How Could Human Nature Have Become This Politicized? – The New York Times

The formulation of what has come to be known as moral foundations theory has been crucial to a deeper understanding of this process. The theory

proposes that the human mind is organized in advance of experience so that it is prepared to learn values, norms, and behaviors related to a diverse set of recurrent adaptive social problems.

Leading proponents argue that there are

five foundations of intuitive ethics: care/harm; fairness/cheating; loyalty/betrayal; authority/subversion; and sanctity/degradation.

The theory is described in detail in Moral Foundations Theory: The Pragmatic Validity of Moral Pluralism, a 2013 paper by Jesse Graham of the University of Utah; Jonathan Haidt of N.Y.U.; Sena Koleva, a research consultant; Matt Motyl of the University of Illinois at Chicago; Ravi Iyer, chief data scientist for Ranker, a consumer internet platform; Sean P. Wojcik, a senior data scientist at the news site Axios; and Peter H. Ditto, of the University of California-Irvine.

What makes moral foundations theory especially relevant now is that in recent decades liberal and conservative partisans have divided over the importance they place on these five moral foundations:

Liberals valued Care and Fairness more than did conservatives, whereas conservatives valued Loyalty, Authority and Sanctity more than did liberals.

These differences mattered little for politics when both parties included liberals and conservatives, but beginning around 1964, this disagreement between left and right on moral values began to coincide more strongly with party affiliation.

A number of scholars have put forth ideas in an effort to understand these developments.

Kevin Smith, a political scientist at the University of Nebraska whose research explores the biology and psychology of individual-level differences in political attitudes and behavior, emailed in response to my inquiry:

Fights about abortion, gay rights, gun rights etc. are less about policy than about underlying core values, values that for many are not up for discussion or compromise because they are deeply held indeed, given the genetic influences on such attitudes, its probably fair to say they are at least partly biologically instantiated.

Smith, who is a co-author of Predisposed: Liberals, Conservatives and the Biology of Political Differences, argues that as political parties have coalesced along ideologically consistent lines, especially on issues related to race, they have

created a political environment where genetically influenced predispositions, what most people would experience as gut feelings that one side or the other is right or wrong on a given set of issues of the day, made partisanship something that was much more likely to become a central part of someones identity.

Smith is quite explicit that he does not posit that there is biological determinism of political views or anything else, but he does contend that

theres little doubt that ideological orientations are genetically influenced, and to a surprisingly high degree studies consistently estimate roughly 40-60 percent of the population level variance in ideology is under genetic influence.

The ideological realignment of the parties that has pushed many liberal Republicans into the Democratic camp and conservative Democrats in the opposite direction, Smith writes, has created a political environment in which

those with strong predispositions to lean one way or the other can readily mate those instinctual feelings to a political party that espouses and affirms those predispositions.

At that point, he continues,

Youve got a recipe for deeply polarized politics that is going to feed on its own dynamics and be hard to change. And that sounds awfully like the political environment we have right now.

In Predisposed, Smith and John Hibbing and John Alford, his co-authors, stress that we are not making a nature versus nurture argument.

Instead, they write, innate forces combine with early development and later powerful environmental events to create attitudinal and behavioral tendencies. A predisposition can be altered. Nonetheless,

predispositions nudge us in one direction or another, often without our knowledge, increasing the odds that we will behave in a certain way, but leaving plenty of room for predispositions to be contravened.

Kevin Arceneaux, a political scientist at Temple, stressed in an email that

It is important to resist the tendency to see heritability of eye color, for example, as the same thing as the heritability of an attitude. I cannot change my eye color, but I can change my attitudes.

Some of the most interesting work in the field of behavioral genetics, Arceneaux continues, shows how

context interacts with genetic influences. If you change the context, the heritability of behavioral constructs changes. So, I would caution against drawing a straight line from heritability to unchanging/intractable.

Along the same lines, Yuan Chang Leong, a postdoctoral fellow in the psychology department at Berkeley, emailed me that

What is heritable is unlikely to be ideology per se, but something more akin to personality traits or a predisposition to respond to certain information in a particular way.

The relationship between these factors and policy positions, Leong continued,

are not set in stone. There is evidence that partisans can be persuaded by political messages, especially when the messages are framed in a manner that appeals to them, so efforts at persuasion are not futile.

Ariel Malka, a professor of psychology at Yeshiva University, believes that religiosity, authoritarianism, and conservative cultural attitudes are rooted in personality traits that have some heritable components.

In an email, Malka noted that

Increased partisan polarization in the U.S. has coincided with the parties placing greater (and opposing) emphases on racial and culture war positions. So its certainly plausible that American polarization stems from partisan conflict having expanded into the racial and cultural areas, aligning this heritable attitude syndrome with partisanship.

Malka cited the work of Amanda Friesen and Aleksander Ksiazkiewicz, political scientists at Indiana University-Purdue University Indianapolis and the University of Illinois-Urbana, who are the authors of Do Political Attitudes and Religiosity Share a Genetic Path?

Friesen and Ksiazkiewicz are persuaded that

certain religious, political, and first principle beliefs on social organization can be explained by genetic and unique environmental components, and that the correlation between these three trait structures is primarily due to a common genetic path.

Malka also points to the work of Steven Ludeke, Wendy Johnson and Thomas J. Bouchard Jr., psychologists at the University of Southern Denmark, the University of Edinburgh and the University of Minnesota, whose findings are described in the title of their 2014 paper, Obedience to traditional authority: A heritable factor underlying authoritarianism, conservatism and religiousness.

In Malkas view, the strength of these predispositions to authoritarianism, religiousness and conservatism has been crucial to the success of Republicans in winning support from white middle-class and working-class voters, many of whom hold strongly liberal views on economic policy.

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How Could Human Nature Have Become This Politicized? - The New York Times

Gaucher Disease Treatment Market 2016 Analysis, Types, Applications, Forecast 2028 – Jewish Life News

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According to the report, thegaucher disease treatment market has been segmented by disease type (type i, type ii, type iii), by treatment type (enzyme replacement therapy (ERT), substrate reduction therapy (SRT)).

Insights about regional distribution of market:

The market has been segmented in major regions to understand the global development and demand patterns of this market.

For gaucher disease treatment market, the segments by region are North America, Asia Pacific, Western Europe, Eastern Europe, Middle East, and Rest of the World. During the forecast period, North America, Asia Pacific and Western Europe are expected to be major regions on the gaucher disease treatment market.

North America and Western Europe have been one of the key regions as they have an established healthcare infrastructure for product innovations and early adaptations. This is estimated to drive demand for gaucher disease treatment market in these regions. In addition to this, some of the major companies operating in this market are headquartered in these regions.

Company profiled in this report based on Business overview, Financial data, Product landscape,Strategic outlook & SWOT analysis:

1. Pfizer Inc.2. Acetelion Pharmaceutical (J&J Ltd.)3. Shire Human Genetics Therapies, Inc.4. Erad Therapeutic Inc.5. JCR Pharmaceuticals Co Ltd.

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Asia Pacific is estimated to register a high CAGR forgaucher disease treatment market. The APAC region has witnessed strategic investments by global companies to cater the growing demand for healthcare solutions in the recent years. Middle East and rest of the World are estimated to be emerging regions for gaucher disease treatment market.

Market Segmentation:By Disease Type:Type IType IIType III

By Treatment Type:Enzyme Replacement Therapy (ERT)Substrate Reduction Therapy (SRT)

By Region:North AmericaNorth America, by CountryUSCanadaMexicoNorth America, by Disease TypeNorth America, by Treatment Type

Western EuropeWestern Europe, by CountryGermanyUKFranceItalySpainThe NetherlandsRest of Western EuropeWestern Europe, by Disease TypeWestern Europe, by Treatment Type

Asia PacificAsia Pacific, by CountryChinaIndiaJapanSouth KoreaAustraliaIndonesiaRest of Asia PacificAsia Pacific, by Disease TypeAsia Pacific, by Treatment Type

Eastern EuropeEastern Europe, by CountryRussiaTurkeyRest of Eastern EuropeEastern Europe, by Disease TypeEastern Europe, by Treatment Type

Middle EastMiddle East, by CountryUAESaudi ArabiaQatarIranRest of Middle EastMiddle East, by Disease TypeMiddle East, by Treatment Type

Rest of the WorldRest of the World, by CountrySouth AmericaAfricaRest of the World, by Disease TypeRest of the World, by Treatment Type

Objectives of this report:o To estimate the market size for gaucher disease treatment market on a regional and global basis.o To identify major segments in gaucher disease treatment market and evaluate their market shares and demand.

o To provide a competitive scenario for the gaucher disease treatment market with major developments observed by key companies in the historic years.o To evaluate key factors governing the dynamics of gaucher disease treatment market with their potential gravity during the forecast period.

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Gaucher Disease Treatment Market 2016 Analysis, Types, Applications, Forecast 2028 - Jewish Life News

World-Renowned Transplant Surgeon to Lead Department of Surgery at NYU Langone Health – NYU Langone Health

Robert Montgomery, MD, DPhil, a pioneering surgeon and director of the NYU Langone Transplant Institute, has been appointed chair of the Department of Surgery. He will assume his new post on September 1. H. Leon Pachter, MD, the George David Stewart Professor of Surgery, who has had a distinguished tenure as chair of the department since 2007, will remain a member of the faculty as chair emeritus.

An internationally renowned surgeon, Dr. Montgomery joined the faculty of NYU Grossman School of Medicine in 2016 from The Johns Hopkins Hospital, where he was part of the team that pioneered a laparoscopic technique for procuring a kidney for live donation that is now standard practice. Under his leadership, the Transplant Institute at NYU Langone has been developing innovative protocols and making significant contributions toward increasing the availability of organs for transplant.

Dr. Montgomery made major headlines himself when, in 2018, the team he assembled performed a heart transplant on him. In yet another example of the game-changing advances he is helping bring about, he accepted a heart that was positive for hepatitis Corgans for which he has strongly advocated for other recipients, including those in the heart, lung, kidney, and liver programs. Thanks to protocols he helped develop, these organs can now be made safe with antiviral medications.

Before joining NYU Langone, Dr. Montgomery developed a system of multiway donor exchanges, also called domino exchanges, facilitating transplants when an intended organ recipient has a donor who is incompatible. He has created techniques such as desensitization therapy to reduce the risk of organ rejection, and has performed groundbreaking research on the possible use of organs from genetically modified animals to address the dire shortages of organs available for transplant.

Dr. Montgomery has made a name for himself in the field of transplant surgery, not only as an innovator and leader, but as a grateful patient, says Robert I. Grossman, MD, dean and CEO of NYU Langone. Under his leadership, the Department of Surgery will continue to push the envelope on behalf of our patients to ensure we continue to provide world-class care.

We thank Dr. Pachter for his leadership of the department, which saw tremendous growthtripling in size during his tenure, says Dr. Grossman. His commitment to patients, trainees, and his faculty embodies the principles of a great leader and outstanding physician.

After graduating magna cum laude with a bachelor of science in biology from St. Lawrence University, Dr. Montgomery graduated with honors from the University of Rochester School of Medicine, and received his doctor of philosophy in molecular immunology from Balliol College at the University of Oxford, England. He completed his general surgical training, postdoctoral fellowship in human molecular genetics, and transplantation surgery fellowship at The Johns Hopkins Hospital.

A prolific researcher and educator, Dr. Montgomery has authored or co-authored more than 275 peer-reviewed publications (cited more than 25,000 times) and given 250 invited or named lectures. In addition to his many academic honors and distinctions, including a Fulbright Scholarship and a Thomas J. Watson Fellowship, in 2019 the Greater New York Hospital Association presented him with the Profile in Courage Award. He appears in the 2010 Guinness Book of World Records for the most kidney transplants performed in one day.

The Department of Surgery at NYU Langone enjoys a distinguished history of discovery and innovation, which has been further enhanced under the exemplary leadership of Dr. Leon Pachter, Dr. Montgomery says. I am extremely excited to accept this new position, and I look forward to this extraordinary opportunity to advance NYU Langones trifold commitment to education, research, and clinical care.

Rob MagyarPhone: 212-404-3500robert.magyar@nyulangone.org

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World-Renowned Transplant Surgeon to Lead Department of Surgery at NYU Langone Health - NYU Langone Health

30% South Asians have Neanderthal gene that increases risk of severe Covid-19: Study – ThePrint

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New Delhi: A piece of the human gene that increases the risk of severe illness from the coronavirus was inherited from Neanderthals over 60,000 years ago, a new study has suggested.The gene in question is carried by 30 per cent of the South Asian population, but is almost completely absent in African people.

In a paper posted on bioRxiv that is yet to be peer-reviewed, scientists from Max Planck Institute for Evolutionary Anthropology in Germany showed that the string of DNA that puts people at increased risk of severe Covid-19 is the same version found in a Neanderthal who lived in Croatia some 50,000 years ago.

Neanderthals are an extinct species of ancient humans who lived in Eurasia until about 40,000 years ago.

We can currently only speculate why the frequency is so high in South Asia, Hugo Zeberg, a co-author of the study, told ThePrint over email.

Zeberg added that the gene variant may have been favourable for the survival of humans earlier, but at this point, it is not clear why it managed to survive 60,000 years.

Also read: Faulty gene linked to dementia doubles risk of severe Covid infection, finds new study

Chromosomes are thread-like structures located inside the nucleus of cells. Each chromosome is made of protein and a single molecule of deoxyribonucleic acid (DNA). The DNA contains the specific instructions or genetic code that makes each individual unique.

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Humans have 23 pairs of chromosomes. People normally have two copies of each chromosome.

In a recent study, researchers found a strong association between severe Covid-19 and two genomic regions: One region on chromosome 3 containing six genes, and one region on chromosome 9 that determines the ABO blood group.

Chromosome 3 spans almost 200 million base pairs or letters, and represents about 6.5 percent of the total DNA in cells. Researchers found that a unique combination of about 50,000 base pairs in chromosome 3 puts people at risk of severe Covid-19.

