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Archive for the ‘Genetics’ Category

what does it mean to be black – Culture, Race & Economy …

Tuesday, June 9th, 2020

Troy

You are equating Black primarily with skin color, with no real relationship to culture.

Exactly

Still, it is not clear given your definition why Obama is not Black. He is basically the same complexion as I am; am I not Black?

I've seen only limited picturesof you but you don't look Obama's complexion to me.Obama is a light brown complexion and you seem to be medium brown.

Also, his features are different than yours.His lips are thinner and his head is more "angular"....larger dome with a smaller jaw line...like most Europeans.

Like most AfroAmericans I'm sure you're mixed with White and Native American ancestry from way back, but sinceyour African features dominate I consider you Black.You don't have to be 100% just to be of a certain race, just be predominant in those traits.

But Obama's African features don't "dominate".....he's pretty even between both races phenotypically speaking.

Look Troy, the thing we must keep in mind is the fact that while Obama is DIRECTLY mixed....meaing one of his parents is actually White....many so-called "Black" people in the United States are INDIRECTLY mixed. Meaning they have a lot of White (and Native American) ancestry and it comes out in their complexion and facial features just like his does.

So when you point to another AfroAmericans and say:"Well THEY are Black andObama looks like THEM so Obama must be Black too!"

Really, all you're doing is comparing 2 mixed raced people!NEITHER ONE is truly"Black" racially speaking but the only difference is one has an immediateWhite parent and the other has Whites ancestorsfurtherback.

Which leads me to my NEXT response....................

My mother and sister are much lighter than Obama, are they also not Black? Let me know

I don't know, I would have to look at them to make that judgment.As I said before, although complexion/skin color is one of the BIGGEST factors in determining race, it's not the ONLY one....other features go into it.

There are groups of Africans in southern Africa known as San and Khoi people who are YELLOW in complexion with slanted eyes but are still "Black" racially speaking.

Speaking of southern Africa.........

If you're sitting back shaking your head and laughing at what I'm saying -Just remember that in South Africa you have millions of people just like us here in the United States but unlike us they all don't consider themselves "Black".

One group calls themselves Black and the other call themselves "Colored".Now the Coloreds look just like many AfroAmericans, light skinned with curly hair and some European features but they don't consider themselves Black!

So don't trip or think it's so ridiculous at my suggesting that many fellow AfroAmericans like Beyonce or Al B Sure or even Prince shouldn't be considered "Black",if this were any other nation besides the United States....trust me they probably wouldn't consider THEMSELVES Black either!

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Christine Taylor Butler, Author Info, Published Books, Bio …

Tuesday, June 9th, 2020

Writing for children is a joyful endeavor. It takes heart, passion, and one endearing story that yearns to be told. As with all things, commit to putting your own ideas on paper. A story left untold will never blossom or touch the heart of a reader. Christine Taylor Butler

Christine Taylor Butler grew up in Ohio surrounded by books and literature. She developed an overwhelming passion for reading and writing at an early age that defined her purpose and who she has become today. She read every opportunity that she got and even made up story filled adventures of her own. Sadly even though she was a gifted and prolific writer she was missing one ingredient in order to step out on her dreams of becoming a writer, and that was courage. Fear gripped her heart and to alleviate the fear of stepping out she became preoccupied with other productive tasks. Some entail a New England boarding school, two MIT degrees (Engineering and Art & Design)and a series of jobs that included working for a start-up software company. Following thereafter was several years at Harvard University and more than a decade as a Graphic Arts Manager at Hallmark Cards. Although she was productive the overwhelming desire to write kept knocking on the doors of her heart until she eventually opened up.

One of the main reasons for her courageously stepping out in pursuit of a career as an author was the love that her two daughters had for reading childrens books. But it saddened her to see their urban peers did not. She came to the conclusion that sadly multicolored children dont see themselves as being relevant in todays society or as having the potential to make a difference. And even though more books are now like never before presenting children of color in a more positive light Christine wanted to really ensure that this continued. As a result of her lending her voice and being an agent of change her writing career soared. Since then she has released 65 commercially published books.(2018)

Christine Taylor Butler is a force to be reckoned with. She genuinely enjoys the journey of childrens book writing and prides in the fact that she was courageous enough to answer the call to write. She has received a countless amount of awards, ranging from Best Childrens Book of the year by Bank Street College Of Education. Best Books Of The Year by Nebraska Library Association, Best Childrens Book of the year by Barnes and Noble Review. As well as Best Multicultural Books list just to name a few. Her accolades attest to the fact that writing, inspiring and captivating the hearts of children through writing is what she was destined to do.

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New Genetic Identification of COVID-19 Susceptibility Will Aid Treatment – SciTechDaily

Tuesday, June 9th, 2020

The clinical presentation of Covid-19 varies from patient to patient and understanding individual genetic susceptibility to the disease is therefore vital to prognosis, prevention, and the development of new treatments.

For the first time, Italian scientists have been able to identify the genetic and molecular basis of this susceptibility to infection as well as to the possibility of contracting a more severe form of the disease. The research will be presented to the 53rd annual conference of the European Society of Human Genetics, being held entirely on-line due to the Covid-19 pandemic, today [Saturday].

Professor Alessandra Renieri, Director of the Medical Genetics Unit at the University Hospital of Siena, Italy, will describe her teams GEN-COVID project to collect genomic samples from Covid patients across the whole of Italy in order to try to identify the genetic bases of the high level of clinical variability they showed. Using whole exome sequencing (WES)[1] to study the first data from 130 Covid patients from Siena and other Tuscan institutions, they were able to uncover a number of common susceptibility genes that were linked to a favorable or unfavorable outcome of infection. We believe that variations in these genes may determine disease progression, says Prof Renieri. To our knowledge, this is the first report on the results of WES in Covid-19.

Searching for common genes in affected patients against a control group did not give statistically significant results with the exception of a few genes. So the researchers decided to treat each patient as an independent case, following the example of autism spectrum disorder. In this way we were able to identify for each patient an average of three pathogenic (disease-causing) mutations involved in susceptibility to Covid infection, says Prof Renieri. This result was not unexpected, since we already knew from studies of twins that Covid-19 has a strong genetic basis.

Although presentation of Covid is different in each individual, this does not rule out the possibility of the same treatment being effective in many cases. The model we are proposing includes common genes and our results point to some of them. For example, ACE2 remains one of the major targets. All our Covid patients have an intact ACE2 protein, and the biological pathway involving this gene remains a major focus for drug development, says Prof Renieri. ACE2 is an enzyme attached to the outer surface of several organs, including the lungs, that lowers blood pressure. It serves as an entry point for some coronaviruses, including Covid-19.

These results will have significant implications for health and healthcare policy. Understanding the genetic profile of patients may allow the repurposing of existing medicines for specific therapeutic approaches against Covid-19 as well as speeding the development of new antiviral drugs. Being able to identify patients susceptible to severe pneumonia and their responsiveness to specific drugs will allow rapid public health treatment interventions. And future research will be aided, too, by the development of a Covid Biobank accessible to academic and industry partners.

