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Archive for the ‘Female Genetics’ Category

Breast cancer and genetics: Can it skip a generation? – Medical News Today

There are a number of genes that can cause a person to develop breast cancer. Some of these genes are inheritable, meaning they pass from parent to child. However, having the gene for breast cancer does not always mean a person develops it.

This article will go into detail about the role of genetics in breast cancer, whether breast cancer can skip a generation, and the next steps for a person who has a breast cancer gene.

The American Cancer Society (ACS) notes that inherited genetic factors do not cause the majority of breast cancers. However, there are certain inherited genes that increase a persons chances of developing breast cancer.

A gene is a sequence of DNA that determines certain traits, such as eye or hair color. Genes are transmitted in pairs from biological parents to their child. A child inherits one copy from each parent. Sometimes, a child can inherit a gene with mutations, which means that the gene does not function correctly.

Approximately 510% of breast cancer cases in people are hereditary.

Learn more about breast cancer genes here.

Other forms of breast cancer can occur due to gradual changes in a persons DNA.

These forms of breast cancer, known as somatic mutations, are not due to inherited factors. Somatic mutations occur for a variety of reasons, such as aging or exposure to certain chemicals.

Inherited breast cancer genes cannot skip a generation.

If a person has inherited a gene that causes breast cancer, they have a 50% chance of passing it on to their children. If a persons child does not inherit the mutated gene, the child cannot then pass it on to their future children.

However, while genes cannot skip a generation, the cancer can. Having a mutated gene is not a guarantee that a person will have breast cancer.

A mutated gene is still inheritable, even if the person does not develop breast cancer. This means that a persons child may inherit the mutated gene from them and could develop breast cancer.

There are various inherited gene mutations that can cause a person to develop breast cancer. The most common causes of inherited breast cancer are mutations in the genes BRCA1 and BRCA2.

The BRCA genes are responsible for repairing damage to cells in a persons body. These genes also help certain cells, such as breast or ovarian cells, to grow as expected.

When mutations occur in these genes, it can lead to atypical cell growth. Atypical cell growth can lead to the development of cancer.

If a female inherits a harmful BRCA gene, their risk of developing breast cancer by age 7080 is between 4569%.

Additionally, the ACS notes that males with the BRCA2 gene have a lifetime risk of 6 in 100 for developing breast cancer. Those with the BRCA1 gene have a lifetime risk of 1 in 100.

However, while there has been extensive research on the risk of breast cancer in females with the BRCA1 and BRCA2 genes, there has been less research on the cancer risk in males. As a result, these statistics might not be a true reflection.

Learn more about the BRCA gene here.

The ACS notes that most females who have breast cancer have no family history of the condition. However, having a family history of breast cancer can increase a persons chances of developing it.

A females chances of developing breast cancer double if they have a first degree relative with the condition. A first degree relative is an immediate family member, such as a sister, mother, or daughter.

Breastcancer.org states that a female has a higher risk of inheriting a genetic mutation linked to breast cancer if they have:

The risk of a person developing breast cancer increases with each additional family member who has it. Additionally, having a male relative who has breast cancer also increases a females chances of having it.

More research is necessary to determine the effects of family history on a males chances of developing breast cancer.

If a person is concerned that they may have inherited a breast cancer gene, they should speak with a doctor. A doctor may suggest for a person to undergo genetic counseling.

Genetic counseling involves a person speaking with a genetic counselor about their chances of developing breast cancer. Genetic counselors can also provide a person with resources and support.

This type of counseling can also help a person decide if they would like to take part in genetic testing or not. Genetic testing involves checking a persons genetic profile for breast cancer-causing genes.

Genetic testing for cancer usually involves a person submitting a blood sample. However, other forms of genetic testing can use cell samples from a persons:

If a person knows they have a BRCA gene, there are various medical options available to them.

These options include the following:

Breastcancer.org suggests that a person with a high risk of developing breast cancer may benefit from having more frequent screenings.

A person can speak with a doctor about how often they should get screened for breast cancer.

This can involve:

There are certain medications that can help reduce a persons chances of developing hormone receptor-positive breast cancer.

Hormone receptor-positive breast cancers contain hormone receptors that are activated by certain hormones. When these hormones bind to the hormone receptors, they can stimulate growth in the cancer.

Hormonal therapy medications reduce the amount of these hormones in a persons body.

These medications include:

A person may choose to have risk-reduction surgery if they have a high risk of developing breast cancer.

According to the National Cancer Institute, risk-reduction surgery for breast cancer can involve removing one or both breasts, ovaries, or both pairs. There are two types of risk-reducing surgeries: bilateral prophylactic mastectomy and salpingo-oophorectomy.

Bilateral prophylactic mastectomies involve removing both breasts, including a persons nipples, which is known as a total mastectomy. The other option is a subcutaneous mastectomy, which involves removing as much breast tissue as possible while leaving a persons nipples intact.

A total mastectomy reduces a persons risk of developing breast cancer better than a subcutaneous mastectomy.

A salpingo-oophorectomy involves the removal of a persons ovaries and fallopian tubes. Removing the ovaries reduces the amount of estrogen in someones body, which can slow the growth of some breast cancers. Estrogen can promote the growth of some types of breast cancer.

For people with a mutation in the BRCA1 and BRCA2 genes, a bilateral prophylactic mastectomy can reduce the risk of breast cancer by at least 95%.

It can also reduce the risk of breast cancer in people with a strong family history of this condition by up to 90%.

A salpingo-oophorectomy can reduce the chances of breast cancer in people with a high risk by 50%.

For people with mutated BRCA genes, premenopausal removal of their ovaries and fallopian tubes can reduce breast cancer risk by 50% and ovarian cancer risk by 8595%.

Ovary removal may also increase a persons chances of survival if they do develop breast cancer due to mutated BRCA genes.

Inherited genetic factors may cause a person to develop breast cancer. However, a person who inherits a breast cancer gene may not always develop cancer.

This means that a breast cancer gene can appear to skip a generation, even though it does not.

If a person has a family history of breast cancer, they are at a higher risk of developing it. A person can speak with a doctor about their risk of breast cancer to see if they may qualify for or benefit from genetic counseling.

A person can then decide if they would like to have genetic testing.

If a person has a mutated BRCA gene, there are various medical options available to them. A person should speak with a doctor about which option is right for them.

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Breast cancer and genetics: Can it skip a generation? - Medical News Today

Gordon Stenhouse, Grizzly whisperer, on humans sharing the world with bears – Maclean’s

Biologist Gordon Stenhouse has observed grizzlies respect for humans. He wishes wed return the favour.

I wanted to be a veterinarian, but I didnt get into vet school. So I went into wildlife biology. In the early 80s, I got a job studying polar bears and, over many years in the Arctic, I was fortunate to also work on many other speciesDall sheep, peregrine falcons, Arctic-nesting geese, barren-ground caribou. Of all the species I worked on, I enjoyed polar bears the most.

I worked for the Northwest Territories government out in Manitobas Cape Churchill, where congregations of polar bears gather every fall waiting for the sea ice to form. My job was to figure out how to keep polar bears and people apartwhat we call bear deterrence. I lived with an assistant in a fire tower, basically an eight-by-eight-foot box on a tower, just watching the bears and taking notes. I couldnt really go down on the ground much, because there were bears all around us. I thought I had the best job in the world.

Later, I moved to Alberta and worked for a forestry company, which was a very good jobI had a pension and benefits, all that. But I left it for a one-year position to work with grizzly bears, getting paid by the hour. Just imagine, coming home and telling your wife that when you have two small kids.

MORE:Arctic narwhals have a new enemy: the noise of passing ships

Scientists had just figured out how to do DNA population inventories. You get hair samples from bears and run DNA profiles on themjust like the CSI stuff you see on TV, but it takes more time. We learned there were fewer bears than expected. After a few years of inventory work, the Alberta government put a stop to the spring bear hunt [in 2006]. We began to think, how do we recover bear populations? We learned about how road densities affect the survival of bears and that we needed to manage roadswhich is really managing people.

(Courtesy of Gordon Stenhouse)

We used radio collars to understand bear movements. In the early days, we would have to fly around in a helicopter and find the bear, then send a signal to the collar to get the data. One day were flying and I see people walking on this trail up the hillside. And going down toward these people is our collared bear, a big male. I thought, oh no, this is going to be a wreck. We were going to stop our work and go chase the bear away, but before we could descend, the bear walked off the trail and sat down about 20 m away, the way a dog would sit, on his haunches. He watched these people walk by, and then he went back to the trail and kept walking. Generally bears want to stay away from people, but theyll share their world with us. And its our responsibility to show them the same respect.

Every time I capture and handle a bear, I think this better be worth it. This bear is minding his own business, and you come in with a helicopter and dart him, put a collar on him and when he wakes up, hes missing a tooth. When someone shoots a collared bear that youve followed for many years, you think, how can humans be like this? Here are bears, sharing their world with us, tolerating us, walking by us on the trail. And this is how we treat them?

I think its possible to balance the needs of humans and bears, but its not easy. We have to make decisions that certain areas are more important for wildlife than for humans. It doesnt mean we cant use those areas, but it has to be controlled usemaybe hiking only, maybe no trucks or quads. Or we cant disturb the landscape for natural resource extraction, we just leave it as it is.

READ:Tseketi, the 100-year-old B.C.sturgeon thats here to save her species

We just finished two inventory projects over the last few years, and the populations in two areas have doubled. Weve also learned that some of the changes made for forestry, like taking big patches of old forest and making them into younger patches, can be good for bears. We have produced, in my view, the most comprehensive database of grizzly bears in North America, and this amazing genetic database. Its a gold mine of data. In my office, I had boxes and boxes stacked to the ceiling. While watching the 2014 Sochi Olympics, I realized that they werent using blood samples to test athletes prior to the Gamesthey were taking hair samples, because hair contains long-term signatures of chemicals. So I thought, we must be able to do something more with this hair. We started looking at hair cortisol, to look at stress and reproductive hormones. Id never imagined that we would be able to do that with hair samples when we collected them.

Sometimes in science, you just happen upon a finding. In grad school, we were taught that grizzlies are a solitary species that only come together when they mate, and then the mom is on her own with the cubs. But one year, in 2012, we had three adult female bears collared. And, from the genetics, we knew they were relateda female, her sister and her daughter. All three of these females had cubs, and they met up on a mountain, and over the course of the next few weeks, those bears were together all the time, with their six little cubs running around. They travelled together, bedded down together. It made me think of a family reunion, when people meet at the summer cottage. And I always say to myself, I wonder if they took the right cubs with them when they left?

Despite all the research, we will likely never know everything about the lives of bears. I find it pleasing that we still have much to learn. Canadians are fortunate to have many wildlife species that other parts of the world dont have. We have an environment that represents wilderness, and bears to me are a symbol of wilderness. I like to think that if we can manage their habitat and give them what they need, they will be around for future generations. I hope that we can conserve them for many, many years to come.

As told to Michelle Cyca

This article appears in print in the November 2021 issue of Macleans magazine with the headline, Here be bears. Subscribe to the monthly print magazine here.

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Gordon Stenhouse, Grizzly whisperer, on humans sharing the world with bears - Maclean's

Care of men with cancer-predisposing BRCA variants – The BMJ

Men and women are equally likely to inherit or pass on a cancer-predisposing BRCA variantfamily history of cancers needs to encompass both sides of the family

Men with cancer-predisposing BRCA variants have an increased risk of developing breast cancer and are advised to be breast aware

Men with cancer-predisposing BRCA2 variants have an increased risk of developing aggressive prostate cancer (men with cancer-predisposing BRCA1 variants may also have an increased risk); it is not yet known whether prostate specific antigen screening reduces mortality in men with cancer-predisposing BRCA variants

The European Association of Urology recommends that PSA screening is offered to men with cancer-predisposing BRCA2 variants from 40 years of age after discussion of the risks and benefits

Around one in 260 men (~0.4%) inherits a cancer-predisposing BRCA variant that increases their risk of developing prostate, pancreatic, and breast cancer and may affect the health of their family.12 Most of these men are currently unaware that they have a cancer-predisposing BRCA variant, but as genetic testing becomes more common, more men will need medical advice about what having such a variant means for them and their families.

Men are just as likely as women to have a cancer-predisposing BRCA variant, but many people perceive these variants as only being relevant to women. Paradoxically, this could lead to women at very high risk of breast and ovarian cancer missing out on screening and risk-lowering treatment despite a concerning paternal family history. Clinicians might also be less attuned to paternal family history of cancer in assessing womens breast cancer risk.3 This practice pointer covers what cancer-predisposing BRCA variants are, who might be tested; and what health issues men and their clinicians need to know about. We refer to men, but the article also applies to transwomen and some non-binary

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Care of men with cancer-predisposing BRCA variants - The BMJ

Cheetah Cubs Are Born at the Smithsonian Conservation Biology Institute – Smithsonian’s National Zoo and Conservation Biology Institute

Carnivore keepers at the Smithsonian Conservation Biology Institutein Front Royal, Virginia, welcomed a litter of fivecheetah cubs today. Five-year-old female Rosalie birthed the cubs at 5:20 a.m., 8:24 a.m., 9:42 a.m., 10:33 a.m and 11:17 a.m. ET. The family can be viewed via the Cheetah Cub Cam. Ten-year-old Nick, who was the first cheetah born at SCBI, sired this litter. Animal care staff will leave Rosalie to bond with and care for her cubs without interference, so it may be some time before they can determine the cubs'sexes. The cubs appear to be strong, active, vocal and eating well. Keepers will perform a health check on the cubs when Rosalie is comfortable leaving them for an extended period of time.

Staff are closely monitoring Rosalie and her cubs behaviors via webcam.Virtual visitors can observe Rosalie and her cubs on this temporary platform until the cubs leave the den. Keepers provided Rosalie with access to multiple dens, so it is possible she may move the cubs to an off-camera location.

"Seeing Rosalie successfully care for this litterher firstwith confidence is very rewarding,"said Adrienne Crosier, cheetah reproductive biologist at SCBI and head of the Association of Zoos and Aquariums'Cheetah Species Survival Plan. "Being able to witness the first moments of a cheetahs life is incredibly special. As webcam viewers watch our cheetah family grow, play and explore their surroundings, we hope the experience brings them joy and helps them feel a deeper connection to this vulnerable species."

SCBI is part of the Cheetah Breeding Center Coalitiona group of 10 cheetah breeding centers across the United States that aim to create and maintain a sustainable North American cheetah population under human care. These cubs are a significant addition to the Cheetah SSP, as each individual contributes to this program.

The SSP scientists determine which animals to breed by considering their genetic makeup, health and temperament, among other factors. Rosalie and Nick were paired and bred July 9 and 10. Keepers trained Rosalie to voluntarily participate in ultrasounds, and SCBI veterinarians confirmed her pregnancy Aug. 16. Since 2007, 16 litters of cheetah cubs have been born at SCBI.

Cheetahs live in small, isolated populations mostly in sub-Saharan Africa. Many of their strongholds are in eastern and southern African parks. Due to human conflict, poaching and habitat and prey-base loss, there are only an estimated 7,000 to 7,500 cheetahs left in the wild. The International Union for Conservation of Nature considers cheetahs vulnerable to extinction.

The Zoos legacy of conservation work extends beyond the public Zoo in Washington, D.C., to SCBI in Front Royal, Virginia. Scientists at SCBI study and breed more than 20 species, including some that were once extinct in the wild, such as black-footed ferrets and scimitar-horned oryx. Animals thrive in specialized barns and building complexes spread over more than 3,200 acres. The sprawling environment allows for unique studies that contribute to the survival of threatened, difficult-to-breed species with distinct needs, especially those requiring large areas, natural group sizes and minimal public disturbance.

SCBI spearheads research programs at its headquarters in Virginia, the Zoo in Washington, D.C., and at field research stations and training sites worldwide. SCBI scientists tackle some of todays most complex conservation challenges by applying and sharing what they learn about animal behavior and reproduction, ecology, genetics, migration and conservation sustainability.

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Cheetah Cubs Are Born at the Smithsonian Conservation Biology Institute - Smithsonian's National Zoo and Conservation Biology Institute

Maryland scientists mapped the DNA of a blue crab for the first time. It could unlock new clues to understanding the species. – Frederick News Post

In the basement of a lab at Baltimores Inner Harbor, The Chosen One was born.

At least, thats what the researchers at the University of Marylands Center for Environmental Science called her. She was the blue crab who would be the foundation of a breakthrough scientific discovery the first map of the species DNA.

Through a process known as genome sequencing, the scientists created a virtual blue crab encyclopedia, which appears on a computer screen as a color-coded network of thousands of nucleotides the genetic building blocks that make a blue crab a blue crab.

The genomes contents, researchers say, hold a range of potential clues to help them better understand and protect the states beloved crustacean. It could help pinpoint what mutations drive disease, for example, or track how climate change affects the species in the wild. It could even provide a blueprint on how to breed the meatiest crabs in a lab for Maryland picnic tables in summers to come.

Scientists had published genome assemblies for 67 different crustaceans, from the Chinese mitten crab to the shrimp. But until this year, the genetic road map of the blue crab remained largely a mystery.

The project took four researchers about four years a timeline that included raising The Chosen One in the lab. Its an arduous process, but one thats become more achievable thanks to technological advancements. By comparison, a first draft of the human genome was unveiled in 2000, but completing it took until this summer.

The work began on the waters of the Chesapeake Bay one day in October 2018. UMCES professor J. Sook Chung boarded a crabbers boat off Pasadena and harvested dozens of young female crabs to bring back to her lab at the Institute of Marine and Environmental Technology in downtown Baltimore.

After years of raising crabs in her lab, one question plagued her: Why is it that one mother crab can produce millions of eggs, but only a lucky few survive to adulthood?

Genomic sequencing could provide the answer.

To get there, the scientists had to raise the chosen crab, which then gave birth in the lab to dozens of healthy babies, proving her genetic viability. Then, they extracted as much blood and soft tissue from that crab and sent those samples to a lab in Rockville for DNA extraction.

Then, Baltimore scientists received a trove of information from the Rockville lab that they had to piece together, bit by bit. It was terabytes upon terabytes of data, which had to be processed by a computer for five to six months at a time. Thats because the results were full of extra, repetitive genetic information, which they had to comb through to craft each individual chromosome.Its a little bit like ads when youre watching Hulu and you get the same ads again and again, said Tsvetan Bachvaroff, another professor at the University of Maryland center.

When the intricate jigsaw puzzle was complete, the group determined that blue crabs have 40 to 50 chromosomes. Thats nearly double the number in humans, but each one is considerably shorter than ours. There are still some small gaps in the blue crab genome, but future research could fill in the holes.

The scientists article was published last month in the peer-reviewed journal G3: Genes, Genomes, Genetics. The entire sequence will soon be available for public viewing.

The Maryland scientists are now able to compare the DNA of other blue crabs to the model theyve created to understand what drives any differences between them. For instance, what genes decide the crabs size and color? What genetic differences separate a Maryland crab from one native to the waters of, say, Venezuela?

In Baltimore, theyve already determined which part of the sequence encodes the hormone that controls molting, when crabs shed their shells so they can grow. Manipulating this gene could pave the way for improvements in large-scale blue crab farming, Chung said. Thats important because when blue crabs grow in a tank, they molt at different times. Crabs with soft bodies are vulnerable to their bloodthirsty brethren.Blue crabs are sort of notorious for cannibalistic behaviors. They dont care if theyre siblings. If you culture them in a communal tank thousands of them eventually, theres just one big crab. They will eat each other, Chung said. If you synchronize all of the animals sharing the water shedding the shell at the same time, you can remove those cannibalistic behaviors.

Molting is also a vulnerable time for crabs in the wild, and the environment theyre in during that time has a profound impact on their future health and size, said Genine McClair, blue crab program manager for the Maryland Department of Natural Resources. Understanding more about what drives the process could help fisheries managers adjust harvest practices in pursuit of the best crabs, she said.

