StemCell Therapy

The ability to modify gene expression in these cells has the potential to lead to new treatments for cancer, autoimmune disease

UCLA Broad Stem Cell Research Center

L-R: Study authors Luke Riggan, Professor Tim OSullivan and Andrew Hildreth.

Sarah C.P. Williams | May 20, 2020

A UCLA research team has successfully usedthe powerful gene-editing tool known asCRISPR-Cas9 toalterthe DNA ofmatureinnate immune cells, some of the bodys first responders to infections. These blood cells have been notoriously difficult to genetically engineer in the past.

While the work was carried out in mice, the ability tomodifythe gene expression of these cells could one day allow clinicians to better harness the power of the immune system in the fight against cancer and autoimmune disease.

The study, published in the journal Cell Reports, was led by senior authorTim OSullivan, an assistant professor of microbiology, immunology and molecular genetics and a member of theEli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Weve figured out a way to genetically edit cells that researchers have had a lot of difficulty with in the past, said OSullivan, who is also a member of theUCLA Jonsson Comprehensive Cancer Center. The real impact will be if we can one day take cells from patients blood, edit them using this approach and put them back in the same patient as an immunotherapy.

Unlike the adaptive immune system, which relies ontheproduction ofantibodiesthattarget specific molecules present on viruses, bacteria, and other pathogens, the innate immune system is the bodysfirst andmoregeneralized line ofdefense. Innate immune cells including macrophages, dendritic cells and natural killer cells recognize and fight offa wide variety offoreign invaders using receptors that seek out common molecular patterns found in pathogens.

Over the past decade, researchers have utilized CRISPR-Cas9 to modify gene expression inside living cells. Adapted from a naturally occurring DNA-editing system in bacteria,the technology relies on a scissor-like protein called Cas9, which can be directed to cut DNA at specific sites on a cells genome to disable, repair or make other alterations to genes.

Typically, the approach uses aharmlessvirus to deliverCas9 and its accompanying moleculesto the inside of cells. It has been successful in editing genes in dozens of cell types, including those of the adaptive immune system. But when researchers including OSullivans team tried to use a similar approach on innate immune cells, the cellsidentifiedthe virus as an invader and activated their defenses, thwarting the efficacy of the approach.

We wanted to figure out a way to edit the innate immune cells without activating them, said UCLA graduate student Andrew Hildreth, cofirst author of the new work.

The groups new method involves zapping theinnateimmune cells with a small pulse of electricity enough to make the outer covering of the cells slightly porous but not enough to harm the cells otherwise. If the Cas9 and the accompanying protein complex used for gene editing are in the liquid surrounding the cells and the electricity pulses just right, the Cas9 complexes can sneak in through the porous membrane of the cells.

We optimized the process so that the Cas9 protein complexes enter the immune cells, go to the nucleus, and edit the target gene with 95% efficiency, said Luke Riggan, a graduate student in OSullivans lab and the other cofirst author of the paper. And we can do all this in less than a week.

To show the utility of the new method for research purposes, OSullivans team used it to delete a gene called MyD88 from the dendritic cells of mice. Without the gene, they showed, mice die from a virus that their immune systems can usually fight off. They also used thenew deliverytechnology to edit the genes of natural killer cells, giving the researchers the ability to test how certain genes contribute to natural killercell proliferation during viral infection. Natural killer cells are a type of white blood cell that have the ability to target cancer cells; boosting their proliferative capabilities could help treat some tumors, the researchers said.

In the future, OSullivan said,the methodcouldbe useful for a range of immunological research quickly deleting many genes from different innate immune cells could help scientists screen for genes that are important for certain immune functions, for instance. But the approach could also be used clinically to edit immune cellstaken directlyfrom patients.

The ability to use this technique in human cells could have major clinical applications, he said, adding that the team is already carrying out experiments on cells from human blood samples.

The research was supported by the National Institutes of Health, including a Ruth L. Kirschstein National Research Service Award.

Originally posted here:
UCLA scientists alter genes of innate immune cells with DNA-snipping tool - UCLA Newsroom

Eurordis, a Paris-based coalition of national rare disease associations across Europe, hosted its first all-virtual conference, bringing some 1,500 delegates from 57 countries together online during the COVID-19 pandemic.