The researchers will now analyze a further 2000 samples from other Italian regions, specifically from 35 Italian Hospitals belonging to the GEN-COVID project.[2]

Our data, although preliminary, are promising, and now we plan to validate them in a wider population, says Prof Renieri. Going beyond our specific results, the outcome of our study underlines the need for a new method to fully assess the basis of one of the more complex genetic traits, with an environmental causation (the virus), but a high rate of heritability. We need to develop new mathematical models using artificial intelligence in order to be able to understand the complexity of this trait, which is derived from a combination of common and rare genetic factors.

We have developed this approach in collaboration with the Siena Artificial Intelligence Lab, and now intend to compare it with classical genome-wide association studies[3] in the context of the Covid-19 Host Genetics Initiative, which brings together the human genetics community to generate, share, and analyze data to learn the genetic determinants of COVID-19 susceptibility, severity, and outcomes. As a research community, we need to do everything we can to help public health interventions move forward at this time.

Chair of the ESHG conference, Professor Joris Veltman, Dean of the Biosciences Institute at Newcastle University, Newcastle upon Tyne, UK, said: We are very excited to have this work on the genetics of COVID19 susceptibility presented as one of our late-breaking abstract talks at the ESHG. Our Italian colleagues present the first insight into the role of genetic susceptibility influencing the severity of the response to a COVID19 infection. It needs to be expanded to encompass much larger populations, but it is impressive to see the speed at which research on this virus has proceeded in just a few months time.

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New Genetic Identification of COVID-19 Susceptibility Will Aid Treatment - SciTechDaily

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Do you have the rocket gene? Why genetics may decide whether you like the peppery veggie – The Independent

Tuesday, June 9th, 2020

Love it or hate it, rocket is popular all over the world. Also known as arugula, roquette and rucola, its known for its pungent and peppery flavours. It might look like an unassuming leafy vegetable, but the reasons for its taste, health benefits and whether we like it all comes down to genetics.

Rocket actually encompasses several species, all of them part of the same family as broccoli, cabbage, kale, mustard and watercress the Brassicales. Its distinctive aroma and flavours are created by chemical compounds produced by its leaves, called isothiocyanates. Some of these compounds can be eye-wateringly hot, whereas others can have a radishy flavour or none at all.

In the wild, isothiocyanates are thought to help defend plants from herbivores and disease, and also help it tolerate environmental stress. But for humans, eating isothiocyanates confers health benefits. Studies have shown them to have anti-cancer properties, and anti-neurodegenerative effects against diseases such as Alzheimers.

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For this reason, plants containing isothiocyanates interest scientists particularly those with little taste and flavour. One such compound is sulforaphane, which is found in rocket and broccoli. Several years ago, researchers produced a super broccoli with high amounts of sulforaphane. Consumers couldnt taste the difference, and it was later shown to be effective in preventing and slowing prostate cancer and in lowering cholesterol.

But one advantage with rocket is that it doesnt need cooked to be eaten. Heating other Brassicales, like broccoli, to over 65C inactivates myrosinase, which is an enzyme in their tissues that converts compounds called glucosinolates into sulforaphane and other isothiocyanates when people chew these plants. If the myrosinase is inactivated, consumers will receive little or none of the associated health benefits, no matter how much is bred into the plants.

Chewing aside, theres some evidence to suggest that our gut microflora possess their own myrosinase and can convert glucosinolates to isothiocyanates for us. The amounts this produces are likely to be quite small, but release may be sustained, exposing our cells to compounds like sulforaphane for longer periods.

But the biggest barrier to people getting these beneficial molecules from rocket is the taste. This depends on when and where rocket crops are grown. In the summer, leaves can be extremely spicy and pungent, whereas in the winter they can be bland and tasteless.

There are many different varieties of rocketiStock)

Growth temperature likely plays a big role in determining the amounts of isothiocyanates released from leaves. Probably a stress response by the plants, it means hotter countries like Italy may produce more pungent leaves.

You can test this effect at home. Get two small pots and some rocket seeds from a local garden centre or supermarket. Plant two or three seeds in each. Keep one well-watered and relatively shaded, and the other in direct sunlight, watering infrequently. After a few weeks, taste the leaves from each pot one should taste much hotter.

The taste and flavour of rocket also varies because of the genetics of different varieties. Not only do leaves contain hot, pungent isothiocyanates, but also sugars (which create sweetness); pyrazines (which can smell earthy and pea-like); aldehydes (which smell like grass); alcohols (one in particular smells just like mushrooms); and many other types yet to be identified.

Recently, the worlds first rocket genome and transcriptome sequence was produced from the Eruca sativa species, allowing researchers to understand which genes may be responsible for making the compounds related to taste and flavour. Its genome contains up to 45,000 genes, which is more than the 42,611 genes humans are thought to have.

The research also found that different varieties produce more isothiocyanates and sugars than others. This explains why leaves can taste so different in the supermarket, even when bought from the same shop at the same time of the year. By knowing which genes are expressed in tissues and when, we can select rocket plants with improved taste and flavour profiles and breed new and improved cultivars.

To further complicate matters, our own genetics mean we dont all taste chemical compounds the same. We have many thousands of different odour receptors in our brains, and many different combinations of taste receptors on our tongues. These genetic differences are one of the reasons why coriander tastes different to different people. Those with a variant of the OR6A2 gene perceive the leaves as having a soapy flavour, which is thanks to the aldehyde compounds in coriander that activate this receptor variant.

Depending on whether you have a functioning or non-functioning copy of certain taste receptor genes, you may not be able to taste certain compounds at all. In the other extreme, if you have two working copies of a particular gene, some foods may taste unbearably bitter and unpleasant.

Another classic example is Brussels sprouts. Some people love them, while others loathe them. This is because of the gene TAS2R38 which gives us the ability to taste the bitter glucosinolate compounds in these vegetables as well as rocket.

Love or loathe? The superfood continues to divide (iStock)

Those people with two working copies of the gene are bitter supertasters. People with only one are medium tasters, while those with no working copies are blind to these compounds. So what is intense and inedible to one person might be pleasant and mild to another.

This partly explains peoples general food preferences and rocket leaves are an excellent example of these processes in action. A consumer study of rocket leaves showed that some people like them hot and pungent, others like them sweet and mild, and others just dont like them at all.

However, peoples culture and life experience probably also determine whether they like rocket and other foods. A previous study of rocket showed that peoples genetic differences are not necessarily an indicator of whether they will like something. Its perfectly possible to be a bitter supertaster and like rocket and Brussels sprouts depending on your upbringing and exposure to them.

Another study showed that preference for flavour and pungency of white radish is linked to differences in geography and culture. Japanese and Korean people liked pungency created by an isothiocyanate much more than Australians. Pickled radish is a common condiment in Asian countries: being regularly exposed to a food may predispose people to like it, irrespective of their taste sensitivity.

Very little is currently known about the interactions between plant and human genotypes. But ongoing research aims to find out which compounds people with different TAS2R38 genotypes are sensitive to. This will make it possible in the future to selectively breed in (or out) certain genes, and produce rocket types tailored to a persons preferences.

Luke Bell is a lecturer in temperate horticulture at the University of Reading. This article first appeared on The Conversation

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Do you have the rocket gene? Why genetics may decide whether you like the peppery veggie - The Independent

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Deep exploration of the genetic dependencies of antibiotic function on SelectScience – SelectScience

Tuesday, June 9th, 2020

Massively parallel microbial strain engineering on a CRISPR-based benchtop platform has enabled the exploration of the genetic dependencies of antibiotic function in unprecedented scale and detail. The ability to design and deliver precisely determined edits throughout the entire E. coli genome has resulted in an unparalleled opportunity to query a diverse population of strain variants for their growth responses to antibiotics from multiple different functional classes.

