Archive for the ‘Male Genetics’ Category

One upside of the COVID-19 disruption is that many people have a bit more time if only because theyre not commuting, looking for a parking space, going for after-work drinks, etc. Ive been encouraging my students to pick up a fun new activity to make good use of this time bonus. Ive chosen to try to learn to draw and am making a start on it. Well, at least Ive bought some instructional books and supplies. Wish me luck!

One activity that we could all benefit from is paying attention to our long-term health. After all, youre far more likely to die from cancer or heart disease than from COVID-19. There are some concrete steps you can take to improve your long term health prospects. If youve been putting off a visit to your doctor for a physical, this might be a good time, even if its a telehealth visit. Some procedures like that dreaded prostate exam do require the hands-on approach. But youd be amazed at how much you and your doctor can sort out over the phone and with lab tests.

To see whats included in a good physical, have a look at the Preventive Care Checklist on the website of the College of Family Physicians of Canada (cfp.ca). It was recently updated, and I learned a lot from it, including that at my age I should be getting the pneumococcal 23-valent polysaccharide vaccine.

Discoveries also highlight the importance of knowing more about our genetic heritage. In a first-of-its-kind genomic study, researchers at Vanderbilt University Medical Center led by William D. Dupont and Joan P. Breyer studied prostate cancer patients with family histories of the disease. They note that prostate cancer heritability is twice that of breast cancer, at roughly 58 per cent. Their latest research focused on the detailed genetic makeup of chromosome 8, which is known to be related to prostate cancer. The Vanderbilt scientists found three mutations that helped protect us from prostate cancer, and four that raised the danger, in one case by 22-fold.

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Keenan: Thinking well beyond COVID-19 - Edmonton Journal

Named Cardamine inseuta, was first spotted in 1972 in the Urnerboden region after the land in the area went from being a forest to a grassland. Now, researchers at the University of Zurich (UZH) have narrowed down the two species of the plants that merged to create the hybrid that is thriving.

One is Cardamine amara, which grows in and around streams and the other is Cardamine rivularis, which inhabits moist, not wet, areas.

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It is the combination of genetic traits from its parents that enabled the new species to grow in a district environmental niche, said Rei Shimizu-Inatsugi, co-author of the study published in Frontiers in Genetics.

The best of both worldsC. inseuta is a so-called triploid plant. It means that it has three sets of chromosomes. Two come from C. rivularis and one set from C. amara.

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From its other parent, C. amara, the new species inherited the trait of submergence tolerance. That means that even if surrounded by water, C. inseuta would survive rather than drown.

Depending on the environmental situation, the plant activates a different set of genes it inherited from its two parent species, said Shimizu-Inatsugi.

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Andrea Ghez is the fourth woman to win the Nobel Prize for Physics found the first signs of the supermassive black hole at the center of the Milky Way

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Scientists unravel the mystery behind new plant species found in the Swiss Alps, which only took 150 years to - Business Insider India

Mathew Knowles, the father of music powerhouses Beyonc Knowles-Carter and Solange Knowles, on Saturday penned an opinion piece encouraging men to get tested for breast cancer.

Knowles wrote the op-ed for USA Today on the one-year anniversary of sharing his diagnosisof Stage 1A breast cancer and called for an inclusive term that doesnt embarrass men or prevent them from seeking the care they need.

It wasnt comforting to walk into my first oncology appointment through doors that read Womens Breast Clinic and to be greeted with the question, am Ihere for my wife? Knowles wrote. Since Ive shared my diagnosis, countless men have secretly shared their male chest cancer diagnosis with me, as they were too ashamed to talk openly about having breast cancer.

The music executive told Good Morning America last year that breast cancer affected several women in his family, including his aunt and cousins.

After his scheduled mastectomy, he learned that he had the BRCA2 gene mutation that put him at a higher risk of breast, prostate and pancreatic cancers and melanoma.

Im grateful to say Im cancer-free today and have the knowledge to make important lifestyle choices that hopefully keep me in remission, such as getting a mammogram every six months, Knowles wrote. Im perhaps even more grateful this discovery spurred my kids to take their own medical genetic tests to learn their own risks and better inform the decisions they make my newfound knowledge also became theirs.

He has since partnered with a medical genetics company, Invitae, and encouraged readers to get screenings done for gene mutations.

Its foolish that so few of us take advantage of this information thats more affordable and accessible than ever. Who doesn't want to be able to get ahead of potentially life-changing diseases or health conditions? Knowledge is power, he wrote.

There will be approximately 2,620 new cases of invasive breast cancer diagnosed in men in the year 2020, according to the American Cancer Society.

Breast cancer is about 100 times less common among white men than among white women.It is about 70 times less common among Black men than Black women, and Black men typically have a worse prognosis.

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Beyonc's father in op-ed urges men to get tested for breast cancer | TheHill - The Hill

Its one of the most important genes in biology: Sry, the gene that makes males male. Development of the sexes is a crucial step in sexual reproduction and is essential for the survival of almost all animal species.

Today in the journal Science, my international collaborators and I report the surprise discovery of an entirely new part of the Sry gene in mice a part we had no idea existed.

I co-discovered Sry in 1990. It is the gene on the Y (male) chromosome that leads to the development of male characteristics in mice, humans and most other mammals. Since then, Sry has been the subject of intense study worldwide because of its fundamental role in mammalian biology.

We have come to understand, in some detail, how Sry acts to trigger a cascade of gene activity that results in the formation of testes, instead of ovaries, in the embryo. Testes then stimulate the formation of other male characteristics.

But its clear we dont have all the answers just yet. Our results published today take us one step further in the right direction.

For 30 years, we have understood the Sry gene is made up of one exon, a segment of a gene used to code for amino acids, the building blocks of proteins. This can be compared to a computer file consisting of one contiguous block of data, on a hard disk.

Our newest research reveals theres actually a second exon in mouse Sry. This is like finding a whole new separate block of previously hidden data.

The mouse genome, like the human genome, has been extensively characterised due to the availability of advanced DNA sequencing and related technologies. Researchers commonly assume all the genes and all the parts of the genes have already been discovered.

But earlier this year, scientists in Japan uncovered what looked like a new piece of the Sry gene in mice. New sequencing approaches revealed what appeared to be two versions of Sry: a short, single-exon form and a longer, two-exon form. They called this two-exon version Sry-T.

They collaborated with my group at the University of Queensland and removed the new exon using CRISPR, a gene editing tool that lets researchers alter DNA precisely. Together we discovered this prevented Sry from functioning: XY mice (which would normally develop as males) developed as females instead.

Conversely, adding Sry-T to fertilised XX mouse eggs (which would normally develop as females) resulted in males.

Importantly, although human Sry does not have the added exon, our discovery may reveal new functions that might be shared between mouse and human Sry.

The DNA sequence of the new exon in Sry-T may point us towards discovering some of the genes and proteins that interact with Sry, something that has been elusive up till now.

And interactions we find in mice may also occur in humans. Studying what human Sry interacts with may help explain some cases of differences in human sex development, otherwise known as intersex development. This is a common but poorly understood group of mostly genetic conditions that arise in humans.

Currently, we dont know the genetics behind a large proportion of intersex conditions. This is partly because we dont yet know all the genes involved in the human sex development pathway.

Read more: Sex, genes, the Y chromosome and the future of men

Scientifically, this discovery is a bit like discovering a new cell type in the body, or a new asteroid in the Kuiper belt. As with many scientific discoveries, it challenges what we thought we knew and raises many questions.

What is the function of the new exon in Sry-T?

Currently, we only have part of the answer. It turns out the first exon of Sry, the one we already knew about, contains instability sequences at its end. These are sequences that cause proteins to fray and degrade.

An important function of the newly discovered second exon is to mask the instability sequences, seal the end of the Sry protein and prevent it from degrading. In other words, this second exon is crucial to the development of male babies.

Whats more, this protection mechanism represents an unusual and intriguing evolutionary mechanism that has acted to help stop vulnerable Y-chromosome genes from literally falling apart.

But its early days yet. The challenge now is to understand whether there are more functions hidden within the newly discovered exon.

If so, this information may provide some of the missing links that have stood in the way of our full understanding of how Sry works at a molecular level and of how males and females come to be.

Read more: Why education about gender and sexuality does belong in the classroom

Read more:
We discovered a missing gene fragment that's shedding new light on how males develop - The Conversation AU

Although rare, men get breast cancer too.

According to the National Breast Cancer Foundation, in 2020, an estimated 2,620 men will be diagnosed with breast cancer this year in the U.S. and approximately 520 will die.

The American Society of Clinical Oncology reports that the 5-year survival rate for men with breast cancer is 84%, with individual survival rates dependent upon various factors, including the stage of the disease when it is first diagnosed. If the cancer is located only in the breast, the 5-year survival rate of men with breast cancer increases to 96%. About 47% of cases are diagnosed at this localized stage. If the cancer has spread to the regional lymph nodes, the 5-year survival rate is 83%.

Breast cancer in men is usually detected as a hard lump underneath the nipple and areola. The mortality rate is higher in men than women because awareness among men is sadly lacking. Men are generally less likely to assume a lump is breast cancer, which may keep them from seeking medical advice. Any delay in seeking treatment can diminish the likelihood of a positive outcome.

Most men diagnosed with breast cancer are over the age of 50.

Here are some important facts about male breast cancer from the American Cancer Society:

Breast cancer is about 100 times less common among white men than among white women; and about 70 times less common among Black men than Black women

As with Black women, Black men with breast cancer tend to have a worse prognosis

For men, the lifetime risk of getting breast cancer is about 1 in 833

Breast cancers can start from different parts of the breast

The most common types of breast cancer are ductal carcinoma in situ, invasive ductal carcinoma, and invasive lobular carcinoma

Breast cancer can spread when the cancer cells get into the blood or lymph system and are carried to other parts of the body

Risk factors for breast cancer in men include the following:

Age The risk of male breast cancer increases as a man ages. The average age of men diagnosed with breast cancer is 72.

Genetics Men with a mutation in the BRCA2 gene have an increased risk of breast cancer.

Klinefelter syndrome This is a congenital condition that affects approximately 1 in 1,000 men. Men with Klinefelter syndrome are more likely to get breast cancer than other men.

Radiation exposure Any man whose chest has been treated with radiation is at an increased risk of developing breast cancer.

Alcohol Excessive consumption of alcoholic beverages increases the risk of breast cancer in men.

Liver disease Men with severe liver disease, such as cirrhosis, run an elevated risk of developing benign male breast growth.

Obesity Studies have shown that obesity is a factor for male breast cancer.

The American Cancer Society encourages men who are or may be at a high risk for male breast cancer to discuss how to manage that risk with their doctor. The American Society of Clinical Oncology goes one step further and urges men to become familiar with the feel of their breast and chest wall tissue, so they can talk with their doctor if they notice any lump or change.

Following is a list of possible symptoms of breast cancer:

A lump or swelling, which is often (but not always) painless

Skin dimpling or puckering

Nipple retraction (turning inward)

Redness or scaling of the nipple or breast skin

Discharge from the nipple

For more information about male breast cancer, visit http://www.nationalbreastcancer.org or http://www.cancer.org.

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Male breast cancer rare, but men should learn risk factors, signs and symptoms - Tampa Bay Newspapers

European wildcats, thought to be extinct 50 or so years ago in the Jura mountains, have since recolonised part of their former territory. This resurgence in an area occupied by domestic cats has gone hand-in-hand with genetic crosses between the two species. The hybridisation between wild and domesticated organisms is known to endanger the gene pool of wild species. In a study to be published in the journal Evolutionary Applications, a team of biologists from the University of Geneva (UNIGE), in collaboration with the University of Zurich and the University of Oxford, modelled the interactions between the two species to predict the future of the wildcat in the mountainous region of the Swiss Jura. The different scenarios modelled by the scientists show that within 200 to 300 years --a very short time in evolutionary terms-- hybridisation will entail the irreversible genetic replacement of wildcats, making it impossible to distinguish them from their domestic cousins, as is already the case in Scotland and Hungary.

Although the European wildcat (Felis silvestris) or forest cat was once very common, it fell victim to intensive hunting in the 19th and 20th centuries and to the massive deforestation that cut back its natural habitat, resulting in its disappearance in some parts of Europe. In Switzerland, the wildcat was deemed practically extinct, with no trace found for 25 years from 1943 to 1968. Thanks to a federal law that has protected the animal since 1962, the wildcat has recolonised the forests and meadows in the Jura range, where it lives side-by-side with the domestic cat (Felis catus) in particular. Although considered two species --or as different subspecies by some-- wildcats and domestic cats can interbreed and have hybrid, fertile kittens. These have the genome of both species and may give birth to offspring carrying the recombinant genes of each species. These hybridisations pose a new threat to the wildcat, since they prompt gene transfers based on a mechanism known as genetic introgression. This mechanism can quickly result in the dissemination of the genes of the more abundant species in the genome of the rarer species. The risk exists in the short term that the genome of the domestic cat will gradually replace the gene of the wildcat, which is markedly less plentiful than its domestic cousin, leading to the extinction of the wildcat.

Recolonising the territory

Scientists from UNIGE and the University of Zurich demonstrated in earlier studies that there is a greater introgression of the wildcat genome by the domestic cat genes than vice versa. The demographic and territorial expansion of wildcats over the last 50 years was identified as the most likely cause of these introgressions, which tallies with observations in the field. This conclusion was reached using bioinformatic simulation models factoring in ecological and genetic characteristics. It was estimated that about 5-10% of contacts between wild and domestic cats produced hybrid kittens. Following these discoveries, the computer model was refined in order to make projections and define the urgency for intervening and preserving the species.

The only solution: stop crossbreeding

The variable factors in the model incorporated in the new article, whose last author is Mathias Currat, senior researcher at the UNIGE Department of Genetics and Evolution, are the hybridisation rate, competition for resources in the environment and the size of the populations. Irrespective of the scenario put forward while acting on these variables, a very strong introgression of the domestic cat's genome into the genome of the wildcat is predicted. Mathias sounds a warning: "This is strongest with population sizes comparable to today's, but is still very high even if we consider more favourable conditions for the wildcat, such as an increase in its population size or a competitive advantage over the domestic cat in the regions where they coexist." Juan Montoya-Burgos, laboratory director in the Department of Genetics and Evolution at UNIGE, and co-author of the study, warns: "The model leads to an irreversible genetic replacement resulting in the ultimate disappearance of the wildcat. Only the end of crossbreeding between the two species predicts the conservation of the wild species."

Action needed now

It follows that the wildcat remains an endangered species in spite of the positive signs of its recent expansion. The dynamic model put forward in the UNIGE study, which combines the demographic and spatial growth of the wildcat populations, can be used to predict the future of the species. Based on the various scenarios, wildcats will be assimilated to domestic cats in as little as 200 to 300 years, as is already the case in Scotland and Hungary. "A hybridisation event has a proportionally much greater impact on the wildcat population, which consists of a few hundred individuals, than in the domestic population, which numbers over one million individuals in Switzerland", points out Mathias Currat.

One initiative suggested by the authors is to drastically reduce the opportunities for hybridisation on the fringes of the wildcat territories. Campaigns to sterilise domestic cats living near farms or close to forests are just one of the proposals. Females should be the primary target since domestic females mate more readily with male wildcats than male domestic cats with wild females. "Early interventions are likely to be less costly both financially and in environmental terms. If we stay passive, the threat to weigh on wildcats in the Jura risks being irreversible," concludes Juan Montoya-Burgos.

Link:
Wildcats threatened by their domestic cousins - Science Codex

Mosquitoes are probably most people's least favorite insect.

Mosquito-borne diseases include malaria, yellow fever, and the Zika virus all of which can cause extreme sickness, birth defects, or death. Per year, malaria is responsible for the deaths of over 400,000 people, while dengue fever causes about 20,000, according to the World Health Organization.

Vaccines have been in development for dengue fever, malaria, and Zika, but production can be very slow and result in low efficacy. Drugs can help, but can be expensive. Insecticides are successful in the short term, but mosquitoes can become resistant, and mass-release insecticide can have health impacts on plants and wildlife.