Now, we have this starting point to ask all these questions, and researchers from all over the country can ask these questions, but they have to reference back to Maryland as where it all began, she said.

All told, the sequencing project cost less than $250,000, much of which came from Maryland-based donors like Mike and Trish Davis of Severna Park. The couple, who ran a software company for decades before their retirement 12 years ago, was looking to support projects that might have trouble getting off the ground without an initial burst of donor funds.Its just a tough project because we dont know exactly what the benefits will be, and people dont like to fund that sort of thing, Mike Davis said.

Slowly, Davis and his wife assembled a group of donors, who collectively gave about $140,000 to the genome project, Davis said.

There was a competitive spirit that helped the scientists in Baltimore make their case, Davis said. The scientists joked about a general rivalry with counterparts in Virginia who also study blue crabs.

They told us: Well, its going to get mapped, its just a matter of who, Davis said. We dont want Virginia to do this, of course, as proud Marylanders.

On a recent afternoon, Chung fed the labs latest crop of blue crabs from the bay, each stored in an orange Home Depot bucket, with oxygen tubes piping bubbles into their watery homes. Its a seven-day-a-week job, she said, to keep the crabs healthy and note their progress.

Sporting a red T-shirt with an image of blue crab sewn on the back, Chung weaved between vast blue tanks to a dark corner of the lab, where minuscule baby crabs grow. Each with their own underwater cubicle, illuminated only by gentle red light, the dime-sized crabs are delicate creatures.

In a way, its fitting Chung was part of the genome sequencing work. Her first name, Sook, is another word for a mature female blue crab, as shes quick to point out. And her earlier work had unveiled some of the creatures more carefully guarded secrets. In 2014, for example, she was part of a team that discovered a new sex hormone in the eyestalks of female blue crabs.

But this recent project feels the most significant, she said the equivalent of passing a baton to the relay runners of tomorrow.

This is a digitized legacy to those who are coming for the next generation of scientists, she said. Thats the way I see it. I left something behind.

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Maryland scientists mapped the DNA of a blue crab for the first time. It could unlock new clues to understanding the species. - Frederick News Post

Weight Loss and Hair Loss: Connection, Prevention, and More – Greatist

Have your luscious locks lost their luster lately? While hair loss can be a normal part of getting older, rapid hair loss could be a sign that somethings up. If youve also been losing weight, its important to understand whether your weight loss and hair loss could be related.

Sudden or rapid weight loss is associated with a condition called telogen effluvium (TE). Its the most common cause of widespread hair loss.

Why does it happen? Stress or trauma may temporarily mess with your hairs growth cycle and cause too much hair to shed at once.

Nutrient deficiencies also seem to be connected to this condition, but that doesnt mean its always a good idea to hit the supplement aisle. In some cases, getting too much of certain vitamins can actually make hair loss worse or put you at risk of toxicity.

A healthcare professional can help you decide whether supplements are right for you.

Keep in mind that TE usually lasts only about 6 months and tends to clear up on its own.

If youre following a very restrictive diet to lose weight, you may be cutting out entire food groups. This can lead to deficiencies in nutrients like zinc, protein, iron, and fatty acids. And those deficiencies can be bad news for your hair health.

A 2015 study of 180 women with hair loss found that iron deficiency and psychological stress were common causes of hair loss.

Research suggests that very low calorie crash diets are another culprit for these nutrient deficiencies. Dieting can also cause psychological stress, which is a major hair loss trigger.

Its important to talk with a healthcare professional before starting a new diet. In general, aim for a balanced diet that includes a variety of fresh fruits, vegetables, grains, and proteins.

Amino acids help your body produce the main structural protein of hair, called keratin. Deficiencies in specific amino acids (like leucine, histidine, valine, and cysteine) are common in folks with hair loss.

A 2017 study in 100 people with hair loss found that a large portion of the participants had leucine and histidine deficiencies. Cysteine and valine deficiencies were also common.

To up your amino acid intake, you can add more protein to your diet. Meat is a solid source of protein, but there are vegetarian and vegan protein options too. Some popular choices are:

Weight loss surgery (such as sleeve gastrectomy) has been linked to low levels of protein, vitamins, and minerals and those deficiencies can lead to hair loss.

A 2018 study of 50 folks who underwent a sleeve gastrectomy found that 56 percent of participants experienced hair loss. Researchers also noted that the peeps who had hair loss also had low levels of vitamin B12 and zinc before and after surgery.

Its tough to say exactly how long hair loss will last after weight loss surgery. In a 2021 study of 112 women who had sleeve gastrectomy surgery, 72 percent of participants experienced hair loss after surgery. In 79 percent of those people, the hair loss started 3 to 4 months after surgery and resolved in about 5.5 months.

Hair loss during weight loss tends to be triggered by rapid weight loss or a diet-related nutrient deficiencies. Try to stick to a sustainable weight loss program instead of an overly restrictive diet. And aim to maintain a balanced diet that includes all the vital vitamins and nutrients your body needs.

Always talk with a healthcare pro before making any major changes to your lifestyle. They can customize a diet or supplement regimen to help get your hair growth back on track.

Hair loss itself isnt a risk to your health, but it can be a sign of an underlying medical condition. Its important to contact a doc ASAP if you experience:

Hair loss is a common side effect of rapid weight loss or nutrient deficiencies. While the hair loss itself isnt dangerous, the underlying cause might be more serious.

Talk with a healthcare pro if you start to notice that your hair is shedding or thinning rapidly, if you notice bald patches, or if clumps of your hair start to fall out. They can help you figure out the cause and the best treatment plan for you.

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Weight Loss and Hair Loss: Connection, Prevention, and More - Greatist

The five biggest threats to our natural world and how we can stop them – The Guardian

The worlds wildlife populations have plummeted by more than two-thirds since 1970 and there are no signs that this downward trend is slowing. The first phase of Cop15 talks in Kunming this week will lay the groundwork for governments to draw up a global agreement next year to halt the loss of nature. If they are to succeed, they will need to tackle what the IPBES (Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services) has identified as the five key drivers of biodiversity loss: changes in land and sea use; direct exploitation of natural resources; climate change; pollution; and invasion of alien species.

1

Changes in land and sea use

Its hidden destruction. Were still losing grasslands in the US at a rate of half a million acres a year or more.

Tyler Lark, from the University of Wisconsin-Madison, knows what he is talking about. Lark and a team of researchers used satellite data to map the expansion and abandonment of land across the US and discovered that 4m hectares (10m acres) had been destroyed between 2008 and 2016.

Large swathes of the United States great prairies continue to be converted into cropland, according to the research, to make way for soya bean, corn and wheat farming.

Changes in land and sea use has been identified as the main driver of unprecedented biodiversity and ecosystem change over the past 50 years. Three-quarters of the land-based environment and about 66% of the marine environment have been significantly altered by human actions.

North Americas grasslands often referred to as prairies are a case in point. In the US, about half have been converted since European settlement, and the most fertile land is already being used for agriculture. Areas converted more recently are sub-prime agricultural land with yields 70% lower than the national average, which means a lot of biodiversity is being lost for diminishing returns.

Our findings demonstrate a pervasive pattern of encroachment into areas that are increasingly marginal for production but highly significant for wildlife, Lark and his team wrote in the paper, published in Nature Communications.

Boggier areas of land, or those with uneven terrain, were traditionally left as grassland, but in the past few decades, this marginal land has also been converted. In the US, 88% of cropland expansion takes place on grassland, and much of this is happening in the Great Plains known as Americas breadbasket which used to be the most extensive grassland in the world.

According to the UNs Convention on Biological Diversity there arefive main threatsto biodiversity. In descending order these are: changes in land and sea use; direct exploitation of natural resources; climate change; pollution and invasive species.

1.For terrestrial and freshwater ecosystems, land-use change has had the largest relative negative impact on nature since 1970.More than a third of the worlds land surface and nearly 75% of freshwater resources are now devoted to crop or livestock production.Alongside a doubling of urban area since 1992, things such as wetlands, scrubland and woodlands which wildlife relies on are ironed out from the landscape.

2. The direct exploitation of organisms and non-living materials,including logging, huntingand fishing and the extraction of soils and water are allnegatively affecting ecosystems.In marine environments, overfishing is considered to be the most serious driver of biodiversity loss.One quarter of the worlds commercial fisheries are overexploited, according to a 2005Millennium Ecosystem Assessment.

3. The climate crisis is dismantling ecosystems at every level. Extreme weather events such as tropical storms and flooding are destroyinghabitats.Warmer temperatures are also changing the timing of natural events such as theavailability of insects and when birds hatch their eggs in spring. The distribution of species and their range is also changing.

4. Many types of pollution are increasing. In marine environments, pollution from agricultural runoff (mainlynitrogen and phosphorus)do huge damage to ecosystems. Agricultural runoff causes toxic algal blooms and even"dead zones"in the worst affectedareas.Marine plastic pollution has increased tenfold since 1980,affecting at least 267 species.

5. Since the 17th century, invasive species havecontributed to 40%of all known animal extinctions. Nearly one fifth of the Earths surface is at risk of plant and animal invasions. Invasive species change the composition of ecosystems by outcompeting native species.

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Hotspots for this expansion have included wildlife-rich grasslands in the prairie pothole region which stretches between Iowa, Dakota, Montana and southern Canada and is home to more than 50% of North American migratory waterfowl, as well as 96 species of songbird. This cropland expansion has wiped out about 138,000 nesting habitats for waterfowl, researchers estimate.

These grasslands are also a rich habitat for the monarch butterfly a flagship species for pollinator conservation and a key indicator of overall insect biodiversity. More than 200m milkweed plants, the caterpillars only food source, were probably destroyed by cropland expansion, making it one of the leading causes for the monarchs national decline.

The extent of conversion of grassland in the US makes it a larger emission source than the destruction of the Brazilian Cerrado, according to research from 2019. About 90% of emissions from grassland conversion comes from carbon lost in the soil, which is released when the grassland is ploughed up.

The rate of clearing that were seeing on these grasslands is on par with things like tropical deforestation, but it often receives far less attention, says Lark.

Food crop production globally has increased by about 300% since 1970, despite the negative environmental impacts.

Reducing food waste and eating less meat would help cut the amount of land needed for farming, while researchers say improved management of existing croplands and utilising what is already farmed as best as possible would reduce further expansion.

Lark concludes: I think theres a huge opportunity to re-envision our landscapes so that theyre not only providing incredible food production but also mitigating climate change and helping reduce the impacts of the biodiversity crisis by increasing habitats on agricultural land.PW

2

Direct exploitation of natural resources

From hunting, fishing and logging to the extraction of oil, gas, coal and water, humanitys insatiable appetite for the planets resources has devastated large parts of the natural world.

While the impacts of many of these actions can often be seen, unsustainable groundwater extraction could be driving a hidden crisis below our feet, experts have warned, wiping out freshwater biodiversity, threatening global food security and causing rivers to run dry.

Farmers and mining companies are pumping vast underground water stores at an unsustainable rate, according to ecologists and hydrologists. About half the worlds population relies on groundwater for drinking water and it helps sustain 40% of irrigation systems for crops.

The consequences for freshwater ecosystems among the most degraded on the planet are under-researched as studies have focused on the depletion of groundwater for agriculture.

But a growing body of research indicates that pumping the worlds most extracted resource water is causing significant damage to the planets ecosystems. A 2017 study of the Ogallala aquifer an enormous water source underneath eight states in the US Great Plains found that more than half a century of pumping has caused streams to run dry and a collapse in large fish populations. In 2019, another study estimated that by 2050 between 42% and 79% of watersheds that pump groundwater globally could pass ecological tipping points, without better management.

The difficulty with groundwater is that people dont see it and they dont understand the fragility of it, says James Dalton, director of the global water programme at the International Union for Conservation of Nature (IUCN). Groundwater can be the largest and sometimes the sole source in certain types of terrestrial habitats.

Uganda is luxuriantly green, even during the dry season, but thats because a lot of it is irrigated with shallow groundwater for agriculture and the ecosystems are reliant on tapping into it.

According to UPGro (Unlocking the Potential of Groundwater for the Poor), a research programme looking into the management of groundwater in sub-Saharan Africa, 73 of the 98 operational water supply systems in Uganda are dependent on water from below ground. The country shares two transboundary aquifers: the Nile and Lake Victoria basins. At least 592 aquifers are shared across borders around the world.

Some of the groundwater reserves are huge, so there is time to fix this, says Dalton. Its just theres no attention to it.

Inge de Graaf, a hydrologist at Wageningen University, who led the 2019 study into watershed levels, found between 15% to 21% had already passed ecological tipping points, adding that once the effects had become clear for rivers, it was often too late.

Groundwater is slow because it has to flow through rocks. If you extract water today, it will impact the stream flow maybe in the next five years, in the next 10 years, or in the next decades, she says. I think the results of this research and related studies are pretty scary.

In April, the largest ever assessment of global groundwater wells by researchers from University of California, Santa Barbara, found that up to one in five were at risk of running dry. Scott Jasechko, a hydrologist and lead author on the paper, says that the study focuses on the consequences for humans and more research is needed on biodiversity.

Millions of wells around the world could run dry with even modest declines in groundwater levels. And that, of course, has cascading implications for livelihoods and access to reliable and convenient water for individuals and ecosystems, he says.PG

In 2019, the European heatwave brought 43C heat to Montpellier in France. Great tit chicks in 30 nest boxes starved to death, probably because it was too hot for their parents to catch the food they needed, according to one researcher. Two years later, and 2021s heatwave appears to have set a European record, pushing temperatures to 48.8C in Sicily in August. Meanwhile, wildfires and heatwaves are stripping the planet of life.

Until now, the destruction of habitats and extraction of resources has had a more significant impact on biodiversity than the climate crisis. This is likely to change over the coming decades as the climate crisis dismantles ecosystems in unpredictable and dramatic ways, according to a review paper published by the Royal Society.

There are many aspects of ecosystem science where we will not know enough in sufficient time, the paper says. Ecosystems are changing so rapidly in response to global change drivers that our research and modelling frameworks are overtaken by empirical, system-altering changes.

The calls for biodiversity and the climate crisis to be tackled in tandem are growing. It is clear that we cannot solve [the global biodiversity and climate crises] in isolation we either solve both or we solve neither, says Sveinung Rotevatn, Norways climate and environment minister, with the launch in June of a report produced by the worlds leading biodiversity and climate experts. Zoological Society of London senior research fellow Dr Nathalie Pettorelli, who led a study on the subject published in the Journal of Applied Ecology in September, says: The level of interconnectedness between the climate change and biodiversity crises is high and should not be underestimated. This is not just about climate change impacting biodiversity; it is also about the loss of biodiversity deepening the climate crisis.

Writer Zadie Smith describes every countrys changes as a local sadness. Insects no longer fly into the house when the lights are on in the evening, the snowdrops are coming out earlier and some migratory species, such as swallows, are starting to try to stay in the UK for winter. All these individual elements are entwined in a much bigger story of decline.

Our biosphere the thin film of life on the surface of our planet is being destabilised by temperature change. On land, rains are altering, extreme weather events are more common, and ecosystems more flammable. Associated changes, including flooding, sea level rise, droughts and storms, are having hugely damaging impacts on biodiversity and its ability to support us.

In the ocean, heatwaves and acidification are stressing organisms and ecosystems already under pressure due to other human activities, such as overfishing and habitat fragmentation.

The latest Intergovernmental Panel on Climate Change (IPCC) landmark report showed that extreme heatwaves that would usually happen every 50 years are already happening every decade. If warming is kept to 1.5C these will happen approximately every five years.

The distributions of almost half (47%) of land-based flightless mammals and almost a quarter of threatened birds, may already have been negatively affected by the climate crisis, the IPBES warns. Five per cent of species are at risk of extinction from 2C warming, climbing to 16% with a 4.3C rise.

Connected, diverse and extensive ecosystems can help stabilise the climate and will have a better chance of thriving in a world permanently altered by rising emissions, say experts. And, as the Royal Society paper says: Rather than being framed as a victim of climate change, biodiversity can be seen as a key ally in dealing with climate change. PW

On the west coast of Scotland, fragments of an ancient rainforest that once stretched along the Atlantic coast of Britain cling on. Its rare mosses, lichens and fungi are perfectly suited to the mild temperatures and steady supply of rainfall, covering the crags, gorges and bark of native woodland. But nitrogen pollution, an invisible menace, threatens the survival of the remaining 30,000 hectares (74,000 acres) of Scottish rainforest, along with invasive rhododendron, conifer plantations and deer.

While marine plastic pollution in particular has increased tenfold since 1980 affecting 44% of seabirds air, water and soil pollution are all on the rise in some areas. This has led to pollution being singled out as the fourth biggest driver of biodiversity loss.

In Scotland, nitrogen compounds from intensive farming and fossil fuel combustion are dumped on the Scottish rainforest from the sky, killing off the lichen and bryophytes that absorb water from the air and are highly sensitive to atmospheric conditions.

The temperate rainforest is far from the sources of pollution, yet because its so rainy, were getting a kind of acid rain effect, says Jenny Hawley, policy manager at Plantlife, which has called nitrogen pollution in the air the elephant in the room of nature conservation. The nitrogen-rich rain thats coming down and depositing nitrogen into those habitats is making it impossible for the lichen, fungi, mosses and wildflowers to survive.

Environmental destruction caused by nitrogen pollution is not limited to the Scottish rainforest. Algal blooms around the world are often caused by runoff from farming, resulting in vast dead zones in oceans and lakes that kill scores of fish and devastate ecosystems. Nitrogen-rich rainwater degrades the ability of peatlands to sequester carbon, the protection of which is a stated climate goal of several governments. Wildflowers adapted to low-nitrogen soils are squeezed out by aggressive nettles and cow parsley, making them less diverse.

About 80% of nitrogen used by humans through food production, transport, energy and industrial and wastewater processes is wasted and enters the environment as pollution.

Nitrogen pollution might not result in huge floods and apocalyptic droughts but we are slowly eating away at biodiversity as we put more and more nitrogen in ecosystems, says Carly Stevens, a plant ecologist at Lancaster University. Across the UK, we have shown that habitats that have lots of nitrogen have fewer species in them. We have shown it across Europe. We have shown it across the US. Now were showing it in China. Were creating more and more damage all the time.

To decrease the amount of nitrogen pollution causing biodiversity loss, governments will commit to halving nutrient runoff by 2030 as part of an agreement for nature currently being negotiated in Kunming. Halting the waste of vast amounts of nitrogen fertiliser in agriculture is a key part of meeting the target, says Kevin Hicks, a senior research fellow at the Stockholm Environment Institute centre at York.

One of the biggest problems is the flow of nitrogen from farming into watercourses, Hicks says. In terms of a nitrogen footprint, the most intensive thing that you can eat is meat. The more meat you eat, the more nitrogen youre putting into the environment.

Mark Sutton, a professor at the UK Centre for Ecology & Hydrology, says reducing nitrogen pollution also makes economic sense.

Nitrogen in the atmosphere is 78% of every breath we take. It does nothing, its very stable and makes the sky blue. Then there are all these other nitrogen compounds: ammonia, nitrates, nitrous oxide. They create air and water pollution, he says. He argues that if you price every kilo of nitrogen at $1 (an estimated fertiliser price), and multiply it by the amount of nitrogen pollution lost in the world 200bn tonnes it amounts to $200bn (147bn) every year.

The goal to cut nitrogen waste in half would save you $100bn, he says. I think $100bn a year is a worthwhile saving.PG

On Gough Island in the southern Atlantic Ocean, scores of seabird chicks are eaten by mice every year. The rodents were accidentally introduced by sailors in the 19th century and their population has surged, putting the Tristan albatross one of the largest of its species at risk of extinction along with dozens of rare seabirds. Although Tristan albatross chicks are 300 times the size of mice, two-thirds did not fledge in 2020 largely because of the injuries they sustained from the rodents, according to the RSPB.