Find out more in this expert webinar as Dr. Dan Held, Director of Synthetic Biology, Microbial Applications Development, Inscripta, outlines how the knowledge garnered through the use of this strain engineering technology has significant potential to lead to the development of novel therapeutics against our most difficult antibiotic-resistant pathogens.

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All webinar participants can request a certificate of attendance, and a learning outcomes summary document for continuing education purposes.

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Expert Insight: Discover the genetic dependencies of antibiotic function – SelectScience

Tuesday, June 9th, 2020

Join us on Friday, June 19, to find out how massively parallel microbial strain engineering may lead to the development of novel therapeutics to combat the most difficult antibiotic-resistant pathogens

Massively parallel microbial strain engineering on a CRISPR-based benchtop platform has enabled the exploration of the genetic dependencies of antibiotic function in unprecedented scale and detail. The ability to design and deliver precisely determined edits throughout the entire E. coli genome has resulted in an unparalleled opportunity to query a diverse population of strain variants for their growth responses to antibiotics from multiple different functional classes.

Find out more in this expert webinar as Dr. Dan Held, Director of Synthetic Biology, Microbial Applications Development, Inscripta, outlines how the knowledge garnered through the use of this strain engineering technology has significant potential to lead to the development of novel therapeutics against our most difficult antibiotic-resistant pathogens.

Key learning objectives

Who should attend?

This webinar will run on Friday, June 19, 2020, at:

Register to watch the full webinar here>>

SelectScience runs 3-4 webinars a month across various scientific topics,discover more of our upcoming webinars>>

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‘We could have waves of infection, waves of lockdown’ says professor of genetics – Irish Examiner

Tuesday, June 9th, 2020

A professor of genetics has warned that there is every possibility of a resurge in Covid-19 and that Ireland could be facing waves of infection and waves of lockdown.

Professor David McConnell of Trinity College, Dublin called for a vigorous, centralised testing system on a massive scale similar to that employed in South Korea.

Speaking on RT radios Today with Sarah McInerney show he said: People think we're out of the woods, it's really quite dangerous. Today we are in the same position as we were on 12th March. What happened on that date - we went into an epidemic. Everything is there for us to resurge to have an equally vigorous epidemic. We could have waves of infection, waves of lockdown.

Prof McDonnell said that the authorities in Ireland should not be happy with what they have done to date.

They say that they have the capacity for 15,000 tests a day, they say they're only using 5,000 - I think there's something quite strange going on. One of the most remarkable things is we don't have a strongly organised, highly centralised, very effective, very fast tracing system or testing system.

We have a distributed system - essentially people in ordinary hospital labs have been repurposed and reassigned to work on the coronavirus testing, this is not what the Koreans had, they had this massive highly centralised, dedicated system, focused on coronavirus.

Our's is adequate for what it is being used for, but it is a very, very weakly organised system, such that it cannot be applied to other major tasks which I suggest it should be applied to.

Prof. McDonnell said he would suggest three measures first the introduction of a really vigorous test and tracing system where contacts could be tracked and traced within a day this would eliminate community-based cases, he said.

Secondly, assuming there was a well-managed system in place then there should be testing of all incoming visitors at all ports. We should have the ability to test all people coming into the country.

His third suggestion was, if there was a large capacity testing system in place then all educational and care facilities (including creches, schools and universities) could reopen if all teachers, carers and children are tested.

There was nothing in place at present he said to even consider this. If we had decided months ago, which we didn't, that we would generate a terrifically powerful testing system, today we would have been able to imagine re opening schools, easily, by September.

You'd do it in stages and you'd have a capacity which would allow you to open the schools and they would be opened under normal circumstances - no question of half of the children in a class coming in the morning, half in the afternoon, and so on.

Prof. McDonnell said that such a system could be in place by September, but it would take a massive administrative policy decision such as establishing a new testing and tracing agency which would be located on a single site, such as IDA factory.

The cost will be a very small price to pay if the prize at the end is the reopening of our economy on a normal basis.

We are running up expenses at the moment of billions of euros - the cost of a massive testing agency set up very quickly would be miniscule, a fraction of the cost which we are bearing at the present time and are likely to continue as our society and economy stutter along into the foreseeable future until a vaccine becomes available and is massively deployed around the country.

My own worry is that each time we introduce a relaxation there will be a minor, or maybe a major surge of the virus and the reaction of our authorities will be to reimpose stricter lockdown regulations, so we'll go up and down, up and down and it will be very frustrating, schools will not be reopening on a normal basis which is a terrible imposition on children and their parents.

Imagine the disappointment in September when we don't have ordinary care facilities open, ordinary creches, ordinary schools, we've put up with it until now, the incredible weather has helped, we've been stoic, people have been absolutely wonderful.

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'We could have waves of infection, waves of lockdown' says professor of genetics - Irish Examiner

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South Australian photographer snaps rare black galah with genetic mutation on the Eyre Peninsula – ABC News

Tuesday, June 9th, 2020

A rare sighting of a galah with a genetic mutation has been snapped by photographer Hoss Bolenski in Port Lincoln, South Australia.

The galah, which is usually grey and pink in colour, was seen at North Point Reserve covered in black feathers with a tinge of pink on its underbelly.

Bird Life Australia coordinator and science writer, Tanya Loos, said the unique colouring is due to a mutation called melanism, which causes an increased development of a dark-coloured pigment.

"The variation that happens in this colour abnormality is really interesting," Ms Loos said.

"Sometimes the bird is completely black and other times it's more of a flush, or a patterning where some parts are darker than usual."

Ms Loos said melanism in galahs is quite rare, making it hard to conduct broad studies on their patterns and behaviours.

"There is some idea that maybe it's a bit harder for them to find a mate, because birds attract each other not only by their behaviours, but also by their beauty and brightness of their feather colours," she said.

"If a galah is looking for a mate and looking for a galah with a really nice bright, pink blush and a deep grey colour the black bird might just seem a little bit out of the ordinary."

In Manjimup, Western Australia, a rare sighting of a black kookaburra with melanism excited bird experts who found little evidence of the bird ever being spotted in WA.

Birds can also display another genetic mutation called 'leucism' where their feathers are completely white.

"Bird Life Australia get enquiries and emails about the white birds much more commonly because leucism happens in a really wide variety of birds including honey eaters and magpies," Ms Loos said.

In 2018, a magpie with leucism was spotted in the Flinders Ranges, South Australia.

"These birds stand out like a beacon and they often get eaten by predators very quickly," Ms Loos said.

She said research suggested birds that are coloured black may have a better advantage when it comes to survival.

"They do note that sometimes the birds that are coloured black are more camouflaged, so it might be an advantage," Ms Loos said.

"But because it happens so rarely in nature it's hard to conduct broad studies on this and get some actual definitive answers."

