University of Chicago.

Alberts didnt feel qualified for the fellowship and called her mentor, Jeanne Altmann, the Eugene Higgins Professor of Ecology and Evolutionary Biology at Princeton University, saying I think they made a mistake!

Altmann told Alberts, It doesnt matter, just dont get immobilized.

Jeannes advice helped me focus, Alberts said. I had to show up and do my best.

First job: Alberts worked at a Seattle bakery called The Little Bread Company after high school. She arrived every morning around 4:30 to knead and mix doughs for whole wheat, rye and sourdough loaves of bread.

I liked working with my hands, Alberts said. I learned so much about how you work with people coming from different backgrounds and who have different expectations, desires and abilities. It really helped me develop.

Something most people dont know about her: Alberts loves jigsaw puzzles. She recently worked on a 500-piece puzzle with the image of a sea turtle.

I dont have much time to do them, but I love them, she said. I love the process of just starting out with a big mess and putting it into a coherent image.

Is there a colleague at Duke who has an intriguing job or goes above and beyond to make a difference?Nominate that personfor Blue Devil of the Week

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Blue Devil of the Week: A Renowned Baboon Scientist - Duke Today

A replacement heifer represents the costliest improvement in the genetics of a herd. Some of the more important influencers that are critical to the success of retaining these genetics over time include hiring the right female, reaching a target breeding weight, proper development, and a defined breeding season.

As we know, reproductive traits are very lowly heritable; 10% controlled by genetics and the other 90% controlled by management and environment. This forces us to be intentional managers within the environment we live. Being better managers naturally forces us to use more data to make decisions that can improve fertility responses from good nutritional management.

Related: Pregnancy check replacement heifers to protect investment

The goal in developing replacement heifers is reaching puberty by the beginning of the breeding season. Puberty in heifers is controlled by three factorsbody weight, age and breed.

With breed, we know that on average Bos taurus cattle reach puberty between 12 to 14 months of age; whereas Bos indicus cattle reach puberty later at approximately 16 to 18 months of age.

Related: Weighing the costs of buying or raising replacement heifers

Heifer body weight has a very influential impact on age at puberty. Research conducted in the 1980s reported that heifers weighing approximately 60-65% of their mature body weight reached puberty prior to breeding.

Not every heifer will make a good replacement heifer. The female you want to hire conceives early in the breeding season. However, to get there we need to make some decisions earlier on in the hiring process.

You need a pool of candidates to start with based on your job description. The job description will lay out minimum requirements the heifer has to have in order to go through the development process.

These requirements should include, at minimum, no freemartins, minimum body weight, minimum age, structural soundness and not out of terminal sires. Throughout the development process, checkpoints need to be in place to monitor the heifers performance of your heifers.

And finally, after the breeding season, is she pregnant and preferably early on in the breeding season? Then, and only then, should we hire her for the job!

To properly develop heifers to 60-65% of mature body weight, you need to know the mature body weight of your cows, otherwise it is just a guess. If you dont know what your cows weigh, you dont know what 65% of mature weight is and what those heifers should weigh at breeding.

At minimum, know what the average weight of your cow herd is so you can determine what her expected mature body weight is. If you have the capabilities to determine this individually, then you can avoid breeding heifers that are too light or too big. The implications of developing heifers too light is not reaching puberty. Developing heifers that are too heavy (or too fat) is a reduction in fertility rates and increased development cost.

Proper development starts with knowing how much she weighs, how much she needs to weigh, how many days you have to get her there and what her nutrient requirements are. Then, you can determine what her average daily gain needs to be and monitor progress to make sure she is on track for breeding.

Typical forage-based development diets for heifers consist of 9% crude protein and 60% total digestible nutrients to achieve a steady rate of gain of 1.5 pounds per head per day. Some programs develop heifers at different rates of gain at different stages of development. Overall, results seem to be similar, regardless of the development stages, as long as she reaches her target breeding weight and is on a positive nutrition plan throughout the development period.

Drastic changes in diets prior to the breeding season can cause wrecks sometimes. Some work out of South Dakota showed significant decreases in pregnancy rates in replacement heifers that were turned out on grass pasture from a dry lot in late spring at the beginning of the breeding season. To avoid this, make sure heifers are on the same forage system (diet) at least 30 days prior to the breeding season.

Without a defined breeding season, we cant manage for fertility. Work out of Clay Center, Neb., in the 2000s reported a higher retention rate across nine calving seasons in replacement heifers conceiving in the first 21 days of their first breeding season compared to heifers conceiving after day 42 of the breeding season.

Preliminary data out of Louisiana State University reported similar results where 28% more heifers conceived to timed-AI during their first breeding season and developed to more than 65% of mature body weight remained in the herd through their fifth calving season, compared to heifers bred by natural service within a 75-day breeding season. In that study, heifers that reached more than 65% of mature body weight at breeding were out of smaller cows, and as a result had a lighter target mature body weight.

The perfect development protocol is one that results in heifers reaching the target age, weighs 60 to 65% of mature body weight, has reached puberty, conceives within the first 21 days of the breeding season and does not require taking out a loan to develop her. Nutrition is critical to ensuring heifers reach puberty by the start of the breeding season. Intentional management plays a major role in achieving high fertility rates during the breeding season at a manageable cost.

Walker is Noble Research Institute livestock consultant. Contact him at rswalker@noble.org.

