Archive for the ‘Male Genetics’ Category

The Division of Human Genetics, in the Department of Internal Medicine, offers outpatient and inpatient consultation services, performs clinical and translational research and participates in community education and outreach. Our physicians and faculty collaborate with colleagues throughout our medical center and around world. Additionally, the Master of Genetic Counseling Graduate Program addresses the rapidly growing need for genetics professionals.

Our comprehensive services include a Clinical Cancer Genetics Program with risk assessments and genetic counseling to 800 patients yearly and, as needed, their families. A Cardiovascular Genetic and Genomic Medicine Program, in conjunction with Ohio States Division of Cardiovascular Medicine, offers consultation for hereditary forms of heart disease at multiple clinics. And the Medical Genetics and Genomics Program provides risk assessment, genetic counseling and, when appropriate, genetic testing for the many different conditions that can run in families. These can range from bleeding and blot-clotting disorders to diseases of the skin, kidney, lung and eye. The Neuroscience Genetics and Genomics Program focuses on neuromuscular disorders, but also provides consultation for a wide array of neurological conditions.

Our program offers risk assessment tools for health care providers, including the interactiveFamily HealthLinkwhich allows you to estimate your own risk by reviewing patterns of cancer, heart disease and related conditions in your family.

Whether originating from a single gene, a chromosome or inherited genetic disorders encompass a broad span of conditions. Ohio State's Division of Human Genetics is a leader in providing the most up-to-date, thorough and advanced information available.

Genetic testing can be provided on a clinical or research basis. Genetic testing is routinely performed on a small sample of blood, saliva or cheek swab.

See original here:
Genetics | Ohio State Medical Center

In the United States, the National Center for Health Statistics estimates the life expectancies of males and females are 74.5 years and 80.2 years, respectively. For healthy aging, the Centers for Disease Control and Prevention (CDC) states that physical activity is key.

To find out whether physical activity had an advantage over genetics in promoting longevity, researchers at the Herbert Wertheim School of Public Health and Human Longevity Science at the University of California San Diego and other institutions conducted a nationwide study.

After analyzing health data of more than 5,000 older postmenopausal women, the researchers found that higher levels of light, moderate, or vigorous physical activity correlated with a lower risk of all-cause deaths. The findings expanded on prior studies that have shown that more sedentary time carries greater health risks.

These associations persisted across varying levels of genetic potential for living longer.

[The] findings support the importance of higher physical activity (PA) and lower sedentary time (ST) for reducing mortality risk in older women, regardless of [their] genetic predisposition for longevity, the researchers wrote.

Their prospective study was recently published in the Journal of Aging and Physical Activity.

From 2012 to 2020, the UC San Diego researchers analyzed data on the physical activity of more than 5,000 ambulatory women ages 63 and older.

Lead author Alexander Posis, MPH, a doctoral student in the San Diego State University/UC San Diego Joint Doctoral Program in Public Health, explained the significance of the OPACH study to Medical News Today:

Our study used pre-existing data from the Objective Physical Activity and Cardiovascular Health (OPACH) study, which is part of the Womens Health Initiative (WHI) that started in the early 1990s because women had not been included in many epidemiologic studies and clinical trials.

Alexander Posis, MPH, lead author of the study

The OPACH study focused on associations between physical activity, cardiovascular disease, and injury risks. The data generated allowed researchers to look at physical activity and the risk of mortality, cancers, cognitive decline, and physical disability as well.

Other research using the OPACH study found associations with physical activity (PA), sedentary time (ST), and mortality during an average follow-up of 3 years. However, no one had explored any possible genetic influence on these associations.

The UC San Diego study aimed to use a follow-up of 6 years and adjust the results with a weighted genetic risk score (GRS) for longevity.

OPACH participants wore an accelerometer 24 hours per day for 7 consecutive days.

The device measured the amount of time the women spent moving or being still and the intensity of any activity.

The researchers defined total PA as movement resulting in energy expenditure. They categorized PA intensity and ST minutes using predetermined cut points applied to the accelerometer counts.

Genome-wide association studies (GWAS) have linked multiple single-nucleotide polymorphisms (SNPs), or genetic variants, to longevity.

The UC San Diego cohort developed a weighted GRS based on three SNPs strongly associated with long life. This metric compared survival to age 90 versus death before age 90.

Covariates, or characteristics among the studys participants, included age, education level, body mass index (BMI), self-reported health status, and other details. Participants race was also a factor but was limited to white, Black, and Hispanic ethnicities.

The study also analyzed chronic conditions present before or after participation, including cancer, depression, frequent falls, and cardiovascular disease.

Of the 5,446 women in the present studys sample, 1,022 passed away during follow-up.

The authors determined that 36% of the total population had a high GRS, 33.1% had a medium GRS, and 30.9% had a low GRS for longevity.

The researchers firstly found that physical activity, of light or moderate-to-vigorous intensity, was associated with a lower risk of death while higher ST was associated with a higher risk of death. Interestingly, these associations persisted regardless of ones genetic predisposition for longevity.

Interestingly, the low-GRS individuals were younger, more active, and had higher physical functioning scores than the other GRS groups. Those with low GRS were also more likely to be of Black race/ethnicity than the medium and high GRS groups.

Our study showed that, even if you arent likely to live long based on your genes, you can still extend your lifespan by engaging in positive lifestyle behaviors such as regular exercise and sitting less, Aladdin H. Shadyab, PhD, the studys senior author and assistant professor at the Herbert Wertheim School of Public Health and Human Longevity Science, said in a news release.

Historically, women have been significantly underrepresented in clinical trials. Using data from the OPACH study was a step forward in inclusive research.

However, the resulting lack of male participation created a limitation on the UC San Diego studys findings.

Based on the design of our study, we were not able to make any inferences on men. But we hope that future studies will examine these associations in study cohorts that include men as well as those in younger age groups, Posis told MNT.

Dr. Scott Kaiser, a geriatrician and director of Geriatric Cognitive Health for the Pacific Neuroscience Institute at Providence Saint Johns Health Center in Santa Monica, CA, told MNT the work is a well-done study [ with] a lot of great data. However, he cautioned that the current study is an association study and not designed to prove causality.

I think this just supports an increasing amount of evidence that our genes are not our destiny [] It shows that there is a stronger association between longevity with physical activity than [with] genetics, Dr. Kaiser said.

Noting that the present study focused on only certain markers of longevity, Dr. Kaiser added that researchers need to determine other such factors. For instance, he said that the SNPs used to calculate the GRS were more common among people of European ancestry.

Dr. Kaiser said the term sedentary time might not be appropriate. It does not account for people who are unable to walk but can still engage in other physical activities such as chair exercises.

Its whether you just have some consistent physical activity versus somebody whos overall physically inactive, he said.

Dr. Kaiser hopes the public will understand that genetics do not trump a healthy lifestyle for reducing disease and mortality risk.

When it comes to healthy aging, exercise is about the closest thing we have to a miracle drug, he said.

The whole take of this [study] is that even if you could go to your doctor and get a fancy genetic test to see whether or not you have markers of longevity, it doesnt matter as much as whether you get up off the couch and exercise on a regular basis.

Dr. Scott Kaiser, geriatrician and director of Geriatric Cognitive Health for the Pacific Neuroscience Institute in Santa Monica, CA

See the article here:
Regular exercise may help women live longer, regardless of their genes - Medical News Today

In my previous article on a similar subject, The Whitaker Family: Horrors of Inbreeding, readers traveled through the horrors of inbreeding. As we talked about how inbred children are at a higher risk of recessive genetic disorders, lets continue the discussion with another popular term, the Habsburg Jaw, which scientists have confirmed is the result of royal inbreeding.

When someone wrote to me that the British Royal Family does not own the patent of inbreeding, I decided to write about Habsburg Jaw, which directly relates to the Habsburgs, one of the most prominent dynasties which ruled a vast European empire for centuries.

Before understanding the Habsburg Jaw, let us turn the pages of history to understand the Habsburgs, who as rulers, archdukes and emperors, did everything in and beyond their powers to keep a tight grip on the empire they ruled. The Habsburg, also known as the House of Austria, ruled Austria from 1282 until 1918. Apart from this, they controlled Hungary and Bohemia from 1526-1918; Spain and the Spanish empire for more than two centuries from 1504-1506 and 1516-1700.

The Habsburgs are also remembered for ruling Slovenia, Slovakia and Croatia, as well as vast parts of Poland, Romania and Italy. If you dont know this, the Habsburgs actually began to rise to power in 1273 as Rudolf I became the German King. Now, as a lover of history, youd remember that Ottokar II Premysl of Bohemia refused to recognize him as a king and the same sparked a major royal beef.

Ottokar managed to become the king of Austria but as he was killed in battle, Rudolf stepped in and granted the land to his sons. That was it, the Habsburgs were unstoppable since that day in history as they spent the next century in empire-building. The family was lifted to A-list Royal status when future emperor Maxmilian married Charles the Bolds daughter Mary and gained control over the Burgundy region.

Now, if we speak of the Habsburg royal clam, it included names like reformer Joseph I; Leopold Wilhelm (emperor, bishop and patron of arts); Rudolf II (Pragues promoter of science and art), Charles VI (Spains ruler who was succeeded by his daughter). This era gave a rise to striking similarities

The Habsburgs came into their full regal power in the 1600s and enjoyed its fruits through the early 1700s. TheHabsburg royal clan included Leopold Wilhelm, an emperor, bishop and patron of the arts; reformer Joseph I whose motto was by love and fear; Charles VI who ruled Spain and set up his daughter to take the crown; and Rudolf II, who decided to live in Prague, where he promoted science and art.

It was during this era that gave rise to a striking similarity in the jawline of the royal members of the Habsburg family, which came to be known as the Habsburg Jaw. Researchers revealed a stark reality that generations of inbreeding among the Habsburgs resulted in Habsburg Jaw, which ultimately caused their downfall.

The best example is that of Charles II, the final male heir, who became physically incapable of having children, and the reasons were plain and simple! The Habsburgs royal familys genetic line progressively deteriorated due to the excessive incest among them. The Habsburg Jaw was more prominent in males than females.

However, Mariana of Austria (Queen of Spain) remains a disturbing yet perfect example of the Habsburg Jaw. Apart from this, one of the most famous Habsburg members, Marie Antoinette of France too could not dodge the Habsburg jaw. She had a projected lower lip which made her look as if she was always pouting.

In the greed to remain Europes most powerful royal family, marriages between biological relatives became a common affair in the ruling houses of Europe. For instance, the Spanish Habsburgs dangerously engaged in incest despite its terrifying consequences. Youd be shocked to know that nine out of the 11 marriages in this family during their 184 years of rule in Spain (1516 to 1700) were incestuous in nature.

To quote famous examples, Charles 1 of Spain and Joseph I were both infamously known for having extremely prominent lower jaws. So what was the consequence? How did they get it? Why were stark similarities amongst the members? The plain and simple answer to the latter is incest. Such revelations were made in the 1988 article Journal of Medical Genetics, which stated that nine successive generations of the Habsburg family were found having this jawline, which came to be commonly known as the Habsburg jaw.

The article reported that at least three generations of this family had similar facial characteristics, called mandibular prognathism, which is a medical term for this kind of jaw. In this condition, the jaw moves so forward that it causes an extreme underbite as the teeth dont line up as they should in a normal human body. They also suffered from the thickened lower lip, misshapen nose, everted lower eyelids and flat malar areas.

The article narrated that this came as a result of constant incestuous relationships in the family and also gave rise to Mandibular Deficiency. The term was described as a pattern of abnormalities, including skeletal, neuromuscular, occlusal and esthetic conditions that can affect a persons speech and ability to eat.

Apart from this, the Habsburgs suffered from numerous ailments like dropsy, asthma, epilepsy, gout, and melancholia. Many accounts reveal that the Habsburg jaw originated among the Polish royals and it was Maximilian 1 (King Of Rome from 1486 and the Holy Roman Empire from 1508 until his death), who was found with this jaw.

For a very long time, there was no research to back the fact that the Habsburg jaw was a result of excessive inbreeding. However, Francisco Ceballos, a geneticist came up with mind-boggling research as the continued to study the facial deformities in 66 portraits of 11 Habsburg family members.

The researchers implemented statistical methods to analyze the effects of inbreeding on the degree of Mandibular Porganathism and Maxillary Deficiency. They found out that the two traits share a common genetic basis. Ceballos stated the following:

The Aha! moment was when we discovered that the MD is affected indeed by inbreeding, and that the Habsburg face is indeed related to their consanguinity. This is the first time that science backs up this statement

Their research revealed that facial deformities, as well as mental illness, are rooted deep in the Habsburg family. So how does inbreeding affect generations? The study revealed that mating between relatives increases the odds of inheriting identical forms of a gene from both parents called genetic homozygosity. This reduces an individuals health.

The best example of such a case is Charles V, who suffered from at least two conditions resulting from recessive mutations in different genes: pituitary hormone deficiency; which can result in infertility; and distal renal tubular acidosis; which causes kidney failure. The Habsburg family basically serves as a complete human laboratory for most researchers on the subject because the range of inbreeding among them was extremely high.

The latest research on the Habsburg family includes a December 2019 paper from Professor Vilas from the University of Santiago de Compostela. Per his research, the Habsburg dynasty was the most influential in Europe but was more famous for inbreeding which caused its downfall. The paper made an alarming conclusion that there is a crystal clear positive relationship between Habsburg Jaw and Inbreeding.

Various scientists and doctors have established that inbreeding leaves the offspring at a greater risk of congenital defects and genetic diseases. Check out this video to understand more about inbreeding.

While it may be true that marrying among relatives may have helped the Habsburgs seize power for a longer time, recessive genes became a reason for the downfall of their empire. Not only this, but inbreeding passed a series of genes that produced birth defects. The Habsburg dynasty came to an end with Charles II, who struggled to eat and speak due to his prolonged lower jaw. He was mocked as the most inbred king of all.

Not only this, but Charles II was short, impotent, weak, mentally handicapped and suffered from numerous intestinal problems. As a child, he could not speak until he turned 4. His feeble mind and physically deformity resulted from a limited gene pool. One French Ambassador wrote about him The Catholic King is so ugly as to cause fear and he looks ill. This was the time when a word was sent for his marriage.

Alexander Stanhope, an 18th-century British envoy wrote about Charles II in his book Spain Under Charles The Second, that he has a ravenous stomach and swallows all he eats whole, for his nether jaw stands so much out, that his two rows of teeth cannot meet; to compensate which, he has a prodigious wide throat so that a gizzard or liver of a hen passes down whole, and his weak stomach not being able to digest it, he voids in the same manner.

As an inbred, Charles II could not have children and many researchers speculated that he may also have been impotent. The last king of the Habsburg dynasty died in 1700 at the age of 38 years. This was the horrific end of a royal who was accumulating two centuries of harmful traits passed down to a single body.

See the article here:
Habsburg Jaw: The Horrific Consequences of 'Royal Inbreeding' in Europe - TheTealMango

For those who have problems maintaining an erection during sexual activity, there is Alpha Beast XL, a potent male enhancement. It will enhance your libido and produce a more pleasurable experience during sex.

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Ingredients of Alpha Beast XL

Men with weak erections can use Alpha Beast XL. It has a potent combination of over thirty non-GMO substances.

L-Arginine: No known negative effects are associated with the amino acid L-Arginine, which serves as a precursor to the vasodilator nitric oxide. Since increased blood flow strengthens and enlarges the penis, it is a crucial component.

Pygeum bark is often used to reduce the size of an enlarged prostate. It is possible for men over the age of 50 to suffer from this problem, and the resultant decrease in blood flow to the vaginal area might contribute to erectile dysfunction.

Saw Palmetto: This plant is well-known for its ability to promote stamina and strength by enhancing testosterone levels, sex desire, and blood flow.

Glutamate: Anti-infective glutamate is regularly recommended by medical professionals. The user's general health will improve, and any ancillary issues with maintaining erections will be lessened.

Quercetin: Another substance that works directly to improve cardiovascular health by maintaining healthy blood pressure is quercetin, which is also absorbed by the body and transported to the penile tissues.