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South Australian photographer snaps rare black galah with genetic mutation on the Eyre Peninsula - ABC News

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Human Genetics Market 2019 Break Down by Top Companies, Countries, Applications, Challenges, Opportunities and Forecast 2026 – Cole of Duty

Tuesday, June 9th, 2020

A new market report by Market Research Intellect on the Human Genetics Market has been released with reliable information and accurate forecasts for a better understanding of the current and future market scenarios. The report offers an in-depth analysis of the global market, including qualitative and quantitative insights, historical data, and estimated projections about the market size and share in the forecast period. The forecasts mentioned in the report have been acquired by using proven research assumptions and methodologies. Hence, this research study serves as an important depository of the information for every market landscape. The report is segmented on the basis of types, end-users, applications, and regional markets.

The research study includes the latest updates about the COVID-19 impact on the Human Genetics sector. The outbreak has broadly influenced the global economic landscape. The report contains a complete breakdown of the current situation in the ever-evolving business sector and estimates the aftereffects of the outbreak on the overall economy.

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The report also emphasizes the initiatives undertaken by the companies operating in the market including product innovation, product launches, and technological development to help their organization offer more effective products in the market. It also studies notable business events, including corporate deals, mergers and acquisitions, joint ventures, partnerships, product launches, and brand promotions.

Leading Human Genetics manufacturers/companies operating at both regional and global levels:

Sales and sales broken down by Product:

Sales and sales divided by Applications:

The report also inspects the financial standing of the leading companies, which includes gross profit, revenue generation, sales volume, sales revenue, manufacturing cost, individual growth rate, and other financial ratios.

The report also focuses on the global industry trends, development patterns of industries, governing factors, growth rate, and competitive analysis of the market, growth opportunities, challenges, investment strategies, and forecasts till 2026. The Human Genetics Market was estimated at USD XX Million/Billion in 2016 and is estimated to reach USD XX Million/Billion by 2026, expanding at a rate of XX% over the forecast period. To calculate the market size, the report provides a thorough analysis of the market by accumulating, studying, and synthesizing primary and secondary data from multiple sources.

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The market is predicted to witness significant growth over the forecast period, owing to the growing consumer awareness about the benefits of Human Genetics. The increase in disposable income across the key geographies has also impacted the market positively. Moreover, factors like urbanization, high population growth, and a growing middle-class population with higher disposable income are also forecasted to drive market growth.

According to the research report, one of the key challenges that might hinder the market growth is the presence of counter fit products. The market is witnessing the entry of a surging number of alternative products that use inferior ingredients.

Key factors influencing market growth:

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Human Genetics Market 2019 Break Down by Top Companies, Countries, Applications, Challenges, Opportunities and Forecast 2026 - Cole of Duty

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BBC edits article on Putins daughter overseeing genetic research project following clarification from Rosneft – Meduza

Tuesday, June 9th, 2020

The BBC Russian Service has edited its article on Putins alleged eldest daughter, pediatric endocrinologist Maria Vorontsova, partnering with Russian energy giant Rosneft to create a new genetic research center in Moscow.

The new version of the article now under the headline Rosneft became a partner in a large-scale Russian genetic project removes claims that Maria Vorontsova and Rosneft CEO Igor Sechin will sit on the new centers board of directors. Mention of Rosneft investing between $500 million and $1 billion in the project has also been removed.

The BBC notes that the aforementioned information was deleted on the basis of clarification on the part of Rosneft, received after the articles publication. The inclusion of this information did not meet the required standards for publication, the statement says.

The names of the journalists who worked on the report have also been removed from the article.

Immediately after the article in question was published, Rosneft said that it contains a baseless lie regarding the company and individuals not involved in the given project. The companythreatened the BBC with a lawsuit, as well.

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BBC edits article on Putins daughter overseeing genetic research project following clarification from Rosneft - Meduza

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How a rare bird and the coronavirus remind us that our safety depends on sciencenot wishful thinking – Genetic Literacy Project

Tuesday, June 9th, 2020

There are worse places to spend a COVID-19 lockdown than next to a sanctuary with one of the worlds rarest birdsthe New Zealand takah. And during this strange moment in history, its wonderful to watch these remarkable relics from the pasttakah were twice declared extinct and twice rebounded unexpectedly from the deadin the shadow of their last wild refuge, the Murchison Mountains in Fiordland National Park.

Indeed, these colorful swamphens and the coronavirus pandemic both exemplify opposite extremes of widely held beliefs about the natural world; attitudes towards nature, moreover, that reflect much popular misunderstanding about evolutionary biologyand genetics in particular.

Given this, the much-regarded bird and the much-reviled virus can usefully illustrate some of the important contradictions and confusions that befuddle broader public appreciation of modern genetic science. So lets begin with a little more detail about the former, the amusingly clumsy-looking takah, the worlds largest rail.

Well-known in pre-contact times to New Zealands indigenous Maori, takah were initially thought extinct by the first European scientists to examine their fossilized remainsan assessment that proved mistaken when a small number of these flightless rails were caught during the latter part of the 19th century, the last in 1898.

Presumed extinct (for the second time) for the following fifty years, takah were famously rediscovered in the rugged and remote Fiordland mountains in 1948an event that triggered both an international avalanche of publicity and intense debate about how best to protect the last remnants of the species. Today considered a national taonga or treasure, this cherished bird is now a darling poster child for New Zealand conservation.

They are also, by all accounts, extremely tastyearly Maori hunted them extensively as a source of much-prized feathers and food, and the sealers who caught and cooked one in 1850 declared it a most delicious dainty.

This then raises a question that is less facetious than might first appear: Would it be okay to eat a takah? And if not, why not? Here we can start to explore the popular beliefs about nature alluded to above, ones that result in wider uncertainty about modern genetic science and, at an extreme, vocal opposition to genetic modification and genetic engineering.

To many nature-lovers, even talking about eating an animal like the takah would likely seem immoral; after all, these birds (like other endangered species everywhere, from black rhinos to gorillas to whales) are special. Yet if we examine this belief, being special appears to amount to little more than being rare. Nor could being wild be a cause for special status; this implies, for instance, that captive-bred rare animals are of less value than their free-living counterparts.

Yet while it is rationally unclear (independent of scarcity) why wild animals should have greater intrinsic value than farmed ones, it is nevertheless a distinction that many people maketreasuring rare or wild animals over well-known domesticated ones. (This inconsistency in attitudes is also evident in the furor over the euthanizing of a single giraffe in 2014 in a zoo in Denmark, an agricultural country where tens of thousands of farm animals are routinely slaughtered each day.) If takah were as common as chickens, sayor whales as widespread as cowswould they still be seen as special?

The old adage familiarity breeds contempt is also evident in antipathy towards genetically modified foods. That is, in the same way that familiar livestock are overlooked in comparison with wild/rare animals, so too are supposedly natural everyday foodstuffs in the vehement rejection of unnatural genetically adulterated Frankenfoods. In reality, of course, all of our staple crops have themselves been genetically modified through selective breeding over time, with manyincluding such common items as corn, peaches and watermelonsveritable monstrosities compared to their wild precursors.

Furthermore, such unexamined beliefs about what is natural and what is unnatural help explain how support for wildlife conservation can morph into opposition to genetic sciencemost especially, in the idea that human activities destroy the delicate balance of nature. Despite having been long-since rejected by ecologists, the romanticized concept of a natural balanceanthropomorphised as a wise and benign Mother Nature, constantly striving to maintain the natural harmonystill holds sway in public consciousness.