The 10th European Conference on Rare Diseases & Orphan Products (ECRD2020) which was set for May 1415 in Stockholm, instead took place via Zoom. Eurordis and its co-organizer, Orphanet, used the occasion to appeal to the European Union in Brussels to urgently approve standardized policies to advance the health and well-being of all Europeans.

Yann Le Cam, CEO of Eurordis, said that as is the case with COVID-19, there is an obvious value to grouping efforts at the EU level in order to tackle rare diseases. But he lashed out at the increasing nationalism shown by various leaders responding to the pandemic.

We must quash this egocentric rhetoric emerging in some countries. It fragments Europe into diverging national-level decisions, Le Cam, of France, said in his welcoming remarks. A lack of EU coordination is both detrimental to the health of people living with a rare disease and has an unnecessary negative impact on the economy.

He urged the EU to take the following concrete steps:

This epidemic has shown that if you fail to prepare, you prepare for failure and we must prepare together across borders, said Terkel Andersen, president of the Eurordis board.

Eurordis is a nonprofit alliance of 900 rare-disease patient organizations from 72 countries that work jointly to improve the lives of Europeans with rare diseases. Orphanet provides high-quality information and data on rare diseases. With its 40-nation network, Orphanet helps to orient patients and doctors to relevant expert resources in Europe and beyond.

The EU considers a disease rare if its incidence is lower than 1 in 2,000 people. About 30 million of the 446 million citizens who live in its 27 member states have a rare disease.

Yet because of the low prevalence of each disease, medical expertise is uncertain, care offerings inadequate, and research limited, said Orphanets director, Ana Rath. She noted that 72% of rare diseases are genetic and that 70% of those genetic conditions begin in childhood.

Now more than ever, the EU has a vital role to play in improving the health of its citizens. ECRD2020 focuses on how to build policies and services over the next decade that will improve the journey of living with a rare disease for patients and families, Rath said.

Attendance at this years virtual conference was up 81% compared to the 850 people who attended ECRD2018 in Vienna. It followed six broad themes, ranging from the future of diagnosis to the digital health revolution.

The online conference program ran 54 pages, with specific breakout sessions covering topics from newborn screening for genetic diseases to how best to bring real life into therapeutic development.

Several top EU officials addressed participants via Zoom, including Stella Kyriakides, the European commissioner for health and food safety. She said ECRD2020 builds on the work of the ongoingRare 2030 Foresight Study, which will conclude in 2021 with a comprehensive set of key recommendations to EU leaders on how to improve rare disease policy.

In the coming years, we will be guided by the Rare 2030 Foresight Study, Kyriakides said. We need now to take lessons from COVID-19. We know that patients will be the driving force of our rare disease policy.Europe currently accounts for more than one-third of the 4.7 million confirmed COVID-19 infections worldwide, with cases stretching from Madrid to Moscow. Infection rates, however, varies widely among EU member states.

Another major theme of ECRD2020 was how to ensure non-discrimination on the basis of health and disability. Officials addressing that theme included David Lega, a Swedish member of the European Parliament; Jana Popova of theBulgarian Association for Neuromuscular Diseases; and Helena Dalli, European commissioner for equality.

All people should be able to participate fully and equally in society and in the economy, Dalli said. It is not only their right. Their participation represents a huge contribution to the whole society.

The ECRD2020 conference was co-chaired by Maria Montefusco, president of Rare Diseases Sweden; Milan Macek, a professor of medical and molecular genetics at Motol University Hospital in Prague; and Violeta Stoyanova-Beninska, chair of the Committee of Orphan Medical Products at the Amsterdam-based European Medicines Agency.

Total Posts: 85

Ana holds a PhD in Immunology from the University of Lisbon and worked as a postdoctoral researcher at Instituto de Medicina Molecular (iMM) in Lisbon, Portugal. She graduated with a BSc in Genetics from the University of Newcastle and received a Masters in Biomolecular Archaeology from the University of Manchester, England. After leaving the lab to pursue a career in Science Communication, she served as the Director of Science Communication at iMM.