Instead, othershave focused their attention on treating the mosquitos, not the symptoms:genetically modifying mosquitos themselves to only produce sterile offspring, effectively wiping out an entire population of insects. Modern genetic modification techniques are fast, and work at thescale of genes but they mimic the plant breedingfocused on phenotype humans have been doing since the beginning of history (like, say, selective breeding of crops, which humans have been doing since agriculture was invented).

There are two general approaches to producing genetically modified mosquitoes: 1) modifying the reproductive ability of male mosquitoes so that they cannot produce offspring, and 2) modifying both male and female mosquitoes so that they are resistant to diseases or incapable of transmitting them to other species. Oxitec, the biotechnology company behind a genetically modified (GM) mosquito Aedes aegypti, has tested the first approach to GM mosquito releases in field trials in parts of Brazil, the Cayman Islands, and Malaysia. These male mosquitoes mate with a female, exchanging a gene mutation that causes the larvae to die unless they are given an antibiotic. These trials have shown to reduce mosquito populations from 80-95%, reducing dengue fever cases by 91%.

GM mosquitoes are successful in reducing mosquito populations, and reducing disease spread. But there are still many scientific questions that haven't been fully answered, including concern over public health, mosquito resistance risks, and environmental consequences associated with genetic modification of a wild-living organism. Many people believe that genetic modification goes against the natural order of the world, or that we don't know the full range of possible outcomes for releasing modified organisms into the environment.

And the skeptics have a point: GM crops, initially thought to reduce our need for pesticide applications, have resulted in increased herbicide applications in the face of the development of resistant weeds and insect pests. In the case of genetically modified corn targeting the European corn borer pest, known as Bt corn, resistance has driven an increase in pesticide use by about 7% over a 15 year period.

A map showing dengue spread in the US as of August 2020, with outbreaks in Puerto Rico, Texas, Florida, and Wisconsin, among others

Via CDC

Studies testing the safety of GM crops are widespread, but the public often sees these announcements coming from huge corporations like General Mills, aiming at selling a GM product. In a 2014 Pew Research Center survey, only 37% of adults felt that GM foods were safe to eat, and only 26% felt GM foods were safe to eat if they stated they had less scientific knowledge than their peers. And yet, multiple science and health organizations have deemed GM crops as safe for human consumption.

But what does all of this uncertainty about GM crops mean for GM mosquitoes? Oxitec is currently the first and only company to be approved to release genetically modified mosquitoes, beginning in 2009 (though not announced until 2010) with the release of 3 million genetically modified mosquitoes in the Cayman Islands in response to high levels of pesticide resistance in the mosquito population. In 2015, in response to an increase in Zika virus in the country, Brazil's National Biosafety Committee approved the release of GM mosquitoes in Juazeiro, in northeast Brazil. The trials were successful, with Oxitec concluding the modified mosquitoes reduced dengue fever mosquito populations by 95%.

It's important to note that Oxitec was not the first to alter the genetics of insects for population control. The genetic approach to render insects infertile or resistant to disease is based on the Sterile Insect Technique (SIT). SIT was developed in the 1930s as a way to reduce insect populations. The technique renders male insects sterile by exposing them to extremely high levels of radiation, before releasing them to mate with females. The technique has great success, eradicating multiple pest species such as the screwworm in the 1950s and reducing pink bollworm moth populations in California beginning in 1967.

A workflow describing proposed stages for developing, testing, and releasing genetically modified mosquitos

Via WHO

Following the success of the initial trials, Oxitec had another GM mosquito release in Jacobina, Bahia, Brazil in 2015. About 450,000 mosquitoes were released each week for 27 months, developed using a strain from Cuba outcrossed with a strain from Mexico. The Brazil trials had little-to-no pushback in the region, with many residents believing the GM mosquito resulted in a drop in dengue fever cases and limiting the success of Zika virus spread.

Oxitec applied to the EPA in the United States to release the modified insect containing a gene in GM male mosquitoes that would spread to and kill offspring in the larval stage in 2012, after outbreaks in 2009 and 2010 of dengue fever in the Florida Keys. But when the public found out about the potential experiment, a petition on Change.org gathered over 100,000 signatures against the project (it's at over 235,000 today). Many skeptics reference Oxitec's rush to use GM mosquitoes in the field in their initial Cayman Island trials without properly consulting the public.

Oxitec scrapped their original release mechanism which would allow female mosquitoes to escape from the release capsule due to public pressure. Instead, they developed a newly branded version of the mosquito technology, coining it "friendly mosquito technology." The new GM mosquito is programmed to only release males from an Oxitec capsule placed in water, and not the biting females. The "safe" name refers to the fact that male mosquitoes do not bite, so the company's release would not increase numbers of female-biting mosquitoes.

A map showing Aedes aegypti's range in the United States and Indigenous reservations

Via CDC

But environmental groups are still unhappy. Many believe the engineered mosquitoes are still putting Floridians at risk, and worry that spreading modified genes from male mosquitoes into the wild mosquito population could cause cascading effects on the food chain. Birds, insects, and mammals all feed on mosquitoes; environmentalists are concerned about any affect the genes could have on these organisms. Many scientists have speculated about whether the elimination of the mosquito would have any impact on other creatures, but others are hesitant to promote the purposeful extinction of a species.

There are also other options for reducing diseases spread by mosquitoes. A non-profit organization in Brazil known as Eliminate Dengue is working to breed mosquitoes that are less likely to spread disease. The group is focused on breeding mosquitoes to carry on a parasite widely found and naturally occurring in mosquitoes, Wolbachia, which has been shown to inhibit the mosquito's ability to spread viruses such as dengue fever or chikungunya. Eliminate Dengue, funded through the Gates Foundation, has released these mosquitoes in 40 areas worldwide. The parasite stays in the population, reducing the need to release modified mosquitoes year after year.

The majority of scientists believe that GM mosquitoes pose no human health risks. However, the possibility of hybridization between GM mosquitoes and wild mosquitoes, passing the genetically modified genetics to wild populations and into the ecosystem, is concerning to many.

The potential good may outweigh the potential bad. But with EPA approval and test releases of genetically modified mosquitoes planned for the Florida Keys and Texas, the future is already here. Only time and data will tell.

More:
You should be excited that scientists are releasing 750 million genetically modified mosquitoes this year - Massive Science

The last seven months or so have been an interesting time to be alive. Lets face it, its not often that we see our grandparents scratching their heads and saying theyve never seen anything like it. From COVID-19 to politics, 2020 has been one of those years that will be referred to in history lessons for decades, if not centuries, to come. Of course all of that upheaval also comes with a record-breaking amount of personal stress, too, manifesting itself in our bodies in all sorts of ways. For a lot of modern men, that tension is working its way out literally through hair loss.

Its perfectly normal to experience some hair loss. Hair goes through phases just like the rest of us. Without getting too technical, theres a growth phase, a transition phase, and a resting phase. Hair can grow for anywhere from five to seven years, depending on your genetics. That transitional phase, on the other hand, only lasts about ten days. The resting phase (the technical term is telogen) can last as long as three months, but thats the point where slowly but surely the hair starts to loosen and come out. After about three months the whole process starts all over again. Usually.

Those of us with Male Pattern Baldness will lose hair due to genetics. The hair follicle starts to shrink and, after a while, that whole growth process just dies out. (Dont despair, there is hope for that.)

Beyond genetics, though the stress of our current times including the stress on your body if you have actually contracted COVID may also lead to premature hair loss. (Editors note: We truly hope that hair loss is the only thing you have to cope with, should you be ill.) In fact, according to Dr Dayal Mukherjee, MD, at The Aura Clinic London, Psychological factors such as stress, anxiety or any significant traumatic episode, may trigger or exacerbate certain types of hair loss.

Dr. Craig Ziering is a hair restoration specialist with clinics in Newport and Beverly Hills, CA, Las Vegas, and New York City. He refers to this circumstance as telogen effluvium. Sure, it sounds like something sticky from Ghostbusters, but its actually the technical term for hair loss that happens after stress. And these past seven months or so have been all about stress.

The coronavirus itself can cause inflammation, so people who are already hypersensitive may find that its bad for their hair, Ziering tells The Manual. Weve even been seeing patients who arent sick suddenly losing more hair than usual. Men particularly are suffering because they are still, traditionally, seen as the head of the household. If they get even a little sick it can cause emotional stress. How will they provide for their families? Compound that with fluctuations in the stock market. Guys who own small businesses may feel it even more because they feel the stress of providing for their families as well as for their employees.

Ziering goes on to point out that a lot of things can unmask underlying genetic hair loss that a patient might not normally experience until later in life. Men who are treated for cancer, for instance, may lose their hair temporarily, but it will grow back. If there is underlying Male Pattern Baldness, however, that may exacerbate hair loss into a more permanent condition.

Sometimes its as simple as giving the patient a sense of control. Everything else in his life is spiraling beyond his power, now its his hair, too? Its about breaking that cycle., says Ziering.

Sometimes that cycle may be as simple as using hair products that are healthier for your hair and scalp. Buildup from styling products can actually clog hair follicles, accelerating that telegenic effluvium response. Here are some of the best natural styling products weve tried.

Dr. Mukherjees comment sparked British grooming brand No Gunk to launch its lighthearted campaign, Dont Be a Receder Peter, in September. The accompanying video shows a young, healthy-haired man transformed into an aged, bald one from using preparations with harsh chemicals and those that leave residue behind. No Gunk is in favor of natural ingredients like lava clay, shea butter, and argan oil.

Winner of 2020 Grooming Awards, Jack Henrys rockstar product only contains four main ingredients beeswax, coconut oil, bentonite clay, and lavender oil to easily shape hair without damaging follicles.

Lots of drugstore shampoos contain some artificial ingredients that can further cause hair damage. Not so with Verbs vegan shampoo, which is infused with hydrating moringa and sunflower seed extracts to thoroughly clean your mane. Plus, its free of harmful sulfates and parabens, and its cruelty-free.

If youve tried changing products and are still experiencing rapid hair loss, dont waste any time getting to a doctor. If a serious hair loss problemis diagnosed in time, it may be reversible within three to six months.

Dr. Ziering starts with topical medications like minoxidil or finasteride, an easy at-home treatment. In some cases he may move on to oral finasteride, which blocks DHT. DHT is a type of testosterone that works wonders for men when were going through puberty, but is not so friendly to your follicles when you get older.

We also use laser therapy, where the patient wears a cap that stimulates the mitochondria, improving cell growth, says Ziering. Finally we also do exosomes injections, which is a form of stem cell therapy. The treatment nourishes the hair and basics all helps wimpy hair grow thicker.

Finally, if it comes down to it, actual surgery may be an option, and doctors like Ziering can help with hair restoration and transplants.

Maybe the most important part of stress-related hair loss is to keep things in perspective.

Im a medical doctor. I deal with the patient as a whole, says Dr. Ziering. Its important to remember that we are all in this together. Find something thats good for your body: Meditation, exercise, rest, yoga, or whatever makes you feel better. Eat a high protein diet with fresh super greens and legumes. Dont keep stress bottled up! Find somebody that you can talk to and share your feelings. Dont be ashamed if its time to do something about losing your hair. Do whats necessary to break that stressful cycle and feel like youre doing something positive for yourself.

Link:
How To Treat Stress-Related Hair Loss During COVID-19 - The Manual

OWINGS MILLS, Md., Sept. 24, 2020 /PRNewswire/ --Chesapeake Urology, an affiliate of United Urology Group, recently welcomed three new physicians to its growing team of specialists and general urologists. The addition of David A. Levy, M.D., Devang Sharma, M.D., and Katherine Smentkowski, M.D., continues to expand Chesapeake Urology's reach into specialties such as prostate cancer, men's sexual and reproductive medicine, reconstructive surgery, as well as general urology.

David A. Levy, M.D. is a recognized expert in prostate cryosurgery, an outpatient curative prostate cancer procedure that he has been performing for the past 15 years. He has published numerous peer-reviewed manuscripts on prostate cryosurgery detailing patient selection criteria, procedure-related side effects and outcomes analyses, as well as the definition of treatment success for the procedure for patients with newly diagnosed prostate cancer and those treated for recurrence following failed radiation therapy.

Dr. Levy also has substantial experience in prostate cancer nutrition and directed a Prostate Cancer Nutrition Genetics Clinic in Cleveland where he treated more than 450 prostate cancer patients in a non-operative manner over the past six years.

He graduated from Washington University in St. Louis in 1985. He received his Doctorate of Medicine degree from the Chicago Medical School and completed his General Surgery Internship and Urology Residency at University Hospitals of Cleveland, Case Western Reserve University. Following his residency, Dr. Levy completed a fellowship in Urologic Oncology at the MD Anderson Cancer Center in Houston, Texas.

Dr. Levy sees patients at Chesapeake Urology's Hanover and Saint Agnes Hospital/Angelos Medical Pavilion offices.

Devang Sharma, M.D. is a comprehensive men's health specialist with fellowship training in male infertility, sexual dysfunction, and reconstructive surgery. In addition to general urology, his practice is focused on men with urinary complaints related to the bladder, prostate, or urethra, erectile dysfunction, Peyronie's disease, low testosterone, fertility concerns, and prostate cancer survivorship. He brings advanced training and expertise in contemporary treatments including no-scalpel vasectomy, Greenlight photovaporization of the prostate, UroLift, penile injection and shockwave therapy, penile implants, artificial urinary sphincters and slings, urethral reconstruction, and microsurgical techniques including vasectomy reversal, varicocele repair, sperm extraction, and spermatic cord denervation.

Dr. Sharma graduated summa cum laude from the University of Maryland with a degree in Bioengineering. He graduated with honors from the Geisel School of Medicine at Dartmouth, then completed Urology Residency and Andrology Fellowship at the University of Virginia.

Dr. Sharma sees patients at Chesapeake Urology's office at Holy Cross Germantown Hospital.

Katherine Smentkowski, M.D.focuses on general urology as well as bladder and kidney cancer, kidney stones and minimally invasive and robotic surgery for upper urinary tract reconstruction. Her fellowship training at Thomas Jefferson University focused on robotic management of both benign and malignant urological conditions. This included prostate, bladder, kidney and ureteral cancers as well as reconstructive techniques for ureteropelvic junction obstruction and ureteral strictures.

Dr. Smentkowski earned her Bachelor of Science degree in Physiology and Neurobiology from the University of Maryland, College Park, MD. She received her Medical Doctorate at Eastern Virginia Medical School (EVMS) in Norfolk, VA where she was involved in community outreach and elected into the Alpha Omega Alpha Honor Society. She went on to complete Urological Residency at EVMS as well as a Fellowship in Minimally Invasive and Robotic Surgery at the Thomas Jefferson University in Philadelphia, PA.

Dr. Smentkowski sees patients in Chesapeake Urology's Columbia office.

About Chesapeake Urology

Chesapeake Urology, an affiliate of United Urology Group, is a fully-integrated urology practice providing a comprehensive array of urologic services to its patients. The Company operates 24 medical offices and 17 AAAHC-certified ambulatory surgery centers in Anne Arundel, Baltimore, Harford, Howard, Carroll, Montgomery, Prince George's, Wicomico, Worchester counties in Maryland, Baltimore City, and Sussex County, Delaware, and has a staff of more than 900 including 90 physicians, 84 who are urologists. Chesapeake Urology has been named one of the top places to work in healthcare nationally by Modern Healthcare magazine and Becker's ASC Review, and locally by the Baltimore Sun, Baltimore magazine and the Baltimore Business Journal. For additional information, please visit ChesapeakeUrology.com.

Media Contact: Patricia Schnably, Senior Vice President, Marketing & CommunicationsUnited Urology Group25 Crossroads Drive, Suite 306, Owings Mills, MD 21117443-738-8107[emailprotected]

SOURCE Chesapeake Urology

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Chesapeake Urology Welcomes Three New Physicians, Expanding Specialty Services in Anne Arundel, Howard, and Montgomery Counties and Baltimore City -...

Hair loss can be the result of complex environmental and genetic processes. In the former camp lies responses to stressful situations and certain cancer treatments. In the genetic camp is androgenetic alopecia - commonly known as pattern baldness. It usually runs in the family, which, on the face of it, seems dispiriting.

Fighting genetics may seem like a losing battle but evidence does suggest you can reverse this form of hair loss.

One strategy that has yielded surprising results is applying a melatonin solution to the scalp.