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Although it is well accepted that low testosterone levels are not the primary cause of erectile dysfunction (ED), there are still a few prerequisites that must be addressed before an erection may be achieved. Taking care of the heart ensures that blood circulates properly throughout the body, including the penile tissues.

If the heart isn't sending blood to the corpora cavernosa, there will be no erection. It's also important that the blood be clean and uncontaminated. Having functioning kidneys is a key factor in reaching this goal.

When people use Alpha Beast XL, they will get nutrients that go straight to the penis, increasing blood flow to the Corpora Cavernosa and stimulating the pineal gland to produce erections. All the nitric oxide compounds have a role in this phenomenon. There is no risk to health from the increased blood flow that occurs naturally due to the presence of nitric oxide.

Benefits:

A benefit is that erections will be as solid as a rock and persist for hours.

This feature enables users to recuperate in bed and spend more time in the snooze chair.

Improves sexual performance

Increased blood flow increases penis size during erection.

It has the potential to improve circulation system-wide.

The user's self-esteem in the bedroom may be restored.

Both the kidneys and heart will benefit to some extent from this.

Negatives

If ED stems from psychological factors, the formula won't assist.

It's important for men to talk to their doctors before starting any new supplement, especially if they are using prescription medication.

Instructions for Using Alpha Beast XL

Users should take two tablets of the supplement daily, one in the morning and one in the evening, with enough water for maximum effect. As with any nutritional supplement, the results will vary depending on the individual using it. The outcomes might vary from one person to the next because of variables such as age, genetics, food, and the environment (such as climate and geography). However, after only a few weeks of use, most men report seeing positive results.

There have been no negative reactions to Alpha Beast XL yet. In a healthy guy, using Alpha Beast XL male enhancement pills is not expected to have any serious negative effects. Men above the age of 18 who are in good health should be the only ones to utilize this supplement. This product should not be used if they are taking any form of medicine. Furthermore, if they have any remaining concerns about the safety of this item, they should see their doctor before taking it.

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Erectile health maintenance strategies

Most men place a high value on preserving their erections into old age.

Not much work is required to keep the reproductive system in good shape. The product's developer recommends five easy steps men should follow to protect their members for the long haul.

But before that can happen, individuals must get an understanding of how their erectile system operates.

To start, the vessels loosen up and make it easier for blood to flow through them. When these cells swell, blood that reaches the corpora cavernosa becomes trapped there, giving rise to an erection.

But there are several prerequisites that must be satisfied before that may happen.

The first step is to ensure a healthy circulation of blood. Of course, it can only happen if the cardiovascular system is in tip-top shape.

The next condition is optimal cardiac health. To provide a stress-free genitourinary system, it must efficiently transport blood to all parts of the body.

And last, the blood itself must be of the highest quality with nothing tainting it; only healthy kidneys can do it.

After all, the brain is the seat of all beliefs. Therefore keeping it in excellent shape is crucial to maintaining an erection. This one has the potential to cause some confusion.

Healthy diet

Because a healthy diet includes vegetables, grains, fibers, protein, and fruits, this is a crucial step toward preserving erectile health.

Maintaining a healthy body is the first step, so try to avoid processed and fatty meals as much as possible.

Improved blood flow

A healthy lifestyle includes a lot of water, avoiding harmful substances like alcohol and drugs, and eating balanced food.

The greatest approach to maintaining the kidneys in tip-top shape, allowing them to better cleanse the blood traveling to the corpora cavernosa, is to drink enough water, as everyone knows. That way, not only will men have greater stamina and energy, but their erections will be more robust as well.

Clear Brain

Having a positive mental attitude may appear counterintuitive, but it really helps one think more clearly and act swiftly when the time is right.

This will make it more susceptible to erection-inducing stimuli.

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Setting up a daily routine might help one become more disciplined and less anxious by giving them a sense of control over their day. This is killing two birds with one stone by doing this for one's mental health.

Routine physical activity

Daily exercise for at least 30 minutes is the key to developing the endurance and strength of a stallion in bed.

Exercises like Kegels and Pilates may work wonders since they increase blood flow to the pelvic region, which in turn promotes hard, lengthy erections.

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Alpha Beast XL will help users have more satisfying sexual encounters. It promises to improve sexual health. If men have trouble with erectile functions and cannot take prescription medication because of the various medical concerns associated with it, they should try taking the Alpha Beast XL male enhancement pill instead. But it should be noted that Alpha Beast XL is not a miracle pill. It has to be taken regularly for results.

If me use the supplement as suggested every day, they should start seeing effects in a matter of weeks. The official website sells Alpha Beast XL. This supplement comes with a risk free refund guarantee, which sweetens the deal.

Go here to read the rest:
Alpha Beast XL Reviews (USA & Canada): Is It Legitimate Or Scammer? Shocking Ingredients Alert! - Deccan Herald

WEDNESDAY, Aug. 10, 2022 (HealthDay News) -- Men are known to be more likely to develop cancer than women, and a new study suggests that this is largely due to biologic differences between the sexes.

After controlling for factors like smoking, alcohol use, diet, physical activity and common medical conditions [that increase cancer risk], the sex bias remained for most cancers, said study author Sarah Jackson, a research fellow at the National Cancer Institutes Division of Cancer Epidemiology and Genetics.

Exactly which biological differences are driving these disparities isnt fully understood yet.

"Wed like to explore the contribution of sex hormones and genetics to cancer incidence in future research, she said.

For the study, researchers looked at differences in risk for 21 cancer sites among 171,000 men and 123,000 women between 50 and 71 years of age who were enrolled in a diet and health study from 1995 to 2011.

During that time, 17,951 new cancers were diagnosed in men, and 8,742 were found in women.

Men had higher risks for most cancers, with the greatest difference in risk seen for cancers of the esophagus (10.8 times higher); larynx and bladder (each 3.5 times higher); as well as gastric cardia, a type of stomach cancer (3.3 times higher).

Men only had lower rates of thyroid and gallbladder cancers, the study showed.

Jackson said men are also more likely to die of cancer than women.

Risk factors such as smoking, alcohol, diet and underlying health issues accounted only for a small fraction of the difference in men's and women's cancer rates. For example, smoking, diet and conditions like diabetes that can increase the risk for some cancers explained only 20% of the male bias in bladder cancer. Men are more than three times as likely to develop bladder cancer than women, Jackson said.

The study was published Aug. 8 in the journal Cancer. Going forward, researchers plan to look at sex differences in cancer rates among racial and ethnic groups.

In an editorial that accompanied the findings, Jangqin Luo said more research is needed to understand why men are more likely than women to develop many cancers.

Sex disparities have been actively studied in the past decades, and the published research findings have deepened our understanding, [but] sex difference in cancer is still an ongoing quest, said Luo, an associate professor of surgery at the Washington University School of Medicine in St Louis.

Understanding these disparities will pave the way toward better prevention and treatment policies, she said.

Dr. Otis Brawley, a professor of oncology at Johns Hopkins University School of Medicine in Baltimore, agreed that it's time to pay more attention to sex differences in cancer rates.

The more cells you have, the more likely one of them is to become malignant, and men tend to be bigger than women, said Brawley, who reviewed the findings.

Some of these differences may be related to hormones. The male sex hormone testosterone may promote the growth of some cancers, and the female sex hormone estrogen may offer protection against others.

When we do epidemiological studies and treatment studies, it is important to look at men versus women, Brawley said.

Eating a healthy diet, maintaining a normal weight, not smoking or drinking alcohol in excess, and other healthy behaviors are still an important part of a cancer prevention strategy for men and women, he said.

More information

The U.S. Centers for Disease Control and Prevention offers more information on how to prevent cancer.

SOURCES: Sarah Jackson, PhD, MPH, research fellow, National Cancer Institute, Rockville, Md.; Jangqin Luo, PhD, associate professor, surgery, Division of Public Health Sciences, Washington University School of Medicine, St. Louis; Otis Brawley, MD, professor, oncology, Johns Hopkins University School of Medicine, Baltimore; Cancer, Aug. 8, 2022

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Men More Prone to Cancer Than Women, But Why? - HealthDay News

Karen Hopkin: This is Scientific Americans 60-Second Science. Im Karen Hopkin.

Its great to have friends. Especially if youre an Indo-Pacific bottlenose dolphin. Because new research shows that the males who are the most popular with the lads are also the most successful with the ladies. Researchers describe how these affable marine mammals maintain and leverage their complex social connections in a pair of papers in the journal Current Biology.

Stephanie King: Male dolphins form lifelong cooperative relationships.

Hopkin: Stephanie King of the University of Bristol. Shes been studying the dolphin population that inhabits Shark Baya UNESCO World Heritage site off the coast of western Australia.

King: By studying populations like the Shark Bay dolphins for many years, we start to see the complex ways they maintain their important social relationships.

Hopkin: These connections are more than casual acquaintanceships. Theyre crucial for the dolphins to be able to fend off rivals and secure mates.

King: When navigating their social world, it is those males that are more adept at building strong friendships that are ultimately more successful.

Hopkin: So what do these aquatic alliances look like?

Livia Gerber: In Shark Bay, every male is embedded in a social network consisting of 4 to 14 males.

Hopkin: Livia Gerberof the University of New South Wales, Sydney.

Gerber: These 4 to 14 males are also known as second order alliances and they are the core social unit of the male bottlenose dolphins in Shark Bay.

Hopkin: This dolphin party consists of unrelated individuals of a similar age that remain together for decades. Now, when one of these dolphins is looking for love, hell select one or two wingmenor maybe fin-pals?... from this larger posse to help him find a fertile female.

Gerber: While it was previously known that males have to cooperate in order to sire offspring in Shark Bay, it wasnt known which male is the most successful one.

Hopkin: Is it the male with the most experience? The one with the largest territory? Or is there something about the bromance that holds the key to reproductive success?

Gerber: To answer this question, I [therefore] looked at the genetic profiles of more than 400 dolphins in Shark Bay and carried out paternity tests.

Hopkin: Once she identified the daddies, she could determine what quality they shared.

Gerber: I was quite surprised by my results because they were contrasting to so many other species, where the oldest males sire the most offspring or the males with the largest territories. As opposed to what we see in these other species, male bottlenose dolphins that have the strongest social bonds and multiple strong social bondsso the most popular malessire the most offspring.

Hopkin: Gerber says that the males with more friends are likely more often invited to cruise for femalesgiving them more opportunities for cooperative canoodling. Ok, so dolphins do better on group dates. But how do they establish and maintain these critical friendships?

King: Through physical contact much like hugging or holding hands in humans.

Hopkin: Or like grooming in other primates, like chimps or monkeys

Emma Chereskin: where individuals will devote a lot of time and energy into grooming their closest friends to strengthen those relationships.

Hopkin: Emma Chereskin of the University of Bristol. She says the problem with all this physical interaction istheres only so many hours in a day.

Chereskin: When group sizes become larger, this places a constraint on how much time is available for an individual to devote to grooming key social partners.

Hopkin: Enter the social bonding hypothesis.

Chereskin: In this hypothesis, vocal exchanges can serve as a replacement for grooming to maintain social bonds.

King: Like us chatting regularly with our circle of friends.

Hopkin: For dolphins, those chats take the form of exchanging signature whistles.

Chereskin: A signature whistle is a vocalization that is completely unique to each dolphin that functions much like a human name.

[Signature whistle from Kooks]

Hopkin: That was Kooksa member of the Alley Cat alliance.

[Signature whistle from Pimento]

Hopkin: And thats his pal Pimento.

Chereskin: So when they use their signature whistle theyre advertising their identity to those around them as a way to maintain group cohesion.

Hopkin: So Chereskin set out to determine which dolphins were getting physicaland which were more or less phoning it in.

Chereskin: The results were surprising. I had anticipated that the way dolphins use their signature whistles would be akin to the way that primates do.

Hopkin: For apes and monkeys, chit chat is more common between besties. But for dolphins?

Chereskin: when we look at just that core alliance group, we see that increased vocal exchanges occur between those with weaker social bonds. So while we do observe that vocal exchanges are indeed occurring between friends, rather than strangers, theyre occurring between distant friends rather than best friends.

[A whistle exchange between Spirit and Guppy]

Hopkin: Like Alley Cats Spirit and Guppy. Which Chereskin says kinda makes sense.

Chereskin: I liken these results to living with a partner. So when you live with someone, you typically dont have to call or text them as much because much of your bonding occurs together in your home.

Hopkin: But for friends who are more far flung, you might be more apt to send a shout outrather than making the effort to get together to bump fistsor fins.

[Dolphin clicks and pops]

For Scientific Americans 60-Second Science, Im Karen Hopkin.

[Signature whistle from Spirit]

[The above text is a transcript of this podcast.]

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For Some Dolphins, the Key to Mating is Rolling with a Tight, Noisy Crew - Scientific American

The man suffered from Primary Hyperoxyluria Type 1. (Representational)

A 22-year-old man from Uttarakhand who has been suffering from a rare genetic condition since the age of seven, received a new lease of life after undergoing double-organ transplant -- for kidney and liver -- at a leading private hospital in Delhi, doctors said on Wednesday.

His 27-year-old sister and 46-year-old mother donated the liver and kidney respectively, they said.

The condition, called Primary Hyperoxyluria Type 1 is a gene defect where a mutation in gene AGXT reduces the capacity of the liver to produce enzymes which helps in maintaining the oxalate level in the body, doctors said.

The absence or defect in this gene leads to the inability to metabolize oxalate leading to its excessive storage in the body, they said.

"This leads to insoluble calcium oxalate crystal accumulation in kidney (kidney stones) and other organs like heart, bones, blood vessels etc causing organ failure," the hospital said in a statement.

Over the years, the patient had been under preventive care and primary clinical management in his native town and had recently started undergoing regular hemodialysis, doctors said.

His condition this time had advanced to end-stage kidney failure following which he was admitted to Apollo hospital here on June 6, they said.

On diagnosis and consultation by Dr Kailash Nath Singh, senior consultant, nephrology and multi-organ transplant unit, at the hospital, he was recommended an "immediate combined kidney and liver transplant surgery (since it was the liver causing complications to other organs)," the hospital said in a statement.

Under the supervision of Dr Sandeep Guleria, senior consultant surgeon in general surgery, GI surgery and transplantation, and Dr Neerav Goyal, senior consultant, liver transplant, at the hospital, a "16-hour long combined kidney and liver transplant surgery was conducted on June 7," it said.

"Primary Hyperoxyluria Type 1 is a rare genetic condition. The calcium oxalate crystals accumulation in the kidney (kidney stones) are the first sign of the disease. The recurrent presence of kidney stones can lead to end-stage renal disease and delay in treatment for such diseases can be life-threatening.

"Hence, the 22-year-old person was immediately recommended for a combined kidney and liver transplant. As we planned, the patient underwent both the procedures together and was discharged after 21 days of the transplantation. The patient has been recovering well since then and has to visit hospital for follow-ups," said Dr Guleria.

The common cause of Primary Hyperoxyluria is genetic. The disease most commonly occurs in the young age and the first symptom of the disease is kidney stone. In spite of recurrent treatment, kidney stones keep developing in the organ due to the deposition of oxalate, it said.

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Sister's Liver, Mother's Kidney Helps Save Uttarakhand Man's Life - NDTV

Dr Shiva Murarka, Senior Scientist-Reproductive Genomics & Vishakha Mali, Genetic Counsellor, Neuberg Centre for Genomic Medicine explains that the usual IVF workup includes commonly recommended genetic tests like- couple karyotype, Y chromosome microdeletion, and sperm DNA fragmentation

Today, IVF or in-vitro fertilization, is a household name. It is the most common assisted conception for couples facing difficulty in achieving a successful pregnancy. IVF entails fusing sperm and eggs outside of the body in a laboratory. The uterus receives the embryo or embryos after they have been formed. This might sound easy theoretically, but there are a lot of complex biological processes that go on in an IVF procedure. Not all IVF cycles end in a successful pregnancy. Thus, many times, in the hope of a healthy pregnancy, couples have to undergo multiple IVF cycles. The usual IVF workup includes commonly recommended genetic tests like- couple karyotype, Y chromosome microdeletion, and sperm DNA fragmentation.

