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Archive for the ‘Male Genetics’ Category

CBD and Blood Pressure: Can It Reduce High BP? – Greencamp

CBD is a natural plant-derived molecule with truly versatile effects on human health, and one of these effects directly causes blood pressure to drop.

The complex legal status of cannabis and hemp continues to cripple CBD research on a global scale, and human studies remain very rare.

While research is still only performed on animals for the majority of conditions, a very important human study was specifically looking into the effects of CBD on blood pressure.

This groundbreaking placebo-controlled, double-blind 2017 research was the first to look into whether CBD reduces blood pressure in humans, and it was inspired by previous preclinical studies which hinted that CBD offers a multitude of cardiovascular benefits.

Nine healthy male volunteers participated in the research, and were given either a 600mg dose of CBD, or a placebo.

The results showed that the participants who received the 600mg CBD dose had:

The data also showed that the participants who were given the CBD dose had:

Finally, in response to cold stress, volunteers who were given 600mg of CBD had:

Researchers concluded that a single administration of CBD reduced resting blood pressure, but also reduced the blood pressure increase associated with stressful situations.

The participants in the study received a considerably large single dose of CBD (600mg), which could be considered as a very expensive treatment method for most people.

On the safety side of things, a 2011 scientific review stated that high doses of CBD are well tolerated in humans (up to 1,500mg per day), and a 2017 follow-up survey also corroborated this claim.

High blood pressure is a very serious health condition, so if youre planning to implement CBD in your regimen, the doses have to be greater compared to less-debilitating conditions such as anxiety or insomnia, for instance.

Not sure how to dose CBD? Download Droppy the app that calculates your perfect dosage based on research studies.

People react differently to CBD, mostly due to the difference in age, overall health, and genetics. These differences make finding the perfect dose of CBD a personal quest, which usually requires some fine-tuning.

For this particular condition, it would be better to start with an intermediate dose (around 60mg of CBD per day) and observe how you are responding. This dose can also be met by consuming two 30mg CBD capsules per day.

Its highly recommended to keep a CBD journal which will help you follow your daily intake and the precise effects of different CBD doses.

Some people feel the effects of CBD right away, while others dont seem to notice any difference whatsoever.

A debate about why exactly this happens still rages on, and as of yet there are no definitive answers.

One of the main hypotheses (and my personal favorite) is the endocannabinoid system deficiency.

The way CBD (and all other cannabinoids) produce their beneficial effects is by enticing the cells of the endocannabinoid system.

Imagine CBD molecules as keys, which upon entering the lock (receptor) of a specific cell trigger a specific reaction of that cell.

The endocannabinoid system is a vast collection of different cells located throughout the body, which is why CBD is able to help with such a large number of different conditions and disorders.

Due to differences in age, unique genetics, overall health, and a variety of other complex factors, some people have a malfunctioning endocannabinoid system.

This means that the cells of a malfunctioning endocannabinoid system wont react in the same way as the cells of a properly-functioning endocannabinoid system.

The theory also suggests that the endocannabinoid system can be restarted, by continually exposing its cells to cannabinoids like CBD. This process usually lasts for several weeks.

The entire endeavor requires some dedication and conviction, but as CBD is completely natural and very well tolerated in most people, its not much of a sacrifice to try it out.

Just like the percentage of people who dont experience relief from CBD right away, some individuals tend to have adverse effects from CBD, while most users dont have any noticeable issues.

This is also most likely due to age, overall health, personal chemistry, and genetic differences.

Luckily, most of the potential side effects of CBD are not too serious and can be considered only a nuisance. They include:

Unfortunately, this entire field of medicine is not yet well understood. The only way to determine which category of users you belong is to try using CBD.

Its important to understand that the potential side effects are not hazardous in any way.

Similarly to grapefruit juice, CBD interferes with the metabolization (the breakdown) of all medications that have a grapefruit warning on their packaging.

This is because CBD is metabolized by an enzyme called CYP3A4.

The CYP3A4 enzyme is also responsible for metabolizing a large percentage of prescription drugs, including some blood pressure medications.

This basically means that if your body is metabolizing both CBD and a different drug at the same time, the CYP3A4 enzyme will have to metabolize both substances at once, which is not a good thing.

The CBD in your system can diminish the metabolization of other drugs in your system, leaving elevated levels of the other drug for too long.

This process can also go the other way around, where the CYP3A4 enzyme focuses more on the other drug, which will leave the CBD molecules lingering in your body.

The interactions of other medications with CBD are very important, so please take them extremely seriously and do your homework by thoroughly researching the medication youre taking.

Some medications dont have a grapefruit warning on their packaging, so check the inserted information for any mention of the CYP3A4 enzyme.

You should also consult with your doctor, but they are still (in most cases) not adequately familiar with CBD and its drug interactions.

High blood pressure is a very serious condition, and its absolutely vital to perform rigorous research if you plan to add CBD to your existing treatment regimen.

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CBD and Blood Pressure: Can It Reduce High BP? - Greencamp

Student Spotlight on Mika Matera-Vatnick ’21: Researching Insect Reproduction Genetics – Cornell University The Cornell Daily Sun

When Mika Matera-Vatnick 21 received President Martha E. Pollacks email in March announcing the closing of campus, her first thought was, What am I gonna do with my flies?

Matera-Vatnick, like many other undergraduate student researchers on campus, had to abandon her honors thesis research project as classes transitioned online for the remainder of the semester.

Last spring, Matera-Vatnick joined the Wolfner lab, led by Prof. Mariana Wolfner, molecular biology and genetics.

Research is the main thing Im involved with on campus. When Im not in class, Im in the lab, she said.

Currently, her research is on pause, since as of March 28, faculty and students are no longer allowed to work in laboratories, barring Matera-Vatnick access to laboratory equipment that is essential to the continuation of her research.

Matera-Vatnick is exploring the genetic basis of sperm competition in fruit flies the competitive process between sperm of two or more different males to fertilize the same egg during sexual reproduction.

Her passion for genetics started during a summer research experience at the bioethics department at the National Institutes of Health after her freshman year, where she learned about personalized medicine.

We are all unique with our own unique genomes and we need to treat patients based on their individual needs and their own genome. This is what led me to take the genetics and genetics lab courses at Cornell, she said.

Specifically, Matera-Vatnick is researching whether there are certain genes linked to mating plug ejection times.

Mating plugs are gelatinous secretions used in the mating in fruit flies and other species, including various primates such as kangaroos and reptiles. These secretions are deposited by a male into a female genital tract and later harden into a plug that glues the tract together. The plugs prevent females from re-mating, making it possible for females to store sperm.

In my experiments, Im comparing how long different strains of flies take to go through the process of mating plug ejection and seeing if there is a genetic basis and where in the gene this might come from, Matera-Vatnik said.

In fruit flies, the female expels the mating plug within five hours of mating in a process called mating plug ejection. The timing of ejection influences the paternity share of the fruit flys mates, playing an important role in mate competition.

Paris Ghazi / Sun Senior Editor

Matera-Vatnick experimenting in the Wolfner lab.

Matera-Vatnik randomly selected genetically diverse types of fruit flies to assess the time it takes for female fruit flies to undergo mating plug ejection. Mating plug ejection times can be compared to genetic variations across these specific fruit fly lines.

This comparison can reveal key genes associated with mating plug ejection, evolutionary histories of neural circuits and the role of these neuronal pathways in female sexual selection when a female chooses a male to mate with.

Understanding the process of sexual selection in insect reproduction may contribute to developing strategies for controlling pests and disease vectors in agriculture and public health.

Matera-Vatnick spent last summer at Weill Cornell Medicine in New York City learning about computational biology, which is the analysis of biological data through computer simulated models. In contrast to the work she did at WCM, Matera-Vatnick typically conducts her research on fruit flies in a wet lab. A wet lab is a lab where experiments are conducted and chemicals are handled, whereas in a dry lab, data is analyzed with computers and other technology.

Not much is known about the genetic basis that underlies the variations in mating plug ejection timing, but Matera-Vatnik is determined to find out.

I learned so much about how computational tools can be used to answer biological questions that are impossible to answer in a wet lab. I think that combining wet lab and computational power together will bring a unique angle to the questions Im interested in answering, she said.

Though research on campus has been put on hold, Matera-Vatnick is hopeful she can finish this project as her honors thesis.

This is the project that will be my senior thesis project. With all the uncertainty of being here, and hopefully the plan is to stay here over the summer, I want to take this project as far as I can before I graduate, Matera-Vatnick said.

Matera-Vatnick is currently in her hometown Washington, D.C. While she is unable to continue her research at the Wolfner Lab, she still attends weekly lab meetings and will be drafting sections of her honors thesis for the rest of the semester. She plans on taking the MCAT at the end of summer, if permitted.

In the meantime, Matera-Vatnick hopes to make the most of her Cornell research experience, upon her return to campus.

Im trying to take as much as I can from campus, Matera-Vatnick said. Thanks to amazing mentorship from my [Principal Investigator], graduate students and other students in the lab, I can say Im very lucky with who Ive surrounded myself with on campus.

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Student Spotlight on Mika Matera-Vatnick '21: Researching Insect Reproduction Genetics - Cornell University The Cornell Daily Sun

Seattle Genetics Announces U.S. FDA Approval of TUKYSA (tucatinib) for People with Advanced Unresectable or Metastatic HER2-Positive Breast Cancer -…

BOTHELL, Wash.--(BUSINESS WIRE)--Seattle Genetics, Inc. (Nasdaq:SGEN) today announced the U.S. Food and Drug Administration (FDA) granted approval to TUKYSA (tucatinib) tablets in combination with trastuzumab and capecitabine for adult patients with advanced unresectable (cannot be surgically removed) or metastatic HER2-positive breast cancer, including patients with brain metastases (disease that has spread to the brain), who have received one or more prior anti-HER2-based regimens in the metastatic setting. The FDA previously granted Breakthrough Therapy designation and Priority Review for TUKYSA and reviewed this application for approval under the Real-Time Oncology Review (RTOR) pilot program. The TUKYSA New Drug Application (NDA) is also part of Project Orbis, an initiative of the FDA Oncology Center of Excellence that provides a framework for concurrent submission and review of oncology drugs among participating international health authorities. TUKYSA is an oral, small molecule tyrosine kinase inhibitor (TKI) of HER2, a protein that contributes to cancer cell growth.1,2

With highly significant and clinically important results for overall and progression-free survival, the addition of TUKYSA to trastuzumab and capecitabine has the potential to become a standard of care for people with HER2-positive metastatic breast cancer after having received one or more previous anti-HER2 therapies in the metastatic setting, said Eric P. Winer, MD, Chief of the Division of Breast Oncology, Susan F. Smith Center for Women's Cancers at Dana-Farber. Cancer spreads to the brain in up to half of patients with HER2-positive metastatic breast cancer; and this approval is based on a unique clinical trial that included patients with active brain metastases, either untreated or progressing. TUKYSA is well tolerated by patients and is a valuable addition to the agents we have for HER2-positive metastatic breast cancer.

Were pleased to have collaborated with the FDA on our second expedited real-time oncology review, enabling us to rapidly bring this new targeted medicine to patients, said Clay Siegall, Ph.D., Chief Executive Officer at Seattle Genetics. TUKYSA has shown impressive results in people with HER2-positive metastatic breast cancer, including in patients with active brain metastases, and offers patients an effective medicine following previous treatment with other anti-HER2 agents in the metastatic setting.

TUKYSA, in combination with trastuzumab and capecitabine, was evaluated in the trial HER2CLIMB, a randomized (2:1), double-blind, placebo-controlled trial that enrolled 612 patients with HER2-positive unresectable locally advanced or metastatic breast cancer who had previously received, either separately or in combination, trastuzumab, pertuzumab, and ado-trastuzumab emtansine (T-DM1). Forty-eight percent of patients in the study had a presence or history of brain metastases. The primary efficacy outcome measure was progression-free survival (PFS) as assessed by blinded independent central review (BICR) in the first 480 randomized patients.1 Additional efficacy outcome measures were evaluated in all randomized patients and included overall survival (OS), PFS in patients with a history or presence of brain metastases, and confirmed objective response rate (ORR).

Patients who received TUKYSA in combination with trastuzumab and capecitabine had a 46 percent reduction in the risk of cancer progression or death (PFS) compared to patients who received trastuzumab and capecitabine alone (hazard ratio (HR)=0.54 [95% Confidence Interval (CI): 0.42, 0.71]; p<0.00001). The addition of TUKYSA reduced the risk of death (OS) by 34 percent compared to trastuzumab and capecitabine alone (HR=0.66 [95% CI: 0.50, 0.87]; p=0.0048). Nearly twice the number of patients who received TUKYSA in combination with trastuzumab and capecitabine had a confirmed objective response compared to those who received trastuzumab and capecitabine alone (40.6 percent (95% CI: 35.3, 46.0) vs. 22.8 percent (95% CI: 16.7, 29.8); p=0.00008). For patients with brain metastases, the addition of TUKYSA reduced the risk of cancer progression or death (PFS) by 52 percent compared to trastuzumab and capecitabine alone (HR=0.48 [95% CI: 0.34, 0.69]; p<0.00001).

Serious adverse reactions occurred in 26 percent of patients who received TUKYSA. Serious adverse reactions occurring in 2 percent or more of patients who received TUKYSA were diarrhea (4%), vomiting (2.5%), nausea, abdominal pain, and seizure (2% each). The most common adverse reactions occurring in 20 percent or more of patients who received TUKYSA were diarrhea, palmar-plantar erythrodysesthesia, nausea, fatigue, hepatotoxicity, vomiting, stomatitis, decreased appetite, abdominal pain, headache, anemia, and rash. Adverse reactions leading to treatment discontinuation occurred in 6 percent of patients who received TUKYSA; adverse reactions leading to treatment discontinuation of TUKYSA (in 1 percent or more of patients) were hepatotoxicity (1.5%) and diarrhea (1%).

The data were published in The New England Journal of Medicine in December 2019.

About TUKYSA (tucatinib)

TUKYSA is an oral medicine that is a tyrosine kinase inhibitor of the HER2 protein. In vitro (in lab studies), TUKYSA inhibited phosphorylation of HER2 and HER3, resulting in inhibition of downstream MAPK and AKT signaling and cell growth (proliferation), and showed anti-tumor activity in HER2-expressing tumor cells. In vivo (in living organisms), TUKYSA inhibited the growth of HER2-expressing tumors. The combination of TUKYSA and the anti-HER2 antibody trastuzumab showed increased anti-tumor activity in vitro and in vivo compared to either medicine alone.1

SeaGen Secure offers access and reimbursement support to help patients access TUKYSA. For more information, go to SeaGenSecure.com.

About HER2-Positive Breast Cancer

Patients with HER2-positive breast cancer have tumors with high levels of a protein called human epidermal growth factor receptor 2 (HER2), which promotes the growth of cancer cells. An estimated 279,100 new cases of breast cancer will be diagnosed in the U.S. in 2020.3 Between 15 and 20 percent of breast cancer cases are HER2-positive.3 Historically, HER2-positive breast cancer tends to be more aggressive and more likely to recur than HER2-negative breast cancer.4,5,6 Up to 50 percent of metastatic HER2-positive breast cancer patients develop brain metastases over time.7,8,9

Important Safety Information

Warnings and Precautions

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

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

Adverse Reactions

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

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

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

Lab Abnormalities

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

Drug Interactions

Use in Specific Populations

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

Conference Call Details

Seattle Genetics management will host a conference call and webcast to discuss the approval of TUKYSA today at 1:00 p.m. Pacific Time (PT); 4:00 p.m. Eastern Time (ET). The live event will be simultaneously webcast and available for replay from the Seattle Genetics website at http://www.seattlegenetics.com, under the Investors section. Investors may also participate in the conference call by calling 888-220-8451 (domestic) or 323-794-2588 (international). The conference ID is 5796578. A replay of the audio only will be available by calling 888-203-1112 (domestic) or 719-457-0820 (international), using conference ID 5796578. The telephone replay will be available until 5:00 p.m. PT on April 20, 2020.