Most people will associate melatonin with sleep - the hormone plays a central role in the bodys sleep-wake cycle.

As the National Sleep Foundation explains, its production increases with evening darkness, promoting healthy sleep and helping to orient our circadian rhythm.

READ MORE:Hair loss treatment - Dr Sara explains the best type of shampoo to stimulate hair growth

Circadian rhythms are 24-hour cycles that are part of the bodys internal clock, governing important processes such as the sleep-wake cycle.

Theres evidence that the benefits of melatonin extend to treating hair loss.

This is because melatonin also affects hair growth, as the hair growth cycle in mammals is under circadian control, according to The Lifespan Research Institute, a research body that focuses on anti-ageing compounds.

"As with other circadian cycles, the hair growth cycle becomes dysregulated and lower in amplitude with age," explains the research body.

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In a randomised double-blind study of 40 women with hair loss, melatonin solution applied to the scalp increased hair growth significantly relative to placebo.

What's more, in a study published in the International journal of trichology, 1891 male and female patients with androgenic alopecia applied a topical melatonin solution for three months.

At three months 61 percent of patients had no hair loss, compared to 12.2 percent at the start; 22 percent had new hair growth at three months compared to four percent at baseline.

The incidence of seborrheic dermatitis also declined, from 34.5 percent at baseline to 9.9 percent at three months.

Seborrheic (seb-o-REE-ik) dermatitis is a common skin condition that mainly affects your scalp.

The skin condition can cause an itchy, flaky rash, which may lead to hair loss due to excessive itching.

According to the NHS, finasteride and minoxidil are the main treatments for male pattern baldness.

"Minoxidil can also be used to treat female pattern baldness. Women shouldn't use finasteride," explains the NHS.

There are a number of drawbacks to consider before taking these treatments.

According to the NHS, these treatments:

These treatments:

Alternatively, some wigs are available on the NHS, but you may have to pay unless you qualify for financial help.

While considering your options, you may benefit from some psychological support.

Your GP may be able to help you get some counselling or you can join a support group, adds the NHS.

The rest is here:
Losing hair fast? Applying this natural solution to the scalp resulted in new hair growth - Express

IRVINE, Calif.--(BUSINESS WIRE)--While studying the genetics of the androgen receptor, a team of scientists discovered a possible breakthrough treatment for COVID-19.

The team led by Andy Goren, MD from Applied Biology, Flavio A. Cadegiani, MD, MSc, PhD from Corpometria Institute in Brazil, along with other collaborators, have published their discovery in several medical journals. The manuscript, What Does Androgenetic Alopecia have to do with COVID-19? An Insight into a Potential New Therapy (doi: 10.1111/dth.13365), elucidates the possible role of androgens in controlling the infectivity of SARS-CoV-2 in human lung cells.

According to Dr. Goren, Our earlier discovery potentially links SARS-CoV-2 infectivity to androgens, the same hormones implicated in male pattern baldness and prostate cancer; thus, anti-androgens originally developed for prostate cancer may prove a breakthrough therapy for COVID-19. One of the most promising anti-androgens is proxalutamide, a next generation anti-androgen.

The study on the effects of proxalutamide on COVID-19 has received national IRB approval and will be conducted in Brasilia, Brazil, in non-hospitalized patients with mild-to-moderate COVID-19 disease. Recruitment of volunteers should start this week.

According to Dr. Cadegiani, We are excited to commence this study that could potentially benefit millions of patients and change the course of COVID-19.

More information about the study (ClinicalTrials.gov Identifier: NCT04446429) is available at clinicaltrials.gov (https://clinicaltrials.gov/ct2/show/NCT04446429?term=NCT04446429&draw=2&rank=1).

The approval was received on September 17th, 2020 from the IRB of the National Board of Ethics Committee (CONEP), from the Brazilian Ministry of Health, under the name The Proxa-AndroCoV Trial, number (CAAE) 36700320.8.0000.0023.

ABOUT APPLIED BIOLOGY

Founded in 2002, Applied Biology, Inc. (www.appliedbiology.com), headquartered in Irvine, California, is a biotechnology company specializing in hair and skin science. Applied Biology develops breakthrough drugs and medical devices for the treatment of androgen mediated dermatological conditions. Applied Biology's R&D pipeline includes a topically applied prophylactic treatment for chemotherapy induced alopecia; a novel diagnostic device that can aid dermatologists in identifying non-responders to topical minoxidil; an adjuvant therapy for non-responders to topical minoxidil; and a novel therapy for female pattern hair loss.

ABOUT CORPOMETIRA INSTITUTE

Corpometria institute was founded in 2013, and is focused on treating, researching and optimizing healthcare of the major unsolved endocrine-related conditions, including patients with obesity, sarcopenia, menopause and andropause, chronic fatigue and burnout, undertrained athletes, and rare metabolic and endocrine diseases.

Corpometria R&D pipeline includes three major clusters: amplifying genetic testing, epigenetic influences and metabolomic analyses of patients with not-fully clarified metabolic and endocrine-related illnesses; development of machine learning and AI-based algorithm for personalized metabolic responses and changes to specific eating, exercising and sleeping characteristics; and full elucidation of endocrine physiology of the sport, including specific hormonal and metabolic responses and adaptations to sports according to intensity, volume, frequency and type of physical activity, and in combination with a variety of nutritional, psychological, social, and sleeping characteristics.

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Applied Biology and Corpometria Institute Receive National IRB Approval to Study a Potential Breakthrough Therapy for COVID-19 - Business Wire

Castrating male piglets has always been quite a controversial topic for farmers and consumers alike, but more pressure is being applied these days by the latter to ban the practice.

It is common knowledge that the meat from uncastrated males can have a rather unpleasant smell or taste when it is cooked: this is known as boar taint. During a recent webinar facilitated by the group Innovative Approaches for Pork Production with Entire Males (IPEMA), a body supported by the EU to look at various methods to producing entire male pigs, a number of alternatives to the surgical castration of piglets were discussed.

Preparations for castration. Will the practice continue as it is? - Photo: Mark Pasveer

Castrated male pigs convert feed to meat less efficiently than entire males but the process of surgical castration without pain relief is painful to the animal. There is a growing consensus within Europe that this process should be discontinued favouring a different approach. In total, 3 different alternatives are available including surgical castration with pain relief, immunocastration and simply leaving the animals as entire males.

IPEMA classifies surgical castration with pain relief as an intermediate short term solution that is inefficient and adds costs. Focusing on the other 2 alternatives, IPEMA found that leaving the pigs uncastrated as entire males increased the aggressive behaviour of the animals and that they mounted their pen mates.

Also, there were issues with boar taint on the meat and other meat quality problems such as lower fat amounts, and being less tender.

During immunocastration, a vaccine is injected that inhibits steroid production by the testes. It is only when a second vaccination is administered, that there is any difference to the animals behaviour and a gradual improvement to meat quality.

There is a number of issues associated with immunocastration including stress during vaccination, and some concerns over meat quality depending on the timing of the second vaccination to the time of slaughter. The biggest challenge though, is that most markets in the European Union are reluctant to accept this as a husbandry process as they assume consumers are against it.

There was discussion as well about how breeding and genetics can be used as tools to reduce boar taint, improve the meat quality and reduce aggressive behaviour of entire male pigs. At the end of the day, whatever method is used going forward will be heavily influenced by consumer and market demands.

During the past 20 years, surgical castration of piglets has been strongly contested by animal welfare organisations. The discussions acknowledged that each of the alternatives has pros and cons but the biggest road blocks to consumer acceptance were boar taint for entire male production and consumer acceptance of immunocastration.

Dutch pig farmer Annechien ten Have-Mellema closed the webinar by recognising there is a lot of work to do on the topic of pig castration. She said: A lot of scientists are working on the alternatives for pig castration. It is a complex issue and it is very nice that there is a collaboration in this network between scientists and stakeholders in the supply chain.

She continued to say, We can see that Europe is moving to pig castration with anaesthesia, immuno vaccination, or towards entire males. We are all on a different stage but the process is irreversible. The work is not ready and has only started. Awareness and knowledge sharing is very important. The European Union also has a responsibility to facilitate this work.

Read the rest here:
Examining the alternatives to piglet castration - Pig Progress

by Nabaa Muhammad and Michael Z. Muhammad | The Final Call | @TheFinalCall

Emphatically no, Walt Boarderly, an entrepreneur and Philadelphia business owner, replied when asked if he would take the Covid-19 vaccine. Mr. Boaderly isnt anti-vaccine, saying he will take the flu shot. There is just too much uncertainty when it comes to this new vaccine, he said.

Blacks do not trust President Trumps Covid-19 vaccine push, and there is plenty of reason to be distrustful. Black people have been the victims of medical experiment, exploitation and abuses by their White enslavers and White doctors from the time the good ship Jesus hit Americas shores. These medical researchers have been like a pack of crazed dogs chasing their helpless prey.

In her comprehensive book Medical Apartheid, Harriett Washington details abuses committed against Blacks and how throughout the 19th century medical schools used Blacks in live surgical demonstrations.

In more recent times, she wrote, Blacks have been disproportionately enrolled in risky, nonbeneficial research in gynecology, oncology, surgery, pediatrics, infectious diseases, and genetics.

Medical Apartheid tells the story of slaves and Black freedmen used in hospitals for experiments without their knowledge or consent. Blacks have historically been victims of grave-robbing, unauthorized autopsies and dissections, Frankenstein-like behavior by White medical researchers.

The American Medical Womens Association sponsored a Sept. 19 Zoom conversation on Medical Apartheid as part of its Racism in Medicine Monthly Discussion.

Primary participants in the discussion were medical students and pre-med students.

The session opened with some basic questions, like whether doctors during slavery focused on the health of enslaved persons. Surprisingly many participants believed those doctors were concerned about slaves healththey werent. The doctors had a pact to inspect slaves to make sure they were fit for work, to determine their value given their ability to work and performed examinations for insurance companies before policies on slaves were issued to slave owners.

Dr. P. Oneeka Williams, a urologist based in Brighton, Mass., was one of two main presenters. She saluted Ms. Washington for her work and talked about the pervasive practice of using enslaved people for experiments.

She focused on Dr. James Marion Sims as the father of gynecology, lionized for his treatments for women. But, said Dr. Williams, These advances along with so many other physicians, really came on the backs of the violations and the atrocities and the disgusting treatment of Black bodies.

Born in 1813 in South Carolina, Dr. Simms underwent one and a half years of medical training, which he considered inadequate and started practicing on Alabama plantations. He experimented on enslaved Black children stricken by tetanus and enslaved Black women. In 1845, he used forceps, despite limited experience, to deliver a child from a slave girl. The baby died and the mother developed a vesicorectal fistula, a devastating condition involving the bladder and the rectum. It was a condition that women, Black and White, often suffered from. He acquired 11 slave women with the condition, housed them and started experimenting with surgical repair. The woman had no consent, no anesthesia and were put on display. The surgeries were painful, frequently broke down and required multiple surgeries with physicians coming to observe his procedures, said Dr. Williams, a Black woman. The enslaved womens piercing screams could be heard, she said.

Dr. Simms developed a procedure to treat the condition, practicing for three years on enslaved Black women. He started publishing articles about his dubious success in 1852 and began operating on White women. As abolitionists objected to using Blacks for medical experimentation, he started to hide the race of his test subjects. He later became president of the American Medical Association and opened the first hospital for women in New York City in 1875. His name is enshrined on buildings, hospitals and statues were erected in his honor.

In 2018, protests led to the removal of his statue in New Yorks Central Park. Officials relocated it to his gravesite in Brooklyn.

Biases and racism would not impact on the medical profession any differently than it impacts on any other categories in life, said Dr. Williams.

Race-based beliefs became seen as real science and are still perpetuated, she added.

Dr. Williams believes educating and raising awareness of medical students and professionals alongside elementary, high school and college students are important to help resolve the problem. She has seen instances today in which physicians have not valued Black lives, though it may not be conscious.

Medical Apartheid chronicles how in the 17th and 18th century enslaved Blacks were used for vaccine trials, smallpox in particular, without their consent and once the vaccines were effective, the cures were released into the general population, said Dr. Williams.

We have to look at history so that when people try to diminish the concerns of Black people about being potentially the unwitting participants of some type of trial that is about using us as guinea pigs that its not a kind of hearsay. Its not oh I think, Im guessing, she continued.

Here its factual information that supports why the skepticism exists and why there has to be a clear set of strategies about how do you really help Blacks to feel confident and reassured that they are not going to be used in a kind of experimentation process that has been done even in our contemporary times. This is not centuries ago, this is within recent history, 10, 20, 30 years, were still seeing situations where Blacks have been used as part of unconsenting experimental protocols to their detriment.

Even the infamous Tuskegee Experiment has aspects that are not generally talked about. In Medical Apartheid, the author reveals how the syphilis study, started in 1932, was based on the belief that racial differences and irresponsible Black behavior accounted for syphilis infections among poor Blacks. Most cases were actually due to disease transmission from mothers to children.

There was a profit motive in the study as the federal government hoped to come out with a lucrative vaccine and wanted to follow the 600 male patients until they died.

When the federal governments wickedness was uncovered, some documents were hidden from a panel that was supposed to look into the genocidal activity and the victims were eventually paid a pittance. In 1943, penicillin, a treatment for syphilis, was discovered but never given to study victims. In addition to the deaths of the men, at least 40 wives and almost 20 children were infected.

In 1965, the study was discovered and a leftist, social activist group tried to stop it, but was ignored. By 1969, 100 men had died from direct and indirect complications from syphilis. Peter Buxton, a Polish immigrant, working within the study called for ending it. In 1972, he shared the nefarious experiment with a friend, who was an AP reporter. Ted Kennedy held hearings, an investigation was opened, but a historian was never involved and a panel was formed to look into the study. The panel was given less than one year to do its work, some documents were deliberately hidden, the panel chair forced a softening of the language of the initial report and submitted it with a cover letter abstaining from agreement with the report.

Tapes of interviews with every victim were kept but destroyed, and in 1995 a doctor determined the studys chief purpose was to create a reliable vaccine and the results of the study were used to create advanced tests for syphilis and vaccines that were marketed globally.

The original U.S. contract with the Alabama Dept. of Health stipulated that the U.S. government owns any invention arising from the Tuskegee Syphilis Study, and so, the U.S. government profited tremendously off the backs of these men and their families and continued to do so, said the moderator for the online session. The CDC also soft pedals the Tuskegee Syphilis Study, though President Clinton apologized for it, she added.

If you look at themes throughout the book, this is all economically driven, commented Dr. Williams. The very agencies that are supposed to be committed to protect the population, to protect the people, the American government, when you look at what was really the motivation for this study.

Even today we are seeing what we are seeing with covid and misinformation, deception, parties that are changing the narrative, changing information, changing things that impact our peoples lives, she said. Things like not testing asymptomatic people have far-reaching effects into the health of the nation, Dr. Williams observed.

Youre exposing people to a potential deadly pathogen, she continued. But who are the people who are disproportionately suffering from that virus? All of these threads when you look at how interwoven the government agencies have been in the deception, in the abuse of Black and Brown bodies, its really very, very disconcerting, said Dr. Williams.

Black only medicine?

Dr. Vanessa Al Rashida, who practices medicine in New Mexico, presented information about the continued use of race as a basis for research based on a chapter in Medical Apartheid.

The public health field has contributed to misinformation going back to slavery, said Dr. Al Rashida. Early U.S. Census studies found free Blacks suffered more from alcoholism and died because of recklessness, she said. The theory was Whites needed to shepherd Black people, the physician added.

In 2005, a drug that the Food and Drug Administration initially denied for wide use was approved for use only in Black Americans with heart failure, she said. The drug was Bidil.

In the 1980s, surveys had found heart failure was twice as common in older Blacks than Caucasians, which is not the case today, she said.

But Blacks dying more often led the company NitroMed to postulate a genetic cause of the disease disparity. FDA approved research for the drug. Clyde Yancey, a Black cardiologist, and others objected to the premise of race-based differences as opposed to differences based on environment and lifestyle. The NitroMed approach ignored these things but a Black cardiologists group approved the study.

Most diseases Blacks suffer are driven by environment, not any inherent difference based on genetics and race, said Dr. Al Rashida.