However, there are upcoming molecular/ genetic tests which are used increasingly in the modern day. Advent of genetic testing in an IVF clinic has increased the rate of healthy pregnancy outcomes. These tests include either testing the embryos or screening the intrauterine environment.

Couples facing infertility, recurrent pregnancy losses or couples who are known to be carriers of a genetic condition can be additionally benefitted from the following tests:

Screening of embryos:

Also termed as Preimplantation Genetic Testing (PGT). The embryos can be screened for the following:

Around 10-15 per cent of first trimester pregnancy losses are attributed to genetic causes, like chromosomal aneuploidies. PGT-A screens for chromosomal aneuploidies in the embryos thereby increasing the chances of a successful pregnancy.

Indications for PGT-A include advanced maternal age, recurrent implantation failure, severe male factor and couples with normal karyotypes who have experienced recurrent miscarriage.

For an individual known to be a carrier of a balanced chromosomal translocation (like inversion, reciprocal translocation or Robertsonian translocation), there is a risk of unbalanced chromosomal translocation in every pregnancy which might lead to pregnancy loss. The test-PGT SR aids in identifying the embryos with unbalanced chromosomal translocation, thereby filtering them out and increasing the chances of implantation of healthy embryos.

This test is useful in cases where a couple has an affected child/ a family history of genetic condition with a known genetic variant and now wants to have a healthy pregnancy. The genetic change present in the affected child/ carrier parents can be tested in the embryos to know their affection status. Based on this report, healthy embryos can then be implanted. The test must be accompanied with appropriate genetic counseling so that the patient makes a well informed decision.

Increasing the rate of implantation:

The journey of a pregnancy from formation of an embryo followed by implantation, and ultimately leading to a live birth is an intricate process and involves synchronisation of multiple systems. One such parameter which is observed to play an important role in implantation is the timing or period of implantation. One third of couples faced with recurrent implantation failure are found to have a displaced Window of Implantation (WOI). WOI is the best suited timing for embryo implantation.

Endometrial Receptivity Testing analyses the transcriptomic signature to determine the best suited time for embryo implantation when the endometrium is most receptive.

A normal endometrial microbiota is important for implantation. The test EndoBiome assesses the levels of endometrial Lactobacillus as well as presence of specific pathogens associated with poor reproductive outcomes. Based on the report, measures can be taken to improve the endometrial microbiota thereby increasing the rate of implantation.

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Role of genetic testing in in-vitro fertilization - Express Healthcare

Study characteristics

Among the 2134 articles retrieved from the databases, 116 articles were finally screened: 96 Chinese articles (Supplementary) and 20 English articles17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36. The articles included a total of 23,396 patients with AD and 25,568 control individuals. Figure1 depicts the literature screening process. The study area source distribution was as follows: a total of 115 studies clearly identified the specific source of cases covering 28 provincial-level regions (Fig.2). Another multicentre study, which could not be consolidated, covered 30 provincial-level regions21. Fifty-one of the studies reported the age distribution of the subjects (Fig.3). In conclusion, the case sources in this meta-analysis covered at least 30 provincial-level administrative regions (including Taiwan and China) out of 34, with good representation.

The study screening process.

115 studies participants from various geographical areas in China.

Age distribution of subjects in 51 studies. *65 is the dividing line between early-onset Alzheimers and late-onset Alzheimers.

Table 1 lists the results obtained for each allele and genotype of ApoE in this meta-analysis. With the exception of the 2 homozygotes and 4 homozygotes, all I2>50% and Q statistics were significant. Therefore, the corresponding random model and fixed model were used for calculating the pooled OR. ApoE 2/4, 3/4 and 4/4 were significantly associated with AD (2/4: OR 1.521, 95% CI[1.2701.823], P<0.001; 3/4: OR 2.491, 95% CI [2.2672.738], P<0.001 and 4/4: OR 5.481, 95% CI [4.8016.257], P<0.001). The 2/2, 2/3 and 3/3 genotypes were also significantly associated with AD (2/2: OR 0.612, 95% CI [0.5040.743], P<0.001; 2/3: OR 0.649, 95% CI [0.5850.714], P<0.001 and 3/3: OR 0.508, 95% CI [0.4680.551], P<0.001). The OR of 4 homozygotes was the largest, and that of 3 homozygotes was the smallest.

Table 1 lists the results obtained for each allele and genotype of ApoE in this meta-analysis. The I2>50% and Q statistics were significant; thus, heterogeneity between studies was significant. The random effect model was applied for calculating the pooled OR. The frequency of the ApoE 4 allele was higher in patients with AD than it was in healthy controls and exhibited a statistically significant positive association between risk factor 4 allele carriers and AD in the Chinese population (OR 2.847, 95% CI [2.6113.101], P<0.001). The frequency of ApoE 3 was lower in patients with AD than it was in healthy controls, and the difference was also statistically significant (OR 0.539, 95% CI [0.5040.576], P<0.001). This finding implies the protective effect of the 3 allele regarding the development of AD in the Chinese population. The 2 and 3 alleles yielded the same result (OR 0.771, 95% CI [0.7050.843], P<0.001). However, the OR of 2 was closer to 1 than that of 3.

Figures3 and 4 show the distribution of the ORs from individual studies in relation to their respective standard deviation in the funnel plot. There was a possibility of a publication bias risk in the meta-analysis. To eliminate any publication bias, the random effect model was selected for most alleles and genotypes. By systematically deleting each study each time and recalculating the results, the OR values were all close to the original results, with a small fluctuation range and significance. All sensitivity analyses were consistent with the primary results.

(a) Funnel plot on the association between 2 Allele and AD in full model. (b) Funnel plot on the association between 3 Allele and AD in full model. (c) Funnel plot on the association between 4 Allele and AD in full model. (d) Funnel plot on the association between 3/3 Genotype and AD in full model. (e) Funnel plot on the association between 3/3 Genotype and AD in subgroup analysis model.

As further verification of the protective effect of the 3 allele, funnel plot results showed high heterogeneity in all studies. A subgroup analysis was performed using the same method for the inclusion of data from the literature that explicitly stated that the study object was sporadic AD. Because of the different genetic relationships between APOE and sporadic AD and familial AD, sporadic AD was predominant in the majority of articles; therefore, studies that clearly stated that the study object was sporadic AD were included in the subgroup analysis. The screening results of 30 references (the sporadic/familial type was not described in the remainder of the articles) were as follows: AD: 11,629 cases, control: 12,394 cases; sex ratio: AD male/female: 5543/5476; control male/female: 5489/6383 (three studies did not provide the sex ratio), gender difference between the two groups, 2=37.900, P<0.001. Figure5a,b report the subgroup analysis of 3 and the 3/3 forest diagram, respectively. The frequency of ApoE 3 in sporadic AD was lower than that in healthy controls, and the differences were statistically significant (OR 0.642, 95% CI [0.5640.731], P<0.001): 2/3 (OR 0.668, 95% CI [0.5550.804], P<0.001) and 3/3 (OR 0.595, 95% CI [0.5100.694], P<0.001). The frequencies of alleles and genotypes were lower than those observed in the healthy controls, and the differences were statistically significant. The OR value of 3/3 was smaller than that of 2/3, which was consistent with the results of the whole model.

(a) Forest plot on the association between 3 allele carriers and AD in subgroup analysis. (b) Forest plot on the association between 3/3 Genotype carriers and AD in subgroup analysis.

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Protective effect of apolipoprotein E epsilon 3 on sporadic Alzheimer's disease in the Chinese population: a meta-analysis | Scientific Reports -...

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PRC1-mediated epigenetic programming is required to generate the ovarian reserve - Nature.com

Actor Ashton Kutcher has gone public with his battle with vasculitis, a rare blood vessel disease that he said left him unable to see, hear, and walk.

On an episode of National Geographics show Running Wild with Bear Grylls: The Challenge, Kutcher said hes lucky to be alive.

Kutcher said on the program that Two years ago, I had this weird, super rare form of vasculitis that, like, knocked out my vision. It knocked out my hearing. It knocked out, like, all my equilibrium.

The 44-year-old actor said it took him about a year to regain those abilities.

You dont really appreciate it until its gone, until you go, I dont know if Im ever going to be able to see again, I dont know if Im ever going to be able to hear again, I dont know if Im ever going to be able to walk again,' Kutcher said.

According to the National Heart, Lung, and Blood Institute, vasculitis also known as angiitis or arteritis includes a group of rare conditions that can take place when swelling affects the walls of your blood vessels. Swelling is your bodys response to tissue injury. Autoimmune disorders or diseases that make your body attack itself, infections, and trauma are some examples of potential causes of swelling in the blood vessels.

Swelling in the blood vessels can lead to serious problems, including organ damage and aneurysms, a bulge in the wall of a blood vessel, the institute said.

There are multiple types of vasculitis, which affect any blood vessels in the body. Symptoms include fever, weight loss, fatigue, pain, and rash.

Drugs can help treat the problem, as the goal is usually reducing the accompanying inflammation, according to the institute. Treatment can push vasculitis into remission.

Vasculitis is an autoimmune condition where your body mistakenly attacks your own blood vessels in addition to other things. This results in loss of blood flow to important areas of your body as these arteries are damaged, Dr. Bing Shue, a vascular surgeon with Connecticut-based The Vascular Experts, told Healthline.

Loss of vision can be a very serious complication of giant cell arteritis, or GCA, Shue said. This is the most common vasculitis that affects people over the age of 65 and can result in permanent blindness. Many patients develop muscle cramps and severe exhaustion that can lead to loss of walking ability. Many forms of vasculitis also cause inflammation in the ear that can cause hearing loss and vertigo.

Shue added vasculitis can be controlled if diagnosed appropriately and treated.

It can be put into remission after initial treatments and your immunologist can monitor for remission long term, Shue said. We perform procedures to diagnose vasculitis and treat damaged blood vessels that result from vasculitis. If untreated it can lead to fatal complications like stroke or loss of kidney function.

There are many different causes, he added. Genetic predisposition is common and diseases can run in the family. Certain vasculitis are more prevalent in certain age ranges We have been seeing more cases of vasculitis but much of this is likely better awareness and diagnosis of these conditions. In the past vasculitis has been notorious for being difficult to diagnose resulting in delayed treatment.

Dr. Robert Koval, a rheumatologist with Texas Orthopedics, told Healthline its not clear what type of vasculitis Kutcher has.

However, vision/hearing loss and coordination difficulties are certainly possible, although rare, Koval said. Vasculitis can present in many different ways, including neurologic complaints, bleeding, rash, or organ failure. Oftentimes fevers, constitutional symptoms, and inflammation in multiple organ systems occur. Lab values, skin or tissue biopsies, and imaging can all be helpful in diagnosing these conditions.

In its most severe forms, vasculitis can be fatal, Koval said. However, there are much improved therapies to treat vasculitis these days that usually can result in remission, or at least minimal symptoms.

Ana Codallo, the chief technology officer of healthcare research website Key Opinion Leaders, told Healthline, that the symptoms of vasculitis are wide-ranging.

There are digestive issues where you might experience pain after eating, and dizziness which affects your hearing as well as weakness in your hands and feet, Codallo said. I would always suggest you seek medical advice if you are experiencing any of the symptoms listed as well as any other symptoms as it is always in your best interest to seek medical opinions. This will help you get the relevant help as soon as possible and it will also prevent you from excess worrying for no reason.

If you are diagnosed with vasculitis, you will be given a corticosteroid drug to control the inflammation, but there are occasions where you might need surgery to unblock arteries, she added. Vasculitis cannot be cured, but it can be managed well and it is no longer considered a fatal illness.

Continue reading here:
Ashton Kutcher and Autoimmune Disease Vasculitis - Healthline

You should read the following discussion and analysis of our financial conditionand results of operations together with the consolidated financial statementsand related notes that are included elsewhere in this Quarterly Report on Form10-Q and our 2021 Form 10-K. This discussion contains forward-looking statementsbased upon current plans, expectations and beliefs that involve risks anduncertainties. Our actual results may differ materially from those anticipatedin these forward-looking statements as a result of various factors, including,but not limited to, those discussed in the section entitled "Risk Factors" andelsewhere in this Quarterly Report on Form 10-Q. In preparing this MD&A, wepresume that readers have access to and have read the MD&A in our 2021 Form10-K, pursuant to Instruction 2 to paragraph of Item 303 of Regulation S-K.Unless stated otherwise, references in this Quarterly Report on Form 10-Q to"us," "we," "our," or our "Company" and similar terms refer to RocketPharmaceuticals, Inc.We are a clinical-stage, multi-platform biotechnology company focused on thedevelopment of first, only and best-in-class gene therapies, with directon-target mechanism of action and clear clinical endpoints, for rare anddevastating diseases. We have three clinical-stage ex vivo lentiviral vector("LVV") programs. These include programs for Fanconi Anemia ("FA"), a geneticdefect in the bone marrow that reduces production of blood cells or promotes theproduction of faulty blood cells, Leukocyte Adhesion Deficiency-I ("LAD-I"), agenetic disorder that causes the immune system to malfunction and PyruvateKinase Deficiency ("PKD"), a rare red blood cell autosomal recessive disorderthat results in chronic non-spherocytic hemolytic anemia. Of these, both thePhase 2 FA program and the Phase 1/2 LAD-I program are in potentiallyregistration-enabling studies in the United States ("U.S.") and Europe ("EU").In addition, in the U.S., we have a clinical stage in vivo adeno-associatedvirus ("AAV") program for Danon disease, a multi-organ lysosomal-associateddisorder leading to early death due to heart failure. Additional work on a genetherapy program for the less common FA subtypes C and G is ongoing. We haveglobal commercialization and development rights to all of these productcandidates under royalty-bearing license agreements.Effective December 2021, a decision was made to no longer pursueRocket-sponsored clinical evaluation of RP-L401; this program was returned toacademic innovators. Although we believe that gene therapy may be beneficial topatients afflicted with this disorder, we have opted to focus availableresources towards advancement of RP-A501, RP-L102, RP-L201 and RP-L301, based onthe compelling clinical data to date and potential for therapeutic advancementin these severe disorders of childhood and young adulthood.

Recent Developments

At-the-Market Offering Program

Gene Therapy Overview

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Index

The chart below shows the current phases of development of Rocket's programs andproduct candidates:

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Index

Analysis of the explanted heart revealed significant fibrosis consistent with

advanced DD.

Myocardial tissue from the explanted heart at 5 months post-treatment displayed

100% LAMP2B protein expression by immunohistochemistry throughout non-fibrotic

cardiac regions including the ventricles and other essential targeted areas

--------------------------------------------------------------------------------

Index

Fanconi Anemia Complementation Group A (FANCA):

--------------------------------------------------------------------------------

Index

Leukocyte Adhesion Deficiency-I (LAD-I):

--------------------------------------------------------------------------------

Index

Pyruvate Kinase Deficiency (PKD):

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Index

Infantile Malignant Osteopetrosis (IMO):

cGMP Manufacturing

Strategy

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Index

Financial Overview

Revenue

Operating Expenses

Research and Development Expenses

Our R&D program expenses consist primarily of external costs incurred for thedevelopment of our product candidates. These expenses include:

expenses incurred under agreements with research institutions and consultants

that conduct R&D activities including process development, preclinical, and

clinical activities on our behalf;

costs related to process development, production of preclinical and clinical

materials, including fees paid to contract manufacturers and manufacturing

input costs for use in internal manufacturing processes;

consultants supporting process development and regulatory activities;

patent fees; and

costs related to in-licensing of rights to develop and commercialize our

product candidate portfolio.

salaries and personnel-related costs, including benefits, travel, and

stock-based compensation, for our scientific personnel performing R&D

activities;

facilities and other expenses, which include expenses for rent and maintenance

of facilities, and depreciation expense; and

laboratory supplies and equipment used for internal R&D activities.

