StemCell Therapy

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

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

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

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.

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

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

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

(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.

Continued here:
Researchers look at the role genetics play in the severity of coronavirus symptoms - WSAW

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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How Spread of Cancer Is Related to Genetics - NewsClick

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

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

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

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

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.

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

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

During the coronavirus crisis, the Los Angeles Times is making some temporary changes to our print sections. The prime-time TV grid is on hiatus in print but an expanded version is available in your daily Times eNewspaper. You can also find a printable PDF online: latimes.com/whats-on-tv.

Americas Got Talent Simon Cowell, Heidi Klum, Howie Mandel and host Terry Crews return with new judge Sofia Vergara in the season premiere of the unscripted competition. 8 p.m. NBC

DCs Stargirl After Courtney (Brec Bassinger) has an unexpected run-in with a member of the Injustice Society of America, Pat (Luke Wilson) reveals the truth to her about their history in a new episode of this superhero series. 8 p.m. CW

Deadliest Catch In this new episode Junior makes the risky decision to venture into Russian waters in his quest for golden crab, while cocaptains Jake and Johnathan try to broker an alliance with longtime rival Keith Colburn. 8 p.m. Discovery

DCs Legends of Tomorrow The Legends are scattered into different TV shows in this new episode. 9 p.m. CW

Chopped The competing chefs get a pork theme in this new episode of the culinary competition. 9 p.m. Food Network

Grant As the Civil War continues, Ulysses S. Grant takes incredible risks and becomes Abraham Lincolns favorite general. 9 p.m. History

World of Dance Contestants must perform in a stripped-down warehouse to prove they have what it takes for this unscripted competition series. Jennifer Lopez, Derek Hough and Ne-Yo are the judges. (N) 10 p.m. NBC

The Genetic Detective Investigative genetic genealogist CeCe Mooreworks with the Seattle areas Snohomish County Sheriffs Office on a double homicide from 1987 in the premiere of this documentary series. (N) 10 p.m. ABC

Supermarket Stakeout Four chefs are handing out cash to shoppers in Glendale as they compete to make the best barbecue dish in this new episode. 10 p.m. Food Network

REAL Sports With Bryant Gumbel This new episode is a virtual roundtable discussion with professional players association officials DeMaurice Smith (NFL), Michele Roberts (NBA) and Tony Clark (MLB) to discuss the impact of the COVID-19 pandemic on their games and the restart of professional sports in America. 10 p.m. HBO

Kingdom of the Mummies A team of archaeologists led by Ramadan Hussein makes the discovery of a lifetime. (N) 10:03 p.m. National Geographic

Space X: Journey To the Future (N) 10 p.m. Discovery

Coronavirus Pandemic (N) 8 and 9 a.m. CNN

Coronavirus Update (N) Noon CW

Pandemic: What You Need to Know Noon ABC

Coronavirus Crisis (N) 7 p.m. Fox

CBS This Morning Sen. Joni Ernst (R-Iowa). (N) 7 a.m. KCBS

Today (N) 7 a.m. KNBC

KTLA Morning News (N) 7 a.m. KTLA

Good Morning America Tracee Ellis Ross; Adam Rippon; Tory Johnson. (N) 7 a.m. KABC

Good Day L.A. (N) 7 a.m. KTTV

Live With Kelly and Ryan Keegan-Michael Key (Game On!); Madison Beer performs. (N) 9 a.m. KABC

The View (N) 10 a.m. KABC

Rachael Ray Clinton Kelly. (N) 10 a.m. KTTV

The Talk (N) 1 p.m. KCBS

Tamron Hall Janelle Mone (Homecoming); dancer Misty Copeland, Swans for a Relief. (N) 1 p.m. KABC

The Real Guest host Eva Marcille. (N) 1 p.m. KTTV

The Kelly Clarkson Show Joel McHale; Grace Byers; Duff Goldman cake demo. (N) 2 p.m. KNBC

The Ellen DeGeneres Show Howie Mandel; Sarah Cooper. (N) 3 p.m. KNBC

Amanpour and Company (N) 11 p.m. KCET; midnight KVCR; 1 a.m. KLCS

The Tonight Show Starring Jimmy Fallon Jennifer Lopez; Michelle Obama; Brad Pitt. (N) 11:34 p.m. KNBC

The Late Show With Stephen Colbert Andrew Cuomo; Christine and the Queens perform. 11:35 p.m. KCBS

