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Where Does Intercept Pharmaceuticals Inc (ICPT) Stock Fall in the Biotechnology Field? – InvestorsObserver

April 23rd, 2020 1:45 pm

Intercept Pharmaceuticals Inc (ICPT) is near the top in its industry group according to InvestorsObserver. ICPT gets an overall rating of 72. That means it scores higher than 72 percent of stocks. Intercept Pharmaceuticals Inc gets a 83 rank in the Biotechnology industry. Biotechnology is number 8 out of 148 industries.

Analyzing stocks can be hard. There are tons of numbers and ratios, and it can be hard to remember what they all mean and what counts as good for a given value. InvestorsObserver ranks stocks on eight different metrics. We percentile rank most of our scores to make it easy for investors to understand. A score of 72 means the stock is more attractive than 72 percent of stocks.

These rankings allows you to easily compare stocks and view what the strengths and weaknesses are of a given company. This lets you find the stocks with the best short and long term growth prospects in a matter of seconds. The combined score incorporates technical and fundamental analysis in order to give a comprehensive overview of a stocks performance. Investors who then want to focus on analysts rankings or valuations are able to see the separate scores for each section.

Intercept Pharmaceuticals Inc (ICPT) stock is trading at $81.86 as of 10:41 AM on Tuesday, Apr 21, a loss of -$0.75, or -0.91% from the previous closing price of $82.61. The stock has traded between $80.53 and $83.30 so far today. Volume today is less active than usual. So far 80,863 shares have traded compared to average volume of 667,682 shares.

To see InvestorsObserver's Sentiment Score for Intercept Pharmaceuticals Inc click here.

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Where Does Intercept Pharmaceuticals Inc (ICPT) Stock Fall in the Biotechnology Field? - InvestorsObserver

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Could genetics explain why some COVID-19 patients fare worse than others? – Live Science

April 23rd, 2020 1:44 pm

Certain genetic differences might separate people who fall severely ill with COVID-19 from those who contract the infection but hardly develop a cough, a new preliminary study suggests.

The research is still in its early days, though, experts say.

The immune system can react to viruses thanks, in part, to specific genes that help cells spot unfamiliar bugs when they enter the body. The genes, known as human leukocyte antigen (HLA) genes, contain instructions to build proteins that bind to bits of a pathogen; those proteins serve as warning flags to alert immune cells. The immune cells, once trained to recognize these bits, jumpstart the process of building antibodies to target and destroy the invasive germ.

Within each individual, HLA genes code for three different classes of proteins; in other words, HLAs come in a variety of flavors, and depending on which HLAs you have, your body may be better or worse equipped to fight off certain germs including SARS-CoV-2, the virus that causes COVID-19.

In a new study, published April 17 in the Journal of Virology, researchers used computer models to predict which combination of HLAs might be best at binding SARS-CoV-2, and which might be worst.

If certain HLAs can bind well to a large proportion of the virus's proteins, "we expect there to be a more protective immune response," authors Abhinav Nellore and Dr. Reid Thompson, who lead a computational biology research group at the Oregon Health and Science University, told Live Science in an email. A better bind means that the viral proteins are more likely to be presented to immune cells and prompt the production of specific antibodies, the authors said.

"If the interaction is not stable, you will not have a proper [immune] response," said Dr. Shokrollah Elahi, an associate professor in the Department of Dentistry and adjunct associate professor in the Department of Medical Microbiology and Immunology at the University of Alberta, who was not involved in the study.

Related: 10 deadly diseases that hopped across species

But a stable bond, alone, does not guarantee the best immune response, Elahi added. If an HLA binds a viral protein that happens to be critical for the germ to replicate and survive, the subsequent antibody activity will likely target the virus more effectively than that prompted by a less important protein, Elahi said.

"This is an issue we did not address in our analysis," the authors noted. Instead, the team focused on predicting how well different HLA types could bind to bits of SARS-CoV-2. Their analysis identified six HLA types with a high capacity to bind different SARS-CoV-2 protein sequences, and three with a low capacity to do so. Specifically, a HLA type known as HLA-B*46:01 had the lowest predicted capacity to bind to bits of SARS-CoV-2.

The same HLA type cropped up in a 2003 study published in the journal BMC Medical Genetics, which assessed patients infected with SARS-CoV, a closely related coronavirus that caused an outbreak of severe acute respiratory syndrome in the early 2000s. The study found that, in a group of patients of Asian descent, the presence of HLA-B*46:01 was associated with severe cases of the infection. In their paper, the research group noted that more clinical data would be needed to confirm the connection and the same goes for the new study of SARS-CoV-2, Nellore and Thompson said.

"The most substantial limitation of our study is that this was conducted entirely on a computer and did not involve clinical data from COVID-19 patients," the authors said. "Unless and until the findings we present here are clinically validated, they should not be employed for any clinical purposes," they added.

"In the body, we have so many things interacting," Elahi said. HLAs represent just one piece of a large, intricate puzzle that comprises the human immune system, he said. To better understand the variety of immune responses to COVID-19, Elahi and his research group aim to assess markers of immune system activity in infected patients and also catalog the ratio of immune cell types present in their bodies. While taking age, sex and other demographic factors into account, these so-called immunological profiles could help pinpoint when and why the illness takes a turn in some patients.

The clinical data could be assessed in parallel with genetic data gathered from the same patients, Elahi added. Similarly, Nellore and Thompson said that "COVID-19 testing should be paired with HLA typing, wherever [and] whenever possible," to help determine how different HLA types relate to symptom severity, if at all. Partnerships with genetic testing companies, biobanks and organ transplant registries could also offer opportunities to study HLA types in larger populations of people, they said.

"We cannot in good conscience predict at this point who will be more or less susceptible to the virus because we have not analyzed any clinical outcomes data with respect to HLA type to know that any of our predictions are valid," the authors said. If future studies support the notion that some HLA genes protect people from the virus, while others place patients at greater risk, those in the latter group could be first in line for vaccination, they added.

"In addition to prioritizing vaccinating the elderly or those with preexisting conditions, one could prioritize vaccinating people with HLA genotypes that suggest the SARS-CoV-2 virus is more likely to give them worse symptoms."

The authors went on to analyze how well HLAs can bind SARS-CoV-2 as compared with other coronaviruses, such as those that cause the common cold and infect humans often. They identified several viral bits shared between SARS-CoV-2 and at least one of these common viruses, suggesting exposure to one germ could somewhat protect the body against the other.

"If someone was previously exposed to a more common coronavirus and had the right HLA types ... then it is theoretically possible that they could also generate an earlier immune response against the novel SARS-CoV-2," the authors said. On the other hand, exposure to a similar virus could leave the body ill-equipped to fight off the new one, if, for instance, "the body is using an old set of tools that aren't ideally suited to address the new problem," the authors said.

Originally published on Live Science.

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Scientists use genetics to study how the world’s three narwhal populations are affected by climate shifts – The Narwhal

April 23rd, 2020 1:44 pm

If you want to learn about your ancestry, you can spit into a test-tube and retrieve your DNA results a month later online.

Scientists seeking to learn about the genetics of the narwhal had to use more elaborate methods to gather DNA samples of the deep-diving whale that lives in the ice-cold waters of the Arctic.

Hoping to unravel the demographic history of the narwhal, often called the unicorn of the sea, the scientists collected narwhal tissue samples from Inuit hunters in Canadas far north and Greenland, and tested narwhal remains from archeological digs in northern Europe and Russia.

They even got permission to take samples of narwhal tusks from the King of Denmarks throne chair, made from Norwegian narwhal tusks and guarded by three life-sized silver lions with manes of real gold.

They had special access to be able to drill little tiny bits of tusk from that throne, said Steven Ferguson, an Arctic marine mammal research scientist with Fisheries and Oceans Canada.

Ferguson is one of 15 co-authors of a study, published on April 21 by the Proceedings of the Royal Society B: Biological Sciences, that helps unwind a little bit more of the mystery and mystique surrounding the narwhal, a close relative of the beluga whale.

Until recently, little was known about the light-coloured cetacean most commonly recognized for its spiralled tusk a tooth extending through its upper lip. Only in 2017 did scientists discover the narwhal uses its tusk, a sensory device, to smack fish before swallowing them.

Using a combination of genetics and habitat modelling, Ferguson and other scientists investigated how past climatic shifts affected the distribution of the narwhal, one of the Arctic species most vulnerable to climate change.

They discovered low levels of genetic diversity among the worlds three narwhal populations, the two largest of which are found in Canada.

The scientists also found that habitat availability has been critical to the success of narwhals over the past tens of thousands of years, raising concerns about the fate of the migratory whale in a rapidly warming Arctic.

There are approximately 200,000 narwhals in the world.

Populations are named for where they summer. The vast majority of narwhals are found in Canada, in two groups known as the Baffin Bay and Hudsons Bay populations. A third population, numbering about 10,000 animals, is found in Greenland, extending to Svalbard an island between Norway and the North Pole and as far as Russia.

Its pretty remarkable that Canada has this resource but its also a lot of responsibility, said Ferguson, who worked with Inuit hunters to gather tissue samples for the study.

We are the ones who are going to have to manage and conserve this species going forward into the future.

DFO scientist Steve Ferguson in the field, conducting research on the worlds narwhal populations. Photo: Steve Ferguson

Narwhals appear only to have ever been an Atlantic species, and all three populations are closely related. Researchers found narwhals have one of the lowest genetic diversities of all marine mammals.

I still dont think weve quite solved that puzzle as to why it is so low, Ferguson said in an interview. Maybe there was some kind of bottleneck way back in the past. This history thats been explained by the genomic study here hasnt really found a good explanation for that.

The study found a long-term, low overall population size that increased when suitable habitat expanded following the last Ice Age. Like other polar marine predators, narwhal populations contracted into smaller areas during the last glaciation.

Its a bit of a mystery as to how fragmented they might have been, Ferguson said.

The study also looked into the future, forecasting what impact global warming might have on populations.

Researchers estimated a 25 per cent decline in habitat suitability by 2100, with a 1.6 degrees northward shift in habitat availability, suggesting narwhal habitat is likely to contract as sea temperatures rise and sea ice continues to melt.

The genetic ghost hunters

Ferguson said there will be a slight decrease in populations, including in the east Greenland group.

Narwhal distribution will be further affected in the near future by increased human encroachment, changes in prey availability, new competitors and increased predation by killer whales, according to the study.

More open water is good for narwhals to some extent, Ferguson said. But they will have competitors and disease and problems coming from the south [and] thats going to continue to push them further north.

Much depends on narwhals having access to the habitat they need to thrive, he said.

Baffin Bay seems to be a perfect spot for them right now, at least in winter. Theyre really deep diving animals, well adapted to diving to extreme depths, up to 2 kilometres. Baffin Bay allows them to do that and has some really good food.

All other Arctic marine mammals are circumpolar, meaning they are found around the world.