Then, a study of 3,199 hospitalised patients by the Covid-19 Host Genetics Initiative, a global consortium of scientists working in genetics, confirmed the association between this genetic string and increased risk for severe SARS-CoV-2 infection and hospitalisation.

The Max Planck Institute study followed, establishing the genes link to Neanderthals, and its team further used an online database to determine which populations are more likely to have it.

Also read: Stanford University develops gene-editing tool that can destroy Covid-19 inside human cells

According to some scientists, modern humans migrated out of Africa and interbred with Neanderthals in Eurasia some 200,000 years ago. Then 140,000 years later, Eurasians with Neanderthal ancestry migrated to Africa, interbreeding with the descendants of the humans who never left.

As a result, about 1-4 per cent of genomes of Eurasians, Native Americans, and North Africans derive from Neanderthals.About 20 per cent of the Neanderthals genes continue to survive today in humans.

The team determining the presence of the gene in modern populations found that while it is almost completely absent in Africa, it occurs in South Asia at a frequency of 30 per cent.

The highest frequency occurs in Bangladesh, where more than half the population (63 per cent) carries at least one copy of the Neanderthal risk variant, and 13 per cent have a similar variant of the gene segment.

About eight per cent of Europeans have this variant, while for mixed-race Americans, the variant is present in 4 per cent of the population.

The researchers conclude that the Neanderthal variant may thus be a substantial contributor to Covid-19 risk in certain populations.

One should stress that at this point this is pure speculation, Svante Paabo, another co-author of the Max Planck Institute study, told New York Times.

Also read: Indian scientists find Covid gene in wastewater a breakthrough in tracking virus outbreak

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30% South Asians have Neanderthal gene that increases risk of severe Covid-19: Study - ThePrint

What’s the science on DNA and RNA vaccines? – DW (English)

Researchers say that gene-based, or DNA and RNA, vaccines are faster and cheaper to produce in large quantities than conventional vaccines.

Conventional vaccines often use "weakened" or "killed" versions of a virus. That means laboratories have to produce huge amounts of the virus. They often also include a protein, which is neededto spark a human immune response. But producing a virus and a viral-protein can be time-intensive and expensive.

A DNA or RNA vaccine, on the other hand, takes a small part of the virus' own genetic information just enough to spark an immune response and the protein can be produced directly at the cell. Experts say the virus' genetic informationcan be replicated and produced relatively easily. And that's what scientists want in a live situation, such as the SARS-CoV-2 / COVID-19 pandemic, where billions of people need protection very quickly.

Read more:Lessons learned: The eradication of smallpox 40 years ago

"That's a great advantage of an RNA vaccine," says Peter Doherty, a Nobel Laureate and professor of immunology at Melbourne University, "if it works well."

Human trials: A Covid-19 vaccine test volunteer receives an injection at a clinic in South Africa

The World Health Organization publishes updates on the so-called "candidate" vaccines for SARS-CoV-2 currently in clinical or pre-clinical evaluation. One of the most recent has about 34 RNA and DNA vaccines on the list. But so far none have been approved for use in humans.

Compared to conventional vaccines

There are many different types of vaccines. "Traditional" or conventional vaccines include live attenuated vaccines, inactivated pathogens (also known as "killed vaccines"), viral-vectored vaccines, and other types known as subunit, toxoid and conjugate vaccines. Some prevent both viral and bacterial infection. The latter two are specific to bacterial infections, such as tetanus and diphtheria.

The oral polio vaccine (OPV), for instance, contains an "attenuated" or weakened version of the polio virus. It activates a human immune response, without making the person fully sick.

But a vaccine-virus is also excreted that is, passed from the body and in communities where there is poor sanitation that can lead to two things.

First, it can spread through the community and provide a form of "passive immunization." That's good, but only a short-lived form of immunity. The body has not learnt to recognize the virus and produce its own antibodies. Which means, the body may become vulnerable to that virus again in the future.

And second, if that vaccine-virus lives on long enough in a community without dying out, as it should, it can become a threat in its own right. The World Health Organization (WHO) says: "In very rare instances, the vaccine-virus can genetically change into a form that can paralyze this is what is known as a circulating vaccine-derived poliovirus."

George Church, a professor of genetics at Harvard Medical School and a pioneer in genetic sequencing says DNA vaccines lie somewhere "between live and dead vaccines," with one pertinent benefit: "They can't replicate, mutate, or escape."

Other advantages of DNA vaccines

DNA vaccines are also said to be more stable than conventional vaccines in warm climates "if kept dry and/or sterile at pH8," says Church.

In Nigeria, children line up for a polio vaccine, but some communities refuse it

"They can be stored at room temperature without losing their activity, whereas traditional vaccines require refrigeration," adds Sarah Gilbert, a professor of vaccinology at the Jenner Institute and Nuffield Department of Clinical Medicine at Oxford University.

They may even be effective against non-infectious conditions such as cancer and autoimmune diseases, where conventional vaccines do not work.

Church says DNA vaccines "could be used widely."

And how do DNA vaccines work?

Instead of using a weakened or dead version of a virus, mixed with protein and other ingredients, the main agent in a DNA vaccine is made from part of the virus' own genetic information. The vaccine uses that DNA or RNA to make the immune system think it's under attack, and that triggers the production of proteins directly in the cell.

That activates the immune response, and in turn antibodies that fight the virus.

"Viruses can only multiply in living cells. But to do that the virus has to make more protein. So, DNA becomes RNA, which becomes messenger RNA, and that makes the protein," says Doherty.

The immune response in a little more detail

There are two elements to the immune response, says Doherty.

The first, he says, is that proteins get turned into small things called "peptides." Those peptides are then presented on the surface of the cell, and they stimulate T cells.

There are CD8T cells, also known as "killer T-cells," and CD4 helper T-cells. You need both to get an antibody response.

Read more:The tide is coming for medicinal cannabis

But you also need protein in the extra-cellular fluid.

RNA instructs the cell to make the protein and "for SARS-CoV-2 vaccines, that's the spike protein," says Prof. Sarah Gilbert

The RNA in a vaccine has to cause the protein to get out of the cell and into the extra-cellular fluid so that B cells, or so-called "memory" cells, can grab hold of it, says Doherty. Because without that, your body will have little or no memory of the virus and will be unable to protect you if you ever get infected for real.

Any downsides to DNA vaccines?

The WHO says many aspects of the immune responses caused by DNA vaccines are not yet fully understood. But that has "not impeded significant progress towards the use of this type of vaccine in humans," it says.

In addition, Gilbert says that DNA vaccines usually only encode one protein from the pathogen. "So, they may not be so good if you need to make an immune response against multiple proteins to get protection, but that can be dealt with by mixing multiple vaccines together," she says.

Arcturus Therapeutics is one of at least 30 labs working on a RNA or DNA vaccine for the novel coronavirus COVID-19

Delivery methods vary and may need to be refined over time and with more experience.

Some use a DNA "plasmid," a molecule that's basically as a transportation vehicle for the vaccine. Others use "electroporation" electric pulses that create temporary openings in the cell membrane to let the vaccine get inside.

"Scary" misconceptions about DNA vaccines

Often when we think of DNA or genetics in any form, we think of scary "designer babies," and worry whether our altered DNA will get passed onto future generations.

Read more:Ebola: Congo declares new epidemic

"Anything to do with genetics, or DNA, is somehow conflated in many people's minds. They look at these technologies, whether it's germline-heritable editing or somatic gene-therapy that isn't heritable but might help with diabetes, or changing the genetics of a plant so that it resists pests, or changing the genetics of an animal so that it produces less phosphorus in its feces," says Alta Charo, a professor of law and bioethics at the University of Wisconsin at Madison.

"And all these things get lumped together in the category of genetics, and very closely linked to genetics is scary. Or at least worrisome. And that's why we have to help people distinguish between the various categories," Charo says.

DNA vaccines aren't heritable

If there are ethical concerns in genetics, they might apply to techniques like human-gene editing, where a person's DNA is altered to cut out a gene that might make you prone to a particular cancer. And those alterations can be passed on through generations.

But that's not the case with DNA vaccines.

"They don't alter a person's DNA at all. They provide a temporary addition in a small number of cells," says Gilbert. "DNA vaccines do not enter the genome."

Prof. Peter Doherty says COVID-19 antibody tests tend to only show antibodies in the blood, but not whether the immune system is sufficiently primed for a secondary attack

They merely imitate what happens when we get infected by a virus. A virus inserts its DNA into our cells to enable it to replicate and spread. And a vaccine has to do that as well, but in a controlled manner. As Charo puts it, you retain "the shell of the virus but take away the guts" the really dangerous stuff that makes you sick.

"When we get a viral infection, genetic material (DNA or RNA) from the virus is there inside our cells, but most viral infections don't then leave DNA that becomes part of the genome, although that does happen in some cases," says Gilbert.

Read more:Does it really matter where your DNA comes from?

HIV, for instance, has a "reverse transcriptase," which copies the viral genetic material back into the genome. But viruses like the coronavirus or influenza don't have that, says Doherty.

"So, we're not going to copy the genetic material back into the human genome. But quite frankly, if you made a RNA vaccine and you gave it to people and it transmitted to other people, that would be a good thing," he says."But I don't see why it should happen anyway."

When will we see gene-based vaccines for COVID-19?

Some DNA vaccines have been approved for veterinary use. And there are many others in clinical trials for human use, including those for SARS-CoV-2.

Many will use what's called an "adaptive clinical trial design" to speed up the process from discovery to development to trial and approval to production.

Charo says adaptive trials are a less "static" approach than conventional ones. They allow researchers to respond to data and adapt as they go along, whereas you would normallytake every step in sequence, and over time.

But in a live pandemic, time is at a premium. An adaptive trial design makes it effectively possible to approve a vaccine before all the testing is complete.

"There would be a requirement to do follow-up research to confirm early indications, known as surrogate markers" says Charo, "and if that research fails to confirm those indications, then the drug or vaccine can be withdrawn."

In any case, you're only likely to see the full effects of a vaccine once it's out in the community. As Doherty puts it, "it's all one enormous experiment. People are trying to be safe, but even a partially effective vaccine might be useful. We'll have to see how that's evaluated by the regulatory bodies and the people making the vaccines."

Courage, curiosity or complete hubris? It's probably a mixture of all these things that causes many scientists to test their own inventions on themselves first. According to the Global Times, a Chinese doctor not only developed an oral vaccine against the SARS-CoV-2 but also tried it out himself. So far, he hasn't seen any side effects.

Scientific knowledge and private pleasure can go hand in hand. The British chemist Sir Humphry Davy experimented with nitrous oxide between 1795 and 1798. With the help of his self-experiments, he discovered not only the pain-relieving effect of the gas but also its intoxicating qualities.

The German physicist Johann Wilhelm Ritter not only discovered ultraviolet radiation in 1801, but also invented the first battery the following year. Ritter was also interested in galvanism a term applied to muscle contractions caused by electric shocks. The fact that he died at the age of 33 is said to have been due in part to the galvanic self-experiments with which he maltreated his body.

The Austrian psychologist and doctor Sigmund Freud is known as the founder of psychoanalysis. His methods are still used, discussed and criticized today. Less well known is that Freud researched the effects of cocaine during his time as a doctor at the Vienna General Hospital. Published letters show that Freud himself consumed coke for a long time and in large quantities.

"I believe that I am on the trail of the true pathogen," wrote the American physician Jesse Lazear on September 8, 1900, in a letter to his wife. Lazear researched malaria and yellow fever. He confirmed that the latter is transmitted by mosquitoes. To study the disease, he intentionally allowed himself to be stung, fell ill and died 17 days after writing the letter. Lazear was only 34 years old.

John Paul Stapp became known as the "fastest man on earth" because of his research on the effects of acceleration forces on the human body including his own: He had himself accelerated on a so-called rocket sled up to more than 1,000 kph (621 mph) and decelerated completely in 1.4 seconds. It is the highest acceleration that a human being has ever voluntarily withstood.

Werner Forssmann was already considered a troublemaker during his medical training. The German surgeon was determined to prove that a long, flexible catheter could be inserted safely from the crook of the arm to the heart. Although his superiors had expressly forbidden him to carry out the experiment, in 1929 Forssmann was the first person to try it out on himself. Secretly, of course.

The Canadian physician Ralph Steinman fell ill with pancreatic cancer and underwent an immunotherapy he developed himself. According to his physician, this therapy was unable to prevent Steinman's death, but contrary to the prognosis could possibly have prolonged his life by over four years. Steinman died in 2011, a few days before the Nobel Prize was awarded, which he received posthumously.

Author: Julia Vergin (fs)

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What's the science on DNA and RNA vaccines? - DW (English)

The Clock Is Ticking: Can Mankind Beat the Extinction? – Interesting Engineering

Have you ever wondered just how long the typical species lasts? After all, it is the fate of every species to one day become extinct.

But could technology possibly save humans from this fate? Or are we also dommed to one day disappear?

Let's take a gander.

RELATED: NEW FOUNTAIN OF YOUTH COCKTAIL PRODUCES LARGEST LIFESPAN INCREASE EVER

Before we start, please note that evolutionary biology and palaeobiology are large and complex fields and that theories on extinction are ever-evolving (excuse the pun). The following article is only intended as a rough and ready overview, not a scientific thesis.

Let's start with a definition.

According to the Merriam-Webster Dictionary, a species is defined as: -

"Acategory of biological classification ranking immediately below the genus or subgenus, comprising related organisms or populations potentially capable of interbreeding, and being designated by a binomial that consists of the name of a genus followed by a Latin or Latinized uncapitalized noun or adjective agreeing grammatically with the genus name."

Simple enough, but at one point can we say that a new species has emerged?At what point can we definitively state, "Yes, now we have a new species"?

New species arise through a process called, appropriately enough, speciation.