Jimmy Kimmel Live! (N) 11:35 p.m. KABC

Nightline (N) 12:06 a.m. KABC

Cry Freedom (1987) 8:48 a.m. Encore

Dont Think Twice (2016) 8:59 a.m. Starz

A Bronx Tale (1993) 9 a.m. AMC

Total Recall (1990) 9 a.m. IFC

I Know Where Im Going! (1945) 9:15 a.m. TCM

Chocolat (2000) 9:35 a.m. HBO

While You Were Sleeping (1995) 10 a.m. Showtime

The Birds (1963) 10 a.m. Sundance

Black Hawk Down (2001) 10:33 a.m. Starz

The Game (1997) 11:29 a.m. Encore

Fury (2014) 11:30 a.m. AMC

Ice Age (2002) 11:30 a.m. Freeform

Jaws (1975) 11:40 a.m. HBO

Overlord (2018) 1:25 p.m. Epix

Hook (1991) 1:30 p.m. Freeform

Far and Away (1992) 1:40 p.m. Cinemax

Undercover Brother (2002) 1:59 p.m. Starz

American Sniper (2014) 2:30 p.m. AMC

Harry Potter and the Deathly Hallows: Part 1 (2010) 2:50 p.m. Syfy

Travels With My Aunt (1972) 3 p.m. TCM

The Cider House Rules (1999) 3:27 p.m. Starz

8 Mile (2002) 3:30 p.m. VH1

Unstoppable (2010) 4 p.m. HBO

The Negotiator (1998) 4 p.m. Ovation

Men of Honor (2000) 4 and 6:30 p.m. WGN America

Despicable Me (2010) 4:40 p.m. Freeform

Crawl (2019) 4:55 p.m. Epix

Incendiary Blonde (1945) 5 p.m. TCM

Wonder Woman (2017) 5 p.m. TNT

Top Gun (1986) 5:30 p.m. AMC

The Meddler (2015) 5:34 p.m. Starz

First Man (2018) 5:35 p.m. Cinemax

Harry Potter and the Deathly Hallows: Part 2 (2011) 6:05 p.m. Syfy

Despicable Me 2 (2013) 6:45 p.m. Freeform

Lady Sings the Blues (1972) 7:15 p.m. TCM

Drag Me to Hell (2009) 7:19 p.m. Encore

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Ghost (1990) 8 and 11 p.m. BBC America

The Cabin in the Woods (2011) 8 p.m. Epix

The Hangover (2009) 8 p.m. IFC

Shrek (2001) 8:55 p.m. Freeform

The Usual Suspects (1995) 9 p.m. Ovation

Funny Girl (1968) 10 p.m. TCM

Star Trek (2009) 11:05 p.m. AMC

The Descent (2005) 11:05 p.m. Epix

The Professional (1994) 11:30 p.m. Ovation

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What's on TV Tuesday: 'The Genetic Detective'; coronavirus - Los Angeles Times

An international research team has identified a candidate thinness gene that could help to explain why some people can seemingly stay slim no matter what they eat. A genetic association study that analyzed data from more than 47,000 people in an Estonian biobank implicated ALK as a key gene that may regulate thinness and play a role in resisting weight gain in metabolically healthy thin people. Further studies in animal models showed that deleting ALK resulted in thinner flies and thinner mice, and demonstrated that ALK expression in the brain may be involved in regulating energy expenditure.

ALK is already a recognized anticancer target, and the researchers suggest that targeting the gene may represent a future therapeutic strategy against obesity. If you think about it, its realistic that we could shut down ALK and reduce ALK function to see if we did stay skinny, said Josef Penninger, PhD, director of the Life Sciences Institute and professor of the department of medical genetics at the University of British Columbia. ALK inhibitors are used in cancer treatments already. Its targetable. We could possibly inhibit ALK, and we actually will try to do this in the future. Penninger is senior author of the teams published paper in Cell, which is titled, Identification of ALK in Thinness. The reported studies involved a multidisciplinary team of researchers in Austria, Switzerland, Estonia, China, Australia, Canada, and Sweden, and the U.S.

Theres considerable variability in how susceptible different people are to putting on weight. We all know these people: its around one percent of the population, said Penninger. They can eat whatever they want and be metabolically healthy. They eat a lot, they dont do squats all the time, but they just dont gain weight.

