Gaucher Disease Treatment Market Global Advance Stimulators, Market Size Composition and Market Subdivision Over the Prediction Period – 3rd Watch…

Most Recent Report On The Global Gaucher Disease Treatment Market

A recent market study reveals that the global Gaucher Disease Treatment market is likely to grow at a CAGR of ~XX% over the forecast period (2019-2029) largely driven by factors including, factor 1, factor 2, factor 3, and factor 4. The value of the global Gaucher Disease Treatment market is estimated to reach ~US$ XX Bn/Mn by the end of 2029 owing to a consistent focus on research and development activities in the Gaucher Disease Treatment field.

The Gaucher Disease Treatment market study is a well-researched report encompassing a detailed analysis of this industry with respect to certain parameters such as the product capacity as well as the overall market remuneration. The report enumerates details about production and consumption patterns in the business as well, in addition to the current scenario of the Gaucher Disease Treatment market and the trends that will prevail in this industry.

Gaucher Disease TreatmentMarket competition by top manufacturers as follows:Genzyme Corporation, Pfizer, Inc., Shire Human Genetics Therapies, Inc., and Actelion Pharmaceuticals Ltd. (acquired by Johnson & Johnson in June 2017). There are various drugs in pipeline of companies such as Lixte Biotechnology Holdings Inc, JCR Pharmaceuticals Co Ltd, Pharming Group NV and Orphazyme ApS, for Gaucher disease treatment.

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Valuable Data included in the report:

In-depth analysis of the sales strategies adopted by domestic as well as global market playersLatest innovations in the Gaucher Disease Treatment market and its impact on market growthAll-round evaluation of the different factors expected to influence the market dynamicsPricing and marketing strategies adopted by top-tier companiesEvaluation of the micro and macro-economic factors that are anticipated to shape the future of the Gaucher Disease Treatment market

Competitive Outlook

The presented business intelligence report includes a SWOT analysis for the leading market players along with vital information including, revenue analysis, market share, pricing strategy of each market players.

Some of the top tier players profiled in the report include:

Market player 1Market player 2Market player 3Market player 4

Product adoption Analysis

A complete assessment of the market share, consumption patterns, and supply-demand ratio of each product is provided backed by insightful tables, figures, and graphs. The products covered in the report include:

Product 1Product 2Product 3Product 4

Regional analysis includes

North AmericaLatin AmericaEuropeSouth AsiaEast AsiaOceaniaThe Middle East and Africa

The researchers have analyzed macro-economic factors such as political, economic, social, technological, environmental, and legal developments, to derive the drivers and restraints of the Gaucher Disease Treatment Market. Over the top investigation of the political and financial scene of every single significant district has been done to introduce the components that will prompt the market income. Then again, customer conduct over the globe has been investigated to comprehend the conceivable development restrictions, notwithstanding other large scale factors. Understanding the restraining factors empowers market players to mitigate the possible risks that they may have to deal with during the forecast period 2016 2026.

The report provides a comprehensive study of the Gaucher Disease Treatment Market, with details ranging from assessment of companies to trends to geography-specific drivers and restraints. Moreover, the examination presents segmental features and serious scene concerning every geology. Authored by researchers after extensive analysis, the report is suffused with key insights into the global Gaucher Disease Treatment Market, and will ensure that the readers gain a comprehensive understanding of the direction the Gaucher Disease Treatment Market is headed in.

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Highlights of TOC:

Overview: Presents a broad overview of the Gaucher Disease Treatment Market, acting as a snapshot of the elaborate study that follows.

Market Dynamics: A straight-forward discussion about key drivers, restraints, challenges, trends, and opportunities of the Gaucher Disease Treatment Market.

Product Segments: Explores the market development of the wide assortment of items offered by associations, and how they charge with end-clients.

Application Segments: This section studies the key end-use applications that contribute to the market growth and the emerging opportunities to the Gaucher Disease Treatment Market.

Geological Segments: Each territorial market with an area explicit investigation of each section is deliberately evaluated for understanding its current and future development situations.

Company Profiles: Leading and emerging players of the Gaucher Disease Treatment Market are thoroughly profiled in the report based on their market share, market served, products, applications, regional growth, and other factors.

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Gaucher Disease Treatment Market Global Advance Stimulators, Market Size Composition and Market Subdivision Over the Prediction Period - 3rd Watch...

Another COVID-19 Vaccine Joins the Race This Time, it’s a Live, Weakened Virus – BioSpace

Another COVID-19 vaccine candidate recently entered the races. The difference this one is a live attenuated (weakened) virus expressing the coronaviruss signature spike protein on its surface. And its delivered nasally, not a shot.

COVID-19 vaccine development will be more of a marathon than a sprint, Martin Moore, Ph.D., co-founder and CEO of Meissa Vaccines, told BioSpace. A live attenuated vaccine may not be first-in-class, but their historically high efficacy could make it the best-in-class.

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Moore spoke with BioSpace about live attenuated vaccines, interim data from their RSV vaccine candidate, and how they are building on their RSV vaccine platform to create a COVID-19 vaccine.

Live attenuated vaccines (LAVs)

Think about it what is the best way to generate an effective vaccine against a virus? Mimic natural infection as close as possible by giving someone a form of the virus that cant make them sick.

This is just what live attenuated vaccines (LAVs) do. LAVs contain a weakened form of a virus that is given to someone the same way that natural infection occurs, such as via a nasal spray (intranasally) for the flu LAV. This provokes all aspects of the immune system: innate local (mucosal), cell-based, and systemic antibody (humoral) responses.

Once inside the body, the weakened virus can replicate at a low level for a few days, but it is easily cleared by the immune system. After just one or two doses, the weakened virus produces strong, long-lasting immune responses that are almost as good as the full-strength virus that causes sickness.

By mimicking infection, LAVs generally provide more robust immune responses compared to injected non-living vaccines that typically only induce the antibody-based immune response. Thats why you usually have to get booster shots of injected vaccines.

This concept is hardly new. In fact, LAVs are already available against multiple viruses, including measles, mumps, rubella (as the combined MMR vaccine); rotavirus; and chickenpox.

The oral polio vaccine is a great example of a live attenuated vaccine, Moore said. Its low cost, able to be given widespread, and easy to administer with no needles or adjuvants needed. From a manufacturing standpoint, its also inexpensive and pretty easy to produce.

Advantages and limitations of live attenuated vaccines (LAVs)

Advantages

Limitations

1-2 doses

Cant be given to immunocompromised people

Lower cost

Need to be refrigerated

Administered through the same route as natural infection (intranasal, oral, etc.)

Genetic stability of virus is important for safety

No needles or adjuvants needed

Strict safety levels to adhere to during development

Induces both cellular and humoral (antibody) immune responses

Need to balance attenuation with potency/immunogenicity

As you can imagine, there is an inherent risk in using the actual (albeit weakened) virus for a vaccine. Viruses constantly mutate, so the weakened virus used in the vaccine has a chance of regaining its ability to be infectious and cause disease.

Creating a LAV is a balancing act the virus must be weakened enough to significantly reduce the risk of it mutating to become infectious, but still close enough to the full-strength virus to create a similar immune response.

The trick is balancing attenuation with immunogenicity, Moore commented.

Moore explained that if a virus is attenuated based on one or two gene mutations, the virus could revert to being infectious in the vaccine recipient and they can shed live virus, spreading it to others. This is the worst-case scenario and why there are such strict safety standards for vaccines, especially LAVs.

Safety is critical, there are no cutting corners with safety, explained Moore. Coronaviruses, in particular, are prone to genetic recombination, so using a live attenuated coronavirus in a vaccine would run the risk of becoming infectious again. Weve mitigated this risk by using RSV, which is more genetically stable, as a backbone.

Building from the foundation of another respiratory vaccine

The backbone of Meissas COVID-19 vaccine comes from another vaccine in their pipeline their respiratory syncytial virus (RSV) vaccine candidate. RSV, a common respiratory virus, usually causes mild cold symptoms; however, infants and the elderly may be hit particularly hard. RSV is infamous for being the culprit behind serious illness and pneumonia in infants less than 1 year old.

To create their intranasal RSV vaccine candidate (called MV-012-968), Meissa genetically engineered RSV to be weakened and safe, yet still potent, by using codon deoptimization.

Codon deopti-what?

Quick genetics review: a codon is a group of three bases in DNA or RNA that encodes a certain amino acid (the building block of proteins). Codons are the genetic code that translates genes into proteins. (Think of bases as the letters of the alphabet, codons as the words, and each gene as a sentence.) There are 64 different codons, but only 20 amino acids that they code for. Almost all amino acids are encoded by multiple codons; some codons for a particular amino acid are used more commonly than the others.