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How to hire the right replacement heifers for your job - Beef Magazine

Contrary to claims made, genes from genetically-modified Aedes aegypti mosquito were found to have been transferred to naturally-occurring A. aegypti mosquito population in three areas in Brazil where transgenic mosquitoes were released. It is unclear if the presence of transgenic mosquito genes in the natural population will affect the disease transmission capacity or make mosquito control efforts more difficult. A.aegypti mosquitoes are responsible for transmitting dengue, chikungunya and Zika virus.

About 4,50,000 transgenic male mosquitoes were released each week for 27 months (June 2013 to September 2015) in three areas in Brazil. Genetic analysis of naturally occurring mosquitoes were done prior to the release and at six, 12, and 27-30 months after the releases.

Researchers from Yale University studied 347 naturally-occurring A. aegypti mosquitoes for transfer of genes from the transgenic insects. The transgenic strains can be distinguished from naturally-occurring mosquitoes by using fluroscent lights and filters. They found that some transgenic genes were found in 10-60% of naturally-occurring mosquitoes. Also, the naturally occurring A. aegypti mosquitoes carrying some genes of the transgenic mosquitoes were able to reproduce in nature and spread to neighbouring areas 4 km away. The results were published in the journal Scientific Reports.

The genetic strategy employed to control A. aegypti population known as RIDL (the Release of Insects carrying Dominant Lethal genes) is supposed to only reduce the population of the naturally occurring A. aegypti mosquitoes and not affect or alter their genetics. Also, offspring are not supposed to grow to adult mosquitoes and reproduce as per claims made by the British company Oxitec Ltd, which had developed the technology and field-tested it in several countries.

The claim was that genes from the release strain would not get into the general population because offspring would die. That obviously was not what happened, senior author Prof. Jeffrey Powell from Yale University was quoted as saying on the University website.

The genetic strategy works on the premise that the transgenic male mosquitoes released frequently in large numbers would compete with the naturally occurring male mosquitoes to mate with the females. Offspring from the mating of transgenic male mosquito and naturally occurring female mosquito do not survive to the adult stage. This is because tetracycline drug, which prevents the dominant lethal gene from producing the lethal protein during rearing in labs, is not present in sufficient quantity in nature. In the absence of tetracycline, there is overproduction of the lethal protein causing the larvae to die.

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Transgenic mosquitoes transfer genes to native mosquito species - The Hindu

On Sunday afternoons a truck filled with cherimoya leaves Stoneacres Farm in the Eastern Cape to travel the almost 900km throughout the night and arrive at the Johannesburg Municipal Market by early Monday morning.

Hopefully by Wednesday it has been sold, notes Alan Stone, cherimoya and kiwi farmer from Stoneacres, Stutterheim, a region better known for its forestry and sheep.

It has a very short shelf life, and the market for it is very restricted. The Portuguese community in South Africa know the fruit. Demand isnt really growing. I dont send to Cape Town because there are one or two cherimoya producers in the Western Cape. I send about sixteen consignments (each about 800kg) of cherimoya to Johannesburg in a good year. More cherimoya wouldnt sell.

He sometimes sends to East London or Port Elizabeth, but 95% goes to Johannesburg in 4kg- and 2kg boxes.

Cherimoyas, known as custard apples in South Africa, seem to break every rule in the commercial fruit production handbook: their flowering period is erratic and difficult to predict it could be in November but last year it was February and March, with disastrous consequences. As a result, its difficult for Alan to predict when hell have a crop, but operating in a very sparsely populated field gives some room for manoeuvre.

The cherimoya, sold as custard apples in South Africa

Weather makes or breaks fruit set Its a problematic plant. Fruit set is another problem. The cherimoya is a very primitive plant with a most unattractive flower. On the first day that the flower opens it is female and on day two it is a male flower. There is an overlap between the female and male state, but there no known pollinator for the flower and it all depends on temperature and humidity, which are critical.

Last year their cherimoya orchards flowered during February and March, when conditions were not suitable: high temperatures were accompanied by low humidity, and there was very low fruit set. Usually if it flowers in November, after its brief springtime deciduous period, the harvest starts in June or July and can go into December, although by that time there is so much summer fruit on South African shelves that Alan winds it down.

Spanish cherimoya geneticsHe has been growing cherimoya for 15 years now, taking its quirks as they come. He was looking for something to supplement his Hayward kiwi orchard dating back to 1992, when prices were very high and everybody was planting kiwis, Alan says.

Kiwis are very labour-intensive, worldwide production has increased and kiwi imports from countries with subsidised farming have had an impact on kiwi price points locally.

The Agricultural Research Council in Nelspruit was testing Spanish Jete cherimoya cultivars. From them Alan obtained his plant material, and being in a high-altitude area that experiences frost Stutterheim is adjacent to the Amathole Mountains he established a modest two hectares, but quite enough for the Gauteng market, mostly South Africans of Portuguese descent, often via Madeira where cherimoya is said to grow wild.

Cherimoya orchard in Stutterheim, Eastern Cape (photo supplied by Stoneacres)

It currently fetches around R70 (4.3 euros) per kilogram at the market, less the agent commission of 14%.

Unfortunately, here, too, its been dry. The worst drought in living memory, Alan calls it, and he notes that the fruit are also much smaller this year. Its an area that receives above-average rainfall by South African standards, approximately 800mm, but there has been no rain for three or four months now, he says. The Stoneacres orchards are irrigated from a spring-fed dam.