Body mass index (BMI), which is commonly used to classify weight categories, is a highly complex trait that is impacted by genes and environmental cues, the researchers wrote. And while more than 700 common single nucleotide polymorphisms (SNPs) have been linked with BMI, only a limited number of genes involved in regulating human body weight have been identified and validated. To date, most studies have focused on susceptibility to obesity, and only a few have looked at the genetic basis of thinness in humans or animal models. Everybody studies obesity and the genetics of obesity, Penninger pointed out. We thought, Lets just turn it around and start a new research field. Lets study thinness.

To do this Penningers team analyzed data from the Estonian Biobank, which includes 47,102 people aged 2044 years. The investigators carried out a genome-wide association study (GWAS) to compare the DNA samples and clinical data of healthy thin individualswho were in the lowest 6th percentilewith normal-weight individuals, in the search for genetic variants linked with thinness. Their results highlighted genetic variants in the ALK gene that were specific to the thin individuals.

Scientists have known that the ALK gene frequently mutates in various types of cancer, and while it is viewed as an oncogene that can drive the development of tumors, the role of ALK outside of cancer isnt understood. ALK has been extensively studied in cancer, but little is known about the biological role of ALK outside the context of cancer, they wrote. The new finding suggested that the ALK gene might play a role as a thinness gene involved in weight-gain resistance.

The researchers investigated the association between ALK and thinness through a series of studies in Drosophila fruit flies, and in mice. Their experiments demonstrated that mice in which the ALK gene was knocked out remained thin and were resistant to diet-induced obesity. Intriguingly, Alk knockout mice were significantly protected against HFD-induced obesity, the researchers wrote. ALK deficiency was also linked with reduced weight gain in a genetic obesity mouse model. Even when the ALK knockout mice had the same diet and activity levels as normal mice, they still demonstrated lower body weight and body fat from an early age, which persisted into adulthood.

Further studies in mice suggested that ALK, which is highly expressed in the brain, plays a role in instructing the fat tissues to burn more fat from food. Expression analysis revealed high Alk mRNA levels in the hypothalamus, especially in the PVN, which is also true for humans, the investigators wrote. Mechanistically, we found that ALK expression in hypothalamic neurons controls energy expenditure via sympathetic control of adipose tissue lipolysis Our genetic and mechanistic experiments identify ALK as a thinness gene, which is involved in the resistance to weight gain.

The findings could help scientists develop therapeutics against ALK as a future strategy against obesity. The team also plans to further study how neurons that express ALK regulate the brain at a molecular level to balance metabolism and promote thinness.

The Estonian Biobank that the team studied was ideal because of its wide age range and its strong phenotype data. We took advantage of the wide age range of the unique Estonian biobank recruitment as well as its strong phenotypic datasets, making ECGUT [Estonian Genome Center of the University of Tartu] an ideal starting point to identify potential variants and genes playing a role in thinness, the scientists noted. Even so, one limitation for replicating these findings is that biobanks that collect biological or medical data and tissue samples dont have a universal standard in data collection, which makes comparability a challenge. The researchers say they will need to confirm their findings with other data banks through meta-analyses. You learn a lot from biobanks, said Penninger. But, like everything, its not the ultimate answer to life, but theyre the starting points and very good points for confirmation, very important links and associations to human health.

The team suggests its work is unique in its combination of populationand genome-wide-scale analyses into the genetic basis of thinness, with in vivo analyses of gene function in mice and flies. Its great to bring together different groups, from nutrition to biobanking, to hardcore mouse and fly genetics, stated Penninger. Together, this is one story including evolutionary trees in metabolism, the evolutionary role of ALK, human evidence, and hardcore biochemistry and genetics to provide causal evidence.

Continue reading here:
Gene for "Thinness" Identified that May Help to Resist Weight Gain - Genetic Engineering & Biotechnology News

Investors focused on the Medical space have likely heard of Applied Genetic Technologies (AGTC), but is the stock performing well in comparison to the rest of its sector peers? Let's take a closer look at the stock's year-to-date performance to find out.

Applied Genetic Technologies is one of 889 companies in the Medical group. The Medical group currently sits at #1 within the Zacks Sector Rank. The Zacks Sector Rank gauges the strength of our 16 individual sector groups by measuring the average Zacks Rank of the individual stocks within the groups.