A surprising example of this concept of purpose and harmony in nature is Pope Franciss recent suggestion that COVID-19 is natures response to climate change. While the Pope is an odd source for such a claim (after all, traditionally God is the one who directs plagues for His own purposes, as many believers still insist), it is nevertheless based on the same belief in a natural (or supernatural) guiding force maintaining natures equilibrium in a world bespoilt by humankind.

Such a notion, of course, stands in stark contrast to the Darwinian concept of life, in which the illusion of harmony merely masks a precarious stalemate in the ceaseless competition between and among species. Moreover, the evolutionary view regards nature as purposeless and amoral, with the ultimate aim of living organisms being simply survival and replication.

In which case, COVID-19 is not natures revenge (or Gods wrath), but rather the mindless spread of an incredibly successful sequence of genes, a contagious virus replicating at the expense of other organisms that just happen to be us. Plagues and pestilence, in other words, are as much a part of nature as wonderful animals like the takah (a point humorously made in Monty Pythons All things dull and ugly).

Potentially, the current coronavirus crisis may disabuse many people of their romanticized notions about benevolent and harmonious nature; at any rate, the overwhelming world reaction is not simply to let nature take its course but rather to act to mitigate its worse effects. And while the unexpectedness and novelty of the pandemic has left many nations floundering over how best to respond, the ultimate solution(s) can only be derived from evidence and factsin other words from empirical science. At the same time, however, the fight against COVID-19 will likely be hindered by the very things that dog the rational application of genetics to human needsmisinformation, conspiracy thinking and pseudo-science.

But before drawing the disparate threads of this argument together, lets return to the takah, itself an excellent example of the pitiless Darwinian account of life. Like much of New Zealands avian fauna, the takahs ancestors were accidental, wind-blown arrivals on these remote South Pacific islands. Lacking competition in their new environment, takah numbers rapidly expanded while at the same time evolutionary processes, including island gigantism, gradually morphed them into the large, flightless and slow-breeding animals we see today. And, like numerous other New Zealand species, the takah were therefore easily out-competed by the next set of arrivals, the fast-breeding mammals introduced by human beings.

Yet while the ensuing tidal wave of bird extinctions was initially viewed as natural and inevitable, modern attitudes have changedand now New Zealands conservation efforts are directed at preserving the surviving native species by eradicating the more recent mammalian invaders. A tragic irony here is that, in the name of conservation, many native species are kept alive only through the mass killing of exotics.

Further ironies abound. Reassured by evidence-based science, the majority of New Zealanders accept the use of 1080 sodium monofluoroacetate poison as the most effective means to control pest speciesyet at the same time, research into more humane genetic alternatives (such as the use of gene drives) are stymied by the countrys vocal anti-GMO movement and its dated and restrictive legislation on genetic technology.

Indeed, the emotional, anti-scientific hostility to 1080 poison captures many of the points raised above, most especially in the belief that native and introduced species can coexist in a natural equilibrium (a notion belied by the estimated 25 million native New Zealand birds killed by introduced predators each year).

As for the takah itself, an initial willingness to let nature take its course was a factor in the species calamitous decline to just over 100 individuals by the 1980s, before more scientifically guided (and better funded) conservation policies began to take effect. Genetics has since played a strong part in hauling the takah back from the brink of extinction, particularly in mitigating the damaging effects of in-breeding. Genetic research has also uncovered surprising findings about the takahs origins; originally divided into two subspeciesone in New Zealands North Island and the other in the South Islandmore recent genetic analysis suggests these were instead two separate species, with the extinct northern variety descended from Australian swamphens and the extant southern species more closely related to South African rails. (Convergent evolution explains the physical similarities between the distinct species on either island.)

And here, takah genetics can usefully illustrate a final point about our conceptions (and misconceptions) of the natural world. Those most attracted to idealized visions of nature (and hence prey to anti-science attitudes), often assume that science robs nature of its glory and wonder. In fact it does the opposite; the more we understand about animals such as the takah (or indeed viruses such as SARS-cov-2), the more we are able to marvel at the wonders of evolved creation. And while romantic wishful thinking wont save the tasty takah from extinction (nor us humans from COVID-19), modern science just might.

Patrick Whittle has a PhD in philosophy and is a freelance writer with a particular interest in the social and political implications of modern biological science. Follow him on his website patrickmichaelwhittle.com or on Twitter @WhittlePM

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Genetic editing of grapes by CRISPR could reduce the use of pesticides in Europe – FreshPlaza.com

Tuesday, June 9th, 2020

The cultivation of grapes in Europe, whose acreage represents 3% of the total cultivable acreage, accounts for up to 65% of the pesticides used by EU growers, given the high incidence of powdery mildew and mildew in the productions. However, this percentage could be drastically reduced if the EU opted for the most advanced plant reproduction technologies, such as CRISPR, which would make it possible to obtain grape varieties resistant to both fungi.

Thus, research has been carried out in this field for several years in order to improve European grape varieties. In the case of Italy, in 2015, ten genetically edited grape varieties were registered in the National Variety Catalog, and in 2018, the first field harvests were carried out. Although still in the pre-commercial phase, the results so far have been positive in terms of resistance to diseases.

The researchers hope that the regulatory uncertainty of CRISPR technologies will be resolved (they are subject to the same regulations as transgenics, despite not being the same). They also hope that both producers and consumers will learn about the potential of these techniques to tackle the agro-food and environmental challenges that humanity is facing.

Source: agronewscastillayleon.com

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Researchers look at the role genetics play in the severity of coronavirus symptoms – WSAW

Wednesday, May 27th, 2020

(WZAW) -- Scientists around the world are racing to understand COVID-19 and the novel coronavirus that causes the disease. Among the questions theyre asking is why do most people who are infected show mild to moderate symptoms, or possibly no symptoms at all, whereas others develop a severe form of the disease.

To help gather more insights, DNA company 23andMe has launched a research study to help determine whether genetics may play a role. 23andMes unique research model, with millions of customers consenting to participate, offers their scientists a powerful tool for potential insight into the role genetics may play in explaining differences in the severity of the novel coronavirus.

With more than 400,000 existing 23andMe customers already enrolled to participate, including several thousand whove confirmed they had the virus, 23andMe is opened enrollment to people who have been hospitalized with the disease but are not currently customers. Opening up the research to individuals with more severe symptoms will increase their ability to learn how genes may play a role in the severity of this disease.

Joyce Tung, vice president of research at 23andMe joined NewsChannel 7 at 4 on Tuesday to talk about how the research is helping to understand the role genetics plays in the severity of COVID-19 symptoms.

Based on our past studies on infectious diseases, for some of those we saw that genes for example that are part of the immune system influence the susceptibility too in severity of those diseases, Tung explained.

Tung said researchers hope genetics can give us insights into the biological pathways in humans that influence the severity of the disease.

And perhaps with this information, we can develop different treatments, she added.

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How Spread of Cancer Is Related to Genetics – NewsClick

Wednesday, May 27th, 2020

Cancer metastasis is a major cause of death which has attracted intense scientific research over the years. Metastasis is the process where cancer propagates to other tissues from where it started initially. It has long been thought that the genetic mutations which occur in the cells that cause cancer in them can also provide these cells with the ability to pervade other tissues further. But a question remainsdoes the inherited genetic make up of a person have a role in metastasis?