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$ 4,507 $ 15,942 $ 8,307Leukocyte Adhesion Deficiency (LVV) RP-L201

$ 5,078 $ 12,511 $ 9,741Stock based compensation expense

$ 24,530 $ 72,150 $ 52,839

(1) Effective December 2021, a decision was made to no longer pursue

Rocket-sponsored clinical evaluation of RP-L401; this program was returned to

the scope, rate of progress, and expense of ongoing as well as any clinical

studies and other R&D activities that we undertake;

future clinical study results;

uncertainties in clinical study enrollment rates;

changing standards for regulatory approval; and

the timing and receipt of any regulatory approvals.

the scope, progress, outcome and costs of our clinical trials and other R&D

activities;

the efficacy and potential advantages of our product candidates compared to

alternative treatments, including any standard of care;

the market acceptance of our product candidates;

obtaining, maintaining, defending, and enforcing patent claims and other

intellectual property rights;

significant and changing government regulation; and

the timing, receipt, and terms of any marketing approvals.

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Index

General and Administrative Expenses

Interest Expense

Interest Income

Interest income is related to interest earned from investments and cashequivalents.

Critical Accounting Policies and Significant Judgments and Estimates

Comparison of the Three Months Ended June 30, 2022 and 2021

-

168

Amortization of premium on investments - net (396 ) (727 )

Research and Development Expenses

General and Administrative Expenses

--------------------------------------------------------------------------------

Comparison of the Six Months Ended June 30, 2022 and 2021

1,052

Research and Development Expenses

General and Administrative Expenses

Other Expense, Net

Liquidity, Capital Resources and Plan of Operations

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Index

20,178

9,907

Net change in cash, cash equivalents and restricted cash $ (45,146 )

Investing Activities

During the six months ended June 30, 2022, net cash provided by investingactivities was $15.8 million, primarily resulting from proceeds of $163.7million from the maturities of investments, offset by purchases of investmentsof $143.0 million, and purchases of property and equipment of $4.8 million.

Financing Activities

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ROCKET PHARMACEUTICALS, INC. Management's Discussion and Analysis of Financial Condition and Results of Operations (form 10-Q) - Marketscreener.com

While many organisms fall into one of two sexes, others are co-sexual, a version of hermaphroditism that involves having both male and female reproductive organs. Multiple species of brown algae (class Phaeophyceae), for example, have evolved over time from a male/female binary into co-sexual hermaphrodites. Susana Coelho, a biologist at the Max Planck Research Institute for Biology Tbingen in Germany, says that while the ability to auto-fertilize results in reduced genetic diversity compared to other mating systems, it can also lessen the pressure to find partners in the vast ocean.

To understand how brown algae switched to hermaphroditism, Coelho and her team studied eight algal species: four that are co-sexual and four closely related species that have retained two sexes. The researchers used RNA-seq to compare gene expression in each species, finding that hermaphrodites shared more sex-biased genesgenes that are typically expressed differently between the sexeswith females than with males, indicating that females most likely made the transition to co-sexuality. It was quite cool . . . to see that it was always the female [that] acquired the male function, Coelho says. The team also found that, as species transitioned, each appeared to experience similar shifts in gene expression. Sixty-one percent of orthologous genes shared across all eight speciessex-biased or notshowed similar changes in patterns of expression in the co-sexual species compared with the binary species.

This was the most interesting result, says Hisayoshi Nozaki, a biologist at the University of Tokyo who was not involved in the study, noting that this research is the first to examine the genetics of the transition to hermaphroditism in these algae. He adds that a further, fruitful step would be to do whole-genome sequencing to learn more about how the seaweeds sex chromosomes have changed.

G.G. Cossard et al., Selection drives convergent gene expression changes during transitions to co-sexuality in haploid sexual systems,Nat Ecol Evol, 6:57989, 2022.

See the rest here:
Meet the Algae That Went from Male/Female to Hermaphroditic - The Scientist

For females of many species, choosing a mate is a weighty decision. You want your offspring to inherit the best possible genes. But how do you judge the genetic quality of a potential mate?

Around 50 years ago, an idea emerged that the extent of deviation from perfect bilateral symmetrythat is, the difference between an animals right and left sidescould indicate genetic quality. Researchers hypothesized that individuals with high-quality genes would be better buffered against stress and instability during development, and thus more likely to turn out symmetric. In order to maximize fitness, then, females should opt for more-symmetric partners.

In the 1980s and 90s, numerous studies across different species tested whether females consider symmetry when choosing a mate. However, these studies produced mixed results, according to Roshan Kumar Vijendravarma, a biologist at the Institut Jacques Monod in Paris. He says that efforts to experimentally induce asymmetry (which included clipping feathers, adding colored rings to the feet, and increasing stresses like temperature during development) often had confounding effects on survival, growth, and behavior. In other words, these studies were unable to separate asymmetry from other factors affecting fitness.

If both wings are equally shaped, each should generate similar sounds.

Eventually, with questions still unanswered, the research buzz around the symmetry-based hypothesis of sexual selection died down. Until, that is, Vijendravarma recently decided to revisit the issue as a postdoc in the lab of Pierre Leopold at the Institut Curie in Paris. Their paper, published in March in PNAS, is clearly an improvement on most or all previous studies in this area, says Laurent Keller, a biologist at the University of Lausanne in Switzerland who was not involved in the study.

Vijendravarma was able to overcome the challenges that had plagued previous attempts with a novel method of inducing asymmetry, which he deployed in Drosophila melanogaster. After unsuccessful attempts at producing wonky fly larvae with the usual ecological stressors, he discovered that altering the direction of gravity with a vertically rotating apparatus reliably disrupted symmetric development. In particular, it influenced the wing area in adults, producing a pool of research subjects whose wings ranged from near-perfect mirror images to very asymmetric but who were otherwise indistinguishablethe treatment had no obvious detrimental effects. The males were all viable and they all reproduced. We were able to uncouple asymmetry from bad quality, he says.

A male fruit fly (Drosophila melanogaster) follows around and sings to a female, using one wing at a time.

COURTESY OF ROSHAM KUMAR VIJENDRAVARMA

Vijendravarma and his colleagues then randomly selected pairs of males raised in altered gravity to compete for a female. Most females opted for males that were more symmetric, the team found. The researchers also performed genetic and surgical manipulations on flies to alter their wing symmetry. While these experiments would not be definitive on their own due to the confounding factors that also plagued earlier studies, they could provide supporting evidence to the results from the gravity experiments, Vijendravarma says. Sure enough, no matter how the wings got to be uneven, females preferred more symmetric males.

The methodology is beautiful, says Marla Sokolowski, a biologist at the University of Toronto who was not involved in the study. I think its a rigorous study, right down to the way the flies were reared, housed, and handled. . . . They came up with almost everything one could think of to induce this asymmetry.

Vijendravarmas second innovation was to look beyond the sense of sight. It struck him that although the literature was full of studies where females were expected to assess the symmetry of males visually, the courtship of most animals is multimodal. Female fruit flies, for instance, use olfactory and auditory cues in addition to visual ones during courtship. Through which of these senses do they perceive asymmetry?

Conducting mate choice experiments under red light, so the females couldnt see, did not make a difference to their behavior, nor did removing their scent-sensitive antennae. However, making the females deaf by removing their antennal sound receptors, or aristae, caused them to lose their preference for symmetric males.

Vijendravarma consequently turned his attention to the Drosophila courtship songs, which males produce by extending and vibrating one wing at a time. If both wings are equally shaped, each should generate similar sounds. But if they are asymmetric, the difference would be reflected in the song, Vijendravarma reasoned. Sure enough, analysis of left wing and right winggenerated sounds revealed that rejected males with asymmetric wings sang songs that varied in amplitude and frequency.

On the face of it, the data are quite convincing, says Michael Ritchie, a biologist at the University of St Andrews who was not involved in the study. However, he says some might be skeptical of whether the study really demonstrates that females evaluate symmetry as a measure of male quality. Theres nothing in the paper about variation in genetic quality. Its an artificially constructed developmental aberration, he says. The question is, does natural variation in genetic quality influence male asymmetry, and would females discriminate against males based on that level of asymmetry?

Keller also wonders about how females may benefit from choosing a symmetric mate. It would be interesting to allow females to choose males based on symmetry and then compare the fitness of the offspring, he says.

In future work, Vijendravarma plans to investigate the link between asymmetry and genetic quality, as well as how altered gravity leads to asymmetry. But he and Leopold also hope to inspire other researchers to think more broadly about asymmetry and sexual selection. In a recent review paper, the pair attempts to address sciences bias toward visual cues by highlighting the many ways that females of different species may assess symmetry nonvisually. The idea is that we need to think more about the ecology of the animal before setting up these types of experiments, rather than impose our own biases onto them, says Vijendravarma.

The authors list auditory, chemosensory, and mechanosensory cues evaluated by females and speculate about how these signals could be affected by asymmetry in physical features such as pheromone glands or legs. They further propose that the structures built for courtship by males of some species, such as the bowers of bowerbirds and nests of certain fish, could amplify minute levels of asymmetry in the builder.

The review is full of useful, fascinating ideas, says Ritchie. I think this deserves to stimulate more work, and it probably will.

Read more here:
The Sex Appeal of Symmetric Songs | TS Digest | The Scientist - The Scientist

Asexual reproduction has been one of the most fascinating biological features of some animals, who can reproduce on their own, hence the derivation of the term.

Unlike sexual reproduction, its counterpart does not rely on conventional mixture of sperm and egg for ovulation and fertilization to take place involving two opposite sexes.

In the process called parthenogenesis, dozens of vertebrate species are capable of asexually reproducing, wherein most animals include fish or lizards.

While it has a beneficial effect for survival, a new study found that asexual reproduction can lead to life-threatening genetic mutations.

The new research led by biologists from the University of Texas at Arlington found new details that support the theory that species have more harmful genes as a result of unnatural genetic changes compared to those utilizing sexual reproduction.

While the mutations are also present in offspring that are byproduct of sexual reproduction, the angle that such genetic alterations are present from asexual reproduction is relatively least explored.

With the new paper, the scientists expounded the premise that the genetic mutations are universal but varies depending on the type of reproduction.

(Photo : Photo by YURI CORTEZ/AFP via Getty Images)

In the study published on the journal Evolutionon May 17, the US-based biologists explored the aspect of sexual reproduction of being ubiquitous in the natural world, implying that sex could have extensive benefits to surpass the coast of males relative to asexual reproduction.

The research used a previous hypothesis that the advantage of reproduction based on sexual intercourse is that it removes faulty genetic mutations from the genome.

The theory predicted that a transition from sexual to asexual increases the risk of the accumulation of "slightly deleterious mutations."

In addition, the paper indicated that such transition suppresses recombination and segregation, which weakens natural selection.

Also Read:Male-less Reproduction: Strange Biological Switch Observed In Shark For The First Time

Authors of the study examined Aspidoscelis, a genus of whiptail lizards, as part of parthenogenesis and as summarized by phys.org.

The team also selected the reptiles due to their abundance and distribution throughout the southwestern part of the United States.

The scientists came up with their conclusion after using mitochondrial genome data from both asexual and sexual whiptail lizards.

The method aimed to test whether their prediction that parthenogenetic lineages result in faster genetic mutations than sexual lineages.

Both sexual and asexual reproduction have their own advantages and disadvantages, which some living things utilize to produce their own offspring, according to the University of Utah.

While some species are capable of both reproduction methods, the new research implies there is still limited data that needs addressing.

Although it was reportedly found that asexual production yielded unwanted genetic changes, it can still serve as a significant method when it comes to survivability and mating challenges.

In particular, previous wildlife documentaries and research showed that there are instances where physical sexual intercourse between two animal species is challenging, especially in hostile environments where competition is prevalent.

Related Article:How Certain Animal Species Survives Without Sexual Reproduction

2022 NatureWorldNews.com All rights reserved. Do not reproduce without permission.

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Asexual Reproduction: Species Reproducing on Their Own are Susceptible to Dangerous Genetic Mutations - Nature World News

Society faces challenges to feed a growing population with a reliable supply of wholesome food, produced to high standards of safety and welfare. The development and adoption of new technologies such as precision breeding can help optimise the balance between productivity, health and welfare in modern livestock farming systems, says aquaculture breeder Alan Tinch.

It was disappointing that a minority of MPs used last weeks Second Reading debate on the Precision Breeding Bill to articulate their prejudice against modern livestock farming by suggesting that the legislation would be a step backwards for farm animal welfare.

Disappointing, but perhaps not entirely surprising given the high-profile campaigns by organisations such as Compassion in World Farming to draw an (unjustified) association between technological advance and worse outcomes for farm animal welfare.

This isnt a debate about whether or not we should farm livestock. We should be considering how new technology can be used to make farming even more sustainable, and deliberating ways to improve the health and welfare of livestock.

Genome editing itself is neutral in terms of animal health and welfare. It is a scientific tool which enables scientists and breeders to make targeted genetic changes more quickly and precisely, based on our improved understanding of genomics and genetic function.

Margaret Beckett, as Environment Secretary, once observed that opposing genetic technologies was like campaigning against the petri dish in other words, what matters is not the existence of specific scientific tools but the way they are used.

As this legislation progresses through Parliament, I hope that future debates will focus on the potential of the science, and avoid provocative references to cramming animals together in unsanitary conditions (Kerry McCarthy MP a vegan), or to intensive factory farming practices (Caroline Lucas MP a vegetarian).

It is also wrong to associate genome editing with any particular farming system or ideology, just as it is wrong to associate scientific innovation and technological advance with poorer animal health or welfare.

We understand from experience that any advance in our scientific knowledge can be deployed to deliver a range of outcomes. We should assess and deploy new technology to improve systems, not dismiss it because there are potential negative consequences. Overzealous precautionary approaches would have prevented use of new technologies such as the printing press, the steam engine, internal combustion engine, vaccines and others. We now consider the Locomotive Act disproportionate with its requirement to wave flags in front of motorised vehicles.

The development of Covid vaccines in record time is a clear example of how genetic technologies such as GM, genome editing and RNAi have unquestionably been used for the enormous benefit of humankind.

Current plans for the use of genome editing in the livestock sector relate either to human health applications or to improved health and welfare in farmed animals, primarily through improved genetic resistance to diseases such as Porcine Reproductive and Respiratory Syndrome (PRRS) and African Swine Fever in pigs, and avian influenza in poultry.

These devastating animal health conditions are not the result of factory farming, as Caroline Lucas suggests. They do not differentiate between animals kept in intensive or extensive systems.

Concern continues about the spread of avian influenza which is transmitted by wild birds and affects outdoor-reared and backyard poultry, and can potentially mutate to infect humans and begin the next global pandemic. Genome editing to control avian influenza infection in chickens has been proposed by scientists in the UK. How can it be ethical not to embrace and encourage scientific innovation which promises solutions to such devastating disease?

The Precision Breeding Bill itself does not set or change existing standards for farm animal welfare.

These standards are addressed through separate regulations applied at both research and farm level and which rightly focus on welfare outcomes, not on production or breeding methods. They are reinforced at farm level by independently accredited assurance schemes such as Red Tractor and RSPCA Assured.

Still often misjudged by the perceptions of 30 or 40 years ago, farm animal breeding today uses a balanced approach to select for a range of traits which optimise performance, health and welfare outcomes in new strains. Organisations such as the European Forum of Farm Animal Breeders (EFFAB) promote the use of a balanced range of traits in farm animal breeding, and UK breeders supported by world-leading livestock research and animal health institutes such as Roslin and Pirbright are recognised for developing novel methods of selecting animals with improved welfare characteristics including IPN resistance in Atlantic salmon, and real-time X-ray assessment of leg strength in broilers.

By using genome editing constructively, animal breeders and farmers can deliver further improvements the health, welfare and sustainability of farmed animals. Personally, I consider it immoral not to deploy technology that can be used to improve the health and welfare of the animals in our care. We wouldnt argue against the development of a new vaccine because farmers might increase stocking density and exactly the same argument applies to precision breeding technologies such as genome editing.

In addition, the Bill makes provision for a separate welfare assessment to be applied specifically to genome edited animals as a further assurance that the welfare of the animal (or its progeny) would not be adversely affected by any trait resulting from precision breeding.

Modern animal breeders welcome objective methods to assess animal welfare and include assessment of welfare-associated traits into their breeding programmes. By open and transparent consideration of precision breeding technology, animal breeders can demonstrate that modern farming continues to improve the health, welfare and sustainability of livestock production.