Codon deoptimization is changing the more common codons into the less common codons for the same amino acid throughout a gene. This introduces many silent mutations, changes in the genetic code that do not alter the resulting proteins being made.

This approach to viral genes has been called death by thousands of cuts, Moore explained. By using rare codons, codon deoptimization can change the expression efficiency of proteins.

The rare codons do not have as many amino acid transporters, called transfer RNA (tRNA), so they can slow down the translation process of turning genes into proteins. The slower the gene is translated, the fewer corresponding proteins is made (the lower the protein expression).

Using codon deoptimization, weve downregulated three RSV genes involved in the viruss ability to inhibit the human immune response to create our attenuated RSV, said Moore. This gives us optimized manufacturability, attenuation, and immunogenicity.

By taking away the viruss ability to inhibit immune pathways, Meissa is engineering attenuated vaccine strains that produce a solid immune response. This is key for viruses that dont provide strong immunity to begin with, like RSV or coronavirus.

Their RSV vaccine candidate, which received Fast Track Designation from the FDA in January, is currently in Phase I trials in healthy adults and young children. Previously, it was shown to produce a robust immune response in rats despite being highly weakened. The company recently provided an interim update announcing that initial clinical data showed the vaccine generate an immune response in healthy adults.

There are three main takeaways from the clinical data: the RSV in the vaccine was heavily weakened (as indicated by the lack of viral shedding from the nose); the vaccine prompted an RSV-specific immune reaction in the nose; and the vaccine was reported to be safe and well-tolerated up to 56 days.

All adults in this study have pre-existing titers of serum neutralizing antibodies systemically, Moore explained. All adults have already been infected with RSV previously. Ideally, we want to give our RSV vaccine to RSV seronegative babies so it will produce nasal and humoral immune responses.

Creating the COVID-19 vaccine candidate

Based off the interim RSV vaccine data, researchers at Meissa thought Could we modify our weakened RSV to create a COVID-19 vaccine?

COVID-19 patients dont seem to have a robust neutralizing antibody response, with lower titers that decrease rapidly over short periods of time, said Moore. This is bad news for developing a live attenuated coronavirus-based vaccine if you weaken the coronavirus further, how are you going to get the immunogenicity needed for a robust immune response?

You would overcome that issue by deeply understanding the biology of the coronavirus, Moore continued. Unfortunately, coronaviruses are some of the largest RNA viruses on the planet (genetically speaking), making them extraordinarily complex. Fortunately, RSV is not nearly as complex (about half of the size of coronaviruses, genetically), making it much easier to work with.

Using an RSV backbone for the COVID-19 vaccine also makes a lot of sense given the similarities between the two viruses: they are both respiratory viruses and inhibit the innate immune response during infection.

To create their COVID-19 vaccine, Meissa removed the surface proteins of their weakened RSV and replaced them with the coronavirus spike protein. The RSV-coronavirus hybrid virus was optimized to express the spike protein. This chimeric virus has the best of both worlds the established, weakened RSV construct and high expression of the coronavirus spike protein. Because this vaccine is RSV-based, they completely avoided the slippery genetic slope of using a weakened coronavirus.

Meissa plans to submit an IND later this year and anticipates a Phase I trial of their COVID-19 LAV to begin at the end of 2020. Moore said that the company is working on scaling up manufacturing now so that the COVID-19 vaccine could be in a large pivotal study in 2021.

Other COVID-19 vaccines in development

We all know that the COVID-19 vaccine development pipeline is becoming quite the rapid race. As of July 8, 2020, there were 165 vaccines in development, according to Bio. You can follow development of the most famous vaccine candidates using the New York Times Coronavirus Vaccine Tracker tool, which is periodically updated with new information.

Out of all the other COVID-19 vaccines being developed, only a few use live attenuated viruses. There arent enough LAV candidates in the broader pipeline, which is dominated by nonreplicating vaccines, commented Moore.

In late January, Yuen Kwok-Yung, Chair of Infectious Diseases at the University of Hong Kong, said his lab modified an intranasal flu vaccine they had previously developed so that the influenza virus also expressed coronavirus surface antigens. (There hasnt seemed to be any updates about that vaccines progress.)

Another company, Codagenix, Inc., is using codon deoptimization (like Meissa) to create vaccines against respiratory diseases like RSV and influenza. Theyve also jumped into the COVID-19 vaccine race with their candidate, called CDX-CoV. They successfully created the vaccine in mid-June and it is still in preclinical studies.

Only 5-7 percent of Americans have been infected and natural immunity doesnt seem to be that robust, so we could be in for quite a slog, Moore concluded.

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Another COVID-19 Vaccine Joins the Race This Time, it's a Live, Weakened Virus - BioSpace

Population genetics of the coral Acropora millepora: Toward genomic prediction of bleaching – Science Magazine

Conservation help from genomics

Corals worldwide are under threat from rising sea temperatures and pollution. One response to heat stress is coral bleachingthe loss of photosynthetic endosymbionts that provide energy for the coral. Fuller et al. present a high-resolution genome of the coral Acropora millepora (see the Perspective by Bay and Guerrero). They were able to perform population genetic analyses with samples sequenced at lower coverage and conduct genome-wide association studies. These data were combined to generate a polygenic risk score for bleaching that can be used in coral conservation.

Science this issue p. eaba4674; see also p. 249

Coral reefs worldwide are suffering losses at an alarming rate as a result of anthropogenic climate change. Increased seawater temperatures, even only slightly above long-term maxima, can induce bleachingthe breakdown of the symbiotic relationship between coral hosts and their intracellular photosynthetic dinoflagellates from the family Symbiodiniaceae. Because these symbionts provide the majority of energy required by the coral host, prolonged periods of bleaching can eventually lead to the death of the colony. In the face of rapidly increasing temperatures, new conservation strategies are urgently needed to prevent future mass losses of coral cover, and these benefit from an understanding of the genetic basis of bleaching.

Bleaching responses vary within and among coral species; in the reef-building coral Acropora millepora, a commonly distributed species across the Indo-Pacific, these differences have been shown to be at least partly heritable. In principle, therefore, interindividual differences in bleaching should be predictable from genomic data. Here, we demonstrate the feasibility of using a genomics-based approach to predict individual bleaching responses and suggest ways in which this can inform new strategies for coral conservation.

We first generated a chromosome-scale genome assembly as well as whole-genome sequences for 237 samples collected at 12 reefs distributed across the central Great Barrier Reef during peak bleaching in 2017. We showed that we can reliably impute genotypes in low-coverage sequencing data with a modestly sized reference haplotype panel, demonstrating a cost-effective approach for future large-scale whole-genome sequencing efforts. Very little population structure was detected across the sampled reefs, which was likely the result of the broadcast spawning mode of reproduction in A. millepora. Against this genomic background, we detected unusually old variation at the heat-shock co-chaperone sacsin, which is consistent with long-term balancing selection acting on this gene. Our genomic sequencing approach simultaneously provides a quantitative measure of bleaching and identifies the composition of symbiont species present within individual coral hosts. Testing more than 6.8 million variants for associations with three different measures of bleaching response, no single site reached genome-wide significance, indicating that variation in bleaching response is not due to common loci of large effect. However, a model that incorporates genetic effects estimated from the genome-wide association data, genomic data on relative symbiont species composition, and environmental variables is predictive of individual bleaching phenotypes.

Understanding the genetics of heat and bleaching tolerance will be critical to predict coral adaptation and the future of coral reef ecosystems under climate change. This knowledge also supports both conventional management approaches and the development of new interventions. Our work provides insight into the genetic architecture of bleaching response and serves as a proof of principle for the use of genomic approaches in conservation efforts. We show that a model based on environmental factors, genomic data from the symbiont, and genome-wide association data in the coral host can help distinguish individuals most tolerant to bleaching from those that are most susceptible. These results thus build a foundation toward a genomic predictor of bleaching response in A. millepora and other coral species.

A. millepora colonies presenting various severity of bleaching during March 2017 at Feather Reef on the Great Barrier Reef. Colonies with a greater severity of bleaching are those with the most pale colors. Prolonged periods of bleaching can lead to the eventual death of the coral host.

Although reef-building corals are declining worldwide, responses to bleaching vary within and across species and are partly heritable. Toward predicting bleaching response from genomic data, we generated a chromosome-scale genome assembly for the coral Acropora millepora. We obtained whole-genome sequences for 237 phenotyped samples collected at 12 reefs along the Great Barrier Reef, among which we inferred little population structure. Scanning the genome for evidence of local adaptation, we detected signatures of long-term balancing selection in the heat-shock co-chaperone sacsin. We conducted a genome-wide association study of visual bleaching score for 213 samples, incorporating the polygenic score derived from it into a predictive model for bleaching in the wild. These results set the stage for genomics-based approaches in conservation strategies.