The African American Heart Failure Trials in 2003 was composed of Blacks only, one group with approved heart medications put against another group of Black Americans using heart medications and Bidil, she explained.

She questioned the methodology of the study, which showed some Bidil benefit in curbing deaths, and FDA approved the drug which is still used today.

The study made me sick for a while, said Dr. Al Rashida.

A non-genetic disease of heart failure, which other studies have shown is often due to high blood pressure caused by environmental factors in Black Americans, is being treated with genetic treatments, she said. That concerns her. Research has shown little genetic difference between people based on race, said Dr. Al Rashida, who read Medical Apartheid in medical school. It was given to her as a gift from a family friend.

The Nitro-Med study would have had more weight if it compared Black Americans to Caucasians, she said. But, it only compared Black Americans and the reason for that was money, she said.

It was not economically feasible for the company to add in Caucasians with African Americans to be compared in the study, said Dr. Al Rashida.

Its also kind of scary to me that future studies are being based on this whole precipice that race is playing a part in diseases that we are seeing in the country. Whereas thats not the case at all. Its environment and its also lifestyle behaviors too that have been rooted back into slavery.

That includes how Black people eat, added Dr. Al Rashida.

I try to be very optimistic and I want to see better for our country, but at the same time, its very scaryespecially with the current leadership that we have in certain institutions. Its going to be a very difficult hill to climb essentially, she said.

If research determines that illness or disorders are based on racial differences, not environment, it is easier to dismiss the need to make changes in society and argue the conditions or illnesses are inevitable.

Prisons, hospitals and the devils playground for reckless research

There are other concerns about vaccines and negative impacts on Blacks. Since 2014, controversy has brewed over a Centers for Disease researcher who charged the agency with hiding research results linking an experimental measles vaccines with increased Black male children developing autism. Dr. William Thompson, who made the charges, has called for an opportunity to testify before Congress. Though CDC denies his charge, there has been no congressional hearing.

Ms. Washington has written about a 1970 Johns Hopkins Free Child Care program for more than 7,000 young boys, 95 percent from underprivileged Negro familieswho used as guinea pigs in a three-year experiment that could have branded them as latent criminals for life. Funded by the National Institutes of Health, the project extracted blood samples, ostensibly to test for anemia and other medical problems. She wrote that testing was done without parental knowledge or consent.

In a piece published in the Baltimore Sun, Ms. Washington wrote, In 1962, Dr. Chester M. Southam of the Sloan-Kettering Institute injected at least 396 inmates at Ohio State Prisonalmost half of them blackwith live humancancercells.

According to Allan Hornblum, author of Acres of Skin: Human Experiments at Holmesburg Prison, Holmesburg Prison became one of Americas largest, nontherapeutic, human research factories. The Pennsylvania prison was about 85 percent Black, and there were very few high school graduates, he wrote.

Dr. Albert Kligman, Ph.D. and M.D., University of Pennsylvania, began dermatology research before 1951 when he visited the prison, said the book author.

Dr. Klingman envisioned using the skin of inmates his dermatology drug trials, trials for anti-obesity drugs, viral infections, and bacterial infections, wrote Mr. Hornblum.

All kinds of tests, foot powder, eye drops, face creams, underarm deodorant, toothpaste, liquid diets, were used, leaving inmates scarred and often suffering. Dr. Klingman reportedly declared, All I saw before me were acres of skin It was like a farmer seeing a fertile field for the first time, according to the book.

In 1979, the Philadelphia Inquirer disclosed that Holmesburg inmates had been used as guinea pigs to test whether mind-altering drugs were useful as Army weapons. In 1981 the paper reported that inmates had been dosed with dioxin to test the herbicides effects on humans.

In American Mengele: Human Radiation Experiments, Ryan Grimm detailed what he called experiments more horrible than Tuskegee. He wrote about experiments conducted by Dr. Eugene L. Saenger at Cincinnati General Hospital from 1960 to 1972. The Department of Defense paid him, and several government agencies used his findings.

What makes radiation experiments like Saengers more horrible than those at Tuskegee is that, in these cases, doctors were not merely watching an already existing disease take its course. Instead, Saenger deliberately injected hundreds of people with potentially lethal doses of radiation, knowing that most of them would die rather quickly, wrote Mr. Grimm.

At least 89 people are acknowledged to have died due to Saengers treatment, although the number is likely well above 200. Dr. Saenger even copped to the crime and openly defended his actions as necessary preparation for nuclear war.He was never charged with a crime.

His average patient had five years of formal education, an average I.Q. of 89 and 62 percent were Black.

A study conducted in part by researchers from the Maryland Center for Health Equity at the University of Maryland-College Park, found many Blacks dont get flu shots because they dont trust the vaccine.

Blackdoctors.org reported 58 percent of respondents to their survey would not take a Covid-19 vaccination as soon as it is available. Fifty-eight percent said no to the vaccine, 22 percent reported they would take the vaccine but had concerns. Eighty percent respondents either said no or had concerns about taking a Covid-19 vaccine, citing mistrust of the health care system.

Read more:
We Can't Trust You: Experimentation, Exploitation and the Hidden History of American Medical Abuses - Final Call News - FinalCall.com News

Researchers say your biological sex affects gene expression in nearly every type of tissue influencing body fat, cancer and birth weight.

Gene expression is the amount of product created by a gene for cell function, the international team of researchers explained.

They said their findings could prove important for personalised medicine, creating new drugs and predicting patient outcomes.

"These discoveries suggest the importance of considering sex as a biological variable in human genetics and genomics studies," said project leader Barbara Stranger, an associate professor of pharmacology at Northwestern University Feinberg School of Medicine in Chicago.

Unreported links

The researchers analysed 44 types of healthy human tissue from 838 people to find out if there were differences between women and men in the average amount of gene expression.

They discovered that 37% of all human genes were expressed at different levels in women and men in at least one type of tissue.

They also identified 369 instances where a genetic variant present in males and females affected gene expression to a different degree in each sex. This led to the discovery of 58 previously unreported links between genes and blood pressure, cholesterol levels, breast cancer and body fat percentage.

Gender differences in gene expression were also found for genes involved in how the body responds to medications, how women control blood sugar levels in pregnancy, how the immune system functions and how cancer develops.

Critical component of personalised medicine

"If specific genes or genetic variants contribute differentially to a given trait in males and females, it could suggest sex-specific biomarkers, therapeutics and drug dosing," Stranger said in a Northwestern news release.

"In the future, such knowledge may form a critical component of personalised medicine or may reveal disease biology that remains obscured when considering males and females as a single group," she said.

The study was published in the journal Science.

Image credit: iStock

Excerpt from:
Your sex affects your genes for body fat, cancer and birth weight - Health24

KENILWORTH, N.J.--(BUSINESS WIRE)--AstraZeneca and Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced final results from the Phase 3 PROfound trial which showed LYNPARZA demonstrated a statistically significant and clinically meaningful improvement in overall survival (OS) versus enzalutamide or abiraterone in men with metastatic castration-resistant prostate cancer (mCRPC) who have BRCA1/2 or ATM gene mutations. Patients had progressed on prior treatment with enzalutamide and/or abiraterone.

Prostate cancer is the second most common type of cancer in men, with an estimated 1.3 million new patients diagnosed worldwide in 2018. Approximately 20-30% of men with mCRPC have an homologous recombination repair (HRR) gene mutation, of which BRCA1/2 and ATM mutations are a subpopulation. Approximately 10-20% of early stage hormone-sensitive prostate cancer cases will develop into CRPC within approximately five years.

In the key secondary endpoint of OS in men with BRCA1/2 or ATM gene mutations, LYNPARZA reduced the risk of death by 31% vs. retreatment with enzalutamide or abiraterone (HR 0.69 [95% CI, 0.50, 0.97], p=0.0175). Median OS was 19.1 months for LYNPARZA vs. 14.7 months for enzalutamide or abiraterone, despite 66% of men on these treatments having crossed over to receive treatment with LYNPARZA following disease progression.

An exploratory analysis also showed a non-statistically significant improvement in OS in the overall trial population of men with HRR gene mutations (BRCA1/2, ATM, CDK12 and 11 other HRR-mutated [HRRm] genes), reducing the risk of death by 21% with LYNPARZA vs. enzalutamide or abiraterone (HR 0.79 [95% CI, 0.61, 1.03]. Median OS was 17.3 months vs. 14 months for enzalutamide or abiraterone.

The most common adverse reactions (ARs) 15% were anemia (50%), nausea (43%), fatigue/asthenia (42%), decreased appetite (31%), diarrhea (21%), vomiting (20%) and constipation (19%). Grade 3 or above ARs were anemia (23%), nausea (2%), fatigue or asthenia (3%), decreased appetite (2%) and diarrhea (1%). Twenty percent of patients on LYNPARZA discontinued treatment due to ARs and 23% had their dose reduced due to an AR.

Dr. Johann de Bono, one of the principal investigators of the PROfound trial and head of drug development at the Institute for Cancer Research and the Royal Marsden Hospital, said, LYNPARZA has demonstrated significant clinical benefit across key endpoints in PROfound and the final overall survival results for men with BRCA1/2 or ATM mutations reinforce its potential to change the standard of care for men with metastatic castration-resistant prostate cancer. The PROfound trial shows that LYNPARZA can play an important role in this new era of precision medicine in prostate cancer, bringing targeted therapy at a molecular level to patients with a historically poor prognosis and few treatment options.

Dr. Jos Baselga, executive vice president, Oncology R&D, AstraZeneca said, These results help to transform the treatment landscape in certain men with metastatic castration-resistant prostate cancer, where overall survival has been very difficult to achieve. LYNPARZA is the only PARP inhibitor to demonstrate overall survival versus enzalutamide or abiraterone for men with BRCA or ATM mutations. We look forward to continuing to bring LYNPARZA to these patients around the world.

Dr. Roy Baynes, senior vice president and head of global clinical development, chief medical officer, Merck Research Laboratories, said, The PROfound trial is the first positive Phase 3 trial using molecular biomarker testing to help identify treatment options for certain men with metastatic castration resistant prostate cancer. These results further underpin the importance of genomic testing for HRR gene mutations to help identify this at-risk patient population and help physicians make treatment decisions. These results demonstrate the potential of LYNPARZA for mCRPC patients with certain HRR mutations.

Final OS results from the PROfound trial were presented on Sunday, Sept. 20, 2020, during the Presidential Symposium at the European Society for Medical Oncology (ESMO) Virtual Congress 2020 and published simultaneously in The New England Journal of Medicine.

Summary of OS results

OS data cut-off date was March 20, 2020.

Men with BRCA1/2 and ATM mutations (Cohort A)Secondary Endpoint

Overall populationof men with HRR mutations(Cohorts A+B)Exploratory Endpoint

LYNPARZA n=162

Control

n=83

LYNPARZA n=256

Control

n=131

Median, months

19.1

14.7

17.3

14.0

Hazard ratio (95% CI)

0.69 (0.50, 0.97)

0.79 (0.61, 1.03)

P-value

0.0175

N/A

The Phase 3 PROfound trial had met its primary endpoint in August 2019, showing significantly improved radiographic progression-free survival (rPFS) in men with mutations in BRCA1/2 or ATM genes, and had met a key secondary endpoint of rPFS in the overall HRRm population, which formed the basis of the U.S. Food and Drug Administration approval in May 2020. Regulatory reviews are ongoing in the EU and other regions.

AstraZeneca and Merck are exploring additional trials in metastatic prostate cancer including the ongoing Phase 3 PROpel trial, with first data expected in 2021, evaluating LYNPARZA as a first-line medicine for patients with mCRPC in combination with abiraterone acetate versus abiraterone acetate alone.

About PROfound

PROfound is a prospective, multi-center, randomized, open-label, Phase 3 trial evaluating the efficacy and safety of LYNPARZA versus enzalutamide or abiraterone in patients with mCRPC who have progressed on prior treatment with abiraterone or enzalutamide and have a qualifying HRR tumor mutation (BRCA1/2, ATM, CDK12, BARD1, BRIP2, CHEK1, CHEK2, PALB2, PPP2R2A, RAD51B, RAD51D, RAD54L).

The trial was designed to analyze patients with HRRm genes in two cohorts: the primary endpoint was rPFS in those with mutations in BRCA1/2 or ATM genes and then, if LYNPARZA showed clinical benefit, a formal analysis was performed of the overall trial population of patients with HRRm genes (BRCA1/2, ATM, CDK12 and 11 other HRR mutated genes; a key secondary endpoint).

In the U.S., patients are selected for treatment with LYNPARZA based on the following FDA-approved companion diagnostics:

IMPORTANT SAFETY INFORMATION

CONTRAINDICATIONS

There are no contraindications for LYNPARZA.

WARNINGS AND PRECAUTIONS

Myelodysplastic Syndrome/Acute Myeloid Leukemia (MDS/AML): Occurred in <1.5% of patients exposed to LYNPARZA monotherapy, and the majority of events had a fatal outcome. The duration of therapy in patients who developed secondary MDS/AML varied from <6 months to >2 years. All of these patients had previous chemotherapy with platinum agents and/or other DNA-damaging agents, including radiotherapy, and some also had a history of more than one primary malignancy or of bone marrow dysplasia.

Do not start LYNPARZA until patients have recovered from hematological toxicity caused by previous chemotherapy (Grade 1). Monitor complete blood count for cytopenia at baseline and monthly thereafter for clinically significant changes during treatment. For prolonged hematological toxicities, interrupt LYNPARZA and monitor blood count weekly until recovery.

If the levels have not recovered to Grade 1 or less after 4 weeks, refer the patient to a hematologist for further investigations, including bone marrow analysis and blood sample for cytogenetics. Discontinue LYNPARZA if MDS/AML is confirmed.

Pneumonitis: Occurred in <1% of patients exposed to LYNPARZA, and some cases were fatal. If patients present with new or worsening respiratory symptoms such as dyspnea, cough, and fever, or a radiological abnormality occurs, interrupt LYNPARZA treatment and initiate prompt investigation. Discontinue LYNPARZA if pneumonitis is confirmed and treat patient appropriately.

Embryo-Fetal Toxicity: Based on its mechanism of action and findings in animals, LYNPARZA can cause fetal harm. A pregnancy test is recommended for females of reproductive potential prior to initiating treatment.

Females

Advise females of reproductive potential of the potential risk to a fetus and to use effective contraception during treatment and for 6 months following the last dose.

Males

Advise male patients with female partners of reproductive potential or who are pregnant to use effective contraception during treatment and for 3 months following the last dose of LYNPARZA and to not donate sperm during this time.

Venous Thromboembolic Events: Including pulmonary embolism, occurred in 7% of patients with metastatic castration-resistant prostate cancer who received LYNPARZA plus androgen deprivation therapy (ADT) compared to 3.1% of patients receiving enzalutamide or abiraterone plus ADT in the PROfound study. Patients receiving LYNPARZA and ADT had a 6% incidence of pulmonary embolism compared to 0.8% of patients treated with ADT plus either enzalutamide or abiraterone. Monitor patients for signs and symptoms of venous thrombosis and pulmonary embolism, and treat as medically appropriate, which may include long-term anticoagulation as clinically indicated.

ADVERSE REACTIONSFirst-Line Maintenance BRCAm Advanced Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for SOLO-1 were: nausea (77%), fatigue (67%), abdominal pain (45%), vomiting (40%), anemia (38%), diarrhea (37%), constipation (28%), upper respiratory tract infection/influenza/ nasopharyngitis/bronchitis (28%), dysgeusia (26%), decreased appetite (20%), dizziness (20%), neutropenia (17%), dyspepsia (17%), dyspnea (15%), leukopenia (13%), UTI (13%), thrombocytopenia (11%), and stomatitis (11%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for SOLO-1 were: decrease in hemoglobin (87%), increase in mean corpuscular volume (87%), decrease in leukocytes (70%), decrease in lymphocytes (67%), decrease in absolute neutrophil count (51%), decrease in platelets (35%), and increase in serum creatinine (34%).