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Unity and EU-wide Efforts Focus of Online Rare Disease Meeting - SMA News Today

Revealing yet another super-power in the skillful squid, scientists have discovered that squid massively edit their own genetic instructions not only within the nucleus of their neurons, but also within the axon the long, slender neural projections that transmit electrical impulses to other neurons. This is the first time that edits to genetic information have been observed outside of the nucleus of an animal cell.

The study, led by Isabel C. Vallecillo-Viejo and Joshua Rosenthal at the Marine Biological Laboratory (MBL), Woods Hole, is published this week in Nucleic Acids Research.

The longfin inshore squid, Doryteuthis pealeii, long established as a research organism for fundamental biological studies. Credit: Elaine Bearer

The discovery provides another jolt to the central dogma of molecular biology, which states that genetic information is passed faithfully from DNA to messenger RNA to the synthesis of proteins. In 2015, Rosenthal and colleagues discovered that squid edit their messenger RNA instructions to an extraordinary degree orders of magnitude more than humans do allowing them to fine-tune the type of proteins that will be produced in the nervous system.

But we thought all the RNA editing happened in the nucleus, and then the modified messenger RNAs are exported out to the cell, says Rosenthal, senior author on the present study. Now we are showing that squid can modify the RNAs out in the periphery of the cell. That means, theoretically, they can modify protein function to meet the localized demands of the cell. That gives them a lot of latitude to tailor the genetic information, as needed. The team also showed that messenger RNAs are edited in the nerve cells axon at much higher rates than in the nucleus.

Top, schematic of squid anatomy showing the location of the giant axon, an unusually large neural projection that partly controls the squids jet propulsion system, used for very fast movement, attacks and escapes. Below, schematic of a neuron, showing the location of the nucleus where all RNA editing was previously thought to occur, and the axon, where local RNA editing was identified in squid. Credit: Vallecillo-Viejo et al, Nucl. Acids Res., 2020.

In humans, axon dysfunction is associated with many neurological disorders. Insights from the present study could accelerate the efforts of biotech companies that seek to harness this natural RNA editing process in humans for therapeutic benefit.

Scientists from Tel Aviv University and The University of Colorado at Denver collaborated with MBL scientists on the study.

Previously, Rosenthal and colleagues showed that octopus and cuttlefish also rely heavily on mRNA editing to diversify the proteins they can produce in the nervous system. Together with squid, these animals are known for strikingly sophisticated behaviors, relative to other invertebrates.

Reference: Spatially regulated editing of genetic information within a neuron by Isabel C Vallecillo-Viejo, Noa Liscovitch-Brauer, Juan F Diaz Quiroz, Maria F Montiel-Gonzalez, Sonya E Nemes, Kavita J Rangan, Simon R Levinson, Eli Eisenberg and Joshua J C Rosenthal, 23 March 2020, Nucleic Acids Research.DOI: 10.1093/nar/gkaa172

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Superpower Discovered in Squids: They Can Massively Edit Their Own Genetics - SciTechDaily

Although scientists don't fully understand it yet, and it varies from person to person, there is a link between genetics and obesity as you've probably figured out if you've got friends who can eat whatever they like while remaining thin.

Now new research has identified one gene that could play a role. It's called ALK (Anaplastic Lymphoma Kinase), and mutations in this gene have previously been linked to certain cancers, and identified as drivers of tumour growth.

The latest study found two particular ALK variations showing up in thin, low BMI individuals - but not in individuals of normal weight. The analysis looked at the DNA of 47,102 people aged 20 to 44 years old, taken from Estonia's 'biobank', a biological database collected from a large percentage of the Estonian population.

"We wanted to understand why," says medical geneticist Josef Penninger, from the University of British Columbia in Canada. "Most researchers study obesity and the genetics of obesity. We just turned it around and studied thinness, thereby starting a new field of research."

In follow-uptests on mice and Drosophila fruitflies, animalsthat had the ALKgene turned off stayed thinner than normal even when the mice were fed what the researchers described to CNN as "a McDonald's diet".

Further tests showed that the mice without the ALK gene had lower than normal body weight and levels of body fat.