The situation on the remote island, 2,600km from South Africa, is a grisly warning of the consequences of the human-driven impacts of invasive species on biodiversity. An RSPB-led operation to eradicate mice from the British overseas territory has been completed, using poison to help save the critically endangered albatross and other bird species from injuries they sustain from the rodents. It will be two years before researchers can confirm whether or not the plan has worked. But some conservationists want to explore another controversial option whose application is most advanced in the eradication of malaria: gene drives.

Instead of large-scale trapping or poisoning operations, which have limited effectiveness and can harm other species, gene drives involve introducing genetic code into an invasive population that would make them infertile or all one gender over successive generations. The method has so far been used only in a laboratory setting but at Septembers IUCN congress in Marseille, members backed a motion to develop a policy on researching its application and other uses of synthetic biology for conservation.

If a gene drive were proven to be effective and there were safety mechanisms to limit its deployment, you would introduce multiple individuals on an island whose genes would be inherited by other individuals in the population, says David Will, an innovation programme manager with Island Conservation, a non-profit dedicated to preventing extinctions by removing invasive species from islands. Eventually, you would have either an entirely all male or entirely all female population and they would no longer be able to reproduce.

Nearly one-fifth of the Earths surface is at risk of plant and animal invasions and although the problem is worldwide, such as feral pigs wreaking havoc in the southern United States and lionfish in the Mediterranean, islands are often worst affected. The global scale of the issue will be revealed in a UN scientific assessment in 2023.

We have to be very careful, says Austin Burt, a professor of evolutionary genetics at Imperial College London, who researches how gene drives can be used to eradicate malaria in mosquito populations. If youre going after mice, for example, and youre targeting mice on an island, youd need to make sure that none of those modified mice got off the island to cause harm to the mainland population.

In July, scientists announced they had successfully wiped out a population of malaria-transmitting mosquitoes using a gene drive in a laboratory setting, raising the prospect of self-destructing mosquitoes being released into the wild in the next decade.

Kent Redford, chair of the IUCN Task Force on Synthetic Biology who led an assessment of the use of synthetic biology in conservation, said there are clear risks and opportunities in the field but further research is necessary.

None of these genetic tools are ever going to be a panacea. Ever. Nor do I think they will ever replace the existing tools, Redford says, adding: There is a hope and I stress hope that engineered gene drives have the potential to effectively decrease the population sizes of alien invasive species with very limited knock-on effects on other species.PG

Find more age of extinction coverage here, and follow biodiversity reporters Phoebe Weston and Patrick Greenfield on Twitter for all the latest news and features

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The five biggest threats to our natural world and how we can stop them - The Guardian

Hunting: How can you tell the age of a deer? Here are some tips – pressherald.com

When most folks talk about aging deer theyre referring to venison, and the process of hanging a deer for an extended period to improve flavor and tenderness. However, with the rise in popularity of trail cameras, increasingly more hunters are sharing photos on social media and asking, How old is this deer?

When it comes to the answers you have to consider the source. A lot of well-meaning keyboard biologists offer their opinions, often of questionable accuracy. Fortunately, there are some fairly reliable though not foolproof methods for properly aging deer on the hoof, or from a photo. Lets start with does as they can only be reliably divided into two or three age classes. Early in the season its easy to distinguish does from fawns but as the youngsters grow it becomes more difficult, especially if you dont have multiple deer present for comparison.

First, look at the head and face. A fawns forehead and nose will appear much shorter (think: 8-ounce soda bottle) in comparison to the adult does longer nose (16-ounce soda bottle) and larger head. Next, look at the body. Fawns also have short, square bodies, short necks and less muscle development. An adult does body will be larger and more rectangular-shaped. Necks appear longer and older does may have swayed backs or sagging bellies.

Yearling does look somewhere in between and are best judged in the presence of older and/or younger deer. Its not uncommon for female deer to travel in family groups consisting of several generations, often a mature doe, her fawns and her yearling female offspring from the previous year. The same guidelines apply to buck fawns, though they may show a more square head than a doe, and sometimes you can distinguish tiny nubs or buttons that will eventually become antlers.

Now for the antlered bucks. Yearling bucks appear dainty, with thin necks, somewhat resembling a doe with antlers. Their legs appear long and slender compared to their body. Antler development can be highly variable depending mostly on nutrition and genetics. Many will sport spikes or forked antlers but some may carry a rack of six or even eight points. Regardless, main beams and points are usually thin and short.

Two-year-old bucks generally look somewhat gangly and awkward, though a healthy Maine buck could fool a lot of folks into thinking its older. Legs also appear long for their body, and theyll have a thin waist and shoulders and limited neck swelling. During the rut, tarsal glands may be dark, but very small and round. Rack size also varies but six-, eight- or even 10-point racks that score in the 120s and even 130s are not unusual, and a 2-year-old might dress out somewhere between 140 and 180 pounds, possibly more further north. Antler beams will still be relatively narrow at the base but thicker than a yearling and possibly have more rounded points.

Three-year-old bucks will have a fuller, thickly-muscled neck. The chest appears deeper than the hindquarters, giving a race horse appearance. Horizontal lines of the back and stomach are still straight and taut. Another good characteristic is that you can usually distinguish where the neck meets the shoulders. Tarsal glands during the rut will be dark but small, and staining does not extend down the leg to the hoof. Antler beams become thicker and could be 3 1/2 inches in diameter at the base.

At age 4, bucks reach maturity. Skeletal structure stops growing so they can direct more nutrition to body weight and antler mass. Their fully muscled neck now blends seamlessly into a deep chest. Their rump appears full and rounded and legs may appear slightly short for the body. The stomach and back do not sag, yet. Jaw skin is tight and tarsal glands will be noticeably large and dark. Rack size still varies but most of these deer will fall into what most hunters would consider the trophy category. The base of the beams will be thick, about the same diameter as a deers eye, and may show more dark staining.

Not many deer make it that long in heavily hunted areas but a few do, more so in the big woods where hunting pressure is less. Their neck and brisket will appear to be one continuous muscle and their neck will show heavy swelling. Now the legs really appear too short for the big, blocky body. Their waistline will be even (parallel) with the chest and they may start to show a pot belly and sagging back. Tarsals appear noticeably large and very dark with staining down the inside of the leg to the hoof during the rut. Again, rack size varies but even if they dont carry a crown of thorns, beams will be thick and heavy, especially at the bases.

There are objective criteria for what distinguishes a trophy buck, but for most hunters its a personal and very subjective judgement. A yearling might be a trophy for an inexperienced or unlucky hunter. Many 2- and 3-year-old bucks eventually make their way to the taxidermist. And a gnarly old north woods buck that wont score well in the record book but will pull the scales down well past the 200-pound mark might make the grade for big woods hunters. Still, if you plan to be selective, its nice to know what to look for.

Bob Humphrey is a freelance writer and Registered Maine Guide who lives in Pownal. He can be reached at:[emailprotected]

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Hunting: How can you tell the age of a deer? Here are some tips - pressherald.com

Alcohol Is the Breast Cancer Risk No One Wants to Talk About – WIRED

Martinez had never organized a social media campaign and doesnt consider herself social media savvy. But after ARG won the $100,000 grant, she was running focus groups, coordinating an advisory group of cancer organizations, building a team of co-investigators and partnering with the ARG communications specialist. The young women made it very clear they did not want to be told what to do, Martinez says of the focus groups. Drink less for your breasts felt more like a helpful suggestion.

Planning for the social media campaign began just as the pandemic forced a national shutdown. As the pandemic dragged on, alcohol consumption rose, especially among women. Days of heavy drinking among women, defined as four or more drinks within a couple of hours, rose by 41 percent, according to a survey by the RAND Corporation. (The study compared a baseline survey of 1,540 adults conducted in the spring of 2019 with their responses during a follow-up in the spring of 2020.)

But pushing back against alcohol consumption isnt simple. As the US found during a disastrous prohibition period from 1920 to 1933, opposing alcohol is not popular. When Sharima Rasanayagam,chief scientist for Breast Cancer Prevention Partnersin San Francisco, gives talks about environmental causes of breast cancer, her audience is raptuntil she mentions alcohol. People like to drink and they dont like to hear that, she says. She tells them that quantity matters: At the very least, drink less.

Its a message she delivers with care, to avoid giving women a reason for self-blame if they develop breast cancer and wonder Why me? Cases of breast cancer cant be tied to alcohol alone, because many factors, including genetics and environmental exposures, contribute to the disease, she explains in a YouTube video linked to the Breast Cancer Prevention Partners website. But Rasanayagam notes that risks add upand alcohol is one that women can reduce. Fewer drinks, whether over time or in one day, mean less exposure to acetaldehyde and potentially less effect on estrogen. Its been shown that the less you drink, the lower your risk, she says. (Breast Cancer Prevention Partners is an advisor to the Drink Less for Your Breasts campaign.)

Its a nuanced message but, in its own way, a bold one, as framed in a social media campaign, says David Jernigan, an alcohol policy expert at Boston University, who has been working in the field for 35 years. What Priscilla is doing in California is groundbreaking, he says.

Jernigan asserts that the harm from alcoholwhich also includes drunk driving and an association with violencewarrants a large-scale response similar to anti-tobacco efforts. He notes that in Estonia, a campaign urging Lets drink less by half! actually lowered per capita consumption by 28 percent. (Estonias alcohol policy also included restrictions on advertising, more enforcement of driving-under-the-influence laws, higher taxes, and a focus on treatment.)

The World Health Organization is also developing a global action plan; the current draft sets a goal of reducing per capita consumption by 20 percent by 2030 (with 2010 consumption levels as the baseline). It urges nations to develop and enforce high-impact policy options, such as higher alcohol taxes, restrictions on advertising, and emphasizes awareness of health risks.

Jernigan calls that effort a good step that doesnt go far enough. He favors the development of an international treaty on alcohol, similar to the Framework Convention on Tobacco Control, the first such negotiated through the World Health Organization. It has been signed by 168 countries that committed to taking steps to restrict tobacco advertising, raise cigarette taxes, and prevent youth smoking.

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Alcohol Is the Breast Cancer Risk No One Wants to Talk About - WIRED

Why Black Women Are Twice as Likely to Die of Endometrial Cancer and What MSK Is Doing to Change It – On Cancer – Memorial Sloan Kettering

When Linda Collins was diagnosed with endometrial cancer in her early 60s, she wanted to find the best treatment possible.

After doing her research, she felt confident she would receive the care she needed at Memorial Sloan Kettering Cancer Center.

She also knew what she needed to give her peace of mind. When I called the MSK Patient Access Service to ask about an appointment, I told them that as a Black woman, I would feel more comfortable with a female doctor who is a person of color.

She explains that years before, I had a white, male gynecologist who dismissed concerns that I had. Respectfully, it seemed like he couldnt be bothered. And I have great insurance!

Linda searched the MSK website and knew she had found the doctor she hoped for in Carol Brown, a gynecologic oncology surgeon and MSKs Chief Health Equity Officer.

Dr. Carol Brown, gynecological oncology surgeon

Dr. Brown has devoted her career to improving cancer disparities that mean some groups of people suffer far worse outcomes, particularly Black people.

In May 2021, she launched an important new initiative as the leader of the Endometrial Cancer Equity Program (ECEP).Endometrial cancer develops in the lining of the uterus (womb) and is also sometimes referred to as uterine cancer.

The programs goals are to educate Black women about endometrial cancer, help those diagnosed find appropriate care, and ultimately find treatments to improve outcomes for all women facing the disease, like Linda.

The numbers are truly shocking.

Black women are nearly twice as likely to die of endometrial cancer as white women, even though the disease is actually slightly more common in white women than in Black women.

The number of cases of endometrial cancer is also on the rise, with the greatest increase among Black women.

Dr. Brown stresses that many factors play a role in the troubling disparity in endometrial cancer, including poorer access to health care in some communities, a lack of awareness among some providers, and research efforts that often have not included enough people who are Black, Hispanic, and Asian.

Dr. Brown says research also suggests another important factor may be a cruel twist of biology.

Dr. Brown points out that the disparity in survival between Black and white women diagnosed with endometrial cancer hasnt changed in four decades. Theres no question that if the difference was only about access to health care, the disparity would have at least narrowed. Thats what weve seen happen in cervical cancer and most forms of breast cancer, when you compare Black and white women. But not endometrial cancer.

One distinction coming into clearer focus is that Black women are more often diagnosed with rare but aggressive forms of endometrial cancer.

Black women are more likely to have papillary serous carcinoma of the endometrium as well as carcinoma sarcoma, Dr. Brown says. Cancers caused by these two types of cancer cells definitely lead to worse outcomes and that in itself is a biologic difference.

Ying Liu is a medical oncologist whose specialty is the genetic component of gynecological cancers. She works alongside Dr. Brown investigating cancer disparities.

Dr. Liu explains that one aspect we are looking at is whether these biological differences in the kinds of cancer more commonly found in Black women are not as well targeted by current treatments. That may explain some of the disparity in survival rates between Black and white patients.

The ultimate goal of research at MSK is to better understand these biological differences in endometrial tumors, down to the molecular level, and then use this knowledge to identify weaknesses in the tumors that are more common in Black women. Then, its about finding therapies to treat them.

Dr. Brown explains at MSK we probably have one of the largest groups of Black female patients in the country where we can analyze the genetics of their endometrial cancer tumors as well as their personal genetics.

Lindas diagnosis was an aggressive papillary serous carcinoma, the type that more commonly affects Black women. Fortunately, the cancer was caught at an early stage.

Linda recalls that within days of our first appointment, Dr. Brown performed a laparoscopic hysterectomy, which involves a much smaller incision, and also removed my fallopian tubes, ovaries, and nearby sentinel lymph nodes. To reduce the chance the cancer could come back, Linda underwent a short course of radiation.

Linda says of her treatment, the staff was just fantastic. And I love Dr. Brown. She was so proactive and always took the time to answer all my questions.

Today, Linda is doing the things she loves. She is a pillar of her community in the Bronx, serving as president of her building association, leading clothing drives for homeless shelters, and serving as a liaison with police associations, among other efforts.

After a 32-year career, most of it in government, she says I just love to serve people.

She also wanted to be sure she was around for her family, retiring from the working world in her mid-50s. She explains as a Black woman, you have the sense that your life expectancy might not be as long as the next person.

Dr. Brown and her colleagues hope their new initiative can help.

Since May 2021, the ECEP has participated in community events that have reached more than 500 women in predominately Black neighborhoods that stretch across Long Island, Brooklyn, and Queens.

In addition, Dr. Brown and colleagues including MSK nurse practitioner Latasha Anderson-Dunkley have screened over 20 women at high risk who have been identified through the ECEP. The goal is to assess whether the women have cancer or precancerous conditions and get them appropriate care.

Dr. Brown says its particularly important that women and their providers are aware of endometrial cancer because as cases rise, the symptoms of the disease are not always clear cut.

Traditionally, providers have focused on symptoms that include bleeding in post-menopausal women, who often have other symptoms such as obesity and diabetes, she explains. But this cancer can present as just a heavier-than-usual period bleeding in your 40s. Thats true of all women and particularly Black women.

For Linda, making women aware of how they can protect their health is just what the doctor ordered. To me, outreach and education is so important, because you dont know what you dont know. Too often, this kind of outreach doesnt happen in communities of color. But if it does, it can save lives.

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Why Black Women Are Twice as Likely to Die of Endometrial Cancer and What MSK Is Doing to Change It - On Cancer - Memorial Sloan Kettering

Murder Island review a contest to solve the killing of a young woman? Bad timing – The Guardian

Its possible that the timing is not propitious for the launch of a new entertainment series centred on the investigation of a young womans murder. The outrage surrounding the conviction of a serving Metropolitan police officer for the rape and killing of Sarah Everard, and the visibility it has given to the endemic violence against women, is a hurdle to overcome. Channel 4s six-part offering Murder Island also has a further point of connection with the case and the context. One of its participants is former chief superintendent Parm Sandhu, who last week gave an interview to Radio 4s World at One about her experience in the Met. She discussed female officers unwillingness to report sexist and misogynist behaviour for fear that the men will close ranks, and said that the fear that most women police officers have got is that when you are calling for help, you press that emergency button on your radio, theyre not going to turn up and youre going to get kicked in the street.

On the other hand, the vulnerability of women to rapists and murderers is not exactly new information and it hasnt curbed appetites for its exploitation as entertainment before now. So maybe this is by the by. Plus, Murder Islands USP is that it is a new genre a hybrid drama/reality show that keeps the involvement of police proper to a minimum. Instead, four pairs of amateur detectives will compete to solve a murder mystery written by Ian Rankin, about the stabbing of Charly Hendricks in a cottage on a remote Scottish island by a person or persons unknown. One team will be eliminated at each stage of the investigation the winners get a 50,000 prize.

Put like that, I am even less sure than I was that this counts for rather than against the new venture.

Context aside, how does the new format fare? The reality show element sings its customary siren song, giving us competitors spanning the full range of capability. At one end of the spectrum are Andrew and Nick, ambitious, articulate and with the lean, hungry look of leopards on the prowl. Andrews father and grandfather were detectives and he is hoping genetics will out. Although they have to be warned like the rest about making assumptions rather than gathering evidence and seeing what it tells them, they seem to have a basic grasp of procedure and, when it comes to assessing timelines and comparing testimonies, logic. If you had money and cared enough, you would bet on them to win.

At the other end there are Dot and Rox, who have to be told not to stand in the blood pool at the crime scene. They became friends when they worked in the same pub, and reckon they know how to read people. This will be very useful once we move to an all-intuition criminal justice system, but, as things stand, makes them merely extremely fun to watch. Told off by Simon Harding, one of the former detectives who is overseeing and evaluating the teams, for taking more photos of the processed crime scene than he would take on holiday, they wonder aloud how boring his holidays must be.

As we cut between the reality show scenes, full drama scenes play out with the fictional characters. As the competitors travel around the village interviewing Charlys friends, acquaintances and other people of interest played by actors, a story builds of a proposed development on the island that is cleaving the community, Charlys activism on behalf of those against the scheme and a possible love triangle between her, Jean the shopkeeper and particularly dour local Hamish. There is also a pregnancy, mysterious events in the far-flung land of Glasgow that have yet to be fully uncovered and the pubs owner Toby looks shifty to us all.

The goal of all hybrid genres is to double the value of watching. On most occasions, however, it simply halves it because neither contribution is fully developed and each undercuts the others momentum. Murder Island, judged on the first episode, falls into the latter camp. Things may improve as teams are eliminated, allowing the hour to tighten up. It will help, too, if the interactions between the detectives and the actors become less stagey and awkward as they relax into the situation and its strange demands.

How much context matters, of course, is up to us.

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Murder Island review a contest to solve the killing of a young woman? Bad timing - The Guardian

One Major Effect Vitamin D May Have in Preventing Breast Cancer, New Study Suggests | Eat This Not That – Eat This, Not That

One question to startOctober: Are you getting enough Vitamin D?The benefits from Vitamin D seem never-ending, and now a new women's health study may point to yet one more. Biology researchers in a region with an "elevated risk of breast cancer" have zeroed in on a specific link between the disease and a nutritional deficiency.

Keep reading to learn more about the possible link between breast cancer and Vitamin D. Also, readThe #1 Best Juice to Drink, Says Nutritionist.

In a new issue of the peer-reviewed journal, Nutrition and Cancer, three genetics and biochemistry researchers in Pakistan have published a new study, in which they state, "Pakistani females are at elevated risk of breast cancer."

They also note that Vitamin D deficiency is "an ignored contributing factor" to the illness, "despite a strong association."

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The study included 154 women who had been diagnosed with breast cancer, and 248 selected at random for the control group.