This is traditionally defined as:

"Speciation is how a new kind of plant or animal species is created. Speciation occurs when a group within a species separates from other members of its species and develops its own unique characteristics." - National Geographic.

Speciation results in reproductive isolation from the original "parent species" population due to the accumulation of genetic differences between the two, or more, groups.

Speciation can occur in several ways. Perhaps the most common is through separation. This may occur whena part of a population becomes separated from the rest of their species, for example, through geological changes. Speciation can also occur without geological effects. In sympatric speciation,two or more descendant species rise from a single ancestral species. This may occur when different populations of a species begin to occupy different niches in the samegeographic location.

Speciation may also be induced artificially, throughanimal husbandry, agriculture, orlaboratory experiments. Genetic driftis another possible, and oft-debated mechanism for speciation. This is when genetic mutations introduce changes to a species over time.

Remember that a group of organisms is only ever considered a species if they can breed and produce viable, fertile offspring.

Of course, speciation doesn't happen overnight. Human action aside, it can take a great deal of time to accumulate enough genetic differences for a new species to emerge. In fact, it may be more appropriate to think of speciation as a continuum, and not a discrete, clear cut event.

The fossil record can also be quite deceptive when it comes to giving us insight into speciation.

Because the fossil record is incomplete, each new species can appear to come out of nowhere. This can be frustrating for paleontologists.

There is also another theory called "punctuated equilibria". Devised by the late Stephen Jay Gouldand his colleague Niles Eldredge, this theory proposes that the evolution of new species can also occur in relatively rapid jumps -- often in response to major cataclysmic events.

This theory is not widely accepted, with prominent figures like Richard Dawkins, a notable critic, but it may occur in some instances.

Now, let's turn our attention to the modern world.

Given the slow rate of change needed for speciation to occur (except for artificial speciation, as when humans deliberately breed new species), it is difficult to "see it in action" today.

One example may be the Hawthorn fly, which some researchers believe may be undergoing speciation. Adistinct population appears to have emerged in North America after apples were introduced in the 19th century. This new populationfeeds only on apples, and not on the fruit ofhawthorns. Researchers have found some evidence that the apple-eating and hawthorn-eating flies now have significant genetic differences and are no longer inter-breeding.

The study of organisms with veryshort lifespans, like bacteriaand viruses, can also sometimes illustrate speciation in action.

Over a long enough time, some antibiotic-resistant bacteria can become a distinctly separate species. Other famous examples include the peppered moth.

And that brings us to a nice segue, namely, what is the natural lifespan of a species?

Let's address the first question, well, first.

You may be tempted to think of any number of so-called "living fossils" when addressing this question. But it is important to bear in mind that the term "living fossil" is a little misleading, and may even be considered a misnomer.

By way of example, let's take one of the most famous "living fossils", the coelacanth. Living examples includeLatimeria chalumnae andLatimeria menadoensis,which are thought to be the last surviving species of the ancient cladeSarcopterygii(lobe-finned fish andtetrapods).

Here, the term "living fossil" is used as shorthand to describe the remaining extant species belonging to a distant ancestral lineage. If we were to analyze the genome of a modern coelacanth and compare it to that of its ancestors, stark differences would appear.

In fact, the term "living fossil" is more one of convenience than accuracy, and in many cases, it is an artefact of previous haphazard taxonomic classifications, and history of discovery, more than a useful concept.

But we digress.

Some of the oldest living species include species of the horseshoe crabs, which have been around for about 150 million years; species of horsetail plants, which may have evolved around 360 million years ago; and cow sharks, which emerged around 175 million years ago.

But what about the longest living individual animals within a species. Here are some common examples: -

All well and good. But what is the longest-living animal known today? The answer is hotly debated, but a few of the candidates are:

Of course, some trees and other plant species are much, much older.

While many people frequently refer to our planet as "Mother Earth", "The Green Planet", or another nickname that conjures up fertility, sanctity, and vitality; the history of life on this planet is actually one of suffering and extinction.

From mass bio-extinction eventsto the daily loss of individual organisms within a population, death hangs above us all.

But, what are the typical "innings" of any particular species here on our home planet?

Setting aside cataclysmic events, like asteroid impacts, ice ages, eruption of super-volcanoes, etc., and human influence, there does appear to be an average species lifespan over geological time. This is referred to as the "background extinction rate" or "normal extinction rate".

It refers to the number of species that would be expected to go extinct over a given period of time, not taking into account human influence. The background extinction rate is generally measured over a particular period of time. It is sometimes given using the unit millions of species years (MSY) which refers to the number of extinctions expected per 10,000 species per 100 years.

The background extinction rate is different for different types of organisms.For example,mammals have an average species lifespan of 1 million years (although some mammal species have existed for more than 10 million). There are around 5,000 mammalian species currently in existence. This means that we can expect one mammal species to go extinct, on average, every 200 years or so.

Most of these calculations are based on the fossils record, which we have already seen in incomplete. In fact, the remains of terrestrial organisms are notoriously less likely to survive the rigors of time due to scavenging, weathering, and other environmental factors.

For this reason, the rate is more of a ballpark figure.

As we have already seen, natural extinction rates are a little tricky to calculate.

Mammals, in general, of which we are a member, tend to have an average species lifespan on the lower end of the scale. Some types of organisms, however, appear to be far more robust. For example, marine invertebrates are thought to have a background level of extinction of 5 to10 million years,while dinoflagellates may have abackground level of extinction of around 13 million years.

These values, however, need to be taken with a pinch of salt. They should not be seen as concrete estimates, and mileage of some species within groups (like mammals) may vary widely.

It is also important to remember that extinction is a natural part of life on Earth.

After all, if the dinosaurs had never been toppled from their pedestal, our early mammalian ancestors would never have been given the chance to thrive and evolve into our very own species.

These historical estimates may also be widely off, as many soft-bodied organisms, especially microscopic ones, are very difficult to identify and track throughout geological history.

It also comes down to how niche-specific species are/were, how adaptable the species is/was, and in which habitats they lived (land or sea, for example), to name but a few issues. With all the problems associated with analyzing taphonomy (the process of fossilization), are there any estimates based on the living species today?

The answer is, of course, yes. But, you will also find widely different estimates for extinction rates here, too.

They range from something like 8,700 species a year (24 a day) by the Mllenum Ecosystem Assessment to somewhere in the region of 150 a day by the U.N. Convention on Biological Diversity.

These estimates are so much higher than historic rates because the extinction rate appears to be increasing rapidly due to human influence on the environment. Remember, scientists estimate extinction rates irrespective of human factors. This is because it is believed by most that humans have had a huge impact on the number of species becoming extinct.

For comparison, we only "really" know of roughly 800 extinctionswhich have occurred over the last 400 years.Of which, about 89 were mammals.

To put that into perspective, this is less than 1 tenth of a percent of the total estimates of global species count of 1.9 million. But, again, these are all guesstimates.

However, we do have another weapon in our arsenal that can help us here for estimating extinction rates ... genetics!

There is a third way that scientists can estimate the lifespan of a species. By comparing the genome of distinct, yet closely related, species, it is possible to estimate, roughly, when they separated from a common ancestor.

Sometimes called sister taxa, the greater the genetic difference between them, the longer ago the split. This method has been termed the molecular clock, and it has proven to be a very useful tool.

In fact, this methodology has helped rewrite some of the long-held beliefs about the evolution of many species.

Using this technique, it has been theorized that humans (specifically the homo genus) split from the line that contains bonobos and chimpanzees betweensix and eight million years ago. Interestingly, bonobos and chimpanzees themselves split from one another around 1 million years ago.

What this means is that the "parent" species of both may have become extinct around that time, which fits the lower estimates for mammals from the fossil record.

Our species, Homo sapiens and our sister taxa, the now-extinct Homo neanderthalensis, split around 800,000 years ago, though new evidence suggests Homo sapiens and Neanderthal may have actually interbred, and thus may not have been separate species, but sub-species.We have yet to find any remains of our common ancestor, though many believe it may have beenHomo heidelbergensis.

But, a recent study may be getting closer to finding out.

There is some evidence to suggest that the proportion of Neandertal-inherited genetic material is around 1.5 to 2.1 % in non-African populations, though some studies indicate it could be as much as 20%.

But this hypothesis is far from widely accepted by the scientific community.

If any of the above-mentioned estimates hold any water, that would mean we have somewhere in the region of at least200,000 years of natural species lifespan left. But, this, of course, ignores completely our ability to adapt and use our technology to extend our time on the planet (or off it).

Homo sapiens have proved to be, so far, a highly adaptable species. According to many scientists, likepaleobiologistDavid Jablonski, the human species is more likely than not to exist for a lot longer than would be otherwise expected, even if there is another mass extinction event.

In fact, we have been there before. There is evidence to show thatHomo sapienswere almost wiped out around 70,000 years ago. The culprit? The eruption of the supervolcano, Toba in Sumatra, Indonesia.

This event is thought to have changed the climate to such a degree that the total human population may have fallen to between 5,000 and 10,000 individuals. Others estimate it could have been as low as 40 breeding pairs (but this is heavily disputed).

But this is, literally, ancient history.

To stave off potential extinction, like from supervolcanic eruptions, somebelieve we will likely need to leave the planet.

The future of humanity is fundamentally going to bifurcate along one of two directions: Either were going to become a multiplanet species and a spacefaring civilization, or were going be stuck on one planet until some eventual extinction event, Elon Musk said during theNational Geographic Channels MARS, a global event series that premieres worldwide on November 14, 2016.

For me to be excited and inspired about the future, its got to be the first option. Its got to be: Were going to be a spacefaring civilization, he added.

An artist's impression of SpaceX's Mars base. Source:SpaceX

If we can find a way off this world and populate the universe, this may be a way of extending our species' lifespan indefinitely. With the work of companies like SpaceX, Blue Origin, or any other of the private space companies currently operating, this may happen sooner than we think.

But even this might not "save" our species. As we have seen with other species on the planet, it may be the case that human colonies will evolve on their own path and quickly become new species in their own right. But that is likely to take another few hundred thousand years or so.

A fascinating thought.

Unless, of course, we wipe ourselves out in a phantasmagorical storm of nuclear fire or wreck the Earth's biosphere beforehand. Or, indeed, we are supplanted by our own creations, likeartificial life.

Only time will tell.

The rest is here:

The Clock Is Ticking: Can Mankind Beat the Extinction? - Interesting Engineering

New Report: Genomic Biomarker Market: Reporting and Evaluation of Recent Industry Developments| Bio-Rad, Beckman Coulter, Myriad Genetics, Thermo…

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HospitalsDiagnostic and research laboratories Global Genomic Biomarker

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Key companies operating in the global Genomic Biomarker market include Bio-Rad, Beckman Coulter, Myriad Genetics, Thermo Fisher Scientific, Roche, QIAGEN, Epigenomics, Almac, Pfizer, Human Longevity, ValiRx, Personalis, Eagle Genomics, Empire Genomics, Agilent, Illumina