Of course correlation isn't causation. But the researchers suggest that the gene, which is highly expressed in the brain, plays a role in telling bodies how much fat to burn and how to use its energy stores.

Still, for now all we've shown is that this direct link exists in fruit flies and mice, not humans. Despite extensive research into the gene's involvement in cancer, our understanding of the ALK gene's role in human physiology remains largely unclear.

But one promising aspect of the discovery is that scientists already know how to inhibit ALK in humans because of its role in cancer development, so testing the link further is doable.

"If you think about it, it's realistic that we could shut down ALK and reduce ALK function to see if we did stay skinny," says Penninger.

"ALK inhibitors are used in cancer treatments already. It's targetable. We could possibly inhibit ALK, and we actually will try to do this in the future."

Further studies are also going to need to take a closer look at how the ALK gene operates in the brain: how it potentially balances metabolism and leads to a skinnier body shape at a molecular level.

Even if a clear link between ALK mutations and a resistance to weight gain is established, it's probably going to only be part of a much larger mix of genetic factors as previous research has hinted at.

While the biobank data and tests on mice and flies are a good starting point at solving the mystery link between genetics and thinness, scientists are going to need a lot more data in the future before we can figure out what's really happening here.

"You learn a lot from biobanks," says Penninger. "But, like everything, it's not the ultimate answer to life, but they're the starting points and very good points for confirmation, very important links and associations to human health."

The research has been published in Cell.

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Researchers Identify a Potential 'Thinness' Gene That Stops Mice Putting on Weight - ScienceAlert

The global scientific community has joined forces in an unprecedented effort to understand, track, forecast, test for, and find a cure for the current coronavirus pandemic. But in a crisis where every second lost means more loss of lives, solidarity alone isnt enough. Supercomputers are enabling a vastly accelerated pace by which scientists can conduct research and collect and analyze data. Never have they proven their value to society more than during this COVID-19 pandemic.

Supercomputers provide scientists with unique capabilities: they can explore the structure and behavior of the virus at the molecular level, and forecast the spread of the disease and design drugs much faster than would otherwise be possible.

The Texas Advanced Computing Center (TACC) began fielding requests for compute time to assist in the fight against COVID-19 in February 2020. In March, the White House enlisted some of the worlds most powerful supercomputers in the battle against COVID-1 through the COVID-19 High Performance Computing (HPC) Consortium, a public-private partnership providing researchers worldwide with massive computing resources.

As part of this effort, we are working closely with teams to provide priority access to supercomputing resources here and across the world. In the U.S. alone, there are more than 100 projects, involving thousands of researchers, using HPC systems to predict the effects of interventions like stay-at-home orders and school closings; to simulate the molecular behavior of the proteins that make the virus virulent; to understand the genetics of the virus and its mutability; to screen potential drugs and vaccines for efficacy; and to visualize and interactively share data with decision-makers.

At TACC, nearly a third of all computing time has been dedicated to accelerating these efforts the equivalent of 40,000 desktop computers churning non-stop. None of this would be possible without federal funding for high performance computing by the National Science Foundation (NSF) and Department of Energy (DOE), who have made open access to supercomputers part of their mission for more than four decades.

Beyond big machines, supercomputing centers employ some of the brightest minds in computational science, and these individuals are collaborating with teams across the nation to fast-track research.

Among these partnerships is the University of Texas at Austin COVID-19 Modeling Consortium, led by Dr. Lauren Ancel Meyers, which developed one of the leading epidemiological models of how the disease spreads based on virus transmission and real-time cell phone data. The White House and CDC, as well as the national media and public, have used the model to inform their understanding and decision-making.

A team from DOEs Argonne and Brookhaven National Laboratories applied several of the most powerful supercomputers in the world to accelerate an AI-based approach to drug docking. Their effort narrowed 6 billion possible small molecules to the 30 with the best chance of binding to one of the virus proteins and disrupting its function. These are now being tested in labs at the University of Chicago.

The TACC-powered COVID-19 Drug Discovery Consortium is collaborating with Enamine, the worlds largest provider of screening compounds, and Boston University, Texas A&M, and the University of Texas Medical Branch, to identify the 600 most promising, readily available, drug-like molecules (out of 2.6 million) and test them in high-containment laboratories in order to find potential drugs in months rather than years.