About Seattle Genetics

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

Forward Looking Statements

Certain statements made in this press release are forward looking, such as those, among others, relating to the therapeutic potential of TUKYSA including its efficacy, safety and therapeutic uses and the potential of TUKYSA in combination with trastuzumab and capecitabine to become a standard of care for people with HER2-positive metastatic breast cancer who have received one or more previous anti-HER2 therapies. Actual results or developments may differ materially from those projected or implied in these forward-looking statements. Factors that may cause such a difference include the possibility that adverse events or safety signals may occur; that utilization and adoption of TUKYSA by prescribing physicians may be limited due to impacts related to the COVID-19 pandemic, including potential difficulties associated with commercializing a new therapeutic agent during the global disruptions created by the COVID pandemic, availability and extent of reimbursement or other factors; and that adverse regulatory actions may occur. More information about the risks and uncertainties faced by Seattle Genetics is contained under the caption Risk Factors included in the companys Annual Report on Form 10-K for the year ended December 31, 2019 filed with the Securities and Exchange Commission. Seattle Genetics disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law.

[1] TUKYSA [package insert]. Bothell, WA: Seattle Genetics, Inc.

[2] Anita Kulukian, Patrice Lee, Janelle Taylor, et al. Preclinical Activity of HER2-Selective Tyrosine Kinase Inhibitor Tucatinib as a Single Agent or in Combination with Trastuzumab or Docetaxel in Solid Tumor ModelsMol Cancer Ther 2020;19:976-987.

[3] Cancer Facts & Figures 2020. American Cancer Society website. https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-and-statistics/annual-cancer-facts-and-figures/2020/cancer-facts-and-figures-2020.pdf. Accessed March 10, 2020.

[3] Loibli S, Gianni L. HER2-positive breast cancer. Lancet. 2017; 389(10087): 2415-29.

[4] Slamon D, Clark G, Wong S, et al. Human breast cancer: correlation of relapse and survival with amplification of the HER-2/neu oncogene. Science. 1987; 235(4785): 177-82.

[5] Breast Cancer HER2 Status. American Cancer Society website. https://www.cancer.org/cancer/breast-cancer/understanding-a-breast-cancer-diagnosis/breast-cancer-her2-status.html. Accessed March 9, 2020.

[6] Freedman RA, Gelman RS, Anders CK, et al. TBCRC 022: a phase II trial of neratinib and capecitabine for patients with human epidermal growth factor receptor 2-positive breast cancer and brain metastases. J Clin Oncol. 2019;37:1081-1089.

[7] Olson EM, Najita JS, Sohl J, et al. Clinical outcomes and treatment practice patterns of patients with HER2-positive metastatic breast cancer in the post-trastuzumab era. Breast. 2013;22:525-531.

[8] Bendell JC, Domchek SM, Burstein HJ, et al. Central nervous system metastases in women who receive trastuzumab-based therapy for metastatic breast carcinoma. Cancer. 2003;97:2972-2977.

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Seattle Genetics Announces U.S. FDA Approval of TUKYSA (tucatinib) for People with Advanced Unresectable or Metastatic HER2-Positive Breast Cancer -...

factors that could make Covid-19 deadly to you – Vanguard

By Sola Ogundipe

SERIES of factors that the majority of COVID-19 patients share have been identified by researchers from eight institutions in China and the United States including the Chinese Peoples Liberation Army General Hospital in Beijing and the University of California.

Their study, published in the American Journal of Respiratory and Critical Care Medicine, throws light on some key factors that people who die from the disease have in common.

The study is based on the data of 85 patients who died of multiple organ failure after having received care for severe Covid-19.

Gender

The novel coronavirus appears to be posing a particular threat to men. The researchers found that 72.9 percent of people who died from the new coronavirus were male. More men are dying than women as a result of some biological and other lifestyle choices.

Hand washing is one of the best ways to prevent infection but multiple studies show that women are much more likely to wash their hands and use soap than men.

Men may have a false sense of security about coronavirus. Also, Chinese men are much more likely to smoke than women, which can lead to a weaker immune system.

China has the largest population of smokers in the world, accounting for nearly a third of the worlds smokers, but just 2 percent of them are women. Smokers are more likely to be killed by the coronavirus. Chinese men also have higher rates of high blood pressure , type 2 diabetesand chronic obstructive pulmonary disease than women.

All of these conditions can increase the risk of complications following infection of coronavirus.

Age

Coronavirus can infect anyone of any age, but adults aged 60 and upwards are more likely to get seriously ill from it, with scientists discovering that those who died from Covid-19 had a median age of 65.8 years old.

Medics say its because our immune systems weaken with age, meaning an older persons body is less able to fight Covid-19.

As you get older, your immune system becomes less efficient thats why older people are at higher risk of serious complications of coronavirus infection. If your immune system isnt strong, its more likely that the virus can multiply deep inside your lung, causing inflammation and scarring.

Your immune system will try and fight it off, and will often destroy healthy lung tissue in the process. This makes you more prone to get secondary infections like pneumococcal pneumonia.

In fact, evidence from China, where the deadly virus originated, shows one in seven of those over 80 known to have contracted coronavirus have died.

Underlying conditions

Those who died from Covid-19 in the study mostly had underlying chronic conditions, such as heart problems or diabetes. The greatest number of deaths in our cohort were in males over 50 with non-communicable chronic diseases.. The study conveys the seriousness of Covid-19 and emphasises the risk groups of males over 50 with chronic comorbid conditions, including hypertension (high blood pressure), coronary heart disease, and diabetes.

Weight

People who are obese or seriously overweight fall into the high risk category for coronavirus. This is because being overweight or obese can weaken the bodys immune system which could make people more likely to catch coronavirus and makes it harder for the body to fight the bug.

People with a BMI of 40 or above have a greater risk of developing complications if they catch the virus. More than 60 percent of patients in intensive care with the virus were overweight or classed as morbidly obese.

Those who were overweight, with a BMI of 25 to 40, made up 64 percent of the 194 coronavirus patients who were in ICU at the time, while 7 percent were classed as obese with a BMI over 40.

Low white blood cells

The research team found that 81.2 percent of those who died from Covid-19 in the study had very low eosinophil counts on admission to the hospital. This is a type of white blood cells, which are specialised immune cells that help fight infection.

The medics suggested that having abnormally low levels of eosinophils may correlate with a greater risk of severe outcomes in people who have contracted Covid-19.

The study, which investigated patients from Wuhan, Chinawho died in the early phases of this pandemic, identified certain characteristics. Yet as the disease has spread to other regions, the observations from these areas may be the same, or different.

Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates, as well. Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

Vanguard

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factors that could make Covid-19 deadly to you - Vanguard

The kkp season of stress and salvation: How scientists and supporters teamed up to take on killer disease – Stuff.co.nz

The vet had bitter news.

"She sounds like she's choking to death," the Auckland Zoo manager of vet services James Chatterton told his radio audience last June.

She was a kkpchick, Nora 1A, suffering cruelly from aspergillosis, a fungal infection that assails the longs and air sacs of a bird's body.

Bryony Hitchcock

Jake Osborne carries Cyndy home.

They operated to remove airway abscesses but she was just too weak, so became the seventh death from the Whenua Hou (Codfish Island) sanctuary off Stewart Island.

READ MORE:* Kkp population reaches record high of 213, despite mystery illness* Kkp disease 'crisis' which garnered $200k in donations remains a mystery* First successful artificial insemination of kkp in a decade

Seven deaths sounds bad, but let's get a sense of scale. By that stage 35 kkphad been helicoptered to receive intensive care, chiefly at Auckland Zoo and also Massey Wildbase, Dunedin Wildlife Hospital and Wellington Zoo.

That was one fifth of the total population of the island where the kkp is making its stand against extinction.

Jake Osborne

Kohittea, the chick.

By September it would be 51 evacuees. Nearly a quarter.

A last chance to see

The UK paper The Guardian, reporting on the aspergillosis battle, described the kkplike this: "Deeply weird. Flightless, nocturnal, with fragrant feathers and a comic waddling run..."

Fair enough on all counts, though the fragrance is more musty than you might assume, once nicely described as like the inside of an old violin case.

The worldwide appeal of these birds cannot solely be attributed to their rarity and size, nor even the worldwide comedic appeal of the footage of Sirocco landing atop zoologist Mark Carwardine and getting carnal with his cranium, to the joyous hooting of onlooking presenter Stephen Fry for the TV series Last Chance to See (the very title of which underscores how imperilled the population is).

Chris McKeen

Margaret Maree is a 34 year old kkp, scanned at Auckland Zoo. She pulled through.

There's something almost mammalian about kkp. Their feathers are especially strokable, their large eyes perhaps more soulful than the average avian, and there's no denying their behaviours suggest wilful character.

The Hitchhiker's Guide to the Galaxy author Douglas Adams found them intriguing, fat birds whose wings were really only good for waggling a bit, though flying is out of the question.

"Sadly, however, it seems that not only has the kkp forgotten how to fly, but it has forgotten that it has forgotten how to fly.

"Apparently a seriously worried kkp will sometimes run up a tree and jump out of it, whereupon it flies like a brick and lands in a graceless heap on the ground."

HAMISH McNEILLY/STUFF

Sirocco the kkp has returned to the limelight as part of a display at Orokonui Ecosanctuary near Dunedin.

Far more seriously, they struggle to breed. There's a real lack of genetic diversity.

Females can get attached to one partner, carrying the same genes into 20 or 30 offspring, which is why it had come as particularly good news last July that the first successful artificial insemination in a decade, courtesy of Sinbad, a male with a rare Fiordland gene, had rendered chicks.

The sole other success, in the 2008/9 season, had been a world first.

Famously, though, the natural breeding season ties in with the berry fruit "mast" in the bush, which happens on a cycle of three years or more.

And the 2019 season had been spectacular. Rimu berries all over the place. The population had risen to its highest in 70 years. It was an exhausting time for the recovery team on the island, but a thrilling one.

Then wham. They were dealing with aspergillosis. Very rare in wild bird populations. Hard to detect early, and brutal in its consequences.

Lydia Uddstrom

Toiora has a CT scan.

"It felt like a real kick in the guts," recalls DOC kkp operations manager DeidreVercoe. "Things had been looking so promising, but changed so quickly."

Her darkest fears were dark indeed - this had the potential to kill so many birds, unravelling decades of conservation effort.

The team had done risk analysis work but aspergillosis was considered very low risk. Only one case had ever arisen, in 2012.

"To suddenly have an outbreak of that scale was a shock. The level of breeding we had that year in itself was new to us - so we were dealing with the biggest ever breeding season and the biggest ever disease event at the same time.

With veterinarians across the country, the team worked to develop a plan, adapting it as they learned more.

Liz Carlson

All 55 birds that remained on Whenua Hou (55) and all the breeding females on Pukenui (21) were health checked and had blood samples taken.

The extent of scientific collaboration grew to something amazing. Veterinarians, scientists, virologists and researchers stepped into important roles via Auckland and Wellington zoos, Massey's Wildbase and Dunedin Wildlife Hospital - and DOC rangers from throughout the country joined in.

The logistics of flying 50 kkp off an offshore island up the length of the country were,Vercoe says, not easy. And all the birds remaining in the wild on Whenua Hou were checked and had blood samples taken - itself a "monumental" undertaking.

But then not much about the crisis effort was, given the intensity of the care that the birds needed - batteries of CT scans, nebulisers, medications feeding, blood tests, some surgery.

On top of which the research needed to face what was effectively a new disease in kkp, and try to understand it in a very short space of time

Chris McKeen/Stuff

Margaret Maree received x-rays at VSA Vets in Mt Wellington.

Scanning the whole population wasn't possible, so they had to prioritise individuals based on their history.

This, says DOC kkp science advisor Dr Andrew Digby, involved quick data analysis, running models in search of clear contributing factors and analysing blood test results to see if this could help predict aspergillosis.

The questions were urgent: Was it due to an unusual set of environmental circumstances, or ana unusually virulent strain perhaps introduced via their management, or an undetected pathogen that made some kkp more susceptible.

From around the world came offers of support from a range of experts in man field, mostly via Twitter. They formed a collaboration of international geneticists, microbiologists, virologists and veterinarians from New Zealand, the UK, the USA, Canada and the Netherlands.

ROBYN EDIE/STUFF

In all, 21 birds were affected by the disease.

"Most of these people don't work in conservation or even with animals - many are medical researchers. They've all dropped current work to tackle this problem, donating time and money to do so."

Digby finds this unity of purpose hugely encouraging, with potential benefits for other studies too, a deeper knowledge of the genetics of the aspergillus fungus involved in this outbreak could help further global understanding of aspergillosis in humans - a serious and growing health problem.

"It's reallydemonstrated the positive power of social media to me too - it's a hugely underrated tool for scientists"

Vercoe agrees. Social media interest was huge from the DOC perspective as well.

"We took a very open approach with our communications, making sure we were keeping people as informed as possible, through the good news and the bad."

Sarah Little

Toiora the kkp sees the outside world for the first time.

The number one question was reliably the same: how can we help. From established programme supporters Meridian and Air New Zealand to a specific donation option that raised $200,000 from countries far and wide.

Gradually the good news was coming back from the exhausted labs.

"I think it was the 17th bird tested who was our first negative. That was a relief - I'd been extremely worried as the positives kept coming back.

Next raft of good news, the affected birds were responding unexpectedly well to treatment.

"It took months of treatment, but birds we thought would surely die were improving."

Jake Osborne

Toiora after being released.

Ultimately, when the last of the evacuees, Margaret Maree, headed home in early February, the crisis had been weathered.

The season that started with147 birds end with 211. Still a small number but on balance, a big step ahead for kkp recovery.

And now, of course, we have Covid-19 and a lockdown of the humans. For the recovery team, the timing has been reasonably fortunate. They'd been winding down monitoring of the breeding season and those birds who had recovered from aspergillosis - all doing reasonably well.

"Outside a breeding season, we're very hands-off with the birds. They're essentially wild birds taking care of themselves. Our rangers are safely at home."

Robyn Edie

DOC Ranger Jake Osborne with five male Kkp chicks, between 63 and 73 days old.

Not to draw too long a bow, but can Vercoe see any lessons applicable to the Covid-19 emergency?

"It can be amazing to see how people really pull together in a crisis. It takes everyone working together to get through, and a clear path of action.

"In our crisis there were times when we didn't fully understand what the best path to take was, but decisions had to be made based on the best information to hand at the time. We couldn't just sit and wait to see what would happen, there was too much to lose... beingprepared to adapt quickly as new information came to light was really important.

Chris McKeen/Stuff

Margaret Maree picked up a fungal lung infection on her home of Codfish Island. She was being treated by Auckland Zoo staff.

"When people feel committed to fighting for something and can clearly see the role they have in that fight - that purpose and connection brings out such strength."

Kkp recovery numbers:

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The kkp season of stress and salvation: How scientists and supporters teamed up to take on killer disease - Stuff.co.nz

The T List: Five Things We Recommend This Week – The New York Times

Welcome to the T List, a newsletter from the editors of T Magazine. Each week, were sharing things were eating, wearing, listening to or coveting now. Sign up here to find us in your inbox every Wednesday. You can always reach us at tlist@nytimes.com.

Buy This

Until last month, I had been a proud but distant observer of the small citrus tree in my apartment. The three-foot-tall semi-dwarf calamondin a plant native to the Philippines that produces sour, compact orange fruit thought to be a hybrid of a kumquat and a mandarin has always thrived despite, rather than because of, my attempts at care. But on my first day of working from home, the small white buds that had spread slowly along its wispy green branches throughout February suddenly burst into constellations of white, star-shaped flowers and its success became the focus of my newly confined existence. In return for more regular waterings, it has filled my apartment with the sweet, subtle, powdery scent of orange blossom for a month. And last week, when its petals finally began to fall, they left behind small green orbs that will soon become new fruit, making it not only the perfect houseplant colorful, fragrant and forgivingly resilient but an ideal houseguest. From $29, fourwindsgrowers.com

In our 2020 Culture issue, out April 19, T celebrates various groups of creative people who, whether united by outlook or identity, happenstance or choice, built communities that have shaped the larger cultural landscape including the now renowned black artists who showed at one or all of three black-owned galleries in the 70s and 80s, the butches and studs whose identity is both its own aesthetic and a repudiation of the male gaze, and the foreign correspondents explaining America to the world. Here, an excerpt from the editors letter by Hanya Yanagihara: Every magazine is by its nature retrospective, a time capsule from the near past. A magazine such as this takes months to photograph, write, edit and research, and a few weeks to print; this means that the things that were true at its conception are sometimes no longer so when its published. Yet while the world around us has changed in ways that were just a few weeks ago once reserved for the realm of fiction, the spirit and thesis of this issue has not. One of the things that has defined our age has been the rise and dominance of what we can colloquially call tribes, groups of people bound not by blood or genetics or law, but by something more profound and just as durable call it an affinity, if you will. Sometimes that affinity has its roots in race, or gender, or sexuality, but its just as often based in something not innate, but developed: taste, say, or sensibility, or experience, or history. These are assemblages of people not born unto one another, but who find one another, and as a result, their bond is more charged, more powerful, more intimate. To see the issue come alive, head to tmagazine.com.