ADVERSE REACTIONSFirst-Line Maintenance Advanced Ovarian Cancer in Combination with Bevacizumab

Most common adverse reactions (Grades 1-4) in 10% of patients treated with LYNPARZA/bevacizumab compared to a 5% frequency for placebo/bevacizumab in the first-line maintenance setting for PAOLA-1 were: nausea (53%), fatigue (including asthenia) (53%), anemia (41%), lymphopenia (24%), vomiting (22%) and leukopenia (18%). In addition, the most common adverse reactions (10%) for patients receiving LYNPARZA/bevacizumab irrespective of the frequency compared with the placebo/bevacizumab arm were: diarrhea (18%), neutropenia (18%), urinary tract infection (15%), and headache (14%).

In addition, venous thromboembolic events occurred more commonly in patients receiving LYNPARZA/bevacizumab (5%) than in those receiving placebo/bevacizumab (1.9%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients for LYNPARZA in combination with bevacizumab in the first-line maintenance setting for PAOLA-1 were: decrease in hemoglobin (79%), decrease in lymphocytes (63%), increase in serum creatinine (61%), decrease in leukocytes (59%), decrease in absolute neutrophil count (35%), and decrease in platelets (35%).

ADVERSE REACTIONSMaintenance Recurrent Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in clinical trials of LYNPARZA in the maintenance setting for SOLO-2 were: nausea (76%), fatigue (including asthenia) (66%), anemia (44%), vomiting (37%), nasopharyngitis/upper respiratory tract infection (URI)/influenza (36%), diarrhea (33%), arthralgia/myalgia (30%), dysgeusia (27%), headache (26%), decreased appetite (22%), and stomatitis (20%).

Study 19: nausea (71%), fatigue (including asthenia) (63%), vomiting (35%), diarrhea (28%), anemia (23%), respiratory tract infection (22%), constipation (22%), headache (21%), decreased appetite (21%), and dyspepsia (20%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the maintenance setting (SOLO-2/Study 19) were: increase in mean corpuscular volume (89%/82%), decrease in hemoglobin (83%/82%), decrease in leukocytes (69%/58%), decrease in lymphocytes (67%/52%), decrease in absolute neutrophil count (51%/47%), increase in serum creatinine (44%/45%), and decrease in platelets (42%/36%).

ADVERSE REACTIONSAdvanced gBRCAm Ovarian Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in clinical trials of LYNPARZA for advanced gBRCAm ovarian cancer after 3 or more lines of chemotherapy (pooled from 6 studies) were: fatigue/asthenia (66%), nausea (64%), vomiting (43%), anemia (34%), diarrhea (31%), nasopharyngitis/upper respiratory tract infection (URI) (26%), dyspepsia (25%), myalgia (22%), decreased appetite (22%), and arthralgia/musculoskeletal pain (21%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA for advanced gBRCAm ovarian cancer (pooled from 6 studies) were: decrease in hemoglobin (90%), mean corpuscular volume elevation (57%), decrease in lymphocytes (56%), increase in serum creatinine (30%), decrease in platelets (30%), and decrease in absolute neutrophil count (25%).

ADVERSE REACTIONSgBRCAm, HER2-negative Metastatic Breast Cancer

Most common adverse reactions (Grades 1-4) in 20% of patients in OlympiAD were: nausea (58%), anemia (40%), fatigue (including asthenia) (37%), vomiting (30%), neutropenia (27%), respiratory tract infection (27%), leukopenia (25%), diarrhea (21%), and headache (20%).

Most common laboratory abnormalities (Grades 1-4) in >25% of patients in OlympiAD were: decrease in hemoglobin (82%), decrease in lymphocytes (73%), decrease in leukocytes (71%), increase in mean corpuscular volume (71%), decrease in absolute neutrophil count (46%), and decrease in platelets (33%).

ADVERSE REACTIONSFirst-Line Maintenance gBRCAm Metastatic Pancreatic Adenocarcinoma

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for POLO were: fatigue (60%), nausea (45%), abdominal pain (34%), diarrhea (29%), anemia (27%), decreased appetite (25%), constipation (23%), vomiting (20%), back pain (19%), arthralgia (15%), rash (15%), thrombocytopenia (14%), dyspnea (13%), neutropenia (12%), nasopharyngitis (12%), dysgeusia (11%), and stomatitis (10%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA in the first-line maintenance setting for POLO were: increase in serum creatinine (99%), decrease in hemoglobin (86%), increase in mean corpuscular volume (71%), decrease in lymphocytes (61%), decrease in platelets (56%), decrease in leukocytes (50%), and decrease in absolute neutrophil count (25%).

ADVERSE REACTIONSHRR Gene-mutated Metastatic Castration Resistant Prostate Cancer

Most common adverse reactions (Grades 1-4) in 10% of patients in clinical trials of LYNPARZA for PROfound were: anemia (46%), fatigue (including asthenia) (41%), nausea (41%), decreased appetite (30%), diarrhea (21%), vomiting (18%), thrombocytopenia (12%), cough (11%), and dyspnea (10%).

Most common laboratory abnormalities (Grades 1-4) in 25% of patients in clinical trials of LYNPARZA for PROfound were: decrease in hemoglobin (98%), decrease in lymphocytes (62%), decrease in leukocytes (53%), and decrease in absolute neutrophil count (34%).

DRUG INTERACTIONS

Anticancer Agents: Clinical studies of LYNPARZA with other myelosuppressive anticancer agents, including DNA-damaging agents, indicate a potentiation and prolongation of myelosuppressive toxicity.

CYP3A Inhibitors: Avoid coadministration of strong or moderate CYP3A inhibitors when using LYNPARZA. If a strong or moderate CYP3A inhibitor must be coadministered, reduce the dose of LYNPARZA. Advise patients to avoid grapefruit, grapefruit juice, Seville oranges, and Seville orange juice during LYNPARZA treatment.

CYP3A Inducers: Avoid coadministration of strong or moderate CYP3A inducers when using LYNPARZA.

USE IN SPECIFIC POPULATIONS

Lactation: No data are available regarding the presence of olaparib in human milk, its effects on the breastfed infant or on milk production. Because of the potential for serious adverse reactions in the breastfed infant, advise a lactating woman not to breastfeed during treatment with LYNPARZA and for 1 month after receiving the final dose.

Pediatric Use: The safety and efficacy of LYNPARZA have not been established in pediatric patients.

Hepatic Impairment: No adjustment to the starting dose is required in patients with mild or moderate hepatic impairment (Child-Pugh classification A and B). There are no data in patients with severe hepatic impairment (Child-Pugh classification C).

Renal Impairment: No dosage modification is recommended in patients with mild renal impairment (CLcr 51-80 mL/min estimated by Cockcroft-Gault). In patients with moderate renal impairment (CLcr 31-50 mL/min), reduce the dose of LYNPARZA to 200 mg twice daily. There are no data in patients with severe renal impairment or end-stage renal disease (CLcr 30 mL/min).

INDICATIONS

LYNPARZA is a poly (ADP-ribose) polymerase (PARP) inhibitor indicated:

First-Line Maintenance BRCAm Advanced Ovarian Cancer

For the maintenance treatment of adult patients with deleterious or suspected deleterious germline or somatic BRCA-mutated (gBRCAm or sBRCAm) advanced epithelial ovarian, fallopian tube or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy. Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

First-Line Maintenance HRD Positive Advanced Ovarian Cancer in Combination with Bevacizumab

In combination with bevacizumab for the maintenance treatment of adult patients with advanced epithelial ovarian, fallopian tube or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy and whose cancer is associated with homologous recombination deficiency (HRD) positive status defined by either:

Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

Maintenance Recurrent Ovarian Cancer

For the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube or primary peritoneal cancer, who are in complete or partial response to platinum-based chemotherapy.

Advanced gBRCAm Ovarian Cancer

For the treatment of adult patients with deleterious or suspected deleterious germline BRCA-mutated (gBRCAm) advanced ovarian cancer who have been treated with 3 or more prior lines of chemotherapy. Select patients for therapy based on an FDA-approved companion diagnostic for LYNPARZA.

gBRCAm HER2-negative Metastatic Breast Cancer

Original post:
LYNPARZA Reduced Risk of Death by 31% vs. Enzalutamide or Abiraterone for Men with BRCA1/2 or ATM-Mutated Metastatic Castration Resistant Prostate...

Male Breast Cancer Treatment Market forecast to 2026

The Global Male Breast Cancer Treatment Market report provides information about the Global industry, including valuable facts and figures. This research study explores the Global Market in detail such as industry chain structures, raw material suppliers, with manufacturing The Male Breast Cancer Treatment Sales market examines the primary segments of the scale of the market. This intelligent study provides historical data from 2015 alongside a forecast from 2020 to 2026.

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Male Breast Cancer Treatment Market size, development, key opportunity, application and forecast to 2026 | Pfizer, Roche, GlaxoSmithKline, Sanofi,...

Its been quite a tough year for our wildlife population.

At least 30,000 koalas across the country lost their lives in last summers devastating bushfires - and in New South Wales alone, up to 71 per cent of the population was wiped out.

Watch the full story above

Now, legislation aimed to protect the species has received backlash from some landowners.

But amongst the bad news, the country has banded together for our furry friends.

State and Federal governments have pledged millions of dollars to the cause, and people all over the country have knitted mittens to aid those affected by the fires.

But theres still a long way to go to save our koalas.

Its not good, to put it very bluntly, said Chad Staples, a zookeeper from Mogo and Featherdale Wildlife Parks.

The fires were devastating for so many species but a tree-dwelling species is going to be affected far worse.

They were already under intense pressure prior to the fires, so its not good.

A tree-dwelling species is going to be affected far worse.

Australian forests need fire to regenerate, and its very natural - but that was a big-scale, high-intensity fire, and that wiped out a lot.

If koala populations were already in big numbers, you would have that flow come back in as the forest comes back.

But because wed already isolated so many of those pockets, for them to breed back to those numbers will take decades.

As part of the rehabilitation process, its important that we keep as much of their habitat as possible.

They will come back if we can allow them to, Staples said.

With the help of zoos, we can always breed koalas to go back - but if theres nowhere for them to go back to, its pretty dire.

Koala corridors are also important so one group of koalas will not get cut off from others.

Koalas need to be able to breed with different groups within their species - and without corridors, they also cant get to new food sources or escape fires.

If you have a pocket of good habitat, that is great for that area, but you need genetic drift, Staples said.

If you have any sort of island population, theres nothing coming in or going out, so youre essentially bottlenecking - and its a very short-term solution.

The corridor allows for males to move between changing genetics and strengthening the whole genome of the population.

In some more uplifting news, Archer, a koala at Featherdale Wildlife Park, has become a dad for the first time.

And the names of Archers two baby joeys have been chosen with a little help from royalty.

The female joey is being named after Princess Eugenie, and the male is being named Jack, after her husband, Staples said.

Theyve been massive supporters and theyre dying to come back out when everyone can travel again.

Go here to read the rest:
Australia's 2020 bushfires wiped out 71 per cent of NSW's koala population - and restoring the numbers will take 'decades' - 7NEWS.com.au

BOTHELL, Wash. & KENILWORTH, N.J.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq: SGEN) and Merck (NYSE: MRK), known as MSD outside the United States and Canada, today announced two new strategic oncology collaborations.

The companies will globally develop and commercialize Seattle Genetics ladiratuzumab vedotin, an investigational antibody-drug conjugate (ADC) targeting LIV-1, which is currently in phase 2 clinical trials for breast cancer and other solid tumors. The collaboration will pursue a broad joint development program evaluating ladiratuzumab vedotin as monotherapy and in combination with Mercks anti-PD-1 therapy KEYTRUDA (pembrolizumab) in triple-negative breast cancer, hormone receptor-positive breast cancer and other LIV-1-expressing solid tumors. Under the terms of the agreement, Seattle Genetics will receive a $600 million upfront payment and Merck will make a $1.0 billion equity investment in 5.0 million shares of Seattle Genetics common stock at a price of $200 per share. In addition, Seattle Genetics is eligible for progress-dependent milestone payments of up to $2.6 billion.

Separately, Seattle Genetics has granted Merck an exclusive license to commercialize TUKYSA (tucatinib), a small molecule tyrosine kinase inhibitor, for the treatment of HER2-positive cancers, in Asia, the Middle East and Latin America and other regions outside of the U.S., Canada and Europe. Seattle Genetics will receive $125 million from Merck as an upfront payment and is eligible for progress-dependent milestones of up to $65 million.

Collaborating with Merck on ladiratuzumab vedotin will allow us to accelerate and broaden its development program in breast cancer and other solid tumors, including in combination with Mercks KEYTRUDA, while also positioning us to leverage our U.S. and European commercial operations, said Clay Siegall, Ph.D., President and Chief Executive Officer of Seattle Genetics. The strategic collaboration for TUKYSA will help us reach more patients globally and benefit from the established commercial strength of one of the worlds premier pharmaceutical companies.

These two strategic collaborations will enable us to further diversify Mercks broad oncology portfolio and pipeline, and to continue our efforts to extend and improve the lives of as many patients with cancer as possible, said Dr. Roger M. Perlmutter, President, Merck Research Laboratories. We look forward to working with the team at Seattle Genetics to advance the clinical program for ladiratuzumab vedotin, which has shown compelling signals of efficacy in early studies, and to bring TUKYSA to even more patients with cancer around the world.

Ladiratuzumab Vedotin Collaboration Details

Under the terms of the agreement, Seattle Genetics and Merck will collaborate and equally share costs on the global development of ladiratuzumab vedotin and other LIV-1-targeting ADCs. The companies have agreed to jointly develop and share future costs and profits for ladiratuzumab vedotin on a 50:50 basis worldwide. Merck will pay Seattle Genetics $600 million upfront and make a $1.0 billion equity investment in 5.0 million shares of Seattle Genetics common stock at a price of $200 per share. In addition, Seattle Genetics will be eligible to receive up to $2.6 billion in milestone payments, including $850 million in development milestones and $1.75 billion in sales milestones.

The companies will jointly develop and commercialize ladiratuzumab vedotin and equally share profits worldwide. The companies will co-commercialize in the U.S. and Europe. Seattle Genetics will be responsible for marketing applications for approval in the U.S. and Canada, and will record sales in the U.S., Canada and Europe. Merck will be responsible for marketing applications for approval in Europe and in countries outside the U.S. and Canada, and will record sales in countries outside the U.S., Europe and Canada. Including the upfront payment, equity investment proceeds and potential milestone payments, Seattle Genetics is eligible to receive up to $4.2 billion.

The closing of the equity investment is contingent on completion of review under the Hart-Scott-Rodino Antitrust Improvements Act of 1976 (HSR Act).

TUKYSA Collaboration Details

Under the terms of the agreement, Merck has been granted exclusive rights to commercialize TUKYSA in Asia, the Middle East and Latin America and other regions outside of the U.S., Canada and Europe. Seattle Genetics retains commercial rights and will record sales in the U.S., Canada and Europe. Merck will be responsible for marketing applications for approval in its territory, supported by the positive results from the HER2CLIMB clinical trial.

Merck will also co-fund a portion of the TUKYSA global development plan, which encompasses several ongoing and planned trials across HER2-positive cancers, including breast, colorectal, gastric and other cancers set forth in a global product development plan. Seattle Genetics will continue to lead ongoing TUKYSA global development planning and operational execution. Merck will solely fund and conduct country-specific clinical trials necessary to support anticipated regulatory applications in its territory.

Seattle Genetics will receive from Merck $125 million as an upfront payment and is eligible to receive progress-dependent milestones of up to $65 million. Seattle Genetics will also receive $85 million in prepaid research and development payments to be applied to Mercks global development funding obligations. In addition, Seattle Genetics would receive tiered royalties on sales of TUKYSA in Mercks territory.

The financial impact of these collaborations is not included in Seattle Genetics 2020 guidance.

Seattle Genetics Conference Call Details

Seattle Genetics management will host a conference call to discuss these collaborations today at 6:00 a.m. Pacific Time (PT); 9:00 a.m. Eastern Time (ET). The event will be simultaneously webcast and available for replay from the Seattle Genetics website at http://www.seattlegenetics.com, under the Investors section. Investors may also participate in the conference call by calling 844-763-8274 (domestic) or +1 412-717-9224 (international). The conference ID is 10147850.