New projects are launching daily.

In many of these cases, long-term research collaborations helped speed the projects out of the gate. The UT Austin Modeling Consortiums projections built on a decade of federally-funded R&D on flu pandemic modeling by Meyers team. The DOE researchers adapted AI-based cancer drug discovery methods for SARS-CoV-2. The Drug Discovery Consortium leveraged tools and methods developed over many years to fight bioterrorism. Our ongoing relationships with these teams has made it possible for them to shift their research focus, expand their scope, and reduce limitations as they work towards a common good.

Academic research is frequently the first step in a long process that requires efforts by government agencies, philanthropic organizations, and industry. Basic science helps decision-makers protect the populace, and informs the creation of vaccines and treatments.

Under normal circumstances, this process takes years or decades. However, time is a luxury we simply do not have. The urgency of the challenge we face makes the application of research accelerators like supercomputers even more critical to help flatten the curve and ultimately solve the greatest crisis we as a society have ever faced.

Dan Stanzione is the director of TACC at The University of Texas at Austin.

A version of this op-ed appeared in The Hill.

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How Supercomputers Are Getting Us Closer to a Covid-19 Vaccine - UT News | The University of Texas at Austin

In 1994, researchers found two chimpanzees dead in Cte dIvoires Ta National Park, which holds West Africas largest rainforest. Autopsies of the chimpanzees revealed signs of hemorrhage resembling those found in humans during outbreaks of ebolavirus that occurred decades earlier in Zaire and Sudan. Indeed, further studies led to the designation of Ta Forest ebolavirus, one of five known strains of the virus that can lead to the ebolavirus disease. One researcher in the park contracted the disease during this time.

This is one of many stories of a zoonotic disease, also referred to as a zoonosis, which is a disease transmitted to humans by animals. Zoonoses are transmitted via direct or indirect contact with an infected individual, consuming contaminated food or water, or through vectors for example, being bitten by a mosquito carrying the disease.

The focus on transmission to humans dominates the global narrative of zoonoses, which include West Nile, rabies, Lyme and others. But certain pockets of the zoological research community focus on the reverse: humans transmitting zoonoses to wildlife, known as zooanthroponosis or anthroponosis.

In the current case of COVID-19, researchers of non-human primates have sounded alarm bells for the risks humans pose for transmitting SARS-CoV-2, the viral pathogen that causes the COVID-19 or coronavirus disease, to species of primates, including monkeys and apes. Being among some of the worlds most endangered species, of particular concern are wild great apes, including bonobos, eastern and western gorillas, orangutans and chimpanzees.

These types of outbreaks can have really devastating effects on primate populations, says says Amanda Melin, a biological anthropologist who runs the Primate Genomics and Ecology lab at the University of Calgary. This is a great example of the risks that we pose to other animals in the earth.

So far, there have been no positive tests of COVID-19 in wild great apes but the deadliness of the disease, should transmission occur, is likely high.

Its the quickest study Ive ever been involved in, says Melin of a study she co-led with Mareike Janiak, a postdoctoral scholar in molecular anthropology, and James Higham, a primate evolutionary biologist at New York University, that helps dispel the guesswork of which non-human primate species are at greatest risk. The study was conducted within about seven days in early April and posted to a preprint server shortly thereafter because of the urgency of its findings, which examine the genetics behind how the SARS-CoV-2 pathogen triggers the COVID-19 disease itself.

In order for a viral pathogen to take hold in a host, the proteins on its surface must bind with certain proteins on the surfaces of a hosts cells. Once the pathogens protein has found its cellular protein match, known as a receptor, the pathogen can enter the cell and trigger the disease. Coronavirus pathogens not just of COVID-19, but of other coronaviruses as well express spike proteins on their surfaces.

If the viruss protein cant find anywhere to bind, then its not going to become infectious, Melin puts simply.

Genes determine which proteins are formed on which cells. Melins study examines the coding sequence of the ACE2gene, which codes the cellular protein (the ACE2 receptor) for the SARS-CoV-2 pathogen. These receptors are found in endothelial tissues throughout the body, including in the lungs, hence the diseases respiratory effects.