But narwhal are unique, Ferguson said. They really seem to have this Atlantic Ocean habitat. So theres an open question as to what might happen as we continue to lose sea ice.

The Arctic is warming at an unprecedented rate. A new study, published in Geophysical Research Letters, predicts summer Arctic sea ice will disappear before 2050, with devastating consequences for the Arctic ecosystem.

Narwhals most vulnerable to increased shipping in Arctic

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Scientists use genetics to study how the world's three narwhal populations are affected by climate shifts - The Narwhal

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Genetic variants linked with onset, progression of POAG – Ophthalmology Times

April 23rd, 2020 1:44 pm

Genetic variants that are unrelated to the IOP are associated with a family history of glaucoma and play a role in the onset of primary open-angle glaucoma (POAG). Genetic variants that are related to the IOP are associated with the age at which glaucoma is diagnosed and are associated with disease progression.

What is known about POAG, the most prevalent form of glaucoma, is that increased IOP and myopia are risk factors for damage to the optic nerve in POAG.

Related: Stent offers IOP stability more than three years after surgery

A family history of glaucoma is a major risk factor for development of POAG, in light of which, therefore, genetic factors are thought to be important in the disease pathogenesis and a few genes mutations have been identified as causing POAG, according to Fumihiko Mabuchi, MD, PhD, professor, Department of Ophthalmology, Faculty of Medicine, University of Yamanashi, Kofu, Japan.

Myopia has been shown to be a risk factor for POAG in several studies. However, it can be difficult to diagnose true POAG in myopic patients and controversy exists over whether it is real risk factor.

Myopic optic discs are notoriously difficult to assess, and myopic patients may have visual field defects unrelated to any glaucomatous process.

The prevalence of POAG increases with age, even after compensating for the association between age and IOP.

Related: Preservative-free tafluprost/timolol lowers IOP well, glaucoma study shows

Part of the storyDr. Mabuchi and his and colleagues, recounted that these factors are only part of the story.

According to Dr. Mabuchi and his colleagues, cases of POAG caused by these gene mutations account for several percent of all POAG cases, and most POAG is presumed to be a polygenic disease.

Recent genetic analyses, the investigators explained, have reported genetic variants that predispose patients to development of POAG and the additive effect of these variants on POAG, which are classified as two types.

The first genetics variants are associated with IOP elevation.

Related: Sustained-release implant offers long-term IOP control, preserved visual function

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Genetic variants linked with onset, progression of POAG - Ophthalmology Times

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The Better Half: On the Genetic Superiority of Women review bold study of chromosomal advantage – The Guardian

April 23rd, 2020 1:44 pm

It was noticeable from the initial outbreak in Wuhan that Covid-19 was killing more men than women. By February, data from China, which involved 44,672 confirmed cases of the respiratory disease, revealed the death rate for men was 2.8%, compared to 1.7% among women. For past respiratory epidemics, including Sars, Mers and the 1918 Spanish flu, men were also at significantly greater risk. But why?

Much of the reason for the Covid-19 disparity was put down to mens riskier behaviours around half of Chinese men are smokers, compared with just 3% of women, for instance. But as the coronavirus has spread globally, its proved deadlier to men everywhere that data exists (the UK and US notably and questionably do not collect sex-disaggregated data). Italy, for instance, has had a case fatality rate of 10.6% for men, versus 6% for women, whereas the sex disparity for smoking (now a known risk factor) is smaller there than China 28% of men and 19% of women smoke. In Spain, twice as many men as women have died. Smoking, then, is unlikely to account for all of the sex disparity in Covid-19 deaths.

Age and co-morbidity (pre-existing health conditions, including diabetes, cardiovascular disease or cancer) are the biggest risk factors, and that describes more older men than women. There may also be a sex difference in how people fight infection, due to immunological or hormonal differences oestrogen is shown to increase the antiviral response of immune cells.

If women are mounting a more effective immune response to Covid-19, it could be because many of the genes that regulate the immune system are encoded on the X chromosome. Everybody gets one X chromosome at conception from their mother. However, sex is determined (for the vast majority) by the chromosome received from their father: females get an additional X, whereas males do not (they receive a Y). According to The Better Half by American physician Sharon Moalem, having this second X chromosome gives women an immunological advantage. Every cell in a womans body has twice the number of X chromosomes as a mans, and so twice the number of genes that can be called upon to regulate her immune response, he says. Only one of the X chromosomes in each cell will be active at any time, but having that diversity of options gives women a better immunological toolbox to fight infections.

Moalem describes the possession of XX chromosomes as female genetic superiority. In the case of Covid-19, for instance, the virus uses its spike protein as a key to unlock a receptor protein on the outside of our human cells, called ACE-2, and gain entry. As the ACE-2 protein is on the X chromosome, men will have identical versions of ACE-2 on all their cells if the virus can unlock one, it can unlock all, he wrote recently in a Twitter thread. Women, though, have two different ACE-2 genes on their two X chromosomes, which may make it harder for the Covid-19 virus to break into all their cells, as it has to unlock two different proteins. Furthermore, once the ACE-2 is unlocked, it cannot perform its function, which, in the case of lung cells, is to clear fluid buildup during infection. So males, with all of their ACE-2 proteins affected, will suffer this more than females, he says. Moalem believes this may be the crucial advantage that XX-carrying women have over XY-carrying men in Covid-19 infection mortality.

Its an intriguing theory, and in his provocative book (written before the Covid-19 outbreak) Moalem expands the XX advantage to explain a whole range of life factors, from womens increased longevity to their lesser incidence of autism. It is incontrovertible that women are far less likely to suffer from X-linked genetic disorders, which include everything from Hunter syndrome to colour-blindness, because they usually have an unaffected X chromosome to fall back on. Indeed, in the case of colour vision, Moalem posits that having a second X chromosome can give some women a visual superpower, enabling them to see 100 times the usual colour range due to the extra diversity of receptors they carry on their multiple Xs.

It is striking that Moalem barely references environmental and social factors in a book about sex differences in health outcomes

However, the evidence for other of Moalems claims for the protective role of a second X chromosome, such as in autism spectrum disorders or behavioural traits, is less convincing. A broad range of genes play complex roles in the workings of the brain, and attributing a simple chromosomal relationship is brave. (It should be noted that Moalem authored the questionable The DNA Restart: Unlock Your Personal Genetic Code to Eat for Your Genes, Lose Weight, and Reverse Ageing in 2016.)

Outside of inherited genetic disorders, such as haemophilia, most conditions are attributable to a range of factors, including cultural norms, behaviours and social and environmental aspects as well as a host of biological factors. For Covid-19, for instance, gender-based norms around smoking and hand-washing, collective or individualistic mindsets that affect compliance with social-distance requests, how polluted your city is, whether you are a caregiver, and poverty and nutrition level all play a part in determining your infection risk and disease outcome. And, as weve seen, a range of co-morbidities increase risk are they too made more likely by absence of a second X chromosome? In many cases, such as cancers and lung disease, Moalem believes so a fascinating theory that surely deserves more study.

It is striking, though, that Moalem barely references environmental and social factors in a book about sex differences in health outcomes. This is particularly problematic when discussing sex differences in the brain, given the history of prejudicial research in this area. Much as this reviewer enjoys the rare pleasure of being described as the stronger, better, and superior sex certainly it is a change from being described as the weaker sex, as women have throughout history it is nevertheless an uncomfortable valuation. Claims for significant innate cognitive or behavioural advantages between the sexes have largely been debunked in the past few years by a range of influential books and research, and while there are differences, in most cases these are at least as great between individuals of each sex as between the sexes.

This is, however, a book that openly champions women, and it is most enjoyable when giving centre stage to female scientists, who have been too often overlooked. Moalems point is that, just as womens discoveries have been ignored, so too has the importance of their second X chromosome. Even today, medical and pharmaceutical research overwhelmingly favours male subjects, blinding us to knowledge that could lead to breakthroughs, and disadvantaging women who suffer inappropriate treatments and dosing. As men continue to fill the Covid-19 morgues faster than women, Moalem is on a quest to draw the worlds attention to a chromosomal tool we might just need.

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Is anxiety genetic? It’s a combination of genes and your environment – Insider – INSIDER

April 23rd, 2020 1:44 pm

Anxiety disorders are the most common type of mental illness. In a given year, 19% of Americans experience an anxiety disorder, according to the National Association on Mental Illness (NAMI).

Among the most common are:

Scientists have long debated the importance of nature versus nurture in terms of human development and illness. We now know that genetics play a significant role in the development of anxiety. Particularly, researchers have found that genes on chromosome 9 are associated with anxiety.

But your experiences within your environment including family upbringing and major life events are also important factors. Here's what you need to know about how genes and life experiences contribute to anxiety.

You're more likely to develop an anxiety disorder if another member of your family also has an anxiety disorder.

Research has indicated that anxiety disorders have a heritability rate of 26% for lifetime occurrence. This heritability rate means that 26% of the variability in whether or not people develop anxiety is caused by genetics.

So, about one-quarter of your risk for developing anxiety is genetic. That means other factors, such as traumatic experiences or physical illnesses, can have a larger impact. And your family can still contribute to anxiety in ways other than genetics.

"Family provides both the genes and the environment. It might be genes or it may be because a family member modeled a very anxious way of being in the world or often a combination of both," says Elena Touroni, PsyD, a psychologist and co-CEO at My Online Therapy. "It can be difficult to disentangle genes and environment."

One 2018 study found that children with anxiety disorders were three times more likely than children without disorders to have at least one parent with an anxiety disorder. The connection was particularly strong for social anxiety.

The study authors suggest that in addition to genetic risk, parents "model" behavior that increases the risk of their child developing social anxiety. For example, a parent who avoids social events might unintentionally teach their child to do the same.

However, adults who were raised by parents with anxiety can mitigate their risk of developing an anxiety disorder by learning how to manage anxiety with effective stress-management techniques. If you're a parent with anxiety, the earlier you teach your kid about this, the better.

"The best thing you can do is be aware of the fact that there is a higher chance that you might be prone to anxiety yourself," Touroni says. "Make a conscious effort to learn techniques to calm the mind, such as mindfulness. Also, having psychological therapy will help you better understand the anxieties of the people in your family, and therefore what they have left you vulnerable to as a result."

You don't need to have a family member with an anxiety disorder in order to develop anxiety. A stressful or traumatic event, for example, can increase the risk of developing an anxiety disorder.

"The main underlying core belief of any anxiety disorder is an exaggerated sense of vulnerability in the world of yourself or the people you care about," Touroni says. "Fundamentally, it's about understanding whether your experiences led you to develop a belief that the world is a dangerous place."

In particular, child sexual abuse and family violence may lead to an increased risk for anxiety. Moreover, having three or more adverse childhood experiences these are somewhat traumatic events for children, ranging from divorced parents to abuse is associated with a higher likelihood of developing anxiety.