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Cherimoya cultivation in the Eastern Cape - FreshPlaza.com

In Florida and Texas, the invasive Aedes aegypti mosquito has posed a serious health threat, carrying the Zika and dengue virus into the state. Traditional insecticides have largely been useless against the mosquito. Outbreaks of Zika virus disease have been recorded in the Americas, Africa, Asia and the Pacific since the epidemic began in 2016, with more than a half million suspected cases and more than 3,700 congenital birth defects. Puerto Rico saw more than 36,000 cases that year. The United States mainland had 224, and its now down to a yearly handful.

With the possibility of future epidemics, the biotech company Oxitec has spent at least a decade testing a transgenic A. aegypti with a gene that kills off newly hatched mosquitos before adulthood. In a recent Brazilian field trial, second-generation GMO mosquitoes led to a reduction of Zika carriers by as much as 96%, Oxitec announced in June. Last week, the U.S. Environmental Protection opened a month-long window for public comments on the companys proposal for releases in Florida and Texas.

Plans for a widespread US release of the genetically altered mosquitoes has met with stiff resistance from anti-GMO organizations, which went door to door to stir up opposition four years ago in the Florida Keys when trials were first proposed. Since then, the fears have faded. There have beensplit reactions from local Floridians in two polls over the years, while other Florida surveys show significant public support. A fiercely-contest referendum in 2016 found Monroe County residents supportive of the releases, with 31 of 33 precincts and 58 percent of country residents voting in favor of the 1st Generation Oxitec mosquito project. Thousands of mosquitoes infected with the Wolbachia bacteria were later released in the Florida Keys as part of a 12-week trial.

Activist environmental groups like Friends of the Earth and Food and Water Watch, who have called the release plans dangerously short-sighted, have spearheaded the opposition in Texas and Florida.Oxitec is awaiting results from the comments and a subsequent ruling by the EPA in hopesof securing permission to fieldtest 20,000 male mosquitoes per acre per week in those two sates. These mosquitoes have been engineered to express a protein called tTAV-OX5034. Female offspring are expected to die before reaching maturity, and thus the A. aegypti population should drop, hopefully significantly.

These carefully cultivated plans were thrown in disarray by a study led by Yale University insect population geneticist Jeffrey Powell and published on September 10 in Scientific Reports. The title alone stirred apocalyptic concerns: Transgenic Aedes aegypti Mosquitoes Transfer Genes into a Natural Population.

Powell and researchers from Brazil monitored a release by Oxitec of 450,000 male A. aegypti mosquitoes in Jacobina, Brazil. The team genotyped the release strain and the population of A. aegyptifor up to 30 months after release. They reported that some parts of the transgenic mosquito genome had been incorporated into the targeted Jacobina mosquito population.

Is that a concern or potential catastrophe? After all, Oxitec had always estimated that about 3 percent of the offspring of the engineered mosquitoes would survive, so the key finding was not surprising. But then the researchers went beyond the data to speculate as to potential causes and implications.

[E]vidently, rare viable hybrid offspring between the release strain and the Jacobina population are sufficiently robust to be able to reproduce in nature. The three populations forming the tri-hybrid population now in Jacobina (Cuba/Mexico/Brazil) are genetically quite distinct, very likely resulting in a more robust population than the pre-release population due to hybrid vigor.

The research team seemed to raise what many readers of the study thought was an apocalyptic take on the data: Had Oxitec just created a new Franken-skeeter? And it was this speculation that caught the attention of the media, anti-GMO groups and more than a few critical scientists.

Anti-GM group GMWatch announced that the mosquitoes in the experiment had escaped human control, and were

now spreading in the environment. The mosquitoes used for the genetic manipulation are originally from Cuba and Mexico. These insects used in the laboratory have now mixed with the Brazilian insects to become a robust population which can persist in the environment over a longer period of time.

Some news reports reported the study straightforwardly, but many others mixed the documentable scientific results (GM mosquitoes mixed with the wild-type mosquitoes and the population of A. aegypti appeared to rebound after an 18-month suppression) with what many considered wild speculation (that new hybrid mosquitoes could be more resistant to suppression and more likely to spread disease).

A ScienceAlert story (quoting a New Atlas article titled Genetic engineering mosquito experiment goes wrong), exemplified this speculative coverage:

The genetically-altered mosquitoes did mix with the wild population, and for a brief period the number of mosquitoes in Jacobino, Brazil did plummet, according to research published in Nature Scientific Reports last week. But 18 months later the population bounced right back up, New Atlas reports and even worse, the new genetic hybrids may be even more resilient to future attempts to quell their numbers.

A story by the German Press Agency, DPA, quoted Christoph Then, head of the well-known European anti-GMO organization Testbiotech:

Oxitecs trials have led to a largely uncontrollable situation. This incident must have consequences for the further employment of genetic engineering.

Scientists responded quickly and sharply to this speculation.Michigan State University plant geneticist Chad Niederhuth tweeted, Some of the claims made by this paper are completely unfounded and the title is downright irresponsible. Despite the papers headline about transferring genes into a natural population, Aedes aegypti is native to Africa, and is an invasive species in all of the western hemisphere (including, naturally, Brazil).