About Ladiratuzumab Vedotin

Ladiratuzumab vedotin is a novel investigational ADC targeted to LIV-1. Most metastatic breast cancers express LIV-1, which also has been detected in several other cancers, including lung, head and neck, esophageal and gastric. Ladiratuzumab vedotin utilizes Seattle Genetics proprietary ADC technology and consists of a LIV-1-targeted monoclonal antibody linked to a potent microtubule-disrupting agent, monomethyl auristatin E (MMAE) by a protease-cleavable linker. This novel ADC is designed to bind to LIV-1 on cancer cells and release the cell-killing agent into target cells upon internalization. Ladiratuzumab vedotin may also cause antitumor activity through other mechanisms, including activation of an immune response by induction of immunogenic cell death.

About TUKYSA (tucatinib)

TUKYSA is an oral, small molecule tyrosine kinase inhibitor (TKI) of HER2, a protein that contributes to cancer cell growth. TUKYSA in combination with trastuzumab and capecitabine was approved by the U.S. Food and Drug Administration (FDA) in April 2020 for adult patients with advanced unresectable or metastatic HER2-positive breast cancer, including patients with brain metastases, who have received one or more prior anti-HER2-based regimens in the metastatic setting. In addition, TUKYSA received approval in Canada, Singapore, Australia and Switzerland under the Project Orbis initiative of the FDA Oncology Center of Excellence that provides a framework for concurrent submission and review of oncology products among international partners. A marketing application is under review in the European Union.

TUKYSA is being evaluated in several ongoing clinical trials and additional studies are planned. Current trials include the following:

For additional information, visit http://www.clinicaltrials.gov.

TUKYSA Important Safety Information

Warnings and Precautions

If diarrhea occurs, administer antidiarrheal treatment as clinically indicated. Perform diagnostic tests as clinically indicated to exclude other causes of diarrhea. Based on the severity of the diarrhea, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Monitor ALT, AST, and bilirubin prior to starting TUKYSA, every 3 weeks during treatment, and as clinically indicated. Based on the severity of hepatoxicity, interrupt dose, then dose reduce or permanently discontinue TUKYSA.

Adverse Reactions

Serious adverse reactions occurred in 26% of patients who received TUKYSA. Serious adverse reactions in 2% of patients who received TUKYSA were diarrhea (4%), vomiting (2.5%), nausea (2%), abdominal pain (2%), and seizure (2%). Fatal adverse reactions occurred in 2% of patients who received TUKYSA including sudden death, sepsis, dehydration, and cardiogenic shock.

Adverse reactions led to treatment discontinuation in 6% of patients who received TUKYSA; those occurring in 1% of patients were hepatotoxicity (1.5%) and diarrhea (1%). Adverse reactions led to dose reduction in 21% of patients who received TUKYSA; those occurring in 2% of patients were hepatotoxicity (8%) and diarrhea (6%).

The most common adverse reactions in patients who received TUKYSA (20%) were diarrhea, palmar-plantar erythrodysesthesia, nausea, fatigue, hepatotoxicity, vomiting, stomatitis, decreased appetite, abdominal pain, headache, anemia, and rash.

Lab Abnormalities

In HER2CLIMB, Grade 3 laboratory abnormalities reported in 5% of patients who received TUKYSA were: decreased phosphate, increased ALT, decreased potassium, and increased AST. The mean increase in serum creatinine was 32% within the first 21 days of treatment with TUKYSA. The serum creatinine increases persisted throughout treatment and were reversible upon treatment completion. Consider alternative markers of renal function if persistent elevations in serum creatinine are observed.

Drug Interactions

Use in Specific Populations

For more information, please see the full Prescribing Information for TUKYSA here.

About KEYTRUDA (pembrolizumab) Injection, 100 mg

KEYTRUDA is an anti-PD-1 therapy that works by increasing the ability of the bodys immune system to help detect and fight tumor cells. KEYTRUDA is a humanized monoclonal antibody that blocks the interaction between PD-1 and its ligands, PD-L1 and PD-L2, thereby activating T lymphocytes which may affect both tumor cells and healthy cells.

Merck has the industrys largest immuno-oncology clinical research program. There are currently more than 1,200 trials studying KEYTRUDA across a wide variety of cancers and treatment settings. The KEYTRUDA clinical program seeks to understand the role of KEYTRUDA across cancers and the factors that may predict a patient's likelihood of benefitting from treatment with KEYTRUDA, including exploring several different biomarkers.

Selected KEYTRUDA (pembrolizumab) Indications

Melanoma

KEYTRUDA is indicated for the treatment of patients with unresectable or metastatic melanoma.

KEYTRUDA is indicated for the adjuvant treatment of patients with melanoma with involvement of lymph node(s) following complete resection.

Non-Small Cell Lung Cancer

KEYTRUDA, in combination with pemetrexed and platinum chemotherapy, is indicated for the first-line treatment of patients with metastatic nonsquamous non-small cell lung cancer (NSCLC), with no EGFR or ALK genomic tumor aberrations.

KEYTRUDA, in combination with carboplatin and either paclitaxel or paclitaxel protein-bound, is indicated for the first-line treatment of patients with metastatic squamous NSCLC.

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with NSCLC expressing PD-L1 [tumor proportion score (TPS) 1%] as determined by an FDA-approved test, with no EGFR or ALK genomic tumor aberrations, and is stage III where patients are not candidates for surgical resection or definitive chemoradiation, or metastatic.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with metastatic NSCLC whose tumors express PD-L1 (TPS 1%) as determined by an FDA-approved test, with disease progression on or after platinum-containing chemotherapy. Patients with EGFR or ALK genomic tumor aberrations should have disease progression on FDA-approved therapy for these aberrations prior to receiving KEYTRUDA.

Small Cell Lung Cancer

KEYTRUDA is indicated for the treatment of patients with metastatic small cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy and at least 1 other prior line of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.

Head and Neck Squamous Cell Cancer

KEYTRUDA, in combination with platinum and fluorouracil (FU), is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent head and neck squamous cell carcinoma (HNSCC).

KEYTRUDA, as a single agent, is indicated for the first-line treatment of patients with metastatic or with unresectable, recurrent HNSCC whose tumors express PD-L1 [combined positive score (CPS) 1] as determined by an FDA-approved test.

KEYTRUDA, as a single agent, is indicated for the treatment of patients with recurrent or metastatic head and neck squamous cell carcinoma (HNSCC) with disease progression on or after platinum-containing chemotherapy.

Classical Hodgkin Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory classical Hodgkin lymphoma (cHL), or who have relapsed after 3 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Primary Mediastinal Large B-Cell Lymphoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with refractory primary mediastinal large B-cell lymphoma (PMBCL), or who have relapsed after 2 or more prior lines of therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. KEYTRUDA is not recommended for treatment of patients with PMBCL who require urgent cytoreductive therapy.

Urothelial Carcinoma

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who are not eligible for cisplatin-containing chemotherapy and whose tumors express PD-L1 [combined positive score (CPS) 10], as determined by an FDA-approved test, or in patients who are not eligible for any platinum-containing chemotherapy regardless of PD-L1 status. 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 confirmatory trials.

KEYTRUDA is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma (mUC) who have disease progression during or following platinum-containing chemotherapy or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy.

KEYTRUDA is indicated for the treatment of patients with Bacillus Calmette-Guerin (BCG)-unresponsive, high-risk, non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors who are ineligible for or have elected not to undergo cystectomy.

Microsatellite Instability-High or Mismatch Repair Deficient Cancer

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic microsatellite instability-high (MSI-H) or mismatch repair deficient (dMMR)

This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with MSI-H central nervous system cancers have not been established.

Microsatellite Instability-High or Mismatch Repair Deficient Colorectal Cancer

KEYTRUDA is indicated for the first-line treatment of patients with unresectable or metastatic MSI-H or dMMR colorectal cancer (CRC).

Gastric Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic gastric or gastroesophageal junction (GEJ) adenocarcinoma whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test, with disease progression on or after two or more prior lines of therapy including fluoropyrimidine- and platinum-containing chemotherapy and if appropriate, HER2/neu-targeted therapy. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Esophageal Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent locally advanced or metastatic squamous cell carcinoma of the esophagus whose tumors express PD-L1 (CPS 10) as determined by an FDA-approved test, with disease progression after one or more prior lines of systemic therapy.

Cervical Cancer

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cervical cancer with disease progression on or after chemotherapy whose tumors express PD-L1 (CPS 1) as determined by an FDA-approved test. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Hepatocellular Carcinoma

KEYTRUDA is indicated for the treatment of patients with hepatocellular carcinoma (HCC) who have been previously treated with sorafenib. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Merkel Cell Carcinoma

KEYTRUDA is indicated for the treatment of adult and pediatric patients with recurrent locally advanced or metastatic Merkel cell carcinoma (MCC). This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials.

Renal Cell Carcinoma

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

Tumor Mutational Burden-High

KEYTRUDA is indicated for the treatment of adult and pediatric patients with unresectable or metastatic tumor mutational burden-high (TMB-H) [10 mutations/megabase (mut/Mb)] solid tumors, as determined by an FDA-approved test, that have progressed following prior treatment and who have no satisfactory alternative treatment options. This indication is approved under accelerated approval based on tumor response rate and durability of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in the confirmatory trials. The safety and effectiveness of KEYTRUDA in pediatric patients with TMB-H central nervous system cancers have not been established.

Cutaneous Squamous Cell Carcinoma

KEYTRUDA is indicated for the treatment of patients with recurrent or metastatic cutaneous squamous cell carcinoma (cSCC) that is not curable by surgery or radiation.

Selected Important Safety Information for KEYTRUDA

Immune-Mediated Pneumonitis

KEYTRUDA can cause immune-mediated pneumonitis, including fatal cases. Pneumonitis occurred in 3.4% (94/2799) of patients with various cancers receiving KEYTRUDA, including Grade 1 (0.8%), 2 (1.3%), 3 (0.9%), 4 (0.3%), and 5 (0.1%). Pneumonitis occurred in 8.2% (65/790) of NSCLC patients receiving KEYTRUDA as a single agent, including Grades 3-4 in 3.2% of patients, and occurred more frequently in patients with a history of prior thoracic radiation (17%) compared to those without (7.7%). Pneumonitis occurred in 6% (18/300) of HNSCC patients receiving KEYTRUDA as a single agent, including Grades 3-5 in 1.6% of patients, and occurred in 5.4% (15/276) of patients receiving KEYTRUDA in combination with platinum and FU as first-line therapy for advanced disease, including Grades 3-5 in 1.5% of patients.

Monitor patients for signs and symptoms of pneumonitis. Evaluate suspected pneumonitis with radiographic imaging. Administer corticosteroids for Grade 2 or greater pneumonitis. Withhold KEYTRUDA for Grade 2; permanently discontinue KEYTRUDA for Grade 3 or 4 or recurrent Grade 2 pneumonitis.

Immune-Mediated Colitis

KEYTRUDA can cause immune-mediated colitis. Colitis occurred in 1.7% (48/2799) of patients receiving KEYTRUDA, including Grade 2 (0.4%), 3 (1.1%), and 4 (<0.1%). Monitor patients for signs and symptoms of colitis. Administer corticosteroids for Grade 2 or greater colitis. Withhold KEYTRUDA for Grade 2 or 3; permanently discontinue KEYTRUDA for Grade 4 colitis.

Immune-Mediated Hepatitis (KEYTRUDA) and Hepatotoxicity (KEYTRUDA in Combination With Axitinib)

Immune-Mediated Hepatitis

KEYTRUDA can cause immune-mediated hepatitis. Hepatitis occurred in 0.7% (19/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.4%), and 4 (<0.1%). Monitor patients for changes in liver function. Administer corticosteroids for Grade 2 or greater hepatitis and, based on severity of liver enzyme elevations, withhold or discontinue KEYTRUDA.

Hepatotoxicity in Combination With Axitinib

KEYTRUDA in combination with axitinib can cause hepatic toxicity with higher than expected frequencies of Grades 3 and 4 ALT and AST elevations compared to KEYTRUDA alone. With the combination of KEYTRUDA and axitinib, Grades 3 and 4 increased ALT (20%) and increased AST (13%) were seen. Monitor liver enzymes before initiation of and periodically throughout treatment. Consider more frequent monitoring of liver enzymes as compared to when the drugs are administered as single agents. For elevated liver enzymes, interrupt KEYTRUDA and axitinib, and consider administering corticosteroids as needed.

Immune-Mediated Endocrinopathies

KEYTRUDA can cause adrenal insufficiency (primary and secondary), hypophysitis, thyroid disorders, and type 1 diabetes mellitus. Adrenal insufficiency occurred in 0.8% (22/2799) of patients, including Grade 2 (0.3%), 3 (0.3%), and 4 (<0.1%). Hypophysitis occurred in 0.6% (17/2799) of patients, including Grade 2 (0.2%), 3 (0.3%), and 4 (<0.1%). Hypothyroidism occurred in 8.5% (237/2799) of patients, including Grade 2 (6.2%) and 3 (0.1%). The incidence of new or worsening hypothyroidism was higher in 1185 patients with HNSCC (16%) receiving KEYTRUDA, as a single agent or in combination with platinum and FU, including Grade 3 (0.3%) hypothyroidism. Hyperthyroidism occurred in 3.4% (96/2799) of patients, including Grade 2 (0.8%) and 3 (0.1%), and thyroiditis occurred in 0.6% (16/2799) of patients, including Grade 2 (0.3%). Type 1 diabetes mellitus, including diabetic ketoacidosis, occurred in 0.2% (6/2799) of patients.

Monitor patients for signs and symptoms of adrenal insufficiency, hypophysitis (including hypopituitarism), thyroid function (prior to and periodically during treatment), and hyperglycemia. For adrenal insufficiency or hypophysitis, administer corticosteroids and hormone replacement as clinically indicated. Withhold KEYTRUDA for Grade 2 adrenal insufficiency or hypophysitis and withhold or discontinue KEYTRUDA for Grade 3 or Grade 4 adrenal insufficiency or hypophysitis. Administer hormone replacement for hypothyroidism and manage hyperthyroidism with thionamides and beta-blockers as appropriate. Withhold or discontinue KEYTRUDA for Grade 3 or 4 hyperthyroidism. Administer insulin for type 1 diabetes, and withhold KEYTRUDA and administer antihyperglycemics in patients with severe hyperglycemia.

Immune-Mediated Nephritis and Renal Dysfunction

KEYTRUDA can cause immune-mediated nephritis. Nephritis occurred in 0.3% (9/2799) of patients receiving KEYTRUDA, including Grade 2 (0.1%), 3 (0.1%), and 4 (<0.1%) nephritis. Nephritis occurred in 1.7% (7/405) of patients receiving KEYTRUDA in combination with pemetrexed and platinum chemotherapy. Monitor patients for changes in renal function. Administer corticosteroids for Grade 2 or greater nephritis. Withhold KEYTRUDA for Grade 2; permanently discontinue for Grade 3 or 4 nephritis.

Immune-Mediated Skin Reactions

Immune-mediated rashes, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN) (some cases with fatal outcome), exfoliative dermatitis, and bullous pemphigoid, can occur. Monitor patients for suspected severe skin reactions and based on the severity of the adverse reaction, withhold or permanently discontinue KEYTRUDA and administer corticosteroids. For signs or symptoms of SJS or TEN, withhold KEYTRUDA and refer the patient for specialized care for assessment and treatment. If SJS or TEN is confirmed, permanently discontinue KEYTRUDA.

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Seattle Genetics and Merck Announce Two Strategic Oncology Collaborations - Business Wire

By Zelda Venter 16h ago

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Fans of the Rietvlei Nature Reserve are looking forward to the day they can be on the lookout for its two new cheetahs.

Njozi, a sub-adult female cheetah which arrived last month, now has a mate, a male sub-adult released in the popular Pretoria city reserve last week.

For now they cannot be seen by the visiting public as they are being kept in a cordoned-off boma to give them a chance to settle.

They will stay together in the reserve until it is time for the male to be relocated the hope is they will produce a litter, as was the case with previous cheetahs in the reserve.

The two took to each other like ducks to water, said Vincent van der Merwe of the Endangered Wildlife Trust (EWT), and they are settling and should be released into the wider reserve by the end of September.

Van der Merwe said it had been an anxious time when the male from Welgevonden was released as they did not know how Njozi would react. She had come from a family in the Western Cape and been skittish at first, but became more confident with time.