Different childhood experiences at home, school and elsewhere can help explain why some family members might develop anxiety while others don't.

For example, a 2018 study followed 49,524 twins for 25 years. The researchers found that as twins aged and their environments became more different, the influence of heritability on their chance of developing anxiety decreased. In short: even though the twins shared genetics, their risk factors for anxiety were affected more by their environment than their genes.

In the end, there's no concrete set of factors that can predict if you will develop anxiety, or not.

"Mental illness is very different to physical illness. We can't always find a concrete link because there are a lot of variables," Touroni says. "Our mental wellbeing is influenced by so many different factors, and because of that, it's difficult to isolate genetic loading from environmental influence."

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Covid-19 Arrived in Seattle. Where It Went From There Stunned the Scientists. – The New York Times

April 23rd, 2020 1:44 pm

SEATTLE As the coronavirus outbreak consumed the city of Wuhan in China, new cases of the virus began to spread out like sparks flung from a fire.

Some landed thousands of miles away. By the middle of January, one had popped up in Chicago, another one near Phoenix. Two others came down in the Los Angeles area. Thanks to a little luck and a lot of containment, those flashes of the virus appear to have been snuffed out before they had a chance to take hold.

But on Jan. 15, at the international airport south of Seattle, a 35-year-old man returned from a visit to his family in the Wuhan region. He grabbed his luggage and booked a ride-share to his home north of the city.

The next day, as he went back to his tech job east of Seattle, he felt the first signs of a cough not a bad one, not enough to send him home. He attended a group lunch with colleagues that week at a seafood restaurant near his office. As his symptoms got worse, he went grocery shopping near his home.

Days later, after the man became the first person in the United States to test positive for the coronavirus, teams from federal, state and local agencies descended to contain the case. Sixty-eight people the ride-share driver at the airport, the lunchmates at the seafood restaurant, the other patients at the clinic where the man was first seen were monitored for weeks. To everyones relief, none ever tested positive for the virus.

But if the story ended there, the arc of the coronaviruss sweep through the United States would look much different.

As it turned out, the genetic building block of the virus detected in the man who had been to Wuhan would become a crucial clue for scientists who were trying to understand how the pathogen gained its first, crucial foothold.

Working out of laboratories along Seattles Lake Union, researchers from the University of Washington and the Fred Hutchinson Cancer Research Center rushed to identify the RNA sequence of the cases from Washington State and around the country, comparing them with data coming in from around the world.

Using advanced technology that allows them to rapidly identify the tiny mutations that the virus makes in its virulent path through human hosts, the scientists working in Washington and several other states made two disconcerting discoveries.

The first was that the virus brought in by the man from Wuhan or perhaps, as new data has suggested, by someone else who arrived carrying a nearly identical strain had managed to settle into the population undetected.

Then they began to realize how far it had spread. A small outbreak that had established itself somewhere north of Seattle, they realized as they added new cases to their database, was now responsible for all known cases of community transmission they examined in Washington State in the month of February.

And it had jumped.

A genetically similar version of the virus directly linked to that first case in Washington was identified across 14 other states, as far away as Connecticut and Maryland. It settled in other parts of the world, in Australia, Mexico, Iceland, Canada, the United Kingdom and Uruguay. It landed in the Pacific, on the Grand Princess cruise ship.

The unique signature of the virus that reached Americas shores in Seattle now accounts for a quarter of all U.S. cases made public by genomic sequencers in the United States.

With no widespread testing available, the high-tech detective work of the researchers in Seattle and their partners elsewhere would open the first clear window into how and where the virus was spreading and how difficult it would be to contain.

Even as the path of the Washington State version of the virus was coursing eastward, new sparks from other strains were landing in New York, in the Midwest and in the South. And then they all began to intermingle.

The researchers in Seattle included some of the worlds most renowned experts on genomic sequencing, the process of analyzing the letters of a viruss genetic code to track its mutations. Before the outbreak, one of the labs had done more sequencing of human coronaviruses than anywhere else in the world 58 of them.

When a virus takes hold in a person, it can replicate billions of times, some of those with tiny mutations, each new version competing for supremacy. Over the span of a month, scientists have learned, the version of the novel coronavirus moving through a community will mutate about twice each one a one-letter change in an RNA strand of 29,903 nucleotides.

The alterations provide each new form of the virus with a small but distinctive variation to its predecessor, like a recipe passed down through a family. The mutations are so small, however, that it is unlikely that one version of the virus would affect patients differently than another one.

The virus originated with one pattern in Wuhan; by the time it reached Germany, three positions in the RNA strand had changed. Early cases in Italy had two entirely different variations.

For each case, the Seattle researchers compile millions of fragments of the genome into a complete strand that can help identify it based on whatever tiny mutations it has undergone.

What were essentially doing is reading these small fragments of viral material and trying to jigsaw puzzle the genome together, said Pavitra Roychoudhury, a researcher for the two institutions working on the sequencing in Seattle.

With some viruses, the puzzles are more challenging to assemble. The virus that causes Covid-19, she said, was relatively well behaved.

Researchers looked closely at the man who had flown in from Wuhan, who has not been publicly identified and did not respond to a request to speak to The New York Times.

They confirmed he had brought a strain of the virus that was already extending broad tentacles from the Wuhan area to Guangdong on Chinas Pacific coast to Yunnan in the mountainous west. Along the way, its signature varied significantly from the version of the virus that spread in Europe and elsewhere: Its mutations were at positions 8,782, 18,060 and 28,144 on the RNA strand.

That gave Dr. Roychoudhury and the scientists around the country she has been working with the unique ability to see what the contact tracers in Seattle had been unable to: the invisible footprints of the pathogen as it moved.

On the hunt for the viruss path through the United States, one of the first signposts came on Feb. 24, when a teenager came into a clinic with what looked like the flu. The clinic was in Snohomish County, where the man who had traveled to China lived. Doctors gave the teenager a nasal swab as part of a tracking study that was already being done on influenza in the region.

Only later did they learn that the teenager had not had the flu, but the coronavirus. After the diagnosis, researchers in Seattle ran the sample through a sequencing machine. Trevor Bedford, a scientist at the Fred Hutchinson Cancer Research Institute who studies the spread and evolution of viruses, said he and a colleague sipped on beers as they waited for the results to emerge on a laptop.

It confirmed what they had feared: The case was consistent with being a direct descendant of the first U.S. case, from Wuhan.

The teenager had not been in contact with the man who had traveled to Wuhan, so far as anyone knew. He had fallen ill long after that man was no longer contagious.

Additional sequencing in the days afterward helped confirm that other cases emerging were all part of the same group. This could only mean one thing: The virus had not been contained to the traveler from Wuhan and had been spreading for weeks. Either he had somehow spread it to others, or someone else had brought in a genetically identical version of the virus.

That latter possibility has become more likely in recent days, after new cases entered into the researchers database showed an interesting pattern. A virus with a fingerprint nearly identical to the Wuhan travelers had shown up in cases in British Columbia, just across the border from Washington State, suggesting to Dr. Bedford that it might not have been the first Wuhan traveler who had unleashed the outbreak.

Either way, the number of cases emerging around the time the teenagers illness was identified indicated that the virus had been circulating for weeks.

On its path through Washington State, one of the viruss early stops appears to have been at a square dance on Feb. 16 in the city of Lynnwood, midway between Seattle and Everett.

It was a full month since the Wuhan travelers arrival. A couple dozen square dancers had gathered for a pie and ice cream social, capping off a series of practices and events from all over the region over the course of a three-day weekend.

Three groups of square dancers swung through promenades and allemandes huffing and sweating to Free Ride and Bad Case of Loving You.

Stephen Cole, who was the dance caller that night, said he did not recall anyone showing signs of illness. But over the next few days, he and a woman who had been cuing the dance fell ill.

Another dancer, Suzanne Jones, had attended a class with Mr. Cole the day before. By the next weekend, Ms. Jones said, she started to feel symptoms she dismissed as allergies, since she had noticed the scotch broom starting to bloom.

After resting for a couple of days, Ms. Jones felt better and drove from her home in Skagit County more than 100 miles south to visit her mother in Enumclaw, helping pack some belongings for storage. On the way back, she visited the strip malls in Renton, then a store in Everett, then a laundromat in Arlington. She stopped to apply for a job with the Census Bureau.

I probably exposed a lot of people that day, she said.

Ms. Jones only realized it could be something more than allergies after getting a notification on March 2 that one of her square-dancing friends had died of the coronavirus as the outbreak began to emerge. She too tested positive.

There was minimal coronavirus testing in the United States during February, leaving researchers largely blind to the specific locations and mutations of the spread that month. The man who had traveled from Wuhan was not at the dance, nor was anyone else known to have traveled into the country with the coronavirus. But researchers learned that the virus by then was already spreading well beyond its point of origin and all the cases of community transmission that month were part of that same genetic branch.

There was another spreading event. On the Saturday after the dance, a group of friends packed the living room of a one-bedroom apartment in Seattle, sharing homemade food and tropical-themed drinks.

Over the following days, several people began coming down with coronavirus symptoms. Among people who attended, four out of every 10 got sick, said Hanna Oltean, an epidemiologist with the Washington State Department of Health.

Several people passed on the virus to others. By late March, the state health department had documented at least three generations of transmission occurring before anyone was symptomatic, Ms. Oltean said.

By then, it was becoming clear that there were probably hundreds of cases already linked to the first point of infection that had been spreading undetected. It left a lingering question: If the virus had this much of a head start, how far had it gone?

As cases of the virus spread, scientists in other states were sequencing as many as they could. In a lab at the University of California, San Francisco, Dr. Charles Chiu looked at a range of cases in the Bay Area, including nine passengers from the Grand Princess cruise ship, which had recently returned from a pair of ill-fated sailings to Mexico and Hawaii that left dozens of passengers infected with the coronavirus.

Dr. Chiu was stunned by his results: Five cases in the San Francisco area whose origins were unknown were linked back to the Washington State cluster. And all nine of the Grand Princess cases had a similar genetic link, with the same trademark mutations plus a few new ones. The massive outbreak on the ship, Dr. Chiu believed, could probably be traced to a single person who had developed an infection linked to the Washington State cluster.

But it did not stop with the Grand Princess. David Shaffer, who had been on the first leg of the cruise with members of his family, said passengers on that leg did not discover until after they disembarked that the coronavirus had been aboard when they learned that a fellow passenger had died.

He and his family felt fine when they returned to their home in Sacramento, he said, and when he started feeling sick the next day, on Feb. 22, he at first assumed it was a sinus infection.

Days later, he was tested and learned he had the coronavirus. His wife later tested positive, too, as did one of his sons and one of his grandsons, who had not been on the cruise.

Dr. Chiu remembers going over the implications in his head. If its in California and its in Washington State, its very likely in other states.

The same day Mr. Shaffer got sick, another person landed at Raleigh-Durham International Airport in North Carolina, having just visited the Life Care Center nursing home in Kirkland, which would become a center of infection. At the time, there were growing signs of a respiratory illness at the facility, but no indication of the coronavirus.