Before proceeding further, let us quickly recapitulate some facts. In most cancers, the genetic mutation occurs in somatic cells. This means that these cancer-causing genetic mutations are not inherited. For a genetic mutation to be called inherited, the mutations must have occurred in the germ cells, that is the cells involved in reproduction. Precisely, the egg cells and the semen.

The somatic mutations occur in a lifetime mostly due to external factors, like life style habits or environmental factors.

Apart from the somatic mutations, what the inherited mutations do in cancer metastasis has been a profound question in cancer research. Now, a Nature Medicinepublication has come out with some elaborated data which indicate the link between cancer metastasis and someones inherited genetics.

This study is based on melanoma, a type of cancer of the skin and finds that a single gene can alter the level of metastasis in this kind of cancer. The researchers also think that this gene and others can have similar effects in other cancer types.

The specific gene in question is the APOE gene, which is present in all types of cells of the body. The production of the gene, a particular protein, appears to have interference in a number of processes that cancer cells undertake to metastasise. The important processes are like forming blood vessels, penetrating deep into other healthy tissues as well as resisting attacks of bodys cancer targeting immune cells.

The APOE gene has three types, namely, ApoE2, ApoE3, ApoE4. An individual carries one type of the APOE gene among its varieties. It has been found that different melanoma patients have different degrees of progression of the cancer. The probable answer to it could be the presence of different APOE genes in different people.

In the latest study, experiments with mice show that those possessing the ApoE4 variety of the gene have the smallest tumour and also the least spread of melanoma. Also, it was found that ApoE4 is the most effective version of the gene that could provide enhanced immune response to tumour cells. In comparison with other types of the APOE gene, mice having the ApoE4 type have higher amount of T cells involved in fighting melanoma tumour along with reduced blood vessels. Benjamin Ostendorf, the first author of the study says, We think that a major impact of the variations in ApoE arises from differences in how they modulate the immune system's attack.

Recruiting genetic data from more than 300 melanoma patients also showed similar results as in the mice. Patients possessing the ApoE4 type could survive the longest and patients with ApoE2 type survived the least. While, the ApoE3 types ability to suppress tumour progression lies in between the other two.

The genetic inheritance and its link to cancer progression is hoped to better development of cancer therapeutics in future.

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Research reveals gene role in both dementia and severe Covid-19 – The Guardian

Wednesday, May 27th, 2020

People with a genetic mutation that increases the risk of dementia also have a greater chance of having severe Covid-19, researchers have revealed.

The study is the latest to suggest genetics may play a role in why some people are more vulnerable to the coronavirus than others, and could help explain why people with dementia have been hard hit: dementia is one of the most common underlying health conditions among those who have died from Covid-19 in England and Wales.

It is not just age: this is an example of a specific gene variant causing vulnerability in some people, said David Melzer, a professor of epidemiology and public health at Exeter University and a co-author of the study.

Writing in the Journal of Gerontology: Medical Sciences, Melzer and colleagues report how they analysed data from the UK Biobank, a research endeavour that has collected genetic and health data on 500,000 volunteers aged between 48 and 86.

The team focused on a gene called ApoE this gives rise to proteins involved in carrying fats around the body, and can exist in several forms. One such variant, called e4, is known to affect cholesterol levels and processes involved in inflammation, as well as increasing the risk of heart disease and dementia.

The researchers found 9,022 of almost 383,000 Biobank participants of European ancestry studied had two copies of the e4 variant, while more than 223,000 had two copies of a variant called e3. The former, the team add, have a risk of dementia up to 14-fold higher than the latter.

The team then looked at positive tests for Covid-19 between 16 March and 26 April when testing for the coronavirus was largely carried out in hospitals, suggesting the cases were severe.

The results reveal 37 people who tested positive for Covid-19 had two copies of the e4 variant of ApoE, while 401 had two copies of the e3 variant. After taking into account various factors, including age and sex, the team say people with two e4 variants had more than double the risk of severe Covid-19 than those with two e3 variants.

Melzer said the findings were not down to people with two e4 variants being more likely to be living in a care home settings that have been hard hit by Covid-19 since the association remained even when the team excluded participants with a diagnosis of dementia. None of the Covid-19 positive participants with two e4 variants of the ApoE gene had a dementia diagnosis.

It is pretty bulletproof whatever associated disease we remove, the association is still there. So it looks as if it is the gene variant that is doing it This association is not driven by people who actually have dementia, said Melzer.

The team say further work is needed to unpick the link.

Prof Tara Spires-Jones, an expert in neurodegeneration at the University of Edinburgh who was not involved in the study, said the large number of Biobank participants meant the association between the ApoE genetic variants and Covid-19 risk was robust, but stressed the study did not prove the former caused the latter. Nevertheless, she said, the study was important.

It is possible that the role of ApoE in the immune system is important in the disease and future research may be able to harness this to develop effective treatments, she said.

Fiona Carragher, a director of research and influencing at Alzheimers Society, said people with dementia and their families were desperately worried, adding the government must take urgent action to protect people with dementia. But, she said, more research was needed to delve into the possible link between the e4 variant of ApoE and severe Covid-19.

Other factors may contribute, so it is difficult to draw firm conclusions at this stage. But clearly much more in-depth research is urgently needed to fully understand why people with dementia seem to be at a higher risk and to what extent factors like ethnicity and genetics might play a role, she said.

But Prof David Curtis, honorary professor at the UCL Genetics Institute, urged caution. He noted that among the studys limitations, diagnoses of dementia in recent years are unlikely to be captured, meaning that the link between the e4 variant and severe Covid-19 may still be driven by more people with two e4 variants having dementia than those with two e3 variants.

Im afraid this study does not really convince me that the ApoE e4 allele [gene variant] is really an independent risk factor for severe Covid-19 infection, he said. I would want to see this tested in a sample where dementia could be more confidently excluded, perhaps a younger cohort. I am sure additional data will soon emerge to illuminate this issue.

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Survey on Genetic Diversity, Biofilm Formation, and Detection of Colis | IDR – Dove Medical Press

Wednesday, May 27th, 2020

Saeed Khoshnood,1,2 Mohammad Savari,1,2 Effat Abbasi Montazeri,1,2 Ahmad Farajzadeh Sheikh1,2

1Infectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; 2Department of Microbiology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Correspondence: Ahmad Farajzadeh SheikhInfectious and Tropical Diseases Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Khuzestan 61357-15794, IranTel +98 9161133491Fax +98 61 3333 2036Email farajzadehah@gmail.com