Eat This

Molly Goddard and Joel Jeffery met in 2011, when she was 19 and he was 23, while skiing in Canada; when she returned to Brisbane, Australia, and he to London, they started a long-distance romance. On Sundays, they would Skype. Because of the time difference, one of us would always be in pajamas, Jeffery says. Thus, the seed was planted for their now five-year-old brand, Desmond & Dempsey, which sells womens, mens and childrens cotton pajamas that are joyfully splashed with brightly colored, vaguely nostalgic prints and retail for $180 a set. The two, who married in 2016, now often eat breakfast together at their Brixton apartment before walking to work. Goddard usually oversees the cooking, favoring a recipe she inherited from her mother, which she has lovingly called spiffy eggs. She makes it regularly on Sunday mornings, and would occasionally make it at the Desmond & Dempsey offices for lunch with their 10-person team. Not long after starting the company, when we didnt know what the rules were, Goddard says, the couple invited an interested buyer from the department store Fortnum & Mason to their apartment and served her Goddards special eggs. It was an unconventional approach, but it worked the buyer picked up the brand. For Goddard, the baked egg dish which includes pumpkin, Parma ham and crumbled feta is appealing not only because it is delicious and filling but also because its made in a single pot and easy to clean up. For the recipe, visit tmagazine.com.

Try This

Like many of you, Ive been spending a lot more time on my couch, a dark gray chenille-tweed settee that was my first big furniture purchase. This fact, along with increased scrolling through design-minded Instagram accounts, has left me wanting a cozy, colorful throw to can get me through springs brisker days and refresh my living room. The Hudson Valley-based brand Alicia Adams Alpaca, which makes ready-to-wear and home goods using wool from its own Alpaca farm, just released a super-soft rainbow-hued throw to celebrate its 10 years in business; 10 percent of the proceeds from each sale will be donated to Glsen, a nonprofit organization that supports the L.G.B.T.Q. community. The Spanish fashion house Loewe offers a vibrantly striped blanket in fuzzy mohair thats also available in solid colors, like this bright pink; one could also turn to Missoni, whose home collection includes an array of throws in the Italian fashion houses familiar chevron motif, like this lightweight polyester version, which is perfect for warmer temperatures. And for a more affordable option, check out Mantas Ezcaray, a small, family-owned business that offers a range of textiles made from luscious mohair in La Rioja, Spain; or these cotton blankets from the lifestyle brand VISO that feature abstract, arty shapes.

Last fall, Sara Gernsbacher and Patrick Walsh accidentally started a candle company: The Los Angeles-based artist couple both are painters and sculptors had been experimenting with folding colorful oil-pastel paintings into rectangular molds, pouring in wax from melted-down thrift-store candles, sticking in wicks and giving the results away to friends. I liked the idea of making sculpture for everyone and stepping outside the commerce of the gallery system, Gernsbacher told me. Then, thanks to Instagram (which is where I spotted their creations), the pair started getting proper sales requests from stores like the womens wear boutique Scout in Los Angeles and the cafe-slash-design-shop Relationships in Brooklyn; thus, Crying Clover Candles was born. Named for a dream Walsh had that featured a tattoo of a sad four-leaf clover, the project has continued to gain momentum, and made an appearance at last months Object & Thing show in New York, which is part of the Independent Art Fair. The allure is no doubt thanks to the candles eye-catching patterns imperfect checkerboards that Gernsbacher likens to skyscraper windows and only heightened now that most of us are stuck inside and in need of calming energy. From $36, cryingclovercandles.org

From Ts Instagram

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The T List: Five Things We Recommend This Week - The New York Times

Hair loss prevention: How to stop it falling out and thinning with stress – Evening Standard

The latest lifestyle, fashion and travel trends

We are living in stressful times.

For some the mask wearing, hand washing, food hoarding and job uncertainty will cause sleepless nights, for others it might trigger, or exacerbate existing, hair loss.

Its well established that hair loss can be related to emotional stress or anxiety, award-winning trichologist Dr. Serkan Aygin tells theStandard. When youre stressed or anxious, your body produces whats known as the fight or flight response. This is when your body is making extra hormones to prepare it to deal with whatever it thinks of as being a potential threat. This change in your hormone levels can have effects all around your body. When these extra hormones are made, they can affect the growth patterns of the hair follicles on your scalp.

Theres usually about a three-month delay between the stressful event or time period and the moment your hair starts falling out. So anyone feeling the Covid-19 anxiety, might not actually notice any hair loss until the end of summer.

The good news though, is that hair loss due to stress tends to be temporary. Unless theres another underlying medical reason for your hair loss, it should only last for as long as youre going through that particular period of stress or anxiety, says Dr. Aygin, who has treated over 10,000 patients for hair loss at his eponymous specialist hair clinic.

During the period of hair loss, more hairs on your head are in whats known as the resting stage. This doesnt mean your hair follicles are dead or that your hair will stop growing permanently. Your usual hair growth and regrowth pattern should return to normal a few months after your stress levels go back down to normal.

How to stop WFH getting in the way of your sleep

If youve lost hair as a result of stress or anxiety, theres every chance it will start to grow back once your stress levels are back to normal. Try working on reducing your stress levels as well as improving your general health and wellbeing. Any hair loss due to stress should grow back on its own in a few months.

So, if youre experiencing hair loss due to stress, the best thing to do is to stay calm, stay healthy and try not to panic. But how do you know if your hair loss is due to stress? And if its hair loss of a more permanent variety, what are the best methods of prevention, detection and treatment?

We asked Dr Aygin to provide some further clarification on the varying causes of hair loss and his preferred methods of treatment.

What causes hair loss?

Possible causes of hair loss include:

1. Genetics

The most common cause of hair loss is a hereditary condition called male-pattern baldness or female-pattern baldness. It usually occurs gradually with ageing and in predictable patterns a receding hairline and bald spots in men and thinning hair in women. Dihydrotestosterone or DHT, a breakdown product of the hormone testosterone, generally triggers male pattern baldness. Hair follicles exposed to DHT begin to shrink and the growth stage becomes shorter. The end result is thinner and shorter hair strands. Over a period of time, hair follicles will reach a phase where they are no longer capable of producing hair.

2. Hormonal Imbalance

A hormonal imbalance can lead to a multitude of annoying health and beauty issues, from adult acne to weight gain. If your hormones are out of balance, the effects will radiate throughout the whole body (and of course, that includes your hair). Hormones play a huge role in regulating the hair growth cycle. "Oestrogens (female hormones) are 'hair friendly' and help to keep hairs in their growth phase for the optimal length of time. Androgens (male hormones) are not very hair friendly, and can shorten the hair growth cycle. An excess of androgens (which could be caused by an endocrine disorder, such as Polycystic Ovarian Syndrome) can cause hair loss. The extent of this is often down to genes - If you have a genetic predisposition to follicle sensitivity, a hormonal imbalance can affect your hair more than it would someone who does not have a predisposition.

3. Medications and supplements

Hair loss can be a side effect of certain drugs, such as those used for cancer, arthritis, depression, heart problems, gout and high blood pressure.

4. Iron Deficiency and Anaemia

One of the most common causes of hair loss in women is an iron deficiency. Iron is essential for producing hair cell protein, without it, your strands will suffer.

5. Thyroid imbalance

The thyroid gland helps to regulate the body's metabolism by controlling the production of proteins and tissue use of oxygen. Any thyroid imbalance can therefore affect hair follicles. Also, if hypothyroidism is left untreated it may result in anaemia, which - as we've just discussed - is another condition that can impact the hair.

6. Vitamin B12 Deficiency

Vitamin B12 deficiency often causes hair loss as it can affect the health of red blood cells, which carry oxygen to your tissues. It's most common in vegans as you can primarily only obtain B12 through animal proteins.

7. Dramatic Weight Loss

A steep drop on the scales can impact your tresses,6-12 weeks after dramatic weight loss, whether it be intentional or unintentional, hair commonly comes out in excess. While our hair is incredibly important to us psychologically, physiologically it is non-essential; we could survive without it with no detriment to our physical health. This means that any nutritional deficiency often first shows up in our hair. Yet another reason to avoid crash dieting and instead try to adopt a healthy, balanced lifestyle.

8. Stress

Many people experience a general thinning of hair several months after a physical or emotional shock. Stress may also trigger scalp problems such as dandruff, disrupt eating habits and mess with the digestive system all of which can have a negative impact on hair. This type of hair loss is generally temporary.

9. Age

For women who are about to enter menopause, changes in their body may also have an effect on their hair. Hair loss becomes more prevalent leading up to and after the menopause. That being said, it's important to realize that our hair ages, and as we get older, hair naturally gets finer. It's a totally normal part of the ageing process.

Is hair loss more common in men?

Although both men and women experience hair loss, it is more common in men.

Androgenetic alopecia, also known as male pattern baldness, is a hereditary condition that is the most common type of hair loss among men. According to the American Hair Loss Association, 95 per centof hair loss in men is caused by androgenetic alopecia. It affects roughly 30 per cent of men by the age of 30, 40 per cent by 40, 50 per cent by 50, and 60 per cent by 60.

This inherited trait that tends to result as a receding hairline and a thinning crown in men, is caused by genetic sensitivity to a by-product of testosterone called dihydrotestosterone (DHT). Because men are constantly producing testosterone throughout their lives, they are also constantly producing DHT. This makes men more likely to lose hair than women, who do not have a similar genetic disposition to hair loss.

The early signs of male pattern baldness are as follows:

Noticeable change in your hairline

Male pattern baldness generally begins in the hairline, when you notice that your mildly receded hairline has turned into a more obvious M-shaped hairline. For most men this begins around the temples and the crown and often starts with thinning rather than total hair loss.

Noticeable thinning of your hair

Not all men experience baldness in their hairline. Some men experience what is defined as diffuse thinning; a type of hair loss that either affects the entire scalp or specific areas like the crown that results in hair loss that starts from the back or top, rather than from the hairline.

Excessive hair loss after showering or brushing

On average, people lose round 50-100 hairs a day, meaning that the five to 10 hairs you notice between your hands after shampooing aren't anything to be concerned about. However, if you start noticing an excessive amount of hair falling out throughout the day, then there is a risk that it could be the result of male pattern baldness.

In general the early signs of hair loss show up in the following ways;

Gradual thinning of the hair on the head

Receding hairline that becomes more visible with each passing year

For women, the first noticeable sign of hair loss is often a widening part or less fullness to their ponytail.

Are there effective preventative measures that can be taken?

Treating hair loss in its early stages can help minimise overall hair loss and increase the treatments efficacy. There are a few ways to control hair loss, but what to do depends on the cause of why you are losing your hair.

Some hair loss conditions such as hair loss experienced after pregnancy (telogen effluvium) are temporary and may resolve on their own. However if your hair loss is persistent you may want to schedule an appointment with your local dermatologist so as to diagnose if your hair loss is caused by conditions such as male pattern baldness, thyroid issues, scalp infections, nutrient deficiencies, stress or simply ageing.

I would recommendfour main hair-loss prevention treatments to consider, all of whichwork to stimulate regrowth on dormant follicles.

1. Finasteride

Finasteride, also sold under the brand name Propecia, is an FDA-approved prescription medication for hair loss prevention in men. Finasteride can be an effective way to prevent your hair from thinning because it prohibits the conversion of testosterone into dihydrotestosterone (DHT). DHT is a powerful hormone that is thought to cause hair follicles to miniaturise and eventually stop growing hair. To get this benefit of finasteride, you need to take it properly and consistently as prescribed by your doctor.

2. Minoxidil

Minoxidil is a vasodilator, meaning its designed to widen blood vessels and improve the flow of blood to certain areas of your body. When applied topically in the form of a serum or foam, Minoxidil increases blood flow to the parts of your scalp where hair grows. By increasing blood flow, more oxygen and nutrients can be transported into each hair follicle, promoting growth and hair health.

3. PRP (Platelet Rich Plasma)

PRP involves taking a small sample of blood and spinning it in a centrifuge to concentrate and separate the platelets and plasma from the other components of your blood, which is then injected back into the scalp. Platelets are the source of growth factors that have the power to promote hair growth and also thicken your existing hair. Growth factor generates new formation of blood vessels in the scalp, which in turn, increases the amount of oxygen and nutrients that are delivered to the hair follicles with subcutaneous blood flow.

The role of PRP is to strengthen the hair and prevent hair loss. PRP aims to promote and enhance tissue repair as well as to stimulate new hair growth.

4. LLLT (Low Level Laser Therapy) or LED Light Therapy

LED light therapy, which is actually known as Low Level Laser Therapy, is a clinically proven, effective treatment for men and women who have mild to moderate hereditary pattern hair loss. Laser hair therapy increases the production of adenosine triphosphate (ATP), which induces the release of nitric oxide. This in turn leads to enhanced hair growth. Additionally, it has been also observed that laser therapy was capable of reducing scalp tissue DHT, which may help slow, or even stop hair loss and improve hair growth.

Can hair grow back after it falls out?

Some forms of hair loss can be naturally reversed, without treatment. Reversible conditions mainly include hair loss caused by medications, prolonged stress, temporary illnesses, inadequate nutrition and improper hair care. In addition to this, hair loss caused by hormonal changes related to pregnancy and deficiencies in the function of the immune system can also be reversible.

What products would you recommend to slow the process of hair loss? And how do they work?

The important criterion to consider for controlling and/or slowing the hair loss process is to always have your hair follicles supplied with additional nutrient substances which, in turn, are requirements for healthy hair growth and hair regeneration. Hair growth can be stimulated as well as enhanced by products aimed at dermatological anti-hair loss care which:

Improve blood supply to the scalp

Serve as an additional source of energy for the hair

Promote hair strengthening

Increase hair resistance

Usinganti-hair loss products depends on the severity of the hair loss condition. For individuals with more defined hair loss patterns it is recommended to use a combination of different products such as shampoo, lotion and capsules for providing the hair with the necessary biological nutrition. At our clinic we recommendPriorin capsules (shop them here) and Sebamed Repair Shampoo (shop it here) to all our clients.

It is important to acknowledge that before trying out any recommendation that has been provided here, you should always first schedule a consultation session with your local dermatologist.

Dr. Serkan Aygin is a hair transplant specialist andmember of the International Society of Dermatology. Currently operating from his eponymous clinic in Turkey, he is due to open a second specialist hair clinic in London in August 2020.

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Hair loss prevention: How to stop it falling out and thinning with stress - Evening Standard

How a Pudgy Porpoise May Save Other Animals From Extinction – WIRED

The ensuing gold rush was catastrophic for fish and porpoise alike. At first, the totoabas were so plentiful that they could be harpooned from the beach, butchered for their mawswhich, when dried, resemble colossal potato chips with unappetizing tendrilsand left to rot. But as the population dwindled, fisherman turned to new methods. Near the Colorado River estuary, they laid gill nets, aquatic weapons of mass destruction designed to hang in the water column and ensnare passing prey. Vaquitas have the fatal misfortune of being nearly the same size as totoabas, so the nets were disastrous for them.

Lorenzo Rojas-Bracho, head of the International Committee for the Recovery of the Vaquita, at his home in Ensenada, Mexico.

The Mexican government banned totoaba fishing in the 1970s, but the killing never really stopped. By 2017, Rojas-Bracho and Taylor faced a difficult decision. With vaquitas stuck in critical decline, what else could be done? They'd talked about setting up a captive breeding program for years, but the expense and complexity had never seemed worth the risk. Now, though, it was time for a Hail Mary. That summer, Rojas-Bracho's boss, the Mexican environment minister, gave him the go-ahead to assemble his armada.

The team had four weeks to pull it all off. Early on in the effort, the vaquitas showed a knack for slipping past the researchers' nets, or just disappearing altogether. Then, with one week remaining, everything changed. It was a gorgeous day, Rojas-Bracho recalled, sinking into his sofa. I was far away from the action, but I could follow by radio. They were saying, We have the vaquita, it's behaving very nicely, it's coming to the net. We've got it on board, it's a female, it's a great animal, it's very calm. Rojas-Bracho motored over to take a look. It was the closest he'd ever been to a live vaquita. I could see my eyes in her eyes, he said.

As the sun set and the sea darkened, the team introduced the vaquita to its temporary home, el Nido. At first, it swam erratically, taking the measure of its new surroundings. Then it started to adapt. Rojas-Bracho was seated on deck, taking it all in. He heard one of the vets say to the vaquita, You're doing well, baby, so he stood up and walked away to call the environment minister. By the time he hung up, the situation had changed dramatically.