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Population genetics of the coral Acropora millepora: Toward genomic prediction of bleaching - Science Magazine

What art history and genetics tell us about fruit and vegetables – Axios

The plants we eat have a long history on Earth, steered in part by human behaviors and preferences for color, taste and size.

How it works: A pair of researchers in Belgium is combining art history and genetics to try to link genetic mutations in fruits, vegetables and other plants to changes in their appearance, or phenotype, over time.

The big picture: The story of plants is intertwined with the history of mankind, says plant biologist Ive De Smet, co-author of an essay detailing the approach this week in Trends in Plant Science.

The challenge: DNA from ancient specimens and written texts can help to trace the natural history of plants.

Instead, they propose using imagery of fruits, vegetables and other plants along with genomic information to pinpoint important changes in plants and tie them to human forces and natural variation.

Yes, but: An artist's interpretation of food from Picasso's abstraction of apples (case in point, I think they are apples) to Beuckelaer's season-defying market offerings could lead to incorrect conclusions.

What's next: The researchers are asking people to provide pictures of paintings to build a public database for their work.

Continued here:

What art history and genetics tell us about fruit and vegetables - Axios

What did our food look like hundreds of years ago? Art history may have the answers – Statesville Record & Landmark

"Images, and in this case artistic depictions, are a good way to provide that missing information," said study coauthor Ive De Smet, the head of the Functional Phosphoproteomics Group at the VIB-UGent Plant Systems Biology Centre in Belgium.

"We are mainly interested in the story that, say, the modern orange carrot made from its humble beginnings as a weed, to its current popular form," he said.

Vogue, June 01, 1975: In the underground art gallery in the home of Happy Rockefeller in New York state, the far wall is covered by a 1970 tapestry version of the 1931 Picasso painting "Pitcher and Bowl of Fruit."

"Genomes of ancient plant-based foods can help us understand what this plant could have looked like for example, color based on the active pathways that produce different colors and which characteristics it might have possessed for example, sweetness," he continued. "This helps us pinpoint the appearance of certain characteristics on a timeline, the same way paintings can."

De Smet and co-author David Vergauwen, who is a lecturer on cultural history at Amarant, a Belgian cultural institution have been friends since high school more than 30 years ago.

Attending the same university they studied disciplines that, until now, seemed worlds apart. But every now and then the friends "take a trip together to visit a region or city we cannot convince our wives to go to," De Smet said.

A few years ago, the duo stood in the Hermitage Museum in Russia, in front of a painting of fruits by the late Flemish painter Frans Snyders. Neither of them recognized the fruits, so the following question was whether the fruit had looked the same in the 17th century, or whether Snyders was merely a bad painter.

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What did our food look like hundreds of years ago? Art history may have the answers - Statesville Record & Landmark

We Are Slowly but Steadily Unraveling the Genetics of This Pandemic – National Review

(WestEnd61/Getty Images)

Today, a team led by scientists at Scripps Research announced they had discovered a common feature found in many of the human antibodies that neutralize SARS-CoV-2:

The scientists, whose study appears July 13 in Science, reviewed data on nearly 300 anti-SARS-CoV-2 antibodies that their labs and others have found in convalescent COVID-19 patients over the past few months. They noted that a subset of these antibodies is particularly powerful at neutralizing the virus and these potent antibodies are all encoded, in part, by the same antibody gene, IGHV3-53.

Genes are likely to play a factor in which antibodies are most effective against the virus, just as genes probably play a factor in who can fight off the virus easily and who succumb to it rapidly.

You probably heard about the New Jersey family that lost four members in rapid succession, including one who had no discernable previous health issues, or the elderly Louisiana woman and her three sons all dying within a week or so, or the three members of a family dying in rapid succession in Florida. Genetics were probably not the only reason these families were struck so severely, but if one parent had genes that made them particularly vulnerable to this particular strain of SARS-CoV-2, they may have passed along those genes to their children.

Yet there are people more than 100 years old sometimes overweight or obese, smokers, and non-exercisers who catch the virus and manage to pull through. Theyre blessed with genetics that makes their immune systems and white blood cells work effectively, even if their health is not ideal otherwise.

At the beginning of June, teams of medical researchers in Germany, Spain, and Italy found variations at two spots in the human genome are associated with an increased risk of respiratory failure in patients with Covid-19. . . . One of these spots includes the gene that determines blood types. Having Type A blood was linked to a 50 percent increase in the likelihood that a patient would need to get oxygen or to go on a ventilator.

The other spot on the genome is six genes on Chromosome 3; earlier this month, additional research determined that this stretch of DNA was passed along from Neanderthals 60,000 years ago. The thinking is, the more this particular gene or genes are in a persons genetic code, the more vulnerable they are to SARS-CoV-2.

From a laymans perspective, genetics is weird and pretty darn unfair; science has determined that some small populations of human beings have near-immunity to anthrax and malaria. Some people might be unnerved at this sort of research, looking for connections between genes and vulnerability to diseases, as it could feed into notions that some people are genetically superior, and represent a step down the road to eugenics. But recognizing the reality of genetic differences does not inherently require one to think of other human beings as lesser in any way. Look hard enough at anybodys genome and youll probably find some gene that puts them at a disadvantage in one circumstance or another.

If were going to beat this virus, we have to understand it as thoroughly as possible including clues as to who might be more vulnerable to it and why.

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We Are Slowly but Steadily Unraveling the Genetics of This Pandemic - National Review

Why does COVID-19 kill some and not others, explores global study – The Peninsula Qatar

19 Jul 2020 - 9:55

Dr. Hamdi Mbarek (left) and Dr. Andrea Ganna

Qatar Foundations Qatar Genome Programme is the first and only active participant from an Arab country in the COVID-19 Host Genetics Initiative, a global initiative to elucidate the role of host genetic factors in the susceptibility and severity of the SARS-CoV-2 virus pandemic.

Why does a 17-year-old with no underlying health conditions succumb to COVID-19 while a 75-year-old great grandmother makes a full recovery?

The wide variation in severity makes it seem like they did not have the same disease, except they did. One of the most mysterious features of this disease, which has killed more than half a million people globally, is the difference in severity. Some people dont even show symptoms, some die and many more are somewhere in the middle.

Age, gender, and underlying health conditions clearly play an important role. But geneticists believe the difference in severity could be linked to the natural variation in peoples genetic code. This is what launched the COVID-19 Host Genetics Initiative (HGI), led by Mark Daly and Andrea Ganna from the Finnish Institute for Molecular Medicine (FIMM) and the Broad Institute in Boston.

The initiative aims to bring together the scientific community to study the role of the human genome in explaining COVID-19 susceptibility and severity. Twenty countries are currently contributing to the study, with the majority of studies being conducted in Europe (55 percent) and the US (28 percent). United Kingdom (10 percent) and Italy (9 percent) being the top two countries in terms of genomes contributed from Europe.

Qatar Genome Programme (QGP), the initiatives only active participant from the Middle East, has so far contributed with over 13,000 genomic results. The contribution of Qatar Genome to COVID-19 HGI is very important because it adds diversity to the initiative and highlights the importance of including populations which are traditionally unrepresented in genetic research, but still highly impacted by the COVID-19 pandemic, said Dr. Andrea Ganna, Co-founder of the COVID-19 HGI and Group Leader at the Institute for Molecular Medicine, Finland.

Results from the latest round of the global study show strong evidence of genetics playing a role in COVID-19 severity. A site on Chromosome 3 has been identified to have a solid link to COVID-19 severity.

The identified site is home to six genes; hence it is not yet possible to say exactly which one of them influences the course of COVID-19. Further investigations are underway to pinpoint exactly which gene this is.

Dr. Hamdi Mbarek, a geneticist, who led QGPs participation said, These results are very interesting and timely. We now have a target region in the genome, and the next challenge is to understand the link between the six genes and COVID-19 severity. Identifying the gene linked to COVID-19 severity will be very valuable in drug development. Now that we now know that genetics is a big factor in determining COVID-19 severity, this information can help the healthcare sector prioritise which group of individuals should be first in line to get a vaccine once one is developed.

If researchers are able to identify exactly which gene is responsible for COVID-19 severity, it could be a potential game-changer in swiftly determining which patients are high-risk and need more aggressive treatment. Previously, this study identified a variation at another spot in the human genome. The identified spot consisted of the gene that determines blood type.

Patients with Type A blood, for example, were found to be at greater risk of being severely affected by COVID-19.