He said they were ready to separate the two if they got in a fight, but it was not necessary. Instead, Njozi called out to the male and when he approached, they licked one another.

They are very relaxed with each other and bonded nicely. Lets see how they adapt to their new surroundings when we release them, he said.

He described the new male as a beautiful animal with a mix of Karoo and Namibian genetics.

Knowledge of cheetahs has grown fast and the EWT has had success with its metapopulation project for the long-term viability of cheetahs in smaller fenced reserves, and with the long-term genetic and demographic integrity of the metapopulation across Africa.

Funds to support the project have come from CRC Industries, Q20 SA, Lions Club of Pretoria City and Strata Logistics.

In 2017, Kiara and Sabona produced a litter of three cubs, the first time cheetah cubs had been born in the reserve, and they were a hit with visitors until their relocation.

Link:
Public will soon be able to spot cheetahs in Rietvlei - IOL

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PfizerRocheGlaxoSmithKlineSanofiNovartisBayerBristol-Myers SquibbEli LillyAstraZenecaTeva PharmaceuticalSun PharmaceuticalBioNumerik PharmaceuticalsSeattle GeneticsAccord Healthcare

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HospitalsClinicsOthers

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Additionally, the report serves as a convenient guide to design and implement potential growth steering activities across select regional pockets in the Male Breast Cancer Treatment market. Frontline players and their effective growth strategies are also enlisted in the report to emulate growth.

North America (U.S., Canada, Mexico)

Europe (U.K., France, Germany, Spain, Italy, Central & Eastern Europe, CIS)

Asia Pacific (China, Japan, South Korea, ASEAN, India, Rest of Asia Pacific)

Latin America (Brazil, Rest of L.A.)

Middle East and Africa (Turkey, GCC, Rest of Middle East)

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Key Points from Table of Content:

1 Market Overview1.1 Product Definition and Market Characteristics1.2 Global Male Breast Cancer Treatment Market Size1.3 Market Segmentation1.4 Global Macroeconomic Analysis1.5 SWOT Analysis

2. Market Dynamics2.1 Market Drivers2.2 Market Constraints and Challenges2.3 Emerging Market Trends2.4 Impact of COVID-192.4.1 Short-term Impact2.4.2 Long-term Impact

3 Associated Industry Assessment3.1 Supply Chain Analysis3.2 Industry Active Participants3.2.1 Suppliers of Raw Materials3.2.2 Key Distributors/Retailers3.3 Alternative Analysis3.4 The Impact of Covid-19 From the Perspective of Industry Chain

4 Market Competitive Landscape4.1 Industry Leading Players4.2 Industry News4.2.1 Key Product Launch News4.2.2 MandA and Expansion Plans

5 Analysis of Leading Companies5.1 Company 15.1.1 Company 1 Company Profile5.1.2 Company 1 Business Overview5.1.3 Company 1 Male Breast Cancer Treatment Sales, Revenue, Average Selling Price and Gross Margin (2015-2020)5.1.4 Company 1 Male Breast Cancer Treatment Products Introduction

5.2 Company 25.2.1 Company 2 Company Profile5.2.2 Company 2 Business Overview5.2.3 Company 2 Male Breast Cancer Treatment Sales, Revenue, Average Selling Price and Gross Margin (2015-2020)5.2.4 Company 2 Male Breast Cancer Treatment Products Introduction

5.3 Company 35.3.1 Company 3 Company Profile5.3.2 Company 3 Business Overview5.3.3 Company 3 Male Breast Cancer Treatment Sales, Revenue, Average Selling Price and Gross Margin (2015-2020)5.3.4 Company 3 Male Breast Cancer Treatment Products Introduction

5.4 Company 45.4.1 Company 4 Company Profile5.4.2 Company 4 Business Overview5.4.3 Company 4 Male Breast Cancer Treatment Sales, Revenue, Average Selling Price and Gross Margin (2015-2020)5.4.4 Company 4 Male Breast Cancer Treatment Products Introduction

6 Market Analysis and Forecast, By Product Types6.1 Global Male Breast Cancer Treatment Sales, Revenue and Market Share by Types (2015-2020)6.2 Global Male Breast Cancer Treatment Market Forecast by Types (2020-2026)6.3 Global Male Breast Cancer Treatment Sales, Price and Growth Rate by Types (2015-2020)6.4 Global Male Breast Cancer Treatment Market Revenue and Sales Forecast, by Types (2020-2026)

7 Market Analysis and Forecast, By Applications7.1 Global Male Breast Cancer Treatment Sales, Revenue and Market Share by Applications (2015-2020)7.2 Global Male Breast Cancer Treatment Market Forecast by Applications (2020-2026)7.3 Global Revenue, Sales and Growth Rate by Applications (2015-2020)7.4 Global Male Breast Cancer Treatment Market Revenue and Sales Forecast, by Applications (2020-2026)

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8 Market Analysis and Forecast, By Regions8.1 Global Male Breast Cancer Treatment Sales by Regions (2015-2020)8.2 Global Male Breast Cancer Treatment Market Revenue by Regions (2015-2020)8.3 Global Male Breast Cancer Treatment Market Forecast by Regions (2020-2026)Continued.

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Male Breast Cancer Treatment Market Size will Observe Substantial Growth by 2026 | Pfizer, Roche, GlaxoSmithKline, Sanofi, Novartis - The Daily...

Sept. 18, 2020 10:45 UTC

BOTHELL, Wash. & TOKYO--(BUSINESS WIRE)-- Seattle Genetics, Inc. (Nasdaq:SGEN) and Astellas Pharma Inc. (TSE: 4503, President and CEO: Kenji Yasukawa, Ph.D., Astellas) today announced that a phase 3 trial of PADCEV (enfortumab vedotin-ejfv) met its primary endpoint of overall survival compared to chemotherapy. The results were reviewed by an independent Data Monitoring Committee following a planned interim analysis. The global EV-301 clinical trial compared PADCEV to chemotherapy in adult patients with locally advanced or metastatic urothelial cancer who were previously treated with platinum-based chemotherapy and a PD-1/L1 inhibitor.

This press release features multimedia. View the full release here: https://www.businesswire.com/news/home/20200918005101/en/

PADCEV (enfortumab vedotin-ejfv) (Photo: Business Wire)

In the trial, PADCEV significantly improved overall survival (OS), with a 30 percent reduction in risk of death (Hazard Ratio [HR]=0.70; [95% Confidence Interval (CI): 0.56, 0.89]; p=0.001). PADCEV also significantly improved progression-free survival (PFS), a secondary endpoint, with a 39 percent reduction in risk of disease progression or death (HR=0.61 [95% CI: 0.50, 0.75]; p<0.00001).

For patients in the PADCEV arm of the trial, adverse events were consistent with those listed in the U.S. Prescribing Information, with rash, hyperglycemia, decreased neutrophil count, fatigue, anemia and decreased appetite as the most frequent Grade 3 or greater adverse event(s) occurring in more than 5 percent of patients. Data from EV-301 will be submitted for presentation at an upcoming scientific congress. Patients in the chemotherapy arm of the trial will be offered the opportunity to receive PADCEV.

The results will be submitted to the U.S. Food and Drug Administration (FDA) as the confirmatory trial following the drugs accelerated approval in 2019. EV-301 is also intended to support global registrations.

These survival results from the confirmatory trial for PADCEV are welcome news for patients whose cancer has progressed after platinum-based chemotherapy and immunotherapy, said Roger Dansey, M.D., Chief Medical Officer at Seattle Genetics. We continue to explore PADCEVs activity across the spectrum of urothelial cancer including its potential for use in earlier lines of therapy.

EV-301 is the first randomized trial to show overall survival results compared to chemotherapy in patients with locally advanced or metastatic urothelial cancer who previously have received platinum-based treatment and a PD-1 or PD-L1 inhibitor, and we are encouraged by the potential this may have in helping patients who have otherwise limited alternatives, said Andrew Krivoshik, M.D., Ph.D., Senior Vice President and Oncology Therapeutic Area Head, Astellas. We look forward to discussing these results with global health authorities.

Globally, approximately 580,000 people will be diagnosed with bladder cancer in 2020.1 Urothelial cancer accounts for 90 percent of all bladder cancers and can also be found in the renal pelvis (where urine collects inside the kidney), ureter (tube that connects the kidneys to the bladder) and urethra.2 Approximately 80 percent of people do not respond to PD-1 or PD-L1 inhibitors after a platinum-containing therapy has failed as an initial treatment for advanced disease.3

About the EV-301 Trial

The EV-301 trial (NCT03474107) is a global, multicenter, open-label, randomized phase 3 trial designed to evaluate PADCEV versus physician's choice of chemotherapy (docetaxel, paclitaxel or vinflunine) in approximately 600 patients with locally advanced or metastatic urothelial cancer who were previously treated with a PD-1 or PD-L1 inhibitor and platinum-based therapies. The primary endpoint is overall survival of participants treated with PADCEV compared to those treated with chemotherapy. Secondary endpoints include progression-free survival, duration of response, and overall response rate, as well as assessment of safety/tolerability and quality-of-life parameters.

For more information about the EV-301 clinical trial, please visit http://www.clinicaltrials.gov.

About PADCEV (enfortumab vedotin-ejfv)

PADCEV was approved by the U.S. Food and Drug Administration (FDA) in December 2019 and is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor and a platinum-containing chemotherapy before (neoadjuvant) or after (adjuvant) surgery or in a locally advanced or metastatic setting. PADCEV was approved under the FDAs Accelerated Approval Program based on tumor response rate. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.4

PADCEV is a first-in-class antibody-drug conjugate (ADC) that is directed against Nectin-4, a protein located on the surface of cells and highly expressed in bladder cancer.4,5 Nonclinical data suggest the anticancer activity of PADCEV is due to its binding to Nectin-4 expressing cells followed by the internalization and release of the anti-tumor agent monomethyl auristatin E (MMAE) into the cell, which result in the cell not reproducing (cell cycle arrest) and in programmed cell death (apoptosis).4 PADCEV is co-developed by Astellas and Seattle Genetics.

PADCEV Important Safety Information

Warnings and Precautions

Adverse Reactions

Serious adverse reactions occurred in 46% of patients treated with PADCEV. The most common serious adverse reactions (3%) were urinary tract infection (6%), cellulitis (5%), febrile neutropenia (4%), diarrhea (4%), sepsis (3%), acute kidney injury (3%), dyspnea (3%), and rash (3%). Fatal adverse reactions occurred in 3.2% of patients, including acute respiratory failure, aspiration pneumonia, cardiac disorder, and sepsis (each 0.8%).

Adverse reactions leading to discontinuation occurred in 16% of patients; the most common adverse reaction leading to discontinuation was peripheral neuropathy (6%). Adverse reactions leading to dose interruption occurred in 64% of patients; the most common adverse reactions leading to dose interruption were peripheral neuropathy (18%), rash (9%) and fatigue (6%). Adverse reactions leading to dose reduction occurred in 34% of patients; the most common adverse reactions leading to dose reduction were peripheral neuropathy (12%), rash (6%) and fatigue (4%).

The most common adverse reactions (20%) were fatigue (56%), peripheral neuropathy (56%), decreased appetite (52%), rash (52%), alopecia (50%), nausea (45%), dysgeusia (42%), diarrhea (42%), dry eye (40%), pruritus (26%) and dry skin (26%). The most common Grade 3 adverse reactions (5%) were rash (13%), diarrhea (6%) and fatigue (6%).

Lab Abnormalities

In one clinical trial, Grade 3-4 laboratory abnormalities reported in 5% were: lymphocytes decreased (10%), hemoglobin decreased (10%), phosphate decreased (10%), lipase increased (9%), sodium decreased (8%), glucose increased (8%), urate increased (7%), neutrophils decreased (5%).

Drug Interactions

Specific Populations

For more information, please see the full Prescribing Information for PADCEV here.

About Seattle Genetics

Seattle Genetics, Inc. is a global biotechnology company that discovers, develops and commercializes transformative medicines targeting cancer to make a meaningful difference in peoples lives. The company is headquartered in the Seattle, Washington area, with locations in California, Switzerland and the European Union. For more information on our robust pipeline, visit http://www.seattlegenetics.com and follow @SeattleGenetics on Twitter.

About Astellas

Astellas Pharma Inc. is a pharmaceutical company conducting business in more than 70 countries around the world. We are promoting the Focus Area Approach that is designed to identify opportunities for the continuous creation of new drugs to address diseases with high unmet medical needs by focusing on Biology and Modality. Furthermore, we are also looking beyond our foundational Rx focus to create Rx+ healthcare solutions that combine our expertise and knowledge with cutting-edge technology in different fields of external partners. Through these efforts, Astellas stands on the forefront of healthcare change to turn innovative science into value for patients. For more information, please visit our website at https://www.astellas.com/en.

About the Seattle Genetics and Astellas Collaboration

Seattle Genetics and Astellas are co-developing PADCEV (enfortumab vedotin-ejfv) under a 50:50 worldwide development and commercialization collaboration that was entered into in 2007 and expanded in 2009.

Seattle Genetics Forward Looking Statements

Certain statements made in this press release are forward looking, such as those, among others, relating to the submission of data from the EV-301 trial for presentation at an upcoming scientific congress; intended regulatory actions, including plans to submit the results of the EV-301 trial to the FDA as the confirmatory trial following the drugs accelerated approval in the U.S. and plans to discuss the results with global health authorities and seek global registrations; conduct of a comprehensive clinical development program for PADCEV, which includes exploring PADCEVs activity in other types of urothelial cancer and its potential for use in earlier lines of therapy; the therapeutic potential of PADCEV, including its efficacy, safety and therapeutic uses, and anticipated development activities, including ongoing and future clinical trials. Actual results or developments may differ materially from those projected or implied in these forward-looking statements. Factors that may cause such a difference include that the data from the EV-301 trial may not be selected for presentation at scientific congresses; the possibility of delays in the submission of results to the FDA; that the results from the EV-301 trial may not be enough to convert PADCEVs accelerated approval in the U.S. to regular approval or to support any other global registrations; that, even if PADCEV receives regular approval in the U.S. or any other global registrations, the product labeling may not be as broad or desirable as anticipated; the possibility that ongoing and subsequent clinical trials may fail to establish sufficient activity; the risk of adverse events or safety signals; and the possibility that adverse regulatory actions may occur. More information about the risks and uncertainties faced by Seattle Genetics is contained under the caption Risk Factors included in the companys Quarterly Report on Form 10-Q for the quarter ended June 30, 2020 filed with the Securities and Exchange Commission. Seattle Genetics disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law.

Astellas Cautionary Notes

In this press release, statements made with respect to current plans, estimates, strategies and beliefs and other statements that are not historical facts are forward-looking statements about the future performance of Astellas. These statements are based on managements current assumptions and beliefs in light of the information currently available to it and involve known and unknown risks and uncertainties. A number of factors could cause actual results to differ materially from those discussed in the forward-looking statements. Such factors include, but are not limited to: (i) changes in general economic conditions and in laws and regulations, relating to pharmaceutical markets, (ii) currency exchange rate fluctuations, (iii) delays in new product launches, (iv) the inability of Astellas to market existing and new products effectively, (v) the inability of Astellas to continue to effectively research and develop products accepted by customers in highly competitive markets, and (vi) infringements of Astellas intellectual property rights by third parties.

Information about pharmaceutical products (including products currently in development), which is included in this press release is not intended to constitute an advertisement or medical advice.

1 International Agency for Research on Cancer. Cancer Tomorrow: Bladder. http://gco.iarc.fr/tomorrow. Accessed 07-31-2020.2 American Society of Clinical Oncology. Bladder cancer: introduction (10-2017).3 Shah, Manasee V., et al Targeted Literature Review of the Burden of Illness in UC (PCN108), Nov 2018.4 PADCEV [package insert] Northbrook, IL: Astellas, Inc.5 Challita-Eid P, Satpayev D, Yang P, et al. Enfortumab Vedotin Antibody-Drug Conjugate Targeting Nectin-4 Is a Highly Potent Therapeutic Agent in Multiple Preclinical Cancer Models. Cancer Res 2016;76(10):3003-13.