The animal started behaving wildly, and then it stopped breathing and it started to kind of sink, he said. Then there was a decision to take it out of the water and do CPR for three hours until it died, and that was painful. Jesus, it was painful. Seeing the best vets in the world trying to prevent the vaquita from dying, saying, Come on sweetie, you can do it, you can do it, it was He sighed quietly and lifted his glasses to wipe his eyes.

Conservationists must ask unpleasant questions: How to triage so many at-risk creatures? How to decide what lives and what dies?

The scientists' terrible night wasn't over. They took the vaquita onshore and performed a necropsy. Rojas-Bracho didn't sleep. The next morning, everyone agreed to shelve the captivity project.

The rest is here:
How a Pudgy Porpoise May Save Other Animals From Extinction - WIRED

Can genetics explain the degrees of misery inflicted by the coronavirus? – Genetic Literacy Project

The single biggest threat to mans continued dominance on the planet is thevirus. Joshua Lederberg, Nobel Prize in Physiology or Medicine, 1958

One of the most terrifying aspects of the COVID-19 pandemic is that we dont know what makes one person die, another suffer for weeks, another have just a cough and fatigue, and yet another have no symptoms at all. Even the experts are flummoxed.

Ive been puzzled from the beginning by the sharp dichotomy of who gets sick. At first it was mostly older people with chronic disease, and then a young person with low risk would show up. It can be devastating and rapid in one individual but mild in another, said Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Disease on a media webinar.

What lies behind susceptibility to COVID-19? Gender? Genetics? Geography? Behavior? Immunity? All of these factors may be at play, and they overlap.

Comedian Bill Maher blames poor immunity on eating too much sugar, and a thriving industry pitches immune-boosters, but much of the strength or weakness of an individuals immune response arises from specific combinations of inherited gene variants. Thats my take as a geneticist, and Dr. Faucis. Perhaps genetics and the immune response play a role in why one person has a mild response, yet another rapidly deteriorates into viral pneumonia and respiratory failure, he said.

During the first weeks of the pandemic, the observation that many victims were either older, had certain chronic medical conditions, or both, fed a sense of denial so widespread that young people flocked to Spring Break beaches as older folks boarded cruise ships in Florida as recently as early March. And then the exceptions began to appear among the young people.

While clinicians on the front lines everywhere are saving as many lives as possible, researchers are racing to identify factors that the most vulnerable, and the most mildly affected, share, especially the asymptomatic carriers. And as the numbers continue to climb and more familiar possible risk factors are minimized or dismissed age, location, lifestyle habits genetics is emerging as an explanation for why otherwise young, strong, healthy people can die from COVID-19.

Following are possible genetic explanations for why some people become sicker than others. These are hypotheses, the language of science: ideas eventually fleshed out with observations and data. Proof is part of mathematics; in science, conclusions can change with new data. The public is getting a crash course in the scientific method.

The most obvious genetic risk factor in susceptibility to COVID-19 is being male. The details of disease demographics change daily, but males are about twice as likely to die if theyre infected as are women: 4.7% versus 2.8%.

At first people blamed the sex disparity on stereotypes, like the riskier habits of many a male compared to females. But the sex difference comes down to chromosomes.

In humans, a gene, SRY, on the X chromosome determines sex. Males have one X and a puny Y; females have two Xs. Fortunately, nature takes care of this fundamental inequality of the sexes, which I detailed hereand in every biology textbook Ive ever written.

To compensate for the X deficit of the male, one X in every cell of a female is silenced beneath a coating of methyl groups, an epigenetic change. But which X is silenced differs, more or less at random. In a liver cell, the turned off X might be the one that the woman inherited from her father; in a skin cell, the silenced X might be the one inherited from her mother.

The immune system seems to benefit from the females patchwork expression of her X-linked genes, with a dual response. Gene variants on one X may recognize viruses, while gene variants on the other X may have a different role, such as killing virally-infected cells.

Women also make more antibodiesagainst several viral pathogens. But some of us pay the price for our robust immune response with the autoimmune disorders that we are more likely to get.

People with type O blood may be at lower risk, and with type A blood at higher risk, of getting sick from SARS-CoV-2, according to results of a recent population-based study. But the idea of type O blood protecting against viral infections goes back years.

We have three dozen blood types. Theyre inherited through genes that encode proteins that dot red blood cell (RBC) surfaces, most serving as docks for sugars that are attached one piece at a time. The RBCs of people with type O blood do not have an extra bit of a sugar that determines the other ABO types: A, B, or AB.

The unadorned RBCs of people with type O blood, like me, are less likely to latch onto norovirus (which explains why I rarely throw up), hepatitis B virus, and HIV.

An investigation of ABO blood types from the SARS epidemic of 2002 to 2003 provides a possible clue to the differences. People with blood types B and O make antibodies that block the binding of the SARS viruss spikes to ACE2 receptors on human cells growing in culture. Since the novel coronavirus enters our cells through the same receptors, are people with type O blood less likely to become infected?

Thats what researchers from several institutions in China have found in the new study. They compared the blood types of 2,173 patients with COVID-19 from three hospitals in Wuhan and Shenzhen to the distribution of blood types in the general population in each area.

People with type A blood were at higher risk than people with type 0 blood for both infection and severity of the illness.

In the general population 31% of the people are type A, 24% are type B, 9% are type AB, and 34% are type O. But among infected individuals, type A is up to 38%, type B up to 26%, AB at 10%, and type O way down to 25%.

The researchers conclude that the findings demonstrate that the ABO blood type is a biomarker for differential susceptibility of COVID-19. I think thats a bit strong for a trend, considering the exceptions. But the researchers suggest that their findings, if validated for more people, can be used to prioritize limited PPE resources and implement more vigilant surveillance and aggressive treatment for people with blood type A.

Immunity and genetics are intimately intertwined. Links between mutations both harmful and helpful and immunity to infectious diseases are well known.

Mutations in single genes lie behind several types of severe combined immune deficiencies (SCIDs), like bubble boy disease. Sets of human leukocyte antigen gene variants (HLA types) have long been associated with increased risk of autoimmune conditions such as celiac disease, type 1 diabetes, and rheumatoid arthritis, and were for many years the basis of tissue typing for transplants.

In HIV/AIDS, two specific mutations in theCCR5 gene remove a chunk of a co-receptor protein to which the virus must bind to enter a human cell. The mutation has inspired treatment strategies, including drugs, stem cell transplants, and using CRISPRto recreate the CCR5 deletion mutation by editing out part of the gene.

Might variants of the gene that encodes ACE2, the protein receptor for the novel coronavirus, protect people in the way that a CCR5 mutation blocks entry of HIV? The search is on.

Another clue to possible genetic protection against the novel coronavirus may come from the SARS experience from years ago and parasitic worm diseases in Africa. (This hypothesis I came up with on my own so Im prepared to be shouted down.)

In a human body, the SARS virus disrupts the balance of helper T cells, boosting the number of cells that fight parasitic worms (the Th2 response) while depleting the cells that protect against bacteria and viruses (the Th1 response). The resulting Th2 immune bias, in SARS as well as in COVID-19, unleashes the inflammatory cytokine storm that can progress to respiratory failure, shock, and organ failure.

In subSarahan Africa alone, a billion people have intestinal infections of parasitic worms, the most common of which is schistosomiasis. Its also called snail fever because the worms are released into fresh water from snails and burrow into peoples feet when they wade in the water.

The worms mate inside our blood vessels, releasing eggs that leave in urine and feces into the water supply. Remaining eggs can inflame the intestines and bladder. The infection begins with a rash or itch, and causes fever, cough, and muscle aches in a month or two. A drug treatment is highly effective.

Genetics determines susceptibility, or resistance to, schistosomiasis. And thats what got me thinking about COVID-19.

People who resist the flatworm infection have variants of eight genes that ignite a powerful Th2 immune response that pours out a brew of specific interferons and interleukins. Could the Th2 immune bias of the novel coronavirus SARS-CoV-2 not be as devastating to people who already have the bias, to resist schistosomiasis? If so, then places in Africa where many people are immune to schistosomiasis might have fewer cases of COVID-19.

So far parts of Africa have reported low incidence of the new disease. On April 7, the World Health Organization reported approximately 10,000 cases in all of Africa. Thats similar to the number of deaths in New York City, although Africa could be on track for the exponential growth seen elsewhere. But if the lower number in Africa persists, then maybe those eight genes are protecting people. Adding to the evidence is that the 8-gene set varies more between West Africans and Europeans than do other sets of genes.

Like the ABO blood type study, if the 8-gene signature that protects against schistosomiasis protects against COVID-19, then the signature should be overrepresented among those exposed to the virus who do not get very sick, and underrepresented among those who do. However, its possible that Africa is just behindthe rest of the world in reporting COVID-19 cases. So, a thought experiment for now.

Before researchers zero in on a highly predictive genetic signature of COVID-19 risk, we can think about how the information would best be used:

I hope that discovery of a genetic basis for COVID-19 vulnerability or resistance will not inspire discrimination unfortunately, genetic information has had a legacy of misuse.

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

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Can genetics explain the degrees of misery inflicted by the coronavirus? - Genetic Literacy Project

Meet Pope Patrick Irish, intersex and pregnant – The Irish Times

The premise of my latest novel, Virgin & Child, will no doubt be seen as so outrageous and provocative that it calls for some explanation.

Its a novel that arose out of a thought experiment, which I wrapped up as a literary thriller. It was long in the writing and brings together all the different aspects of my own life and work, and yet the idea came to me in one instant, more than 10 years ago.

I was studying for my masters in theology, having come to faith after a long struggle between my head and my heart, wanting to understand it better. We had a task: to review the then Pope Benedicts first encyclical, Deus Caritas Est (God is Love). What was praised by the Catholic Church and many commentators for what Ruth Gledhill called its beautiful and passionate writing and theological rigour seemed to me to set up such an idealised nature of love that no human being could possibly come close to it.

An encyclical is addressed to the world, not just the Catholic Church, and this one had nothing to say to anyone who doesnt support the churchs position that only in a heterosexual marriage and when open to procreation can sex be approved.

The encyclical failed to address any of the new approaches to gender, embodiment, sexuality and sexual orientation in our postmodern or transmodern world. There was nothing either to help or offer guidance with all the difficult and complex moral and ethical dilemmas faced in the modern age by us imperfect beings in an imperfect world. In short, it was an epic fail.

I had spent a great deal of my early career involved in womens reproductive rights. I worked for various charities and sat on the Committee to Defend the 1967 Abortion Act, and worked with Spanish groups trying to set up contraception and abortion services after Francos death.

I saw at first hand the very real pain and suffering and the struggles faced by women who found themselves unwantedly pregnant, and the moral conflicts they faced. The language used by the Catholic Church around abortion, as well as on issues such as homosexuality and transgender, is dismissive and horrible.

What could happen to shake these popes and cardinals in the Vatican, wrapped in their dogma, surrounded by medieval walls and completely divorced from the reality of peoples ordinary lives, desires and problems? How, in particular, could they ever understand a womans lived experience, what it is like to be unwantedly pregnant, or the lives of those who feel different?

And then the idea came to me. It was only if one of them became mysteriously pregnant, I thought, if they desired to end it and were afraid of childbirth, if they discovered that they were not male as they had thought, that they would understand. And I liked the idea that they could be intersex, since I had been a tomboy as a child and had felt frustrated with the gender roles in our society when I was growing up, especially since my then ambition was to become an astronaut.

Yes, this seemed an absurd idea for a novel. Was this even possible? Could I make it convincing? Happily, my first degree was in biochemistry, which included a module in molecular genetics. I looked at scientific papers and found that a rare condition exists where two early embryos fuse, one male and one female, and then go on to develop as one individual, but with a random distribution of male and female cells and characteristics.

One case study caught my eye a person with one ovary and one testis, who appeared to be male. And there had been 11 live births to such people. So, while of course it was extremely unlikely, it was indeed possible and so it neednt be a miracle, though of course people would suspect that it was.

My Pope, Patrick, is the first Irish Pope. I chose an Irish Pope because there has never been one, so I felt that he couldnt be thought to be based on anyone specific; and because I have always identified as a Celt rather than English, as my Welsh, Scottish, and distant Irish ancestry far outweighs my English blood.

It also seemed appropriate in terms of the enormous changes that have taken place in Irish society in the last few years, with the diminishing power of the church, tarnished by child abuse scandals, and the legalisation of abortion, which happened towards the end of the writing of the novel.

At first, it was hard to like my Pope Patrick. He started off as dogmatic, rigid, fussy, a bit like Benedict himself. And then Benedict resigned and we had Pope Francis a different kind of character altogether. My Pope changed too as I recreated his childhood.

As I wandered round Cork where my cousin lives, and where it was therefore convenient for Patrick to have grown up, he began to become human. I realised that as a child he had been mocked for being different, something I had always felt at school. He was desperate for human love and connection, and found himself in a position where this was impossible to achieve.

This human love is of course mediated through touch, something withheld from him by his mother and father; his difficult relationship with his parents rested on secrets which he uncovered only after his fathers death.

As the cardinals in my novel opposed him and threatened his position, even took steps to remove him, I felt more and more sympathy with his predicament. And as the story unfolded, and his faith was shaken, it reflected my own struggles with Christianity, something which as a scientist I had always found hard to believe, and yet which constantly tugged at my heart till I could no longer resist it.

I tried to write the book with humanity, and respect. I dont have any wish to denigrate religion, and indeed, there are passages in the book based on my own experience of prayer and Gods presence. The Catholic Church today is torn, as is my novel, between those who want things to stay as they are and those who want to make the faith more relevant in the modern world. My novel is a way of engaging with this debate, asking questions and inviting people to share in the experience, rather than giving any definitive answers.Virgin & Child is published by Barbican Press, priced 16.99

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Meet Pope Patrick Irish, intersex and pregnant - The Irish Times

The 5 factors people who die of coronavirus have in common – The Scottish Sun

THE number of people dying from coronavirus across the world is continuing to rise every day - with just under 130,000 deaths in 210 countries.

And in the UK alone,the total of deathspushed past the 12,000 barrier yesterday - with the grim total expected to be 15 per cent higher than reported due to people dying outside of hospital.

4

However, scientists have now revealed that there are some key factorsthat people who pass away from Covid-19have in common.

A team of researchers from eight institutions in China and the United States including the Chinese Peoples Liberation Army General Hospital in Beijing, and the University of California Davis recently looked at the data of 85 patients who died of multiple organ failure after having received care for severe Covid-19.

All individuals whose data the study used received care at either the Hanan Hospital or the Wuhan Union Hospital between January 9 and February 15, 2020.

And the researchers who conducted the study,that appears in the American Journal of Respiratory and Critical Care Medicine,uncovered a series of factors that the majority of these patients shared.

Here, we outline these key factors...

The killer new coronavirus appears to be posing a particularly deadly threat to men.

In fact, the researchers found that 72.9 per cent of those who died from the new coronavirus were male.

Experts believe there are a few reasons for more men dying than women, including some biological and other lifestyle choices.

Hand washing is one of the best ways to prevent infection - but multiple studies show that women are much more likely to wash their hands and use soap than men.

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Akiko Iwasaki, a professor of immunology at Yale University, told the New York Times that men may have a "false sense of security" about coronavirus.

Meanwhile, Chinese men are much more likely to smoke than women, which can lead to a weaker immune system.

In fact China has the largest population of smokers in the world - accounting for nearly a third of the world's smokers - but just two per cent of them are women.

Meanwhile, in the UK 16.5 per cent of men - around 3.9 million - and 13 per cent of women - around 3.2 million - reported being current smokers.

Chinese men also have higher rates of high blood pressure, Type 2 diabetes and chronic obstructive pulmonary disease than women.

All of these conditions can increase the risk of complications following infection of coronavirus.

Then new strain of deadly coronavirus doesn't discriminate and can infect anyone of any age.However, it's older adults - aged 60 and upwards - who are more likely to get seriously ill from it - with the scientists discoveringthat those who died from Covid-19 had amedian age of 65.8 years.

Medics say it's because our immune systems weaken with age, meaning an older person's body is less able to fight Covid-19.

Dr Sarah Jarvis, GP and Clinical Director of Patient Access, told The Sun: "We know that as you get older, your immune system becomes less efficient thats why older people are at higher risk of serious complications of coronavirus infection.

4

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"If your immune system isnt strong, its more likely that the virus can multiply deep inside your lung, causing inflammation and scarring.