We are glad to have contributed to this initiative with the genomes of an Arab population, which has added valuable diversity to the study. The diversity in the participating genomes strongly indicates that COVID-19 indiscriminately affects populations from all around the world, added Dr. Said Ismail, Director of Qatar Genome Programme

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Why does COVID-19 kill some and not others, explores global study - The Peninsula Qatar

Demand for Functionalized Polyolefins to Scale New Heights as Market Players Focus on Innovations 2019 2029 Bulletin Line – Bulletin Line

Evaluation of the Global Functionalized Polyolefins Market

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The competitive outlook assessment provides an in-depth understanding related to the business proceeding of top-tier market players in the global Functionalized Polyolefins market. The product portfolio, sales strategy, marketing & promotional strategy, and sales footprint of each market player is scrutinized thoroughly in the report. Some of the leading players evaluated in the report include:

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Demand for Functionalized Polyolefins to Scale New Heights as Market Players Focus on Innovations 2019 2029 Bulletin Line - Bulletin Line

Study of Over 1 Million People Finds Intriguing Link Between Iron Levels And Lifespan – ScienceAlert

A massive new study has found evidence that blood iron levels could play a role in influencing how long you live.

It's always important to take longevity studies with a big grain of salt, but the new research is impressive in its breadth, covering genetic information from well over 1 million people across three public databases. It also focused on three key measures of ageing: lifespan, years lived free of disease (referred to as healthspan), and making it to an extremely old age (AKA longevity).

Throughout the analysis, 10 key regions of the genome were shown to be related to these measures of long life, as were gene sets linked to how the body metabolises iron.

Put simply, having too much iron in the blood appeared to be linked to an increased risk of dying earlier.

"We are very excited by these findings as they strongly suggest that high levels of iron in the blood reduces our healthy years of life, and keeping these levels in check could prevent age-related damage," says data analyst Paul Timmers, from the University of Edinburgh in the UK.

"We speculate that our findings on iron metabolism might also start to explain why very high levels of iron-rich red meat in the diet has been linked to age-related conditions such as heart disease."

While correlation doesn't necessarily mean causation, the researchers used a statistical technique called Mendelian randomisation to reduce bias and attempt to infer causation in the data.

As the researchers note, genetics are thought to have around a 10 percent influence on lifespan and healthspan, and that can make it difficult to pick out the genes involved from all the other factors involved (like your smoking or drinking habits). With that in mind, one of the advantages of this new study is its sheer size and scope.

Five of the genetic markers the researchers found had not previously been highlighted as significant at the genome-wide level. Some, including APOE and FOXO3, have been singled out in the past as being important to the ageing process and human health.

"It is clear from the association of age-related diseases and the well-known ageing loci APOE and FOXO3 that we are capturing the human ageing process to some extent," write the researchers in their published paper.

While we're still in the early stages for investigating this association with iron metabolism, further down the line we could see the development of drugs designed to lower the levels of iron in the blood - which could potentially add extra years to our lives.

Besides genetics, blood iron is mostly controlled by diet and has already been linked to a number of age-related diseases, including Parkinson's and liver disease. It also affects our body's ability to fight off infection as we get older.

We can add this latest study to the growing evidence that 'iron overload', or not being able to break it down properly, can have an influence on how long we're likely to live, as well as how healthy we're likely to be in our later years.

"Our ultimate aim is to discover how ageing is regulated and find ways to increase health during ageing," says Joris Deelenwho studies the biology of ageing at the Max Planck Institute for Biology of Ageing in Germany.

"The 10 regions of the genome we have discovered that are linked to lifespan, healthspan, and longevity are all exciting candidates for further studies."

The research has been published in Nature Communications.

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Study of Over 1 Million People Finds Intriguing Link Between Iron Levels And Lifespan - ScienceAlert

Setting the bar in education – The Star Online

Cheahs belief in working with the best and learning from the best also birthed the appointments of the Jeffrey Cheah distinguished professors.

Under the collaboration between Jeffrey Cheah Foundation and globally acclaimed academic institutions, eminent experts and scholars - who have contributed to solving critical global issues in health, disease and economy amongst others - are appointed to share their knowledge and expertise with Malaysian academics, students and the general public.

Among the prominent names on the list are:

Prof Jeffrey David Sachs

As a world renowned economist and director of the UN Sustainable Development Solutions Network, Prof Sachs is one of the worlds most influential experts on sustainable economic development.

A passionate leader in the fight against poverty and the special advisor to the UN secretary-general on sustainable development, he has advised heads of states and governments on economic strategy for more than a quarter century.

Appointed as an honorary Jeffrey Cheah distinguished professor of sustainable development at Sunway University this year, he is also the chairman of the Jeffrey Sachs Centre on Sustainable Development.

Prof Sir Leszek Borysiewicz

The chairman of Cancer Research United Kingdom (UK) since 2016, Prof Borysiewicz is an Honorary Jeffrey Cheah distinguished professor who is now the emeritus vice-chancellor of the University of Cambridge, after serving as its vice-chancellor from 2011 to 2017.

A founding fellow of the Academy of Medical Sciences, he has been chief executive of the UKs Medical Research Council since 2007 and was knighted in 2001 for his breakthroughs in vaccines, including developing Europes first trial of a vaccine to treat cervical cancer.

Prof Sir Alan Fersht

World leading protein scientist Prof Fersht, also an honorary Jeffrey Cheah distinguished professor and life fellow of Gonville and Caius College Cambridge, is widely regarded as one of the main pioneers of protein engineering, which is a process to analyse the structure, activity and folding of proteins.

His current research involves a fusion of protein engineering, structural biology, biophysics and chemistry to study the structure, activity, stability and folding of proteins, as well as the role of protein misfolding and instability in cancer and disease.

Prof Kay-Tee Khaw

Prof Khaw, a leading expert in the field of health and disease, is a Jeffrey Cheah professorial fellow in Gonville and Caius College, Cambridge. She is currently one of the principal UK scientists working on the European Prospective Investigation into Cancer and Nutrition, a Europe-wide project investigating the links between diet, lifestyle and cancer.

Appointed as a Commander of the order of the British Empire in 2003, Prof Khaw has been recognised for developing improved methods for collecting information on peoples diets and levels of exercise and relating this to the number of diagnosed cancer cases.

Prof Rema Hanna

A highly distinguished economist, Prof Hanna is the Jeffrey Cheah professor of South East Asia Studies and chair of the Harvard Kennedy School International Development Area, as well as the faculty director of evidence for policy design at Harvards Centre for International Development and the co-scientific director of the Abdul Latif Jameel Poverty Action Lab South East Asia office in Indonesia.

Her focus is on improving overall service delivery, understanding the impacts of corruption, bureaucratic absenteeism and discrimination against disadvantaged minority groups on delivery outcomes.

Prof Ketan J Patel

Prof Patel is a Jeffrey Cheah professorial fellow in Gonville and Caius College, Cambridge and the principal research scientist at the famous MRC Laboratory of Molecular Biology in the University of Cambridge.

His research, which focuses on the molecular basis of inherited genomic instability and the role it plays in the biology of stem cells, has been recognised through prestigious awards and prizes, including being elected as a fellow of the Royal Society of London, a member of the European Molecular Biology Organisation and a fellow of the Academy of Medical Sciences UK.

Prof John Todd

The Jeffrey Cheah fellow in medicine at Brasenose College, Oxford and professor of precision medicine, Prof Todd is a leading pioneer researcher in the fields of genetics, immunology and diabetes. His research areas include Type 1 diabetes genetics and disease mechanisms with the aim of clinical intervention.

In his former role as a professor of human genetics and a Wellcome Trust principal research fellow at Oxford, he helped pioneer genome-wide genetic studies, first in mice and then in humans.

Prof William Swadling

Prof Swadling, a Jeffrey Cheah professorial fellow, is a senior law fellow at Brasenose College, Oxford and Professor in the Law of Property in the Oxford University Law School.

An expert on the Law of Restitution, he is a contributor to Halsburys Laws of England, wrote the section on property in Burrows (ed) English Private Law and is widely cited in the British courts.

Prof William James

A Jeffrey Cheah professorial fellow emeritus and fellow in medicine at Brasenose College, Oxford, Prof James is a virologist with a background in genetics and microbiology.

As the professor of virology with the University of Oxford, he is the principal investigator at the Stem Cell Research Institute of Oxford, running a research lab studying HIV-macrophage biology using stem cell technology.

Prof Mark Wilson

Prof Wilson, the dean of Brasenose College, is a Jeffrey Cheah professorial fellow at the college and the professor of physical chemistry in the University of Oxfords physical and theoretical chemistry department.

The primary focus of his research interest is on the construction, development and application of relatively simple potential models to assess a wide range of systems with potentially unique properties.

Prof Jarlath Ronayne

Appointed in 2010 as the first Jeffrey Cheah distinguished professor, Prof Ronayne is a key member of Sunway Universitys board of directors and has played a pivotal role in establishing links between Sunway, Oxford and Cambridge.