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1 Market Overview of Genomic Biomarker1.1 Genomic Biomarker Market Overview1.1.1 Genomic Biomarker Product Scope1.1.2 Market Status and Outlook1.2 Global Genomic Biomarker Market Size Overview by Region 2015 VS 2020 VS 20261.3 Global Genomic Biomarker Market Size by Region (2015-2026)1.4 Global Genomic Biomarker Historic Market Size by Region (2015-2020)1.5 Global Genomic Biomarker Market Size Forecast by Region (2021-2026)1.6 Key Regions, Genomic Biomarker Market Size YoY Growth (2015-2026)1.6.1 North America Genomic Biomarker Market Size YoY Growth (2015-2026)1.6.2 Europe Genomic Biomarker Market Size YoY Growth (2015-2026)1.6.3 Asia-Pacific Genomic Biomarker Market Size YoY Growth (2015-2026)1.6.4 Latin America Genomic Biomarker Market Size YoY Growth (2015-2026)1.6.5 Middle East & Africa Genomic Biomarker Market Size YoY Growth (2015-2026) 2 Genomic Biomarker Market Overview by Type2.1 Global Genomic Biomarker Market Size by Type: 2015 VS 2020 VS 20262.2 Global Genomic Biomarker Historic Market Size by Type (2015-2020)2.3 Global Genomic Biomarker Forecasted Market Size by Type (2021-2026)2.4 Protein Marker2.5 Nucleic Acid Marker2.6 Other 3 Genomic Biomarker Market Overview by Application3.1 Global Genomic Biomarker Market Size by Application: 2015 VS 2020 VS 20263.2 Global Genomic Biomarker Historic Market Size by Application (2015-2020)3.3 Global Genomic Biomarker Forecasted Market Size by Application (2021-2026)3.4 Hospitals3.5 Diagnostic and research laboratories 4 Global Genomic Biomarker Competition Analysis by Players4.1 Global Genomic Biomarker Market Size (Million US$) by Players (2015-2020)4.2 Global Top Manufacturers by Company Type (Tier 1, Tier 2 and Tier 3) (based on the Revenue in Genomic Biomarker as of 2019)4.3 Date of Key Manufacturers Enter into Genomic Biomarker Market4.4 Global Top Players Genomic Biomarker Headquarters and Area Served4.5 Key Players Genomic Biomarker Product Solution and Service4.6 Competitive Status4.6.1 Genomic Biomarker Market Concentration Rate4.6.2 Mergers & Acquisitions, Expansion Plans 5 Company (Top Players) Profiles and Key Data5.1 Bio-Rad5.1.1 Bio-Rad Profile5.1.2 Bio-Rad Main Business5.1.3 Bio-Rad Products, Services and Solutions5.1.4 Bio-Rad Revenue (US$ Million) & (2015-2020)5.1.5 Bio-Rad Recent Developments5.2 Beckman Coulter5.2.1 Beckman Coulter Profile5.2.2 Beckman Coulter Main Business and Companys Total Revenue5.2.3 Beckman Coulter Products, Services and Solutions5.2.4 Beckman Coulter Revenue (US$ Million) (2015-2020)5.2.5 Beckman Coulter Recent Development and Reaction to Covid-195.3 Myriad Genetics5.5.1 Myriad Genetics Profile5.3.2 Myriad Genetics Main Business5.3.3 Myriad Genetics Products, Services and Solutions5.3.4 Myriad Genetics Revenue (US$ Million) & (2015-2020)5.3.5 Thermo Fisher Scientific Recent Developments5.4 Thermo Fisher Scientific5.4.1 Thermo Fisher Scientific Profile5.4.2 Thermo Fisher Scientific Main Business5.4.3 Thermo Fisher Scientific Products, Services and Solutions5.4.4 Thermo Fisher Scientific Revenue (US$ Million) & (2015-2020)5.4.5 Thermo Fisher Scientific Recent Developments5.5 Roche5.5.1 Roche Profile5.5.2 Roche Main Business5.5.3 Roche Products, Services and Solutions5.5.4 Roche Revenue (US$ Million) & (2015-2020)5.5.5 Roche Recent Developments5.6 QIAGEN5.6.1 QIAGEN Profile5.6.2 QIAGEN Main Business5.6.3 QIAGEN Products, Services and Solutions5.6.4 QIAGEN Revenue (US$ Million) & (2015-2020)5.6.5 QIAGEN Recent Developments5.7 Epigenomics5.7.1 Epigenomics Profile5.7.2 Epigenomics Main Business and Companys Total Revenue5.7.3 Epigenomics Products, Services and Solutions5.7.4 Epigenomics Revenue (US$ Million) (2015-2020)5.7.5 Epigenomics Recent Development and Reaction to Covid-195.8 Almac5.8.1 Almac Profile5.8.2 Almac Main Business5.8.3 Almac Products, Services and Solutions5.8.4 Almac Revenue (US$ Million) & (2015-2020)5.8.5 Almac Recent Developments5.9 Pfizer5.9.1 Pfizer Profile5.9.2 Pfizer Main Business5.9.3 Pfizer Products, Services and Solutions5.9.4 Pfizer Revenue (US$ Million) & (2015-2020)5.9.5 Pfizer Recent Developments5.10 Human Longevity5.10.1 Human Longevity Profile5.10.2 Human Longevity Main Business5.10.3 Human Longevity Products, Services and Solutions5.10.4 Human Longevity Revenue (US$ Million) & (2015-2020)5.10.5 Human Longevity Recent Developments5.11 ValiRx5.11.1 ValiRx Profile5.11.2 ValiRx Main Business5.11.3 ValiRx Products, Services and Solutions5.11.4 ValiRx Revenue (US$ Million) & (2015-2020)5.11.5 ValiRx Recent Developments5.12 Personalis5.12.1 Personalis Profile5.12.2 Personalis Main Business5.12.3 Personalis Products, Services and Solutions5.12.4 Personalis Revenue (US$ Million) & (2015-2020)5.12.5 Personalis Recent Developments5.13 Eagle Genomics5.13.1 Eagle Genomics Profile5.13.2 Eagle Genomics Main Business5.13.3 Eagle Genomics Products, Services and Solutions5.13.4 Eagle Genomics Revenue (US$ Million) & (2015-2020)5.13.5 Eagle Genomics Recent Developments5.14 Empire Genomics5.14.1 Empire Genomics Profile5.14.2 Empire Genomics Main Business5.14.3 Empire Genomics Products, Services and Solutions5.14.4 Empire Genomics Revenue (US$ Million) & (2015-2020)5.14.5 Empire Genomics Recent Developments5.15 Agilent5.15.1 Agilent Profile5.15.2 Agilent Main Business5.15.3 Agilent Products, Services and Solutions5.15.4 Agilent Revenue (US$ Million) & (2015-2020)5.15.5 Agilent Recent Developments5.16 Illumina5.16.1 Illumina Profile5.16.2 Illumina Main Business and Companys Total Revenue5.16.3 Illumina Products, Services and Solutions5.16.4 Illumina Revenue (US$ Million) (2015-2020)5.16.5 Illumina Recent Development and Reaction to Covid-19 6 North America6.1 North America Genomic Biomarker Market Size by Country6.2 United States6.3 Canada 7 Europe7.1 Europe Genomic Biomarker Market Size by Country7.2 Germany7.3 France7.4 U.K.7.5 Italy7.6 Russia7.7 Nordic7.8 Rest of Europe 8 Asia-Pacific8.1 Asia-Pacific Genomic Biomarker Market Size by Region8.2 China8.3 Japan8.4 South Korea8.5 Southeast Asia8.6 India8.7 Australia8.8 Rest of Asia-Pacific 9 Latin America9.1 Latin America Genomic Biomarker Market Size by Country9.2 Mexico9.3 Brazil9.4 Rest of Latin America 10 Middle East & Africa10.1 Middle East & Africa Genomic Biomarker Market Size by Country10.2 Turkey10.3 Saudi Arabia10.4 UAE10.5 Rest of Middle East & Africa 11 Genomic Biomarker Market Dynamics11.1 Industry Trends11.2 Market Drivers11.3 Market Challenges11.4 Market Restraints 12 Research Finding /Conclusion 13 Methodology and Data Source 13.1 Methodology/Research Approach13.1.1 Research Programs/Design13.1.2 Market Size Estimation13.1.3 Market Breakdown and Data Triangulation13.2 Data Source13.2.1 Secondary Sources13.2.2 Primary Sources13.3 Disclaimer13.4 Author List

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10-year plan hopes to give western chimpanzees a fighting chance – Mongabay.com

Western chimpanzees are the most threatened of the four confirmed chimpanzee subspecies. Conservationists estimate that populations of the western chimpanzee (Pan troglodytes versus) declined by 80% between 1990 and 2014. Large tracts of chimpanzee habitat have already been lost, and much of what remains is in the crosshairs of agriculture, industry and infrastructure development.

Adding to the pressure, in their West African home, the subspecies shares its space with the worlds fastest-growing human population. Without immediate action, the IUCN warns the western chimpanzee may soon become extinct.

The IUCN recently released its latest 10-year action plan, setting out nine key strategies to protect chimpanzees. On the agenda are improved legal protection, raising awareness, and more research into their distribution, genetics and behavior. The plan also highlights the need for chimpanzees to be considered at all levels of the land use planning process if they are to have a future in the rapidly developing West Africa region.

The western chimpanzee is in dire need of coordinated and effective conservation action right now, said Erin Wessling, a postdoctoral fellow at Harvards Department of Human and Evolutionary Biology and lead editor of the IUCN plan.

The western chimpanzees range extends across eight countries in West Africa: Cte dIvoire, Ghana, Guinea, Guinea-Bissau, Liberia, Mali, Senegal and Sierre Leone. The subspecies is already locally extinct in Benin, Burkino Faso and Togo.

The exact challenges western chimpanzees face vary by location, but the IUCN has identified common key threats across the region: poaching, habitat loss, and disease.

According to U.N. population data, almost half of West Africas 367 million inhabitants were 15 or younger in 2015, making it highly likely that the regions current rapid population growth will continue in the near future. Agricultural production in West Africa has been growing even faster than population growth in the last 30 years, allowing the region to greatly reduce undernourishment.

While vital for West Africas food security, this rapid agricultural expansion has had unfortunate consequences for chimpanzees. Much of their habitat has been lost to subsistence and industrial agriculture, and what remains has become increasingly fragmented.

In Cte dIvoire, once home to one of the largest populations of western chimpanzees, widespread agricultural expansion for coffee, cacao and palm oil has seen the chimpanzees range cut by 70%. Researchers now believe that only small remnant populations of a few hundred individuals remain in two of Cte dIvoires national parks.

Large portions of the remaining chimpanzee habitat in West Africa as much as 80% in Liberia are also suitable for oil palm production, a valuable export crop. Without a voice for chimpanzees in the land use planning process, experts fear the lure of foreign exchange may well override any conservation concerns.

As well as agriculture, artisanal and industrial mining, logging, new roads and development projects all have an impact on chimpanzee habitat. According to a study modeling western chimpanzee distribution, 10% of chimpanzees live within 25 kilometers (16 miles) of four major development corridors planned in West Africa.

As large-scale land-use change is occurring across West Africa, this action plan points out the need for integrated land-use planning that involves chimpanzee experts, said Stefanie Heinicke, a postdoctoral researcher with the Potsdam Institute for Climate Impact Research and one of the authors of the IUCN plan.

At present, chimpanzees are sometimes considered in environmental impact assessments for individual projects in the region. However, the IUCN plan argues that unless the cumulative impact of multiple projects is considered, the full impact of development on chimpanzees cant be seen.

Chimpanzee experts need to have a voice in the planning practice, argues the action plan, which was developed following a four-day workshop in Monrovia that included representatives from the governments of all eight range countries as well as NGOs and researchers.

The authors propose that environmental assessments be carried out at both a national and range-wide level to assess the impact of development and land use change on chimpanzee populations and identify important no-go zones to protect. The IUCN plan also emphasizes the importance of ensuring land use planners have accurate information on the likely impact of developments on chimpanzee populations. As a last resort, the IUCN suggests establishing offset programs to counteract the impact of development projects on chimpanzees.

In addition to fragmenting habitat, infrastructure projects like roads also make chimpanzee habitat more accessible to poachers 60% of western chimpanzees already live within 5 km (3 mi) of a road. Bushmeat consumption is the main driver of direct killing of chimpanzees in West Africa, with researchers documenting the availability of chimpanzee meat in both rural and urban bushmeat markets. Chimps are also killed for their body parts and as a result of human wildlife conflict, or are captured live for the exotic pet trade.

Heinickes modeling study calculated that 83% of the estimated 52,800 remaining western chimpanzees live outside protected areas, leaving them especially vulnerable.

As less than 20% of western chimpanzees occur in high-level protected areas, the strengthening and extension of protected areas is a central strategy of this new conservation action plan, she said.

And even living in a protected area is not a guarantee of safety. A study surveying hunters around Liberias Sapo National Park recorded 74 chimpanzees killed and eight infants captured alive in two months.

To tackle this, the action plan calls for increased legal protection for chimpanzees and international coordination to improve the enforcement of wildlife laws.

Laws and protected areas dedicated to protecting this subspecies havent been as effective as we need them to be, Wessling said. To do so will require that chimpanzee conservationists have a seat at the table in the discussions.

There are also other consequences to the growing proximity between chimpanzees and humans.

An increasing spatial overlap can increase the risk of disease transmission between humans and chimpanzees, and can also increase the likelihood of conflicts, Heinicke said.

With many physiological similarities, chimpanzees are susceptible to a number of human diseases, and vice versa. Chimpanzees are known to have caught human respiratory diseases, including a type of human coronavirus, that can prove fatal. Another disease of major concern in the West Africa region is Ebola. While there is no evidence that chimpanzees have been affected in the worst outbreak, from 2014-16, gorilla and chimpanzee populations have been severely affected in the past.

The action plan calls for disease monitoring and risk analysis to understand and mitigate the risks of disease transmission between humans and chimpanzees, an issue that has recently shot to prominence in light of the current COVID-19 pandemic.

Another area the plan focuses on is the need to fill gaps in scientific knowledge about the distribution, behavior and genetic diversity of western chimpanzees an area also highlighted in the previous action plan.

Since the last conservation action plan many areas across West Africa have been surveyed, Heinicke said. However, there are still gaps, especially in terms of chimpanzee density and distribution.

The remaining strategies in the action plan call for an increased awareness of the plight of western chimpanzees at both the local and international level, and the need for effective long-term financing for chimpanzee conservation.

With rising competition for chimpanzee habitat and increasing proximity to West Africas growing human population, the future for the western chimpanzee is precarious. Wessling and Heinicke say they are hopeful that the nine strategies the IUCN plan sets out can offer a glimmer of hope for the western chimpanzees.

Theres an urgent need to make calculated efforts to give this subspecies a chance, Wessling said. [T]he consequences if we arent effective are immense.

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10-year plan hopes to give western chimpanzees a fighting chance - Mongabay.com

Explained: A new calculation to find out your dogs age in human years – The Indian Express

Written by Kabir Firaque, Mehr Gill | New Delhi | Updated: July 11, 2020 5:08:29 pm There exists a very simple thumb rule, used frequently over the years. The new research, however, has described it as a myth

Dogs live shorter lives than humans, and so a six-year-old dog is at a far later stage of its life than a six-year-old child. A dog can even be a grandparent at age six. What, then, is its age in human years? New research, published in the journal Cell Systems has come up with a formula and a graph to determine that.

Was there not a formula already?

There exists a very simple thumb rule, used frequently over the years. The new research, however, has described it as a myth. According to the popular rule, you multiply a dogs age by 7, and you supposedly get its equivalent age in human years: For example, a four-year-old dog is 28 in human years. Only, its not so simple.

Why not?

The new research, which is based on epigenetics, has found the comparison between human years and dog years is not perfectly linear which would have been the case had the 1:7 thumb rule been reliable. The relationship, in fact, follows the red curve shown in the figure.

How can I use this curve to determine my dogs age in human years?

First, find your dogs age along the horizontal (X) axis. Suppose your dog is four years old. Locate 4 on the horizontal axis, then trace your finger upwards until you reach the red curve. From that point, move left towards the vertical (Y) axis, where you have human years (illustrated with Tom Hanks at various ages). Your finger will touch the vertical axis at, in this case, 52 years.

So, a four-year-old dog is equivalent in physiological age to a 52-year-old Tom Hanks (or any 52-year-old human). This is almost twice as much the age you would get (28) if you followed the 1:7 thumb rule.

What is the basis of this new calculation?

It is based on molecular changes in the human genome and dog genome over time. Researchers at the University of California at San Diego analysed patterns over time in methylation a term that refers to specific chemical changes in the genome.

This is the field that is known as epigenetics, which studies chemical modifications that influence which genes are off or on, without altering the original genetic sequence itself. The new formula, the researchers said, provides a new epigenetic clock for determining the age of a cell, tissue or organism.