Introduction: Acinetobacter baumannii is an opportunistic pathogen responsible for nosocomial infections. The emergence of colistin-resistant A. baumannii is a significant threat to public health. The aim of this study was to investigate the molecular characterization and genotyping of clinical A. baumannii isolates in Southwestern Iran.Methods: A total of 70 A. baumannii isolates were collected from patients admitted to Imam Khomeini Hospital in Ahvaz, Southwestern Iran. Minimum inhibitory concentration test was conducted by using Vitek 2 system. The presence of biofilm-forming genes and colistin resistance-related genes were evaluated by PCR. The isolates were also examined for their biofilm formation ability and the expression of pmrA and pmrB genes. Finally, multilocus sequence typing (MLST) and PCR-based sequence group were used to determine the genetic relationships of the isolates.Results: Overall, 61 (87.1%) and 9 (12.8%) isolates were multidrug-resistant (MDR) and extensively drug-resistant (XDR), respectively. Colistin and tigecycline with 2 (2.8%) and 32 (45.7%) resistance rates had the highest effect. Among all the isolates, 55 (78.5%), 7 (10%), and 3 (4.3%) were strong, moderate, and weak biofilm producers, respectively. The frequency rates of biofilm-related genes were 64 (91.4%), 70 (100%), 56 (80%), and 22 (31.42%) for bap, ompA, csuE, and blaPER1, respectively. Overexpression of pmrA and pmrB genes was observed in two colistin-resistance isolates, but the expression of these genes did not change in colistin-sensitive isolates. Additionally, 37 (52.8%) and 8 (11.4%) isolates belonged to groups 1 (ICII) and 2 (IC I), respectively. MLST analysis revealed a total of nine different sequence types that six isolates belonged to clonal complex 92 (corresponding to ST801, ST118, ST138, ST 421, and ST735). Other isolates were belonging to ST133 and ST216, and two colistin-resistant (Ab4 and Ab41) isolates were belonging to ST387 and ST1812.Conclusion: The present study revealed the presence of MDR and XDR A. baumannii isolates harboring biofilm genes and emergence of colistin-resistant isolates in Southwestern Iran. These isolates had high diversity, which was affirmed by typing techniques. The control measures and regular surveillance are urgently needed to preclude the spread of these isolates.

Keywords: Acinetobacter baumannii, drug resistance, colistin, MLST, clonal complex

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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New analysis may rewrite the history of Washington states coronavirus outbreak – Seattle Times

Wednesday, May 27th, 2020

A Snohomish County man who was the countrys first confirmed COVID-19 patient was probably not the source of the coronavirus outbreak in Washington state, according to a new genetic analysis by an international group of scientists.

The finding upends one of the most compelling scientific narratives of the pandemics arrival in the United States, but it also showcases the power of quick public-health action, said Michael Worobey, lead author of the report and head of the University of Arizonas Department of Ecology and Evolutionary Biology.

As researchers learn more about the pandemics roots, its becoming clear that the virus entered the United States via multiple paths and at multiple times. But Washington still seems to be the place where it first took hold in this country and flared into a community outbreak, said co-author Joel Wertheim, a molecular epidemiologist at the University of California, San Diego.

The Snohomish County man, sometimes erroneously referred to as patient zero, started feeling sick after he returned Jan. 15 from a visit to Wuhan, China the pandemics birthplace. He was confirmed positive Jan. 20. Public-health officials tested and isolated everyone they could identify who came into contact with him, and found no other infections.

So it was baffling when a second case emerged Feb. 28 and genetic analysis showed it was similar to the first, differing by only two mutations. Trevor Bedford, a computational biologist at the Fred Hutchinson Cancer Research Center, and his colleagues, concluded that the two cases were linked with the Snohomish County man as the original source. They also estimated the virus had been spreading silently for six weeks.

But the new analysis, which was posted Monday on the preprint site bioRxiv and has not been peer-reviewed, says its more likely that quick action by public-health officials succeeded in stamping out any spread from the first infection, turning it into a dead end. The outbreak that eventually flared in late February and early March was probably the result of a separate introduction from China around Feb. 13, either directly or by way of British Columbia, Worobey and his colleagues argue.

To reach that conclusion, the team examined many more viral genomes than had been available earlier in the outbreak and found none in Washington that exactly matched the earliest known infection. They also found none of the expected missing link genomes, intermediate between the first case and subsequent infections.

They then used computer simulations to, as Worobey put it, rerun the tape of evolution over and over again. Thousands of times, in fact, to see how the viral genomes would be expected to change and evolve. Again, they found no indication that the viral strain carried by the Snohomish County man was the source of the states spreading outbreak.

To understand how a closely related strain might have been introduced separately, the team examined travel patterns and found that the Feb. 2 ban on air travel from China was actually quite leaky, with an estimated 40,000 U.S. residents returning to the United States from China via airports including Seattle-Tacoma International Airport.

The remaining influx likely provided ample opportunity for a second introduction to Washington State, the report says. It is also possible that the virus entered via nearby Vancouver, British Columbia, which is closely linked to both China and Washington state.

But Dr. Jared Roach, a senior research scientist at the Institute for Systems Biology in Seattle, said the new analysis is not likely to be the final word. Among other things, the model the researchers used for their simulations didnt appear to account for super-spreader events, like a choir practice where many people were infected, which could affect the virus evolutionary path, he said. Nor did it account for other possible variations in the way the virus spread, with some lineages fizzling out and others catching fire.

They are far too confident their answer is the only answer, Roach said. I think there are other explanations they didnt consider.

In a series of 18 tweets Monday, Bedford said he now agrees a second introduction was probably responsible for Washingtons outbreak. However, hes still convinced that second seed was planted fairly early, sometime between Jan. 18 and Feb. 9.

The exact timing is difficult to determine, Worobey said. But the implications are important.

If the virus had a six-week head start, spreading unseen and, thus, untouchable by public-health measures, then it was essentially hopeless theres not much anyone could have done to prevent the eventual flare-up.

But if, as the new analysis suggests, the virus didnt take hold until mid-February, then control might have been possible if the country hadnt fumbled the rollout of testing and tracing capacity.

The timing suggests strongly that those weeks that were lost were pretty consequential weeks, and that we did have more of a chance (of stopping it) than we realized, Worobey said.

The paper also criticized the U.S. Food & Drug Administration for halting the Seattle Flu Study, which could have provided valuable insights into the early spread of the virus. The project, funded by Bill Gates, had been collecting nasal swabs from volunteers across King County to study the spread of respiratory disease. Their samples represented a potential wealth of information, but researchers were initially barred from accessing that information because the project lacked specific approval to test the samples for the coronavirus.

The timeline of the pandemics spread is being revealed in bits and pieces, and a full picture probably wont emerge for quite some time. At least two Washington residents who were sick in December later tested positive for antibodies to the new coronavirus, though its not clear when their infections occurred. The first recorded death in the United States occurred in Snohomish County on Feb. 26, but posthumous analyses in California confirmed two earlier fatalities, the first on Feb. 6.

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Genetic Mutation Appears to Link COVID-19 to Dementia, Study Finds – The Daily Beast

Wednesday, May 27th, 2020

Dementia is one of the most common underlying health conditions in people who have died from the novel coronavirus in England and Walesnow British researchers say they might know why. A study has found that people with a specific genetic mutation known to increase the risk of dementia also have a much greater chance of having severe COVID-19, according to The Guardian. Its the latest study to suggest genetics may play a role in why some people are hit harder by the coronavirus than others, and could help explain why people with dementia appear to be particularly vulnerable. It is not just age: This is an example of a specific gene variant causing vulnerability in some people, said study co-author David Melzer, a professor of epidemiology and public health at Exeter University. The team found that having the gene that raises the risk of dementia could make people twice as likely to suffer badly from the virus.