"Your immune system will try and fight it off, and will often destroy healthy lung tissue in the process.

"This makes you more prone to get secondary infections like pneumococcal pneumonia."

In fact, evidence from China, where the deadly virus originated, shows one in seven of those over 80 known to have contracted coronavirus have died.

Those who died from Covid-19 in the study mostly had underlying chronic conditions, such as heart problems or diabetes.

The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the researchers said.

We hope that this study conveys the seriousness of Covid-19 and emphasizss the risk groups of males over 50 with chronic comorbid conditions, including hypertension (high blood pressure), coronary heart disease, and diabetes, they added.

4

In fact, another study recently revealed that your risk of dying from coronavirus is 80 per cent higher if you have just one underlying health issue.

For those with two pre-existing conditions or more, the chances of being admitted to intensive care are even higher, experts warned.

Some of the chronic conditions said to heighten the risk among patients are asthma, cancer, cystic fibrosis, chronic obstructive pulmonary disease (COPD), diabetes and HIV and AIDS.

People who are obese or seriously overweightfall into the high risk category for coronavirus.

This is because being overweight or obese can weaken the bodys immune system which could make people more likely to catch coronavirus and makes it harder for the body to fight the bug.

The NHS has said people with a BMI of 40 or above have a greater risk of developing complications if they catch the virus.

More than 60 per cent of patients in intensive care with the virus were overweight or classed as morbidly obese, arecent NHS survey found.

Those who were overweight, with a BMI of 25 to 40, made up 64 per cent of the 194 coronavirus patients who were in ICU at the time, while seven per cent were classed as obese with a BMI over 40.

BMI is a measure of whether youre a healthy weight for your height, you can calculate yours on the NHS website.

In the past, studies have shown overweight and obese people are at greater risk of serious complications or death from infections, like flu.

The extra weight on obese people's diaphragms puts pressure on lungs and makes it harder to breathe, starving them of oxygen.

Clogged up arteries can also make it harder for blood carrying immune cells to circulate and travel to fight infection around the body.

In terms of other potentially relevant information, the research team found that 81.2 per cent of those who died from Covid-19 in the study had very low eosinophil counts on admission to the hospital."

This is a type of white blood cells, which are specialised immune cells that help fight infection.

The medics suggested that having abnormally low levels of eosinophils a condition known as eosinophilopenia may correlate with a greater risk of severe outcomes in people who have contracted Covid-19.

While the scientists hope that their current findings may help other doctors better understand and prepare for fighting coronavirus, the researchers nevertheless urge other experts to keep on recording all possible information about people receiving care for this new illness.

Our study, which investigated patients from Wuhan, China, who died in the early phases of this pandemic, identified certain characteristics, the researchers said.

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"Yet as the disease has spread to other regions, the observations from these areas may be the same, or different.

They added: Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates, as well.

"Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

We pay for your stories and videos! Do you have a story or video for The Scottish Sun? Email us at scoop@thesun.co.uk or call 0141 420 5300

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The 5 factors people who die of coronavirus have in common - The Scottish Sun

[Discussion] Dealing with shitty male genetics. : steroids

Why Young People Should Not Take AAS

Adapted from the r/steroids Wiki

Nandrolone has been reported to induce psychiatric side effects such as aggression and depression. Adolescence represents an extremely sensitive neurodevelopmental period to influence by detrimental effects.

Side Effects of Drugs Annual (2015)

AAS use by teenagers is a primary concern because of the potential side effects where remodeling of the brain and behavioral maturation occurs.

Journal of Behavioral Processes (2015)

Until you're around the age of 25, your brain and endocrine system are still developing. This should be obvious as you are still going through the end of puberty, getting acne, etc. During this time period, supplementing with exogenous hormones is extremely dangerous.

Taking anything before you are completely finished with puberty can have negative side effects. While you are maturing, your brain, organs, and cells are consistently gauging the overall development of your body. When you introduce a foreign substance, you risk your bodys ability to truly judge how far along your maturation is, resulting in the possibility of premature shutdown or stunting your growth and development processes.

Natural Blast

Your body is already pumping out blast levels of testosterone as part of the natural course of late adolescence. It's the highest that it's ever going to be in your lifetime.

Why prematurely shut that down and ruin a great thing? You're essentially on free steroids right now. Don't take that opportunity for granted and abort your own physiological development by injecting additional variables that short-circuit the whole equation.

Sides

There's a serious potential for long-term side effects. People oft-say I've stopped growing, so it's okay. No: it's not okay. The rest of you hasn't finished developing yet. There are many other potential side effects besides simply your growth plates. Here are a few.

Brain Function, Memory, Alzheimers Disease

It's well known that hormones play a role in the development of cognitive brain function. Your neuroendocrine system is still developing until the age of 25. Adding external hormones when your brain is still developing can stunt normal development and maturation.

Many steroids are neurotoxic.

They lead to depression, memory loss and learning difficulties.

They cause longstanding dysfunction in brain reward systems.

They give rise to the accumulation of amyloid plaques, which leads to Alzheimers.

Do you really want to add these variables to a still-growing and developing brain? How can you know many years down the road there won't be even more problems?

Cancer, Liver, Kidney Disease

You hear all the time teenagers say Well my friends it and they got big and nothing happened to them. Really? How do you know? Have they been to a doctor and had their liver and kidney values checked? Just because a person looks okay on the outside, doesn't mean that they don't already host serious problems on the inside. If treated improperly or in an untimely manner, liver and kidney damage can prove to be fatal.

Premature Closing of Growth Plates

This one is the most known about. Even if you think you've stopped growing, there still is a potential for height increase over time. Scientists have found that growth plates don't fuse completely in some cases until individuals are past 22. Don't be deterred just because you haven't grown taller in awhile. You grow out as well as up. Do you want broader shoulders, or do you want to stay stuck with what you've got now?

Impotence

Your neuroendocrine system is still developing. Supplementing with hormones while you are still growing can potentially cause permanent impotence and fertility issues in teenagers. When you add testosterone, estrogen and a wealth of other synthetic androgens to your body it can cause problems with your normal testicular growth and function. Remember, some of these effects are more than just temporary.

Gyno, or Bitch Tits

Androgen usage in teens increases the risk of gyno. Gyno has already been known to happen naturally in many teenagers because of fluctuating hormones. When you add more hormones to the mix, you dramatically increase the problems. Remember once you have gyno, it's very hard to get rid of. Unless you take the proper precautions up front, you'll have to resort to surgery and go under the knife.

Hair Loss, Acne, Prostate Dysfunction

All of these can be accelerated and aggravated with exogenous androgen use.

Have you seen a 20-year old already going bald?

What about permanent scarring from severe cystic acne?

How about being unable to use the bathroom due to the excruciating pain involved in the process? It's not pretty.

Don't think it can't happen to you.

References

A few references.

Trenbolone neurotoxicity:

Deca, or Nandrolone, is eleven times more damaging to blood vessels than Testosterone. It causes longstanding changes in the brain reward system, affects learning and memory, and induces genetic damage across multiple organ systems.

Nandrolone impaired spatial learning and memory, and this effect was not rescued by exercise. The harmful effects of ND and other AAS on learning and memory should be taken into account when athletes decide to use AAS for performance or body image improvement.

Adapted from the r/steroids Wiki

Originally posted here:
[Discussion] Dealing with shitty male genetics. : steroids

Insight: What those dying of COVID-19 have in common – P.M. News

A team of researchers from eight institutions in China and the U.S. has offered a fresh insight into why 85 patients died of multiple organ failure after suffering severe COVID-19.

All individuals whose data the team studied received care at either the Hanan Hospital or the Wuhan Union Hospital between January 9 and February 15, 2020.

The researchers came from the Chinese Peoples Liberation Army General Hospital in Beijing, and the University of California Davis and six other institutions.

Their study uncovered a series of factors that the majority of these patients shared.

The study has been published by the American Journal of Respiratory and Critical Care Medicine.

The majority were older malesThe research team was able to access and analyze the deceased patients medical histories, including whether they had any underlying, chronic conditions.

The researchers were also able to find out what symptoms the patients experienced once they had contracted the virus and access information from laboratory tests and CT scans.

They also accessed information about the medical treatment they received while in the hospitals.

They found that 72.9% of those who died with COVID-19 were male, with a median age of 65.8 years and underlying chronic conditions, such as heart problems or diabetes.

The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the investigators note.

They found that 72.9% of those who died with COVID-19 were male, with a median age of 65.8 years and underlying chronic conditions, such as heart problems or diabetes. The greatest number of deaths in our cohort were in males over 50 with noncommunicable chronic diseases, the investigators note.

We hope that this study conveys the seriousness of COVID-19 and emphasises the risk groups of males over 50 with chronic comorbid conditions, including hypertension (high blood pressure), coronary heart disease, and diabetes, they have commented.

The team also notes that, among the 85 patients whose records it analyzed, the most common COVID-19 symptoms were fever, shortness of breath, and fatigue.

Some important observationsIn terms of other potentially relevant information, the research team found that 81.2% of the study individuals had very low eosinophil [a type of white blood cells, which are specialized immune cells that help fight infection] counts on admission.

Among the complications that the patients experienced while hospitalised with COVID-19, some of the most common were respiratory failure, shock, acute respiratory distress syndrome, and cardiac arrhythmia, or irregular heartbeat.

As part of their treatment, the majority received antibiotics, antivirals, and glucocorticoids, and some received intravenous immunoglobulins (also known as antibodies), or interferon alpha-2b, which is also a stimulant for the immune response.

Yet, the researchers note, the effectiveness of medications, such as antivirals or immunosuppressive agents, against COVID-19 is not completely known.

Based on their observations, the authors indicate that treatments, including combinations of antimicrobial drugs, did not appear to have much of a positive effect.

Perhaps our most significant observation is that while respiratory symptoms may not develop until a week after presentation, once they do there can be a rapid decline, as indicated by the short duration between time of admission and death (6.35 days on average) in our study, they write.

They also suggest that having abnormally low levels of eosinophils a condition known as eosinophilopenia may correlate with a greater risk of severe outcomes in people who have contracted SARS-CoV-2.

While they hope that their current findings may help other doctors better understand and prepare for fighting COVID-19, the researchers nevertheless urge the global scientific community to keep on recording all possible information about people receiving care for this new illness.

Our study, which investigated patients from Wuhan, China, who died in the early phases of this pandemic, identified certain characteristics, the researchers say, yet as the disease has spread to other regions, the observations from these areas may be the same, or different.

They continue: Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates, as well.

Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

*Originally published by Medical News Today

View post:
Insight: What those dying of COVID-19 have in common - P.M. News

COVID-19: Young Boys At Higher Risk Of Infection and Severe Illness From Coronavirus, Says Study – Yahoo Singapore News

In recent reports, it has been said that the coronavirus takes a higher toll on menwith some experts warning that being male may be a risk factor for COVID-19, as much older age is.

In fact, a scientist who studies sex difference in viral infections at Johns Hopkins Bloomberg School of Public Health, Sabra Klein told the New York Times: Being male is as much a risk factor for the coronavirus as being old. People need to be aware that there is this pattern. Just like being old means youre at higher risk, so does being male. Its a risk factor.

She also said the vulnerability could be biological or behavioural, adding that women have more robust immune systems than men.

But a new study from the Centers for Disease Control and Prevention (CDC) is suggesting it may have more to do with biology than lifestyle. In particular, it may even have to do with genetics.

Male COVID-19 patients are more common than females, study finds. | Image source: iStock

In CDCs Morbidity and Mortality Weekly Report published on Monday (6 April), it is found that there is a higher prevalence of COVID-19 in males across every pediatric age groupincluding newborns and infants.

Specifically, in the study of over 2,500 childrenaged 0 to 18with COVID-19, some 57 percent were male, suggesting that biological factors could make men more susceptible to the virus.

Based on the study, among the cases in children, the median age was 11 years, with nearly one-third of reported pediatric cases of cases involving teens between the ages of 15 and 17.

Among pediatric cases for which sex was known, 57 percent occurred in malesmuch higher in percentage compared to adult cases, in which 53 percent occurred in males.

The study also found that most of the children reported symptoms of cough or fever, only 5.7 percent were hospitalized.

These data support previous findings that children with COVID-19 might not have reported fever or cough as often as do adults, the report said.

Children who were hospitalised reported at least one underlying health condition, with most common being chronic lung diseases (such as asthma), cardiovascular diseases.

Meanwhile, in Singapore, a quick check on the summary of made available since the beginning of April shows that among the 21 reported pediatric patients who tested positive for COVID-19, 16 are male. Furthermore, based on this online dashboard, among the 49 pediatric cases reported here as of 11 April, 29 are male.

Still, it is noted that the research is still in its preliminary stages and that the authors are working with limited information. It is noted that the research did not suggest that parents should now be more concerned about their male childrenmore than their female childrengetting severely ill from COVID-19. Experts said it is no reason for parents of boys to panic, and for parents of girls to think they are immune to the virus.

24 hour clinics in singapore, Male COVID-19

Image source: iStock

They also reiterated that the risk for children remains very low. In fact, though there have been multiple reports from all over the world about coronavirus-related death in children recently, only 0.1 percent of the children infected died.

Story continues

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COVID-19: Young Boys At Higher Risk Of Infection and Severe Illness From Coronavirus, Says Study - Yahoo Singapore News

Exploring the gourd family of cucumbers, squashes and melons – Las Cruces Sun-News

Marisa Thompson, Southwest Yard and Garden Published 3:12 a.m. MT April 12, 2020

Small fruit are developing at the base of the female flower (bottom left), but not on the male flower (top left). Pollen from the stamens in the center of the open male flower (top right) can be translocated to the stigma in the center of the open female flower (bottom right) by pollinating insects or by humans.(Photo: Abrahami, Wikimedia Commons)

Question: I would love to be able to grow both zucchini and watermelon this year, but I am hesitant because of problems with cross-pollination in the past. Any tips?

Seed to Supper online course participant, somewhere in New Mexico

Answer: First of all, for readers who dont already know about New Mexico State University'sSeed to Supper program through ICAN (Ideas for Cooking & Nutrition), this is a free, online, self-paced beginning gardening course that was first developed by the Oregon State University Extension Service and modified by our own NMSU Food Systems Specialist Sally Cassady to be web-based and New Mexico-oriented (https://ican.nmsu.edu/seedtosupper.html).

It sounds like the problems youve had in the past with zucchinis and watermelons may have been more about fruit set issues which could include pollination problems than cross-pollination. Cross-pollination can only occur within plants of the same species. The old gardening tip dont plant cucumbers next to squash or melons because theyll cross-pollinate and form bad fruit isnt true. NMSU Extension Vegetable Specialist Stephanie Walker confirmed: As long as the cucurbits are different species, its very unlikely theyll cross-pollinate. Zucchini is Cucurbita pepo and watermelons are Citrullus lanatus, so they wont cross-pollinate to produce viable seed.

Marisa Y. Thompson(Photo: Courtesy)

Plants in the cucurbit (gourd) family include melons, pumpkins, squashand cucumbers. Each of those different cucurbits includes plants of different species and genera (plural of genus). Remember, the scientific names of plants consist of two parts: the genus and the species. So musk melons scientific or botanical name is Cucumis melo, with Cucumis as the genus and melo as the species. Cucumber is Cucumis sativus, so even though musk melons and cucumbers are in the same genus (Cucumis), they are not the same species and wont be likely to cross-pollinate. Even if they did cross-pollinate, the evidence would not be visible in this years crop. If you saved seed from cross-pollinated fruit and grew it next year, you might get something cool and yummy, although its more likely to be undesirable. Pumpkins with green bumps could be the result of seeds that were saved from normal pumpkins crossed with green-warted gourds.

Its not just that plants from different species arent likely to cross-pollinate based on their genetics. Amanda Skidmore, NMSU Extension integrated pest management specialist for urban and small farms, explains that our pollinators are picky too: Interestingly, different pollinators will visit each plant because of the flower shape and inflorescence. For example, squash bees will visit zucchini, but not watermelon.Skidmore encourages gardeners to take some time to watch and see what different pollinators are visiting the two plants. There will be some overlap (honey bees, bumble bees), but some cool differences too.

For information, check out our NMSU Extension Guide collection for vegetables. Related titles include Starting Plants Early Outdoors, Spices and Herbs for the Home Garden, Home Vegetable Gardening in New Mexico and Growing Zones, Recommended Crop Varieties, and Planting and Harvesting Information for Home Vegetable Gardens in New Mexico.