How did the researchers derive the formula?

The UC San Diego team had previously published epigenetic clocks for humans. For the new study, they collaborated with dog genetics experts at UC Davis and the US National Human Genome Research Institute. They analysed blood samples from 105 Labrador retrievers for changes with age.

Only Labradors?

Indeed, that is one limitation of the new epigenetic clock, acknowledged by senior author Trey Ideker himself. (The first author is Tina Wang, Idekers former graduate student, who first suggested the idea for such a study.) In a statement, Ideker acknowledged that the new epigenetic clock was developed using a single breed of dog, and some dog breeds are known to live longer than others. More research will be needed, he said.

Will it work for my dog if it is not a Labrador?

Ideker said it is accurate for humans and mice, as well as Labrador retrievers. He predicts that the clock will apply to all dog breeds. As such, it may provide a useful tool for veterinarians and even for evaluating anti-ageing interventions, the researchers suggest.

How so?

There are a variety of anti-ageing interventions in the market, with some of these standing on a more solid scientific foundation than others. But, as Ideker noted in the statement, how do you know if a product will truly extend your life without waiting 40 years or so?

If you refer to the new epigenetic clock, you need not wait, he suggested. What if you could measure your age-associated methylation patterns before, during and after the intervention to see if its doing anything?

The Indian Express is now on Telegram. Click here to join our channel (@indianexpress) and stay updated with the latest headlines

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Explained: A new calculation to find out your dogs age in human years - The Indian Express

Scores forecast effects of mutations in autism gene – Spectrum

Mutation rating: Scores may help researchers identify changes in the gene PTEN most likely to play a role in autism.

CRAFTSCI / Science Photo Library

A new analysis links individual mutations in a gene called PTEN to a persons odds of having autism, cancer or other conditions1. The findings may help clinicians and researchers predict the effects of various mutations in the gene.

PTEN controls cell growth and regulates the strength of connections between neurons. Mutations in the gene are associated with a variety of conditions, including autism, macrocephaly (enlarged head size), benign tumors and several types of cancer. It is still unclear how different mutations cause such varied effects.

Scientists cannot easily predict the consequences of a PTEN mutation based on its type whether it involves a single amino acid change or a larger interruption to the gene, for example or its impact on the protein the gene encodes. Researchers have developed methods to examine the molecular effects of PTEN mutations within cells in a dish, but these approaches do not link mutations to specific conditions in people.

In the new analysis, the researchers probed the effects of 7,657 PTEN mutations, representing all possible changes to each amino acid in the genes sequence. They built on the findings from a previous study in which they used yeast cells to calculate a fitness score for 7,244 PTEN mutations2. They combined this dataset with another in which researchers had given an abundance score to 4,112 PTEN mutations based on how those mutations affect protein levels in human cells in a dish3.

The team used machine learning on the combined dataset to calculate abundance and fitness scores for mutations that lacked them. They then compared these scores with data they gathered from 421 people with PTEN mutations 165 controls and 256 people with a PTEN-related condition, such as autism, developmental delay, intellectual disability, macrocephaly, or benign or malignant tumors.

People with the largest head size tend to have mutations with the lowest fitness and abundance scores, the researchers reported in June in the American Journal of Human Genetics. Similarly, low scores track with having PTEN-related conditions that are severe or appear at a young age.

By comparing mutations in individuals with PTEN-linked traits and those in controls, the researchers also found that fitness scores can predict whether a mutation is likely to lead to a PTEN-related condition.

Together, these findings suggest that abundance and fitness scores may help predict the consequences of PTEN mutations, the researchers say.

The team also split single amino acid changes into three classes based on the severity of their effects on protein function and abundance.

The most severe mutations are linked to a higher likelihood of cancer diagnosis by age 35 compared with the least severe mutations, the researchers found. Greater severity also tracks with an increased likelihood of tumor-like growths.

However, the severity of the variants effects is not tied to a persons likelihood of having autism or developmental delay. This suggests that even a small decrease in PTEN activity may be enough to significantly increase the odds of having a neurodevelopmental condition, the researchers say.

The analysis may help tease apart PTEN mutations different effects, the researchers say. It may also help researchers identify the mutations most likely to play a role in autism and prioritize them for further research.

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Scores forecast effects of mutations in autism gene - Spectrum

Herd Immunity Is A Distant Dream- Antibodies May Disappear From An Individual’s Body Within Weeks – Inventiva

It will take around five months for the US, 22 months for the UK, and about one year in Italy for the people to attain herd immunity.

Now if you are completely oblivious to the fact of what herd immunity is, let us help you out. When a persons immune system is attacked with an unknown virus, the antibody production starts at a mass level. When the person recovers from the ailment, and immunity is developed known as the herd immunity. So for the herd immunity to develop as a whole, in a population of about 100 percent, about 80 percent of people have to be attacked with the same virus so that they can produce rapid antibodies.

The novel coronavirus continues to spread at an alarming speed and has infected near 12 million individuals. There is, while the pros are studying more about the operation of the contagion with each day. The fresh price of research has suggested that achieving a level of herd immunity among the crowd can be pretty difficult to attain in a few weeks or even months. While there is an ongoing debate going on among experts, most of them are split about the decision or the time limit as to when shall herd immunity be the only option among crowds. It is surely an achievable foot but it will take time to happen as more and more population are suspected to be tested as positive.

In a study performed in Belgium, scientists assessed the feasibility of creating herd resistance in a population without burdening the ICUs. The investigators used an online tool out of about-the-curve. Net along with also the SIR (Susceptible-Infected-Recovered) version for the spread of illness to estimate that without burdening the ICUs, it might take about 5 weeks to the US, 22 weeks to the UK and roughly a year for Italy to grow herd immunity.

The team works on human genetics, bioinformatics, AI, and machine learning. Besides, he teaches bioinformatics focusing on approaches in biology.

The UK had suggested the idea of herd immunity when the number of cases improved in the nation, but there was a lockdown set in place. The research is still in development and peers are asked to review it before it can be sent to the officials.

Its thought that herd immunity could be achieved for specific ailments when most cases have grown immune and 40 percent of the populace is infected with the disease. But in the majority of cases at 80 to 90 percent of the populace should grow immunity (through vaccination or becoming infected) to halt the illness from spreading farther. Experts around the globe hoped to go in effect to allow its contagion, for the novel coronavirus.

In a recent study which is conducted in Spain, about only 5% of the people have developed protective antibodies for the novel coronavirus. But this is completely on the papers and not published yet. Since the figures were drawn on a previously based study, scientists are still counting the number of people who are yet to develop rapid antibodies inside them. It is even suspected that 40 percent of the people are slowly healing without having to develop symptoms.

The study underlines that although Spain is still one of those nations that are worst-hit by the coronavirus from the entire world, 95 percent of its inhabitants are prone to the book coronavirus. The report further reads, Spain is taken as an example since the extreme outbreak of the coronavirus pandemic happened initially at this place. Now that the curve is flat, scientists are finding it that if the population have achieved levels of herd immunity or not. At the Moment, herd resistance is hard to reach without accepting the security damage of deaths in the vulnerable people and overburdening of health programs

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Herd Immunity Is A Distant Dream- Antibodies May Disappear From An Individual's Body Within Weeks - Inventiva

Explained: A new calculation to find your dogs age in human years – The Indian Express

Written by Kabir Firaque, Mehr Gill | New Delhi | Updated: July 9, 2020 7:34:11 am There exists a very simple thumb rule, used frequently over the years. The new research, however, has described it as a myth

Dogs live shorter lives than humans, and so a six-year-old dog is at a far later stage of its life than a six-year-old child. A dog can even be a grandparent at age six. What, then, is its age in human years? New research, published in the journal Cell Systems has come up with a formula and a graph to determine that.

Was there not a formula already?

There exists a very simple thumb rule, used frequently over the years. The new research, however, has described it as a myth. According to the popular rule, you multiply a dogs age by 7, and you supposedly get its equivalent age in human years: For example, a four-year-old dog is 28 in human years. Only, its not so simple.

Why not?

The new research, which is based on epigenetics, has found the comparison between human years and dog years is not perfectly linear which would have been the case had the 1:7 thumb rule been reliable. The relationship, in fact, follows the red curve shown in the figure.

How can I use this curve to determine my dogs age in human years?

First, find your dogs age along the horizontal (X) axis. Suppose your dog is four years old. Locate 4 on the horizontal axis, then trace your finger upwards until you reach the red curve. From that point, move left towards the vertical (Y) axis, where you have human years (illustrated with Tom Hanks at various ages). Your finger will touch the vertical axis at, in this case, 52 years.

So, a four-year-old dog is equivalent in physiological age to a 52-year-old Tom Hanks (or any 52-year-old human). This is almost twice as much the age you would get (28) if you followed the 1:7 thumb rule.

What is the basis of this new calculation?

It is based on molecular changes in the human genome and dog genome over time. Researchers at the University of California at San Diego analysed patterns over time in methylation a term that refers to specific chemical changes in the genome.

This is the field that is known as epigenetics, which studies chemical modifications that influence which genes are off or on, without altering the original genetic sequence itself. The new formula, the researchers said, provides a new epigenetic clock for determining the age of a cell, tissue or organism.

How did the researchers derive the formula?

The UC San Diego team had previously published epigenetic clocks for humans. For the new study, they collaborated with dog genetics experts at UC Davis and the US National Human Genome Research Institute. They analysed blood samples from 105 Labrador retrievers for changes with age.

Only Labradors?

Indeed, that is one limitation of the new epigenetic clock, acknowledged by senior author Trey Ideker himself. (The first author is Tina Wang, Idekers former graduate student, who first suggested the idea for such a study.) In a statement, Ideker acknowledged that the new epigenetic clock was developed using a single breed of dog, and some dog breeds are known to live longer than others. More research will be needed, he said.

Will it work for my dog if it is not a Labrador?

Ideker said it is accurate for humans and mice, as well as Labrador retrievers. He predicts that the clock will apply to all dog breeds. As such, it may provide a useful tool for veterinarians and even for evaluating anti-ageing interventions, the researchers suggest.

How so?

There are a variety of anti-ageing interventions in the market, with some of these standing on a more solid scientific foundation than others. But, as Ideker noted in the statement, how do you know if a product will truly extend your life without waiting 40 years or so?

If you refer to the new epigenetic clock, you need not wait, he suggested. What if you could measure your age-associated methylation patterns before, during and after the intervention to see if its doing anything?

The Indian Express is now on Telegram. Click here to join our channel (@indianexpress) and stay updated with the latest headlines

For all the latest Explained News, download Indian Express App.

The Indian Express (P) Ltd

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Explained: A new calculation to find your dogs age in human years - The Indian Express

SETI in the News Media Roundup May 16 June 30, 2020 – SETI Institute

Martian Moons Orbit Hints at an Ancient Ring of Mars

Scientists from the SETI Institute and Purdue University have found that the only way to produce Deimoss unusually tilted orbit is for Mars to have had a ring billions of years ago. While some of the more massive planets in our solar system have giant rings and numerous big moons, Mars only has two small, misshapen moons, Phobos and Deimos. Although these moons are small, their peculiar orbits hide important secrets about their past.

Researchers from the University of California Berkeley and other organizations, including the SETI Institute, released the most extensive collection of images showing debris discs around young stars, providing a glimpse of what our solar system might have looked like when its planets were forming. The images were part of data collected over four years by the Gemini Planet Imager (GPI), located on the Gemini South Telescope in Chile.

Citizen science pioneers recently made two contributions to a better knowledge of outer space. Backyard astronomers of the SETI Institute and Unistellar network conducted in April citizen science observations, and their discoveries will improve our understanding of asteroids and exoplanets. Thanks to their work, we know precisely the location of the main-belt asteroid 2000 UD52 and have confirmed an exoplanet transit of Qatar-1b.

Its anyones guess how many alien civilizations could be out in the cosmos. Experts recently weighed in with numbers ranging from 36 to a thousand.

According to a new analysis from scientists at the University of Nottingham, we dont have a lot of alien company. On June 15, two researchers published a paper in the Astrophysical Journal arguing that the Milky Way which sports about 250 billion stars could host as few as 36 alien societies. Thats a small number, and rather less than the number of races that have appeared in Star Trek. The authors supplement their piddling tally with a second, more generous analysis in which they say that, OK, the count might be as many as a thousand. (Seth Shostak, SETI Institute Senior Astronomer)

Frank Drake, who recently turned 90, is a pioneer in the search for extraterrestrial life (SETI). 60 years ago, in 1960, he used an 85-foot radio telescope at the National Radio Astronomy Observatory (NRAO) in Green Bank, West Virginia, to make humanitys first attempt to detect interstellar radio transmissions.

He was the first to probe the skies in an unprecedented way in an experiment he called Project Ozma. Drake was looking for signs of cosmic company: the presence of other intelligent beings on planets around other stars. (Seth Shostak)

A historic piece of intergalactic communication will soon be ready for our listening pleasure.

A message that was first used in an attempt to contact intelligent life is now being turned into music. That's right, if you thought you'd seen it all when it comes to clever sampling and creative audio to MIDI conversions, Australian electronic duo,The Avalanches, are about to take things a step further.

It's unknown whether Frank Drake, creator of the 1974 Arecibo Message, envisioned his work being turned into a song several decades later, but that is exactly what's been teased in The Avalanches' latest post. (EDM.com)

Check out Weekly Space Hangout with astrophysicist Dana Backman, who manages the NASA Airborne Astronomy Ambassadors (AAA) program for the SETI Institute.

Rock from outer space is usually referring to a solid object, but not in this case. Researchers recently announced receiving radio transmissions from space in the form of classic rock music.