Jason Rasgon, an entomologist and epidemiologist at Pennsylvania State University, dissected the papers problem in more detail. In a series of tweets, as well as in a story in Science magazine, Rasgon wrote:

Rasgon and other scientists have started asking why these speculative conclusions were in an otherwise solid paper on the population genetics of mosquitoes, why a notable group of researchers would make such statements and why Scientific Reports would publish them.

Shortly after the papers release, after a firestorm of criticism of the paper, the magazine (Nature Publishing) posted this:

In the Talking Biotech podcast by University of Florida Kevin Folta, Oxitec research and development and operations lead Kelly Matsen said that the Aedes mosquito is invasive worldwide, and has resisted other efforts. The companys genetic-based sterile insect technique turns away from traditional x-ray/irradiation methods, to genetically modify insects so that they can have the effect of reducing populations, and then remove the genes from the environment when we have done our work, Matsen said.

However this is resolved, the paper and the reaction to it illustrate the structure of conflict over genetic modifications some scientists who support the careful use of technology, others who fall victim to hype and speculation and non-government organizations (NGOs) which stringently oppose any such technology. As the GLP reported in a previous article, this opposition is based on speculative risks, those that have no established theory or evidence data, according to Canadian researchers who surveyed experts on their views of genetic modification.

Andrew Porterfield is a writer and editor, and has worked with numerous academic institutions, companies and non-profits in the life sciences.BIO. Follow him on Twitter@AMPorterfield

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Oxitec's GMO mosquitoes spread their genes in the wild? Separating science from hype after controversial new study - Genetic Literacy Project

Jacobina, Brazil, where hundreds of thousands of genetically modified mosquitoes were released from 2013 to 2015. Image: Ari Rios (CC BY-SA 3.0

An experimental trial to reduce the number of mosquitoes in a Brazilian town by releasing genetically modified mosquitoes has not gone as planned. Traces of the mutated insects have been detected in the natural population of mosquitoes, which was never supposed to happen.

The deliberate release of 450,000 transgenic mosquitoes in Jacobina, Brazil has resulted in the unintended genetic contamination of the local population of mosquitoes, according to new research published last week in Scientific Reports. Going into the experimental trial, the British biotech company running the project, Oxitec, assured the public that this wouldnt happen. Consequently, the incident is raising concerns about the safety of this and similar experiments and our apparent inability to accurately predict the outcomes.

The point of the experiment was to curb the spread of mosquito-borne diseases, such as yellow fever, dengue, chikungunya, and Zika, in the region. To that end, Oxitec turned to OX513Aa proprietary, transgenically modified version of the Aedes aegypti mosquito. To create its mutated mosquito, Oxitec took a lab-grown strain originally sourced from Cuba and genetically mixed it with a strain from Mexico.

The key feature of these bioengineered mosquitoes is a dominant lethal gene that (supposedly) results in infertile offspring, known as the F1 generation. By releasing the OX513A mosquitoes into the wild, Oxitec hoped to reduce the population of mosquitoes in the area by 90 percent, while at the same time not affecting the genetic integrity of the target population. The OX513A strain is also equipped with a fluorescent protein gene, allowing for the easy identification of F1 offspring.

Starting in 2013, and for a period of 27 consecutive months, Oxitec released nearly half a million OX513A males into the wild in Jacobina. A Yale research team led by ecologist and evolutionary biologist Jeffrey Powell monitored the progress of this experiment to assess whether the newly introduced mosquitoes were affecting the genes of the target population. Despite Oxitecs assurances to the contrary, Powell and his colleagues uncovered evidence showing that genetic material from OX513A did in fact trickle to the natural population.

The claim was that genes from the release strain would not get into the general population because offspring would die, Powell, the senior author of the new study, said in a press release. That obviously was not what happened.

That genetic material from OX513A has bled into the native species does not pose any known health risks to the residents of Jacobina, but it is the unanticipated outcome that is concerning, said Powell. Based largely on laboratory studies, one can predict what the likely outcome of the release of transgenic mosquitoes will be, but genetic studies of the sort we did should be done during and after such releases to determine if something different from the predicted occurred.

Indeed, lab tests conducted by Oxitec prior to the experiment suggested that around 3 to 4 percent of F1 offspring would survive into adulthood, but it was presumed these lingering mosquitoes would be too weak to reproduce, rendering them infertile. These predictions, as the new research shows, were wrong.

To conduct the study, Powell and his colleagues studied the genomes of both the local Aedes aegypti population and the OX513A strain prior to the experiment in Jacobina. Genetic sampling was performed six, 12, and 27 to 30 months after the initial release of the modified insects. The researchers uncovered clear evidence showing that portions of the genome from the transgenic strain had incorporated into the target population, the authors wrote in the new study. The project resulted in a significant transfer of genetic materialan amount the authors described as not trivial. Depending on the samples studied, the researchers found that anywhere from 10 to 60 percent of mosquitoes analyzed featured genomes tainted by OX513A.

As the researchers note in the study, the Oxitec scheme worked at first, resulting in a dramatic reduction in the size of the mosquito population. But at the 18-month mark, the population began to recover, returning to nearly pre-release levels. According to the paper, this was on account of a phenomenon known as mating discrimination, in which females of the native species began to avoid mating with modified males.