As retired NMSU Extension Horticulture Specialist Curtis Smith explained in a 2008 column, cucurbits have separate male and female flowers on the same plant. You can recognize the male flowers because they do not have a small fruit behind them (more on this later). They produce the pollen needed to form the fruit, but they do not produce the fruit. The female flower, on the other hand, has a small fruit behind the flower even before it opens. The female flower cannot produce the pollen needed to cause the fruit to develop and is dependent upon insect (or human) pollinators to transport the pollen from the male flower. The male flowers begin forming before the female flowers form. So, it is possible to have cucurbits blooming, but not producing fruit. The time between the first development of male flowers and the female flowers depends on plant variety and environmental conditions. Your problem may just be that the female blossoms have not formed yet. They should be forming soon. However, if you see the female flowers on your cucurbit plants, but they are not "setting" fruit, then the problem may be that you do not have pollinators.

Smith also offers tips on how to pollinate your cucurbit flowers yourself: Each morning, collect pollen from the stamens in the center of the male flowers and then transfer that pollen to the stigma in the center of the female flowers. Use a small, soft-bristled paintbrush to do this. If you are successful, you should see small fruit forming within a few days. Leave some female flowers unpollinated (by you), so you can watch for the return of the natural pollinators to relieve you of the early morning effort of pollination.

A few years ago, I wasnt convinced that Id be able to tell the difference between male and female flowers on a squash plant. That is, until I looked closer. Both flower types are huge and bright orange-yellow, but if you look just behind the flowers, youll know when you find a female versus a male because theres a swollen fruit structure developing at the base of female flowers. In some cucurbits, that baby fruit will be more rounded, and in others more like a small pickle.

For gardening information, including decades of archived Southwest Yard & Garden columns, visit the NMSU Extension Horticulture page (http://desertblooms.nmsu.edu/), follow us on social media (@NMDesertBlooms), or contact your County Extension office (https://aces.nmsu.edu/county).

Marisa Thompson, PhD, is the Extension Horticulture Specialist for New Mexico State University and is based at the Agricultural Science Center at Los Lunas.

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The Unpredictable Genetics Of Male-Pattern Baldness

What are the genetics of male pattern baldness? originally appeared on Quora: the knowledge sharing network where compelling questions are answered by people with unique insights.

Answer by Adriana Heguy, Director of the NYUMC Genome Technology Center and Professor of Pathology, on Quora:

Unfortunately the genetics of androgenetic alopecia (male-pattern baldness) is not really well understood. The more complex the biology behind a phenomenon is, the more difficult is going to be to find all the genetic factors. Regulation of hair growth in mammals is extremely complicated and poorly understood, in spite of this subject being a very active area of research. Hair is very important to mammalianthermoregulation thus it makes sense for its biology to be very complex.

It is clear that male-pattern baldness is a highly heritable condition [1], although there is also some evidence for the involvement of epigenetic factors [2]. There are a few genes implicated in androgenetic alopecia from different studies [3]. Unsurprisingly, the androgen receptor (AR) gene is one of them, as it is well known that the condition is dependent on testosterone (an androgen). The androgen receptor is on the X chromosome, which is why some people propagate the myth that male-pattern baldness comes from the mother's side of the family (a male inherits the X chromosome from mom, the Y chromosome from dad). But it is not the only gene involved, or even the main gene involved. There are genes in basically all chromosomes that have been implicated in androgenetic alopecia, and this is what makes it so difficult to unravel, as we would have to examine the overall contribution that each gene variant (single nucleotide polymorphism, or SNP) play in hair loss, and also how these genes interact with each other and the environment to result in the phenotype.

Position of genes implicated in male pattern hair loss, from [4].

Some of these genes code for transcription factors or histone deacetylases. TheWnt pathway appears to be involved. Even though we know a fair amount about transcription factors, the Wnt pathway, etc., this still does not tell us much about what's actually going on in androgenetic alopecia and why the hair follicles shrink and die. The hope is that identifying these genes will provide targets for therapeutic intervention. But so far, we are still far from a definitive "cure" for androgenetic alopecia.

If there is any consolation for men (or at least, heterosexual men) distressed about hair loss, if it was a phenotype that was repulsive to females, the gene variants would have been weeded out a long time ago, by sexual selection. Many of us find bald heads very manly and attractive.

Footnotes

[1] Genetic basis of male pattern baldness.

[2] Eleven pairs of Japanese male twins suggest the role of epigenetic differences in androgenetic alopecia.

[3]Hunting the genes in male-pattern alopecia: how important are they, how close are we and what will they tell us?

[4] Hunting the genes in male-pattern alopecia: how important are they, how close are we and what will they tell us?

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Everything you need to know about fatal cases of COVID-19 – Ladders

Nearing COVID-19s fatality peak means having a larger pool of severe cases to draw correlates from.

A new study published in The American Journal of Respiratory and Critical Care Medicine has successfully identified several clinical similar sites linking fatal reactions to SARS-Cov-2 infection.

The global death toll from COVID-19 virus exceeds 21000. The risk factors for death were attributed to advanced age and comorbidities, but havent been accurately defined, the authors wrote in the new paper. Medical records of 85 fatal cases of COVID-19 between January 9 and February 15, 2020, were collected. The information recorded included medical history, exposure history, comorbidities, symptoms, laboratory findings, CT scans, and clinical management.

The researchers were not only able to determine the underlying factors that lead to acute COVID-19 symptoms, but they were also able to link onset symptoms with critical outcomes.

According to the data, the majority of COVID-19 deaths occur as a result of multiple organ failure. Patients on ventilators do not receive enough oxygen in their bloodstream to sustain vital biological functions or combat accompanying effects of prolonged illness like inflammation, pneumonia and acute respiratory distress syndrome (ARDS). Between 30% and 40% of patients who experience ARDS do not survive

The median age of the patients involved in the new study who succumbed to COVID-19 was 65.8 years old and 72.9% were male. The common symptoms in cases that went on to become fatal were fever, shortness of breath, fatigue, and dyspnea (labored breathing).

Early onset of shortness of breath may be used as an observational symptom for COVID-19 exacerbations. Eosinophilopenia may indicate a poor prognosis. The combination of antimicrobial drugs did not offer considerable benefit to the outcome of this group of patients, the report continued.

Symptoms were not the only instructive element of case severity. Hypertension, diabetes and coronary heart disease were the most common comorbidities in the cases analyzed.

Eighty-one percent of patients who had low white blood cell counts at admission developed fatal cases of COVID-19. Complications associated with these predictors included respiratory failure, shock, ARDS, and arrhythmia.

Antibiotics were administered the most often for patients under intensive care, followed by antiviral therapeutics and glucocorticoid treatments.

As the disease has spread to other regions, the observations from these areas may be the same, or different. Genetics may play a role in the response to the infection, and the course of the pandemic may change as the virus mutates as well, the authors conclude. Since this is a new pandemic that is constantly shifting, we think the medical community needs to keep an open mind as more and more studies are conducted.

Danish researchers from Aarhus University collaborated with scientists from the University of Siena for an independent study premised by the high COVID-19 mortality rates in Italy.

The researchers compellingly establish a correlation between air pollution and coronavirus-related deaths in two regions of Northern Italy: Lombardy and Emilia Romagna.

These areas evidence a mortality rate of 12%, which is considerably higher than any other impacted community (16,000 coronavirus deaths as of April 7th).

Lombardy and Emilia Romagna rank among the most heavily air-polluted areas in all of Europe. After reviewing air data collected by the NASA satellite Aura and comparing it with the European Environment Agencys Air Quality Index, Lombardy and Emilia Romagna ranked as one of the most heavily air-polluted areas in the entire continent of Europe.

It stands to reason that turbulent air has a hand to play considering SARS-Cov-2 targets lung cells and damages the hairlike projections that keep our airways clear of mucus and debris.

The authors are quick to point out that the findings published in the journal Environmental Pollution do not wholly account for the disproportionately high mortality rates observed in the regions studied, but they should not be counted outbecause at this stage nothing should be counted out.

There are several factors affecting the course of patients illness, and all over the world, were finding links and explanations of what is important. Its very important to stress that our results are not a counter-argument to the findings already made. At the moment, all new knowledge is valuable for science and the authorities, and I consider our work as a supplement to the pool of knowledge about the factors that are important for the course of patients illness, says environmental scientist Dario Caro in a release.

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Why its too early to start giving out immunity passports – MIT Technology Review

You can read our most essentialcoverage of the coronavirus/covid-19 outbreakfor free, and also sign up for ourcoronavirus newsletter. But pleaseconsider subscribingto support our nonprofit journalism.

About six to 10 days after viral exposure,the body begins to develop antibodies that bind and react specifically to the proteins found on SARS-CoV-2. The first antibody produced is called immunoglobulin m (IgM), which is short-lived and only stays in the bloodstream for a few weeks. The immune system refines the antibodies and just a few days later will start producing immunoglobulins G (IgG) and A (IgA), which are much more specific. IgG stays in the blood and can confer immunity for months, years, or a lifetime, depending on the disease its protecting against.

In someone who has survived infection with covid-19, the blood should, presumably, possess these antibodies, which will then protect against subsequent infection by the SARS-CoV-2 virus. Knowing whether someone is immune (and eligible for potential future certification) hinges onserological testing,drawing blood to look for signs of these antibodies. Get a positive test and, in theory, that person is now safe to walk the street again and get the economy moving. Simple.

Except its not. There are some serious problems with trying to use the tests to determine immunity status. For example, we still know very little about what human immunity to the disease looks like, how long it lasts,whether an immune response prevents reinfection, and whether you might still be contagious even after symptoms have dissipated and youve developed IgG antibodies. Immune responses vary greatly between patients, and we still dont know why. Genetics could play a role.

Weve only known about this virus for four months, says Donald Thea, a professor of global health at Boston University. Theres a real paucity of data out there."

SARS-CoV-1, the virus that causes SARS and whose genome is about 76% similar to that of SARS-CoV-2, seems toelicit an immunity that lasts up to three years. Other coronaviruses that cause the common cold seem to elicit a far shorter immunity, although the data on that is limitedperhaps, says Thea, because there has been far less urgency to study them in such detail. Its too early to tell right now where SARS-CoV-2 will fall in that time range.

Even without that data, dozens of groups in the US and around the world are developing covid-19 tests for antibodies. Many of these are rapid tests that can be taken at the point of care or even at home, and deliver results in just a matter of minutes. One US company, Scanwell Health, has licensed a covid-19 antibody test from the Chinese company Innovita that can look for SARS-CoV-2 IgM and IgG antibodies through just a finger-prick blood sample and give results in 13 minutes.

There are two key criteria we look for when were evaluating the accuracy of an antibody test. One is sensitivity, the ability to detect what its supposed to detect (in this case antibodies). The other is specificity, the ability to detect the particular antibodies it is looking for. Scanwells chief medical officer, Jack Jeng, says clinical trials in China showed that the Innovita testachieved 87.3% sensitivity and 100% specificity(these results are unpublished). That means it will not target the wrong kind of antibodies and wont deliver any false positives (people incorrectly deemed immune), but it will not be able to tag any antibodies in 12.7% of all the samples it analyzesthose samples would come up as false negatives (people incorrectly deemed not immune).

By comparison, Cellex, which is the first company to get a rapid covid-19 antibody test approved by the FDA, has a sensitivity of 93.8% and a specificity of 95.6%. Others are also trumpeting their own tests vital stats. Jacky Zhang, chairman and CEO of Beroni Group, says his companys antibody test has a sensitivity of 88.57%, for example. Allan Barbieri of Biomerica says his companys test is over 90% sensitive. The Mayo Clinic is making available its own covid-19 serological test to look for IgG antibodies, which Elitza Theel, the clinics director of clinical microbiology, says has 95% specificity.

The specificity and sensitivity rates work a bit like opposing dials. Increased sensitivity can reduce specificity by a bit, because the test is better able to react withanyantibodies in the sample, even ones you arent trying to look for. Increasing specificity can lower sensitivity, because the slightest differences in the molecular structure of the antibodies (which is normal) could prevent the test from finding those targets.

It really depends on what your purpose is, says Robert Garry, a virologist at Tulane University. Sensitivity and specificity rates of 95% or higher, he says, are considered a high benchmark, but those numbers are difficult to hit; 90% is considered clinically useful, and 80 to 85% is epidemiologically useful. Higher rates are difficult to achieve for home testing kits.

But the truth is, a test that is 95% accurate isnt much use at all. Even the smallest errors can blow up over a large population. Lets say coronavirus has infected 5% of the population. If you test a million people at random, you ought to find 50,000 positive results and 950,000 negative results. But if the test is 95% sensitive and specific, it test will correctly identify only 47,500 positive results and 902,500 negative results. That leaves 50,000 people who have a false result. Thats 2,500 people who are actually positiveimmunebut are not getting an immunity passport and must stay home. Thats bad enough. But even worse is that a whopping 47,500 people who are actually negativenot immunecould incorrectly test positive. Half of the 95,000 people who are told they are immune and free to go about their business might never have been infected yet.

Because we dont know what the real infection rate is1%, 3%, 5%, etc.we dont know how to truly predict what proportion of the immunity passports would be issued incorrectly. The lower the infection rate, the more devastating the effects of the antibody tests inaccuracies.The higher the infection rate, the more confident we can be that a positive result is real.

And people with false positive results would unwittingly be walking hazards who could become infected and spread the virus, whether they developed symptoms or not. A certification system would have to test people repeatedly for several weeks before they could be issued a passport to return to workand even then, this would only reduce the risk, not eliminate it outright.

As mentioned, cross-reactivity with other antibodies, especially ones that target other coronaviruses, is another concern. There are six different coronaviruses known to infect humans, says Thea. And its entirely possible if you got a garden-variety coronavirus infection in November, and you did not get covid-19, you could still test positive for the SARS-CoV-2 antibodies.

Lee Gehrke, a virologist and biotechnology researcher at Harvard and MIT, whose company E25Bio is also developing serological tests for covid-19, raises another issue. It's not yet immediately clear, he says, that the antibodies these tests pick up are neutralizing. In other words, the antibodies detected in the test may not necessarily actagainstthe virus to stop it and protect the bodythey simply react to it, probably to tag the pathogen for destruction by other parts of the immune system.

Gehrke says he favors starting with a smaller-scale, in-depth study of serum samples from confirmed patients that defines more closely what the neutralizing antibodies are. This would be an arduous trial, but I think it would be much more reassuring to have this done in the US before we take serological testing to massive scale, he says.

Alan Wells, the medical director of clinical laboratories at the University of Pittsburgh Medical Center, raises a similar point. He says that some patients who survive infection and are immune may simply not generate the antibodies youre looking for. Or they may generate them at low levels that do not actually confer immunity,as some Chinese researchers claim to have found.

I would shudder to use IgM and IgG testing to figure out whos immune and whos not, says Wells. These tests are not ready for that.

Even if the technology is more accurate, it might still simply be too early to start certifying immunity just to open up the economy. Chris Murray from the University of Washingtons Institute for Health Metrics and Evaluationtold NPRhis groups models predict that come June, at least 95% of the US will still be susceptible to the virus, leaving them vulnerable to infection by the time a possible second wave comes around in the winter. Granting immunity passports to less than 5% of the workforce may not be all that worthwhile.

Theel says that instead of being used to issue individual immunity passports, serology tests could be deployed en masse, over a long period of time, to see ifherd immunity has set inlifting or easing restrictions wholesale after 60 to 70% of a communitys population tests positive for immunity. There are a few case studies that hold promise. San Miguel County in Colorado has partnered with biotech company United Biomedical in an attempt to serologically test everyone in the county. The community is small and isolated, and therefore easier to test comprehensively. Iceland has been doing the same thing across the country.

This would require a massively organized effort to pull off well in highly populated areas, and its not clear whether the decentralized American health-care system could do it. But its probably worth thinking about if we hope to reopen whole economies, and not just give a few individuals a get-out-of-jail-free card.

Not everyone is so skeptical about using serological testing on a case-by-case basis. Thea thinks the data right now suggests SARS-CoV-2 should behave like its close cousin SARS-CoV-1, resulting in an immunity that lasts for a maybe a couple of years. With that in mind, its not unreasonable to identify individuals who are immune from reinfection, he says. We can have our cake and eat it too. We can begin to repopulate the workforcemost importantly the health-care workers. For instance, in hard-hit cities like New York that are suffering from a shortage of health-care workers, a serological test could help nurses and doctors figure out who might be immune, and therefore better equipped to work in the ICU or conduct procedures that put them at a high risk of exposure to the virus, until a vaccine comes along.