Expressing excitement over what could be a landmark discovery in the search for extraterrestrial life, scientists at the SETI Institute announced Tuesday they had received a mysterious radio transmission from space that repeats 50-minute intervals of nonstop classic rock blocks. We detected a signal emanating from hundreds of thousands of lightyears away that, once deciphered, we realized was all the best hits from Zeppelin, Aerosmith, and the Doors in a back-to-back commercial-free format, said SETI researcher Duane Hess, confirming that the transmission could potentially originate from an alien civilization of die-hard 60s, 70s, and 80s rock fans. (The Onion, satirical news)

In a recent Reddit Ask-Me-Anything (AMA), Pascal Lee of the SETI Institute and NASAs Haughton-Mars Project at NASA Ames Research Center described genetic testing on samples from beneath the surface as the best way to find alien life on Mars.

The only way to establish that life found on Mars is alien would be to do genetics on it and show that it does not belong to Earth's Tree of Life. In order to do genetics on it, we have to find it alive (or dead only very recently; not fossilized), he explained.

Until we explore the interiors of Mars' volcanoes (lava tubes) and/or drill deep into the Martian subsurface, we are unlikely to find any signature of life we can establish as alien, which is the main point of the search to begin with, he stated. No amount of fossil finding at the surface of Mars will tell you for sure that you've found alien life.

Big Picture Science

Laughing rats, sorrowful elephants, joyful chimpanzees.The more carefully we observe, and the more we learn about animals, the closer their emotional lives appear to resemble our own.Most would agree that we should minimize the physical suffering of animals, but should we give equal consideration to their emotional stress?Bioethicist Peter Singer weighs in. Meanwhile, captivity that may be ethical: How human-elephant teamwork in Asia may help protect an endangered species. Join guests Peter Singer, Frans de Waal, Jacob Shell and Kevin Schneider as we take a look at universal emotions in Animals Like Us.

Crowded subway driving you crazy? Sick of the marathon-length grocery store line? Wish you had a hovercraft to float over traffic? If you are itching to hightail it to an isolated cabin in the woods, remember, we evolved to be together. Humans are not only social, were driven to care for one another, even those outside our immediate family. Join guests Adam Rutherford, Patricia Churchland and Mark Moffett as we look at some of the reasons why this is so from the increase in valuable communication within social groups to the power of the hormone oxytocin.Plus, how our willingness to tolerate anonymity, a condition which allows societies to grow, has a parallel in ant supercolonies in Let's Stick Together.

Sexist snow plowing?Data that guide everything from snow removal schedules to heart research often fail to consider gender.In these cases, reference man stands in for average human.Human bias also infects artificial intelligence, with speech recognition triggered only by male voices and facial recognition that cant see black faces.Join guests Caroline Criado-Perez, Kade Crockford and Amy Webb as we question the assumptions baked into these numbers and algorithms in Skeptic Check: Data Bias.

While citizens take to the streets to protest racist violence, the pandemic has its own brutal inequities. Black, Latino, and Native American people are bearing the brunt of COVID illness and death. Join guests Marcella Nunez Smith, Utibe Essien, Nina Jablonski, Robert Sapolsky and Harold Frazier as we look at the multitude of factors that contribute to this disparity, most of which existed long before the pandemic. Also, how the Cheyenne River Sioux tribe maintained their coronavirus safeguards in defiance of the South Dakota governor. And, the biological reasons why we categorize one another by skin color in Race and COVID.

Some safeguards against COVID-19 dont require a medical breakthrough. Join guests Cody Cassidy, Nina Jablonski and Eti Ben Simon as they discuss catching sufficient Zs, sending viruses down the drain and how your first line of defense, your skin, is also neglected in Soap, Skin, Sleep.

Will Alexa laugh at your jokes or groan at your puns? In this episode, find out whats involved in tickling A.I.s funny bone with guest Julia Rayz, Steve Adler, Doug Vakoch and Richard Wrangham, as well as an interstellar communication challenge in Gained in Translation.

When can we expect a COVID vaccine? Guests Nigel Brown, Ian Haydon, Bonnie Maldonado and Paul Offit discuss timelines, how it would work, whos involved and the role of human challenge trials in Vaccine, When?

SETI Live

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SETI in the News Media Roundup May 16 June 30, 2020 - SETI Institute

Idorsia announces positive results in the second Phase 3 study of daridorexant – GlobeNewswire

Allschwil, Switzerland July 6, 2020Idorsia Ltd (SIX: IDIA) today announced positive top-line results of the second pivotal Phase 3 study investigating 10 and 25 mg doses of its dual orexin receptor antagonist, daridorexant, in 924 adult and elderly patients (39.3% 65 years) with insomnia. The study confirms the findings of the first pivotal study, demonstrating efficacy of treatment with daridorexant on objective and subjective sleep parameters and showed positive effects on daytime functioning, with patients reporting no morning sleepiness and no evidence of rebound or withdrawal symptoms upon treatment discontinuation.

On April 20, 2020, the company reported (media release) the results of the first pivotal study with daridorexant where both 25 and 50 mg daridorexant significantly improved both sleep onset and sleep maintenance. Daridorexant 50 mg also significantly improved daytime functioning. All results were sustained over the 3 months of the trial.

In the second study, daridorexant 25 mg significantly improved sleep maintenance as measured objectively in a sleep lab by polysomnography. Daridorexant 25 mg also significantly improved subjective total sleep time as measured daily with a patient diary at home. The results were statistically significant at month 1 and at month 3 for these sleep measures, showing sustained benefit.

Furthermore, the effect of daridorexant 25mg on sleep onset and daytime functioning were numerically consistent with the effects seen in the first study. However, due to the control of the Type 1 error rate for 16 comparisons, these endpoints despite the low p values did not reach statistical significance.

The 10 mg dose of daridorexant showed numerical improvements, across all efficacy measures, of a smaller magnitude than observed on 25 mg, none of which reached statistical significance.

The results of the two large pivotal studies, testing daridorexant at three doses from 10 to 50 mg, now provide a deep understanding of its efficacy and tolerability profile. Furthermore, the similar design of the two Phase 3 studies allows for the twogroups of25 mgandplaceboto be pooledanda pre-planned analysis to be made. This pooled analysis willfurthercharacterize the effect of daridorexant.

Guy Braunstein, MD and Head of Global Clinical Development of Idorsia, commented:

I want to start with a thank you to the study participants, investigators and their support staff, and the Idorsia team for delivering another comprehensive set of robust data. I am delighted to see the replicated effect of 25 mg of daridorexant in this large confirmatory study. The consistency of the treatment effect across both studies is remarkable. I believe the fact that daridorexant improves daytime functioning is a real breakthrough for patients. I am looking forward to the integration of all aspects of the program, including the pooled data, the long-term extension data, the clinical pharmacology program, and all that we can learn from the patient reported outcome instruments. There is a lot of work for us to do as we interact with the health authorities and share the data with the scientific community.

About safety in the studyThe safety profile was consistent with the results of the first study. Treatment-emergent adverse events (TEAEs) during the double-blind study period were reported in 38.2% and 39.3% of the patients treated with 10 and 25 mg daridorexant, respectively (32.7% for placebo). The most frequent TEAEs reported over 3% incidenceand higher on 25 mg of daridorexant than placebo were nasopharyngitis, headache, somnolence and fatigue. The number of patients experiencing serious adverse events was low and balanced across treatment groups (10 mg, 3 patients; 25 mg, 3 patients; placebo, 4 patients). Based on independent blinded adjudication committee assessment, the number of patients reporting excessive daytime sleepiness as AE was low (10 mg, 1 patient; 25 mg, 4 patients; and placebo, 1 patient); 3 patients had AEs of special interest related to sleep paralysis and hallucination. No events denoting cataplexy-like events were reported or adjudicated. There was no next-morning residual effectas assessed every morning by the patients using a visual analog scale; 2 patients reported suicidal ideation (10 mg, 1 patient; 25 mg, 1 patient) with clear alternative causes; no suicide or self-injury were observed. There was no evidence of rebound insomnia, and no withdrawal symptoms upon discontinuation.

EmmanuelMignot,MD and Professor of Psychiatry and Behavioral Sciences at Stanford University, commented:The daridorexant program demonstrates the full potential of orexin receptor antagonism excellent effect and a good safety profile. It is exciting to see this, 20 years after the discovery of the role of orexin in sleep regulation. For me, the improved daytime functioning seen with daridorexant is most impressive. What is important to patients is not only to improve their night sleep but also how they feel during the day. By measuring the benefits of the drug through the day as well as through the night, the program has put patients back at the center of the equation and raised the standard for what we need to see with sleep medications. This ensures the patient need is at the center of prescription decisions when treating insomnia.

Jean-Paul Clozel, MD and Chief Executive Officer of Idorsia, commented:I was stunned by the excellent results of the first study with daridorexant, this time Im struck by the consistency of the efficacy results, including daytime functioning and the safety profile. I am very proud of the great science behind daridorexant and that Idorsia has designed and executed such a comprehensive program, focused on patients, in such a short time. I am convinced that with daridorexant, Idorsia has a unique drug which is going to have a disruptive impact on the insomnia market. The whole company is united in the effort to file the NDA with the US FDA around the end of this year and to prepare for a successful launch. There is certainly a lot of work to be done, but we are already making great progress on all fronts.

Detailed results of the Phase 3 studies will be made available through scientific disclosure at upcoming congresses and in peer-reviewed publications.

About the Phase 3 registration program

The Phase 3 registration program comprises two confirmatory studies of 3-month duration, together with a long-term extension study. Both pivotal studies are complete, having enrolled around 1,850 patients with insomnia at over 160 sites across 18 countries. As insomnia often presents later in life, around 40% of the recruited population was aged 65 years or older. The confirmatory multi-center, double-blind, randomized, placebo-controlled, parallel-group, polysomnography studies investigated three doses of daridorexant (10 mg, 25 mg, and 50 mg) on sleep and daytime functioning parameters, objectively in a sleep lab by polysomnography and subjectively with a daily patient diary at home. The impact of insomnia on patients daytime functioning was measured daily using the sleepiness domain score from the Insomnia Daytime Symptoms and Impacts Questionnaire (IDSIQ) a Patient Reported Outcome (PRO) instrument, validated according to the US Food and Drug Administration (FDA) Guidance for Industry. 806 patients decided to continue treatment in the ongoing 40-week extension study which will measure the effect of all three doses vs. placebo, generating data for long-term treatment of insomnia.

Investor webcastOn April 20, 2020, the company held an investor webcast to discuss the results of the first Phase 3 study with daridorexant. On that occasion, Martine Clozel, MD, Chief Scientific Officer presented a brief overview of the tailored drug discovery efforts that led to the synthesis of daridorexant. This was followed by Guy Braunstein providing an overview of insomnia, the objectives of the Phase 3 program, the methodologies used to measure the effect of daridorexant on patients with insomnia, and the results of the first study. This webcast is available for replay on the corporate website.

The company will hold an investor conference call and webcast to discuss the results of the second Phase 3 study with daridorexant. On the call, Guy Braunstein will present the study results, followed by a Q&A session with Jean-Paul Clozel, Guy Braunstein, and Martine Clozel.

Date: Monday July 6, 2020Time: 14:00 CEST | 13:00 BST | 08:00 EDT

Webcast participants should visit Idorsia's website http://www.idorsia.com 10-15 minutes before the webcast is due to start.

Conference call participants should start calling the number below 10-15 minutes before the conference is due to start.

Dial-in CH: +41 (0)44 580 65 22 / UK: +44 20 3009 2470 / US: +1 (877) 423-0830PIN: 24890393#

Notes to the editor

About insomniaInsomnia is a condition of overactive wake signaling that can have a profound effect on the lives of patients. Insomnia can be defined as difficulty falling asleep and / or staying asleep, occuring at least three times a week for a minimum of three months.

It is estimated that as many as one in ten people suffer from insomnia and its impact is often underestimated. In reality, it can be a distressing condition that can impair quality of life. Sleepless nights can leave people feeling irritable and out of sorts this may affect many aspects of daily life, from studying and employment to social activities and relationships. People who suffer from insomnia may lack the energy or motivation to exercise or to take part in social activities. It can also have a significant economic impact as it increases the risk of accident and injury on the road or in the workplace, and is a leading cause of absenteeism and reduced productivity at work. People with insomnia are more likely to experience feeling down or depressed, lack concentration, and suffer from poor energy levels during the day compared with people who sleep well. In addition, worrying about sleep can cause stress and may lead to negative thought patterns which may in turn make it more difficult to sleep, setting up a vicious circle. Chronic insomnia is associated with cardiovascular and cerebrovascular diseases, and increased mortality.

The goal of treatments for insomnia is to improve sleep quality and quantity, as well as reducing insomnia-related impaired daytime functioning, while avoiding adverse events and next morning residual effect. Current treatment of insomnia includes cognitive behavioral therapy, sleep hygiene recommendations, and pharmacotherapy. The most widely prescribed products on the market that are indicated for insomnia enhance the effects of gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Such medications are only approved for short-term use and are associated with side effects such as next-morning residual effects, anterograde amnesia, and risk of tolerance and dependence.

About the orexin systemWake and sleep signaling is regulated by intricate neural circuitry in the brain. One key component of this process is the orexin system, which helps promote and consolidate wakefulness. There are two forms of orexin neuropeptides Orexin A and OrexinB. Orexin promotes wakefulness through its receptors OX1R and OX2R. In combination, these neuropeptides and receptors comprise the orexin system. The orexin system stimulates target neurons in the wake system leading to the release of several chemicals (Dopamine, Serotonin, Histamine, Acetylcholine, Norepinephrine) which promote wakefulness. Under normal circumstances, orexin levels rise throughout the day as wakefulness is promoted and then consolidated and fall at night. Overactivity of the orexin system is thought to be an important driver of insomnia.

Idorsias research team has been working on the science of orexin and orexin receptors since they were first described in 1998. The teams initial work led to the conclusion that antagonism of the orexin system was the key to preserving a natural sleep architecture for patients with insomnia. With this as the target the team started to design a dual antagonist with a rapid effect, and a duration of action sufficient for the night but short enough to avoid any negative residual activity the following morning at optimally effective doses.