A few days later, the traveler began feeling ill, but with no sign that it might be anything serious, he went out for dinner at a restaurant in Raleigh. Just then, officials in Washington State began to report a coronavirus outbreak at Life Care Center. The person in North Carolina tested positive a few days later the first case in the state.

By the middle of March, a team at Yale gathered nine coronavirus samples from the Connecticut region and put them through a portable sequencing machine. Seven came back with connections to Washington State.

I was pretty surprised, said Joseph Fauver, one of the researchers at the lab. At the time, he said, it suggested that the virus had been spreading more than people had initially believed.

In sequencing more recent cases, the researchers have found cases emanating from a larger cluster, with its own distinct genetic signature, originating in the New York area.

A group of cases throughout the Midwest, first surfacing in early March, appears to have roots in Europe. A group of cases in the South, which emerged around the same time, on March 3, appears like a more direct descendant from China.

But of all the branches that researchers have found, the strain from Washington State remains the earliest and one of the most potent.

It has surfaced in Arizona, California, Connecticut, the District of Columbia, Florida, Illinois, Michigan, Minnesota, New York, North Carolina, Oregon, Utah, Virginia, Wisconsin and Wyoming, and in six countries.

And new cases are still surfacing.

One of the enduring mysteries has been just how the virus managed to gain its first, fatal foothold in Washington.

Did the contact tracers who followed the steps of the man who had traveled from Wuhan miss something? Did he expose someone at the grocery store, or touch a door handle when he went to the restaurant near his office?

In recent days, the sequencing of new cases has revealed a surprising new possibility. A series of cases in British Columbia carried a genetic footprint very similar to the case of the Wuhan traveler. That opened up the possibility that someone could have carried that same branch of the virus from Wuhan to British Columbia or somewhere else in the region at nearly the same time. Perhaps it was that person whose illness had sparked the fateful outbreak.

But who? And how? That would probably never be known.

Mike Baker reported from Seattle and Sheri Fink from New York.

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Covid-19 Arrived in Seattle. Where It Went From There Stunned the Scientists. - The New York Times

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Is It Too Late to Buy Shares of Seattle Genetics? – Motley Fool

April 23rd, 2020 1:44 pm

As the overall market declined amid the coronavirus outbreak, Seattle Genetics (NASDAQ:SGEN) shares resisted, climbing22% since the start of this year. The reason is simple: It's all about products. Seattle Genetics started the year with a newly approved drug -- Padcev, for the most common form of bladder cancer -- and investors were hopeful the U.S. Food and Drug Administration would soon approve the company's breast cancer drug, tucatinib, to be commercialized as Tukysa. Last week, that approval came -- four months earlier than expected.

Now the question is: Can Seattle Genetics move higher, or is the good news priced into the shares at this point? A look at approved treatments and market sizes can offer us some clues.

Image source: Getty Images.

Just a year ago, Seattle Genetics was a one-product company. That product -- Adcetris, for Hodgkin lymphoma -- had a particularly strong 2019 thanks to label expansions, posting a 32% increase in net salesto $627.7 million in the U.S. and Canada. Now, Seattle Genetics forecasts a slowdown in Adcetris' sales for 2020, with an increase in the range of 8% to 12%. Still, long-term growth isn't necessarily over for Adcetris as the company works to establishthe treatment as the standard of care in Hodgkin lymphoma and expand its uses.

A slowdown in growth for Adcetris is also less of a concern given the approvals of Padcev in December and Tukysa more recently, though it will take several quarters before these drugs can truly contribute to revenue. My eyes will be on Seattle Genetics' earnings reportApril 30 to see how Padcev fared during its first full quarter on the market.

Padcev is a treatmentfor locally advanced or metastatic urothelial (bladder) cancer. The approval pertains to adult patients who have previously been treated with both platinum-based chemotherapy and inhibitors of proteins that help cancer cells survive. The FDA recently granteda breakthrough therapy designation for an additional use, and after discussions with the regulatory body, Seattle Genetics is optimistic about a potential accelerated approval registration. That would be for the use of Padcev along with an immune therapy called pembrolizumab as a first-line treatment for patients with advanced forms of urothelial cancer who can't receive chemotherapy treatments that use a common treatment called cisplatin.

If sales predictions are correct, Padcev may be poised to be a blockbuster. Analysts from SVB Leerink Research predict peak sales of more than $5 billion, according to press reports. And according to Grand View Research, the global urothelial cancer drug market will reach $3.6 billion by 2023, with a compounded annual growth rate of 23%.

Tukysa might be another blockbuster opportunity. SVB Leerink expectsthat drug to generate peak sales of $1.2 billion by 2030. Tukysa is approvedin combination with trastuzumab and capecitabine for advanced or metastatic HER2-positive breast cancer. In HER2-positive breast cancer, high levels of the HER2 protein within tumors lead to the spread of cancer cells. Tukysa inhibits enzymes that activate this type of protein. A GlobalData report shows the market for HER2-positive breast cancer is set to increase 54% to $9.89 billion by 2025 from 2015.

Seattle Genetics also has about 15 programs in phase 1 or phase 2 trials among its pipeline, adding to future revenue prospects.

Seattle Genetics has steadily grown its revenuesince 2011, when Adcetris was first approved. The company's net lossnarrowed last year to $158.7 million from $222.7 million in 2018, and after fiveconsecutive quarterly losses, Seattle Genetics posted a profit in the last quarter of 2019. The company also reported an increase in cash levels, starting this year with $868.3 million in cashand investments compared with $459.9 milliona year earlier. The financial picture is brightening for Seattle Genetics, and the additions of Padcev and Tukysa should give it a further boost.

So, is it too late to buy Seattle Genetics stock? No. Though the shares only have to rise5.5% to reach Wall Street's average price estimate, for the long-term biotech investor, there is more to gain as the newly approved drugs begin adding to the company's revenue.

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Earth Day: The relevance of land genetics in the time of COVID-19 – CNBCTV18

April 23rd, 2020 1:44 pm

April 22 is celebrated as Earth Day across the world since 1970 after a UNESCO conference in San Francisco proposed a day in honour of the mother Earth a year earlier. On this day in 2016, a landmark Paris agreement -- The draft Climate Protection Treaty -- was signed by the US, China and 120 other countries to protect the planet.

Come 2020 and we're all fighting an unexpected war. What is ironic, is that this war is being fought by sitting at home. Yes, the worldwide lockdown due to the coronavirus pandemic has a majority of people on the planet indoors. The condition is likened to land genetics and part of it is neuroarchitecture, which is a discipline that studies how the physical environment surrounding us can modify our brains and consequently out behavior.

Despite making ourselves busy at homes by indulging in news and entertainment on screens, most of us are facing anxiety issues.

Like the human body, planet Earth too has its anatomy, which can be positive or become sick. So while were at home, lets make use of land science and come out of this lockdown to a healthier planet. This science is purely based on geology, geography and human behaviour. Moreover, the application of land genetics can have a positive effect of our health and lives overall. The theory of land genetics suggests changes in our lifestyle -- the way we use the planet -- which can bring about a long lasting positive change.

With over 80 percent of humans locked indoors, lets consider our homes as the universe and energise the land where we live.

Here are some dos and donts according to the importance of directions that you could practice.

Sleep with your head towards the south. The head is the heaviest part of the body and acts as the North Pole and theory of physics suggests that opposite poles attract each other, this would have a calming effect on you.

If sitting for long, face the east or north, it helps you concentrate better.

A family should sleep from west to east or south to north beginning with the eldest member. The wavelength of land is bigger for elders and smaller for younger members.

If a member of the family is unwell, keep him in the first quadrant of the house which is in the north-east direction. They should sleep facing the south. It will help them fight the diseases effectively. The north-east wavelength is the smallest of all.

While cooking, one should face the north or east. This is similar to the flow of blood within the body and the magnetic force of the Earth. It helps focus and the food turns out delicious.

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Genetic analysis suggests that the coronavirus was already circulating in Spain by mid-February – EL PAS in English

April 23rd, 2020 1:44 pm

Four pages of newsprint have the same number of letters as the genetic code of the new coronavirus: 30,000. In that brief text, there is enough information to bring the whole of humanity to its knees and force billions of people to hide away in their homes. Once the virus infects a human cell, in the throat for example, the virus is capable of reproducing up to 100,000 times in just 24 hours. Each copy can contain small errors of one letter for another and the new viruses inherit these. The history of the pandemic can be reconstructed by studying these errors.

A team of scientists from Madrids Carlos III Health Institute has analyzed the first 28 genomes of the virus in Spain. The trail of the errors does not lead to a single patient zero, but confirms that there were a multitude of entries by people who had been infected in other countries during the month of February, according to the bioinformatic specialist Francisco Dez, the first signatory of the study.

Based on the information we have today, we believe that there were at least 15 different entries in Spain

On February 23, Fernando Simn, the director of the Health Ministrys Coordination Center for Health Alerts, stated that the virus is not in Spain, nor is the disease being transmitted, nor do we currently have any cases. But it would appear that by that point the virus was already spreading unimpeded.

Dezs team has studied the nearly 1,600 complete virus genomes read by the international scientific community up until the end of March. The analysis shows that the 28 Spanish genomes belong to the three main virus families identified in the rest of the world, which are named S, G and V.

All of the viruses are very similar, in principle, with few mutations that differentiate them, which is good news, with all due care, explains Dez, who is now working at the Clnic Hospital in Barcelona. The experimental vaccines that are being investigated today are being conceived for the current genetic sequence of the virus. A high rate of mutation could ruin the efficiency of the first vaccines, which are due to arrive within a year at the earliest.

The new analysis, which has been published in an open repository and has not been externally reviewed, suggests that the common ancestor of the 1,600 viruses was in the Chinese city of Wuhan around November 24. Thirteen of the Spanish genomes belong to the S family and 11 are linked to a prior case detected on February 1 in Shanghai. The first three S viruses identified in Spain are from samples taken on February 26 and 27 in Valencia. A week before, 2,500 soccer fans from the region had traveled to Milan to see Atalanta play Valencia, an event that was described as a biological bomb by the mayor of Bergamo, Giorgio Gori.

However, genetic analysis suggests that the coronavirus from the S family was already circulating in Spain, around February 14. Another group of half a dozen cases in Madrid suggest that the G family was already circulating in the capital around February 18.

It would appear that by February 23 the coronavirus was already spreading unimpeded in Spain

The study allows for the invisible and explosive dissemination of the virus to be seen. The case of Shanghai on February 1 is apparently related to another two samples taken in France on February 25 and 26, another in Madrid on March 2, another in Chile on March 3, another in the United States on March 4, another in Georgia on March 8 and another in Brazil on March 16. The probable transmission routes become more complicated until they form a web on the world map. Dez believes that this specific branch of the virus went from Spain to another six countries.