And at the very least, serological testing is potentially useful because many covid-19 cases present, at most, only mild symptoms that dont require any kind of medical intervention. About 18% of infected passengers on theDiamond Princesscruise shipshowed no symptoms whatsoever, suggesting there may be a huge number of asymptomatic cases. These people almost certainly arent being tested (CDC guidelines for covid-19 testing specifically exclude those without symptoms). But their bodies are still producing antibodies that should be detectable long after the infection is cleared. If they develop immunity to covid-19 thats provable, then in theory, they could freely leave the house once again.

For now, however, there are too many problems and unknowns to use antibody testing to decide who gets an immunity passport and who doesnt. Countries now considering it might find out they will either have to accept enormous risks or simply sit tight for longer than initially hoped.

Correction: The initial version of the story incorrectly stated: "The higher the infection rate, the more devastating the effects of the antibody tests inaccuracies." A higher infection would actually produce more confident antibody test results. We regret the error.

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XX male syndrome – Wikipedia

Rare congenital condition

XX male syndrome, also known as De la Chapelle syndrome, is a rare congenital intersex condition where an individual with a 46 XX karyotype (otherwise associated with females) has phenotypically male characteristics that can vary among cases.[2] In 90 percent of these individuals, the syndrome is caused by the Y chromosome's SRY gene, which triggers male reproductive development, being included in the crossing over of genetic information that takes place between the pseudoautosomal regions of the X and Y chromosomes during meiosis in the father.[2][3] When the X with the SRY gene combines with a normal X from the mother during fertilization, the result is an XX male. Less common are SRY-negative XX males, which can be caused by a mutation in anautosomalor X chromosomal gene.[2] The masculinization of XX males is variable.

This syndrome is diagnosed through various detection methods and occurs in approximately 1:20,000 newborn males, making it much less common thanKlinefelter syndrome.[2][4][5] Treatment is medically unnecessary, although some individuals choose to undergo treatments to make them appear more male or female.[1][6]

The appearance of XX males can fall into one of three categories: 1) males that have normal internal and external genitalia, 2) males with external ambiguities, and 3) males that have both internal and external genital ambiguities (true hermaphrodites).[7] External genital ambiguities can include hypospadias, micropenis, and clitoromegaly.[7] Typically, the appearance of XX males differs from that of an XY male in that they are smaller in height and weight.[2] Most XX males have smalltestes,are sterile, and have an increase in maldescended testicles compared to XY males.[2][8] Some XX male individuals have decreased amounts of body hair and decreased libido.[8] Individuals with this condition sometimes have feminine characteristics, with varying degrees ofgynecomastiabut with no intra-abdominalMllerian tissue.[8] According to research at theUniversity of Oklahoma health science centers, despite XX males exhibiting feminine characteristics, their behaviours are usually representative of masculinity in their culture.[9]

The degree to which individuals with XX male syndrome develop the male phenotype is variable, even among SRY-positive individuals.[10] A completely male phenotype usually develops in the presence of the SRY gene but, in some cases, the presence of the SRY gene can result in internal and/or external genitalia ambiguities.[10] Normal XX females undergo X inactivation during which one copy of the X chromosome is silenced. It is thought that X inactivation in XX males may account for the genital ambiguities and incomplete masculinization seen in SRY-positive XX males.[11][10] The X chromosome with the SRY gene is preferentially chosen to be the active X chromosome 90% of the time, which explains complete male phenotype being observed often in SRY-positive XX males.[11][10] In the remaining 10%, X inactivation spreads to include a portion of the SRY gene, resulting in incomplete masculinization.[11][10]

Masculinization of SRY-negative XX males is dependent upon which genes have mutations and at what point in development these mutations occur.[12]

Males typically have one X chromosome and one Y chromosome in eachdiploidcell of their bodies. Females typically have two X chromosomes. XX males that are SRY-positive have two X chromosomes, with one of them containing genetic material from the Y chromosome, making them phenotypically male but genetically female.[2]

The SRY gene plays an important role in sex determination by initiating testicular development. In most XX males the SRY gene is present. The tip of the Y chromosome contains the SRY gene and, during recombination, a translocation occurs in which the SRY gene on the Y chromosome is moved to become part of an X chromosome.[7][13] The presence of the translocated SRY gene leads to an XX embryo developing male characteristics.

In 10% of cases, an XX male does not have the SRY gene, causing variations in their levels of masculinity.[2] The exact cause of this condition is unknown but it has been proposed that mutations in the SOX9 gene may contribute to this syndrome since SOX9 plays a role in testes differentiation during development.[14][12] Another proposed cause is mutations to the DAX1 gene which encodes a nuclear hormone receptor.[15][16] DAX1 represses masculinizing genes, therefore, if there is a loss of function of DAX1 then testes can develop in an XX individual.[16] Mutations in SF1 and WNT4 genes are also being studied in connection with SRY-negative XX male syndrome.[16]

Hypothesis that XX occurs in males because of the interaction of the testis-determining portion of the Y chromosome and part of the X chromosome, called the Xg gene, is generally supported by various data.[17] The frequency of the Xg phenotype in XX males is closer to normal males' frequency than normal females' frequency.[17] There have been at least four cases where XX males have inherited the Xg allele from their father, and at least nine cases where XX males did not inherit the allele from their father.[17]

In cases where the individual is being evaluated for ambiguous genitalia, such as a small phallus, hypospadias, or labioscrotal folds, exploratory surgery may be used to determine if male and/or female internal genitalia is present.[18]

A standard karyotype can be completed to cytogenetically determine that an individual with a partial or complete male phenotype has a XX genotype.[7][18]

FISH analysis determines the presence or absence of the SRY gene.[10]

Localization of the SRY gene can by determined using fluorescent in situ hybridization.[2]

Indicators include two testes which have not descended the inguinal canal, although this is seen in a minority of XX males, and the absence of Mllerian tissue.[8] External indicators include decreased body weight and small testes.[2]

As of 2010, only 200 cases have been reported it is estimated that 1 of every 20,000 to 30,000 males has a 46,XX karyotype.[19][20]

XX males are sterile due to no sperm content and there is currently no treatment to address this infertility.[21] Genital ambiguities, while not necessary to treat for medical reasons, can be treated through the use of hormonal therapy, surgery, or both. Since XX male syndrome is variable in its presentation, the specifics of treatment varies widely as well. In some cases gonadal surgery can be performed to remove partial or whole female genitalia. This may be followed by plastic and reconstructive surgery to make the individual appear more externally male.[22] Conversely, the individual may wish to become more feminine and feminizing genitoplasty can be performed to make the ambiguous genitalia appear more female.[23] Hormonal therapy may also aid in making an individual appear more male or female.[22][23]

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Androgen insensitivity syndrome – Genetics Home Reference …

Androgen insensitivity syndrome is a condition that affects sexual development before birth and during puberty. People with this condition are genetically male, with one X chromosome and one Y chromosome in each cell. Because their bodies are unable to respond to certain male sex hormones (called androgens), they may have mostly female external sex characteristics or signs of both male and female sexual development.

Complete androgen insensitivity syndrome occurs when the body cannot use androgens at all. People with this form of the condition have the external sex characteristics of females, but do not have a uterus and therefore do not menstruate and are unable to conceive a child (infertile). They are typically raised as females and have a female gender identity. Affected individuals have male internal sex organs (testes) that are undescended, which means they are abnormally located in the pelvis or abdomen. Undescended testes have a small chance of becoming cancerous later in life if they are not surgically removed. People with complete androgen insensitivity syndrome also have sparse or absent hair in the pubic area and under the arms.

The partial and mild forms of androgen insensitivity syndrome result when the body's tissues are partially sensitive to the effects of androgens. People with partial androgen insensitivity (also called Reifenstein syndrome) can have genitalia that look typically female, genitalia that have both male and female characteristics, or genitalia that look typically male. They may be raised as males or as females and may have a male or a female gender identity. People with mild androgen insensitivity are born with male sex characteristics, but they are often infertile and tend to experience breast enlargement at puberty.

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Why women are better than men at beating the coronavirus – New York Post

As the novel coronavirus cuts its relentless swath across the globe, doctors have identified one grim constant: COVID-19 has men, more than women, in its sights.

In Italy, men account for at least 70 percent of all coronavirus deaths. While South Korea has seen more confirmed COVID-19 cases in female patients than in males, a higher percentage of men have been felled by it. Here in New York City, more men than women are testing positive for coronavirus, with 55 percent of all cases. They also are dying of it at even higher rates. As of Friday, 1,159 men in the five boroughs had been killed by COVID-19 62 percent of the citys 1,867 deaths.

The phenomenon has stumped medical experts. In their rush to make sense of the data, many are pointing fingers at men and their behavior. Some speculate that higher male smoking rates leave them vulnerable to the respiratory infection. Others guess that men are blowing off social-distancing guidelines, or are neglecting to wash their hands.

I find that so offensive, genetic researcher Sharon Moalem, MD, told The Post. Talk about blaming the victim.

Sure, there are some behaviors that might affect the number of infections, he said. But why should poor hand-washing lead to death for a patient whos already in intensive care? Its ridiculous.

In fact, the coronavirus bulls-eye on men is consistent across age groups, regardless of underlying risk factors.

What we are actually seeing is that males do not do well once infected, Moalem said. So it comes down to genetics. There is a genetic component to this illness.

As a clinical researcher studying genetic disease, Moalem spent years working with patients at both ends of the human life span from babies in the neonatal intensive care unit to seniors grappling with Alzheimers. In both groups he noticed that his female patients were more resilient than males, better at fighting off infections and recovering from injuries.

The hardest thing a human being can do is surpass the age of 110, he noted. And 95 percent of those supercentenarians are women. Meanwhile, around the world, more girls than boys make it to their first birthdays.

That brought Moalem to a startling conclusion contradicting centuries worth of conventional wisdom: Men, not women, are the weaker sex.

In The Better Half (Farrar, Straus and Giroux), out Tuesday, Moalem explains that from the time they are still in the womb to their final breaths, womens immune systems outperform those of men an inherent advantage that lengthens their lives and improves their overall health.

And when it comes to outwitting COVID-19, Moalem says, womens genes provide an even bigger edge.

With this virus, there is immense risk simply due to the fact of being male.

Its not just that females have a stronger immune system to fight this infection, he said. Its that their genes give them a better defense at the cellular level.

Every human, male and female, carries a set of 46 chromosomes in our cells. One of those 23 chromosome pairs determines a humans biological sex. A mans cells contain an X chromosome inherited from his mother and a Y chromosome provided by his father. A womans cells carry two X chromosomes one from each of her parents.

The genes within our chromosomes contain the code that builds our bodies. The Y chromosome, with only about 70 genes, is a specialist that fashions the male reproductive system. But the X chromosome, with nearly 1,000 genes, does much more.

The X chromosome has the genes that go into making the brain and the immune system, the two crucial things you need to survive as a human being, Moalem said.

Both of a females X chromosomes are present in all her cells. But within each cell, only one of the Xs calls the shots. Half of a womans cells are dominated by the X chromosome that came from her mother, half by the X contributed by her father.

That genetic diversity is really valuable, Moalem explained. One of the immune systems most important weapons is the ability to recognize a virus. Well, genes on the X chromosome are involved in viral recognition. Right away, women have two different populations of immune cells that are best at spotting invaders.

Meanwhile, maybe the other X has a gene thats very good at identifying and killing infected cells, he said. So womens immune cells function like a tactical unit. They specialize, then they interact and cooperate to fight the invaders.

Men, with their single X chromosome, have a far less nimble immunological army at their command.

As a man, I dont have all those options, Moalem said. I can only hope that my one X has the genes that can recognize the virus and can kill it, too.

It gets worse for men in the age of COVID-19: The new coronavirus takes direct aim at their single-X vulnerability.

What we researchers are seeing right now is the way this coronavirus gets into our lung cells, Moalem said. It has a key: a spike protein we think it uses to break in. And the lock it picks to enter is called ACE2 an enzyme attached to the outer surface of the cell membrane.

The gene that makes ACE2 is on the X chromosome, he continued. So if the coronavirus has the right key, it can unlock every one of a males lung cells. But females have two Xs so half of their lung cells use one ACE2 lock, and the other half use a slightly different ACE2 lock. The chance that the virus has the perfect key to unlock both of them is not great. So thats another enormous advantage for females.

The virus lock-picking action damages the ACE2 so badly that it can no longer perform one of its crucial functions: preventing the buildup of fluid in the lungs during the infection.

Its the lungs filling up with fluid that happens in COVID-19 that can lead to the breathing difficulties experienced by so many, Moalem said. The severest lung injury were seeing with this infection is not likely to occur unless all your locks get picked. In females, the virus cant usually get into enough of their cells to do that amount of damage and that may be the reason why were seeing so many men dying.

If that idea is correct, he said, we should expect more tragedies like that of the Fusco family of New Jersey, who lost four closely related members 73-year-old matriarch Grace Fusco, two of her sons, and a daughter to the coronavirus last month.

We will likely see siblings or families that are particularly susceptible to this virus, because their cells share the same lock that the coronavirus is picking, Moalem said. We will see young people succumbing very quickly, very likely because they were born with a genetic version of the ACE2 lock that the coronavirus easily picks.

And yet he sees reason to hope as research laboratories around the world home in on ACE2 to thwart the coronavirus attack.

In that effort we can learn from the superimmunity of females, he said.

Moalems own lab was in the midst of investigating new antibiotics when the crisis hit.

We quickly switched our research efforts to find out if we can repurpose a drug that already exists, he said. There are a lot of drugs available, drugs whose safety profile we know, that could be used. Im hopeful we can find something already in the toolkit that will be effective.

Until then, he said, understanding the genetic risk factors of COVID-19 should spur us to safeguard those who are most in danger.

We should be shielding all our seniors, but we should actually be protecting our male elders most of all, he said. With this virus, there is immense risk simply due to the fact of being male.

The homogenous chromosomes benefit other animals too.

Human females are not the only ones that benefit from the double-X advantage. Across the animal kingdom, in all kinds of creatures whose sex is determined by their chromosomes, researchers are learning that the sex that has the doubled chromosome is almost always the one that lives longer.

Essentially Im proposing a new biological law, genetic researcher Sharon Moalem told The Post. The sex that gets two of same chromosomes will have an immense genetic advantage.

Moalem calls it the Law of Homogameity (same-gene).

In a study published just last month, researchers from Australias University of New South Wales found new evidence to support his thesis. Biologists analyzed life-span data on 229 different animal species mammals, birds, insects, fish, spiders, and more.

We found that across that broad range of species, the heterogametic sex does tend to die earlier than the homogametic sex, and its 17.6 percent earlier on average, lead researcher Zoe Xirocostas said.

It isnt always the female of a species that gets the edge. Birds, some reptiles and butterflies dont have the X and Y chromosomes that humans and other mammals share. Instead, they have whats called a ZW sex-determination system. Female birds cells contain Z and W chromosomes; males get the double-Z.

Just as Moalem suspected, its the males in those animal species that gain the longevity edge.

Across the animal kingdom, these creatures benefit from a double chromosome hit

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Why women are better than men at beating the coronavirus - New York Post

A framework for high-resolution phenotyping of candidate male infertility mutants: from human to mouse. – Physician’s Weekly

Male infertility is a heterogeneous condition of largely unknown etiology that affects at least 7% of men worldwide. Classical genetic approaches and emerging next-generation sequencing studies support genetic variants as a frequent cause of male infertility. Meanwhile, the barriers to transmission of this disease mean that most individual genetic cases will be rare, but because of the large percentage of the genome required for spermatogenesis, the number of distinct causal mutations is potentially large. Identifying bona fide causes of male infertility thus requires advanced filtering techniques to select for high-probability candidates, including the ability to test causality in animal models. The mouse remains the gold standard for defining the genotype-phenotype connection in male fertility. Here, we present a best practice guide consisting of (a) major points to consider when interpreting next-generation sequencing data performed on infertile men, and, (b) a systematic strategy to categorize infertility types and how they relate to human male infertility. Phenotyping infertility in mice can involve investigating the function of multiple cell types across the testis and epididymis, as well as sperm function. These findings will feed into the diagnosis and treatment of male infertility as well as male health broadly.

PubMed

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A framework for high-resolution phenotyping of candidate male infertility mutants: from human to mouse. - Physician's Weekly

With hair loss on the rise, Asia’s men grapple with what it means to be bald – CNN

Written by Oscar Holland, CNNHong Kong

Despite his father having an "m-shaped" hairline, Alex Han from northeast China never thought he'd experience hair loss in his 20s.