About dual orexin receptor antagonismDual orexin receptor antagonists or DORAs are an entirely different approach to treating insomnia than previous drug classes, turning down overactive wakefulness by blocking the activity of orexin. DORAs specifically target the orexin system by competitively binding with both receptors and thereby reversibly blocking the activity of orexin. It is hypothesized that blocking orexin receptors reduces the downstream activity of the other wake promoting neurotransmitters that are overactive in insomnia, leading to the clinical efficacy demonstrated by orexin receptor antagonists.

Data supporting daridorexant in insomnia Results of the first Phase 3 study, investigating daridorexant doses 25 and 50mg, were reported in April 2020. The study demonstrated efficacy of treatment with daridorexant on objective and subjective sleep parameters and daytime functoning with no residual effect in the morning, and no evidence of rebound or withdrawal symptoms upon treatment discontinuation.

Daridorexant at both 25 and 50 mg significantly improved sleep onset and sleep maintenance as measured objectively in a sleep lab by polysomnography. Daridorexant also significantly improved subjective total sleep time as measured daily with a patient diary at home. The results were consistently statistically significant at month 1 and at month 3, indicating sustained benefit. Furthermore, treatment with daridorexant improved patients daytime functioning from baseline at month 1 and month 3.

The rate of adverse events was comparable between placebo and daridorexant at both treatment doses. Treatment-emergent adverse events (TEAEs) during the double-blind study period were reported in 37.7% and 37.7% of the patients treated with 25 and 50 mg daridorexant, respectively (34.0% for placebo). The most frequent TEAE reported over 3% incidence and higher than placebo was nasopharyngitis, headache.

Prior to the Phase 3 program, the safety and efficacy of daridorexant in adult and elderly patients with insomnia was evaluated in a comprehensive Phase 2 program, comprising two studies, one of which included zolpidem 10 mg as an active reference. Both studies showed the desired effect on sleep maintenance and onset, with a significant dose-response relationship; treatment was generally well tolerated.

A comprehensive clinical pharmacology program is being conducted totaling approximately 20 studies and including, amongst others, studies assessing abuse liability, drug-drug interactions, next-morning driving, the effect of daridorexant on respiratory function in patients with chronic obstructive pulmonary disease (COPD) or obstructive sleep apnea (OSA), and the pharmacokinetics of daridorexant in patients with liver and renal impairment.

EmmanuelMignot,MD and Professor of Psychiatry and Behavioral Sciences at Stanford University

He is a former student of the Ecole Normale Superieure (Ulm, Paris, France) and received his M.D. and Ph.D. from Paris V and VI University in France. He practiced medicine in France for several years before joining Stanford as a faculty member in 1991 and was named Director of the Stanford Center for Narcolepsy in 1993. Dr. Mignot was named the Craig Reynolds Professor of Psychiatry and Behavioral Sciences in 2001. He served as the Director of the Stanford Center of Sleep Sciences and Medicine from 2009 to 2019.

Dr. Mignot is internationally recognized for discovering the cause of narcolepsy. His findings led to the development of new hypnotics that block the hypocretin (orexin) receptor and is likely to have other therapeutic applications as well. His research also demonstrated that narcolepsy is a selective autoimmune disease of the hypocretin system showing the involvement of molecular mimicry in humans with influenza A.

He has received numerous research grants and honors including National Sleep Foundation and National Institute of Health Research Awards, Howard Hughes Medical Institute Investigator and McKnight Neuroscience awards, the Narcolepsy Network professional service award, the Drs. C. and F. Demuth 11th Award for Young Investigators in the Neurosciences, the WC Dement Academic Achievement Award in sleep disorders medicine, the CINP and ACNP awards in neuropharmacology and the Jacobaeus prize.

Dr. Mignot is an elected member of the Association of American Physicians, the Institute of Medicine, and of the National Academy of Sciences (USA). He is the co-author of more than 200 original scientific publications, and he serves on the editorial board of scientific journals in the field of sleep and biology research. Dr. Mignot is an active member of several professional and governmental organizations. He has served as President of the Sleep Research Society, Chair of the National Center on Sleep Disorders Research Advisory board of the National institutes of Health, and Chair of the Board of Scientific Counselors of the National Institute of Mental Health.

Most of Dr. Mignot's current research focuses on the neurobiology, genetics and immunology of narcolepsy, a disorder caused by hypocretin (orexin) cell loss, with indirect interest in the neuroimmunology of other brain disorders. His laboratory uses state of the art human genetics techniques, such as genome wide association, exome or whole genome sequencing in the study of human sleep and sleep disorders, with parallel studies in animal models. His laboratory is also interested in web-based assessments of sleep disorders, computer-based processing of polysomnography (PSG), and outcomes research. Dr. Mignot serves as a consultant to Idorsia.

References

About IdorsiaIdorsia Ltd is reaching out for more - We have more ideas, we see more opportunities and we want to help more patients. In order to achieve this, we will develop Idorsia into one of Europes leading biopharmaceutical companies, with a strong scientific core.

Headquartered in Switzerland - a biotech-hub of Europe - Idorsia is specialized in the discovery and development of small molecules, to transform the horizon of therapeutic options. Idorsia has a broad portfolio of innovative drugs in the pipeline, an experienced team, a fully-functional research center, and a strong balance sheet the ideal constellation to bringing R&D efforts to business success.

Idorsia was listed on the SIX Swiss Exchange (ticker symbol: IDIA) in June 2017 and has over 800 highly qualified specialists dedicated to realizing our ambitious targets.

For further information, please contactAndrew C. WeissSenior Vice President, Head of Investor Relations & Corporate CommunicationsIdorsia Pharmaceuticals Ltd, Hegenheimermattweg 91, CH-4123 Allschwil+41 58 844 10 10www.idorsia.com

The above information contains certain "forward-looking statements", relating to the company's business, which can be identified by the use of forward-looking terminology such as "estimates", "believes", "expects", "may", "are expected to", "will", "will continue", "should", "would be", "seeks", "pending" or "anticipates" or similar expressions, or by discussions of strategy, plans or intentions. Such statements include descriptions of the company's investment and research and development programs and anticipated expenditures in connection therewith, descriptions of new products expected to be introduced by the company and anticipated customer demand for such products and products in the company's existing portfolio. Such statements reflect the current views of the company with respect to future events and are subject to certain risks, uncertainties and assumptions. Many factors could cause the actual results, performance or achievements of the company to be materially different from any future results, performances or achievements that may be expressed or implied by such forward-looking statements. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those described herein as anticipated, believed, estimated or expected.

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Idorsia announces positive results in the second Phase 3 study of daridorexant - GlobeNewswire

Human genetics – Wikipedia

Human genetics is the study of inheritance as it occurs in human beings. Human genetics encompasses a variety of overlapping fields including: classical genetics, cytogenetics, molecular genetics, biochemical genetics, genomics, population genetics, developmental genetics, clinical genetics, and genetic counseling.

Genes are the common factor of the qualities of most human-inherited traits. Study of human genetics can answer questions about human nature, can help understand diseases and the development of effective disease treatment, and help us to understand the genetics of human life. This article describes only basic features of human genetics; for the genetics of disorders please see: medical genetics.

Inheritance of traits for humans are based upon Gregor Mendel's model of inheritance. Mendel deduced that inheritance depends upon discrete units of inheritance, called factors or genes.[1]

Autosomal traits are associated with a single gene on an autosome (non-sex chromosome)they are called "dominant" because a single copyinherited from either parentis enough to cause this trait to appear. This often means that one of the parents must also have the same trait, unless it has arisen due to an unlikely new mutation. Examples of autosomal dominant traits and disorders are Huntington's disease and achondroplasia.

Autosomal recessive traits is one pattern of inheritance for a trait, disease, or disorder to be passed on through families. For a recessive trait or disease to be displayed two copies of the trait or disorder needs to be presented. The trait or gene will be located on a non-sex chromosome. Because it takes two copies of a trait to display a trait, many people can unknowingly be carriers of a disease. From an evolutionary perspective, a recessive disease or trait can remain hidden for several generations before displaying the phenotype. Examples of autosomal recessive disorders are albinism, cystic fibrosis.

X-linked genes are found on the sex X chromosome. X-linked genes just like autosomal genes have both dominant and recessive types. Recessive X-linked disorders are rarely seen in females and usually only affect males. This is because males inherit their X chromosome and all X-linked genes will be inherited from the maternal side. Fathers only pass on their Y chromosome to their sons, so no X-linked traits will be inherited from father to son. Men cannot be carriers for recessive X linked traits, as they only have one X chromosome, so any X linked trait inherited from the mother will show up.

Females express X-linked disorders when they are homozygous for the disorder and become carriers when they are heterozygous. X-linked dominant inheritance will show the same phenotype as a heterozygote and homozygote. Just like X-linked inheritance, there will be a lack of male-to-male inheritance, which makes it distinguishable from autosomal traits. One example of an X-linked trait is CoffinLowry syndrome, which is caused by a mutation in ribosomal protein gene. This mutation results in skeletal, craniofacial abnormalities, mental retardation, and short stature.

X chromosomes in females undergo a process known as X inactivation. X inactivation is when one of the two X chromosomes in females is almost completely inactivated. It is important that this process occurs otherwise a woman would produce twice the amount of normal X chromosome proteins. The mechanism for X inactivation will occur during the embryonic stage. For people with disorders like trisomy X, where the genotype has three X chromosomes, X-inactivation will inactivate all X chromosomes until there is only one X chromosome active. Males with Klinefelter syndrome, who have an extra X chromosome, will also undergo X inactivation to have only one completely active X chromosome.

Y-linked inheritance occurs when a gene, trait, or disorder is transferred through the Y chromosome. Since Y chromosomes can only be found in males, Y linked traits are only passed on from father to son. The testis determining factor, which is located on the Y chromosome, determines the maleness of individuals. Besides the maleness inherited in the Y-chromosome there are no other found Y-linked characteristics.

A pedigree is a diagram showing the ancestral relationships and transmission of genetic traits over several generations in a family. Square symbols are almost always used to represent males, whilst circles are used for females. Pedigrees are used to help detect many different genetic diseases. A pedigree can also be used to help determine the chances for a parent to produce an offspring with a specific trait.

Four different traits can be identified by pedigree chart analysis: autosomal dominant, autosomal recessive, x-linked, or y-linked. Partial penetrance can be shown and calculated from pedigrees. Penetrance is the percentage expressed frequency with which individuals of a given genotype manifest at least some degree of a specific mutant phenotype associated with a trait.

Inbreeding, or mating between closely related organisms, can clearly be seen on pedigree charts. Pedigree charts of royal families often have a high degree of inbreeding, because it was customary and preferable for royalty to marry another member of royalty. Genetic counselors commonly use pedigrees to help couples determine if the parents will be able to produce healthy children.

A karyotype is a very useful tool in cytogenetics. A karyotype is picture of all the chromosomes in the metaphase stage arranged according to length and centromere position. A karyotype can also be useful in clinical genetics, due to its ability to diagnose genetic disorders. On a normal karyotype, aneuploidy can be detected by clearly being able to observe any missing or extra chromosomes.[1]

Giemsa banding, g-banding, of the karyotype can be used to detect deletions, insertions, duplications, inversions, and translocations. G-banding will stain the chromosomes with light and dark bands unique to each chromosome. A FISH, fluorescent in situ hybridization, can be used to observe deletions, insertions, and translocations. FISH uses fluorescent probes to bind to specific sequences of the chromosomes that will cause the chromosomes to fluoresce a unique color.[1]

Genomics is the field of genetics concerned with structural and functional studies of the genome.[1] A genome is all the DNA contained within an organism or a cell including nuclear and mitochondrial DNA. The human genome is the total collection of genes in a human being contained in the human chromosome, composed of over three billion nucleotides.[2] In April 2003, the Human Genome Project was able to sequence all the DNA in the human genome, and to discover that the human genome was composed of around 20,000 protein coding genes.

Medical genetics is the branch of medicine that involves the diagnosis and management of hereditary disorders. Medical genetics is the application of genetics to medical care. It overlaps human genetics, for example, research on the causes and inheritance of genetic disorders would be considered within both human genetics and medical genetics, while the diagnosis, management, and counseling of individuals with genetic disorders would be considered part of medical genetics.

Population genetics is the branch of evolutionary biology responsible for investigating processes that cause changes in allele and genotype frequencies in populations based upon Mendelian inheritance.[3] Four different forces can influence the frequencies: natural selection, mutation, gene flow (migration), and genetic drift. A population can be defined as a group of interbreeding individuals and their offspring. For human genetics the populations will consist only of the human species. The HardyWeinberg principle is a widely used principle to determine allelic and genotype frequencies.

In addition to nuclear DNA, humans (like almost all eukaryotes) have mitochondrial DNA. Mitochondria, the "power houses" of a cell, have their own DNA. Mitochondria are inherited from one's mother, and their DNA is frequently used to trace maternal lines of descent (see mitochondrial Eve). Mitochondrial DNA is only 16kb in length and encodes for 62 genes.

The XY sex-determination system is the sex-determination system found in humans, most other mammals, some insects (Drosophila), and some plants (Ginkgo). In this system, the sex of an individual is determined by a pair of sex chromosomes (gonosomes). Females have two of the same kind of sex chromosome (XX), and are called the homogametic sex. Males have two distinct sex chromosomes (XY), and are called the heterogametic sex.

Sex linkage is the phenotypic expression of an allele related to the chromosomal sex of the individual. This mode of inheritance is in contrast to the inheritance of traits on autosomal chromosomes, where both sexes have the same probability of inheritance. Since humans have many more genes on the X than the Y, there are many more X-linked traits than Y-linked traits.However, females carry two or more copies of the X chromosome, resulting in a potentially toxic dose of X-linked genes.[4]

To correct this imbalance, mammalian females have evolved a unique mechanism of dosage compensation. In particular, by way of the process called X-chromosome inactivation (XCI), female mammals transcriptionally silence one of their two Xs in a complex and highly coordinated manner.[4]

GeneticChromosomal

[35]

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Human genetics - Wikipedia

Genetic Mutations as a Tool To Predict Lifespan and Fertility – Technology Networks

Differences in the rate that genetic mutations accumulate in healthy young adults could help predict remaining lifespan in both sexes and the remaining years of fertility in women, according to University of Utah Health scientists. Their study, believed to be the first of its kind, found that young adults who acquired fewer mutations over time lived about five years longer than those who acquired them more rapidly.The researchers say the discovery could eventually lead to the development of interventions to slow the aging process.