There was no patient zero in Spain, says virologist Jos Alcam, who supervised the study along with his colleague, Inmaculada Casas. There is no patient zero when an epidemic is already so widespread. The team of geneticist Fernando Gonzlez Candelas, from the Valencian foundation Fisabio, sequenced the first three Spanish genomes of the virus on March 17. His group has now read more than a hundred. Based on the information we have today, we believe that there were at least 15 different entries in Spain. Something similar has happened in other countries, such as the US and Iceland, where multiple entries of the virus have also been identified, Gonzlez explains. Patient zero does not exist.

Gonzlez points to the limitations of these genetic studies, which are based on the complete genomes of the virus published by the scientific community in the Gisaid open repository. There are already 11,000 complete genomes from half of the world, 150 of them from Spain. But there are essential pieces missing. There are no relevant sequences from Italy in order to reach conclusions, Gonzlez complains. Without these genomes, possible routes of transmission from Italy to the rest of the world are invisible. Whats more, the image is always incomplete: there are 2.4 million confirmed cases on the planet, according to the latest data from the World Health Organization (WHO).

The Fisabio geneticist, who did not take part in the new study, is also optimistic on seeing the low diversity of the virus. SARS-CoV-2 has a mutation rate that is a thousand times slower than the flu or HIV, he says. In principle, this is good news.

Just 82 days have passed since, on February 1, the first coronavirus case was detected in Spain. The patient in question was a German tourist on the Canary Island of La Gomera. The man was linked to one of the first known outbreaks in Europe, that of a group of employees from the motor vehicle product company Webasto, who had taken part in a training course in Munich together with a Chinese colleague who had family in Wuhan.

The coronavirus, however, had already been circulating for some days, according to the genetic and epidemiological data. No border has been able to stop the virus, explains geneticist Fernando Gonzlez Candelas, from the Fisabio foundation.

The European Center for Disease Prevention and Control warned on January 18 that Wuhan airport had six weekly direct flights to Paris, three to London and another three to Rome. That was how a multitude of patient zeros traveled.

English version by Simon Hunter.

Given the exceptional circumstances, EL PAS is currently offering all of its digital content free of charge. News related to the coronavirus will continue to be available while the crisis continues.

Dozens of journalists are working non-stop to bring you the most rigorous coverage possible and meet their mission of providing a public service. If you want to support our journalism, you can do so here for 1 for the first month (10 from June). Subscribe to the facts.

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Seattle Genetics (NASDAQ:SGEN) Is In A Strong Position To Grow Its Business – Yahoo Finance

April 23rd, 2020 1:44 pm

We can readily understand why investors are attracted to unprofitable companies. For example, biotech and mining exploration companies often lose money for years before finding success with a new treatment or mineral discovery. But the harsh reality is that very many loss making companies burn through all their cash and go bankrupt.

So, the natural question for Seattle Genetics (NASDAQ:SGEN) shareholders is whether they should be concerned by its rate of cash burn. In this report, we will consider the company's annual negative free cash flow, henceforth referring to it as the 'cash burn'. We'll start by comparing its cash burn with its cash reserves in order to calculate its cash runway.

View our latest analysis for Seattle Genetics

A company's cash runway is calculated by dividing its cash hoard by its cash burn. When Seattle Genetics last reported its balance sheet in December 2019, it had zero debt and cash worth US$811m. In the last year, its cash burn was US$234m. That means it had a cash runway of about 3.5 years as of December 2019. Notably, however, analysts think that Seattle Genetics will break even (at a free cash flow level) before then. In that case, it may never reach the end of its cash runway. The image below shows how its cash balance has been changing over the last few years.

NasdaqGS:SGEN Historical Debt April 22nd 2020

Some investors might find it troubling that Seattle Genetics is actually increasing its cash burn, which is up 4.3% in the last year. The silver lining is that revenue was up 40%, showing the business is growing at the top line. On balance, we'd say the company is improving over time. While the past is always worth studying, it is the future that matters most of all. For that reason, it makes a lot of sense to take a look at our analyst forecasts for the company.

There's no doubt Seattle Genetics seems to be in a fairly good position, when it comes to managing its cash burn, but even if it's only hypothetical, it's always worth asking how easily it could raise more money to fund growth. Issuing new shares, or taking on debt, are the most common ways for a listed company to raise more money for its business. One of the main advantages held by publicly listed companies is that they can sell shares to investors to raise cash to fund growth. We can compare a company's cash burn to its market capitalisation to get a sense for how many new shares a company would have to issue to fund one year's operations.

Since it has a market capitalisation of US$24b, Seattle Genetics's US$234m in cash burn equates to about 1.0% of its market value. That means it could easily issue a few shares to fund more growth, and might well be in a position to borrow cheaply.

It may already be apparent to you that we're relatively comfortable with the way Seattle Genetics is burning through its cash. In particular, we think its cash runway stands out as evidence that the company is well on top of its spending. While its increasing cash burn wasn't great, the other factors mentioned in this article more than make up for weakness on that measure. Shareholders can take heart from the fact that analysts are forecasting it will reach breakeven. After considering a range of factors in this article, we're pretty relaxed about its cash burn, since the company seems to be in a good position to continue to fund its growth. Taking an in-depth view of risks, we've identified 2 warning signs for Seattle Genetics that you should be aware of before investing.

Story continues

Of course, you might find a fantastic investment by looking elsewhere. So take a peek at this free list of companies insiders are buying, and this list of stocks growth stocks (according to analyst forecasts)

If you spot an error that warrants correction, please contact the editor at editorial-team@simplywallst.com. This article by Simply Wall St is general in nature. It does not constitute a recommendation to buy or sell any stock, and does not take account of your objectives, or your financial situation. Simply Wall St has no position in the stocks mentioned.

We aim to bring you long-term focused research analysis driven by fundamental data. Note that our analysis may not factor in the latest price-sensitive company announcements or qualitative material. Thank you for reading.

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Seattle Genetics (NASDAQ:SGEN) Is In A Strong Position To Grow Its Business - Yahoo Finance

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Rapidly Revealing COVID-19s Journey and Evolution With Genetic Tracing Barcode – SciTechDaily

April 23rd, 2020 1:44 pm

Researchers have reported a method to quickly identify mutated versions of SARS-CoV-2, the virus that causes COVID-19. Credit: Drexel University

Drexel University researchers have reported a method to quickly identify and label mutated versions of the virus that causes COVID-19. Their preliminary analysis, using information from a global database of genetic information gleaned from coronavirus testing, suggests that there are at least six to 10 slightly different versions of the virus infecting people in America, some of which are either the same as, or have subsequently evolved from, strains directly from Asia, while others are the same as those found in Europe.

First developed as a way of parsing genetic samples to get a snapshot of the mix of bacteria, the genetic analysis tool teases out patterns from volumes of genetic information and can identify whether a virus has genetically changed. They can then use the pattern to categorize viruses with small genetic differences using tags called Informative Subtype Markers (ISM).

Major SARS-CoV-2 genetic subtypes in countries/regions with the most sequences (indicating date subtype was firstsequenced in that country/region). Subtypes with less than 5% abundance are plotted as OTHER. Credit: Drexel University

Applying the same method to process viral genetic data can quickly detect and categorize slight genetic variations in the SARS-CoV-2, the novel coronavirus that causes COVID-19, the group reported in a paper recently posted on the preliminary research archive, bioRxiv. The genetic analysis tool that generates these labels is publicly available for COVID-19 researchers on GitHub.

The types of SARS-CoV-2 viruses that we see in tests from Asia and Europe is different than the types were seeing in America, said Gail Rosen, PhD, a professor in Drexels College of Engineering, who led the development of the tool. Identifying the variations allows us to see how the virus has changed as it has traveled from population to population. It can also show us the areas where social distancing has been successful at isolating COVID-19.

Relative abundance of ISMs in DNA sequences from Canada as sampled over time. Credit: Drexel University

The ISM tool, developed by Rosen and a focused team including doctoral studentZhengqiao Zhao and Bahrad A. Sokhansani, PhD, an independent researcher and intellectual property attorney, is particularly useful because it does not require analysis of the full genetic sequence of the virus to identify its mutations. In the case of SARS-CoV-2, this means reducing the 30,000-base-long genetic code of the virus to a subtype label 17 bases long.

Its the equivalent of scanning a barcode instead of typing in the full product code number, Rosen said. And right now, were all trying to get through the grocery store a bit faster. For scientists this means being able to move to higher-level analysis much faster. For example, it can be a faster process in studying which virus versions could be affecting health outcomes. Or, public health officials can track whether new cases are the result of local transmission or coming from other regions of the United States or parts of the world.

While these genetic differences might not be enough to delineate a new strain of virus, Rosens group suggests understanding these genetically significant subtypes, where theyre being found and how prevalent they are in these areas is data granular enough to be useful.

Stacked plot of the number of sequences of the reference sequence ISM subtype (CCCCGCCCACAGGTGGG). Credit: Drexel University

This allows us to see the very specific fingerprint of COVID-19 from each region around the world, and to look closely at smaller regions to see how it is different, Rosen said. Our preliminary analysis, using publicly available data from across the world, is showing that the combination of subtypes of virus found in New York is most similar to those found in Austria, France and Central Europe, but not Italy. And the subtype from Asia, that was detected here early in the pandemic has not spread very much, instead we are seeing a new subtype that only exists in America as the one most prevalent in Washington state and on the west coast.

In addition to helping scientists understand how the virus is changing and spreading, this method can also reveal the portion of its genetic code that appears to remain resistant to mutations a discovery that could be exploited by treatments to combat the virus.

Were seeing that the two parts of the virus that seem not to be mutating are the ones responsible for its entry into healthy cells and packaging its RNA, Rosen said. Both of these are important targets for understanding the bodys immune response, identifying antiviral therapeutics and designing vaccines.

Rosens Ecological and Evolutionary Signal-Processing and Informatics Laboratory will continue to analyze COIVD-19 data as it is collected and to support public health researchers using the ISM process.

Reference: Characterizing geographical and temporal dynamics of novel coronavirus SARS-CoV-2 using informative subtype markers by Zhengqiao Zhao, Bahrad A. Sokhansanj and Gail Rosen, 10 April 2020, bioRxiv.DOI: 10.1101/2020.04.07.030759

This research is supported in part by the National Science Foundation.

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Rapidly Revealing COVID-19s Journey and Evolution With Genetic Tracing Barcode - SciTechDaily

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A coronavirus strain from Washington state was one of the earliest and most potent found and it’s in Utah – Salt Lake Tribune

April 23rd, 2020 1:43 pm

Seattle As the coronavirus outbreak consumed the city of Wuhan in China, new cases of the virus began to spread out like sparks flung from a fire.

Some landed thousands of miles away. By the middle of January, one had popped up in Chicago, another one near Phoenix. Two others came down in the Los Angeles area. Thanks to a little luck and a lot of containment, those flashes of the virus appear to have been snuffed out before they had a chance to take hold.