The researchers note that out of these 402 women, 51.5% "were completely ignorant of their [Vitamin D] level." Between the women who weren't aware of their Vitamin D intake versus those who held some awareness, the researchers noted higher incidence of breast cancer among those who were entirely uncertain.

RELATED:These Foods May Increase Your Breast Cancer Risk, Says New Study

Upon analysis, the team discovered a couple insightful trends. They found that women ages 41 to 50 years old were most prone to a Vitamin D deficiency.

Interestingly, women in cities were 12% more likely to suffer a Vitamin D deficiency than women who lived in rural areas.

A possible explanation for this may be greater outdoor exposure to sunlight, which triggers the body to produce Vitamin D. Perhaps more importantly, the higher Vitamin D levels among rural woman might highlight the importance of having access to fresh, nutritious foods, thanks to their proximity to agriculture.

RELATED:The #1 Way to Tell If You Need More Vitamin D, Says Dietitian

The researchers state: "It was concluded that [Vitamin D] deficiency is a highly contributing factor for breast cancer so every female must be aware of the importance of [Vitamin D] and should maintain a sufficient level of this crucially important vitamin."

For more Vitamin D wisdom, readSimple Ways to Avoid Vitamin D Deficiency, Say Experts.

Also, keep reading:

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One Major Effect Vitamin D May Have in Preventing Breast Cancer, New Study Suggests | Eat This Not That - Eat This, Not That

Wisconsin Dairy Expo: Faye and Faroh finish first at the International Brown Swiss Show – Wisbusiness.com

MADISON, WIS. Cutting Edge Thunder Faye was crowned the Grand Champion Female at the International Brown Swiss Show at World Dairy Expo. Faye won the Aged Cow, Six-Year-Old & Over Class before taking the Senior Champion Female title. Faye was also awarded the $1,000 Udder Comfort Grand Champion Cash Award, the Alan Hetts Memorial Trophy, the Vid Vye Memorial Trophy and the Swiss Bell. Following Faye, the Reserve Grand Champion Female was won by Cutting Edge F Faroh-ETV. Faroh won the Senior Three-Year-Old Class before winning Intermediate Champion Female. Both Faye and Faroh are owned by Ken Main and Kenny Joe Manion of Copake, New York.

Reserve Senior Champion Female honors were awarded to Iroquois Acres Jong Cali, the second-place Aged Cow Six-Year-Old & Over Class exhibited by Matthew Pacheco of Kerman, California. Reserve Intermediate Champion Female, Siegrets Damian Pinapple, was second place in the Senior Three-Year-Old Cow Class and was shown by Leslie & Linda Bruchey of Westminster, Maryland.

Pit-Crew Formula Tawny, leased by Abby Foss and owned by Pit-Crew Genetics of Cambridge, Minnesota, was the Junior Champion Female. Tawny was the winning Winter Yearling Heifer while the first-place Fall Heifer Calf, Wright-Way Famous Tik Tok-ET, exhibited by Landree & Dakota Fraley of Muncy, Pennsylvania, was named Reserve Junior Champion Female.

Elite Dairy 2 of Copake, New York was awarded Premier Breeder and was presented the Ira Inman Award. Winning both Premier Exhibitor and Premier Exhibitor of the Heifer Show, in addition to Premier Breeder of the Heifer Show, was Pit-Crew Genetics of Cambridge, Minnesota. Voelkers Td Carter was named Premier Sire and Premier Sire of the Heifer Show.

Official judge Lynn Harbaugh of Marion, Wisconsin, and associate judge Phillip Topp of Botkins, Ohio placed a total of 343 animals in the 2021 International Brown Swiss Show.

Complete class results can be found atworlddairyexpo.com.

Serving as the meeting place of the global dairy industry, World Dairy Expo brings together the latest in dairy innovation and the best cattle in North America. The dairy industry will return to Madison, Wis. for the 54thevent, September 28 October 2, 2021, when the worlds largest dairy-focused trade show, dairy and forage seminars, world-class dairy cattle show and more will be on display. Download the World Dairy Expo mobile event app, visitworlddairyexpo.comor follow WDE onFacebook,Twitter,LinkedIn,Spotify,InstagramorYouTubefor more information.

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Wisconsin Dairy Expo: Faye and Faroh finish first at the International Brown Swiss Show - Wisbusiness.com

‘We’re Angry’: Medical Journal Apologizes for Referring to Biological Women with Trans-Inclusive Phrase – CBN News

The editor of a leading medical journal has apologized in the wake of outrage stemming from a recent cover of the publication referring to biological women as bodies with vaginas.

In the latest issue of The Lancet, the British-based journal featured a quote on the front cover from a peer-reviewed piece on the anatomy and physiology of bodies with vagina.

Richard Horton, editor-in-chief of the journal,issued a statementthis week in response to the backlash the publication faced for the terminology.

[W]e have conveyed the impression that we have dehumanized and marginalized women, he said. [I] apologize to our readers who were offended by the cover quote and the use of those same words in the review. At the same time, I want to emphasize that transgender health is an important dimension of modern health care, but one that remains neglected.

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Horton defended the article by stating the article in question calls for greater efforts to overcome the lack of knowledge and stigma too often associated with menstruation.

These are serious issues that demand serious actions, he explained. We encourage people to read the full review and support a growing movement against menstrual shame and period poverty.

Critics saw the terminology as demeaning and an erasure of the female experience.

David Curtis, an honorary professor of genetics, evolution, and environment at University College London,arguedits difficult to imagine why any medical researcher would want to submit their paper to The Lancet journal when they are happy to refer to women on their front cover with language which would be considered inappropriate even in a red light district.

Another critic, Claire Heuchan, an author who describes herself as a black radical feminist,condemned the characterizationas sexist and hypocritical, noting The Lancet has not referred to biological males as bodies with penises.

This framing makes it sound like a coincidence that bodies with vaginas have been neglected medicine, as if it were not the product of a discrimination and oppression specific to the female sex, she wrote. Medical misogyny exists and refusing to acknowledge women perpetuates it.

Dr. Jane Clare Jones, who classifies herself as a philosopher and a feminist, took issue with Hortons apology,writingshe is not offended, as the editor suggested.

Were angry with your colluding with the political erasure of women, she explained. Especially in a context when you are supposed to be rectifying that historic erasure.

The dustup over The Lancets description of women came the same week people on social media rebuked the left-leaning American Civil Liberties Unionfor censoring a pro-abortion quoteby the late U.S. Supreme Court Justice Ruth Bader Ginsburg.

In 1993, as part of her written responses to questions submitted during her Senate confirmation hearing, Ginsburg wrote: The decision whether or not to bear a child is central to a womans life, to her well-being and dignity. It is a decision she must make for herself. When government controls that decision for her, she is being treated as less than a fully adult human responsible for her own choices.

The ACLU, however, edited her quote to be more trans-inclusive by removing any reference to women or female pronouns.

***As the number of voices facing big-tech censorship continues to grow, please sign up forFaithwires daily newsletterand download theCBN News appto stay up-to-date with the latest news from a distinctly Christian perspective.***

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'We're Angry': Medical Journal Apologizes for Referring to Biological Women with Trans-Inclusive Phrase - CBN News

The 2021 winners: Cool Science Image Contest – University of Wisconsin-Madison

Ten images and two videos created by University of WisconsinMadison students, faculty and staff have been named winners of the 2021 Cool Science Image Contest.

A panel of nine experienced artists, scientists and science communicators judged the scientific content and aesthetic and creative qualities of scores of images and videos entered in the 11th annual competition. The winning entries showcase animals and plants, the invisibly small structures all around us, and stars and nebulae millions of millions of miles away.

An exhibit featuring the winners is open to the public at the McPherson Eye Research Institutes Mandelbaum and Albert Family Vision Gallery on the ninth floor of the Wisconsin Institutes for Medical Research, 111 Highland Ave., through December. A reception open to the public for the contest entrants will be held at the gallery on Oct. 7 from 4:30 to 6:30 p.m.

Winning submissions were created with point-and-shoot digital cameras, cutting-edge microscopes, and telescopes of both the backyard and mountaintop variety.

Because sometimes, theres no substitute for the visual.

An image often can convey meaning more effectively than words, says Ahna Skop, a longtime contest judge, artist and UWMadison professor of genetics and active ambassador for science. We know from marketing and education research that adding a picture with words to a slide increases retention of knowledge by 65 percent. The visual communication of science is critical for the transference of knowledge broadly.

Story continues after gallery

1 A winterover one of the two staff members who stay through the minus-100-degree Fahrenheit nights of Antarcticas coldest months hikes underneath the stars and aurora to the South Pole home of IceCube, a UWMadison-led neutrino telescope frozen in a cubic kilometer of ice.

Yuya Makino,assistant scientist, IceCube Neutrino Observatorydigital camera

2 The large holes in this cross-section of a stalk of desert stringybark, Eucalyptus arenacea, are conduits through the plant tissue that help researchers quantify the way the plant native to dry parts of Australia adapts to a new, wetter environment.

Kennah Konrad,undergraduate student, Botany;Duncan Smith,graduate student, Botanycompound microscope

3 Fluorescent antibodies highlight the extensive nervous system of a mouse heart. By creating maps of cardiac nerves with unprecedented accuracy, researchers can explore how those nerves influence heart function.

Rebecca Salamon,graduate student, Cell and Regenerative Biologyconfocal microscope

4 Messier 42, known as the Orion Nebula, is in the sword of the constellation Orion and is one of the brightest nebulae in the sky. At just 1,400 light-years away and 24 light-years across, it is one of the closest and largest regions of dense gas and dust in which stars are formed.

Jeffrey E. Shokler,associate director, Office of Undergraduate Advisingrefractor telescope and CCD camera

5 The carnivorous sundew plant snags insect meals with armloads of tentacles that it can move to tighten its grip and bog down prey in sticky secretions. The leaves roll up around a meal to facilitate digestion by enzymes and absorption of the nutrients.

Nisha Iyer,postdoctoral fellow, Wisconsin Institute for Discoverydigital camera

6 Mazes of tiny structures less than 15 billionths of a meter across and made of some of the smallest ribbons of graphene layers of carbon just a single atom thick ever fabricated represent an important step toward graphene-based telecommunications devices.

Joel Siegel and Margaret Fortman,graduate students, Physics;Jian Sun,graduate student, Materials Science;Jonathan Dwyer,PhD alumnus, Chemical Engineeringscanning electron microscope

7 A pair of mating dragonflies pause on the surface of a Minnesota pond. Dragonfly coupling begins with the male (with blue markings) gripping the female with claspers at the very end of his abdomen. To complete the act, the female will bend her abdomen underneath her body to meet the males abdomen and create a characteristic heart shape.

Shin-Tsz (Lucy) Kuoundergraduate student, Computer Science and Economicsdigital camera

8 White matter, the connective nerve tissue of the brain, has been colored according to the predominant orientation of fibers red, right-left; green, front-back; blue, up-down in different regions of the human brain to reveal pathways traversing the regions. Understanding white matter organization may offer insights into normal brain development as well as into the study of neurological disorders.

Jose Guerrero,postdoctoral fellow, Medical Physics;Andrew Alexander,professor, Medical Physics;Peter Ferrazzanoprofessor, Pediatricsmagnetic resonance imaging scanner

9 The yellow connecting arms, called axons, of diseased human brain cells grow willy-nilly across boundaries of inhibitory chemicals (the red stripes). Healthy axons would precisely follow the dark lanes, giving researchers the opportunity to test the effects of disease-causing mutations on axon growth.

Timothy Catlettgraduate student, Cell and Molecular Biology;Timothy Gomez,professor, Neuroscienceconfocal microscope

10 By varying the exact size and shape of these micrometer-wide, star-shaped pillars etched into a silicon wafer, researchers can carefully manipulate light passing through a lens to correct for aberrations that would otherwise focus different wavelengths of light on different points in space.

Gregory Holdman,graduate student, Physicsfocused ion beam and scanning electron microscope

Recurrent neural networks are the computing engines behind state-of-the-art applications from self-driving cars to speech recognition like Amazons Alexa. The behavior of these networks is challenging to characterize, but it can be visualized for small networks. This video displays the behavior of a network with just three neurons, showing the way their output evolves by mapping their values in blue. The result, a fractal structure called a strange attractor, could help researchers better understand the behavior and characteristics of these kinds of networks.

David J. Nowak, alumnus and auditing student; Robert D. Nowak, professor, Electrical and Computer Engineering

Captured at 20,000 frames per second, this video shows the shock-wave-induced mixture of two gasses raw imagery on the left; adjusted to better reflect concentration of the lighter gas on the right. Experiments like this are run in the 9-meter-tall Wisconsin Shock Tube, depicted at left, to simulate and explore mixing at the interface of materials in extreme conditions like nuclear fusion, supernovae and hypersonic propulsion.

Josh Herzog, postdoctoral fellow, and Professor David Rothamer, both of Mechanical Engineering; Riccardo Bonazza, professsor, Engineering Physics

Continued from above gallery

There can be an ineffable sort of something that makes a particularly effective science image its the Cool in Cool Science Image Contest but the good ones have much in common.

Youll know it when you see it. Its like seeing Starry Night or the Mona Lisa for the first time, in person. They hit you deep and quickly, Skop says. They are beautiful to the eye, simple, and convey meaning. Some images just take your breath away.Looking deeper they exquisitely communicate the secrets of science beautifully.

The Cool Science Image Contest recognizes the technical and creative skills required to capture images or videos that capably reveal something about science or nature while also leaving an impression with their beauty or ability to induce wonder. The contest is sponsored by Madisons Promega Corp., with additional support from the UWMadison Division of the Arts.

Winning entries are shared widely on UWMadison websites, and all entries are showcased at campus science outreach events and in academic and lab facilities around campus throughout the year. Because there was no opportunity to show off the 2020 contest winners in-person, this years exhibit is a double-feature for both the 2020 and 2021 contests. See last years winners.

The contest judges were:

Steve Ackerman, professor of atmospheric and oceanic sciences and vice chancellor for research and graduate education

Terry Devitt, emeritus director of research communications, University Communications

Kevin Eliceiri, director, Laboratory for Optical and Computational Instrumentation

Michael King, visual communications specialist, College of Agricultural and Life Sciences

Steve Paddock, former scientist, Molecular Biology

Kara Rogers, science writer and editor, Encyclopedia Britannica

Ahna Skop, professor of genetics

Kelly Tyrrell, director of research communications, University Communications

Craig Wild, videographer, University Communications

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The 2021 winners: Cool Science Image Contest - University of Wisconsin-Madison

Bear incidents are rising in the North Bay. Biologists sent in a wildlife tracker to find out why – San Francisco Chronicle

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Meghan Walla-Murphy stooped to examine a twisted pile of dried poop, obscured by golden grass on an arid ridge in eastern Napa County. It may have belonged to one of the feral pigs that run rampant in the area. Or it may have been evidence of black bears, whose presence in Wine Country appears to be on the rise.

Walla-Murphy picked it up for a closer look.

No undigested identifiers, she said. Probably pig. She set it down and kept hiking.

Walla-Murphy, 46, is an ecological consultant and wildlife tracker who lives in western Sonoma County. Two years ago, she started the North Bay Bear Collaborative, an effort to bring together state wildlife experts, land managers, property owners, nonprofits, tribes and researchers for discussions about cultivating a bear culture in California.

On a recent survey near Atlas Peak in Napa County, Walla-Murphy and a pair of volunteers found 13 signs of bear scat and claw marks on the trunk of an oak.

Volunteer Alan Studley holds what appears to be a charred deer skull found in the slopes of Foss Valley.

The bears are here in the North Bay now, Walla-Murphy said. So, how do we figure out how to live with them?

Incidents involving black bears are escalating in the mountainous areas of Napa, Sonoma and Marin counties, and state wildlife biologists want to know why. Nuisance reports have jumped from an average of about 67 per year from 2010 to 2016 to more than 200 last year and upward of 200 so far this year, according to the California Department of Fish and Wildlife.

Sightings reported to the department have also climbed significantly in the past decade. One of the creatures was even spotted two years ago sauntering through downtown Napa highly unusual behavior.

A running theory is that the rise signals the southern expansion of a large black bear population in Mendocino and Humboldt counties, which could portend more bear-human encounters to come in the greater Bay Area.

If the bears are getting pushed toward the Bay Area, thats their southern limit. Theres real potential for human-wildlife conflicts, said Stacy Martinelli, a wildlife biologist at Fish and Wildlife. Were trying to understand whats going on, so we can make some management decisions before that happens.

Ecological consultant Meghan Walla-Murphy (left) of Sonoma County leads volunteers on a hunt for bear scat in the hills above Foss Valley in Napa County.

First, they need to know how many bears are roaming around.

In decades past, wildlife managers divined population estimates from the number of unique bear teeth provided by hunters and aerial surveys via helicopter crude, imperfect tactics at best. Estimates from Fish and Wildlife put the state black bear population at 30,000 to 40,000 in 2016, up from 10,000 to 15,000 in 1992. Activity around Lake Tahoe, the unofficial black bear capital of California where the animals live about one per square kilometer, is fairly well documented, but its a mystery most everywhere else.

We really dont know as much as we should know about whats happening with bears in different places around the state, Martinelli said.

In the past two years, Fish and Wildlife has embarked on a study that uses genotyping to identify and sex individual black bears in the North Bay by their DNA. Its a relatively new and much less disruptive method that has helped the state more accurately monitor populations of deer, elk and the Sierra Nevada red fox, which was recently listed as an endangered species.

State biologists hope to eventually track bears movements and plot their home ranges as well, which could help the North Bays rural residents better prepare to coexist with their furry new neighbors. Bears have been known to show up at vineyards this time of year to munch ripe grapes off the vine and suck down water from irrigation ponds.

This approach hinges, in part, on the expertise of Walla-Murphy and participation from the bear collaboratives volunteers: The biologists need DNA samples, and the best way to get them is by finding bear excrement. Another way to gather DNA is by setting out hair snares in bear territory designed to snag fur from the animals. But that involves the labor-intensive process of lugging bales of barbwire into remote areas.

Meghan Walla-Murphy hikes into Foss Valley in Napa County during a recent scat survey.

For the past year, Walla-Murphy has orchestrated volunteer surveys in Sonoma, Napa and Marin, and collected hundreds of scat specimens. The samples are processed at UC Davis and logged into a growing database of individuals with identifiers such as Sonoma Female 1 as well as their locations. The more samples Walla-Murphy and her revolving group of volunteers collect, the clearer the picture of bear activity becomes.

With a robust flow of these data points, we can study reproductions, survival, their space use and if theyre concentrating, say, near places where people are leaving their trash out, said Ben Sacks, a UC Davis professor of mammalian genetics who is handling the DNA analysis. There is tremendous potential for these noninvasive genetic methods and a lot of untapped applications.

A deeper dive into the scat specimens could illuminate the bears diets and show whether a given female is pregnant, Sacks said. But thats beyond the scope of the current study. For now, the goal is to get an accurate count and a snapshot of where theyre ranging.

Several factors could be pushing more black bears south toward the Bay Area: drought, food shortages, wildfires or just steady growth of a healthy population.

Usually its not one reason, its multiple reasons, Martinelli said.

Back on the scat hunt in Napa, Walla-Murphy led two volunteers across a ridgeline above Foss Valley, a narrow avenue largely given over to grape-growing, which partially burned in the Glass Fire last year. Amid the blackened landscape, new plant life was emerging: Wildflowers blossomed, and bright, leafy tufts of oak resprouted from charred root crowns.

Walla-Murphy has surveyed this area for years and noticed that the fire didnt chase away the bears for long, like one might have assumed. The animals were present before the fire and returned almost immediately afterward.

Wildlife tracker Meghan Walla-Murphy (second from right) and two volunteers look across vineyards in Napa Countys Foss Valley. The North Bays black bear population is growing.