View source version on businesswire.com: https://www.businesswire.com/news/home/20200918005101/en/

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Seattle Genetics and Astellas Announce PADCEV (enfortumab vedotin-ejfv) Significantly Improved Overall Survival in Phase 3 Trial in Previously Treated...

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Rita Colwell is a pioneering microbiologist whose work on cholera helped illuminate the interplay between the environment and public health. She was also the first woman to serve as director of the National Science Foundation, and is currently a Distinguished University Professor at both the University of Maryland and Johns Hopkins Universitys Bloomberg School of Public Health.

In her half-century-plus in the sciences, Colwell has also seen very clearly the array of obstacles confronted by women as they try to navigate a traditionally male world. (When she applied for a graduate fellowship in bacteriology, she says was told, We dont waste fellowships on women.)

A Lab of Ones Own: One Womans Personal Journey Through Sexism in Science, by Rita Colwell and Sharon Bertsch McGrayne (Simon & Schuster, 288 pages).

Colwells new book, A Lab of Ones Own, co-authored with writer Sharon Bertsch McGrayne, documents much of what she has seen and heard over the years, from sexual harassment to the invisible structural obstacles placed in the way of women working in the sciences. (The books subtitle is One Womans Personal Journey Through Sexism in Science.)

Not long ago, women were discouraged from studying science at all; those who did pursue such studies were seen as oddities. Later, when the numbers of women earning science degrees began to rise, they found themselves receiving less funding than their male colleagues, and less likely to land a position as a professor or a lab director. (It wasnt that long ago, Colwell recalls, when a grant application could be turned down because a man on the granting committee simply didnt like women scientists.) But Colwell also found allies along the way, and her book is something of a celebration of what can be achieved when science strives for inclusivity.

The following interview has been edited for length and clarity.

UNDARK: Though sexism has a long history, you write that the 1950s and 60s saw unprecedented levels of sexism in the sciences. What was going on at that time?

Rita Colwell: The attitude was, a woman worked in the home period. A woman couldnt even get a credit card in her own name; she had to have her husband, or her father, vouch for her. In general, the understanding was, if you were [a woman] interested in science, that was peculiar. It wasnt unusual for women to go to college but most did not go from there into any kind of work, unless it was nursing or teaching. It was a very limiting time, for women. A lot of this was unspoken; it was just sort of assumed.

UD: Regarding graduate education, you say that women were simply seen as not worth investing in. What does that mean?

RC: The expectation was that you would get married and have children. If you werent there, with your children, you were seen as a bad mother. You went to college to find a husband; that was the expectation.

UD: You point out that not only could one face obstacles for being a woman Ph.D. student, you could face a backlash if you supervised too many women Ph.D. students. What was that about?

RC: The assumption was that anyone who was really brilliant, with great ideas, would work for a male professor. So if you took women students, it was assumed they werent the best and the brightest. Having women students would mark you as not serious; your students were just going to get married, and youre just wasting all this time.

UD: As you say, a lot of this was unspoken but eventually there was solid data to quantify this discrimination. How did that come about?

RC: It was in the 90s that Nancy Hopkins at MIT carried out her now-famous experiment: She measured the labs, and discovered that the men had almost twice as much space; they also got the bulk of the research money. More women were entering these careers [in the sciences], but men got most of the funding and most of the space.

Later, Jo Handelsman did the experiment where they sent identical letters to male researchers [from recent graduates applying to be a lab manager], the only difference was that some were signed John and others were signed Jennifer. The question was, would you hire this person, and what would you pay them? Far fewer said they would hire the woman; and the salary they were prepared to offer was much, much lower.

But Id like to emphasize one thing: Once I was able to break through, at each stage of my career, there was tremendous support. My father was very education-minded; it didnt matter if you were a girl or a boy; everyone went to school. My husband, a physicist, was a fantastic supporter; we were married for 62 very happy years. And my Ph.D. supervisor, John Liston, was absolutely the best. He was a newcomer to the University of Washington, starting a new program in marine microbiology so I ended up being the first graduate student with a Ph.D. in marine microbiology, possibly in the whole United States.

The assumption was that anyone who was really brilliant, with great ideas, would work for a male professor. So if you took women students, it was assumed they werent the best and the brightest.

UD: Youre known for your groundbreaking work on cholera, but it was also fascinating to read about your work investigating the 2001 anthrax attacks, in which a number of politicians and journalists were mailed packages containing the deadly substance in the weeks following the 9/11 attacks. How did you end up on the front lines of that investigation?

RC: I was appointed [as director of the National Science Foundation] by Bill Clinton, and I served two years under Clinton and four under George W. Bush. In October or November [of 2001], we heard about anthrax attacks. I remember saying, Weve got to sequence that bacterium, or well never know who did it.

I had been working on an advisory board for the CIA, so I was able to call on some colleagues, and we formed an inter-agency group. We decided not to make the group official, so that we could keep it a secret. And we worked for five years on this classified project. And using molecular genetics, we tracked down the source. Now, well never know whether the perpetrator was in fact Bruce Ivins, and if he worked alone, or with others. [Ivins died in 2008.] He was an anthrax microbiologist, and the source turned out to be in his lab.

UD: You were using a computer in the late 1950s, long before they became ubiquitous in the life sciences. Did you have a sense that computers would eventually impact every branch of science?

RC: At the University of Washington, I wrote a computer program the first in the country, for bacteriology using the old IBM 650, which has less power than the chip in your microwave oven. When I was working with that computer, I had to program it, and I didnt know diddly. But in my husbands lab, there was a postdoc named George Constabaris, who taught me. And there was another chap who was using the IBM to do pipe-fitting for the ships in Seattle harbor. He was programming how to cut and fit pipe most efficiently.

So it was clear to me that this was an amazing tool. I used the computer for taxonomic purposes, for identification which now everybody does. Its amusing I used to give talks about species of bacteria, and people would yawn. But now the hotshots in Silicon Valley know the differences between different kinds of bacteria. It was clear to me that we had to have massive computation [in the sciences]. I was able to get into the NSF budget, over my term, $2 billion, for computation, for universities to start building the internet railway, so to speak.

UD: So much has changed in science, and in the culture of science, over your career. Today, are you optimistic or at least, more optimistic?

RC: I would say its cautious optimism. I dont know whats going to happen in the next administration; it could be a disaster for women. I strongly encourage girls to go into science. I abhor the assumption that girls cant do math; its absurd. Or that if youre African American you cant do math or you cant do science its crazy. Theres still sexism, which ranges from the criminal to the clueless. Like when someone comments to a woman scientist as shes going up to the podium to give a talk, that she looks attractive. Thats the last thing you want to hear. You want to hear Thats a great idea, or Can we collaborate on the next stage of this experiment?

More:
The Undark Interview: A Conversation with Rita Colwell - Undark Magazine

When I was younger, the Hollywood blockbuster The Mummy enraptured and captured my attention like few other movies did. Its mesmerising mixture of Egyptian myth and cinematic mayhem sparked a lifelong fascination in me for mysterious, ancient civilisations.

However, one thing I noticed over the years was how Malaysia and Southeast Asia were largely absent from the discussion when it came to ancient civilisations. There were tales about the Sumerians, Babylonians, Egyptians, Indians, and Chinese but never Malaysians or rather those who inhabited Malaysia at the time.

For a long time, we were thought to be at the periphery of prehistory, so we were often relegated to a footnote, and sometimes not even that. Our history textbooks certainly didnt help they concentrated the bulk of their focus on the Malacca sultanate and the events that followed after (post-1400 AD), dedicating just a few cursory sections to powerful regional kingdoms that predated it such as Langkasuka, Majapahit, Srivijaya, and Kedah Tua. Their details on prehistory are even abysmally scantier.

When I dug deeper, I realised why. In addition to there being little archaeological, geological, and literary evidence to go by, the prevailing scientific consensus was that those who came to inhabit the Malay peninsula and Borneo were descendants of ancient argonauts from Taiwan who colonised Malaysia and other parts of Southeast Asia only as recently as 4,000 years ago.

Called the Out-of-Taiwan Theory, it was largely based on exiguous archaeological findings and linguistic population mapping. Since we were considered a relatively young offshoot culture who inherited agriculture and other neolithic technology from the seafaring ancient aboriginal Taiwanese (the Formosans), we were not of much interest to many prehistorians and archaeologists.

But a potentially paradigm-shifting theory posited by Oxford geneticist Stephen Oppenheimer threatens to upend this long-standing view. While his predecessors used archaeology, geology, and linguistics to investigate the subject, Oppenheimer and his colleagues have added a new, powerful tool to the mix genetics.

The key to the theory is the study of the often marginalised and sometimes even criminally disenfranchised Orang Asli.

Oppenheimer and his colleagues pored through the Orang Aslis female mtDNA (mitochondrial DNA) and the male Y chromosome the two components of the human genetic code that dont get shuffled like nuclear DNA does during reproduction, hence maintaining their purity and making them powerful portals into our past.

Thanks to this study and the discovery of many other geological, linguistic, and archaeological markers, a new theory that reverses and predates the Out-of-Taiwan Theory has emerged. Its called the Out-of-Sundaland Theory.

This groundbreaking theory puts Malaysia and Southeast Asia at the heart of prehistoric innovation and civilisation and makes the Orang Asli the probable progenitors of the ancient cultures that would go on to dominate the world.

According to the theory, there was a single migration of anatomically modern humans out of Africa around 80,000 years ago. These pioneering beachcombers traversed the Arabian and Indian coasts, eventually making it to the lands now known as Malaysia and Southeast Asia around 60,000 years ago.

Oppenheimer says: The ancestors of the three Orang Asli groups (the Senai, Semang, and Proto-Malays) in the Malay peninsula arrived in the vanguard. They (the Orang Asli) descended from the very first people who put foot in this region in Malaya.

But when the ancestors of the Orang Asli set foot here, Malaysia didnt look like it does now far from it. At the time, it wasnt a snaking peninsula with a large island on the east.

Instead, it was part of a gargantuan, trunk-like subcontinent double the size of India the result of sea levels being at least 120 metres lower than they are currently. This means that modern-day Malaysia, Thailand, Indonesia, Singapore, and all the now-submerged land between them were connected and formed one solid, massive peninsula.

This majestic, prehistoric landmass is aptly called Sundaland Sund being the Sanskrit term for an elephants trunk.

Thanks to its fortuitously strategic geography, where it hugs the equator and is flanked by the sea, it was Eden-like full of dense, life-sustaining vegetation, frequent rainfall, and populated by animals of all kinds. Many of our ancestors, presumably enamored of this newly-found Suvarnabhumi, stayed put.

But all that changed around 14,000 years ago when rapidly melting ice unleashed cataclysmic floods, and maybe even tsunamis, which inundated many parts of the world. Large swaths of the low-lying coasts of Sundaland were especially badly battered and permanently submerged due to it.

Subsequently, two more massive flooding events took place around 11,500 years ago and 8,000 years ago, further swallowing up the elephantine landmass and eventually turning it into what it is today Peninsular Malaysia, the island of Borneo, the Indonesian Archipelago, and Singapore.

These bouts of cosmic angst unsurprisingly caused a mass exodus from the region. Genetic marker links indicate that migrant bands from Sundaland travelled to and colonised many parts of the world, including Eastern Europe, the Middle East, India, China, Korea, and New Guinea.

And when they did, they carried with them the seeds of civilisation that might have gone on to fertilise the great ancient cultures of the world, including Mesopotamia, Egypt, and India.

Dr Sangkot Marzuki of the Eijkman Institute in Jakarta encapsulates it well when he says: Southeast Asia is the place of origin from which modern man spread out to the rest of the world, after Africa.

Oppenheimer zeroes in on the location of the dispersion even further, saying that the genetic evidence for the spread of people from Southeast Asia round the Pacific Rim points to two Aboriginal areas, Sabah in northeast Borneo and the jungles of the Malay Peninsula.

In light of this groundbreaking scientific revelation, its about time we celebrated the Orang Asli and their ancient way of life, instead of looking at them as irrelevant relics of the past and relegating them to the sidelines of society.

Its about time we embraced and learned from these genetic and cultural time-capsules. After all, the Orang Asli provide a window into our forgotten past and are the proud custodians of tens of thousands of years of wisdom something few other cultures can lay claim to today.

And its definitely about time we invested a lot more money and dedicated a lot more academic firepower into studying the rich prehistory of our homeland. If we did, who knows what we would uncover next.

The views expressed are those of the author and do not necessarily reflect those of FMT.

Link:
Is Malaysia the cradle of civilisation? | Free Malaysia Today - Free Malaysia Today

By: Lifestyle Desk | New Delhi | Updated: September 19, 2020 12:36:00 pmPCOS is so common in women intheir 20s that every 1 in 5 women go through it, while endometriosis is diagnosed in women, who are inbetween their 30s and 40s, said the expert. (Photo: Getty Images/Thinkstock)

Women often end up ignoring their health, and this can sometimes lead to serious issues like a reproductive disorder. It has been seen that health conditions like PCOS (Polycystic Ovarian Syndrome) and endometriosis are often gone undiagnosed as women feel that certain symptoms are variations of a normal menstrual cycle. PCOS is so common in women in their 20s that every 1 in 5 women go through it, while endometriosis is diagnosed in women, who are in between their 30s and 40s, said Dr Sandeep Chadha, consultant obstetrician and gynecologist, Motherhood Hospital, Noida.

Here are some differences and similarities between the two, and when its time to visit your doctor:

What is PCOS?

PCOS is a common hormonal disorder in women in which ovaries produce too many male hormones resulting in irregular or absent menstrual periods, weight gain, hair growth in unusual places like your face, neck, or abdomen, thinning hair on your scalp, acne on your face, chest, or back, and infertility issues.

But with the changing times, there has been difficulty in diagnosis of the condition. Experts suggest that they have been seeing many such women, who do not have all the classic symptoms but they still have been diagnosed with PCOS. While the cause of PCOS is still unclear, but genetics are thought to play a role and high levels of insulin and androgens exacerbate the problem. Excess insulin, which can lead to weight gain, is thought to boost androgen production in the ovaries. So, you are more prone to developing this disorder if you have a family history of PCOS, obesity or diabetes, she told indianexpress.com.

What is endometriosis?

Endometriosis is a condition in which the lining of the uterus, known as endometrium, grows outside the uterus or on other areas such as the ovaries, the outer surface of the uterus, the fallopian tubes, the vagina, the cervix, or even on the bladder or rectum. If a woman has the condition, she will have immensely painful periods with pelvic and lower back pain, pain during or after intercourse, pain while using the bathroom, excessive bleeding, digestive problems, and infertility are also common symptoms.

With a typical menstrual cycle, your endometrium thickens, breaks down, bleeds, and exits your body through the uterus each month. Like PCOS, endometriosis can be difficult to diagnose. Endometriosis is also challenging to diagnose because some women will have no symptoms, and other women who have all of the symptoms above may not necessarily have endometriosis. The exact reason behind endometriosis is also unknown. There are several theories, but none explain all aspects of the disorder, she explained.

Can you have both?

Unfortunately, you can have both, said the expert. She added that many mix-and-match possibilities can present themselves in women suffering from both, but the most common overlapping symptom is infertility.

ALSO READ | Count on these handy tips to prevent and manage polycystic ovarian syndrome

The regularity of your menstrual cycle and hormone testing can help differentiate between the two conditions. It is more common to see endometriosis present in women with regular cycles. However, if a patient with PCOS reports significant pelvic pain, this raises the possibility of another condition being present with PCOS, such as uterine fibroids or endometriosis, since PCOS does not cause pain during periods, she said.

However, any time if you experience especially painful or irregular cycles, notice abnormal hair growth, or struggle with infertility, then its time to visit your doctor.

What you can do

There are no known cures for PCOS or endometriosis, but both are treatable and the symptoms can be managed once correctly diagnosed. PCOS can be managed through hormonal birth control pills, which can help level hormones and therefore regulate periods. If youre trying to get pregnant and cant take birth control, then a doctor suggests some hormone therapy medications. For endometriosis, you can take an extended-cycle pill, which means you have a few periods or eliminating your period completely. A hormonal intrauterine device (IUD) is another option. It can be inserted to help reduce pain and bleeding. Surgery for endometriosis may improve your chances of pregnancy, depending on how extensive the condition has become, she said.

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PCOS and Endometriosis: How to spot the signs - The Indian Express