Alan Tinch receiveda Ph.D. in genetics from the University of Edinburgh, and has been the VP of the Center for Aquaculture Technologies. During his career he has worked with aquatic and terrestrial species such as Atlantic salmon, chickens and pigs in the UK and worldwide. Follow Alan on Twitter @aetinch

A version of this article was posted at Science for Sustainable Agriculture and is used here with permission. Check out Science for Sustainable Agriculture on Twitter @SciSustAg

More:
Viewpoint: Why genetic engineering of livestock is compatible with the sustainable and human treatment of animals - Genetic Literacy Project

Everybody gets older, although not everyone ages in the same way. For many people, late life includes a deterioration of health brought on by age-related disease. Yet there are also people who retain a more youthful vigor, and around the world, women typically live longer than men. Why is that? In this episode, Steven Strogatz speaks with Judith Campisi and Dena Dubal, two biomedical researchers who study the causes and outcomes of aging to understand how it works and what scientists know about postponing or even reversing the aging process.

Listen on Apple Podcasts, Spotify, Google Podcasts, Stitcher, TuneIn or your favorite podcasting app, or you can stream it from Quanta.

Steven Strogatz (00:03): Im Steve Strogatz, and this is The Joy of Why podcast from Quanta Magazine that takes you into some of the biggest unanswered questions in science and math today. In this episode, were going to be talking about aging. Why exactly do we age? Whats happening at the cellular level as our bodies get older?

(00:22) Scientists are still chasing many of the answers, but there have been some important advances in understanding the distinctive changes we call aging. Someday, that progress might not only help us live longer, but live better too. After all, living many years may not be much of a bargain if it means suffering from diseases like Alzheimers or Parkinsons. Well ask what role do our genes play in aging? And why do women tend to live longer than men on average? And also, what is research finding out about the ways we might slow down the process of aging?

(01:00) Later in this episode, well be hearing from Dr. Dena Dubal, associate professor in the department of neurology at the Weill Institute for Neurosciences at the University of California, San Francisco. But first, joining me now is Dr. Judith Campisi, a biochemist and cell biologist and professor at the Buck Institute for Research on Aging. Her lab there focuses on cellular senescence, a concept that well be unpacking very shortly. She is co-editor in chief of the Aging journal. Judy, thanks so much for joining us today.

Judith Campisi (01:34): My pleasure.

Strogatz (01:35): Im very excited to be talking to you about this. Well, of course, all of us are getting older, and we all feel it. It raises so many questions, though, like why is it happening? Is it something that nature is doing on purpose? Is it that our bodies are kind of wearing out like an old machine? Or how should we think about it?

Campisi (01:54): I think the way we have to think about it is in the context of evolution. If you think about humans, our lifespan, over the course of our evolution, aging never happened. There was no Parkinsons disease, no Alzheimers disease, there was no cancer. Everybody was dead by the age of 40 or 45. So evolution put into place ways of keeping young, reproductively fit organisms healthy for only a few decades, certainly not for the larger number of decades that were living through.

(02:35) Now, many of the processes that happen during aging really happen as a consequence of the declining force of natural selection. That is, there was no natural selection for these diseases. The process we study, cellular senescence, its now clear and certainly in mouse models that this process, the cellular process, drives a large number of age-related diseases, everything from macular degeneration, to Parkinsons disease, cardiovascular disease, and even late-life cancer, but it evolved to protect young organisms from cancer.

(03:19) So we certainly dont want to stop it when were young. It also helps fine-tune certain structures during embryogenesis. And it initiates labor in women in the placenta. So these are the things that evolution is selecting for. And this is why we have to be careful in how we intervene. And thats true for almost everything that happens with age. Evolution didnt try to make us old. Evolution tried to make us young and healthy. And sometimes that came at a cost.

Strogatz (03:56): Its a fascinating perspective, actually, that the things that are healthy for us when were young and that would be selected by evolution can have this inadvertent consequence. That as weve been able to extend lifespan I suppose through better diet or medicine, all kinds of things that now what used to help us can hurt us.

Campisi (04:15): Yes, this idea that whats good for you when youre young, can be bad for you when youre old. It was proposed in the 1950s by a guy named George Williams, an evolutionary biologist named George Williams. There was no molecular data at that time, you know. No genomes had been sequenced. He pointed out evolution never had to fine-tune the prostate. If you dont have a good prostate, you dont have good babies. You dont make good babies. On the other hand, almost inevitably with age, over the age of, say, 50 or so, the prostate begins to enlarge and of course it becomes a possibility of developing into cancer. Yet that didnt happen for most of our evolutionary history.

Strogatz (05:02): Wow. So lets go into cells because this its so rich and wonderful what you and your students and colleagues have been discovering at the cellular level. So could you please define what it means for a cell to be senescent?

Campisi (05:17): It is a state that the cell enters, in which it adopts three new traits. One of them is it gives up almost forever, almost forever, the ability to divide. It will tend to resist dying. And most important, it tends to secrete a lot of molecules that can have effects on neighboring cells, and also in the circulation. Not that many cells have been studied when they become senescent. And almost everything else we know about senescence is slowly changing as we learn more and more about different cell types and different ways that cells enter senescence.

(06:00) Okay, so they stopped dividing. And that makes sense that that would prevent cancer. The other thing is they become relatively resistant to cell death. That is they stick around. And this could explain why they increase with age, and they do. Many people now have looked in many, many vertebrate tissues. And it just seems that the older the tissue, the more senescent cells are present.

(06:29) The caveat to that statement is, there are still very few of them even in very old and very diseased tissue. A few percent at the most. So why do people think this has anything to do with aging? That has to do with the third thing that happens when cells become senescent is they begin to secrete a large number of molecules that have biological activity outside the cell. And that means that those senescent cells can call immune cells to the site where they are, it can cause neighboring cells to fail to function. And it basically causes a situation that is classically termed chronic inflammation. You know, and of course, chronic inflammation is also a great risk for developing age-related cancer. Not so much childhood cancers, but age-related cancers.

Strogatz (07:26): So a certain small subset of cells that stopped dividing hang around for a long time, dont dont die, and yet secrete molecules that call immune cells or other parts of the immune system to come. And what I mean, are they signaling come and kill me? Or whats going on? Why are they, what are they secreting for?

Campisi (07:50): Yeah, so theyre secreting a large number of molecules. So some of them are growth factors. And we reported some time ago, that at least on a mouse, if you make a wound, like a skin wound just a little punch biopsy on the back of the mouse at the site of that wound, senescent cells form within a few days, and they secrete growth factors that help the wound heal.

(08:17) This is why evolution selected for this phenotype. Its not all bad. On the other hand, if you have a pre-cancerous cell nearby, and those growth factors are now being secreted, and this cancer cell sees them, its possible that that cancer cell will wake up and start to form a tumor. So again, good for you when youre young, bad for you when youre old.

Strogatz (08:44): Well, let me ask some basics while were talking about senescent cells, because I think there are some things Im curious about. For instance, should I think of them as having started out like any other kind of cell and something set them on a pathway to become senescent? Or are we born with them? Or whats, whats the right way to think about this?

Campisi (09:04): I think where the field is right now is were beginning to realize that all senescent cells are not equal. And then the question is, why would what starts out as a normal cell so youre right, you start out with a normal cell. What would make it enter this strange state where it doesnt divide? And its got all these molecules it has to make and secrete. And the answer is, the kinds of stresses that we tend to associate with both cancer and aging. So for example, anything that damages the genome or even damages what we now call the epigenome. The way genes are organized within the nucleus, anything that damages that has the potential to drive a cell into this senescent state.

(09:51) On the other hand, there are also stresses that we dont think about as normally associate certainly, not associated with cancer. But things, for example, like advanced glycation end products, the chemical reactions that take place when glucose levels are too high. And so this is a big problem with people who have diabetes or pre-diabetic conditions. So those, those chemicals can also cause the cell to become senescent. So its more appropriate to call it a stress response, except not all stresses result in senescence.

Strogatz (10:30): Let us, if we could, talk about the mouse experiments that you and your, your group have done really pioneering experiments where youve used the technique in molecular biology of transgenic mice. Maybe first, you should tell us what they are, and then how you use them as a kind of testbed for how to get rid of bad senescent cells.

Campisi (10:49): So right now in biology, its pretty straightforward and easy to insert DNA into the genome of a mouse, and then have that mouse develop into a full-blown adult mouse and have that adult mouse make babies. And so the mouse that we made, this trans. So thats called a transgene, the transgenic mouse we made, carried a piece of DNA that had a foreign protein made when cells become senescent. And that foreign protein had three parts. A molecule that was what we call luminescent, meaning we could image the cells in a living animal. It had a fluorescent protein, which meant that we could sort senescent cells from the tissues of that mouse. But most importantly, it had a killer gene, a gene that would normally be totally benign. But if you feed a drug, which is also very benign, that drug and the presence of that foreign gene will cause senescent cells to die.

(12:01) So we made this mouse quite a while ago. And weve shared it with dozens and dozens of academic labs that are studying different diseases of aging: Alzheimers disease, Parkinsons disease, cardiovascular disease, age-related cancers, osteoporosis, osteoarthritis, et cetera. And the results are just astounding.

(12:27) If you eliminate senescent cells, it is possible to do one of three things to an age-related pathology: You either make it less severe, or you postpone its onset, or and this is, of course, the one we all love in a few cases, you can even reverse that pathology.

Strogatz (12:49): Oh wow.

Campisi: I know. Thats true for osteoarthritis so far. And so this has now sort of given meat to the idea that developing drugs that can do what our transgenes can do. Its too late for any adult to get their transgenes. But if you have an unborn baby, it may be possible.

Strogatz (13:09): Oh, I see where youre going with that. I mean, thats, of course, thats a big can of worms for us, isnt it to think that, you know

Campisi (13:15): I know, its too political. Its already been done.

Strogatz (13:17): Oh, really?

Campisi (13:19): Well, its been done. Its been done in China. Right?

Strogatz (13:22): Youre saying that fetuses or before fetuses

Campisi (13:25): Thats correct. Was engineered. Yeah. I dont know the guy who did it, the Chinese guy who did it was condemned by the community because there were not enough controls there. No oversight, et cetera, et cetera. But its possible. Theres no intellectual reason why we cant make transgenic people. And my guess is, its not just China.

Strogatz (13:45): Okay, in terms of what was actually we know that youve done in you and the other people doing transgenic mice, if I just make sure I got that. You said there were three parts to the transgene, two of which it sounds like were for detecting. So theres the luminescent and the fluorescent part. But the, the killer part is the part that is playing the role of in the future drugs, I suppose, that could kill off the bad senescent cells. You had this genetic mechanism

Campisi (13:46): Thats exactly right. So the drug that we use to kill senescent cells in the mouse would not work in humans because humans are not transgenic. But the idea would be now to develop new drugs. And they are being developed. There, there are already some that are being used in mice, and even a few in early-stage clinical trials in people with the idea that they would mimic what our transgene can do in the presence of this otherwise benign drug.

Strogatz (14:13): And so the punchline here is that if this really comes to pass, this gives us hope for, as you said, postponing, ameliorating or in some cases maybe again, were dreaming, but its like theres science behind this or possibly reversing some of these many age-related diseases. Just that you told us about. Yes. Wow.

Campisi (15:01): Youll die on the tennis court at 110. But youll be winning.

Strogatz (15:06): Thank you very much, Judy. This has been just a delightful conversation, my pleasure.

Announcer (15:14): Explore more science mysteries in the Quanta Magazine book Alice and Bob Meet the Ball of Fire, published by The MIT Press. Available now at Amazon.com, Barnesandnoble.com or your local bookstore. Also, make sure to tell your friends about The Joy of Why podcast and give us a positive review or follow where you listen. It helps people find this podcast.

Strogatz (15:39): Why we age and what happens to our bodies as we age are two of the biggest mysteries about aging. Another mystery has to do with sex differences. Women tend to live longer than men. Its often said that they live three to five years longer. But really, if you look at the global statistics, you see that in some places, women live more than 10 years longer. So what is it about being female that makes women more resilient? The body of a 70-year-old woman may be younger than her 70 years biologically when compared to that of a 70-year-old man. Researchers on aging say that an epigenetic clock runs differently for each.

(16:19) If we can understand why a womans brain might also age differently than a mans, we might be able to develop therapies to help everyone. Research into this question gets us into proteins and sex chromosomes and hormones. The goal is to understand all of this better. Can we slow down the aging process somehow?

(16:39) Joining me now to discuss all this is Dr. Dena Dubal. Shes an associate professor of neurology at the University of California, San Franciscos Weill Institute for Neurosciences. Her lab studies female longevity and the aging brain. What makes it resilient against cognitive decline? Dr. Dubal is also an investigator with the Simons Collaboration on Plasticity and the Aging Brain. Dena, thank you so much for joining us today.

Dena Dubal (17:06): My pleasure. Thank you for inviting me.

Strogatz (17:08): Well, Im really pumped up by this. You know, I think in my own family about how sharp some of the women were in their 90s, even. I recently had an aunt who just passed away just shy of her 100th birthday. She had smoked her whole life. But she was sharp. And I dont know how she could have managed to live so long. The men were all gone, the husbands had all died.

Dubal (17:32): Yeah, I noticed something similar in my family of origin, when I was very young, and that is that women live longer than men. And every summer growing up, my parents would take me back to India, their country of origin. Theyre immigrants from India. And we would spend time in a very small village in western Gujarat. And it was really remarkable that the elderly were, were really mostly women. And I had a great-grandmother, whose name was Rumba, who was just a remarkable woman, not educated, but really smart. And she lived almost to her 90s. And her husband, my great grandfather, despite being robust, tall, handsome and also very smart, he died in his early 40s. And so her lifespan was nearly double that of his. And this was seen really throughout my extended family, that the women live longer than the men and I always wondered why that was.

Strogatz (18:41): I mean, Im sure that many of our listeners are thinking the same thing. Its a pretty commonplace experience that the, the women outlive the men. Of course, its not universal. There are exceptions for all kinds of reasons, but, but its just an amazing general trend.

Dubal (18:55): So in every society that records mortality across the world, women live longer than men. From Sierra Leone, where lifespan is lower, to Japan and Sweden, where lifespan is much longer. But heres a really interesting piece of information: When we look historically across multiple countries and societies, at times of extreme mortality, like famine and like epidemics, the girls will live longer than the boys and the women will live longer than the men.

(19:34) And this, this really suggests to us that there is a biologic underpinning for female longevity, because even when there is very high and equal stress in the environment with very high mortality, the girls are outliving the boys and the women are outliving the men. Theres some very, very sad and really remarkable times that, that demonstrate this including the Irish famine and many, many other examples in our world history.

Strogatz (20:04): Its, its really fascinating to think that its somehow so intrinsic, that theres something you know, youve mentioned the cultural aspects, but it does feel like theres something purely biological also going on. And I wonder if we could get into that. I mean, is there something happening in the body itself that could account for these differences?

Dubal (20:26): There can be, really I would say, four main reasons. If we think about this, biologically, why there could be sex differences and human longevity. One has to do with sex chromosomes, our genetics, our genetic code, and every single one of our cells in our bodies. And that is that female mammals and certainly female human mammals have two X chromosomes in every cell. One of them is inactivated during development, but there are two X chromosomes, and that is the sex chromosome complement of women and girls. In contrast, boys and men have one X and one Y.

(21:12) And so here already at the outset, there is a very clear and striking difference in our genetics. And so with this difference, and XX in females compared to XY in males, there, there arises for biologic reasons, for sex differences in longevity. One is that in males, theres a presence of a Y. And it is thought, although not experimentally shown, that maybe there are toxic effects or deleterious effects of the presence of a Y chromosome.

Strogatz (21:48): Wow, what an idea. Well, why do living things get old at all? Why dont we live forever? What causes aging in the first place?

Dubal (21:56): Thats a very simple yet philosophical question. I would say that aging is what happens with the passage of time to the biology of cells. There is a change in biologic functions that leads to dysfunction and vulnerability to diseases. One major cause is genetic instability. So over time, our genetic code becomes more unstable. Some mutations will occur. Parts of our genes kind of jump around those are called transposons and disrupt other parts of our genetic code. There are changes that occur epigenetic, that means on top of our genes that ultimately change the way that our cells express themselves. And that becomes dysregulated and more dysfunctional over time with aging.