The fires are often creating more food forage-ability for bears, Walla-Murphy said. We see deer and foxes and bobcats come back right away as well. The animals know how to live with fire.

Within that simple observation is an insight Walla-Murphy hopes will steer the direction of bear management in California: A more natural landscape supports more natural animal behavior, which makes living with wildlife easier for humans.

If we can really begin to steward and tend our landscapes better so that theres more diversity and theyre regenerative and they have more forage for wildlife, that ideally will keep the bears in their natural habitat rather than pushing them into cities for food, she said.

Gregory Thomas is The San Francisco Chronicles editor of lifestyle a outdoors. Email: gthomas@sfchronicle.com Twitter: @GregRThomas

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Bear incidents are rising in the North Bay. Biologists sent in a wildlife tracker to find out why - San Francisco Chronicle

Pune-based J K Trust to soon attain 100 IVF pregnancies from Gir cow Samadhi – The Indian Express

Samadhi, a cow, is likely to become the proud mother of 100 calves with the application of in-vitro fertilisation. At Phaltan in Satara district, farmer Dayaram Thengil, is overjoyed that eight surrogate cows from his herd, are carrying the pregnancies through IVF of Samadhi, a Gir cow.

Dr Shyam Zawar, chief scientist at J K Trust a city-based NGO working in the field of animal husbandry, which has set up a state-of-the-art in-vitro fertilisation-embryo transfer laboratory at Vadgaon Rasai told The Indian Express that a cow in its lifespan of 15-16 years will give birth to a maximum of 8-10 calves. Our lab was set up in 2016 to produce IVF embryos from elite indigenous cows such as Gir and Sahiwal, Zawar said. The cattle IVF and ET technology, which is being widely used around the world, can be customised and adapted to suit Indian climatic conditions, Zawar said.

The Trust has succeeded in establishing 74 IVF pregnancies from Samadhi in just 12 months and plans to reach 100 IVF pregnancies in the next two months.

Of these 74 IVF pregnancies, 30 IVF calves have already taken birth at various farms across the country, including Pune, Ahmednagar and Satara districts.

Of the 10 recipient cows, eight are confirmed pregnant and they are about to calve in a weeks time. The semen used for IVF was that of the famous Brazilian Gir bull namely Espanto, Zawar told The Indian Express.

Stay updated with the latest Pune news. Follow Express Pune on Twitter here and on Facebook here. You can also join our Express Pune Telegram channel here.

Dayaram, too, said he was amazed when eight of his cows were confirmed pregnant in such a short time. IVF is a reproductive technique where matured eggs are harvested from a female and fertilised with sperm in a laboratory. The fertilised egg is planted in the body of the female animal after 6-7 days when cell division starts. The embryo develops normally after its gestation period.

IVF is mostly used in bovine animals to plant an embryo of superior genetics into a surrogate mother. After the normal gestation period of nine months, the calves that are reared have the traits of the original mother and father. Normally, in such cases, the egg is harvested from an animal with proven milk yielding capacity and crossed with the sperm of a male whose mother has well documented genetics. Once fertilised, the zygote is planted in the womb of the surrogate mother, whose qualities the calf does not inherit.

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Pune-based J K Trust to soon attain 100 IVF pregnancies from Gir cow Samadhi - The Indian Express

Israeli group to research link between menstrual changes and COVID vaccines – Haaretz

A little over a week after S., 34, received her second vaccination against COVID, at a time when she was menstruating, she was surprised to discover that she had begun menstruating again.

It was strange because my period is as regular as a Swiss watch. At first, I didnt give it any thought, but two weeks later I got my period again for seven days. Two weeks after that, bleeding that lasted four days. It turned out that for almost six months there were more days when I bled than when I didnt. After I talked to my friends, I realized the phenomenon is much more widespread, she said.

Growing evidence from Israel and abroad is showing that the phenomenon extends much beyond S.s social circle. In February, shortly after women of childbearing age began receiving the second shot, many of them posted on social media that they were experiencing changes in their menstruation shortly after the shot, such as irregularity and increased bleeding. Other women reported that they had begun bleeding years after menopause.

The medical establishment could not explain the phenomenon or associate it with the vaccination, among other things because irregular menstruation is common and influenced by many factors. It is usually not considered exceptional. However, the mounting complaints and increased concern women were showing over taking the shots due to the phenomenon, has spurred the medical community to look into the matter. Preliminary research has been published in Britain and the United States, and the U.S. government has allocated $1.67 million for research on the subject.

Prof. Roni Maimon, chairman of the Israel Society of Obstetrics and Gynecology, is moving ahead on the first Israeli study of the subject. In terms of biochemistry and endocrinology, we havent found a connection between disruption of menstruation and the vaccination. However, because we live in an age of evidence-based medicine, we decided to look into the phenomenon among a large number of women in Israel, he said. The exact number of women who will participate in the study is not yet decided.

The Health Ministry said it doesnt have exact data on the extent of the phenomenon in Israel. It has received reports, but because the condition is common and does not require hospitalization, there is no way to know how common it was in the population [before the vaccinations] and whether it is now more common. The ministry said similar reports have been received by major healthcare agencies abroad, and that the phenomena appear to be temporary and carry no risk.

The issue has become a topic of discussion on social media in terms of whether to take the third shot. For example, on the Facebook page Medicine for Women in Israel, one woman wrote: The two first shots brought on my period early, and six months later I began to experience bleeding between periods and irregular periods, and at the moment they cant figure out why Im very undecided about the booster.

The matter has also raised concerns aboutpossible damage to fertility. As H., 39, told Haaretz: After the first and second shots I had some irregularities in my period . The doctor explained that its because the immunological system is connected to the hormonal system, and its not really dangerous. However, H. added, In June, I started trying to get pregnant by artificial insemination. When they started talking about the booster, I was in the middle of hormone treatment. I asked the doctor whether to get the booster, and he said he didnt recommend it, that if I got pregnant, I should take it only after they see a heartbeat. When the insemination didnt work, I took got the booster.

Based on the data that has been collected, the theory is that the symptoms are connected to the vaccination but that they apparently do not stem directly from a specific vaccination. Experts believe this is the immune systems response to various vaccinations, including those not based on mRNA, like those of Pfizer and Moderna.

Dr. Ido Solt, head of Maternal Fetal Medicine at Rambam Health Care Campus in Haifa, said that although the phenomenon is connected to vaccination, it is apparently insignificant because it appears with Pfizer, Moderna and other vaccinations even though they use a different method of immunization. The theory is that this is not about a specific component of the vaccine, but rather another manifestation of an immunological response, he said.

Solt added that the papillomavirus vaccine is also known to cause menstrual irregularity. At present, women of childbearing age who contracted COVID reported phenomena of this type, Solt said.

In light of this, the treatment policy is that if the changes go one for more than two or three periods, or if a woman in menopause begins to menstruate, the case is treated as if she had not been vaccinated, Solt explained.

Its true that the vaccination impacts menstruation and can cause bleeding, but there is no evidence that this harms menstruation or fertility, Solt added. He said the symptoms had been compared to occurrences in the general population and in clinics and no negative effect had observed.

Conclusions so far

In Britain, health care authorities and researchers have said that data collection in a published study was based on voluntary reporting by women, which makes it difficult to reach definitive conclusions. Different research approaches need to be used to examine the differences between vaccinated and unvaccinated women with these symptoms.

The study, published about two weeks ago in the medical journal BMJ examined more than 30,000 reports of women with irregular menstrual symptoms from the beginning of the vaccination drive and until September 2. Most of the women who reported irregularities said things returned to normal by their next period, according to the researchers, who are from the Imperial College School of Medicine and Westminster Hospital. Unplanned pregnancies occurred at similar rates among vaccinated and unvaccinated women, and pregnancy rates at fertility clinics were similar in vaccinated and unvaccinated women.

The research indicated that the symptoms appeared among women vaccinated with vaccines using different means of immunization. The study concluded that if there is a connection between vaccination and menstruation, it is not due to a specific component in the vaccine.

In response to the study, Dr. Joe Mountfield, vice chancellor of the Royal College of Obstetrics and Gynecology, was quoted as saying there is no proof that the temporary changes would impact a womans future fertility. He recommended that taking the vaccination was important especially if a woman was planning to get pregnant, because of the higher risk pregnant women run of contracting COVID.

The Israeli Fertility Association will be holdings its annual conference on Monday, at which the impact of the vaccination on male and female fertility will be discussed. Dr. Talia Eldar-Geva, head of endocrinology and genetics at Shaare Zedek Medical Center and a former head of the association said, There is still no work dealing with long-term effects on fertility, but in the short term, there is no difference in response to fertility treatments, the number of eggs or the quality of the fetuses among men and women who have been vaccinated.

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Israeli group to research link between menstrual changes and COVID vaccines - Haaretz

NIH awards Brown $10.8M to expand data-informed research to fight human disease – Brown University

PROVIDENCE, R.I. [Brown University] Five years after an $11.5 million federal grant launched the COBRE Center for Computational Biology of Human Disease at Brown University, the National Institutes of Health has awarded $10.8M in new funds to Brown to build on the centers early success.

The center a federal Center of Biomedical Research Excellence funded by the NIHs National Institute of General Medical Sciences uses sophisticated computer analyses to advance research aimed at understanding and fighting human diseases.

Director David Rand, a professor of biology at Brown, said the renewal funds will enhance the centers research infrastructure, enable strengthened collaboration among scientists working with computational and bioinformatics tools, and support four new research projects. Rand said there is a computational revolution happening in the biomedical sciences, as researchers need computational analyses to help them make sense of massive amounts of available data.

Even those working in wet labs or clinics who dont use computers in their daily work will at some point need assistance in analyzing complex data sets, he said.

Rand compared the current moment to the molecular biology revolution thats been changing science since the 1970s, when DNA cloning and sequencing became standard tools used by researchers across diverse fields. Computational analysis is bringing groups together today in a similar way, he said. For example, people working in engineering, computer science, basic biology and medicine will face situations where they need to convert data sets into information that can help them find solutions and answer questions. While their research projects are highly distinct, he said, the data analysis work shares common themes.

In addition to helping researchers with individual projects, we view the Center for Computational Biology of Human Disease as a vehicle for raising the level of computational ability for researchers in the community overall, Rand said.

To provide that service to COBRE project leaders and researchers across Brown, the center is home to a Computational Biology Core a group of four scientists, data analysts and software engineers who support data-intensive research. With the renewal grant, center leaders will work to build sustainable support for the group through continued funding to its scientists and support to ensure that four members are at the Ph.D.-level (past budget included support for two Ph.D.s and two masters-level scientists).

Everyone has large data sets and needs to convert these into useful information, and we aim to help people achieve that goal, Rand said. The center brings together researchers in the lab and clinic with exceptionally skilled and creative data scientists to turn data into information.

Funds from the grant will also support the research of junior faculty investigators and help position them to earn additional, longer-term funding for their work enabling them, Rand said, to build upon discoveries and continue their research while freeing up center funds to seed innovative new projects. With the initial $11.5 million from the NIH in the centers first phase, faculty projects at the Center for Computational Biology of Human Disease generated an additional $17.9 million in grants in areas of research such as human genomics, immunology and infectious disease, microbiome and machine learning approaches to complex genetics.

Read more:
NIH awards Brown $10.8M to expand data-informed research to fight human disease - Brown University

Genetic mapping of subsets of patients with fragile X syndro | TACG – Dove Medical Press

Introduction

Fragile X syndrome (FXS), OMIM # 300624, is a X-linked inherited genetic disease classified as a triplet repeat condition. FXS is the most common cause of inherited intellectual disability and autism in the world. It has a prevalence of 1 in 5000 men and 1 in 8000 women. Affected individuals are characterized by intellectual disability, autism, language deficit, typical facies, and macroorchidism.1,2

Alterations in the FMR1 gene with locus Xq27.3 are causative of Fragile X Syndrome and other disorders. This gene harbors a CGG repeat within the 5 untranslated region and, depending on the number of repetitions, 4 types of alleles are defined with different clinical manifestations:3 Normal alleles, which have up to 44 CGG repeats; grey zone or intermediate alleles that contain between 45 and 54 repeats; premutation (PM) alleles with between 55 and 200 repeats; and full mutation (FM) alleles, with more than 200 repeats. In most cases, this is due to an expansion of the CGG triplet from one generation to the next.4

The Fragile Mental Retardation Protein (FMRP) is coded by the FMR1 gene. The absence of FMRP expression is usually secondary to the methylation of the FMR1 gene that occurs when more than 200 CGG repeats are present in the 5UTR region; this can also be explained by a point mutation in the coding region for FMR1 or a deletion that includes this gene, but these changes have only been reported in a few cases. The absence of FMRP is related to the classic FXS phenotype.5,6

FMRP expression is slightly lower in the carriers of a PM allele. Lower levels of FMRP are found particularly in the upper premutation (PM) range however, they typically do not present the classic FXS syndrome phenotype.7 Furthermore, they have elevated FMR1 mRNA levels between 2 to 8 times normal levels, which also leads to RNA toxicity. These elevated levels of mRNA are a risk for a number of medical conditions that are not explained by decreased FMRP.2,4,8

FMRP has roles in chromatin dynamics, RNA binding, mRNA transport, and mRNA translation9,10 and for certain subgroups of cerebral transcripts.11

This protein is involved in the regulation of RNA stability, subcellular transport and translation of neural mRNAs that codify proteins involved in synapsis development, neural plasticity and brain development.8

In addition, FMRP interacts with at least 180 proteins expressed in the brain and connective tissue. This interactome comprises known FMRP-binding proteins, including the ribosomal proteins FXR1P, NUFIP2, Caprin-1, and other novel FMRP-interacting candidate proteins located in different subcellular compartments, including CARF, LARP1, LEO1, NOG2, G3BP1, NONO, NPM1, SKIP, SND1, SQSTM1 and TRIM28. This interactome suggests that, besides its known functions, FMRP is involved in transcription, RNA metabolism, ribonucleoprotein stress granule formation, translation, DNA damage response, chromatin dynamics, cell cycle regulation, ribosome biogenesis, miRNA biogenesis and mitochondrial organization.9

Several studies have shown that in the absence of FMRP, a wide range of neural mRNAs are affected, boosting neural protein synthesis, which results in dendritic spine dysmorphogenesis and glutamate/GABA imbalance, which in turn produce variations in neural excitation/inhibition, phenomena that are present in FXS. Dendritic spine dysmorphogenesis plays a role in the intellectual deficits and behavioral problems, due to the weak synaptic connections found in this syndrome.12,13

Fragile X syndrome (FXS) has incomplete penetrance and variable expressivity and biological sex is a decisive factor of the phenotype. Full mutation of the FMR1 gene has a 100% penetrance of intellectual disability in males and 60% in females. Other characteristics associated with FXS Appear with varying frequencies in affected individuals. Autism spectrum disorder (ASD) symptoms appear during early childhood in 50% to 60% of males and 20% of females with FXS.1417

Physical features include elongated face, large and prominent ears (7578% of affected males), mandibular prognathism (80% of adult men), hyperlaxity and macroorchidism (95% of adult men). Other characteristics also vary in their frequency of presentation: seizures (23%), strabismus (8%), and cardiac abnormalities such as abnormal aortic root dimensions (18%) and mitral valve prolapse (55%). In general, the female phenotype is less severe and less specific.4,18

The variation in the phenotype of monogenic diseases is common,19,20 it is explained by a combination of genetic, environmental, and lifestyle factors,21 and FXS is not an exception.

Here, we present a review of the knowledge about the molecular factors involved in the variable expressivity of FXS.

The presence of a full mutation in FMR1 is associated with the hypermethylation of a CpG island located in the promoter of the FMR1 gene. Methylation of DNA regions (mDNA) is one of the main epigenetic modifications related to transcription regulation.22 A CpG island is located proximal to the CGG repeat tract, which is expanded in FXS. Hypermethylation of the CpG island generates transcriptional silencing of the FMR1 gene.23 As a consequence, the Fragile Mental Retardation Protein (FMRP), codified by the FMR1 gene, is not produced24 and in turn, the absence or low expression of FMRP causes FXS.

CGG tract repetition expansion in the untranslated region (UTR) of exon 1 in the FMR1 gene generates instability of that region during the replication process, inducing size mosaicism, which is defined as the presence of premutation and mutation alleles in several cells.25

In males with FXS caused by full mutation, the detection of FMR1 mRNA levels in peripheral blood lymphocytes is common. This phenomenon is due to both size mosaicism and mDNA in the CpG island and nearby regions that vary between cells and tissues.26 Furthermore, longitudinal studies in women with FXS have shown that levels of mRNA transcribed from FMR1 decrease significantly with age.23 Complicating even more the behavior of mDNA and FXS, it has been found that in premutation alleles, a considerable number of cells have mDNA.27 The variation between methylation states of the CpG island and nearby regions among different cells and tissue of the same person is known as methylation mosaicism.28 It is estimated that around 50% of people with FXS have this type of mosaicism.29 In cells where mutated alleles are not methylated, they are transcriptionally active and can be expressed.30 However, in these cells there is no FMRP synthesis since mRNA with CGG expansion greater than 200 repeats is not translated efficiently in ribosomes.31,32

The absence or low levels of FMRP is a decisive factor for FXS development, as several studies have aimed to discover the relationship between protein levels and phenotypic characteristics of the patients. Since the late 1990s, correlations between FMRP levels and the neurological phenotype of FXS have been established.29,33,34 The first studies about this topic established the standard levels of FMRP in peripheral blood leucocytes through immunoblotting. When comparing protein levels with the allele type and the presence of size mosaicism, it was demonstrated that people with the lowest FMRP levels were males with FM. Males with size mosaicism and females with FM had slightly higher levels of FMRP than males with FM.33,35,36 Via multiple regression models, it was found that FMRP levels were significantly correlated with the intelligence quotient (IQ) of the patients in the study.33 However, studies did not identify the same relation between FMRP levels and behavioral symptoms.34,37 More recent evidence supports a partial overlap between the pathogenic mechanisms that lead to FXS and ASD.38 Lower FMRP levels have been documented in samples of individuals with FXS and ASD compared to patients with FXS only.29,34 The relation between FMRP levels and IQ in males and females with different expansions in CGG repeats was studied recently.39 This last study has two important advantages compared with previous studies: firstly, the use of fluorescence resonance energy transfer (FRET), which has a higher sensibility when measuring protein levels, and also FMRP levels were measured in dermal fibroblasts. Unlike leucocytes, fibroblasts derive from the ectoderm, the same germ layer from which nervous system cells originate. Researchers found a strong and positive relation between FMRP levels and cognitive skills in patients with levels below 30% of the standard levels in controls. Interestingly, above this level, there was a higher dependence between low FMRP levels and low IQ.39

In parallel with the aforementioned studies, researchers reported the incidence of size and methylation mosaicism in cognitive impairment severity.4042 The classic definition of premutation alleles behavior as non-methylated alleles, and mutated alleles as methylated or partially methylated ones in order to categorize premutation carriers and patients with FXS has been extended progressively to include a detailed classification that takes into account the existence of size and methylation mosaicisms.

Regarding size mosaicisms, different combinations have been described, including patients with some FM cells and other cells with PM. Indeed, patients with FM, PM, grey zone alleles and even alleles with normal size have been reported.40 The presence of size mosaicisms with PM and FM alleles is related with a less severe phenotype and a higher risk of developing fragile X-associated tremor/ataxia syndrome (FXTAS).43

When exploring the possible relation between size mosaicisms and the intellectual functioning of patients with FXS disregarding sex, it was found that patients with FM/PM had better intellectual functioning and less maladaptive behavior, compared with FM-affected individuals.42 Interestingly, the same study found that ASD features and maladaptive behaviors were similar between FM-only and PM/FM mosaics within each sex, after controlling for overall intellectual functioning. A limitation of this study is that they used venous blood and real time PCR and Southern blot analysis to quantify the level of methylation.