The Zacks Rank emphasizes earnings estimates and estimate revisions to find stocks with improving earnings outlooks. This system has a long record of success, and these stocks tend to be on track to beat the market over the next one to three months. AGTC is currently sporting a Zacks Rank of #1 (Strong Buy).

Over the past three months, the Zacks Consensus Estimate for AGTC's full-year earnings has moved 11.64% higher. This is a sign of improving analyst sentiment and a positive earnings outlook trend.

According to our latest data, AGTC has moved about 1.77% on a year-to-date basis. Meanwhile, the Medical sector has returned an average of -1.66% on a year-to-date basis. This means that Applied Genetic Technologies is outperforming the sector as a whole this year.

To break things down more, AGTC belongs to the Medical - Biomedical and Genetics industry, a group that includes 382 individual companies and currently sits at #16 in the Zacks Industry Rank. On average, this group has gained an average of 8.25% so far this year, meaning that AGTC is slightly underperforming its industry in terms of year-to-date returns.

Investors in the Medical sector will want to keep a close eye on AGTC as it attempts to continue its solid performance.

Want the latest recommendations from Zacks Investment Research? Today, you can download 7 Best Stocks for the Next 30 Days. Click to get this free reportApplied Genetic Technologies Corporation (AGTC) : Free Stock Analysis ReportTo read this article on Zacks.com click here.

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Is Applied Genetic Technologies (AGTC) Outperforming Other Medical Stocks This Year? - Yahoo Finance

The difference in COVID-19 death rates between white people and black, Asian and minority ethnic (BAME) people in the UK is shocking. One recent report found that, between the beginning of February and the end of April 2020, black people in England were 71% more likely than white people to die from COVID-19. And Asian people were 62% more likely.

This disparity has led to an inquiry by Public Health England and funding for urgent academic research into the issue. We expect many factors to be involved, including the disadvantages that BAME people face due to greater chances of poverty and health issues.

But its important that we examine whether there may also be a genetic component to the problem in order to fully understand whats going on. My colleagues and I are conducting research among frontline healthcare workers to try to see if there are any innate differences in the way different peoples immune systems respond to this specific virus, including genetic differences that may be associated with ethnicity.

Researchers have identified a greater chance of dying from COVID-19 among BAME people in several countries aside from the UK, including Norway and the US. There are many social reasons why ethnic minorities may generally be more vulnerable to disease, including a greater chance of malnutrition, more exposure to pollution due to where they live, or greater likelihood of working in less healthy environments.

Inequality and poverty also play a role in the fact that BAME people are more likely to suffer conditions that we know are linked to a greater chance of dying from COVID-19, such as diabetes and heart disease.

Initial data suggests that BAME healthcare workers are more likely to die from COVID-19 than their white colleagues. British Medical Association research has found that BAME doctors are twice as likely as white doctors to feel pressured into working with inadequate PPE when they are at risk of infection. And they are twice as likely not to feel confident enough to raise concerns about workplace safety.

However, all these established facts alone dont seem to explain why the risks of COVID-19 vary between different ethnic groups and are lowest among white people. This is particularly the case when we compare it with other forms of viral pneumonia that do not lead to such a difference.

The study that found BAME people in England were more likely to die from the disease accounted for differences in some underlying health conditions that are strongly linked to social issues, suggesting these werent the main factor. But the preliminary results from another study suggest ethnic minorities arent more likely to die once other factors linked to deprivation are taken into account.

To clarify this issue, its important to examine whether there may be some genetic component that predisposes ethnic minorities to a higher risk to COVID-19, while still recognising the critical role of other factors.

The way peoples immune systems work depends on genetic factors, not just environmental and social ones. There are effectively two parts to our immune systems. One is the part that produces antibodies, called the adaptive immune system. When our body has never seen a virus before, it can take several days for it to produce them, which is why some people get sick in the first place.

We also have an innate immune system that acts before our body has had time to make antibodies. This system is strong in children and young people, but not very good after the age of 65. This is likely to be one reason why older people are at higher risk of dying of COVID-19.

When a virus like the coronavirus SARS-CoV-2 enters a cell, molecules called toll-like receptors, or TLRs, alert the immune system that something potentially harmful is present. Interestingly, many of the bodys TLRs that can detect viruses come from genetic instructions found in the X chromosome, for which men have only one copy and women two.

We know that women can have a more effective innate immune response to other viruses such as HIV than men, and that oestrogen, the female hormone, enhances this type of immune response. We also know that women are less likely to die from COVID-19 than men.