The new evidence also suggests that some members of the F1 generation were not weakened as predicted, with some individuals clearly strong enough to reach adulthood and reproduce. The mosquitoes in Jacobina now feature genetic traits from three distinct mosquito populations (Cuba, Mexico, and local), which is a potentially troubling development. In nature, the intermingling of traits between different species can sometimes provide an evolutionary boost in a phenomenon known as hybrid vigor. In this case, and as the researchers speculate in the new study, the added genetic diversity may have resulted in a more robust species, a claim Oxitec denies.

Powell and his team tested the hybrid mosquitoes to determine their susceptibility to infection by Zika and dengue. The researchers found no significant differences, as noted in the study, but this is for just one strain of each virus under laboratory conditions, and that under field conditions for other viruses the effects may be different. Its also possible that the intermingling of genetic traits might have also introduced entirely new characteristics, such as increased resistance to insecticides, the authors warned in the new paper.

An Oxitec spokesperson told Gizmodo the company is currently in the process of working with the Nature Research publishers to remove or substantially correct this article, which was found to contain numerous false, speculative and unsubstantiated claims and statements about Oxitecs mosquito technology. The spokesperson provided a three-page document detailing Oxitecs concerns with the research, noting that the new paper did not identify any negative, deleterious or unanticipated effect to people or the environment from the release of OX513A mosquitoes.

According to Oxitec, the OX513A self-limiting gene does not persist in the environment, and that the limited 3-5% survival of the OX513A strain means that, within a few generations, these introduced genes are completely eliminated from the environment.

Oxitec also disputes the researchers claim that female mosquitoes began to avoid mating with modified males, saying, Selective mating has never been observed in any releases of close to 1 billion Oxitec males worldwide. The authors provide no data to support this hypothesis.

Gizmodo reached out to Powell for comment did not hear back by the time of posting.

German broadcaster Deutsche Welle reports that the news that the Oxitec experiment didnt go as planned is raising alarms among scientists and environmentalists:

Biologists critical of genetic engineering go one step further with their criticism, among them the Brazilian biologist Jos Maria Gusman Ferraz: The release of the mosquitos was carried out hastily without any points having been clarified, Ferraz told the newspaper Folha de S. Paulo.

The Munich-based research laboratory Testbiotech, which is critical of genetic engineering, accuses Oxitec of having started the field trial without sufficient studies: Oxitecs trials have led to a largely uncontrollable situation, CEO Christoph Then told the German Press Agency, dpa. This incident must have consequences for the further employment of genetic engineering, he demanded.

That this project didnt go as planned is legitimately troubling. The episode demonstrates that releasing genetically modified organisms into the wild can have unintended, unpredictable consequences and that independent scientific monitoring of the outcomes is crucial.

Update: September 17, 12:33 p.m. ET: Scientific Reports, the journal in which the research article appears, added the following editors note to the paper on September 17:

Readers are alerted that the conclusions of this paper are subject to criticisms that are being considered by editors. A further editorial response will follow the resolution of these issues.

We have reached out to the journal for more information and will update when we hear back.

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Genetically Modified Mosquitoes Are Breeding in Brazil, Despite Biotech Firm's Assurances to the Contrary - Gizmodo

One night at a watering hole outside of Seattle, Ralph Taylor overheard a man a few beers in bragging about how easy it was to get certified as a minority business owner, thus gaining access to potentially millions of dollars worth of state contracts.

Taylors ears perked up. He asked the man exactly how this all went down, and the man told him the Office of Minority and Womens Business Enterprises (OMWBE) the Washington state office that certifies small businesses for these government contracts had a relatively lax application process. All Taylor had to do to get a Minority Business Enterprise (MBE) certificate, the man said, was provide a sworn affidavit that he belonged to a specific minority class and submit a photo ID. Then hed get approved.

There was a potentially huge payoff: Washington state agencies have a budget of almost$3 billion per year to contract with businesses. Right now, small businesses with white owners get more than six times as much money as small businesses with black owners. But as part of an initiative by Washington Gov. Jay Inslee (D), the state is attempting to level the playing field and award more money to women and people of color. Last year, minority- and women-owned businesses were awarded around $154 million, with nearly $90 millionspent on contracts with certified MBEs.

A few years after that bar conversation, Taylor, who works in the risk management industry, applied to have his own business, Orion Insurance, certified as minority-owned. And in 2014, Washington state awarded him an MBE certificate. It was a remarkable turn of events because, for most of his life, Taylor has been treated as a white man.

HuffPostRalph Taylor took a test that showed he had 4% African DNA. He now wants his small business certified as minority-owned.

That hasnt stopped Taylor from launching a crusade to be legally recognized as Black, based on his own sense of identity and the results of a genealogy test that revealed that he has 4% African DNA.

When Taylor applied to the very same office for a similar federal certificate(a Disadvantaged Business Enterprise, or DBE), his application was rejected on the grounds that he didnt meet their criteria of someone belonging to a minority group.

In a letter to Taylor informing him of the denial, the office wrote, The laws governing the state and federal certification are different. While OMWBE has certified an application by your Firm to the Washington State MBE program, that certification is not binding on the Federal DBE certification program.

Flummoxed, he says he contacted the OMWBE by email and phone to fight the denial. I asked, What is the Black culture? he recalls one afternoon in Seattle when we meet downtown outside the federal courthouse, at his behest, so he can demonstrate to me how his racial status changes from Black on state property to white on federal property. He asked the OMWBE to clarify why they excluded him from the program even after, he says, he provided additional evidence of his proposed blackness, including his DNA test results.