Recently, methylation mosaicism has been taken into account as an important variable in phenotype traits. The most frequent mosaicism found in males is the presence of FM-methylated alleles and non-methylated FM and PM alleles (combination of size and methylation mosaicism).25,44 However, in patients with FM and not PM mosaicisms, methylated alleles do not express mRNA, while non-methylated alleles do. An aspect that highlights the importance of detecting the presence of this kind of mosaicism is the influence on phenotype severity. Additionally, according to some case reports, the presence of synthesized mRNA from PM and FM alleles increases the odds of developing the FXTAS phenotype.45,46 The final consequence of methylation mosaicism is the cells reduced ability to express FMR1 mRNA, measure mRNA and determine if there is a relation with phenotypic traits. When analyzing mRNA levels between males and females, it was found that females had higher levels. Also, in females, higher levels of FMR1 mRNA were related positively with age but not with intellectual functioning and autistic features. Males with FM that express FMR1 mRNA had significantly higher ADOS calibrated severity scores, when compared with males with fully methylated FM. Interestingly, no differences were found regarding intellectual functioning.41 Likewise, when contrasting FMR1 mRNA levels and scores on the Aberrant Behavior Checklist-Community-FXS version (ABC-CfX) it was found that in males with FM, higher values of FMR1 mRNA were related with elevated irritability and lower health-related quality of life scores.47 This association was not found in males with PM/FM, suggesting that for improved genotype/phenotype associations, it is essential to take into consideration not only sex but also size and methylation mosaicism.

Recent investigations explored simultaneously how FMR1 mRNA levels of FMRP are related to phenotypic alterations in males with PM and FM.48 In a study composed of 14 cases of patients with PM or PM and FM mosaicism and mental illnesses such as bipolar disorder, schizophrenia and psychosis, among others, low levels of FMRP and increased FMR1 mRNA were evident in these patients. This combination of characteristics in patients with FM, decreased FMRP, PM and increased FMR1 mRNA represents a dual mechanism of clinical significance that may generate characteristics of both FXS and FXTAS.48 In a clinic-based ascertained group of patients with FXS of both gender, a significant difference was found between FXS with ASD and low levels of FMRP when comparing concentrations of the protein in patients with FXS without ASD.29 They found that the mean full scale IQ and adaptive skills composite scores were significantly lower in males than in females (p = 0.016 and p = 0.001, respectively, MannWhitney). Additionally, all individuals with moderate or severe ID were males. Not surprisingly, ASD was present more frequently in males with FXS (46% vs 20% females). This association was not found in males with PM/FM, suggesting that for improved genotype/phenotype associations is essential to take into consideration not only sex but size and methylation mosaicism.29

There is a small proportion of FXS patients without expansions in the CGG-repeat tract. In this group, the condition is caused by missense or nonsense mutations,5,16 or deletions in FMR1.1,6 Patients with these mutations have similar physical, cognitive and behavioral characteristics to FXS patients. With the increasing availability of diagnostic methods based on next-generation sequencing and comparative genomic hybridization, a higher rate of diagnosis of mutations causing FMR1 function loss is expected. This will allow a clear delimitation of the phenotype caused by the loss of the protein in the absence of CGG tract expansions.

For many monogenic diseases it is known that, besides the allelic variance, the effect of modifier genes has an important role in incomplete penetrance and variable expressivity. The identification of modifier genes that affect the phenotype in monogenic diseases has many challenges that complicate their description. A genetic variant can modify the effect in the phenotype of another variant in many ways, including epistasis and genetic interactions.49,50

In studies using FXS murine models, important new evidence was acquired in order to establish the importance of potential modifier genes and their impact on FXS phenotype development. The knockout mouse model for FXS was generated in the last decade of the XX century. Fmr1 KO mice had learning deficits, abnormal synaptic connections, seizures, hyperactivity and macroorchidism.51,52 When describing the mouse phenotype in detail, it was evident that abnormal phenotypic characteristics depend, at least in some proportion, on their genetic background.53

During the identification of modifier genes in the FXS phenotype, a large proportion of the research has aimed towards the susceptibility to developing certain clinical behavioral characteristics, such as aggression, ASD and seizures.34,5459 All of the studies use a similar methodological design: they arrange groups of people with or without a specific phenotypic trait and establish the frequency of specific variants in modifier gene candidates.

The possibility that Val66Met polymorphism in the brain-derived neurotrophic factor (BDNF) gene may modulate the epilepsy phenotype in FXS patients has also been investigated. The replacement of a methionine for a valine in the 66th position of the BDNF protein interferes with normal intracellular traffic and BDNF dependent secretory activity in cortical neurons.60 This polymorphism has been related to cerebral anatomy alterations61 and neuropsychiatric disorders.62,63 In a sample of 27 males with FXS from Finland, it was found that all the patients with epilepsy (15%) had the Met66 allele, whereas the prevalence of this allele is 20% in the normal population. Research suggests that the Met66 allele in BDNF interacting with FM in FMR1 may partially explain the higher incidence of seizures in patients with FXS.56 In a more recent study with a higher number of males with FXS (77 patients), the results were not replicated and there was no association between seizures and Val66Met polymorphism.58 These results show the importance of validating studies about modifier genes in different populations.

In research about genes that affect mood and aggression, such as the serotonin transporter (5-HTTLPR), the monoamine oxidase A (MAOA-VNTR) and COMT, conflicting results were found. All of those genes are involved in regulatory pathways for different neurotransmitters, and their variants have been associated with the development of behavioral phenotypes in different contexts other than FXS. In one group of 50 males with FXS, the relationship of 5-HTTLPR and MAOA-VNTR polymorphisms with the frequency/severity of aggressive/destructive, self-injurious and stereotypic behaviors was studied. It was found that the high-transcribing long (L/L) genotype in 5-HTTLPR was related with a higher frequency of aggressive/destructive and stereotypic behavior, while patients with the short (S/S) genotype had less aggression. The MAOA-VNTR genotype had no effect on behavior.55 On the other hand, in a study of 64 males with FXS where the COMT gene was also included, the results of the previous study were not replicated. There was no association between behavioral characteristics and either 5-HTTL PR (serotonin) or MAOA genotypes. Nevertheless, the A/A genotype in COMT that modifies dopamine levels was associated with greater interest and pleasure in the environment, and with less risk of property destruction, stereotyped behavior and compulsive behavior.54 The authors of the study suggest that the non-reproducibility of the results regarding MAOA-VNTR can be explained by differences in the prevalence of aggressive and stereotyped behavior among the studied populations or by differences in the measurements used to characterize each behavior.

The importance of identifying potential modifier genes was explored in a clinical trial. The researchers investigated the relation between polymorphisms in several genes and the response of sertraline in 51 children. They found that BDNF, MAOA, 5-HTTLPR, Cytochrome P450 2C19 and 2D6 polymorphisms had significant correlations with treatment response.64

Currently the knowledge about molecular causes of the variable phenotype in patients with FXS include characteristics associated with the FMR1 gene itself and to secondary, modifying gene effects.

Regarding FMR1, when the diagnosis is established, the type of mutation causing FXS is identified: CGG repeat tract expansion vs pathological variant causing loss of function in FMR1.

When the CGG is identified, is it expected that about half of the patients have size or methylation mosaicism or both.29 The presence of any of those mosaicisms determines the expression or not of FMR1 mRNA and FMRP. The quantity of FMRP is directly related with IQ.34,37,39 While the presence of size mosaicism is related with better intellectual functioning and less maladaptive behavior,29,42 elevated concentrations of FMR1 mRNA in patients with FM have been associated with a higher risk of developing FXTAS45,46,48 and with the severity of behavioral symptoms.47

The search for modifier genes affecting the phenotype has been carried out using the candidate genes strategy. Because high impact clinical manifestations in FXS are related with neurologic phenotypes, the studied candidate genes are involved in CNS development and the appearance of seizures (BNDF)56,6062 and associated with mood and aggression (5-HTTLPR, MAOA-VNTR y COMT).54,55 Recent research has been done with small groups of patients and there are no conclusive results about the importance of these variants in modifier genes.

Scientific and clinical evidence about molecular causes of variable expressivity in FXS is growing quickly. It is evident that aspects of the mutation type in FMR1 and the behavior of the CGG repeat tract are relevant in the presentation of the condition. Research about modifier genes is still emerging. There are important limitations such as sample size and comparability of different studies, mainly due to smaller groups of selected patients and the use of different tools for measuring the phenotypes.

Independent cohorts of patients with FXS across different continents have shown evidence that mosaicism, FMR1 mRNA or FMRP quantification are associated with the severity of the phenotype. However, this information cannot currently be used effectively in the integral management of patients. When intervention strategies become available in order to prevent the development of FXTAS, or when certain molecules can regulate levels of FMRP expression to measure FMR1 mRNA and FMRP, they could be crucial for selecting patients and identifying the best therapeutic intervention.

In clinical trials there is an important window of opportunity. Identifying mosaicism, measuring transcription/translation activity of FMR1 and stratifying patients by modifier genotypes29,65 will permit the identification of subgroups of patients with greater potential to respond to specific treatments.

The authors report no conflicts of interest in this work.

1. Coffee B, Keith K, Albizua I, et al. Incidence of Fragile X syndrome by newborn screening for methylated FMR1 DNA. Am J Hum Genet. 2009;85(4):503514. doi:10.1016/j.ajhg.2009.09.007

2. Saldarriaga W, Tassone F, Gonzlez-Teshima LY, Forero-Forero JV, Ayala-Zapata S. Fragile X Syndrome. Colomb Med. 2014;190198. doi:10.25100/cm.v45i4.1810

3. Bagni C, Tassone F, Neri G, Fragile HR. X syndrome: causes, diagnosis, mechanisms, and therapeutics. J Clin Invest. 2012;122(12):43144322. doi:10.1172/JCI63141

4. Salcedo-Arellano MJ, Dufour B, McLennan Y, Martinez-Cerdeno V, Hagerman R. Fragile X syndrome and associated disorders: clinical aspects and pathology. Neurobiol Dis. 2020;136:104740. doi:10.1016/j.nbd.2020.104740

5. Sitzmann AF, Hagelstrom RT, Tassone F, Hagerman RJ, Butler MG. Rare FMR1 gene mutations causing fragile X syndrome: a review. Am J Med Genet Part A. 2018;176(1):1118. doi:10.1002/ajmg.a.38504

6. Coffee B, Ikeda M, Budimirovic DB, Hjelm LN, Kaufmann WE, Warren ST. Mosaic FMR1 deletion causes fragile X syndrome and can lead to molecular misdiagnosis: a case report and review of the literature. Am J Med Genet Part A. 2008;146A(10):13581367. doi:10.1002/ajmg.a.32261

7. Tassanakijpanich N, Hagerman RJ, Worachotekamjorn J. Fragile X premutation and associated health conditions: a review. Clin Genet. 2021;99(6):751760. doi:10.1111/cge.13924

8. Hagerman RJ, Berry-Kravis E, Hazlett HC, et al. Fragile X syndrome. Nat Rev Dis Prim. 2017. doi:10.1038/nrdp.2017.65

9. Taha MS, Haghighi F, Stefanski A, et al. Novel FMRP interaction networks linked to cellular stress. FEBS J. 2021;288(3):837860. doi:10.1111/febs.15443

10. Siomi H, Siomi MC, Nussbaum RL, Dreyfuss G. The protein product of the fragile X gene, FMR1, has characteristics of an RNA-binding protein. Cell. 1993;74(2):291298. doi:10.1016/0092-8674(93)90420-U

11. Ashley CT Jr, Wilkinson KD, Reines D, Warren ST. FMR1 protein contains conserved RNP-family domains and demonstrates selective RNA binding. Science (80-). 1993;262(5133):563566. doi:10.1126/science.7692601

12. Bear MF, Huber KM, Warren ST. The mGluR theory of fragile X mental retardation. Trends Neurosci. 2004;27(7):370377. doi:10.1016/j.tins.2004.04.009

13. Gatto CL, Broadie K. Genetic controls balancing excitatory and inhibitory synaptogenesis in neurodevelopmental disorder models. Front Synaptic Neurosci. 2010. doi:10.3389/fnsyn.2010.00004

14. Budimirovic DB, Haas-Givler B, Blitz R, et al. Consensus of the fragile X clinical and research consortium on clinical practices: autism Spectrum Disorder in Fragile X Syndrome. 2014;115.

15. Budimirovic DB, Subramanian M. Neurobiology of Autism and Intellectual Disability: fragile X Syndrome. 2 ed. In: Johnston M, Adams H, Fatemi A, editors. London: Oxford University Press;2016.doi:10.1093/med/9780199937837.001.0001

16. Saldarriaga W, Payn-Gmez C, Gonzlez-Teshima LY, Rosa L, Tassone F, Hagerman RJ. Double genetic hit: fragile X syndrome and partial deletion of protein patched homolog 1 antisense as cause of severe autism spectrum disorder. J Dev Behav Pediatr. 2020;41(9):724728. doi:10.1097/DBP.0000000000000850

17. Sherman SL, Kidd SA, Riley C, et al. Forward: a registry and longitudinal clinical database to study fragile X syndrome. Pediatrics. 2017;139(Supplement 3):S183S193. doi:10.1542/peds.2016-1159E

18. Loehr JP, Synhorst DP, Wolfe RR, Hagerman RJ. Aortic root dilatation and mitral valve prolapse in the fragile X syndrome. Am J Med Genet. 1986;23(12):189194. doi:10.1002/ajmg.1320230113

19. Rahit KMTH, Tarailo-Graovac M. Genetic modifiers and rare mendelian disease. Genes (Basel). 2020;11(3):239. doi:10.3390/genes11030239

20. Li D, Yu J, Gu F, et al. The roles of two novel FBN1 gene mutations in the genotypephenotype correlations of marfan syndrome and ectopia lentis patients with marfanoid habitus. Genet Test. 2008;12(2):325330. doi:10.1089/gte.2008.0002

21. Fahed AC, Wang M, Homburger JR, et al. Polygenic background modifies penetrance of monogenic variants for tier 1 genomic conditions. Nat Commun. 2020;11(1). doi:10.1038/s41467-020-17374-3

22. Kim M, Costello J. DNA methylation: an epigenetic mark of cellular memory. Exp Mol Med. 2017;49(4):e322e322. doi:10.1038/emm.2017.10

23. Kraan CM, Baker EK, Arpone M, et al. Dna methylation at birth predicts intellectual functioning and autism features in children with fragile x syndrome. Int J Mol Sci. 2020;21(20):7735. doi:10.3390/ijms21207735

24. Pieretti M, Zhang F, Fu YH, et al. Absence of expression of the FMR-1 gene in fragile X syndrome. Cell. 1991;66(4):817822. doi:10.1016/0092-8674(91)90125-I

25. Nolin SL, Glicksman A, Houck GE, Brown WT, Dobkin CS. Mosaicism in fragile X affected males. Am J Med Genet. 1994;51(4):509512. doi:10.1002/ajmg.1320510444

26. Stger R, Genereux DP, Hagerman RJ, Hagerman PJ, Tassone F, Laird CD. Testing the FMR1 promoter for mosaicism in dna methylation among cpg sites, strands, and cells in FMR1-expressing males with fragile x syndrome. PLoS One. 2011;6(8):e23648. doi:10.1371/journal.pone.0023648

27. Pretto DI, Mendoza-Morales G, Lo J, et al. CGG allele size somatic mosaicism and methylation in FMR1 premutation alleles. J Med Genet. 2014;51(5):309318. doi:10.1136/jmedgenet-2013-102021

28. Jiraanont P, Kumar M, Tang H-T, et al. Size and methylation mosaicism in males with Fragile X syndrome. Expert Rev Mol Diagn. 2017;17(11):10231032. doi:10.1080/14737159.2017.1377612

29. Budimirovic DB, Schlageter A, Filipovic-Sadic S, et al. A genotype-phenotype study of high-resolution FMR1 nucleic acid and protein analyses in fragile X patients with neurobehavioral assessments. Brain Sci. 2020;10(10):694. doi:10.3390/brainsci10100694

30. Tassone F, Hagerman RJ, Loesch DZ, Lachiewicz A, Taylor AK, Hagerman PJ. Fragile X males with unmethylated, full mutation trinucleotide repeat expansions have elevated levels of FMR1 messenger RNA. Am J Med Genet. 2000;94(3):232236. doi:10.1002/1096-8628(20000918)94:3<232::aid-ajmg9>3.0.CO;2-H

31. Dolskiy AA, Yarushkin AA, Grishchenko IV, et al. miRNA expression and interaction with the 3UTR of FMR1 in FRAXopathy pathogenesis. Non-Coding RNA Res. 2021;6(1):17. doi:10.1016/j.ncrna.2020.11.006

32. Primerano B, Tassone F, Hagerman RJ, Hagerman P, Amaldi F, Bagni C. Reduced FMR1 mRNA translation efficiency in fragile X patients with premutations. RNA. 2002;8(12):14821488. doi:10.1017/S1355838202020642

33. Kaufmann WE, Abrams MT, Chen W, Reiss AL. Genotype, molecular phenotype, and cognitive phenotype: correlations in fragile X syndrome. Am J Med Genet. 1999. doi:10.1002/(SICI)1096-8628(19990402)83:4<286::aid-ajmg10>3.0.CO;2-H

34. Loesch DZ, Bui QM, Dissanayake C, et al. Molecular and cognitive predictors of the continuum of autistic behaviours in fragile X. Neurosci Biobehav Rev. 2007. doi:10.1016/j.neubiorev.2006.09.007

35. Backes M, Gen B, Schreck J, Doerfler W, Lehmkuhl G, Von Gontard A. Cognitive and behavioral profile of fragile X boys: correlations to molecular data. Am J Med Genet. 2000;95(2):150156. doi:10.1002/1096-8628(20001113)95:2<50::aid-ajmg11><50::aid-ajmg11>3.0.CO;2-1

36. Tassone F, Hagerman RJ, Ikl DN, et al. FMRP expression as a potential prognostic indicator in fragile X syndrome. Am J Med Genet. 1999;84(3):250261. doi:10.1002/(SICI)1096-8628(19990528)84:3<250::aid-ajmg17>3.0.CO;2-4

37. Hall S, DeBernardis M, Reiss A. Social escape behaviors in children with fragile X syndrome. J Autism Dev Disord. 2006;36(7):935947. doi:10.1007/s10803-006-0132-z

38. Bagni C, Zukin RS, Synaptic A. Perspective of Fragile X syndrome and autism spectrum disorders. Neuron. 2019. doi:10.1016/j.neuron.2019.02.041

39. Kim K, Hessl D, Randol JL, et al. Association between IQ and FMR1 protein (FMRP) across the spectrum of CGG repeat expansions. PLoS One. 2019;14(12):e0226811. doi:10.1371/journal.pone.0226811

40. Aliaga SM, Slater HR, Francis D, et al. Identification of males with cryptic fragile x alleles by methylation-Specific quantitative melt analysis. Clin Chem. 2016;62(2):343352. doi:10.1373/clinchem.2015.244681

41. Baker EK, Arpone M, Aliaga SM, et al. Incomplete silencing of full mutation alleles in males with fragile X syndrome is associated with autistic features. Mol Autism. 2019;10(1). doi:10.1186/s13229-019-0271-7

42. Baker EK, Arpone M, Vera SA, et al. Intellectual functioning and behavioural features associated with mosaicism in fragile X syndrome. J Neurodev Disord. 2019;11(1). doi:10.1186/s11689-019-9288-7

43. Kraan CM, Godler DE, Amor DJ. Epigenetics of fragile X syndrome and fragile X-related disorders. Dev Med Child Neurol. 2019;61(2):121127. doi:10.1111/dmcn.13985