Strogatz (22:54): All right, well, so theres, the story of why we age then is a very multi-faceted one, apparently.

Dubal (23:01): Yeah, yeah, and the loss of what we call homeostasis. But really, what that is, is housekeeping of proteins. How theyre turned over, how theyre modified, how theyre folded, what is done with the proteins in our cells. And the housekeeping of these proteins declines with aging. And so then theres this buildup of essentially gunk, of like clutter, that really jams up cellular processes and contributes to aging as well. Mitochondria are the powerhouses of our cells, and they have more dysfunction with aging.

(23:40) This brings us back to another possible biologic reason for female longevity, it brings me to something called the mothers curse. So all the mitochondria in all of your cells, Steve, and all of mine, are inherited from our mothers. So in the process of, of cellular division and the creation of a zygote, mothers pass on their mitochondria, not fathers. And so this, this becomes really important because mitochondria can only undergo evolution in a female body. Males will never pass their mitochondria on.

(24:24) And so at the end of the day, what that predicts is that mitochondrial function is more evolved to female physiology, when compared to male physiology. And this may make a difference with aging when things begin to go awry. The female cells may be more fit because their mitochondria are more evolved to the female cells compared to male cells. For males, that would be a mothers curse.

Strogatz (24:50): And then a mothers blessing for females, maybe. Interesting. This is this is an interesting thing. Wow. So that gives me a very good big picture about whats happening. So living longer, though, is just one aspect of what well be discussing here. Theres also the issue of living better, right? In terms of not in the case of people, not experiencing the cognitive decline that we or reducing that, that we all associate with getting older.

Dubal (25:18): Yeah. So, lifespan is one thing, right? How, how long does one live? And right now the oldest recorded person in history has lived to approximately 122 years old. But then health span is really a measure of how many healthy years of life is one living. Thats what we really aspire to, is really good healthy health span, where we are not suffering from cancers, cardiovascular disease, neurodegenerative diseases, like Alzheimers, cognitive decline and more that happens with aging.

(25:58) So with a very good health span, one lives a healthy life without these chronic debilitating conditions until, lets say, 100 and then one dies peacefully in ones sleep from pneumonia, lets say. But that is health span. Its really life lived without diseases. And, you know, the reason that we are so interested in lifespan is that the things that help us to live longer tend to help us to live better.

(26:32) So if we can understand the molecules that work together to conspire toward longevity, we can harvest those molecules to help fight disease. And thats why were so interested in, Wow, why is it that women live longer than men? Is there some biology of aging that can be discovered, learned and then harvested toward better health span in males and females?

Strogatz (27:02): Well, let us start getting into that, then. I mean, I suppose our common sense would say that its got to be about sex hormones. That we associate testosterone with men, estrogen with women. Is it estrogen thats the secret here that, that thats somehow protective? Or lets, lets start with that. Is it, is this a story of estrogen?

Dubal (27:24): Yeah, its a golden question. So this brings me to the fourth biologic reason for sex differences in longevity. One was, could it be the presence of a Y that increases mortality? Is it an extra X in females that extends lifespan? Is it a mothers curse of mitochondrial inheritance from mothers only that works against males? And fourth, what about sex hormones? Could it be that testosterone is decreasing lifespan in males and estrogen is increasing it in females?

(27:58) I think this is a really important possibility and considering sex differences in biology and in longevity. And we have some very interesting clues from natural human experiments and experiments in animals.

(28:16) There is some support that removing testosterone prolongs life. The Korean Chosun dynasty had a population of Korean eunuchs, that were castrated. They were useful and respected members of the dynasty and of the imperial court. And they lived a very long life, a significantly longer life than men of the same socio-economic status that lived at the same time on average, 15 years longer.

Strogatz (28:49): This is amazing.

Dubal (28:51): Right?

Strogatz (28:52): Wow!

Dubal (28:52): It suggests that decreasing testosterone prolongs life. And we do see this, actually. There have been animal studies in which sheep are castrated and will live longer compared to those that are not. And some very robust studies in dogs. Of course, we spay our dogs and castrated male dogs will live longer than non-castrated male dogs.

(29:16): But, Steve, I have to tell you that this question that you asked was burning me for many, many years. Could it be the hormones that contribute to female longevity? Is it estrogen, or could it be sex chromosomes that contribute to longevity? And to that point, we did a really neat experiment to be able to dissect out those two causes, and Id love to explain it if this is a good time.

Strogatz (29:42): Its perfect and, and I like that you, you describe it as neat because I read in reading about it to prepare for our conversation. I thought this was such an elegant and you know, this is like primo science. This is the scientific method, to ask this tricky question and find a way to get a good approximation to an answer to it.

Dubal (30:04): It was a really exciting experiment to do. And it mattered not what the results were, we were to follow the science and the science would tell us something about the cause of sex differences in longevity.

(30:18) And so to be able to dissect out whether female longevity was driven by hormones, or by sex chromosomes, we used a really elegant, as you said, animal model, called the FCG model, the four core genotypes model. And in these mice, theres, theres a genetic manipulation, theres a genetic engineering thats taken place. And that is on the Y chromosome, there is this SRY, or a testis-determining factor, theres a gene that causes male differentiation and the production of testes and testosterone.

(30:58) So in this model, SRY is taken off of the Y chromosome and added to any other autosomes, the non-sex chromosomes. And what this allows is the inheritance of this testicular determining factor, the SRY, the inheritance of it by males that are XY or by females that are XX. So at the end of the day, this genetic engineering enables the creation of mice that have four sexes: XX mice with ovaries, that is the typical female biologic genotype and phenotype. XX mice that have developed as male with testes. And thats again, because they inherited the testicular determining factor SRY and they have differentiated as males and they, they cannot be distinguished from other male mice, except that theyre XX. So they have testes, they have male reproductive behaviors, they ejaculate. They fight in their cages. They are male mice, except theyre XX.

Strogatz (32:10): Hmm. So Ive got it. I want to make sure everyone listening has got it because its so incredible this way of doing things that the, you can make. I mean, let me put it crudely I think its approximately right phenotypically, on the outside, they look like males but inside, in terms of their chromosomes, they look like females.

Dubal (32:29): Thats right. Thats right. And then we do the same in males, in that we produce XY males that lack the testis determining factor and have developed by default as females that is, that they are indistinguishable from other female mice. They have ovaries, they have a uterus, they cycle, they have female reproductive behaviors, they are female mice, except their genetics are XY. And then we have the typical male, that is XY male that has developed a male phenotype.

(33:08) So this model produces four sex genotypes with males and females, XX and XY that developed with either ovaries or testes. And this allows us to really track which mice will live longer. Is it the mice that have ovaries regardless of being XX or XY? Or is it the mice that are XX, that have female genetics, regardless of growing up with ovaries or testes?

Strogatz (33:37): Before you reveal the answer? Let me ask the question a different way because I want everyone to mull this question over in their head, and guess what the answer is. So the question is, youve created this thing thats a little hard to wrap our minds around, but I think weve got it. These four sexes, a traditional male, a traditional female, a male genetically, but I dont know which one you call the male. Do you call you call, you refer to male as anything thats XY, is that right?

Dubal (34:07): I do. But its, its a matter of taste and, and style.

Strogatz (34:11): Okay, but so its an, its an organism thats XY but has ovaries, yes. Or you can have an organism thats X. Its not an organ. Its a mouse that has XX, but has testes.

Dubal (34:24): Its, its sudoku. Its like this is scientific sudoku.

Strogatz (34:30): Thats great.

Dubal (34:30): Yeah, we actually didnt have a specific hypothesis, we were going to follow the science. And what we found very clearly, is that the mice with two X chromosomes lived longer than those that were XY. So the XX mice, regardless of growing up with ovaries and having lots of estrogen, or regardless of having testes and lots of testosterone, it was the XX mice that lived longer compared to the XY. So this was a decisive genetic experiment that showed us really for the first time that sex chromosomes contribute to female longevity.

(35:14) Now, there was more that the experiment taught us too. The mice that lived the longest of all the groups, or the mice that had ovaries combined with the XX chromosomes, those lived to maximal longest lifespan, suggesting that the hormones produced by the ovaries, that ovaries and the hormones also contribute to female longevity. And that maybe testosterone is deleterious. So the answer was, the main statistical effect was that sex chromosomes contribute to female longevity. However, the hormones did have an effect in there as well.

Strogatz (35:56): So of the four sexes that we could choose from in this sudoku that you created, the traditional female, if I can keep referring to it as that, seems to be the winner?

Dubal (35:56): In living the longest. Yes.

Strogatz (36:12): What about the worst? What about the one living the shortest is what I would guess?

Dubal (36:16): The XY with testes? The XX mice, whether they grew up with ovaries or testes, lived longer than the XY mice that grew up with ovaries or testes. XX mice lived about 15 to 20% longer than XY mice.

Strogatz (36:33): Thats an enormous difference. It really, I mean, I assume by any statistical measure was considered significant. Your statisticians must have said, is that right?

Dubal (36:41): Absolutely. Very, very clearly significant, a very clear sex chromosome effect.

Strogatz (36:47): Well, thank you on that very inspiring and thoughtful note, Dena. You know, this was a really just an outstanding discussion. Thanks so much for joining us today.

Dubal (36:55): My pleasure.

Announcer (36:58): Wants to know whats happening at the frontiers of math, physics, computer science and biology? Get entangled with Quanta Magazine, an editorially independent publication supported by the Simons Foundation. Our mission is to illuminate basic science and math research through public service journalism. Visit us at quantamagazine.org.

Steve Strogatz (37:22): The Joy of Why is a podcast from Quanta Magazine, an editorially independent publication supported by the Simons Foundation. Funding decisions by the Simons Foundation have no influence on the selection of topics, guests, or other editorial decisions in this podcast or in Quanta Magazine. The Joy of Why is produced by Susan Valot and Polly Stryker. Our editors are John Rennie and Thomas Lin, with support by Matt Carlstrom, Annie Melchor and Leila Sloman. Our theme music was composed by Richie Johnson. Our logo is by Jackie King, and artwork for the episodes is by Michael Driver and Samuel Velasco. Im your host, Steve Strogatz. If you have any questions or comments for us, please email us at quanta@simonsfoundation.org. Thanks for listening.

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Why Do We Get Old, and Can Aging Be Reversed? - Quanta Magazine

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Ten years ago, Hanna Rosins book, The End of Men, argued that feminism had largely achieved its aims, and that it was time to start worrying about the coming obsolescence of men. American women were getting more undergraduate and graduate degrees than American men, and were better placed to flourish in a feminized job market that prized communication and flexibility. For the first time in American history, they were outnumbering men in the workplace. The modern economy is becoming a place where women hold the cards, Rosin wrote.

The events of the past decadethe rise of Trump, the emergence of the #MeToo movement, the overturning of Roe v. Wadehave had a sobering effect on this sort of triumphalism. The general tone of feminist rhetoric has grown distinctly tougher and more cynical. Cheerful slogans about the femaleness of the future have receded; the word patriarchy, formerly the preserve of womens-studies professors, has entered the common culture. Last year, in an article about womens exodus from their jobs during the pandemic, Rosin recanted her previous thesis and apologized for its tragic navet. Its now painfully obvious that the mass entry of women into the workforce was rigged from the beginning, she wrote. American work culture has always conspired to keep professional women out and working-class women shackled.

Men, especially conservative men, continue to wring their hands over the male condition, of course. (Tucker Carlson appropriated the title of Rosins book for a documentary, advertised this past spring, about plummeting sperm counts.) But feminist patience for twilight of the penis stories has run out. All that time they spend snivelling about how hard it is to be a poor persecuted man nowadays is just a way of adroitly shirking their responsibility to make themselves a little less the pure products of patriarchy, Pauline Harmange wrote in her 2020 screed, I Hate Men. More recently, the British journalist Laurie Penny, in her Sexual Revolution (Bloomsbury), notes the systemic underpinnings of such snivels: The assumption that oozes from every open pore of straight patriarchal culture is that women are expected to tolerate pain, fear and frustrationbut male pain, by contrast, is intolerable. Penny is careful to distinguish hatred of masculinity from hatred of men, but she nonetheless defines the fundamental political struggle of our time as a contest between feminism and white heterosexual male supremacy. In Daddy Issues (Verso), Katherine Angel calls for #MeToo-era feminists to turn their attention to long-overlooked paternal delinquencies. If the patriarchy is to be defeated, she argues, womens reluctance to criticize their male parents must be interrogated and overcome. Even the modern, civilized father must be kept on the hook, she recommends, and daughters must reckon with their desire for retribution, revenge and punishment.

The combative tone taken by these writers is hardly a surprise. One might argue that a movement currently scrambling to defend some vestige of womens reproductive rights can be forgiven for not being especially solicitous of mens sperm counts. One might argue that it isnt feminisms job to worry about how men are doingany more than its the job of hens to fret about the condition of foxes. But two recent books claim otherwise. A History of Masculinity: From Patriarchy to Gender Justice (Allen Lane), by the French historian Ivan Jablonka, and What Do Men Want?: Masculinity and Its Discontents (Allen Lane), by Nina Power, a British columnist with a background in philosophy, both contend that the drift toward zero-sum war-of-the-sexes language is a bad thing for feminism. Although their diagnoses of the problem are almost diametrically opposed, both authors make the case for a more generous and humane feminist discourse, capable of recognizing the suffering of men as well as of women. Hens, they acknowledge, have legitimate cause for resentment, but foxes have feelings, too.

Jablonkas dense, copiously researched book, which became a surprise best-seller in France when it was published there, in 2019, takes an ambitious, key-to-all-mythologies approach to its subject. Jablonka, who is a professor at the Universit Sorbonne Paris Nord, begins in the Upper Paleolithic, examining its mysterious, corpulent Venus figurines, and moves suavely across the millennia all the way to the successive waves ofmodern feminism. He has an eye for striking, often grim, detailsunder the Babylonian Code of Hammurabi, a daughter might be killed as punishment for a murder committed by her fatherand relishes drawing parallels across eras. From ancient times to the present day, it seems, the central totems of masculinityweapons, locomotive vehicles, and meat (particularly rare meat)have remained remarkably consistent. Likewise, from the fall of Rome to the Weimar Republic, men have consistently attributed political disaster and cultural decline to the corrupting influence of feminine values.

Jablonkas thesis about how patriarchy arose is a fairly standard one. Paleolithic societies already had a sexual division of laborSpanish cave paintings from as early as 10,000 B.C. show male archers hunting and women gathering honeybut it was relatively benign. In the Neolithic era, with the advent of agriculture and the move away from nomadic existence, birth rates increased and women became confined to the domestic sphere, while men started to own land. From then on, each new development, be it metal weapons, the rise of the state, or even the birth of writing, further entrenched the power of men and the subjugation of women.

Until now, that is. Patriarchy has declined, according to Jablonka, but men remain caught in pathologies of the masculine, trying to live up to a symbolic role that doesnt reflect their reduced dominance. The result is an almost tragic level of alienation, he writes, and feminists, instead of mocking or dismissing male anguishthereby leaving men vulnerable to the revanchist fantasies of Tucker Carlson and his ilkshould recognize this moment as a crucial recruitment opportunity. Now is the time to convince men that their obligatory model of virility has immiserated them far more than it has empowered them. The masculinity of domination pays, but it comes at a high cost: an insecure ego, puerile vanity, disinterest in reading and the life of the mind, atrophied inner life, the narrowing of social opportunities... and to top it all, a diminished life expectancy.

Feminism has been slow to empathize and collaborate with men, Jablonka claims, because too many in the movement remain wedded to a Manichean world view of male oppressors and female victims. Some feminists are unreconstructed leftist types, who reject any evidence of womens progress as mystification designed to hide the persistence of male domination. Others are duped by a pro-women romanticism into believing that women are innately nicer and more progressive than men. Jablonka rejects this sort of essentialist thinking, which he says provides a spurious biological rationale for traditional gender roles. If women are naturally kinder and more nurturing than men, and if men are intrinsically imbued with a culture of rape, why bother trying to change the status quo? Testosterone and other androgens may have something to do with a male propensity for aggression, he concedes, but human beings are hostage neither to their biology nor their gender. Mens history of brutish behavior is the product of patriarchal culture, and only by insisting on the fundamental identity between men and women can feminism realize its proper aima redistribution of gender, in which new masculinities abound and the selection of any given way of being a man becomes a lifestyle choice.