Under his leadership, the Jeffrey Cheah Professorial Fellowships at Gonville and Caius College, Cambridge as well as Brasenose College, Oxford and the Jeffrey Cheah Scholar-in-Residence programmes in both colleges were established, alongside the prestigious Oxford University-Jeffrey Cheah Graduate Scholarship launched by the British High Commissioner in 2018. All these initiatives are in perpetuity.

Prof Sibrandes Poppema

A medical expert on Hodgkins disease, Prof Poppema has published more than 200 articles that have been cited more than 17,000 times.

The Jeffrey Cheah distinguished professor is also the co-owner of 12 patents and the founder of two biotechnology companies, as well as the advisor to the chancellor at Sunway University, especially on the establishment of a new medical school at the university.

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Setting the bar in education - The Star Online

How Old Is Your Dog? New Equation Shows How to Calculate Its Age in Human Years – NBC New York

Common wisdom has long held that each dog year is equivalent to seven human years. But a new equation developed to measure how a dog ages finds the family pup may be a lot older than we realize.

Researchers studying chemical changes to canine DNA found that dogs age very quickly during their first five years and much more slowly later on.

The findings, published recently in the journal Cell Systems, calculate that a 5-year-old dog would be pushing 60 in human years.

Puppies age super quickly, said Trey Ideker, the studys senior author and a professor of genetics at the University of California, San Diego, School of Medicine. By the time a dog is a year old, at a molecular level, hes much more like a 30-year-old human. Retrospectively, we did know these things. It didnt make any sense that the equivalent to a 7-year-old human would be able to have puppies.

Read the full story on NBCNews.com

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How Old Is Your Dog? New Equation Shows How to Calculate Its Age in Human Years - NBC New York

How genetic studies will become the holy grail to find cancer biomarkers in future – Express Healthcare

Dr Villoo Morawala-Patell, Founder, Avesthagenand her team has been researching on genetic basis of disease risk associated with longevity and the endogamy prevalent within various communities. Theirpurpose is to deliver population-specific qualified biomarker targets to achieve the holy grail of genomics predictive, preventive, and personalised medicines. In an interview withRaelene Kambli, Dr Patell reveals more on their research and its application in the development and validation of cancer biomarker. She also delved into explaining theneed for a cross-disciplinary integration of scientific and clinical expertise for research especially in the field of cancer

What according to you is the most promising area of your current research?

The most promising area of our current work in terms of innovation is the significant and prolific outcomes from the Avestagenome Project for cancers, neurodegenerative conditions, and rare diseases. Our recent work on the genomics of the Zoroastrian-Parsis converges, ancient history, human migration, endogamous population genetics, social behaviour and customs that express in genetic signatures of wellness and health.

Specifically, we present a population genetics study wherein we assembled the first,de novoZoroastrian-Parsi Mitochondrial Reference Genome from one individual and the first Zoroastrian-Parsi Mitochondrial Consensus Genome derived from the assembly of 100 complete mitochondrial genomes of the dwindling, endogamous, non-smoking Zoroastrian-Parsi community of India. Phylogenetic analysis of the 100 Parsi mitochondrial genome sequences, showed a largely Persian origin for the Parsi community of India.Disease association mapping showed that the majority of the mitochondrial variants to be linked longevity and its associated conditions revealing the genetic basis for many of the heritable diseases in the community like cancer, neurodegenerative diseases like Parkinsons, Alzheimers and many rare genetic conditions.Our study is a first in tackling the genetic basis of disease risk associated with longevity and the endogamy prevalent within the community. The outcome of this study has an impact on all populations

So, your paper suggests that Zoroastrian-Parsi genes may help scientists characterise biomarkers predictive of diseases caused by tobacco use, such as lung, head and neck, and oesophagus cancers. Can you elaborate on the same?

We found 420 mitochondrial variants in our analysis of the 100 Zoroastrian-Parsi mitochondrial genomes. The detailed analysis brought to light the absence in the Zoroastrian-Parsi samples variants in mitochondrial genes like ND5, ND6 and tRNA that are shown to be associated with lung cancer and non-small cell lung cancer in other non-Parsi populations. Many of these reported genes have been associated with smoking-induced lung cancer and other smoking-induced cancers. Our study thus serves as a biological validation ofa well-known cultural phenomenon, reflecting the practice of abstinence from smoking in Zoroastrian-Parsis whose origins date back a millennium.

How helpful is this information for your research and what does it imply?

Our study is unique and provides a road map for understanding the genetic factors that underlie ageing and longevity associated diseases. A vast majority of the 420 mitochondrial variants are associated with longevity and conditions like Parkinsons disease, Alzheimers disease as well as breast, colon, prostate, ovarian cancer, infertility disorders like asthenozoospermia and rare neuronal diseases associated with mitochondrial dysfunction. Indeed, epidemiological studies of the community do show a preponderance of these diseases and a strong bias for the inheritance of these genetic disease variants owing to the practice of endogamy within the community. Our current study will complement our research goals as we accelerate our whole-genome analysis of the Parsi community to identify from the control population, alongside other comparative population subjects. The purpose is to deliver population-specific qualified biomarker targets to achieve the holy grail of genomics predictive, preventive, and personalised medicines.

What are the key findings of this study?

Our insights from the assembly of the archetypical Zoroastrian-Parsi mitochondrial genome extend from human migration to the genetic basis of disease prevalence. Our phylogenetic analysis showsalargely Persian origin for the Parsi community and revealed the presence of seven major haplogroups and 25 sub-haplogroups in our study group.We believethe strict endogamy practised by the Zoroastrian-Parsi community, has meant that their maternally inherited mitochondrial genome has remained largely unchanged from that of their ancestors in Old Persia. We also see the prevalence of genetic variants, specifically 217 unique variants linked to longevity and 41 longevity associated conditions like cancers, neurodegenerative disease, and rare diseases. We did not find any mitochondrial variants previously reported for lung cancer in our study and found an extremely low frequency of mutational signatures linked to tobacco carcinogens, reflective of the strong disapproval of smoking in the Zoroastrian religion. Another exciting outcome of our study is the discovery of 12 unique mitochondrial gene variants distributed across 27 subjects that have not been reported in public databases that index mitochondrial variants discovered thus far in other studies. We are currently in the process of investigating their function in the context of diseases.

So, you mean the gene expression picked from this study can be implemented to tailor adjuvant therapy among common cancers?

Mutations in mitochondrial DNA (mtDNA) can cause a range of incurable and life-limiting metabolic diseases in humans. Our current study has identified crucial disease associated with genetic variants in the mitochondrial genomes of the Zoroastrian-Parsi community. Our study is a necessary first step to tailor therapeutic strategies that involve targeting validated mitochondrial biomarkers involved in diseases. Given the advent of technologies that enable precise genome editing like CRISPR, we believe our study will benchmark crucial mitochondrial disease-associated variants, classify its prevalence and risk outcomes to complement and tailor therapies that can correct genetic mutations, thus improving patient outcomes in the case of complex genetic diseases like cancers.

How much of your study will pave the path to an era of personalised medicine?

It may be fortuitous that our current study is published on the heels of another study published describing important milestone in editing mitochondrial genomes. Mok, BY et al (Nature, July 2020) has demonstrated the ability to enable precise editing of mtDNA. Our study and its future outcomes will provide a database of mitochondrial variants associated with various conditions to further enhance the possibility of precisely editing the inheritable mutations in mitochondrial genomes, moving the needle towards personalised medicines.

Are there any indicators that may raise caution?

Indeed, any disease associations in a dwindling population is a cause for concern. We show an increased association of variants with conditions like Parkinsons disease, prostate, colon and ovarian cancers, rare diseases resulting in an inherited visual disability like LHON, hearing disability, muscular dystrophy like diseases and infertility. Understanding the molecular mechanisms of these variants resulting in clinical manifestations is extremely important in framing healthcare policies that include precise diagnostic platforms for early disease diagnosis and therapy, steps necessary to arrest the declining numbers in communities like the Zoroastrian-Parsis and other close-knit communities across the world.

What are your predictions for the next five years in cancer biomarker development and validation?

In the next five years, understanding of most cancers would be linked to population genetics and would be individualised into specific groups for treatment. Specific targeted drugs linked to a subset of biomarkers found in each individual patient leading to precision individualised therapies would be the order of the day.

Do you think that there is a need for a cross-disciplinary integration of scientific and clinical expertise for research especially in the field of cancer?

Cross-disciplinary research, especially in cancer, is increasingly relevant and important to reducing that gap in what is identified as best practice and what happens in clinical care. Narrowing this knowledgepractice gap continues to be a slow, complex, and poorly understood process, particularly for research that encompasses the notion of transdisciplinarity, as in the case of complex diseases like cancers. The assimilation of diverse perspectives, research approaches, and types of knowledge is important in helping research teams tackle real-world patient care issues, create more practice-based evidence, and translate the results to clinical and community care settings.