According to Taylor, the office questioned whether he was truly part of a minority group.Taylor says he tried to clarify again: Is it Condoleezza Rice, is it Snoop Dogg? Is it Dr. Dre? Or is Ludacris? Or is it Colin Powell? I mean, thats a wide variety of people there, so what is Black culture? They said something to the effect that, If you dont know what it is, thats because youre not Black.

So, he sued the OMWBE. Beyond his own racial status, Taylor claims to be fighting for a greater good, exposing flaws with affirmative action programs.

DNA tests complicate perceptions of race.

HuffPostDNA tests are becoming increasingly popular, though they only look at a small fraction of our genetic materials.

DNA test kits are often marketed as novelty items something fun to bring up at a dinner party or romanticized as a means to unlock fairy tales hidden in our past. Or theyre the subject of true-crime sagas, with podcasts like Serial inspiring Reddit pages fixated on convicted murderer Adnan Syeds case. DNA tests have even gotten glossy Netflix treatment with documentaries like Making A Murderer.

More recently, these kits entered our politics when Democratic presidential candidate Elizabeth Warren revealed the results of a genetic ancestry test to back up earlier claims of indigenous heritage. Warren was criticized by some tribal leaders for implying a relation between DNA and tribal citizenship, and she subsequently apologized.

These controversies aside, DNA kits have become cheaper and more popular; 23andMe, for instance, was originallypriced at $999 when it came to market, but now kits cost around $99. And yet, University of Pennsylvania sociologist Wendy Roth says we still dont fully understand what happens when we send our saliva off to a laboratory and we dont know how to properly interpret the results.

Right now I dont think that [companies selling at-home genealogy kits] are generally doing a good enough job of explaining how these tests should be interpreted and what the limitations are and what some potential negative impacts could be, says Roth, whose work is focused on DNA as it intersects with culture and identity.

Humans share 99.9% of the same genetic makeup, so at-home genealogy kits only look at a small fraction of our genetic materials. These tests are then further limited by the fact that the majority of people who have taken them have predominantly European ancestry (white people love this stuff!) so they are less accurate for other groups.

HuffPostUniversity of Pennsylvania sociologist Wendy Roth says we still dont fully understand what happens when we send our saliva off to a laboratory.

Still, companies are getting frighteningly good at identifying Americans of European descent who have never even taken a genetic test themselves. Law enforcement agencies, for example, use existing samples to triangulate information and solve crimes; it was a distant relatives DNA that led to the capture of the suspected Golden State Killer.

Despite all this, Roth says these tests are not particularly accurate as a means of determiningracial ancestry. Race is not something that is just genetic. Genetics play a part, but only a part, Roth explains. The way that sociologists define race is something that is socially determined, that refers to aspects of your biology or your ancestry. But its only referring to them.

Black cultural theorist and author Mychal Denzel Smith agrees. DNA is not telling you your race, because race is not a biological fact, he says. Race is a social and political construct. It is something that is lived.

For his part, Taylor tells me that he has always considered himself multiracial and sees race as fluid. DNA, he says, will prove that our racial makeup is just genetic mutations at the end of the day.

Roth says that understanding race as a social construct can sometimes lead people to think that they can pick and choose their race as they like, without consequence. In a qualitative study she conducted in 2018, Roth found that white respondents were most eager, of all respondents, to change their ethnic or racial identity. They wanted to discover ancestry that made them distinctive or exotic, or they wanted a more specific tradition to distinguish themselves. Roth called this phenomenon symbolic race.

People want to be able to enjoy the privileges or the benefits of a racial group without any of the costs, she says, adding that shes working on quantitative studies to further explore these patterns. They dont experience any discrimination, and because they dont have to tell anyone that they have this ancestry or this identity, they can just use it when its advantageous for them and hide it when its not.

Could DNA impact affirmative action laws?

All 50 states have an OMWBE or equivalent. The amount that each state allocates to minority contractors varies, as does the impact of each program. One recent report commissioned by Washington state discovered that some MBEs felt that certification was actually a detriment because it can be viewed by other firms and agencies as a stigma.

Butthe majority of the country still sees a benefit to affirmative action, and the number of Americans saying they favor such programs has risen in the last few years.

Affirmative action programs are trying to adjust for a specific form of oppression which has to do with racial hierarchies, the legacy of slavery, the legacy of Jim Crow, the legacy of lynching, the legacy of redlining. It is specifically meant to address that, cultural theorist Smith explains, adding that race is something that is lived.

Similarly, writer and HuffPost Black Voices Editor Taryn Finley sees affirmative action programs like the OMWBE to be a sort of corrective to historic racial injustices. Its not a fix-all, but it levels the playing field for people of color, for marginalized people.

Finley takes umbrage with Taylors method of exposing what he says are flaws with the system, and says the ends do not justify his means. If you look at a lot of the loudest voices, the folks who are going up against affirmative action are people like Ralph Taylor, who dont know how to use their privilege or relinquish their power in ways to actually help marginalized folks.

HuffPost"Being able to tip-toe back and forth across a line between 'now Im Black, now Im white, now Im multiracial' -- thats not identity. Youre playing a game," says HuffPost Black Voices Editor Taryn Finley.

So how might DNA tests impact whos eligible for affirmative action programs? The truth is, the issue has not yet been legally tested.