Just as there are variations in DNA that are responsible for the differences in response of immune cells between the sexes, there can also be variations between people of different ethnic backgrounds. For example, the amount and type of genes that immune cells produce when the TLR-virus pathway is stimulated, are very different between people of African and of European origin.

This is not surprising, because we know that human populations from different parts of the planet have had to adapt to different types of infections. Ethnic differences in the risk to other respiratory viral diseases have been linked to genetic variation, and these variants are different in BAME groups and white people in these same pathways. However, the role of ethnicity in genetic susceptibility to viral diseases is still controversial.

We want to see if it could be a factor in the higher rate of BAME deaths from COVID-19. To do this, we are taking blood from frontline healthcare workers of a variety of ethnic backgrounds, assessing DNA differences and measuring the various substances the samples contain. The results could indicate if differences in the innate immune systems of BAME groups result in higher risk of developing severe COVID-19.

If there is some genetic element to the different death rates from COVID-19 between ethnic groups, its important that we understand it to give us the best chance of fighting the disease. For example, if we do find that the way the innate immune system works plays a role, we can advise people on ways to improve that system, such as through what we eat.

But that wont change the fact that the generally worse health among BAME groups in western societies is strongly linked to socioeconomic factors that are known to play a very significant role in this pandemic.

Read more:
Coronavirus: BAME deaths urgently need to be understood, including any potential genetic component - The Conversation UK

A 12-year-old girl is on a diet 'stricter than vegan' after a routine eye examination led to her being diagnosed with a rare genetic condition.

Hallie Melling from Old Swan in Liverpool, was initially believed to have been suffering from dyspraxia because she was disorientated and always falling at school.

When school staff advised her 30-year-old mum Amy-Lea to get her eyes tested it lead to a referral to Alder Hey hospital where medics discovered she had Homocystinuria (HCU).

HCU is a metabolic disorder that prevents the normal breakdown of protein and can affect the brain, eyes, skeleton and the vascular system, Liverpool Echo reports.

Amy-Lea said: Since 2015, they have had a heel prick test that babies get to get tested for it, but they didnt have it when Hallie was born.

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Shes had six years of this building up in her system and has had to face the consequences.

When she was in reception school they said she had dyspraxia because she was always falling, not very good at PE and was getting disorientated.

Then that led on to them telling us to get her eyes checked because shes making up what the pictures are in the stories.

So we went to a regular Specsavers appointment and got sent away with a sealed envelope to go to Alder Hey.

The ophthalmologist described the effects the condition has had on Hallies sight as if her eye was a trampoline and the supporting strings had been cut.

Over a year, Hallies sight deteriorated to the point where her glasses prescription was minus 21, and eventually, the lenses in her eyes had to be removed.

After genetic tests, the results came back that Hallie had the rare condition HCU.

According to the NHS, it needs to be treated to avoid serious complications so Hallie will be on medication for the rest of her life and a restricted diet to limit the amount of protein she eats.

Amy-Lea said: The only things she can eat unchecked are fruit and some vegetables.

The rest is prescription food from the chemist and only 18 grams of natural protein a day.

She could go to McDonalds and get a veggie burger meal but that would add up of three-quarters of her daily allowance so we would have to keep her on prescription food for the rest of the day.

She used to be a brilliant eater, she would go to her nans and eat liver and everything.

Now her diet is more strict than a vegan diet.

Amy-Lea said that when Hallie was first diagnosed in 2015 it felt like a life sentence but the way her daughter takes the condition has given her hope.

She said: Within a year of going to Specsavers we were under ophthalmology, genetics and cardiology because it affects your heart.

It also affects her visual memory and she has low bone density.

Were trying to strengthen her bones now because if she doesnt use them they will become very brittle.

When she was doing PE first at school after being diagnosed we were concerned but we were encouraged not to wrap her in cotton wool.

She added: Its all down to Hallie. We were all doom and gloom at first but the way she deals with it makes us deal with it."

Read the rest here:
Girl, 12, diagnosed with rare genetic condition following visit to Specsavers - Mirror Online

There is ongoing debate among policymakers and the general public about where SARS-CoV-2, the virus that causes COVID-19, came from. While researchers consider bats the most likely natural hosts for SARS-CoV-2, the origins of the virus are still unclear.