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Israeli Lab: Drugs For Gaucher Disease May Work Against Coronavirus, Other Viral Infections | Health News – NoCamels – Israeli Innovation News

Wednesday, May 27th, 2020

Israeli scientists at the Israel Institute for Biological Research (IIBR) have found that a combination of two existing antiviral drugs for Gauchers disease appears to inhibit the growth of SARS CoV-2, the virus that leads to COVID-19 and may work against other virus infections, including a common flu strain.

The IIBR is a governmental research center specializing in biology, chemistry and environmental sciences that falls under the jurisdiction of the Prime Ministers Office. During the pandemic, announcements have been issued by the Defense Ministry.

According to a press announcement on Tuesday, scientists at the secretive bio-defense lab tested an analog of the FDA-approved drug Cerdelga, and an analog of a second drug, Venglustat, currently in advanced trials. They found that, in combination, the drugs led to a significant reduction in the replication capacity of the coronavirus and to the destruction of the infected cells.

The two drugs are used to treat Gaucher disease, an inherited genetic condition most common in people of Ashkenazi Jewish descent that leads to the buildup of fatty substances in certain organs, particularly the spleen and liver, and can affect their function. The disease can also lead to skeletal abnormalities and blood disorders, In rare cases, Gauchers disease can also lead to brain inflammation, according to the Mayo Clinic. The disease is unrelated to COVID-19.

The Israeli researchers tested the drugs on mouse models using four different RNA viruses: Neuroinvasive Sindbis virus (SVNI), an infection transmitted via mosquitos that can lead to years of debilitating musculoskeletal symptoms; West Nile virus (WNV), also a mosquito-borne disease that can cause neurological disease and is potentially fatal; Influenza A virus, a strain of the flu; and SARS-CoV-2.

The researchers found that the two drugs were effective in all four cases. They work by inhibiting glucosylceramide synthase *GCS), an enzyme involved in the production of glucocerebroside, a lipid that accumulates in the tissues of patients affected with Gaucher disease. In the lab setting, they inhibited the replication of the viruses, and in the case of mice infected with SVNI, increased their survival rate.

In the case of COVID-19, the drugs have an antiviral effect on the SARS-CoV-2 clinical isolate in vitro, with a single dose able to significantly inhibit viral replication within 2448 h.

The two drugs are currently being tested for their effectiveness in treating animals infected with the coronavirus.

The study, published in bioRxiv, has not yet been peer-reviewed. The authors are all from the IIBRs Department of Infectious Diseases

The data suggests that GCS inhibitors can potentially serve as a broad-spectrum antiviral therapy and should be further examined in preclinical and clinical trial, the scientists wrote, adding that repurposing approved drugs can lead to significantly reduced timelines and required investment in making treatment available.

Treatment of a new disease such as COVID-19 using an existing, approved drug may serve as an effective short-term solution considering that one of the major challenges in addressing such a pandemic is the length of time it takes for both the research and approval phases of new drugs, the Defense Ministry wrote in the announcement.

The lab has been conducting various research into COVID-19 for several months, including studies on possible treatment and a vaccine. Israeli Prime Minister Benjamin Netanyahu tapped the institute in early February to begin development on inoculation. In early April, the center reported significant progressand trials on animals.

The institute has also been involved in plasma collection from Israelis who have recovered from COVID-19 to research antibodies, proteins made by the immune system that can attack the virus.

Earlier this month, the IIBR said it completed a groundbreaking scientific development toward a potential treatment based on an antibody that neutralizes SARS-CoV2. The development had three key parameters, according to the IIBR: first, the antibody is monoclonal (lab-made identical immune cells that are all clones of a unique parent cell), and contains a low proportion of harmful proteins; second, the institute has demonstrated the ability of the antibody to neutralize the coronavirus; and third, the antibody was specifically tested on SARS CoV-2.

The Ness Ziona-based institute said it is now pursuing a patent for its development after which it will approach international manufacturers.

A number of Israeli scientific teams and over 100 groups worldwide are currently working to develop a vaccine or a treatment for COVID-19.

At least 10 candidate vaccines are in clinical evaluation, including those of Massachusetts-based company Moderna which was the first to develop an experimental vaccine that went into trial quickly, and California-based biotech firm Gilead Sciences, which is evaluating the safety and efficacy of its novel antiviral drug Remdesivir, developed originally for Ebola, in adults diagnosed with COVID-19.

Last month, Israeli scientists at theMigal Galilee Research Institute formed a new company, MigVax, to further adapt a vaccine they developed for a deadly coronavirus affecting poultry for human use. The scientists had been working for four years to develop a vaccine for IBV (Infectious Bronchitis Virus) which affects the respiratory tract, gut, kidney and reproductive systems of domestic fowl.

Also in April, an Israeli scientist wasawarded a US patent for his innovative vaccine design for the corona family of viruses and indicated that he was on track to develop a vaccine for SARS CoV2.

Meanwhile, two Israeli bio-medical companies nabbed FDA approval for separate trials in the US with their respective solutions for COVID-19 as part of a compassionate use program, a treatment option that allows for the use of not-yet-authorized medicine for severely ill patients.

BothRedHill BioPharma, a publicly-traded specialty biopharmaceutical company, andPluristem Therapeutics, also a public company that specializes in placental cell therapy, were given the green light for their imminent separate studies with the investigational drug, opaganib, and the placental cell therapy PLX, respectively.

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The possible link between genetics and coronavirus – CBS19.tv KYTX

Monday, May 25th, 2020

SAN ANTONIO Scientists around the world are racing to understand coronavirus and why most people who are infected show mild to moderate symptoms or sometimes no symptoms at all and others develop a severe form of the disease, in some cases resulting in death.

23andMe has provided personalized genetic reports for years. But now he biotechnology company is switching gears to help battle coronavirus with a new study, and they're looking for those with a positive diagnosis to take part.

"Given that COVID-19 has taken a turn of turning our lives upside down so very, very quickly, at this stage we just don't know to what extent genetics plays a role in determining the severity of outcomes," said Adam Auton, the principal scientist of statistical genetics at 23andMe.

To participate in the study, you must be over 18 years of age and live in the U.S., be willing to provide a saliva sample for DNA testing, complete an online survey, have a positive coronavirus diagnosis, and you must have been hospitalized due to coronavirus-related symptoms. The stronger your symptoms, the likelier you could play a big part in the research.

"In order to maximize our abilities to make a discovery, we would really like to provide people with severe outcomes (the opportunity) to come into the study and participate in the study," Auton said.

This study could even shed some light on a phenomenon known as the COVID cliff when patients who seem to be improving suddenly get worse and whether or not genetics play a role. Dr. Diego Maselli, the Medical Director of respiratory therapy at University Hospital told us,

"Unfortunately, some of these patients, when this happens or this phenomenon starts to happen, then they get sicker and they end up in the ICU and sometimes on a ventilator," said Diego Maselli, the medical director of respiratory therapy at University Hospital.

"The hope (is) that our study can help provide information that will provide some answers to those sorts of questions," Auton said.

So far, 600,000 Americans have agreed to participate, but only 9,000 say they had COVID-19. 23andMe is looking for thousands more.

"It's the nature of genetic studies that we really need very large numbers of people to participate," Auton said.

If you would like more information about the study or to participate, click here.

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The possible link between genetics and coronavirus - CBS19.tv KYTX

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