If the results from this small study are validated by other independent research, it would have tremendous implications, says Lynn B. Jorde, Ph.D., chair of the Department of Human Genetics at U of U Health and a co-author of the study. It would mean that we could possibly find ways to fix ourselves and live longer and better lives.

"Young adults who acquired fewer mutations over time lived about five years longer than those who acquired them more rapidly."

Scientists have long known that DNA damage constantly occurs in the body. Typically, various mechanisms repair this damage and prevent potentially harmful mutations, according to lead and corresponding author Richard Cawthon, M.D., Ph.D., a U of U Health research associate professor of human genetics.

As we get older, these mechanisms become less efficient and more mutations accumulate. Older parents, for instance, tend to pass on more genetic mutations through their germline (egg and sperm) to their children than younger parents.

However, Cawthon and colleagues theorized that these mutations could be a biomarker for rates of aging and potentially predict lifespan in younger individuals as well as fertility in women.

The researchers sequenced DNA from 61 men and 61 women who were grandparents in 41 three-generational families. The families were part of the Centre d'Etude du Polymorphisme Humain (CEPH) consortium, which was central to many key investigations that have contributed toward a modern understanding of human genetics.

The researchers analyzed blood DNA sequences in trios consisting of pairs of grandparents from the first generation and one of their children from the second generation. Thats because germline mutations are passed on to their offspring. Mutations found in the childs blood DNA that were not present in either parents blood DNA were then inferred to have originated in the parents germlines. The researchers were then able to determine which parent each germline mutation came from, and, therefore, the number of such mutations each parent had accumulated in egg or sperm by the time of conception of the child.

Knowing that allowed the researchers to compare each first-generation parent to others of the same sex and estimate their rate of aging.

So, compared to a 32-year-old man with 75 mutations, we would expect a 40-year-old with the same number of mutations to be aging more slowly, Cawthon says. Wed expect him to die at an older age than the age at which the 32-year-old dies.

The scientists found that mutations began to occur at an accelerating rate during or soon after puberty, suggesting that aging begins in our teens.

Some young adults acquired mutations at up to three times the rate of others. After adjusting for age, the researchers determined that individuals with the slowest rates of mutation accumulation were likely to live about five years longer than those who accumulated mutations more rapidly. This is a difference comparable to the effects of smoking or lack of physical activity, Cawthon says.

Women with the highest mutation rates had significantly fewer live births than other women and were more likely to be younger when they gave birth to their last child. This suggests that the high rate of mutation was affecting their fertility.

The ability to determine when aging starts, how long women can stay fertile, and how long people can live is an exciting possibility, Cawthon says. If we can get to a point where we better understand what sort of developmental biology affecting mutation rates is happening during puberty, then we should be able to develop medical interventions to restore DNA repair and other homeostatic mechanisms back to what they were before puberty. If we could do that, its possible people could live and stay healthy much longer.ReferenceCawthon et al. (2020). Germline Mutation Rates in Young Adults Predict Longevity and Reproductive Lifespan. Scientific Reports. DOI: https://doi.org/10.1038/s41598-020-66867-0

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Genetic Mutations as a Tool To Predict Lifespan and Fertility - Technology Networks

Human Genetics Market Analysis with Key Players, Applications, Trends and Forecasts to 2026 – Farmers Ledger

The Human Genetics market report Added by Market Study Report, LLC, enumerates information about the industry in terms of market share, market size, revenue forecasts, and regional outlook. The report further illustrates competitive insights of key players in the business vertical followed by an overview of their diverse portfolios and growth strategies.

The research report on Human Genetics market offers a thorough analysis of this industry vertical, while evaluating all the segments of the market. The study provides significant information concerning the key industry players and their respective gross earnings. Additionally, crucial insights regarding the geographical landscape as well as the competitive spectrum are entailed.

Request a sample Report of Human Genetics Market at:https://www.marketstudyreport.com/request-a-sample/2468209?utm_source=farmersledger&utm_medium=RV

Highlighting the main pointers of the Human Genetics market report:

In-depth analysis of the regional scope of Human Genetics market:

Emphasizing on the competitive spectrum of Human Genetics market:

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Other insights associated with the Human Genetics market research report:

This report considers the below mentioned key questions:

Q.1. What are some of the most favorable, high-growth prospects for the global Human Genetics market?

Q.2. Which products segments will grow at a faster rate throughout the forecast period and why?

Q.3. Which geography will grow at a faster rate and why?

Q.4. What are the major factors impacting market prospects? What are the driving factors, restraints, and challenges in this Human Genetics market?

Q.5. What are the challenges and competitive threats to the market?

Q.6. What are the evolving trends in this Human Genetics market and reasons behind their emergence?

Q.7. What are some of the changing customer demands in the Human Genetics Industry market?

Table of Contents:

Executive Summary: It includes key trends of the Human Genetics market related to products, applications, and other crucial factors. It also provides analysis of the competitive landscape and CAGR and market size of the Human Genetics market based on production and revenue.

Production and Consumption by Region: It covers all regional markets to which the research study relates. Prices and key players in addition to production and consumption in each regional market are discussed.

Key Players: Here, the report throws light on financial ratios, pricing structure, production cost, gross profit, sales volume, revenue, and gross margin of leading and prominent companies competing in the Human Genetics market.

Market Segments: This part of the report discusses about product type and application segments of the Human Genetics market based on market share, CAGR, market size, and various other factors.

Research Methodology: This section discusses about the research methodology and approach used to prepare the report. It covers data triangulation, market breakdown, market size estimation, and research design and/or programs.

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Human Genetics Market Analysis with Key Players, Applications, Trends and Forecasts to 2026 - Farmers Ledger

China Is Collecting DNA From Tens of Millions of Men and Boys, Using U.S. Equipment – The New York Times

The impetus for the campaign can be traced back to a crime spree in the northern Chinese region of Inner Mongolia. For nearly three decades, the police there investigated the rapes and murders of 11 women and girls, one as young as 8. They collected 230,000 fingerprints and sifted through more than 100,000 DNA samples. They offered a $28,000 reward.

Then, in 2016, they arrested a man on unrelated bribery charges, according to the state news media. Analyzing his genes, they found he was related to a person who had left his DNA at the site of the 2005 killing of one of the women. That person, Gao Chengyong, confessed to the crimes and was later executed.

Mr. Gaos capture spurred the state media to call for the creation of a national database of male DNA. The police in Henan Province showed it was possible, after amassing samples from 5.3 million men, or roughly 10 percent of the provinces male population, between 2014 and 2016. In November 2017, the Ministry of Public Security, which controls the police, unveiled plans for a national database.

China already holds the worlds largest trove of genetic material, totaling 80 million profiles, according to state media. But earlier DNA gathering efforts were often more focused. Officials targeted criminal suspects or groups they considered potentially destabilizing, like migrant workers in certain neighborhoods. The police have also gathered DNA from ethnic minority groups like the Uighurs as a way to tighten the Communist Partys control over them.

The effort to compile a national male database broadens those efforts, said Emile Dirks, an author of the report from the Australian institute and a Ph.D. candidate in the department of political science at the University of Toronto. We are seeing the expansion of those models to the rest of China in an aggressive way that I dont think weve seen before, Mr. Dirks said.

In the report released by the Australian institute, it estimated that the authorities aimed to collect DNA samples from 35 million to 70 million men and boys, or roughly 5 percent to 10 percent of Chinas male population. They do not need to sample every male, because one persons DNA sample can unlock the genetic identity of male relatives.

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China Is Collecting DNA From Tens of Millions of Men and Boys, Using U.S. Equipment - The New York Times

Researchers identify environmental components that affect gene expression in cardiovascular disease – The South End

A research team led by Francesca Luca, Ph.D., and Roger Pique-Regi, Ph.D., both associate professors of the Wayne State University Center for Molecular Medicine and Genetics, and of the Department of Obstetrics and Gynecology, has published a study that annotated environmental components that can increase or decrease disease risk through changes in gene expression in 43 genes that could exacerbate or buffer the genetic risk for cardiovascular disease.

The results of the study, whose first authors are Anthony Findley, an M.D./Ph.D. student, and Allison Richards, Ph.D., a research scientist, highlight the importance of evaluating genetic risk in the context of gene-environment interactions to improve precision medicine.

Interpreting Coronary Artery Disease Risk Through GeneEnvironment Interactions in Gene Regulation was published in Genetics, the journal of the Genetics Society of America.

The study, said Dr. Luca, illustrates that combining genome-wide molecular data with large-scale population-based studies is a powerful approach to investigate how genes and the environment interact to influence risk of cardiovascular disease.

By identifying regions of DNA important for endothelial cell response to different common environmental exposures, the researchers discovered that caffeine can influence the risk of cardiovascular disease. The study demonstrates the potentially beneficial and/or detrimental effects of certain environmental exposures on the cardiovascular disease risk differ depending on individual DNA sequence.

The study focused on cardiovascular disease, the research team said, because it is the leading cause of death, both in the United States and worldwide. Also, the disease is highly multifactorial, with large contributions from both environmental and genetic risk factors. By treating endothelial cells under a controlled environment, we can discover how these genetic and environmental risk factors influence each other at the molecular level, she said. Our lab has developed expertise in cardiovascular research, with additional projects using endothelial cells to develop new assays to test the regulatory activity of genetic variants. The approach outlined in this paper can be applied to many different diseases; for example, our lab has also focused on how bacteria in the human gut affect gene expression in the colon, and also on the effect of psychosocial stress on asthma.

While the work identified regions of the genome important for how endothelial cells respond to the environment and can influence the risk of cardiovascular disease, the researchers do not yet know exactly which genetic variants are directly responsible. A former graduate student, Cynthia Kalita, developed an assay to test thousands of genetic variants for gene regulatory activity. The researchers can test the variants discovered in their study using that assay to validate and explore the mechanisms by which they exert their effects, Dr. Luca said. They also are developing computational/statistical methods that can yield better personalized risk scores.

We have extended our approach to study cardiomyocytes, which are the muscle cells of the heart. Healthy heart tissue is difficult to obtain, so we have collaborated with researchers at the University of Chicago to derive cardiomyocytes from stem cells, Dr. Luca said. This will allow us to shift our focus from the vasculature to the heart itself, where we can study diseases like cardiomyopathies and arrhythmias.

As the cost of DNA sequencing continues to decrease, the research teamexpects that genetic testing will play a greater role in preventive health care. To fully realize the potential of precision medicine, we need to consider both genetic and environmental risk factors of disease, and how they interact. While there are already direct-to-consumer tests that prescribe an individualized diet based on DNA, these products currently offer no demonstrated clinical value. However, with very large numbers of individuals for whom we have both DNA sequencing and information on diet and lifestyle, we may one day be able to offer better recommendations.

Other members of the research team include Cristiano Petrini, of the Center for Molecular Medicine and Genetics; Adnan Alazizi, lab manager; Elizabeth Doman, of the Center for Molecular Medicine and Genetics; Alexander Shanku, Ph.D., research scientist; Gordon Davis, of the Center for Molecular Medicine and Genetics; Nancy Hauff, Department of Obstetrics and Gynecology; Yoram Sorokin, M.D., professor of Obstetrics and Gynecology; and Xiaoquan Wen, of the Department of Biostatistics at the University of Michigan.

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Researchers identify environmental components that affect gene expression in cardiovascular disease - The South End

China collects DNA from millions of men and boys – BioNews

22 June 2020

Chinese authorities are collecting blood samples from across the country to build a genetic map of its roughly 700 million males.

A new Australian Strategic Policy Institute (ASPI) reportdescribes how Chinese law enforcement has been collecting samples to build a DNA databaseto track a man's male relatives using only his blood, saliva or other genetic material.

Thereport states: 'A police-run Y-STR database containing biometric samples and detailed multigenerational genealogies from all of China's patrilineal families is likely to increase state repression against the family members of dissidents and further undermine the civil and human rights of dissidents and minority communities.'

The Chinese Ministry of Public Security allowed the expansion of genetic collection in 2017 from all males in the population, irrespective of criminal records, in at least 22 of the 31 administrative regions of China.

The police argue that the database is key for controllingcriminal activity, and that all genetic donors fully consent to the data collection. However, Chinese nationals have suggested that the collection is being done involuntarily as they do not have the right to refuse under an authoritarian state.

According to the New York Times, Jiang Haolin, a computer engineer from a rural county in northern China, donated a blood sample after being told by authorities that if he did not comply his household would be blacklisted and could losethe right to travel and accessto hospital treatments.

Theproject is a continuation of China's efforts to use genetics to control its people, which had been focused on tracking ethnic minorities and other, more targeted groups. It adds to the surveillance methods police are deploying across the country including advanced cameras, facial recognition systems and artificial intelligence.

Human rights groups have actively condemned these developments. Concerned that individuals have no control over how their genetic information is used and where it is stored, they argue that the database violates China's own laws and human rights codes.

'The ability of the authorities to discover who is most intimately related to whom, given the context of the punishment of entire families as a result of one person's activism, is going to have a chilling effect on society as a whole,'Maya Wang, a China researcher for Human Rights Watch told the New York Times.

Meanwhile, Massachusetts-basedfirm Thermo Fisher, has come under fire from US lawmakers for selling Chinathe custom-tailored DNA kits for its data collection scheme, in a deal estimated to be worth over 23 billion dollars.

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China collects DNA from millions of men and boys - BioNews