But on Jan. 15, at the international airport south of Seattle, a 35-year-old man returned from a visit to his family in the Wuhan region. He grabbed his luggage and booked a ride-share to his home north of the city.

The next day, as he went back to his tech job east of Seattle, he felt the first signs of a cough not a bad one, not enough to send him home. He attended a group lunch with colleagues that week at a seafood restaurant near his office. As his symptoms got worse, he went grocery shopping near his home.

Days later, after the man became the first person in the United States to test positive for the coronavirus, teams from federal, state and local agencies descended to contain the case. Sixty-eight people the ride-share driver at the airport, the lunchmates at the seafood restaurant, the other patients at the clinic where the man was first seen were monitored for weeks. To everyones relief, none ever tested positive for the virus.

But if the story ended there, the arc of the coronaviruss sweep through the United States would look much different.

As it turned out, the genetic building block of the virus detected in the man who had been to Wuhan would become a crucial clue for scientists who were trying to understand how the pathogen gained its first, crucial foothold.

Working out of laboratories along Seattles Lake Union, researchers from the University of Washington and the Fred Hutchinson Cancer Research Center rushed to identify the RNA sequence of the cases from Washington state and around the country, comparing them with data coming in from around the world.

Using advanced technology that allows them to rapidly identify the tiny mutations that the virus makes in its virulent path through human hosts, the scientists working in Washington and several other states made two disconcerting discoveries.

The first was that the virus brought in by the man from Wuhan or perhaps, as new data has suggested, by someone else who arrived carrying a nearly identical strain had managed to settle into the population undetected.

Then they began to realize how far it had spread. A small outbreak that had established itself somewhere north of Seattle, they realized as they added new cases to their database, was now responsible for all known cases of community transmission they examined in Washington state in the month of February.

A genetically similar version of the virus directly linked to that first case in Washington was identified across 14 other states, as far away as Connecticut and Maryland. It settled in other parts of the world, in Australia, Mexico, Iceland, Canada, Britain and Uruguay. It landed in the Pacific, on the Grand Princess cruise ship.

The unique signature of the virus that reached U.S. shores in Seattle now accounts for a quarter of all U.S. cases made public by genomic sequencers in the United States.

With no widespread testing available, the high-tech detective work of the researchers in Seattle and their partners elsewhere would open the first clear window into how and where the virus was spreading and how difficult it would be to contain.

Even as the path of the Washington state version of the virus was coursing eastward, new sparks from other strains were landing in New York, in the Midwest and in the South. And then they all began to intermingle.

The researchers in Seattle included some of the worlds most renowned experts on genomic sequencing, the process of analyzing the letters of a viruss genetic code to track its mutations. Before the outbreak, one of the labs had done more sequencing of human coronaviruses than anywhere else in the world 58 of them.

When a virus takes hold in a person, it can replicate billions of times, some of those with tiny mutations, each new version competing for supremacy. Over the span of a month, scientists have learned, the version of the novel coronavirus moving through a community will mutate about twice each one a one-letter change in an RNA strand of 29,903 nucleotides.

The alterations provide each new form of the virus with a small but distinctive variation to its predecessor, like a recipe passed down through a family. The mutations are so small, however, that it is unlikely that one version of the virus would affect patients differently than another one.

The virus originated with one pattern in Wuhan; by the time it reached Germany, three positions in the RNA strand had changed. Early cases in Italy had two entirely different variations.

For each case, the Seattle researchers compile millions of fragments of the genome into a complete strand that can help identify it based on whatever tiny mutations it has undergone.

What were essentially doing is reading these small fragments of viral material and trying to jigsaw puzzle the genome together, said Pavitra Roychoudhury, a researcher for the two institutions working on the sequencing in Seattle.

With some viruses, the puzzles are more challenging to assemble. The virus that causes COVID-19, she said, was relatively well behaved.

Researchers looked closely at the man who had flown in from Wuhan, who has not been publicly identified and did not respond to a request to speak to The New York Times.

They confirmed he had brought a strain of the virus that was already extending broad tentacles from the Wuhan area to Guangdong on Chinas Pacific coast to Yunnan in the mountainous west. Along the way, its signature varied significantly from the version of the virus that spread in Europe and elsewhere: Its mutations were at positions 8,782, 18,060 and 28,144 on the RNA strand.

That gave Roychoudhury and the scientists around the country she has been working with the unique ability to see what the contact tracers in Seattle had been unable to: the invisible footprints of the pathogen as it moved.

On the hunt for the viruss path through the United States, one of the first signposts came on Feb. 24, when a teenager came into a clinic with what looked like the flu. The clinic was in Snohomish County, Washington, where the man who had traveled to China lived. Doctors gave the teenager a nasal swab as part of a tracking study that was already being done on influenza in the region.

Only later did they learn that the teenager had not had the flu, but the coronavirus. After the diagnosis, researchers in Seattle ran the sample through a sequencing machine. Trevor Bedford, a scientist at the Fred Hutchinson Cancer Research Institute who studies the spread and evolution of viruses, said he and a colleague sipped on beers as they waited for the results to emerge on a laptop.

It confirmed what they had feared: The case was consistent with being a direct descendant of the first U.S. case, from Wuhan.

The teenager had not been in contact with the man who had traveled to Wuhan, so far as anyone knew. He had fallen ill long after that man was no longer contagious.

Additional sequencing in the days afterward helped confirm that other cases emerging were all part of the same group. This could only mean one thing: The virus had not been contained to the traveler from Wuhan and had been spreading for weeks. Either he had somehow spread it to others, or someone else had brought in a genetically identical version of the virus.

That latter possibility has become more likely in recent days, after new cases entered into the researchers database showed an interesting pattern. A virus with a fingerprint nearly identical to the Wuhan travelers had shown up in cases in British Columbia, just across the border from Washington state, suggesting to Bedford that it might not have been the first Wuhan traveler who had unleashed the outbreak.

Either way, the number of cases emerging around the time the teenagers illness was identified indicated that the virus had been circulating for weeks.

Exposing a lot of people

On its path through Washington state, one of the viruss early stops appears to have been at a square dance on Feb. 16 in the city of Lynnwood, midway between Seattle and Everett.

It was a full month since the Wuhan travelers arrival. A couple dozen square dancers had gathered for a pie and ice cream social, capping off a series of practices and events from all over the region over the course of a three-day weekend.

Three groups of square dancers swung through promenades and allemandes huffing and sweating to Free Ride and Bad Case of Loving You.

Stephen Cole, who was the dance caller that night, said he did not recall anyone showing signs of illness. But over the next few days, he and a woman who had been cuing the dance fell ill.

Another dancer, Suzanne Jones, had attended a class with Cole the day before. By the next weekend, Jones said, she started to feel symptoms she dismissed as allergies, since she had noticed the scotch broom starting to bloom.

After resting for a couple of days, Jones felt better and drove from her home in Skagit County more than 100 miles south to visit her mother in Enumclaw, helping pack some belongings for storage. On the way back, she visited the strip malls in Renton, then a store in Everett, then a laundromat in Arlington. She stopped to apply for a job with the Census Bureau.

I probably exposed a lot of people that day, she said.

Jones only realized it could be something more than allergies after getting a notification on March 2 that one of her square-dancing friends had died of the coronavirus as the outbreak began to emerge. She too tested positive.

There was minimal coronavirus testing in the United States during February, leaving researchers largely blind to the specific locations and mutations of the spread that month. The man who had traveled from Wuhan was not at the dance, nor was anyone else known to have traveled into the country with the coronavirus. But researchers learned that the virus by then was already spreading well beyond its point of origin and all the cases of community transmission that month were part of that same genetic branch.

There was another spreading event. On the Saturday after the dance, a group of friends packed the living room of a one-bedroom apartment in Seattle, sharing homemade food and tropical-themed drinks.

Over the following days, several people began coming down with coronavirus symptoms. Among people who attended, 4 out of every 10 got sick, said Hanna Oltean, an epidemiologist with the Washington State Department of Health.

Several people passed on the virus to others. By late March, the state health department had documented at least three generations of transmission occurring before anyone was symptomatic, Oltean said.

By then, it was becoming clear that there were probably hundreds of cases already linked to the first point of infection that had been spreading undetected. It left a lingering question: If the virus had this much of a head start, how far had it gone?

As cases of the virus spread, scientists in other states were sequencing as many as they could. In a lab at the University of California, San Francisco, Dr. Charles Chiu looked at a range of cases in the Bay Area, including nine passengers from the Grand Princess cruise ship, which had recently returned from a pair of ill-fated sailings to Mexico and Hawaii that left dozens of passengers infected with the coronavirus.

Chiu was stunned by his results: Five cases in the San Francisco area whose origins were unknown were linked back to the Washington state cluster. And all nine of the Grand Princess cases had a similar genetic link, with the same trademark mutations plus a few new ones. The massive outbreak on the ship, Chiu believed, could probably be traced to a single person who had developed an infection linked to the Washington state cluster.

But it did not stop with the Grand Princess. David Shaffer, who had been on the first leg of the cruise with members of his family, said passengers on that leg did not discover until after they disembarked that the coronavirus had been aboard when they learned that a fellow passenger had died.

He and his family felt fine when they returned to their home in Sacramento, California, he said, and when he started feeling sick the next day, on Feb. 22, he at first assumed it was a sinus infection.

Days later, he was tested and learned he had the coronavirus. His wife later tested positive, too, as did one of his sons and one of his grandsons, who had not been on the cruise.

Chiu remembers going over the implications in his head. If its in California and its in Washington state, its very likely in other states.

The same day Shaffer got sick, another person landed at Raleigh-Durham International Airport in North Carolina, having just visited the Life Care Center nursing home in Kirkland, which would become a center of infection. At the time, there were growing signs of a respiratory illness at the facility, but no indication of the coronavirus.

A few days later, the traveler began feeling ill, but with no sign that it might be anything serious, he went out for dinner at a restaurant in Raleigh. Just then, officials in Washington state began to report a coronavirus outbreak at Life Care Center. The person in North Carolina tested positive a few days later the first case in the state.

By the middle of March, a team at Yale gathered nine coronavirus samples from the Connecticut region and put them through a portable sequencing machine. Seven came back with connections to Washington state.

I was pretty surprised, said Joseph Fauver, one of the researchers at the lab. At the time, he said, it suggested that the virus had been spreading more than people had initially believed.

In sequencing more recent cases, the researchers have found cases emanating from a larger cluster, with its own distinct genetic signature, originating in the New York area.

A group of cases throughout the Midwest, first surfacing in early March, appears to have roots in Europe. A group of cases in the South, which emerged around the same time, on March 3, appears like a more direct descendant from China.

But of all the branches that researchers have found, the strain from Washington state remains the earliest and one of the most potent.