44. Rousseau F, Heitz D, Biancalana V, et al. Direct diagnosis by DNA analysis of the fragile X syndrome of mental retardation. Obstet Gynecol Surv. 1992;47(5):306308. doi:10.1097/00006254-199205000-00008

45. Loesch DZ, Sherwell S, Kinsella G, et al. Fragile X-associated tremor/ataxia phenotype in a male carrier of unmethylated full mutation in the FMR1 gene. Clin Genet. 2012;82(1):8892. doi:10.1111/j.1399-0004.2011.01675.x

46. Santa Mara L, Pugin A, Alliende MA, et al. FXTAS in an unmethylated mosaic male with fragile X syndrome from Chile. Clin Genet. 2014;86(4):378382. doi:10.1111/cge.12278

47. Baker EK, Arpone M, Kraan C, et al. FMR1 mRNA from full mutation alleles is associated with ABC-CFX scores in males with fragile X syndrome. Sci Rep. 2020;10(1). doi:10.1038/s41598-020-68465-6

48. Schneider A, Winarni TI, Cabal-Herrera AM, et al. Elevated FMR1-mRNA and lowered FMRP a double-hit mechanism for psychiatric features in men with FMR1 premutations. Transl Psychiatry. 2020;10(1). doi:10.1038/s41398-020-00863-w

49. Dipple KM, McCabe ERB. Phenotypes of patients with Simple mendelian disorders are complex traits: thresholds, modifiers, and systems dynamics. Am J Hum Genet. 2000;66(6):17291735. doi:10.1086/302938

50. Schffer AA. Digenic inheritance in medical genetics. J Med Genet. 2013;50(10):641652. doi:10.1136/jmedgenet-2013-101713

51. Mineur YS, Sluyter F, De Wit S, Oostra BA, Crusio WE. Behavioral and neuroanatomical characterization of the Fmr1 knockout mouse. Hippocampus. 2002;12(1):3946. doi:10.1002/hipo.10005

52. Bakker CE, Verheij C; The Dutch-Belgian Fragile X Consorthium, et al. Fmr1 knockout mice: a model to study fragile X mental retardation. Cell. 1994. doi:10.1016/0092-8674(94)90569-X

53. Errijgers V, Kooy RF. Genetic modifiers in mice: the example of the fragile X mouse model. Cytogenet Genome Res. 2004;105(24):448454. doi:10.1159/000078218

54. Crawford H, Scerif G, Wilde L, et al. Genetic modifiers in rare disorders: the case of fragile X syndrome. Eur J Hum Genet. 2021;29(1):173183. doi:10.1038/s41431-020-00711-x

55. Hessl D, Tassone F, Cordeiro L, et al. Brief report: aggression and stereotypic behavior in males with fragile X syndrome - Moderating secondary genes in a single gene disorder. J Autism Dev Disord. 2008;38(1):184189. doi:10.1007/s10803-007-0365-5

56. Louhivuori V, Arvio M, Soronen P, Oksanen V, Paunio T, Castrn ML. The Val66Met polymorphism in the BDNF gene is associated with epilepsy in fragile X syndrome. Epilepsy Res. 2009;85(1):114117. doi:10.1016/j.eplepsyres.2009.01.005

57. Stepniak B, Kstner A, Poggi G, et al. Accumulated common variants in the broader fragile X gene family modulate autistic phenotypes. EMBO Mol Med. 2015;7(12):15651579. doi:10.15252/emmm.201505696

58. Tondo M, Poo P, Naud M, et al. Predisposition to epilepsy in fragile X syndrome: does the Val66Met polymorphism in the BDNF gene play a role? Epilepsy Behav. 2011;22(3):581583. doi:10.1016/j.yebeh.2011.08.003

59. Wassink TH, Hazlett HC, Davis LK, Reiss AL, Piven J. Testing for association of the monoamine oxidase a promoter polymorphism with brain structure volumes in both autism and the fragile X syndrome. J Neurodev Disord. 2014;6(1). doi:10.1186/1866-1955-6-6

60. Chen ZY, Patel PD, Sant G, et al. Variant Brain-Derived Neurotrophic Factor (BDNF) (Met66) alters the intracellular trafficking and activity-dependent secretion of wild-type BDNF in neurosecretory cells and cortical neurons. J Neurosci. 2004;24(18):44014411. doi:10.1523/JNEUROSCI.0348-04.2004

61. Szeszko PR, Lipsky R, Mentschel C, et al. Brain-derived neurotrophic factor val66met polymorphism and volume of the hippocampal formation. Mol Psychiatry. 2005;10(7):631636. doi:10.1038/sj.mp.4001656

62. Chen ZY, Jing D, Bath KG, et al. Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior. Science (80-). 2006;314(5796):140143. doi:10.1126/science.1129663

63. Gratacs M, Gonzlez JR, Mercader JM, de Cid R, Urretavizcaya M, Estivill X. Brain-derived neurotrophic factor Val66Met and psychiatric disorders: meta-analysis of case-control studies confirm association to substance-related disorders, eating disorders, and schizophrenia. Biol Psychiatry. 2007;61(7):911922. doi:10.1016/j.biopsych.2006.08.025

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Genetic mapping of subsets of patients with fragile X syndro | TACG - Dove Medical Press

‘Star Wars: The Bad Batch’ Who Is Omega? Inside the Magic – Inside the Magic

Michelle Angs Omega joins the Star Wars universe in the latest Disney+ television series from Lucasfilm, Star Wars: The Bad Batch. With voice actor veteran, Dee Bradley Baker, back as the titular Bad Batch, Angs character is stirring up some big questions for Star Wars fans namely, who is Omega in The Bad Batch?

Here is your guide to the new female clone in the Star Wars universe.

The Bad Batch premiere launched on Star Wars Day (May 4) and tells the story of a group of defective, genetically modified clones called Clone Force 99, or the Bad Batch. Made up of five mutated clone troopers Hunter, Tech, Echo, Crosshair, and Wrecker the squad partakes in numerous mercenary missions on behalf of the Republic, and are quickly becoming some of the best characters in the galaxy.

Dave Filonis (Star Wars Rebels, Star Wars Resistance) new animated series crosses over the events of Star Wars: The Clone Wars and Star Wars: Episode III Revenge of the Sith (2005) in the time before the original trilogy began. The season began with a feature-length episode titled, Aftermath, highlighting the historic moment of the Galactic Empires rise to power. Despite The Bad Batch controversy early on, the new series seems to have already built its fandom like many of the other Star Wars spinoffs.

When Chancellor Palpatine executed Order 66, overriding the Clone Armys programming to turn on their Jedi generals, Clone Force 99 was seemingly unaffected due to their enhancements. Although, as time wore on, some of the squad members did succumb to the Order 66 protocol before being saved by their brothers.

Omega, like the member of Clone Force 99, is a genetically enhanced clone. Essentially made from the DNA of bounty hunter Jango Fett, Omegas existence at least at first was seemingly unknown, but as the series progresses more and more is coming to light about the new character.

In the ninth episode of The Bad Batch, Bounty Lost, Omega was revealed to be a direct replica of Jango Fett, at least in terms of genetics. Only one other clone has this same link the bounty hunter, Boba Fett.

Arguably the new Grogu of Star Wars, Omega was introduced as a wide-eyed child intent on seeking a more adventurous life. Raised under the guidance of the Kaminoans on Kamino, Omegas first appearance came when the elite soldiers of Clone Force 99 returned to Kamino following the execution of Order 66. She was the medical assistant to Nala Se.

Hunter had just saved the Padawan Caleb Dume Kanan Jarrus in Star Wars Rebels after the murder of Jedi Master Depa Billaba, and upon returning to Kamino stumbled upon Omega. When Admiral Tarkin arrived on Kamino, Omega bonded with Hunter and the rest of Clone Force 99 before escaping the planet with them after Crosshairs chip activated, making him turn on his squad.

Many theories point to Omega being Force-sensitive. Her skill targeting a weapon in the premiere episode of the Star Wars animation, and more recently her ability to win every opponent at a game of dejarik, suggests there may be more than meets the eye with this honorary Bad Batch member.

What Star Wars fans do know, however, is that Omega is the daughter of Jango Fett and sister to Boba Fett. In Bounty Lost, after a near-death situation with the notorious Cad Bane and Fennec Shand, Tech revealed that Omegas genetic makeup is a direct replication of Jango Fetts. While the clone trooper armys genetics were slightly modified to grow quicker, Omega and Boba Fett were left completely untouched.

While Star Wars fans dont know much else other than this familial connection to two of the galaxys most notorious bounty hunters, her relationship to Boba Fett provides the most interesting detail, and not just for Filonis The Bad Batch. With only six episodes left of the first season, her backstory could point to the animated reprisal of Boba Fett or likewise the live-action debut of Omega in a Star Wars series down the line like Robert Rodriguezs The Book of Boba Fett.

Back to The Bad Batch though, we know the Kaminoans have hired bounty hunters to capture and protect Omega reasons unknown so her existence in the animated series suggests that trouble isnt far away for Clone Force 99.

As well as discovering what she is, Omega is slowly building a life outside of Kamino. Still under the shadow of those who made her, Omegas burgeoning connection to the members of the Bad Batch is how she seems to be writing her own history. The character is always one to dive into adventure, and even though this causes despair for Hunter and the gang, she is proving herself to be a valuable part of this formidable crew.

From helping in the mission on Corellia to find and secure a tactical droid to being present for the removal of the clones inhibitor chips on Bracca, Omegas Star Wars story has only just begun.

Omega is sharp-minded and headstrong. Sometimes a little nave, the character often heads into trouble with the right intentions but not the military skill to back it up. However, her way to find good in everyone as well as passing no judgments on what Clone Force 99 has had to do to stay alive makes her one of the galaxys warmest hearts.

Omegas personality has been shaped by those around her. The individual members of the unique squad, all of which have their own personalities seem to have rubbed off on the young clone. It is in her difference now to when she first met Clone Force 99, that fans can get an idea of how sheltered her life was back on Kamino. Much like how Grogu was in hiding for so long in The Mandalorian, Omegas entry into the big wide galaxy is a point of much character exploration.

From the Bad Batch, she learned about teamwork and survival, and even from characters like Cid (Rhea Perlman) has Omega developed new traits for this example, it seems Cids abrupt nature and aloofness has given Omega some new street smarts if her dejarik winning streak is anything to go by.

While Omega is the one Clone Force 99 protects most of the time, her calmness and quality to not see everything from a military perspective has aided the group on many occasions. Her competitive kinship with Rafa and Trace Martez on Corellia helped bring the sisters and the Bad Batch together to battle the army of police droids.

Omegas caring nature and inability to leave those she loves also highlight how the young clone is adding something new to the squad. Even after Wrecker set out to kill her after his inhibitor chip activated, Omega stayed by his side following the chip removal surgery and wouldnt rest until her squadmate woke up.

Omega has learned much since joining Clone Force 99. On Bracca, Wrecker taught her how to disarm explosives while on Ord Mantell, she acquired a Zygerrian energy bow. Although at first a novice in combat, Omega has quickly learned new skills in order to survive the attacks of Crosshair and the Galactic Empire as well as the relentless confrontations with the galaxys most nefarious bounty hunters.

Omega picked up her energy bow on Ord Mantell and has become an adept user at handling the weapon, although she still needs much practice to use it confidently. As StarWars.com describes:

Firing sizzling laser bolts instead of arrows, a Zygerrian energy bow is a formidable weapon in a firefight if you have a sharp eye and strong arms to lend the weapon unwavering accuracy.

It is perhaps the mystery surrounding the possibility of Omega being Force-sensitive that is most interesting in her skillset. Some might say its beginners luck or youthful charm, but the way she successfully aimed, possibly the first weapon she has ever wielded, in the premiere episode or managed to win numerous back-to-back games of dejarik, alludes to the fact that Omega may not be any regular clone.

Whether she is connected to the Force or not, Omegas skills at negotiating with her team members and other allies, as well as her ability to quickly pick up military talents make her more than suitable to take up the opening Crosshair left in Clone Force 99 and become one of the new rebels of the galaxy.

With more yet to discover, Omega is perhaps one of Star Wars most interesting new characters, and with many more upcoming projects, fans might not have to wait long for some answers.

What is your favorite thing about Omega? Let us know in the comments!

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'Star Wars: The Bad Batch' Who Is Omega? Inside the Magic - Inside the Magic

Hair: Types and care instructions – Medical News Today

There are many different types of hair, including straight, curly, wavy, and coily.

Depending on a persons hair type, they may need to follow different care instructions.

This article will provide some general information about hair types and detail some specific care instructions.

Hair type typically refers to the shape of a persons hair. Hair can be straight, wavy, curly, or coily.

According to one 2020 article, hair consists of two structures: the strand of hair itself, or the hair shaft, and the hair follicle.

The hair shaft consists of different layers, including the cortex, the surrounding cells, and, in thicker hair, a central medulla.

A 2017 study notes that the shape of the hair follicle determines the shape of a persons hair. For example, the hair follicles for curly hair are in the shape of an S.

Genetic factors play a role in deciding the shape of a persons hair follicle.

Learn more about what determines hair shape here.

Hair shape refers to the degree of curliness of a persons hair.

One review article notes that different researchers have used different hair shape categorization systems in their research about hair. For example, some have used use labels such as:

Some hairstylists like to distinguish hair shapes into four categories. However, scientists do not use this categorization system in medicine or scientific research.

Hairstylists use the following categorization system:

Hair density refers to the number of hairs that a person has on their head. The more hairs a person has, the higher that persons hair density.

Hair structure refers to the thickness of the strands of hair. A persons hair can be:

According to the World Trichology Society (WTS), hair thickness varies depending on the person. Some people have finer hairs than others. The WTS also notes that the hair fibers become shorter and finer as a person ages.

Hair porosity is a measure of the amount of moisture that a persons hair can absorb.

Hair porosity depends on how many gaps or tears are present in the cuticle layer. The cuticle is the outer layer of the hair, which protects it from wear and tear.

According to one 2015 article, hair is naturally porous. However, hair that has sustained damaged due to bleaching or chemical treatments is more porous than untreated hair.

People may find it helpful to avoid strong chemical and high heat treatments to let their hair recover.

According to the American Academy of Dermatology (AAD), people can try the following when caring for their hair:

People should select their shampoo and conditioner based on their hair type.

If possible, they should try to limit:

There is some evidence to suggest that straight hair carries sebum more easily than curly hair. Sebum is a waxy, oily substance that a persons skin produces. This means that people with straight hair may be more likely to get oily hair than those with curlier hair.

For this reason, people with straighter hair may wish to avoid the excessive use of certain hair products. These include:

People with straight hair may also wish to wash their hair more frequently.

According to a 2015 article, a person with straight hair may need to use a more gentle approach to caring for their hair. This may involve:

Over-brushing can damage curl definition. Therefore, people with curly hair may need to experiment to find the right amount of brushing for their hair.

Some other care tips for curly hair include:

Some people may also wish to use hair mousses and gels that are intended for curly hair to maintain curl definition.

The AAD suggests the following tips for Black hair:

Additionally, people may wish to take care when using weaves or extensions. To prevent hair damage, they may wish to try:

Tight hairstyles can also lead to traction alopecia, which results in hair loss. People may wish to consider giving the hair a break after 23 months of wearing a weave or extension.

Learn more about Black hair care tips here.

People with thick hair may find it helpful to use denser hair products, such as:

Additionally, people with greater hair density may find it beneficial to use brushes that are designed for thick hair. These brushes have fewer spokes than others, which helps people remove knots without breaking the hairs.

There is anecdotal evidence to suggest that denser hair products, such as oils and butters, can weigh down thinner hair. For this reason, people with thin hair may wish to avoid these products.

People with thinner hairs may also benefit from:

The WTS notes that people shed approximately 50150 hairs per day. This can occur through hair washing, brushing, and combing. However, some people lose more hair than they can grow.

This can happen for various reasons. One common cause is androgenetic alopecia. This is a genetically predetermined condition that affects around 50% of people. In males, hair loss occurs at the temples and the top of the head. In females, hair loss can affect the crown.

Hair loss can also occur in females due to other health conditions, including:

A person should contact a doctor if they:

Some anecdotal evidence suggests that people can use certain shampoos, essential oils, and dietary supplements to thicken the hair. However, there is no scientific evidence to prove that hair care can prevent thinning hair.

That said, a person can take measures to help prevent some causes of hair loss, such as traction alopecia.

Learn more about stopping hair loss here.

Everyones hair is slightly different. A persons hair can be straight, curly, coily, or wavy, and each type benefits from different methods of care.

Although some hair loss is common, a person should contact a healthcare professional if they are concerned.

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Hair: Types and care instructions - Medical News Today

New laws hit the books in Mississippi on Thursday – Yall Politics

Check out what laws go into effect on July 1, 2021.

Dozens of Mississippi laws will go into effect on Thursday, July 1, 2021. Take a look at some of the most talked about bills of the 2021 session and how these new or revised laws could impact you.

Teacher Pay Raise

Probably one of the most talked about bill that passed from the House of Representatives was a raise for teachers and teaching assistants. HB 852, which had a nearly identical companion bill in the Senate, provided for a $1,000 raise for teachers at the start of the 2021-2022 school year and $1,100 for assistant teachers.

A teacher pay raise was on everyones mind entering the 2021 session and COVID-19 made it particularly important to lawmakers to see these funds diverted to teachers. In total, the raise made up an additional $50 million to education in the FY2022 budget.

Occupational Licensing Recognition

Workers in Mississippi and those who would like to come to the state but are licensed in other states, just got a helping hand. HB 1263, authored by Rep. Becky Currie, instated the Universal Recognition of Occupational Licensing Act. This bill allows individuals who work in other states and have a license that is in good standing with that agency to transfer for work to Mississippi with no additional loopholes.

RELATED: Governor Reeves on Universal Occupational Licensing Act: Mississippi is open for business

Just days before going into law, Governor Tate Reeves commented that this bill would allow workforce development to continue and labor shortages from the pandemic to decrease. He also said that it will reduce the red tape many professionals have to go through in order to work in Mississippi. That will include teachers coming from out of state to work here.

Election Qualifying

Planning to run for office in Mississippi? Well, take note of this bill lawmakers passed this session. HB 1048 effectively changes the qualification deadline to February 1 for some statewide, state district, county and county district offices.

Previously the deadline was not until March 1. This will bump the decision up for candidates considering a run for elected office by one month.

Appropriations bills

Mississippis budget was set during the 2021 session. The bills that pertain to appropriations for state agencies and such will all go into effect July 1, 2021. This marks the start of a new fiscal year in the state.

You can read more of those bills from the Senate and House here.

Alcohol Delivery

Many Mississippians have been pushing for more accessible ways to get their alcohol. The Legislature listened with HB 1135. This bill will allow the delivery of a particular wine, spirit or beer from a licensed retailer to a consumer. The retailer must also have a delivery service permit to participate in this service.

Those delivering can be current employees or contracted individuals who are at least 21 years old and receive proper training consistent with current programs. To place an order, you must be at least 21 years old.

Executive Sessions for Public Bodies

Speaker of the House Philip Gunn authored a bill, HB 1323, that will allow any public body to enter into executive session in order to develop a strategic plan to combat, eliminate, reduce or respond to human trafficking or the commercial sexual exploitation of children.

The reason these meetings would be necessary is to address a particular trafficking issue and attempt to provide an immediate solution.

MAEP Calculations

Over in the Senate, many lawmakers set their sights on improving education as well as helping the Mississippi Department of Education operate in unprecedented times.

SB 2149, which was authored by Sen. Dennis DeBar, provided that typical daily attendance rolls would not count against schools from the 2020-2021 school year.

Mississippis MAEP funding formula is calculated in part by daily attendance. Due to the unprecedented nature of the pandemic and virtual learning, daily attendance was unpredictable and, for many schools, impossible in-person during portions of the last year.