Whats saved to the cloud gets printed in Hell.

Cartoon by Michael Shaw

To claim that masculinity is a patriarchal construct, however, is not so much an explanation as the postponement of an explanation. Who or what created the patriarchy? Evolutionary biologists maintain that our earliest male ancestors had an evolutionary incentive to maximize the spread of their genes by violently competing for, and monopolizing access to, women. Jablonka is eager to avoid such biological imperatives, but in doing so he reaches for a kind of just-so story that renders much of the history he has laid out beside the point. Patriarchy, he speculates, was motivated by simple resentment of womens wombs. Deprived of the power that women have, men reserved all the others for themselves, he writes. This was the revenge of the males: their biological inferiority led to their social hegemony.

Thus it is that successive patriarchal lites have spent the past several millennia shoring up their illegitimate rule, by defining manliness as a set of superior qualities denied to women. Not that Jablonka thinks there is only one, eternal masculine style; rather, all models of masculinity since antiquity have been mechanisms for asserting and imposing patriarchal power. The extroversion and swagger of the toreador look very different from the gallantry of the Victorian gentleman, which is, in turn, quite distinct from the laconic glamour of the cowboy, but they are all equally culpable expressions of the masculine-superiority complex.

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New Feminist Considerations of Masculinity, Reviewed - The New Yorker

Hari Jones, six, from Gwynedd, has X Linked Myotubular Myopathy (XLMTM), which affects about one in every 50,000 male births - he cannot walk or sit up and is connected to a life support machine that needs constant monitoring

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Wales: Boy with rare genetic disorder desperately needs care

A family says they are at a "breaking point" as they wait for a full care package for their son who has a rare genetic disorder.

Hari Jones, six, from Gwynedd, has X Linked Myotubular Myopathy (XLMTM), which affects about one in every 50,000 male births.

He cannot walk or sit up and is connected to a life support machine that needs constant monitoring.

The parents say they've been told he would get a full care package, but because of "ongoing issues" they have stepped up as Hari's carers while they wait.

Hari is unable to attend school and requires constant supervision in case the tube in his throat blocks or his breathing stops.

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Dad Michael Jones had told the BBC that "poor management" has "let them down as a family" and it is harming their physical and mental health as they have to step up as carers.

He says that he also has health conditions and was in a coma in 2018, which means a lot of care has fallen onto Hari's mum Ellen.

Mr Jones said: "She's with him day and night, mainly because I'm still really unwell so Ellen's life is basically next to Hari, she can't go out of the house, she's constantly with him and making sure he's safe.

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"She's a nurse for him, a doctor, a physiotherapist, she manages all his stock, she does absolutely everything for him day and night - to the point where she doesn't sleep for days and days so it's a lot of stress for her.

"At the worst, Ellen's done 12 days and 12 nights non-stop and her basic hours are 36 hours without sleep, so it's a lot of work."

Mr Jones added: "They should just find answers - it's not something that happened overnight for them.

"They've known that this was going to happen, and happening, since March last year so they should have had something in place to help us by now."

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The health board has said it would need time to recruit and train staff said due to Hari's complex needs it would take time to recruit and train staff.

A spokeswoman said the board was recruiting more staff and "continuing to work closely" with the family.

Hari spent four years on and off at Alder Hey Children's Hospital in Liverpool.

He was then assigned a care package that included carers being with the family almost 24 hours a day.

The health board took over from a private company in early 2021 - and the family say it reduced contact hours and used agency staff who were unable to fulfil the hours.

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The family say they were offered respite care at a hospice in Chorley, Lancashire, which is three hours from their home.

Neeru Naik, of Muscular Dystrophy UK - a charity which supports more than 60 conditions including XLMTM - said there were "inconsistencies" in regards to care packages.

Dr Catrin Edwards from the Carers Trust said there was "huge pressure" on families and unpaid carers.

"There's no doubt that our health and social care system is totally dependent on unpaid carers and we have to acknowledge the strain on them.

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"We have to remember that carers have legal rights and an individual has to be willing and able to provide care. However, when there are so many gaps existing in the workforce, many carers feel they have no choice but to continue, despite the personal strain."

Betsi Cadwaladr health board said Hari's care needs were set at 168 hours per week, a plan which had been agreed upon by a multidisciplinary team and the family.

It said it "compares favourably with other packages of care across the country".

Liz Fletcher, Assistant Area Director for Childrens Services in the West of Betsi Cadwaladr University Health Board, told The Mirror: We are continuing to work closely with Haris parents, Mr and Mrs Jones, to discuss the plans we have made to ensure that Hari has safe and ongoing care.

We are fully committed to providing the package of care for Hari and his family as an in-house arrangement, rather than via an external provider.

"We have taken this decision due to the complexity of the package required and the lack of suitable agencies and care providers nationally that can fulfil the familys needs.

"However, due to Haris complex needs, it will take time for us to recruit and train the number of appropriately skilled staff required to deliver this care package in full.

Two Health Care Support Workers and three registered nurses are now providing regular consistent care and we are actively recruiting more staff who will work as a team to support Hari.

"The team will be gradually introduced over a phased period according to a plan that has been discussed and shared with Mr and Mrs Jones.

We recognise there are challenges at times with staffing and when this occurs it is communicated to the family, who are updated regularly throughout the week.

"We do continue to offer meetings with Mr and Mrs Jones to discuss the package of care and any ongoing concerns they have.

We continue to look at all possible ways to support Hari at home recognising the challenges for everyone involved.

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Rocio Cifuentes, the children's commissioner for Wales, told The Mirror: "For children and young people throughout Wales who have complex needs, there are often difficulties in accessing the help and support they need.

"We want care to be much easier to access for children, and we want it to fit around them and their needs.

"Access to robust support at home, and regular short breaks is a hugely important part of any care package - so improving access to this for children and families across Wales must be a focus for services going forward."

A Welsh Government spokesperson told The Mirror: "We are investing heavily to support the recruitment and retention of social care staff in Wales, including paying social care workers the real living wage.

"Local authorities are also working closely with health boards to increase the number of domiciliary care workers. We've delivered record numbers of NHS staff - a 54% increase over the last 20 years - and more qualified nurses, hospital consultants and ambulance staff than ever before."

The Mirror contacted the Carers Trust for comment.

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JOB VIGIL North Platte Telegraph

NORTH PLATTE Across Nebraska, corn tassels wave in the breeze as the crop moves toward pollination and on into harvest.

Managing that pollination specifically for seed or field corn determines the quality for the following season. Randy Lloyd, research facility coordinator at West Central Research, Extension and Education Center in North Platte, said getting the most out of the harvest depends on a lot of factors, one of which is hybridization.

Hybrids are a cross of two parents to create a new, stronger seed. Corn that self-pollinates inbred Lloyd said, is not high producing or high quality.

When you cross dog breeds or whatever it is, you get what they call hybrid vigor, which means the offspring is stronger than the parents, Lloyd said. Thats why sometimes you get these purebred dogs that have all these problems like hip (dysplasia) and such.

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A similar situation occurs with corn, Lloyd said, in that hybrid corn is much stronger because the best DNA from each plant is combined to produce stronger seed.

Back in the late 1800s, farmers just grew their corn, Lloyd said. The pollen (interacted) with whatever was around it and the seed developed on the ear and thats what they collected.

What geneticists found is there is an inherent improvement when you cross two parents creating hybrid seeds.

Corn is really a neat plant, because you can hybridize it so easily, Lloyd said.

To make hybrid strands, farmers and researchers have to separate male and female plants. The tassel is the male part of the plant and the ear is the female. Detasseling a plant ensures a female plant, Lloyd said.

What farmers will do is they will plant typically two or four rows of male and then upwards of eight rows of the female, Lloyd said. Theyll put them side by side through the field and youll see them alternate like that.

In hybridization, the farmer wants to ensure the proper pollen is being used and that is the reason for detasseling, so the plants cant self-pollinate.

Historically, detasseling was all done by hand, Lloyd said. Certainly in Nebraska where a lot of seed is produced in that Doniphan, York area, Ive heard stories of multi-generational detasselers.

The industry has developed some mechanical ways to detassel as well.

Corn production in the United States from the 1870s to the mid-1930s was mostly static. The average yield was about 25 bushels per acre.

A lot of the reason was, one, we didnt need that much corn back then, Lloyd said. If you think of what was available from a farming perspective we had no equipment, we had no fertilizers, we had no herbicides, we had nothing.

The way farmers collected seed for the next year in the early days of field corn production was to walk their fields and pick out what appeared to be the healthiest-looking ears.

That was their selection for seed and it was all open pollinated, Lloyd said. They planted it, the pollen came from this field, and it just pollinated whatever plant was ready to receive pollen.

When researchers began to develop hybrids, farmers saw their yields start to grow significantly.

(Hybridization) really didnt catch on that much with farmers until the Dust Bowl, Lloyd said.

Farmers saw yields going up due to drought-tolerant hybrids that were being developed at the time.

For a little while there, we started gaining about .9 bushels per acre until about the mid-1950s, Lloyd said. Then in the mid-1950s there was kind of an explosion of both technology and genetics, so we really started focusing on hybridization.

Along with continuing to improve hybrid seeds after World War II, Lloyd said equipment got better, fertilizers got better and herbicides came into the picture. Since that time, the way science manages genetics is improving each year.

Almost 95%-plus of the corn today is hybrid corn, Lloyd said, and the reason detasseling hybrid corn is important is for control that improves the quality of the corn.

Tassels have begun to show at the tops of corn around the area. Lloyd said the tassel, if its a good tassel, will have anywhere from 2 million to 5 million pollen grains. As the ear develops, it will have small kernels on it and it starts sending out silks.

It always starts at the bottom, Lloyd said. These (silks) are going to start to elongate up through the husk and then theyre going to come out the top of the ear.

Once the kernels are pollinated, the silks drop off.

If you have 30,000 plants per acre, which is a typical population, Lloyd said, youre getting 2 to 5 million pollen grains per tassel. Thats why when you come out of the fields youre covered in pollen, because theres so much of it.

With farmers paying almost $300 a bag for seed corn, Lloyd said, the farmer wants to be sure what he is purchasing is pure and gives him the best opportunity to produce a quality crop. Field corn is big business and companies work with farmers directly.

Typically a company will go to the farmer and say, we want you to grow this seed in your field and when you harvest it we want the seed, Lloyd said. Theyll take it back to their plant, clean it, do whatever they have to do to it, treat it and put it in a bag. This is almost all contract work.

The companies are particular about the types of herbicides, fungicides and fertilizer used to produce the crop.

Typically the company will send out a consultant to go look at the field several times during the year to make sure things are going well, Lloyd said.

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There are valid reasons so many Nebraska kids have spent their summers detasseling corn - Scottsbluff Star Herald

image:One of the samples of ancient herpes DNA used in the study came from a male of 26-35 years old, excavated near the banks of the Rhine. The man was a fervent smoker of clay pipes. Traces of the habit are visible in multiple places on the teeth, where the hard clay pipe, usually put in the same place in the mouth, has worn the teeth. view more

Credit: Dr Barbara Veselka

Ancient genomes from the herpes virus that commonly causes lip sores and currently infects some 3.7 billion people globally have been uncovered and sequenced for the first time by an international team of scientists led by the University of Cambridge.

Latest research suggests that the HSV-1 virus strain behind facial herpes as we know it today arose around five thousand years ago, in the wake of vast Bronze Age migrations into Europe from the Steppe grasslands of Eurasia, and associated population booms that drove rates of transmission.

Herpes has a history stretching back millions of years, and forms of the virus infect species from bats to coral. Despite its contemporary prevalence among humans, however, scientists say that ancient examples of HSV-1 were surprisingly hard to find.

The authors of the study, published in the journal Science Advances, say the Neolithic flourishing of facial herpes detected in the ancient DNA may have coincided with the advent of a new cultural practice imported from the east: romantic and sexual kissing.

The world has watched COVID-19 mutate at a rapid rate over weeks and months. A virus like herpes evolves on a far grander timescale, said co-senior author Dr Charlotte Houldcroft, from Cambridges Department of Genetics.

Facial herpes hides in its host for life and only transmits through oral contact, so mutations occur slowly over centuries and millennia. We need to do deep time investigations to understand how DNA viruses like this evolve, she said. Previously, genetic data for herpes only went back to 1925.

The team managed to hunt down herpes in the remains of four individuals stretching over a thousand-year period, and extract viral DNA from the roots of teeth. Herpes often flares up with mouth infections: at least two of the ancient cadavers had gum disease and a third smoked tobacco.

The oldest sample came from an adult male excavated in Russias Ural Mountain region, dating from the late Iron Age around 1,500 years ago.

Two further samples were local to Cambridge, UK. One a female from an early Anglo-Saxon cemetery a few miles south of the city, dating from 6-7th centuries CE. The other a young adult male from the late 14th century, buried in the grounds of medieval Cambridges charitable hospital (later to become St. Johns College), who had suffered appalling dental abscesses.

The final sample came from a young adult male excavated in Holland: a fervent clay pipe smoker, most likely massacred by a French attack on his village by the banks of the Rhine in 1672.

We screened ancient DNA samples from around 3,000 archaeological finds and got just four herpes hits, said co-lead author Dr Meriam Guellil, from Tartu Universitys Institute of Genomics.

By comparing ancient DNA with herpes samples from the 20th century, we were able to analyse the differences and estimate a mutation rate, and consequently a timeline for virus evolution, said co-lead author Dr Lucy van Dorp, from the UCL Genetics Institute.

Co-senior author Dr Christiana Scheib, Research Fellow at St. Johns College, University of Cambridge, and Head of the Ancient DNA lab at Tartu University, said: Every primate species has a form of herpes, so we assume it has been with us since our own species left Africa.

However, something happened around five thousand years ago that allowed one strain of herpes to overtake all others, possibly an increase in transmissions, which could have been linked to kissing.

The researchers point out that the earliest known record of kissing is a Bronze Age manuscript from South Asia, and suggest the custom far from universal in human cultures may have travelled westward with migrations into Europe from Eurasia.

In fact, centuries later, the Roman Emperor Tiberius tried to ban kissing at official functions to prevent disease spread, a decree that may have been herpes-related. However, for most of human prehistory, HSV-1 transmission would have been vertical: the same strain passing from infected mother to newborn child.

Two-thirds of the global population under the age of 50 now carry HSV-1, according to the World Health Organisation. For most of us, the occasional lip sores that result are embarrassing and uncomfortable, but in combination with other ailments sepsis or even COVID-19, for example the virus can be fatal. In 2018, two women died of HSV-1 infection in the UK following Caesarean births.

Only genetic samples that are hundreds or even thousands of years old will allow us to understand how DNA viruses such as herpes and monkeypox, as well as our own immune systems, are adapting in response to each other, said Houldcroft.

The team would like to trace this hardy primordial disease even deeper through time, to investigate its infection of early hominins. Neanderthal herpes is my next mountain to climb, added Scheib.

Ancient herpes simplex 1 genomes reveal recent viral structure in Eurasia

27-Jul-2022

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Prehistoric roots of 'cold sore' virus traced through ancient herpes DNA - EurekAlert

In an age of universal communications via satellites circling the globe when any human on the planet who has a capable device may offer up opinions and speculations about any subject known to humankind it is not unreasonable, given the testimony of history, to assume some of these ideas will be of such content so as to stretch the mind to its furthest capacity of acceptance.

In short, there is a lot of crazy stuff on the internet. Let me pass along a couple of these offerings as they may, or may not, have passed through the ether:

Do you ever wonder how some people become famous but have zero talent? It is a known fact in the late 1930s three scientists in a country that cannot be named for fear of reprisal discovered a small entity within our solar system, which they first thought was nothing more than collected gases, but upon further investigation they discovered it was of a gelatinous nature, more blob than solid matter, but seemed to be inhabited by creatures with the same jelly-type body.