It has surfaced in Arizona, California, Connecticut, the District of Columbia, Florida, Illinois, Michigan, Minnesota, New York, North Carolina, Oregon, Utah, Virginia, Wisconsin and Wyoming, and in six countries.

And new cases are still surfacing.

One of the enduring mysteries has been just how the virus managed to gain its first, fatal foothold in Washington.

Did the contact tracers who followed the steps of the man who had traveled from Wuhan miss something? Did he expose someone at the grocery store, or touch a door handle when he went to the restaurant near his office?

In recent days, the sequencing of new cases has revealed a surprising new possibility. A series of cases in British Columbia carried a genetic footprint very similar to the case of the Wuhan traveler. That opened up the possibility that someone could have carried that same branch of the virus from Wuhan to British Columbia or somewhere else in the region at nearly the same time. Perhaps it was that person whose illness had sparked the fateful outbreak.

But who? And how? That would probably never be known.

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A coronavirus strain from Washington state was one of the earliest and most potent found and it's in Utah - Salt Lake Tribune

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Childhood Psychopathology Linked to Higher Levels of Genetic Vulnerability of Adult Depression – Clinical OMICs News

April 23rd, 2020 1:43 pm

Emotional, social, and psychiatric problems in children and adolescents have been linked to higher levels of genetic vulnerability for adult depression, according to University of Queensland scientists. They made the finding Genetic Associations Between Childhood Psychopathology and Adult Depression and Associated Traits in 42998 Individuals: A Meta-Analysis, which appears inJAMA Psychiatry, while analyzing the genetic data of more than 42,000 children and adolescents from seven cohorts across five European countries.

Christel Middeldorp, MD, PhD, a child and adolescent psychiatrist at the Child Health Research Centre at the University of Queensland, said that researchers have also found a link with a higher genetic vulnerability for insomnia, neuroticism, and body mass index.

By contrast, study participants with higher genetic scores for educational attainment and emotional wellbeing were found to have reduced childhood problems, she pointed out.

We calculated a persons level of genetic vulnerability by adding up the number of risk genes they had for a specific disorder or trait, and then made adjustments based on the level of importance of each gene. We found the relationship was mostly similar across ages.

Adult mood disorders are often preceded by behavioral and emotional problems in childhood. It is yet unclear what explains the associations between childhood psychopathology and adult traits. To investigate whether genetic risk for adult mood disorders and associated traits is associated with childhood disorders, write the investigators.

This meta-analysis examined data from 7 ongoing longitudinal birth and childhood cohorts from the U.K., the Netherlands, Sweden, Norway, and Finland. Starting points of data collection ranged from July 1985 to April 2002. Participants were repeatedly assessed for childhood psychopathology from ages 6 to 17 years. Data analysis occurred from September 2017 to May 2019.

Individual polygenic scores (PGS) were constructed in children based on genome-wide association studies of adult major depression, bipolar disorder, subjective well-being, neuroticism, insomnia, educational attainment, and body mass index (BMI).

Results from this study suggest the existence of a set of genetic factors influencing a range of traits across the life span with stable associations present throughout childhood. Knowledge of underlying mechanisms may affect treatment and long-term outcomes of individuals with psychopathology.

The results indicate there are shared genetic factors that affect a range of psychiatric and related traits across a persons lifespan. Around 50 percent of children and adolescents with psychiatric problems, such as attention deficit hyper-activity disorder (ADHD), continue to experience mental disorders as adults, and are at risk of disengaging with their school community among other social and emotional problems, added Middeldorp.

Our findings are important as they suggest this continuity between childhood and adult traits is partly explained by genetic risk, she continued. Individuals at risk of being affected should be the focus of attention and targeted treatment. Although genetic vulnerability is not accurate enough at this stage to make individual predictions about how a persons symptoms will develop over time, it may become so in the future, in combination with other risk factors.

Middeldorp believes that this study and others may support precision medicine by providing targeted treatments to children at the highest risk of persistent emotional and social problems.

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Lozier praises promising, and ethical, blindness study – OneNewsNow

April 23rd, 2020 1:43 pm

New research results show promise in treating people who are blind.

The National Eye Institute funded the study, which is research considered to be ethical.

Dr. David Prentice of the Charlotte Lozier Institute says there have been discussions over using adult stem cells to restore sight, which he calls a different tack for advancing science and medicine.

It's still an ethical way to go about this, he observes. There's no embryonic stem cells, no fetal tissue, none of this unethical type of research direction.

What the scientists did was turn a skin cell directly into a photoreceptor for vision then transplanted it.

Prenticeadvises the testing is very preliminary after the experiment on mice.

But what they find was when they transplanted this newly formed type of vision cell into the eyes of these blind mice, he says, they restored their vision.

The researchers applied chemicals that transformed one cell type into another needed for vision, and there is now potential to help people with all forms of vision blindness or vision correction, which would include macular degeneration and other retinal disorders.

Editor's note: Original posting attribute comments to wrong person.

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Very low-dose Avastin effective for preventing blindness in preterm infants – National Institutes of Health

April 23rd, 2020 1:43 pm

News Release

Thursday, April 23, 2020

Babies born prematurely who require treatment to prevent blindness from retinopathy of prematurity (ROP) could be treated with a dose of Avastin (bevacizumab) that is a fraction of the dose commonly used for ROP currently. Results from the dose-finding study were published April 23 in JAMA Ophthalmology. The study was conducted by the Pediatric Eye Disease Investigator Group (PEDIG) and supported by the National Eye Institute (NEI), part of the National Institutes of Health.

Preterm babies are at high risk of abnormal blood vessel growth in the retina, the light-sensitive tissue in the back of the eye. These abnormal blood vessels are fragile and prone to leaking. If left untreated, vessel growth can lead to scarring and retinal detachment, the main cause of ROP-related vision loss. ROP is one of the leading causes of blindness in children.

Established ROP treatments include laser therapy and cryotherapy. Both interventions work by causing the abnormal blood vessels to stop growing before they can cause scarring and retinal detachment.

Avastin is one of several available drugs that inhibit abnormal blood vessel growth by suppressing the overproduction of a signal protein called vascular endothelial growth factor (VEGF).

The U.S. Food and Drug Administration approved Avastin in 2004 as a cancer therapy. Since then, ophthalmologists have used it off-label to inhibit abnormal blood vessel growth in ROP, as well as in other ocular disorders. Results from a clinical trial published in 2011 confirmed the benefit of using Avastin over laser therapy for treating the most severe cases of ROP, which occur in a region of the retina known as posterior zone 1.

As a faster and easier treatment option, anti-VEGF eye injections were a welcomed alternative to laser therapy for treating severe ROP, said the new studys protocol chair, David Wallace, M.D., MPH, chair of ophthalmology at the Indiana University School of Medicine. Laser therapy requires sedating the baby for as long as 90 minutes; an Avastin injection takes much less time and is generally less stressful to the infant.

But we know that anti-VEGF agents injected into the eye also get into the bloodstream, and doctors worry that inhibiting VEGF systemically could interfere with normal development of brain, lung, bone, and kidney tissues, he said. Evidence suggests that injections of anti-VEGF in the eye reduce levels of VEGF in the bloodstream.

In this study, Wallace and colleagues in the NEI-funded PEDIG hoped to pinpoint the lowest possible therapeutic dose of Avastin by testing progressively lower doses in 10-14 infants per dose. We didnt want to start by testing an ineffective dose and risk a child going blind, so we started with 40% of the dose commonly used for ROP. When a dose was successful, we halved it and then tested that dose. Eventually we cut the dose in half seven times, he said.

In the current study, we found that 0.004 mg of Avastin a dose thats merely 0.6% of the dose used in the 2011 study of Avastin for ROP may be the lower limit to be effective for most infants with ROP, said Wallace. The findings set the stage for a randomized controlled trial comparing long-term effects of low-dose Avastin with laser therapy for treating ROP, he said.

They plan to follow children over time to compare the long-term effects of each strategy on vision and organ development. Previous studies suggest that babies treated with Avastin versus laser may be less likely to become myopic and require glasses for nearsightedness as they grow older.

The study involved 59 preterm infants with type 1 ROP, the most severe form. Each infant had one eye treated by a single injection containing 0.016 mg, 0.008 mg, 0.004 mg, or 0.002 mg of Avastin. If the other eye required treatment, it received twice the concentration (one dose level higher). By comparison, currently used doses of Avastin for ROP range from 0.25 mg to 0.625 mg.

Treatment was considered a short-term success if ROP improved by day four after therapy, and if there was no recurrence or need for additional treatment within four weeks. Such success was achieved in all eyes treated with the 0.016 mg and 0.008 mg doses, and in 9 of 10 eyes receiving 0.004 mg, but only in 17 of 23 eyes receiving 0.002 mg, resulting in the conclusion that 0.004 mg may be the lowest effective dose.

The study was supported by NEI grants EY011751, EY023198, and EY018810. The clinicaltrials.gov record is NCT02390531.

NEI leads the federal governments research on the visual system and eye diseases. NEI supports basic and clinical science programs to develop sight-saving treatments and address special needs of people with vision loss. For more information, visit https://www.nei.nih.gov.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

Wallace DK, Kraker RT, Freedman SF, Crouch ER, Bhatt AR, Hartnett ME, Yang MB, Rogers DL, Hutchinson AK, VanderVeen DK, Haider KM, Siatkowski RM, Dean TW, Beck RW, Repka MX, Smith LE, Good WV, Kong L, Cotter SA, Holmes JM for the Pediatric Eye Disease Investigator Group (PEDIG). Short-term Outcomes After Very Low-Dose Intravitreous Bevacizumab for Retinopathy of Prematurity. Published April 23, 2020 in JAMA Ophthalmology.

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Clear vision, many smiles: How a non-profit is helping children in India see better – YourStory

April 23rd, 2020 1:43 pm

India is home to 472 million children. According to a study published by the National Centre for Biotechnology Information, out of 668 hospitals, only 192 (28.7 percent) reported that they provided pediatric eye care services a handful in a country as vast as India.

Primary and quality eye care is a necessity, and to make it accessible, Orbis International, a non-profit non-governmental organisation, started its saving initiative in India with its flagship Flying Eye Hospital. Orbis International was founded in 1982 in the United States. After running multiple Flying Eye Hospital programmes in Hyderabad and New Delhi, Orbis India established an office in New Delhi in 2000.

Orbis India launched India Childhood Blindness Initiative (ICBI) flagship programme in 2002. Its aims to ensure that Indias children across geographies have access to quality eye care for generations to come.

Dr Rishi Raj Borah has been an integral part of the Orbis journey for the last 12 years and has developed innovative, impactful, and sustainable home-grown eye care initiatives for millions of children in Indian and Nepalese communities. He is the Country Director of Orbis India.

Before working in the field of eye care, Dr Rishi worked with UNICEF, CORDAID and Don Bosco Institute. He is also a Board Member of VISION 2020: The Right to Sight India.