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How genetic studies will become the holy grail to find cancer biomarkers in future - Express Healthcare

Demand for Functionalized Polyolefins to Scale New Heights as Market Players Focus on Innovations 2019 2029 – Bulletin Line

Evaluation of the Global Functionalized Polyolefins Market

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The competitive outlook assessment provides an in-depth understanding related to the business proceeding of top-tier market players in the global Functionalized Polyolefins market. The product portfolio, sales strategy, marketing & promotional strategy, and sales footprint of each market player is scrutinized thoroughly in the report. Some of the leading players evaluated in the report include:

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Demand for Functionalized Polyolefins to Scale New Heights as Market Players Focus on Innovations 2019 2029 - Bulletin Line

Researchers Discover Two Paths of Aging and New Insights on Promoting Healthspan – UC San Diego Health

Yeast cells with the same DNA under the same environment show different structures of mitochondria (green) and the nucleolus (red), which may underlie the causes of different aging paths. Single and double arrowheads point to two cells with distinct mitochondrial and nucleolar morphologies.

Molecular biologists and bioengineers at the University of California San Diego have unraveled key mechanisms behind the mysteries of aging. They isolated two distinct paths that cells travel during aging and engineered a new way to genetically program these processes to extend lifespan.

The research is described July 17 in the journal Science.

Our lifespans as humans are determined by the aging of our individual cells. To understand whether different cells age at the same rate and by the same cause, the researchers studied aging in the budding yeast Saccharomyces cerevisiae, a tractable model for investigating mechanisms of aging, including the aging paths of skin and stem cells.

The scientists discovered that cells of the same genetic material and within the same environment can age in strikingly distinct ways, their fates unfolding through different molecular and cellular trajectories. Using microfluidics, computer modeling and other techniques, they found that about half of the cells age through a gradual decline in the stability of the nucleolus, a region of nuclear DNA where key components of protein-producing factories are synthesized. In contrast, the other half age due to dysfunction of their mitochondria, the energy production units of cells.

The cells embark upon either the nucleolar or mitochondrial path early in life, and follow this aging route throughout their entire lifespan through decline and death. At the heart of the controls the researchers found a master circuit that guides these aging processes.

To understand how cells make these decisions, we identified the molecular processes underlying each aging route and the connections among them, revealing a molecular circuit that controls cell aging, analogous to electric circuits that control home appliances, said Nan Hao, senior author of the study and an associate professor in the Section of Molecular Biology, Division of Biological Sciences.

Having developed a new model of the aging landscape, Hao and his coauthors found they could manipulate and ultimately optimize the aging process. Computer simulations helped the researchers reprogram the master molecular circuit by modifying its DNA, allowing them to genetically create a novel aging route that features a dramatically extended lifespan.

UC San Diego biologists and bioengineers identified a master aging circuit that opens the door to genetically engineered prolonged life. Erik Jepsen/UC San Diego Publications

Our study raises the possibility of rationally designing gene or chemical-based therapies to reprogram how human cells age, with a goal of effectively delaying human aging and extending human healthspan, said Hao.

The researchers will now test their new model in more complex cells and organisms and eventually in human cells to seek similar aging routes. They also plan to test chemical techniques and evaluate how combinations of therapeutics and drug cocktails might guide pathways to longevity.

Much of the work featured in this paper benefits from a strong interdisciplinary team that was assembled, said Biological Sciences Professor of Molecular Biology Lorraine Pillus, one of the studys coauthors. One great aspect of the team is that we not only do the modeling but we then do the experimentation to determine whether the model is correct or not. These iterative processes are critical for the work that we are doing.

The research team included Yang Li (postdoctoral scholar, Biological Sciences), Yanfei Jiang (postdoctoral scholar, Biological Sciences), Julie Paxman (graduate student, Biological Sciences), Richard OLaughlin (former bioengineering graduate student, Jacobs School of Engineering), Stephen Klepin (laboratory assistant, Biological Sciences), Yuelian Zhu (visiting scholar), Lorraine Pillus (professor, Biological Sciences and Moores Cancer Center), Lev Tsimring (research scientist, BioCircuits Institute), Jeff Hasty (professor, Biological Sciences, Jacobs School of Engineering and BioCircuits Institute) and Nan Hao (associate professor, Biological Sciences and BioCircuits Institute).

The National Institutes of HealthNational Institute on Aging (AG056440) and National Science Foundation Molecular and Cellular Biosciences (1616127 and 1716841) supported the research. Julie Paxman was supported by UC San Diegos Cellular and Molecular Genetics training program, (5T32GM007240).

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Researchers Discover Two Paths of Aging and New Insights on Promoting Healthspan - UC San Diego Health

Polish scientist involved in breakthrough work linking coronavirus effects to genes – The First News

Doctor Karolina Chiakowska: part of team researching the link between the virus and genes. Uniwersytet Medyczny w Biaymstoku/Facebook

A Polish researcher has helped make a breakthrough in coronavirus research linking how people react to the virus to their genes.

As countries around the world struggle to control the COVID-19 epidemic, teams of researchers are busy trying to understand the virus, from who is most at risk to it to how people become immune to it. The outcome of this research could help protect vulnerable groups and save thousands of lives around the world.

Now an international team, which includes Polish bio-technologist Doctor Karolina Chiakowska, has made an important discovery: peoples susceptibility to the coronavirus depends on their genes.

Based at the Medical University of Biaystok in eastern Poland and the company Imagene.me, which is also located in that city, Chwiakowska specialises in the analyses of disease-related changes in gene expression levels and DNA methylation, especially cancers and metabolic disorders. She is also interested in epigenetic age perturbation.

Her work is part of an international effort looking into why people react differently to the coronavirus.Jakub Kaczmarczyk/PAP

Recently, Chwiakowska has been working with international research consortium the COVID-19 Host Genetics Initiative (HGI), a bottom-up collaborative effort in the human genetics community to generate, share and analyse data to learn the genetic determinants of COVID-19 susceptibility, severity and outcomes. The research was conducted in 50 countries simultaneously.

This means that a team of researchers from one side of the world has ongoing access to the results of other scientists working on the same problem, said Chwiakowska.

The researchers found that genes located in the third human chromosome could be key to determining why people react differently after being infected with the SARS-COV-2 coronavirus and experience the COVID-19 illness in different ways. This was discovered by analysing the DNA of 2,000 infected people in Spain and Italy.

The large-scale genomic analyses confirmed the relationship between genetic variability in this region of the human genome and severe COVID-19, she said.

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Polish scientist involved in breakthrough work linking coronavirus effects to genes - The First News

How old is your dog? New equation shows how to calculate its age in human years – NBC News

Common wisdom has long held that each dog year is equivalent to seven human years. But a new equation developed to measure how a dog ages finds the family pup may be a lot older than we realize.

Researchers studying chemical changes to canine DNA found that dogs age very quickly during their first five years and much more slowly later on.

The findings, published recently in the journal Cell Systems, calculate that a 5-year-old dog would be pushing 60 in human years.

Puppies age super quickly, said Trey Ideker, the studys senior author and a professor of genetics at the University of California, San Diego, School of Medicine. By the time a dog is a year old, at a molecular level, hes much more like a 30-year-old human. Retrospectively, we did know these things. It didnt make any sense that the equivalent to a 7-year-old human would be able to have puppies.

Ideker and colleagues noticed that dogs, just like humans, have chemical marks on their DNA, called methylation marks, that change with age.

The genome itself doesnt change with age, Ideker said. "What does change is marks on the genes that control a dog or human's growth pattern."

The methylation marks, or as Ideker calls them wrinkles on the genome, change in predictable ways as we and dogs age.

We are able to quantify this at the molecular level and tell how fast someone is aging, and we can align it across dogs and humans, Ideker said. But we dont know exactly what it all means.

To find the mathematical relationship connecting dog aging to human aging, Ideker and his colleagues studied 104 Labrador retrievers whose ages ranged from weeks-old puppies to 16-year-old dogs.

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When they compared the dog DNA data to information from humans, the researchers came up with a new equation to figure out the dog's comparable human age.

The equation: 16 ln(dog age) + 31 = human age.

For iPhone calculators that have the natural logarithm, or "ln," function, first type in the dog's age. Then hit the "ln" button. Multiply that result by 16; then add 31.

If you're using Googles scientific calculator: First, hit "ln," then type in the dogs age, then equal it out. Next, multiply by 16, and then add 31.

Using that equation:

By this time, dog aging has slowed down, so an 8-year-old dog is like a 64-year-old human.

According to this equation, the average 12-year Labrador lifespan is equivalent to a human living to about 70.