Teacher License Reciprocity

Similar to the removal of red tape for all occupational licensing, SB 2267 will allow reciprocity for teachers.

This bill will apply to any teacher coming from another state who already possess a teacher license and can pass a background check. Under the law, the Department of Education can grant a one-year extension to June 2022 to allow for that teacher to meet requirements in Mississippi.

The bill also implements the creation of a licensing and certification committee that will assist in streamlining the process for teacher certification in the state.

Earned Parole Eligibility

Possibly one of the most talked about pieces of legislation in general this year centered around the criminal justice system in Mississippi. SB 2795, or the Earned Parole Eligibility Act, was offered by Sen. Juan Barnett. He brought forward a similar bill in 2020 but it was vetoed by Governor Reeves.

Barnett said he took those critiques and perfected the language in order to have an agreement.

The Earned Parole Eligibility Act allows for particular non-violent, and some violent offenders, to be eligible for parole after a certain amount of their sentence has been served. The hesitation in 2020 centered around murderers being considered in the eligibility category, a move Barnet said was removed in the 2021 bill.

RELATED: Senate passes Mississippi Earned Parole Eligibility Act

Those not eligible include sex offenders, human traffickers, murderers, capitol, and habitual offenders. It is important to note that the bill does not grant any offenders parole; it only allows the possibility of parole in the event the individual has met the proper criteria for consideration.

The bill passed in both chambers and was later signed into law by Governor Reeves.

Medicaid Tech Bill

Every three years lawmakers are tasked with reconfiguring the guidelines for the Mississippi Division of Medicaid. This year it almost looked as if lawmakers would leave the 2021 session without a Medicaid Tech bill. However, at the final hour they were able to come to an agreement on the program with SB 2799.

RELATED: Medicaid will live on in the Governors office and with a budget

Though some attempts were made to remove the Division of Medicaid from under the Governors office, it remained housed there in the 2021 legislation. But the House did remove language that would have provided 12 months of postpartum care for mothers who receive the benefits.

Sen. Kevin Blackwell, Chairman of Medicaid, said the final bill included a 5% reimbursement for some providers, restored crossover claims for hospitals, nursing home and immediate care facility reimbursement days, and provided an additional 5% bump for dentists in 2022-2024 to cover preventative services.

RELATED: Senate passes bill to increase TANF benefits for Mississippians

Dept. of Public Safety

Many changes were made in regard to law enforcement and the Department of Public Safety. Perhaps the largest of note was the transfer of the Capitol Police from the Department of Finance and Administration to the Department of Public Safety. The law came by way of SB 2434.

The duties and abilities of the Capitol Police did not change with the bill, only the overseeing agency. The bill was offered by Sen. Brice Wiggins, Sen. Angela Hill and Sen. John Horhn.

Capitol Police monitor the Capitol Complex in Jackson.

Mississippi Fairness Act

Mississippi gained national attention with the passage of SB 2536, entitled the Fairness Act. The legislation, offered by Sen. Angela Hill, would prevent biologically male individuals from competing in female sports. This law will apply to K-12 schools as well as institutions of higher learning.

When defending her bill to those who claimed it was non-inclusive to transgendered athletes, Hill said those who were born physically a male have an advantage over female athletes simply due to genetics.

RELATED: Mississippi Governor signs Fairness Act into law barring biological men participating in women, girls sports

The bill was up in the air until the last minutes of the session when it was passed. Sen. Hill said the legislation was necessary in order to protect girls sports in the state under the current federal position toward transgendered persons competing among athletes that do not share their at-birth genetic makeup.

Name, Image, Likeness

Another bill that could impact Mississippi athletes is SB 2313. This bill will allow Mississippi collegiate athletes to receive compensation if their image, name or likeness is used in advertising.

RELATED: Reeves signs bill to allow college athletes compensation when their name, image or likeness is used

Mississippi lawmakers believe passing this legislation will keep Mississippi schools competitive in the event the U.S. Supreme Court rules in current court cases to allow for the compensation.

Weight Limits

Senator Jennifer Branning presented SB 2825, the Mississippi Infrastructure Act of 2021 which tackled several road, bridge and transportation issues the state faces.

Probably the most considerable change was that of the harvest weight limits being raised from 84,000 pounds to 88,000 pounds. The bill goes into effect July 1, 2021, but the harvest permit increase does not take effect until July 1, 2023. These weight limits would only apply to commercial truckers carrying a harvest permit.

The bill was argued by many in the Senate as it moved through the process.

While this story only highlights some of the more impactful bills going into effect on July 1, you can access information on all bills passed from the 2021 session, and when they will take effect you can visit the Mississippi Legislatures website HERE.

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Lawmakers will officially head back to the Capitol in January for the 2022 session.

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New laws hit the books in Mississippi on Thursday - Yall Politics

PATHWAY to Northern PROFITABILITY with Seifert Belmont Reds – Queensland Country Life

This article is branded content for Seifert Belmont Reds

Profit-making genetics are readily apparent in the 90 bulls and 10 PTIC heifers' that husband and wife team Ian Stark and Jeanne Seifert, have selected for their third annual Seifert Belmont Reds Sale.

Seifert Belmont Reds is the largest breeder of purebred registered Breedplan recorded Belmont Reds in Australia. Their aggregation of five properties totals approximately 10,000ha and is a mix of ticky and clean country from marginal iron bark breeder country to brigalow backgrounding country.

Mrs Seifert is particularly proud of their females who continue to naturally rebreed, even on the back of two of the driest years on record.

"Our genetics are produced from a tough, unpampered cow herd where females are managed under a single sire mating program, using Belmont Red bulls at 1 per cent - 2 per cent, for a nine or a twelve-week joining period.

"Our cattle are never ever treated for tick or fly, are rarely handled, and every female must wean a calf every year, off native pasture, without any special care," she said.

"Under this regime and dry years, our wet cows and heifers returned from 93.2 per cent to 98.5 per cent pregnancy rates this year."

Early puberty bulls are also used from 14 months old to produce higher fertility daughters and sons. These stringent 'survival of the fittest' breeding principles, ensure that the young bulls catalogued for the 2021 sale will provide valuable heritable traits including phenomenal fertility, excellent growth and carcase attributes, genuine docility, and the highest levels of environmental adaptation.

Of the 90 bulls, 44 are Homozygous Polls (PP) and offer phenomenal fertility, truetropical adaptation and parasite resistance, with muscling and marbling.

"To top it off , 44 bulls of the 90 bulls are homozygous (PP) polls, and an impressive 73 per cent of them are at or above the 50th percentile for the Breedplan export $index."

Mr Stark said their emphasis on real fitness for purpose, and their ability to reliably meet volume demand, plus JBAS 7 status, ensures Seifert Belmont Reds can sell Australia-wide including into the Northern Territory and Western Australia.

"The reputation for our bulls to deliver consistent lines of calves, stems from many decades of breeding, where our pedigrees can be traced back to the original CSIRO Africander cross breeding trials of 1954," Mr Stark said.

"I'm especially pleased with the progress our herd has made with respect to type, muscling, and eye muscle area.

"IVF (invitro fertilization), ET (embryo transfer), AI (artificial insemination) and cloning are used to create optimum genetic combinations and accelerate genetic progress."

The demand for tropically adapted Bos Taurus Seifert Belmont Red genetics is emphasised by their exportation to Papua New Guinea, New Caledonia, the Philippines, and South America.

In 2020 the stud also established a satellite purebred Belmont Red herd with partners in Paraguay.

"Our focus on personal and professional integrity, combined with trustworthy data, provides peace of mind to our buyers," he said.

"We have every confidence in this draft, and we're sure they will make a valuable contribution to your herd and your profitability."

The demand for tropically adapted Bos Taurus Seifert Belmont Red genetics is emphasised by their exportation to Papua New Guinea, New Caledonia, the Philippines, and South America.

The catalogue is available now on http://www.seifertbelmontreds.com with hardcopies mailed on request. Inspections are welcome at any time, on any day - call, text or email Ian 0439 632 113 or Jeanne 0427 632 113, jeanne@seifertbelmontreds.com.

Click here for sale catalogue.

Videos will be on the website and AuctionsPlus two weeks before the sale. The sale will be on AuctionsPlus and by Helmsman auction, from 12 noon Monday, August 2, on property at 'Wonga' Jandowae. Attendees are welcome from 7am with complimentary morning tea and lunch.

Free delivery to Charters Towers, Rockhampton, Roma and Dalby saleyards will be available. Outside agents welcome, contact Elders Michael Smith 0428 541 711 or Anthony Ball 0428 275 499.

This article is branded content for Seifert Belmont Reds

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PATHWAY to Northern PROFITABILITY with Seifert Belmont Reds - Queensland Country Life

In Memoriam: Jean Wilson, M.D., made scientific discoveries that led to effective prostate treatments, insights into sexual differentiation – UT…

DALLAS June 21, 2021 Jean D. Wilson, M.D., an internationally known endocrinologist whose scientific discoveries led to profound insights into the mechanisms underlying sexual differentiation and led to now widely used treatments for prostate disease, died June 13. He was 88.

Wilson, seen here in 1962, graduated from UTSouthwestern Medical School in 1955 and joined the faculty in 1960, where he began his studies of testosterone.

Wilson, professor emeritus of internal medicine at UTSouthwestern, was largely responsible for current understanding of the mechanisms by which steroid hormones induce male sexual differentiation. He also was instrumental in identifying the scientific underpinnings of a widely prescribed class of drugs known as 5-alpha-reductase inhibitors which include finasteride (Proscar, Propecia) and dutasteride (Avodart) to treat enlarged prostate and balding in men.

Wilsons discovery of 5-alpha-reductase and the identification of dihydrotestosterone as the primary hormone associated with the growth of the prostate transformed our understanding of prostate gland growth and paved the way for new effective treatment of prostate disease, says Daniel K. Podolsky, M.D., president of UTSouthwestern. His findings led to the first medical therapy for benign prostatic hyperplasia, and also provided the basis for understanding of the mechanism underlying the differentiation of male and female genital development. His legacy will be found in the legions of patients who have benefited from the therapy made possible by his discoveries.

Wilson, seen in 1978, was a popular and highly sought-after attending physician on the wards of Parkland Memorial Hospital, valued for his vast expertise in endocrinology and medicine in general.

Jean Wilson was one of the most critical and helpful sources of information concerning the development of two important drugs we were developing at Merck the statins, for control of LDL cholesterol, and Proscar, for treatment of benign prostate enlargement. Wilson was always available to wrestle with problems that often arise in drug development. I needed expert friends in those early days, and probably still do, says P. Roy Vagelos, M.D., former chairman, president, and chief executive officer of Merck & Co. and now chair of the board of Regeneron Pharmaceuticals.

Wilsons research included the study of cholesterol metabolism and steroid hormone action. The UTSouthwestern Medical School graduate and former National Institutes of Health (NIH) researcher earned international prominence for his investigations of testosterone including its formation from cholesterol as well as its metabolism and action. His efforts elucidated disorders resulting from genetic defects that lead to disruption in sex hormone biosynthesis with corresponding alteration in development.

Collaborations at UTSouthwestern with David Russell, Ph.D., professor of molecular genetics, led to the cloning of the 5-alpha-reductase (5AR) gene, development of animal models for 5AR deficiency, and eventually the finding that a 5AR inhibitor blocked prostate growth, which resulted in clinical trials led by Claus Roehrborn, M.D., chair of urology. The human androgen receptor later was cloned in 1989, allowing Wilson and colleagues to identify the receptor as a transcription factor that could regulate both the receptor and 5AR expression in prostate cancer. Other scientists at UTSouthwestern expanded upon his research, identifying androgen involvement in virtually all aspects of prostate development, alternate mechanisms of androgen synthesis, and other forms of androgens related to castrate-resistant prostate cancer.

Among his numerous awards, Wilson received the Kober Medal from the Association of American Physicians (1999); the Fred Conrad Koch Award from The Endocrine Society (1993); Gregory Pincus Award from the Worcester Foundation for Experimental Biology (1992); Henry Dale Medal from the Society for Endocrinology (1991); Amory Prize from the American Academy of Arts and Sciences (1977); and the Eugene Fuller Award from the American Urological Association. He was elected as a member of the American Academy of Arts and Sciences (1982), the National Academy of Sciences (1983), and the National Academy of Medicine (1994) as well as the American Philosophical Society and served as president of the Endocrine Society, the American Society for Clinical Investigation, and the Association of American Physicians.

Wilson, seen in 1992, was elected as a member of the American Academy of Arts and Sciences (1982), the National Academy of Sciences (1983), and the National Academy of Medicine (1994).

Wilson, who had held the Charles Cameron Sprague Distinguished Chair of Biomedical Research, was known as a collaborative colleague and empathetic adviser to students and fellows. His approach with students and trainees was threefold find out what they want to do, encourage them to do it, and develop pathways to fulfill their goals, he said in an interview with The Journal of Clinical Investigation. He also noted that some of the most difficult students to counsel turned out to be late bloomers who really were worth an investment of time and effort.

At UTSouthwestern, he served as the first director of the Medical Scientist Training Program, and it was recently announced that the Physician Scientist Training Program in Internal Medicine would be known as the Jean Wilson Society. The Jean D. Wilson Center for Biomedical Research and The Jean D. Wilson, M.D. Award, which honor excellence in scientific research mentorship, are named in his honor. The center was established with support from Dr. Wilson and his sister, the late Dr. Margaret Sitton, to promote research in endocrinology, developmental biology, and genetics, along with the J.D. and Maggie E. Wilson Distinguished Chair in Biomedical Research. In addition, he served among editors of two landmark medical textbooks Williams Textbook of Endocrinology and Harrisons Principles of Internal Medicine and as editor for The Journal of Clinical Investigation, among other journals. He authored The Memoir of a Fortunate Man, which chronicles his life growing up in the Texas Panhandle through his rise to pioneering academic physician and researcher.

Jean was a popular and highly sought-after attending physician on the wards of Parkland Memorial Hospital, valued for his vast expertise in endocrinology and medicine in general, say Nobel Laureates Joseph Goldstein, M.D, chair of molecular genetics, and Michael Brown, M.D., director of the Erik Jonsson Center for Research in Molecular Genetics and Human Disease. He founded a diabetic foot clinic at Parkland and spent hours each week clipping toenails and treating ulcers on the feet of elderly diabetic patients. After long days on the wards, he would retire to his modest laboratory where he would spend half the night meticulously dissecting rabbit fetuses. Often, when we were just starting our careers, we would sit by his side while he dissected, receiving sage advice about our careers as physician-scientists and life in general. Later, he extended his fatherly role to generations of M.D./Ph.D. students when he became the founding director of our M.D./Ph.D. program.

He had a rich life outside of the Medical Center as well. An avid opera buff, Wilson collected antique gramophones that could play every type of recording that had ever been produced. His extensive collection of 3,500 old 78-rpm operatic recordings included a 1917 disc of Enrico Caruso singing songs of Irving Berlin the only record that Caruso ever recorded in English, they note.

An avid opera buff, Wilson, seen in 2019, collected antique gramophones. His extensive collection of 3,500 old 78-rpm operatic recordings included a 1917 disc of Enrico Caruso singing songs of Irving Berlin the only record that Caruso ever recorded in English.

He took memorable trips to places like the North Pole, Antarctica, the Galapagos Islands, and the Easter Islands. He often incorporated science into his trips, visiting the Kangaroo Island in Australia to study sexual development in wallabies, and to Kenya to biopsy the phallus of the spotted hyena. Fearless in the pursuit of knowledge, he performed a rectal examination on a lion to estimate the size of the prostate, Goldstein and Brown say. A dedicated bird watcher, he traveled the world to many exotic places, hoping to spot that rare bird. But in the end, the rarest of that rare bird was Jean Wilson himself.

Born in Wellington, Texas, in 1932, Wilson obtained an undergraduate degree in chemistry from UT Austin and graduated from UTSouthwestern Medical School in 1955. As a student, he studied the control of urinary acid secretion by adrenal hormones, and as a resident, he investigated cholesterol metabolism. After residency, he spent two years at the NIH, where he studied ethanolamine biosynthesis. He joined the UTSouthwestern faculty in 1960 where he began his studies of testosterone, and worked in 1970 at Cambridge University. In all, he spent 60 years at UTSouthwestern and was named professor emeritus of UTSouthwesterns storied internal medicine department in 2011.

Jean Wilson leaves us with a remarkable legacy a quintessential physician-scientist whose scholarship both inspires and continues to serve as a foundation for new advances, says Podolsky, also professor of internal medicine.

In a career spanning six decades at UTSouthwestern, Dr. Jean Wilsons discoveries included:

Cholesterol metabolism

Dr. Wilson developed methods for quantifying cholesterol synthesis, absorption, degradation, and excretion in lab animals. Together, these analytical methods served as tools for understanding the feedback control of cholesterol synthesis and turnover. In addition, Dr. Wilson demonstrated that plasma cholesterol is synthesized in the intestinal wall and liver, findings that helped researchers define the contributions of diet and endogenous synthesis to cholesterol turnover in humans and other primates.

Male androgens

Concurrently, Dr. Wilson studied the action of male androgens, focusing on testosterone and its metabolite, dihydrotestosterone. Starting with a collaboration with his postdoctoral fellow, Nicholas Bruchovsky, in 1966, the researchers discovered that testosterone is converted inside prostate cells into dihydrotestosterone, a more potent androgen that is responsible for most of male sexual maturation and male sexual function. Dr. Wilson and his colleagues later showed that mutations that impair either the synthesis of testosterone, the conversion of testosterone to dihydrotestosterone, or the function of this metabolites receptor protein are the most common cause of birth defects associated with incomplete development of the male urogenital tract, affecting about four in every 1,000 boys. Cloning these responsible genes eventually allowed researchers to identify asymptomatic carriers of these mutations.

Dihydrotestosterone

Dr. Wilson also discovered that excess dihydrotestosterone is responsible for benign prostatic hyperplasia (BPH), or prostate enlargement, a condition that affects about 210 million men worldwide. Dihydrotestosterone is responsible for prostate growth in all male mammals, but in humans and dogs, prostate growth continues throughout life. Wilson and his colleagues showed that local excess of this potent androgen leads to prostate overgrowth. By curbing its production by inhibiting 5a-reductase, the enzyme that converts testosterone to dihydrotestosterone, they were able to prevent BPH in dog models of this condition. These findings have been developed into multiple 5a-reductase-inhibiting pharmaceuticals to treat this condition in human patients.

Brown, a Regental professor and director of the Erik Jonsson Center for Research in Molecular Genetics and Human Disease, holds The W.A. (Monty) Moncrief Distinguished Chair in Cholesterol and Arteriosclerosis Research, and the Paul J. Thomas Chair in Medicine.

Goldstein, a Regental professor and chair of molecular genetics, holds the Julie and Louis A. Beecherl, Jr. Distinguished Chair in Biomedical Research, and the Paul J. Thomas Chair in Medicine.

Podolsky holds the Philip OBryan Montgomery, Jr., M.D. Distinguished Presidential Chair in Academic Administration, and the Doris and Bryan Wildenthal Distinguished Chair in Medical Science.

Russell holds the Eugene McDermott Distinguished Chair in Molecular Genetics.

About UTSouthwestern Medical Center

UTSouthwestern, one of the premier academic medical centers in the nation, integrates pioneering biomedical research with exceptional clinical care and education. The institutions faculty has received six Nobel Prizes, and includes 24 members of the National Academy of Sciences, 16 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 2,800 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UTSouthwestern physicians provide care in about 80 specialties to more than 117,000 hospitalized patients, more than 360,000 emergency room cases, and oversee nearly 3 million outpatient visits a year.

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In Memoriam: Jean Wilson, M.D., made scientific discoveries that led to effective prostate treatments, insights into sexual differentiation - UT...

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