In 2003, when these tests were in their infancy and still costly, Alan Moldawer, a father of adopted twin boys, made headlineswhen he said he was considering using the outcomes of a genealogy test to try and secure financial aid for his kids on the grounds of their minority status. While white-presenting, his twin boys were 9% Native American and 11% North African, according to the tests Moldawer commissioned. It was one of the first reported instances where DNA tests were raised as a possible entry point to affirmative action programs.

More recently,a judge this year allowed Princeton student Nicole Katchurs lawsuitagainst the Sidney Kimmel Medical College of Thomas Jefferson University to proceed. Katchur, who is white, is suing for racial discrimination, claiming that an admissions officer told her that if she were to take a DNA test and discover Native American or African-American lineage, her chances of getting accepted into the medical school program would go up. (The medical school is seeking to dismiss the suit.)

The case was reminiscent of Fisher v. University of Texas, in which Abigail Fisher sued the University of Texas in 2008 for what she perceived to be anti-white bias in its admissions process. Fisher lost in 2016 when the Supreme Court upheld the universitys use of race in admission decisions.

What Taylors case and these college-based lawsuits have in common are the questions they raise about the gatekeepers of these programs who gets to decide whether someone is a deserving applicant or not. And more often than not, the first barrier to entry is phenotype (what we look like) rather than genotype (what our genes reveal).

When it comes to race, how we see ourselves isnt always how others see us.

Despite attempts to codify race, it is not as static an idea as many would like. In her book The Limits of Whiteness, sociologist Neda Maghbouleh explores how Iranians and other Middle Eastern Americans moved across the color line and documents how the U.S. Supreme Court used Iranians as a racial litmus test to determine the classification of other Middle Eastern or Arab people. Drawing on work by Middle East historian Nina Farnia, Maghbouleh shows how between 1909 and 1939, Iranians skin color was classified and reclassified as white and nonwhite by claimants in eight separate Supreme Court cases.

In 1896, in the landmark case Plessy v. Ferguson that led to the infamous separate but equal principle, the Supreme Court drew the color line in a different place. Justice Henry Billings wrote a majority opinion that refers to the one-drop rule or the idea that any person could be Black even if not discernible to the naked eye.

Taylors case somewhat oddly and uncomfortably evokes Plessy. A small amount of centiMorgans (the unit of measure of DNA) reveals some distant African ancestry, allowing him to claim access to an affirmative action program.

Smith cautions against this protocol. Thats just getting us into another position in which we are trying to scientifically determine something that does not exist scientifically, he says.

HuffPostDNA is not telling you your race, because race is not a biological fact, saysBlack cultural theorist and author Mychal Denzel Smith.

Roth further notes that the sheer volume of African-informed DNA has no bearing on how race is constructed socially. Should Taylors 4% be enough for society to accept him as Black? What if his results came back with 44%, or 64%?

I think what makes the difference is how the person is seen by others within their community. If the person is seen by others within their community as a white person, then the percentage doesnt matter, Roth argues. In the case of somebody who has a very small percent, like 4%, its very unlikely that that is going to be visible enough that its going to influence peoples interactions with them.

Roths position is one that has historically guided government agencies.

Take the U.S. census. The census was originally filled out by an enumerator who went door to door and filled out the survey for you. As Roth points out, these people were often neighbors who may have known your family history chances are, they might have known if your grandfather was a Mulatto or a person who was white and so may have filled out the forms based on their knowledge of your family history, in addition to how they took in your appearance.

This changed in the 1960s and 70s with mailouts and that simple shift in data collection had a more profound sociocultural impact. The meaning of this race question just completely shifted without anyone really paying any attention to it at all, Roth explains. It really went from something that was all about how youre seen by others to how you mark yourself.

There are many more recent instances where how we are viewed by other people has been instructional as to how were viewed in the eyes of the law. A recentLos Angeles Times investigation revealed businesses in at least 18 states won certification as minority contractors by claiming Native American status, even though birth, census and other government records identified the firms owners or their ancestors as white.In response, two House committees are investigating.

In Brazil, eyeing someones racial makeup has been at the heart of a protracted legal battle, after the government introduced a quota system for federal jobs and made the postings public. People started hunting down and searching peoples Facebook and social media profiles, sleuthing and cross-checking to see if their named racial backgrounds matched with how they appeared in photographs.

Taylor went through a similar process in his quest to be awarded federal minority designation after he was denied. He attempted to submit scores of Excel spreadsheet data with the names of people who were awarded federal minority status alongside hyperlinks to the LinkedIn profiles or company websites, in an effort to reveal how many people were, he says, gaming the system. Taylor claims that his own research into states minority business owner programs shows that 65% of enrollees were white, based on his perception of their photos. The spreadsheet was ultimately disallowed by the 9th Circuit court as evidence.

When I asked the OMWBE over email about the validity of Taylors claims, they said: This is not an area of fraud our program has seen.When I asked about whether it ever turns down applicants, the office said, Each year is different depending on the number of applications we receive.

HuffPostTaylor believes he should qualify as a minority.

Is being Black about more than DNA?

Taylor is tall and surprisingly soft-spoken. He rarely raises his voice, even for emphasis. Nonetheless, he has loudly advertised his identity with contemporary stereotypes. To flex his Black culture bonafides, Taylor argued that he was a member of the NAACP, subscribes to Ebony Magazine and takes a great interest in black social causes. In 2017, he changed his birth certificate to reflect what he says is his multiracial status of Black, Native American and Caucasian.