Ideker suspects there will be some variation based on dog breed but that they will all follow a similar pattern.

The new dog-age math has given Ideker some pause when he thinks about taking his own dogs on runs: He now realizes his 6-year-old dog is actually pushing 60 in human years.

Margret Casal, a specialist in veterinary genetics, said the new calculations match what shes observed in her dog patients.

It validates what a lot of other researchers have been saying, said Casal, a professor of medical genetics, pediatrics and reproduction at the University of Pennsylvania School of Veterinary Medicine.

Researchers knew the 1-to-7 comparison was off, but they did not know what the specific relationship was, she added.

It will be interesting to look at different breeds," Casal said. "We know that some smaller breeds live longer and some larger ones dont live quite as long.

For owners hoping to help a beloved dog live as long as possible, Casal offered a few tips:

Lastly, take your dog for yearly wellness visits.

Thats really important, Casal said. I can say as an owner of a dog, sometimes you dont see something is wrong and your vet might be able to see it better.

Linda Carroll is a regular health contributor to NBC News and Reuters Health. She is coauthor of "The Concussion Crisis: Anatomy of a Silent Epidemic" and "Out of the Clouds: The Unlikely Horseman and the Unwanted Colt Who Conquered the Sport of Kings."

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How old is your dog? New equation shows how to calculate its age in human years - NBC News

Have any of Earth’s creatures stopped evolving? – Genetic Literacy Project

Thegoblin shark, duck-billed platypus, lungfish, tadpole shrimp, cockroach, coelacanths and the horseshoe crab these creatures are famous in the world of biology, because they look as though they stopped evolving long ago. To use a term introduced by Charles Darwin in 1859, they are living fossils. And to their ranks, some have added humans, based on the idea that technology and modern medicine has, for all intents and purposes, eliminated natural selection by allowing most infants to live to reproductive age and pass on their genes.

It may be tempting to conclude from the sharks, horseshoe crabs and other creatures that evolution does often stop, and that Darwins living fossil term makes sense. But such a conclusion would be wrong.

Some argue that Darwin never intended the phrase to be used seriously. The term is over-simplifying and leads to people believing that some things havent evolved, which is so wrong, noted Africa Gmez, a biologist at Hull University in the United Kingdom who led a genetic analysis of the tadpole shrimp that in 2013 demonstrated that this living fossil is no fossil at all. They have been evolving non-stop and speciating and radiating, so why on earth are they called living fossils?

The same is true if one looks closely at the other living fossils. They are all evolving, humans included. This is partially because there is more to biology than meets the eye, with things changing constantly at the cellular and biochemical level. But its also because Darwins watershed discovery, natural selection, known in popular language as survival of the fittest is not the only evolutionary force.

Death prior to reaching reproductive age and lack of reproductive capability are not the only factors controlling biological change. Mathematics also plays a role here. Keep the environmental conditions the same around a biological group, remove selective pressures, but mess with the numbers of individuals in a population, and evolution still happens. Living things evolve, whether you see it on the surface or not.

Natural selection is the best-known evolutionary force and there are numerous examples of it operating quickly in recent times. To illustrate how natural selection works to biology students, teachers and textbook writers typically use examples of creatures with physically obvious changes. Among the more popular is the peppered moth of England. Early in the Industrial Revolution, peppered moths were light-colored. This camouflaged them against the white bark of birch trees around industrializing cities. Over a half-century, as the soot from burning coal in factories darkened the bark of the trees, the moths darkened their coloring too. It happened through natural selection. If youre black moth on a white tree, youre likely to get eaten by a bird, but when the trees darkened, now the dark moths had the advantage.

Another textbook example of natural selection is the high incidence of sickle cell disease in humans in places where malaria is endemic. Malaria and sickle cell disease are both deadly without modern medicine, but to have sickle cell disease one must carry two copies of a gene for defective hemoglobin, one from each parent. Having one defective copy, and one normal copy of the relevant gene however protects an individual from the parasite that causes malaria. But it causes no sickle cell crises, unless the individual engages in extreme exercise, or travels to high altitudes.

The lesson from these examples is that natural selection, due to environmental factors, leads to overt changes, but that a biological status quo should persist as long as everything in the environment remains copacetic.

In the mid to late 19th century, Darwin enjoyed a fair amount of publicity in England, and throughout the world. That publicity was well deserved, but Darwins contemporary, Gregor Mendel, was effectively invisible. Working from a monastery in a region that is now part of the Czech Republic, Mendel made fundamental discoveries about inheritance that eventually would put him in chapter one of every genetics text book. Darwin thought that children were a blend of their parents. But using plant models, Mendel figured out that this was not the case. Rather, he found that traits often disappeared from parents to offspring, only to reappear in future generations.

Early in the 20th century, a British researcher named Reginald Punnett was asking a lot of questions about inheritance to himself and also to his colleagues. Together with biologist William Bateson, Punnett would end up co-founding the Journal of Genetics in 1910. But Punnett also had a mathematician friend named Godfrey Hardy. Together, Punnett and Hardy used to play a lot of cricket, and one day on the cricket field Punnett mentioned that the problem of inheritance might be understood best in light of mathematics.

This led Hardy to publish what was called Hardys Law in June of 1908. It was an algebraic expression showing how the numbers and ratios of genes and traits should stay the same, or shift over time. It would have made Hardy the sole founder of population biology, if not for the fact that somebody else had already discovered it six months earlier. That man was Wilhelm Weinberg, a German physician who had derived a similar equation of population genetics in January, 1908. When this was realized, geneticists began referring to what we now call the Hardy-Weinberg Principle, and an equation by the same name.

The Hardy Weinberg Principle illustrates that there is an equilibrium that is maintained the ratios alleles, alternate forms of each gene remain the same, so there is no evolution if selective pressure is removed, but there are a couple of other requirements. The population must be reproductively isolated (separated from other organisms that can produce offspring with it), and the population must be infinitely large.

If the number of individuals in an isolated, successful population is not infinity, then a force called genetic drift comes into play. Like the increasing chances of getting more heads or more tails as the number of random coin tosses is decreased, genetic drift increases as the size of a population decreases. Other things that happen in nature are founder effects and bottlenecks, both of which you can equate to drawing a handful of gumballs from a jar and ending up holding gumballs with a ratio of colors that differs from the color ratio in the jar, due to the randomness of sampling.

With a founder effect, a small group of individuals gets isolated, and due to chance the ratio of alleles for various genes is different from the mother population. The same is true in a bottleneck effect, which happens when the bulk of a population gets killed off, and due to to chance, the ratio of different alleles in the surviving gene pool is different from what it was in the mother population.

Whereas founder effects and bottlenecks remove diversity from the gene pool of a population, the opposite can happen when migration and other factors bring populations together. Thus, while in the case of humanity, modern medicine and other technologies may indeed be reducing the impact of natural selection, migration and founder effects has been playing a major roles as transportation and other technologies have developed. And these phenomena may play a still more influential role if human colonization of the Moon, Mars, or free space becomes reality. In nature all phenomena that change the gene pool operate in concert, affecting the course of evolution, whether in tadpole shrimp, lungfish, or humans.

This article was originally published on November 27, 2017.

David Warmflash is an astrobiologist, physician and science writer. BIO. Follow him on Twitter @CosmicEvolution

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Have any of Earth's creatures stopped evolving? - Genetic Literacy Project

There is a strong genetic component to asthma, but it’s not the only risk factor – Insider – INSIDER

Asthma is a chronic condition that causes your airways to become inflamed leading them to swell and narrow. This makes it harder for you to breathe and can cause dangerous asthma attacks.

Asthma is often linked to other health conditions like hay fever and environmental factors including air pollution. However, research also shows that carrying certain genes can put you at greater risk of developing asthma.

Here's what you need to know about what causes asthma and how it can be passed down through families.

Scientists have identified more than one hundred specific genes that may play a role in whether or not a person develops asthma. In fact, a person with at least one biological parent with asthma is 3 to 6 times more likely to develop the condition than someone whose parents don't have asthma.

However, even if you are born with asthma-related genes, you may not develop asthma unless those genes are "turned on," likely by something in your environment. "Multiple genes may be involved and they could be triggered by a number of factors, such as viral infections," says Stanley Szefler, MD, the Director of the Pediatric Asthma Research Program at Children's Hospital Colorado.

This means that if you have asthma-related genes and suffer a bad respiratory infection as a child, this could kickstart a lifelong asthma condition. However, experts say that more research is needed to fully understand how these genes interact with the environment to cause asthma in the first place.

Doctors have identified several different types of asthma including adult-onset asthma, allergic asthma, and exercise-induced asthma. Scientists have not linked any specific genes to a particular type of asthma, Szefler says. However, there is evidence that every type of asthma has a genetic component.