After months of observation the scientists documented that the populace of what was now deemed, by them, a planet was amorphous and could, chameleon-like, replicate whatever object they observed; much like the shape shifters of some Native American cultures. According to the scientists global rotation calculations, the planet would pass closest to Earth on Feb. 4, 1944, its closest point directly above a hospital in Los Angeles, Calif., USA. It is believed that on this occasion a creature from the planet occupied the body of a newborn male infant at that facility.

In the early morning hours of New Years Day 1944, after a night of celebration, an unexplained fire took the lives of the three scientists and destroyed all compiled data. A short note naming the planet written to a friend by one of the scientists was the only remaining evidence of their undisclosed discovery, and as result the world would never learn what became of the planet the scientists dubbed Kardashia.

There is no known phenomenon between a verified body in space and the birth of Robert George Kardashian (1944-2003).

There is an explanation of what creature these unsuspecting hikers came across, but governments around the world have hidden the true story. It is a known fact that just after the turn of the 20th century at a convention of genetic scientists in Paris, France, there was a paper submitted that outlined a process by which human genes could be spliced with primate genes thus producing a human being with the capabilities of a primate; a combination thought by the geneticist author to produce a manageable race to be used as working class for menial labor and soldiering.

The author of the paper, a scientist from China, had his paper and his ideas rejected by the scientific community, but volumes of his research and initial findings of experiments were copied by some of those attending the conference and were taken with them back to their home countries. What the research revealed was that the Chinese scientist had separated the DNA from a creature found frozen in a cave about 26 miles (41 kilometers) east of Mount Everest in Nepal.

Based on findings from other parts of China, speculation is the creature may have been a preserved Bunopithicus sericus. It is then believed he attempted to cross this DNA with tribesmen of the area for a number of years before submitting his findings at the 1912 convention. The scientist died in 1916 and a subsequent search of his abandoned facility, the Yuang Experimental and Testing Institute, led authorities to believe there were numerous studies done on human subjects, and subsequently the facility and all documents were destroyed by government authorities.

But oral history recounts testimony of local residents who reported hearing loud primal screams and odors described as musky and like a dirty wet dog coming from the compound where barracks sat alongside the laboratory. A handful of Sherpas had for years reported smells and sounds in the upper reaches of the Himalayas, and of seeing large human-like footprints in the snow. It is not known how many foreign scientists who availed themselves of the Yuang research papers conducted their own experiments nor what if any results may have occurred.

There is no known evidence of any research by any genetic scientists in the early part of the 20th century in any country involving gene splicing humans with other species (see Myths: Abominable Snowman, Sasquatch, Bigfoot, Yeti).

It is a known fact in the witch haven of Bad Durkheim Palatinate in Rhineland-Germany that a sorceress by the name of Juliana Maria Rodenroth (born circa 1667-70) pronounced a curse upon the family of her grandson when he married below his station in life and moved from the ancient land of his ancestors, many of whom were considered practitioners of occultism and witchery, to Kallstadt Palatinate of the Kingdom of Bavaria.

Oral tradition of the area relates the curse was that within her grandsons lineage there would be one born who would by inherited bounty and nefarious means rise to great power only to use that power to bring about great shame upon her grandsons name and the name of his heirs for generations to come.

As yet all data has yet to be compiled upon the generations of Juliana Maria Rodenroth, the mother of Johann Sebastian Trump (1699-1756) (see Select Committee Hearing to Investigate the January 6 Attack on the United States Capitol).

***

I dont usually get political, but cmon folks, sometimes there is just an abundance of honest people giving honest account about a dishonest human being.

Take care. Peace.

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Funny Papers Again Column | Idiotologies vs The Review and Research Posse - King City Rustler

The US has an abundance of national parks of varying shapes and sizes. From the grandeur of Colorados best national parks to the beauty of Californias stunning parks, they are home to hundreds (if not thousands) of plants and animals. Thus, nature-loving and adventure-seeking tourists have ample opportunity to witness these creatures thrive in their natural habitats when visiting national parks in the US. Whether one goes backcountry camping, hiking, or even kayaking, these US parks offer opportunities for viewing wildlife in its natural habitat!

Yosemite National Park is familiar with crowds of tourists wanting to visit its majesty and whimsy. This California park receives hundreds of thousands of visitors annually, providing an array of activities for many to enjoy its natural wonders. Take a guided tour of the park while riding a horse, bike through the trails, or get some bait to try some fishing at Yosemite. This famous national park is also home to over 165 species of birds, making it an ideal destination for avid birdwatchers.

Michigans Isle Royal National Park is nothing to scoff at; being an archipelago, it encompasses over 400 islands! With 36 campgrounds and approximately 165 miles (or 266 km) of trails, experienced backpackers can take a backcountry trip to Michigans massive park, exploring its many nooks and crannies. Otherwise, this natural area is also great for families, offering activities like scuba diving, fishing, paddling, and canoeing. Plus, its possible to spot local wildlife here, including red foxes, squirrels, bats, and certain reptiles.

Located 290 miles (or 470 km) away from Las Vegas, the Great Basin National Park provides a quieter hangout compared to the bright lights of The Strip. The park is known for the strenuous Wheeler Summit Trail and the Lehman Caves. However, nature-loving tourists can also find a plethora of wildlife at the Great Basin National Park. Hikers may spot species like the bighorn sheep, pygmy rabbit, water shrews, porcupines, and beavers.

The most beautiful wildflowers are found in Alaskas Katmai National Park. Thus, plant lovers who visit this Northern national park can find vascular plants like fireweeds, Kamchatka lilies, and Alaskas Nootka lupine. However, despite its faunal diversity, tourists flock to Katmai for one reason: brown bears! With their population in the thousands (particularly about 2,200), backcountry campers and curious tourists love watching these cuteyet mightymammals at Katmai every year. Bear-watching usually occurs between June to September, so travelers wishing to see these beautiful beasts can book a bear-watching trip through a reputable local tour operator.

RELATED: A Guide On Where To Find All The Summer Action In Virginia Beach

Sitting near the US-Mexican border, the Big Bend National Park lies far away from bustling cities. However, this desert park, located in Far West Texas, offers breathtaking views of the Chisos Mountains and its dramatic canyons. While backcountry camping or kayaking along the Rio Grande, visitors may spot local critters like jackrabbits, deer, bobcats, or the collared peccary.

Colorados Rocky Mountain National Park is a popular attraction for wildlife viewing year-round. Whether visitors take a relaxing road trip through the Rocky Mountains or embark on its 350+ mile worth of hiking trails, the Rocky Mountain National Park has an abundance of flora and fauna. Regardless of how travelers explore this Colorado park, from a distance, they may spot some unique wildlife like the yellow-bellied marmot, bighorn sheep, black bears, coyotes, or the white-tailed ptarmigan.

Covering over 1.5 million acres of wetland, this south Floridian national park is a must-visit for nature-loving travelers. Thus, the Everglades National Park offers visitors many opportunities to appreciate its wildlife. Go birdwatching in Homestead to see mangrove cuckoos, purple gallinules, or warblers in their natural habitat, or venture to the Everglades City entrance to witness bald eagles and wood storks. Alternatively, canoeing (or kayaking) is a fun way to explore the mangrove forests and marshes in the park while spotting local alligators, crocodiles, or manatees!

RELATED: Not Everyone Enjoys The Summer, And These U.S. Destinations Always Feel Like Fall

The Grand Canyon National Park is undoubtedly beautiful and a popular tourist attraction in Arizona. However, theres something beautiful about the Saguaro National Park. Home of the giant saguaro cacti, visitors can take a scenic road trip around the park or hike along its trails with picnic areas. Plus, depending on the month of ones visit, those exploring the parkespecially during the warmer monthsmay spot some local amphibians and reptiles, including canyon treefrogs, leopard frogs, Gila monsters, tortoises, and rattlesnakes.

Just a stone's throw away from the Yellowstone National Park, Grand Teton features breathtaking views of the Teton Range, alongside countless lakes and rivers. Its expansive size and lush surroundings make it an ideal destination for passionate, experienced backcountry campers. Simultaneously, Grand Teton National Park is home to hundreds of animals and flora that can be easily spotted while driving (or camping), such as mule deer, bears, moose, elk, bison, and grizzly bears.

Known as the worlds first national park (and in the US), Yellowstone National Park welcomes millions of nature-seeking tourists every year. Visit this national park by entering one of its five entrances to appreciate some of natures best sites (and wildlife)! This UNESCO World Heritage Site always dazzles visitors with its incredible views of the Grand Canyon and the world-famous Grand Prismatic Spring. Additionally, Yellowstone is rich in biodiversity, where visitors (at a respectable distance) can watch animals like buffalo, moose, grizzly bears, wolves, and bald eagles thrive in their natural habitat.

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10 US Parks Where You Can Watch Wildlife In Its Natural Habitat - TheTravel

Heart disease is the leading cause of death among men in the U.S., according to the Centers for Disease Control and Prevention (CDC). Over 380,000 men die from heart disease annually, accounting for about one in every four male deaths. By now, most of us are aware that various risk factors can make you especially vulnerable to heart-related death: being obese, smoking, or having diabetes or high blood pressure, for example. Now experts are warning men about a little-known risk factor you'd never suspect. Read on to learn why certain men are at an outsized risk of life-threatening heart disease, and the one thing you can do to reduce your chances of a problem.

READ THIS NEXT:Doing This at Night Could Lead to Heart Failure, Study Warns.

Composed of proteins and DNA, chromosomes are structures found within the nuclei of cells that contain your genes. Within each human cell, there are two pairs of 23 chromosomes (a total of 46), two of which can differ depending on biological sex. Women have two X chromosomes, while men have one X and one Y chromosome.

However, experts say many men begin losing their Y chromosomes as they age, a phenomenon known among scientists as hematopoietic mosaic loss of Y chromosome (mLOY). "At least 40 percent of males lose the Y chromosome from some of their blood cells by age 70. And by age 93, at least 57 percent have lost some of it," The New York Times recently reported.

READ THIS NEXT:If This Happens to You in the Bathroom, Get Checked for Heart Failure.

Though researchers have been aware of mLOY for decades, much was still unknown about its impact on the body. Now, they're exploring its link to age-related disease and higher risk of mortality in men.ae0fcc31ae342fd3a1346ebb1f342fcb

To do so, one group of researchers studied genetically engineered male mice, who were "reconstituted with bone marrow cells lacking the Y chromosome." They found that as the mice lost their Y chromosomes, they developed scar tissue on the heart, resulting in "reduced cardiac function," heart failure, and increased mortality from heart disease.

Though the study, published in the Jul. 2022 issue of the journal Science, used mice as subjects, the researchers behind the study believe their findings are applicable to human males. Other studies have supported this notion, having found a causal link between loss of Y chromosomes and chronic illnesses such as cancer and heart disease.

Some scientists say this could help explain the difference in life expectancy between men and women. According to the CDC, women live an average of five years longer than men. According to a 2020 report by the health authority, women live an average of 80 years, while men live an average of 75 years.

A 2014 study on the subject published in the journal Nature Genetics reviewed data from 1,153 men in Sweden. The team discovered that men who were missing the Y chromosome in a large percentage of their blood cells were at notably heightened risk of mortality in the years that followed. "I saw that men with loss of Y in a large proportion of their blood cells survived only half as long, 5.5 years versus 11.1 years," Lars Forsberg, a researcher at Uppsala University and one of the study's lead authors, told the Times.

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The New York Times reports that having low testosterone levels is unrelated to loss of Y chromosome, and testosterone supplements do not benefit men with mLOY.

However, experts say there is one known way to reduce your risk of Y chromosome loss: quitting smoking. In fact, according to a separate study published in Science, smokers are up to four times more likely to lose all Y chromosomes in the blood cells, compared with non-smokers.

Addicted to nicotine? Speak with your doctor for tips on how to quitand to learn more about the benefits of doing so.

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Men Missing Y Chromosome Have High Heart Disease Risk Best Life - Best Life

Summary: In males, sun exposure activates the p53 protein which signals to the body to produce the appetite-associated ghrelin hormone. In women, estrogen blocks the interaction between p53 and ghrelin, reducing the urge to eat following sun exposure.

Source: Tel Aviv University

A new study from Tel Aviv University reveals that solar exposure increases appetite in males, but not in females. Conducted on lab models, the study unravels the differences between males and females in the activation of the metabolic mechanism.

The researchers explain that in males of both animal species and humans, sun exposure activates a protein called p53, in order to repair any DNA damage in the skin that might have been caused by the exposure. The activation of p53 signals the body to produce a hormone called ghrelin, which stimulates the appetite.

In females, the hormone estrogen blocks the interaction between p53 and ghrelin, and consequently does not catalyze the urge to eat following exposure to the sun.

The groundbreaking study was led by Prof. Carmit Levy and PhD student Shivang Parikh of the Department of Human Genetics and Biochemistry at TAUs Sackler Faculty of Medicine.

It was conducted in collaboration with many researchers in Israel and worldwide, including contributors from Tel Aviv Sourasky (Ichilov), Assuta, Meir, and Sheba Medical Centers, along with Dr. Yiftach Gepner and Dr. Lior Bikovski from TAUs Sackler Faculty of Medicine, and Prof. Aron Weller of Bar-Ilan University.

The paper was published in the prestigious journalNature Metabolism.

The study was based on epidemiological data collected in a year-long survey about the eating habits of approximately 3,000 Israelis of both sexes, including self-reports from students who had spent time in the sun, combined with the results of a genetic study in a lab model.

The findings identify the skin as a primary regulator of energy and appetite (metabolism) in both lab models and humans.

The researchers explain that there is a dramatic metabolic difference between males and females, impacting both their health and their behavior. However, so far it has not been established whether the two sexes respond differently to environmental triggers such as exposures to the suns UV radiation.

Prof. Levy: We examined the differences between men and women after sun exposure and found that men eat more than women because their appetite has increased.

Our study was the first gender-dependent medical study ever conducted on UV exposure, and for the first time, the molecular connection between UV exposure and appetite was deciphered.

Gender-dependent medical studies are particularly complex, since twice the number of participants are required in order to find statistically significant differences.

Prof. Levy concludes: As humans, we have cast off our furand consequently, our skin, the largest organ in our body, is exposed to signals from the environment. The protein p53, found in the skin, repairs damage to the DNA caused by sun exposure, but it does more than that. It signals to our bodies that winter is over, and we are out in the sun, possibly in preparation for the mating season.

Our results provide an encouraging basis for more research, on both human metabolism and potential UV-based therapies for metabolic diseases and appetite disorders.

Author: Noga ShaharSource: Tel Aviv UniversityContact: Noga Shahar Tel Aviv UniversityImage: The image is in the public domain

Original Research: Open access.Food-seeking behavior is triggered by skin ultraviolet exposure in males by Carmit Levy et al. Nature Metabolism

Abstract

Food-seeking behavior is triggered by skin ultraviolet exposure in males

Sexual dimorphisms are responsible for profound metabolic differences in health and behavior. Whether males and females react differently to environmental cues, such as solar ultraviolet (UV) exposure, is unknown.

Here we show that solar exposure induces food-seeking behavior, food intake, and food-seeking behavior and food intake in men, but not in women, through epidemiological evidence of approximately 3,000 individuals throughout the year.

In mice, UVB exposure leads to increased food-seeking behavior, food intake and weight gain, with a sexual dimorphism towards males.

In both mice and human males, increased appetite is correlated with elevated levels of circulating ghrelin.

Specifically, UVB irradiation leads to p53 transcriptional activation of ghrelin in skin adipocytes, while a conditional p53-knockout in mice abolishes UVB-induced ghrelin expression and food-seeking behavior. In females, estrogen interferes with the p53chromatin interaction on the ghrelin promoter, thus blocking ghrelin and food-seeking behavior in response to UVB exposure.

These results identify the skin as a major mediator of energy homeostasis and may lead to therapeutic opportunities for sex-based treatments of endocrine-related diseases.

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Going to the Beach? Planning a Hike? Be Prepared: Men Will Be Much Hungrier! - Neuroscience News