"I was prepping my masters entrance examinations and there was a lot of pressure, so I probably didn't sleep very well," Han said in a phone interview. "At that time, (my receding hairline) was under control, but after three years in Beijing getting my masters, I moved to Germany for PHD study ... and not only me, but other Asian students there, had a problem with hair loss."

Commuters crowd the subway in Beijing in July 2008. China has traditionally had some of the world's lowest rates of baldness, though changes to people's lifestyles are contributing to an increase in hair loss. Credit: Guang Niu/Getty Images

Han opted to travel to Thailand for the transplant, which sees thousands of hair follicles grafted from other parts of the body -- such as the chest, or back of the neck -- onto the head. The eight- to 10-hour procedure cost him around $9,000, though he found clinics in China quoting "a sixth of that." The transplant may take months to take effect, though Han expressed hope that he will "see the results and see my hair return to normal in the next two or three months," adding, "then I'll behave as if nothing has happened."

Navigating stigmas

Han's fears mirror those experienced by men with receding hairlines around the world, namely the impact on his confidence, professional prospects and first impressions. "Hairstyles, for me, are critically important for men's first impressions," he said.

But losing your hair may be especially difficult in countries where it's less common. The male beauty standards in East Asian popular culture -- from Korean K-pop to Hong Kong's movie industry -- often favor big hair and boyish looks. "In Asian cultures the younger generation really like idols like (Chinese pop band) TFBoys," Han said, adding that standards for white or black men are often different.

"Whenever there is a precedent, people tend to feel (more confident) to follow," he said in an email interview.

A man looks at a robotic hair transplant machine at the China International Import Expo in Shanghai in 2019. Credit: China News Service/Visual China Group/Getty Images

Chinese American entrepreneur Saul Trejo, who has lived in various cities around Asia since 2011, began losing his hair while studying in Beijing. The 30-year-old said he "definitely noticed" the lower proportion of bald men in the city, compared to the US, and "it probably bothered me, but I tried to not let it." He also found that people were more comfortable than those in the West to pass comment -- even if in an entirely observational way.

"People will tell you straight out," he said in a phone interview from Taipei, recounting instances when his loss of hair was casually pointed out to him. "Normally when they're saying it they're not trying to be mean, they're just commenting, so I can't be mad. But you remember.

"I tried to shave my head, but I didn't think it was suitable for my head and body shape," he added, naming Dwayne "The Rock" Johnson and actor Jason Statham as non-Asians who can pull off the look. "I think Asian people, including myself, tend to be a little slimmer, so if I had to choose between bald and slim versus bald and athletic, or even muscular, then I think it looks better with the more size you have."

In 2018, Trejo underwent a hair transplant in Bangkok, where he was based at the time. While it took almost a year to see the final results, Trejo said his new hairline is "a major blessing," that "massively improved my dating life." Before-and-after images shared with CNN show a remarkable amount of hair restoration at the top and sides of his head.

Chinese American Saul Trejo, pictured before and after undergoing a hair transplant in Thailand. Credit: Saul Trejo

The doctor behind Trejo's procedure, Damkerng Pathomvanich, is a leading researcher into hair loss. He said that the number of hair transplant clinics in Asia is "skyrocketing," and that business among Chinese patients at his clinic is "booming."

Alternative approaches

A judge examines finalists at a 1957 baldness competition in Japan, where rates of hair loss have historically been among the world's lowest. Credit: Keystone Features/Hulton Archive/Getty Images

In Korea, meanwhile, houttuynia cordata -- also known as fish mint, or chameleon plant -- can be brewed into a black liquid that is applied to the scalp, according to the journalist, David Ko, who received some from his concerned mother-in-law.

"I used it like a shampoo whenever I washed my hair," he said. "After wetting my hair, I poured a handful of the plant-steeped water on my scalp, finger-massaged my scalp for about one minute, then rinsed it off with fresh water.

"But as time went by without seeing any clear sign of improvement, I got so tired of the remedy that I dumped more of (it) on my hair each time to finish the jar faster and get the practice over with." He then tried other suggested home remedies. "My wife also nudged me to sprinkle some sea salts over my scalp instead of the plant water, and one of my co-workers told me her balding father benefitted from eating lots of black sesame seeds as a snack."

Related video: Beauty is protest for young North Korean women

While New York dermatologist Norman Orentreich is widely known as the father of hair transplants, Japanese doctor Shoji Okuda is believed to have performed the very first procedure in 1937 (though the breakout of World War II meant that his research was largely overlooked). With baldness on the rise in Asia, it's perhaps no surprise that the continent's scientists -- Japan's and South Korea's in particular -- are again leading some of the field's most promising research.

Like 'a triad'

But, still, Asia poses unique challenges for receding men. Undergoing the scalp tattoo procedure requires patients to permanently sport a shaved-head look, which, as the Korean study suggested, may be "stereotyped in Asian cultures as (being like) a gangster or criminal." According to Ko, however, such labels are a thing of the past.

"Back in the day, when young males shaved their heads, seniors would mildly chide them with a totally unproven and absurd hypothesis," he said, suggesting that elders once saw a skinhead as a sign that someone was a rebel, or had "a problem with society."

"Nowadays (these attitudes) almost never exist, but it is still true people look at bald males with a certain awe."

A model with a shaved head walks the runway at China Fashion Week in 2017. The rise of street style may be helping popularize the skinhead look. Credit: Visual China Group / Getty Images

Eric But of Synergy Model Management, which has offices in Hong Kong and Guangzhou, said that clients are still often looking for Asian models to be "cute (with) long hair -- that Korean drama, perfect boyfriend kind of look." But while he distinguishes between shaved and bald heads, the modeling agent said that the rise of street fashion is gradually normalizing the skinhead look in Asia.

"For our parents' generation, a skinhead in Asia is kind of like a gangster -- if you want to be a triad, or if you go to prison, you have to shave your head," he said over the phone. "But now, for people born in the '90s or later, they see having a skinhead as a streetwear trend. And streetwear is massive in Asia."

Even in the home of coiffed K-pop, visibility may be growing gradually. Ko cited restaurateur Hong Seok-cheon (below), rapper Gill and actor Kim Kwang-kyu as examples of a slowly-growing number of high-profile bald celebrities in South Korea.

"It would be more helpful if there were more Koreans with hair loss --- if there were more cases (people) could look up to and think they are not alone out there."

Top image: Chinese artist Fang Lijun pictured with one of his paintings, which since the 1990s have often featured bald-headed protagonists. The artist uses the hairless figures as symbols of disillusionment and rebellion in modern China.

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With hair loss on the rise, Asia's men grapple with what it means to be bald - CNN

CDC: Coronavirus is more prevalent in young boys than girls – Yahoo Lifestyle

For weeks, infectious disease experts have been investigating why the coronavirus is proving particularly devastating to males, with early theories from China suggesting that higher rates of smoking among men may be to blame. But a new study from the Centers for Disease Control and Prevention (CDC) is suggesting it may have more to do with biology specifically, genetics than lifestyle.

The research, released on Monday in the CDCs Morbidity and Mortality Weekly Report, found a higher prevalence of COVID-19 in males across every pediatric age group including infants. Fifty-seven percent of the more than 2,572 pediatric cases of COVID-19 studied (out of 149,750 cases overall) were found in males, ranging in age from newborns to 18.

To be clear, the research did not suggest that parents should now be concerned about their male children or female children getting seriously ill from COVID-19. The risk for children remains very low.

Most of the children reported symptoms of cough or fever, but only a small fraction (five percent) were hospitalized, bolstering reports that kids often develop a mild case of the virus. Those hospitalized were far more likely to report underlying health conditions than those who werent, including asthma, chronic lung disease and cardiovascular disease. Only 0.1 percent of the children infected died.

The median age of the more than 2,500 children with COVID-19 was 11, with over a third of cases involving teens between the ages of 15 and 17. But the most striking statistic for the researchers was that 57 percent of cases occurred among males an even higher number than the adult group, in which 53 percent of the cases involved males. The researchers conclude that the higher rate of boys testing positive in every pediatric age groupsuggests that biologic factors might play a role in any differences in COVID-19 susceptibility by sex.

So what exactly may be driving the higher incidence in young boys, and should parents take this as a concern? GregoryA.Poland,MD, an infectious diseases expertandheadofthe Mayo Clinic's Vaccine ResearchGroup, tells Yahoo Lifestyle that the study is no reason to panic, and shouldnt be taken as a roadmap for parents with boys. Instead, Poland helps unpack what the new research can teach us.

Poland says the concept that females are less susceptible to disease is a generalizable phenomenon beyond just infectious diseases (such as COVID-19). In fact, women also tolerate starvation and dehydration and survive longer than men do in austere environments, Poland tells Yahoo Lifestyle. So there does appear to be a sex advantage on the side of females that males don't have, meaning a better immune response.

Although the gender disparity may lead to theories about hormones, Poland says studies like this one are the reason researchers dont consider hormones to be the source. These are children who are absent the kind of hormonal levels or differences that we would see post-pubertal, Poland says, adding that the disparity in infection is one seen in post-menopausal women, too. That doesn't mean there couldn't be some still fine hormonal differences. But it leads to the idea that while hormones are important, it's again just one factor in this complex web that still needs to be teased apart.

Its still unclear to experts exactly why women respond better to certain diseases and harsh environments, but Poland says that genes may inform the answer. We don't fundamentally understand this... but what we do know is that females depending on the virus will tend to activate or suppress different genes than males do when their cells are exposed to these viruses, says Poland. So we think a strong driver of this is going to be just genetic, not just hormonal.

There is no evidence that females may be better equipped to fight disease due to evolution, but Poland says the idea has been floated. We don't have any evidence but people always postulate ... the idea has been in general: Is it this way for the primary reason of propagation of the species? he says. You need women to have children. You can have a lot of children with a few men, but you can only have them one by one with women.

An immunologist at the Heinrich Pette Institute in Hamburg, Germany, Marcus Atlfeld, raised another theory in a Scientific American piece from 2016 suggesting that women might have evolved a particularly fast and strong immune response to protect developing fetuses and newborn babies. Poland says that, in the absence of evidence, it may not be possible to form a conclusion.

Poland says males facing disease at higher rates than women is something currently being studied through the lens of vaccines. When you give males versus females of any age a vaccine, females almost always respond better than males, Poland says. He says that it shows females, even when faced with a small viral load of an inactivated disease, are often able to respond better than males something seen with vaccines against smallpox, measles and influenza.

Women responding more efficiently to disease may be beneficial in the midst of a coronavirus pandemic, but Poland says it has a negative side, too a higher likelihood that the immune system will overreact. This supercharged immune system has a negative side to it, says Poland. And that is women have higher rates of autoimmune diseases diseases where their own immune system attacks their own body. (According to the National Institutes of Health, roughly eight percent of the population has an autoimmune disease; 78 percent of them are women).

Like the authors of the CDC study, who note many limitations of the research, Poland says the study doesnt necessarily mean that more young boys are getting the virus. Instead, it could be showing that they do not have the same quality of immune response that girls do. There could be a lot of girls out there who had it but had zero symptoms, says Poland. So she may not even go and be tested to know that she has COVID-19. The boy is more likely to have symptoms [and] that may drive testing.

For that reason and many others, Poland says the new research should not be a reason for parents of boys to panic, nor for parents of girls to consider them immune. I would not want this to give false reassurance to a parent because yes, there were girls that got sick, Poland tells Yahoo Lifestyle. There were girls that had severe illness. So I would put it in the category of, that's interesting. More research needs to be done. But for me as a parent, I put whatever appropriate layers of protection around my children, regardless of their gender.

For the latest coronavirus news and updates, follow along at https://news.yahoo.com/coronavirus. According to experts, people over 60 and those who are immunocompromised continue to be the most at risk. If you have questions, please reference the CDC and WHOs resource guides.

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CDC: Coronavirus is more prevalent in young boys than girls - Yahoo Lifestyle

The Why of the Fly Y: Reflections on Junk DNA – Discovery Institute

In April 1980, almost exactly forty years ago, the journal Nature published a pair of highly influential articles on the topic of what has become known as junk or selfish DNA. Both reflected the key concept of The Selfish Gene, the highly influential 1976 book by Richard Dawkins, namely, that organisms are merely DNAs way of making more DNA. The first was authored by W. Ford Doolittle and Carmen Sapienza and titled Selfish genes, the phenotype paradigm and genome evolution.1 The second was authored by Leslie Orgel and Francis Crick and titled Selfish DNA: the ultimate parasite.2 Together they posited an easy-to-grasp way to conceive of excess nucleotides along chromosomes repetitive sequences in general and transposable elements in particular. In short, it was proposed that most such DNA elements neither had nor have (developmental) effects or functions (in general) in the shaping of an organisms traits (its phenotype). And because they have no phenotypic expression (as Doolittle and Sapienza put it) or little or no effect on the phenotype (as Orgel and Crick put it), the only role that can be ascribed to them is that of replicative survival.

But there are two problems with this outlook, one empirical and one formal. That which is empirical involves the organization of (eukaryotic) chromosomes, whereas that which is formal involves how to define effect, expression, and function when it comes to repetitive DNA sequences of any type. And so to narrow our focus on these problems, let us give some thought to the Y chromosome of Drosophila melanogaster, that engaging fly which is the bond-servant of genetics, as it is replete with a junk and selfish typography. Note that I will only be briefly touching on the first problem in this piece.

Now the Y chromosome of this species is approximately 40,000,000 bases in length, and that is significant for it makes up around 20 percent of the male haploid DNA content.3-4 While it is essential for male fertility, it has but few protein-coding regions and these are interrupted by or surrounded by vast tracks of (often degenerated) transposable elements, tandemly arranged runs of satellite units (such as AACAC, AATAG, AATAT, and so forth), a block of ribosomal-RNA genes, and various other sequence families.5 In addition, its various components are densely compacted in somatic-cell nuclei, and this heterochromatin is supposedly inert until around the stage the primary spermatocytes are formed. I hasten to mention also that its composition of DNA varies from strain to strain of D. melanogaster, even though its protein-coding sequences are stable throughout.6 What all of this seems to suggest, then, is that the bulk of this chromosome may have no phenotypic expression or little or no effect on the phenotype in males of this species.

Recall, however, that I said that there are two problems with this outlook, one of which is empirical. Concerning that, let us note that by the mid 1950s it was well-established that introducing a Y chromosome into a female D. melanogaster (by the feats of fruit-fly genetics) leads to a broad range of phenotypic effects, as does increasing the copies or dosage of a Y chromosome in a male of the same.7 Not only that, but with the sixty-plus years that have elapsed, we are much closer to understanding how such phenotypic effects due to junk or selfish DNA sequences take place. For one thing, it is now clear that different Y-chromosome sequence variants can differentially alter the expression of hundreds of genes in the somatic cells of male flies.8-10 For another, the characters that are affected are those of interest to the population geneticist including such things as male reproductive traits. Then again, many of the genes so modulated by the Y chromosome in this Drosophila species are positioned in so-called repressed chromatin domains.11

Apropos is an in-press work by Emily Brown, Alison Nguyen, and Doris Bachtrog that tests a hypothesis to explain such Y-chromosomal-based phenotypic effects.12 Some have suggested that long stretches of repetitive elements on that chromosome (which again is millions of bases long) can serve as a sink that titrates out heterochromatic proteins, thereby depleting the latter in other domains of a nucleus.13 Congruent with this hypothesis, Brown and colleagues showed that a consequence of introducing a Y chromosome into a female, or by decreasing or increasing the copies or dosage of a Y chromosome in a male line, is a widespread redistribution in nuclei of histone markers that are specific for heterochromatin, but not for those that are specific for active euchromatin. This means that the Y-sequences do make their absence or presence and (if present) quantities known in morphogenesis. What is more, the balance of chromatin domains in female versus male flies is likely to be en masse modulated by such parameters.

We can thus rephrase what Doolittle and Sapienza or Orgel and Crick asserted back in 1980 in this manner: Seemingly excess nucleotides do have phenotypic expressions be they ever so indirect, which is to say that they do have major effects on the phenotype. It thus looks like there is a why to the fly Y, though it does not fit the axioms with which the junk DNA advocates beset us. Yet we should note that such a possibility was never actually excluded, for as Doolittle and Sapienza claimed: We do not deny thatrepetitive and unique-sequence DNAs not coding for protein in eukaryotes may have roles of immediate phenotypic benefit to the organism.2

Photo: Drosophila melanogaster, an engaging fly, bySanjay Acharya / CC BY-SA.

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The Why of the Fly Y: Reflections on Junk DNA - Discovery Institute

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