He says he has received death threats as a result of his story. In order to prove to his detractors that hes not pursuing his case for financial gains, he took a polygraph test, which he shared with me: It was never about the money, he says, adding he hasnt benefitted financially from his MBE status.

When he talks to me about this in the bar, the conversation turns, inescapably, for a moment to Rachel Dolezal. Dolezal, who now goes by Nkechi Diallo, was the woman who sparked outrage in 2015 when it was revealed that she had been posing as a Black woman for most of her adult life, despite being born white. Taylor says he feels sorry for Dolezal, and wished he could have told her that all she had to do was identify.But this kind of physical code-switching is typically only a one-way street.

Being able to tip-toe back and forth across a line between now Im Black, now Im white, now Im multiracial thats not identity. Youre playing a game, says Finley of HuffPost Black Voices. Its a very nefarious way of using your privilege, and I dont think that youre genuinely trying to expose a flaw in the system.

Nicholas K. Geranios/APThis July 24, 2009, file photo shows Rachel Dolezal, who made headlines for saying she was Black, even though she had been born white.

Finley, who took a DNA test herself to uncover her own previously unknown family history, is 10% European. But, she says, Im a Black woman. My lived experience as a Black woman cannot be passed [as white].

Smith also takes exception to Dolezal and Taylors claims to Blackness. He roots Black culture in a community of people with shared experiences.

Theres the common experience that all of our ancestors had of slavery. They formed culture out of that. You have the common experience of segregation. They formed culture out of that, he says. If you cannot point to your life as a shared experience with those people, then how can you claim that status?

Taylor, however, sometimes claims that affirmative action entry points shouldnt be focused on race at all. Instead, he says equal opportunity programs should look more at socioeconomics in part because, in his telling, we are all multiracial. Simultaneously, Taylor claims that his 4% African DNA results mean that he should be considered Black enough to qualify for the OMWBE program anyway.

In December 2018, the 9th Circuit judges unanimously ruled against Taylor, and in favor of the OMWBE, which the court argued did not act in an arbitrary and capricious manner when it determined it had a well founded reason to question Taylors membership claims.

Smith expresses some sympathy for the gatekeepers of these affirmative action programs. What were trying to determine is if you are a part of a class of people that has been discriminated against and therefore you are eligible for the corrective program, right? Its really, really confusing and tricky to do, he says. What were asking then is for you to prove a history of discrimination on the basis of how you look. Thats difficult for anybody to suss out.

Is this just trolling to make a point?

Speaking with Taylor at the bar outside of Seattle, its hard not to wonder if, frankly, he isnt just trolling us all and the government.

Taylor says he has already spent hundreds of thousands of dollars litigating his case. He jokes that hes willing to live out of his car if it means seeing this through to the end, though what that end looks like is at this stage unclear. The U.S. Supreme Court declined to hear his case over the summer, and he has run out of appeals to the 9th Circuit. But he says he plans to reapply to the OMWBE for certification later this month.

In a June 2019 email to the director of the Washington state OMWBE, which he shared with HuffPost, Taylor inquired about resubmitting the paperwork to get his DBE certification and be recognized federally as a minority business owner. In the note, he states that hes sending in his newly amended birth certificate, but asks should I have the certificate amended to state that I am black without any other ethnicities and adds I can also have the certificate amended to state female if that will help.

The glibness is part of Taylors point he wants to expose the flaws in the process of becoming minority certified, and more broadly with what he says is the somewhat arbitrary nature of the affirmative action system.

The system the way it is now needs to break, he says.

Kayvon Afshari, Lindsey Davis and Emily Bina contributed reporting.

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A DNA Test Revealed This Man Is 4% Black. Now He Wants To Abolish Affirmative Action. - HuffPost

A study designed to determine differential characteristics between bipolar disorder (BD)-I and BD-II and published in Psychiatry Research found that being female, having a family history of psychiatric conditions, and having higher illness severity were associated with a diagnosis of BD-II.

Gianluca Serafini, MD, PhD, of the Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, Section of Psychiatry, University of Genoa, Italy, and colleagues conducted a study of bipolar subtype characteristics among patients with currently euthymic bipolar disorder. Patients were receiving only maintenance treatment.

The investigators found that those with BD-II were more likely to be female (odds ratio [OR], 0.289), to have other family members with psychiatric conditions (OR, 0.273), and to experience a higher severity of illness (OR, 0.604). In addition, patients with BD-II were more likely to have psychotic symptoms at first episode and to have substance abuse/dependence issues. Those with BD-I were more likely to have higher depressive, manic, anxiety, and symptoms severity and to have been younger at illness onset.

Limitations of the study include the use of a single psychiatric sample population and the relatively small sample size, making it difficult to generalize these findings to other existing patient populations. In addition, the subgroups compared included both outpatients and inpatients, possibly biasing the results.

The investigators concluded that BD is a heterogeneous condition and there is a need to identify valid and reliable BD subtypes according to phenotypic BD characteristics. These findings also challenge the assumption that BD-II is a less severe and disabling BD subtype.

Reference

Serafini G, Gonda X, Aguglia A, et al. Bipolar subtypes and their clinical correlates in a sample of 391 bipolar individuals. Psychiatry Res. 2019;281:112528.

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Sex, Higher Illness Severity Associated With Bipolar Disorder II - Psychiatry Advisor