In a study, published in 2008 in Twin Research and Human Genetics, researchers compared the incidence of asthma in twins to determine how strongly genes affect the likelihood of developing asthma, compared with environmental factors. The results showed that genetics plays a very large role the genes account for about 70% of your risk of developing asthma.

It's important to remember that even though genes are an important risk factor for asthma:

About half of all asthma sufferers start having symptoms as children age 5 and younger. But for people who develop asthma later in life, genes are less likely to play a role. This may be because some older people develop asthma due to lifestyle choices like smoking.

In addition to genetics, asthma may be caused by:

In many cases, experts don't know why some people develop asthma while others don't. However, there are risk factors that can increase your risk. These include:

There is no way to prevent asthma, even if you start treatment early on after your symptoms develop, says Szefler. Researchers are starting to look at whether using biologic medications containing live bacteria could work to prevent asthma, Szelfer says, "but the results are several years off."

However, even if you can't prevent asthma, there are steps you can take to prevent asthma attacks:

Asthma is an ongoing condition and you should "maintain good medical follow-up to keep the disease under control," Szefler says. You will need to make an individual treatment plan with your doctor, designed to target your symptoms and help avoid your asthma triggers.

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There is a strong genetic component to asthma, but it's not the only risk factor - Insider - INSIDER

Alzheimer’s disease: protective gene uncovered in human cell model bringing promise for new drug discoveries – The Conversation UK

Every three seconds, someone in the world develops dementia. The most common form of dementia is Alzheimers disease. While researchers have identified a number of risk factors that are linked to dementia including genetics, smoking, and high blood pressure there is currently still no cure.

Part of the reason for this is because of how complicated it is to test potential Alzheimers drugs. In order to conduct clinical trials participants need to have symptoms. But by the time symptoms appear, its usually too late for treatments to have a large effect as many of their brain cells have already died.

But our latest research developed a new human cell model that is able to rapidly simulate the development of Alzheimers disease in the lab. This allowed us to identify a gene, called BACE2, that is naturally able to suppress the signs of Alzheimers disease in human brain cells. Our research is the result of around five years work, and was the collaborative effort of teams based in London, Singapore, Sweden and Croatia.

Researchers already know a lot about which genes cause Alzheimers disease or make someone more likely to develop it. These genes contribute to certain toxic proteins accumulating in the human brain. So our team thought that the opposite must also be true: our brain cells must also have proteins that can naturally slow down the development of Alzheimers.

One gene that can definitely cause Alzheimers disease is a gene found on the 21st pair of human chromosomes that is responsible for making the amyloid precursor protein (APP). Research shows that 100% of people born with just one extra copy of the APP gene (called DupAPP) will develop dementia by age 60.

People with Downs syndrome are born with three copies of APP because they have a third 21st chromosome. But by age 60, only 60% of them will develop clinical dementia. We wanted to know why some people with Downs syndrome have delayed development of or never develop Alzheimers dementia compared to those who have one extra DupAPP gene.

The simple answer for this is because they have an extra dose of all other genes located in chromosome 21. We believed that there could be some dose-sensitive genes on chromosome 21 that, when triplicated, protect against Alzheimers disease by counteracting the effects of the third APP gene.

These genes must then appear to delay the onset of clinical dementia in some people with Downs syndrome by approximately 20 years. Studies have even shown that any future drug able to delay dementia onset by just five years would reduce the prevalence of Alzheimers in the general population by half.

To study the potential of the extra genes, we took hair follicle cells from people with Downs syndrome and re-programmed the cells to become like stem cells. This allowed us to turn them into brain cells in a Petri dish.

We then grew them into 3D balls of cells that imitated the tissue of the grey matter (cortex) of the human brain. The 3D nature of the culturing allowed misfolded and toxic proteins to accumulate, which are crucial changes that lead to Alzheimers disease in the brain.

We found all three major signs of Alzheimers disease (plaque build-up in the brain, misfolded tau proteins and dying brain neurons) in cell cultures from 71% of people with Downs syndrome who donated samples. This proportion was similar to the percentage of clinical dementia among adults with Downs syndrome.

We were also able to use CRISPR a technology that allows researchers to alter DNA sequences and modify a genes function to reduce the number of BACE2 genes from three copies to two copies on chromosome 21. This was only done in cases where there were no indications of Alzheimers disease in our cellular model. Surprisingly, reducing the number of BACE2 genes on chromosome 21 provoked signs of the disease. This strongly suggest that having extra copies of a normal BACE2 gene could prevent Alzheimers.

The protective action of BACE2 reduces the levels of toxic amyloid proteins. This was verified in our cellular models, as well as in cerebrospinal fluid and post-mortem brain tissue from people with Downs syndrome.

Our study provides proof that natural Alzheimers-preventing genes exist, and now we have a system to detect new potential protective genes. Importantly, recent research showed the protective action of BACE2 might also be relevant to people who dont have Downs syndrome.

Our results also show that all three signs of Alzheimers disease can be potentially detected in cells from live donors. Though this requires a lot more research, it means we may be able to develop tests that identify which people are at higher risk of Alzheimers disease by looking at their cells.

This would allow us to detect the disease before it starts developing in a persons brain, and could make it possible to design personalised preventative treatments. However, we are still a long way from reaching this goal.

Most importantly, our work shows that all three signs of Alzheimers disease detected using our model could be prevented by drugs known to inhibit the production of the toxic amyloid protein and this can be detected in as little as six weeks in the lab. We hope our discovery could lead to the development of new drugs aimed at delaying or preventing Alzheimers disease, before it causes brain cell death.

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Alzheimer's disease: protective gene uncovered in human cell model bringing promise for new drug discoveries - The Conversation UK

Four Rivers Wildlife: The color of my skin – Murray Ledger and Times

You mean our skin color is controlled by just a few genes? The question came from the front row. There is simply nothing better for a teacher than seeing the imaginary light bulb go on. In this case, the bulb burned bright, as the science had social implications.

Skin color in humans is controlled by the amount of melanin our cells produce. The more melanin, the darker the skin, and melanin production is controlled by the genes we have inherited from our parents. Although there are multiple genes involved, melanin genetics is relatively simple compared to some other traits. Because each gene has alternative forms, there is a diverse, continuous distribution of possible skin colors. We use labels like black and white but skin color is much more precise than that, because humans are a lot more variable than the categories our minds want to place each other in.

Consider my niece, whose ivory skin is a consequence of her German ancestry. She married a darkly skinned gentleman from India. Because of the multiple genes involved, their sons skin color could have been very white like his mother or very dark like his father, although those options were extremely unlikely. In fact, he is somewhere intermediate in the distribution of possibilities, exactly where you would expect. In contrast, my own skin had little chance of being different than my parents, because both them had very similar skin color.

The genetics that underlie human skin color, eye color, and even whether your earlobes are attached or not follow the same basic mechanisms that we see in other organisms, from microbes to wildlife. All life shares the same general process, although the specific mechanisms producing color patterns vary across species.

For example, gray squirrels come in three color morphs, or forms, and this occurs in part because the genetics of squirrel color is simpler than in humans. Most are gray on top with a white belly, but because of variation at a single gene, some are completely jet-black, and a few are black on top but brown underneath.

In contrast, ladybugs have more than 200 color patterns, although the ones we see in North America are usually reddish with about 20 black spots. In their native Asia, there are many more colors, including all red without spots, and all black with red spots. Like squirrels, this variation is controlled by a single gene, but this gene is turned on or off in specific places by other genes, producing one of the most variable color patterns of any animal.

These examples support one basic idea: the color of many organisms, from ladybugs to humans, is genetically determined. However, humans differ from other animals in how we perceive and react to these colors. Squirrels do not treat each other differently based on color. Most mammals, including squirrels, use smell rather than vision as their primary sense. Similarly, insect behavior is influenced more by chemical cues than vision. In these species, color patterns are used for hiding from predators or regulating temperature, not for determinations of social status.

Our color vision has social implications that we cannot ignore. Perhaps as we consider such questions, and the social changes that we are a part of, we will realize that the heart of the matter is unchanging: we are all one species.

The color of our skin is a genetically-determined trait, like those of squirrels and ladybugs. Our skin color is beyond our control, just like we cannot determine whether our earlobes are attached or not. But our behavior is not. How we perceive and respond to skin color and other traits is what makes us human. And no matter what the color of my skin, or yours, we are all related, whether we are brothers and sisters, nieces and nephews, or very distant cousins.

Humans do not treat each other differently based on earlobes, nor should we do so based on the color of our skin. Its easy to write that, but much harder to do. But understanding that skin color is just one of many traits that are a result of basic genetic principles might turn on imaginary light bulbs throughout the world, brightening all of our lives.

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Four Rivers Wildlife: The color of my skin - Murray Ledger and Times