Recently, in the journal Current Biology, researchers describe a recently identified bat coronavirus that is SARS-CoV-2s closest relative in some regions of the genome and which contains insertions of amino acids at the junction of the S1 and S2 subunits of the viruss spike protein in a manner similar to SAR-CoV-2. While its not a direct evolutionary precursor of SARS-CoV-2, this new virus, RmYN02, suggests that these types of seemingly unusual insertion events can occur naturally in coronavirus evolution, the researchers say.

Since the discovery of SARS-CoV-2 there have been a number of unfounded suggestions that the virus has a laboratory origin, says senior author Weifeng Shi, director and professor at the Institute of Pathogen Biology at Shandong First Medical University in China. In particular, it has been proposed the S1/S2 insertion is highly unusual and perhaps indicative of laboratory manipulation. Our paper shows very clearly that these events occur naturally in wildlife. This provides strong evidence against SARS-CoV-2 being a laboratory escape.

The researchers identified RmYN02 from an analysis of 227 bat samples collected in Yunnan province, China, between May and October of 2019. Since the discovery that bats were the reservoir of SARS coronavirus in 2005, there has been great interest in bats as reservoir species for infectious diseases, particularly as they carry a very high diversity of RNA viruses, including coronaviruses, Shi says. RNA from the samples was sent for metagenomic next-generation sequencing in early January 2020, soon after the discovery of SARS-CoV-2.

Across the whole genome, the closest relative to SARS-CoV-2 is another virus, called RaTG13, which was previously identified from bats in Yunnan province. But RmYN02, the virus newly discovered here, is even more closely related to SARS-CoV-2 in some parts of the genome, including in the longest encoding section of the genome called 1ab, where they share 97.2% of their RNA. The researchers note that RmYN02 does not closely resemble SAR-CoV-2 in the region of the genome that encodes the key receptor binding domain that binds to the human ACE2 receptor that SARS-CoV-2 uses to infect host cells. This means its not likely to infect human cells.

The key similarity between SARS-CoV-2 and RmYN02, is the finding that RmYN02 also contains amino acid insertions at the point where the two subunits of its spike protein meet. SARS-CoV-2 is characterized by a four-amino-acid insertion at the junction of S1 and S2; this insertion is unique to the virus and has been present in all SARS-CoV-2 sequenced so far. The insertions in RmYN02 are not the same as those in SARS-CoV-2, which indicates that they occurred through independent insertion events. But a similar insertion event happening in a virus identified in bats strongly suggests that these kinds of insertions are of natural origin. Our findings suggest that these insertion events that initially appeared to be very unusual can, in fact, occur naturally in animal betacoronaviruses, Shi says.

Our work sheds more light on the evolutionary ancestry of SARS-CoV-2, he adds. Neither RaTG13 nor RmYN02 is the direct ancestor of SARS-CoV-2, because there is still an evolutionary gap between these viruses. But our study strongly suggests that sampling of more wildlife species will reveal viruses that are even more closely related to SARS-CoV-2 and perhaps even its direct ancestors, which will tell us a great deal about how this virus emerged in humans.

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Reference: A Novel Bat Coronavirus Closely Related to SARS-CoV-2 Contains Natural Insertions at the S1/S2Cleavage Site of the Spike Protein by Hong Zhou, Xing Chen, Tao Hu, Juan Li, Hao Song, Yanran Liu, Peihan Wang, Di Liu, Jing Yang, Edward C. Holmes, Alice C. Hughes, Yuhai Bi and Weifeng Shi, 10 May 2020, Current Biology.DOI: 10.1016/j.cub.2020.05.023

This work was supported by the Academic Promotion Programme of Shandong First Medical University, the Strategic Priority Research Programme of the Chinese Academy of Sciences, the Chinese National Natural Science Foundation, the National Major Project for Control and Prevention of Infectious Disease in China, the High-End Foreign Experts Program of Yunnan Province, the Taishan Scholars Programme of Shandong Province, the NSFC Outstanding Young Scholars, Youth Innovation Promotion Association of CAS, and an ARC Australian Laureate Fellowship.

Current Biology, Zhou et al.: A novel bat coronavirus closely related to SARS-CoV-2 contains natural insertions at the S1/S2 cleavage site of the spike protein

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Close Genetic Relative of SARS-CoV-2 Found in Bats Offers More Evidence It Evolved Naturally - SciTechDaily