As part of Orbis Comprehensive Childhood Blindness Project, their partner, Akhand Jyoti Eye Hospital (AJEH) conducts school screenings in some of Bihars districts. Several children with vision problems were identified and prescribed spectacles during the school screening in the village of Dariyapur.

In one of Dariyapurs schools where the screening was conducted, a girl named Rinky was identified to have poor vision. The AJEH team discovered that the 13-year-old had been suffering for the last two years.

Rinky

Her poor vision would also hinder her daily activities and despite being scolded in class for being unable to read, Rinky was largely unaware of her problems. Due to uncorrected refractive error, which was blurring her vision, Rinky would be uncomfortable while watching the television and identifying objects in low light conditions. She even had difficulties in seeing under bright light.

Rinky and her friends

The Orbis-AJEH team came to Rinkys rescue. They identify cases like Rinkys, while generating awareness for teachers in these schools. The team also actively engages with the parents of children who go on to get treatments done via the screenings.

Rinky was identified with myopia, which is the inability to see objects at a distance, and was prescribed with a pair of spectacles by the team.

Rinky in her classroom

Rinky was glad about wearing spectacles and soon realised that, like her friends, she was also able to see things clearly.

As of today, Orbis India has presence in Delhi, Punjab, Uttar Pradesh, Uttarakhand, Chhattisgarh, West Bengal, Odisha, Bihar, Maharashtra, Rajasthan, Gujarat, Madhya Pradesh, Kerala, Karnataka, Andhra Pradesh, Arunachal Pradesh, and Assam.

Millions of childrens lives have been positively affected by programs similar to the one in Rinkys school. 33 Childrens Eye Centers (CEC) have been established across the country, which are supported and equipped with quality partners and teams.

How has the coronavirus outbreak disrupted your life? And how are you dealing with it? Write to us or send us a video with subject line 'Coronavirus Disruption' to editorial@yourstory.com

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Why Julia’s Eyes Is Better Than Bird Box (& Is Overlooked) – Screen Rant

April 23rd, 2020 1:43 pm

While the film description, a horror movie where the protagonist wears a blindfold, would conjure 2018 sci-fi horror Bird Box in most peoples minds, it also serves to describe the 2010 Spanish movie,Julias Eyes.

Released on Netflix, Bird Box depicts a post-apocalyptic world where humans are forced to wear blindfolds to avoid seeing madness-causing monsters. Starring Sandra Bullock as Malorie, the movie leans heavily into its star power. It came out the same year A Quiet Place hit theaters, and many were quick to point out the similarities between the two. WhileA Quiet Placewas the higher-rated movie,Bird Boxbecame something of a viral, meme-worthy hit, garnering significant acclaim and attention. Despite all eyes being on the Sandra Bullock-led thriller, which was based off a novel by Josh Malerman, a lesser-known foreign horror is the more direct choice for comparisons, notA Quiet Place.

Related: Why Bird Box 2 Shouldn't Happen

Julias Eyes was directed by Spanish director Guillem Morales and produced by two-time Oscar-winner Guillermo del Toro. A horror thriller, it follows the story Julia, a woman who is slowly losing her sight. Played by the extremely talented Beln Rueda, Julia investigates her sisters suicide while also undergoing an eye surgery that temporarily blinds her.

In both movies, the blindfold serves both a mechanical and symbolic purpose. In Bird Box, supernatural monsters take the shape of ones worst fear, leading those who see them to either madness or suicide; blindfolds are a protective measure. The audience never sees the monsters outright, only their effect. It represents a fear of the unknown.

In Julias Eyes, the blindfold is a necessary measure to ensure her eye operation takes. Here, the blindfold represents sacrifice, a running theme through the movie: a moment of darkness for a brighter future. Much of the tension comes not just from knowing that something sinister is happening around Julia, but that if she peeks to look at it, it condemns her to permanent blindness. It exchanges one kind of blindness for another.

In terms of reception, Julias Eyes has Bird Box beat. Its 90% score on Rotten Tomatoes is leagues ahead of Bird Boxs 63%. The blindfold mechanic in Julias Eyes is much more organic as well. In eschewing any sci-fi elements, Julias Eyes grounds its horror in humanity. It is a story that weaves its concept with its horror, developing multiple levels of tension. The film leans into dramatic irony; from the first scene, the audience knows something is amiss, while Julia is left to grope in the dark.

Related: Every Sci-Fi Horror Movie Releasing In 2020

It is also an extremely beautiful movie. Its high caliber cinematography and acting put it in the realm of horror like Silence Of The Lambs and Psycho. Julia's Eyes alsoincludes one of the most arguably tense scenes in horror history, combining open eyes and a knifes edge to capture many of humanitys innate fears, while developing character-specific tension.

Spanish-language cinema has had a lot to offer horror. The Orphanage balances a terrifying atmosphere with supernatural dread. [REC] uses high stakes zombie horror to make one of the most tense found footage films. The acting is one of the strongest points of Julias Eyes, something that would be lost in an adaptation.

Julias Eyes rarely makes it onto top ten horror lists. It released at a time when horror and foreign language horror were generally still treated as separate. There is a bias in the film world towards English language movies; instead of distributing East Asian horror globally as is, it is usually adapted and translated in the West, often to the detriment of the story. Limiting horror to a single language limits the scope of imagination and possibility.

Fortunately, this trend is slowly disappearing, as exemplified by Korean thriller Parasite becoming the first non-English film to win the Oscar for Best Picture. The future holds hope for movies like Julias Eyes, which have the merit but still deserve to one day reach the scope of films like Bird Box.

Next: Netflix Is Adding So Much Foreign Horror (& What That Means For Streaming)

Jennifer's Body: Every Similarity To 2000's Ginger Snaps

Shannon Lewis is a features and news writer on Screen Rant. She has experience in editorial working as the deputy editor for Specialty Food, an online and print magazine, curating its news section and social media. She has worked as a freelance writer since 2017, writing articles, features, and profiles in a wide range of topics, from business and tech to pop culture and media. Previously, she has also worked as a ghost writer for a fiction manuscript, and co-founded arts-and-literature magazine, Octarine.Hailing from Queretaro, Mexico, she is a graduate of the University of East Anglia's English Literature with Creative Writing program. An avid reader and fan of writing, she leverages her love of literature to dissect movies in her favorite genres, including horror, rom-coms, and superhero movies. Her focus is on the cross-section between story, cultural background, and character development. When she isn't busy reading everything ever published under the mantle of Image Comics, you might find her writing fiction, rock climbing, or putting together a horror anthology with friends.

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Why Julia's Eyes Is Better Than Bird Box (& Is Overlooked) - Screen Rant

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Glaucoma can be successfully treated with gene therapy – Daijiworld.com

April 23rd, 2020 1:43 pm

London, Apr 22 (IANS): A common eye condition, glaucoma, could be successfully treated with a single injection using gene therapy, which would improve treatment options, effectiveness and quality of life for many patients, say researchers.

Glaucoma affects over 64 million people worldwide and is a leading cause of irreversible blindness. It is usually caused by fluid building up in the front part of the eye, which increases pressure inside the eye and progressively damages the nerves responsible for sight.

Current treatments include either eye drops, laser or surgery, all of which have limitations and disadvantages.

"At present, there is no cure for glaucoma, which can lead to loss of vision if the disease is not diagnosed and treated early," said study researcher Dr Colin Chu from the University of Bristol in the UK.

For the findings, published in the journal Molecular Therapy, the research team tested a new approach that could provide additional treatment options and benefits.

The researchers designed a gene therapy and demonstrated proof of concept using experimental mouse models of glaucoma and human donor tissue.

The treatment targeted part of the eye called the ciliary body, which produces the fluid that maintains pressure within the eye.

Using the latest gene-editing technology called CRISPR, a gene called Aquaporin 1 in the ciliary body was inactivated leading to reduced eye pressure.

"We hope to advance towards clinical trials for this new treatment in the near future. If it's successful it could allow a long-term treatment of glaucoma with a single eye injection, which would improve the quality of life for many patients whilst saving the NHS time and money," Chu said

The researchers are currently in discussion with industry partners to support further laboratory work and rapidly progress this new treatment option towards clinical trials.

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Ivermectin emerges as possible treatment option for Covid-19 – The Irish Times

April 23rd, 2020 1:42 pm

Could a drug discovered in the 1970s help to tackle the Covid-19 pandemic? New evidence from research in Australia shows that the anti-parasitic drug ivermectin can inhibit the virus that causes Covid-19 from replicating in cells in the lab.

While findings show promise, the news should be greeted with caveats, according to Donegal scientist Professor William C. Campbell, who shared a Nobel Prize for his role in the discovery of ivermectin.

The report is, in itself, of great importance, says Prof Campbell of the study, which was carried out by scientists at Monash University in Melbourne. But perspective is needed, even though perspective can be boring when the results are exciting.

The researchers in Melbourne grew mammalian cells in the lab and infected them with the Sars-CoV-2 virus that causes Covid-19. Then they exposed the cells and viruses in the lab to ivermectin, a drug that has been widely used for decades to control parasitic worms and insects in livestock, pets and humans.

One of the best known uses of ivermectin in humans is against the worm that causes river blindness - the pharmaceutical company Merck donated the drug for that use for millions of people in affected areas.

Prof Campbell, a graduate of Trinity College Dublin, shared the Nobel Prize in Physiology or Medicine in 2015 for his part in the discovery and development of ivermectin and its use in treating river blindness.

While he was working at Merck Research Laboratories in New Jersey, he was part of an extensive team that identified a substance called avermectin, which was produced by bacteria and could stop parasitic worm infections.

The compound was enhanced and developed as ivermectin, becoming a treatment for parasitic diseases such as heart worm in dogs and river blindness in humans. The Royal Irish Academy will publish Campbells memoir this June.

While ivermectin has not been approved as a drug against viruses, it is known to be effective in the lab against a broad range of viruses including HIV, Dengue and Influenza.

The Australian research showed that ivermectin resulted in a 5,000-fold reduction of Sars-CoV-2 RNA within 48 hours. Ivermectin therefore warrants further investigation for possible benefits in humans, explains the study authors in the journal Antiviral Reports.

The experiments used high concentrations of ivermectin, notes Proff Campbell: the concentration of drug needed to kill the virus in the lab was many times higher than the concentration of ivermectin found in the blood of people in the normal use of ivermectin to control parasitic disease.

So the probability of ivermectin being used safely to kill the virus in people must be considered low, he says.

On the other hand, there is, as the authors of the report point out, the possibility that a safe dosage of ivermectin might reduce the rate of viral replication in the mammalian body, or affect the virus in other ways that might be revealed by further research. That is a more positive prospect.

Commenting on the study, lead researcher Dr Kylie Wagstaff from the Biomedicine Discovery Institute at Monash University says: Ivermectin is very widely used and seen as a safe drug. We need to figure out now whether the dosage you can use it at in humans will be effective - thats the next step.

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