As is the case concerning most forms of life, less diversity means less resilience to threat, and so too does it go for genetic predisposition to COVID-19.

Proteins are made of amino acids. Genes can vary in the sequences of their comprising DNA, and the variants of a gene will code protein receptors with different structures of their amino acids. Receptors with a range of structures make it more difficult for a pathogen to find its match.

With that context, consider this statement from Melins study: Here, we show that all apes, including chimpanzees, bonobos, gorillas, and orangutans, and all African and Asian monkeys, exhibit the same set of twelve key amino acid residues as human ACE2.

In other words, we and many of our primate cousins are in the same boat of being highly susceptible because we have highly similar ACE2 genes and receptors, making it easier for the SARS-CoV-2 pathogen to find its binding match on our cells.

Interestingly, the study found that monkeys in the Americas, and some tarsiers, lemurs and lorisoids, had more ACE2 genetic variation, indicating that many species are likely less susceptible. However, Melin warns, some lemur species are also likely to be highly susceptible, which is worrying as they are also among the most endangered primates.

(Bats, notorious for being hosts and spreaders of coronaviruses, have exceptionally high ACE2 genetic variation. Within just the handful of bat species that we looked at, we saw genetic variation equivalent to the variation we saw across the entire range of other mammals we included, says Melin.)

Its easy to imagine that were closely related to other non-human primates, and so we should be careful with diseases. But knowing that they have the exact same sites and should be equally susceptible to us, and seeing what its doing to humans around the world its really concerning.

At the end of 2016 and into early 2017, chimpanzees in the Ta forest were seen with cold-like symptoms. While it did not prove deadly, the illness was found by researchers to have been a coronavirus passed to the chimpanzees from humans, likely poachers.

Similar to Gombe, disease is the leading challenge for conservation of chimpanzees at Ta, says Thomas Gillespie, whose work with wild great apes in Africa includes directing theGombe Ecosystem Health Project, in addition to running the Gillespie Lab at Emory University. Because of that, were always alert to the risk of disease exposure from people. The Ta team, 10 years ago or so, had a major respiratory outbreak that killed all the young chimpanzees

The tell-tale signs of COVID-19 are likely also the same for human and non-human primates, namely dry cough and fever.

We expect to see human-like symptoms, or more extreme versions of those. Laboratory-based infection of macaques resulted in similar disease progression to what were seeing in humans, says Gillespie.

Because best practices of wildlife conservation, and especially with wild great apes, demand limited human interaction, researchers rely on technology to check animals for symptoms from a safe and hidden distance. Laser thermometers are used to check fecal masses immediately after defecation to determine body temperatures. Blood meals from mosquitos are tested to keep track of pathogens circulating between them and animals. Carrion flies, which feast on dead animals, can give insights on mortality.

The Cross River gorillas, for example we never see them because theyre very cryptic, says Gillespie of the critically endangered species. Only an estimated 200 or 300 remain, residing at the border of Nigeria and Cameroon. But the flies are still going to find them. Flies are going to let us know if theres a spike in mortality. And then that can alert us to potential issues.

Should COVID-19 begin to be found in wild great apes, there is good and bad news. The bad is that quarantining isnt an option. Because of group dynamics, individual animals within most groups cannot be removed They dont respond well it tends to go quite badly, says Gillespie making the likelihood of virus spreading to the entire group of a single infected animal quite high.

And, once a wild animal has left the wild, he adds, there are tremendous threats involved with putting them back in the wild because we might have exposed them to additional pathogens in the sanctuary setting.

So we cant think about things like darting individuals, removing them from the group, quarantining them. We have to really focus on them not becoming infected. And thats the most important thing.

Gillespie nonetheless expects the virus to make its way into at least some populations of wild apes populations. The key now is to understand how it is likely to spread among species, based on exposure as well as the apes behavior and ecology. For example, in some places, habituated apes those accustomed to proximity to humans might be exposed to SARS-CoV-2, but will likely never come into contact with non-habituated apes. In other areas, this might not be the case.

And in yet other areas, monkeys that share habitats with apes baboons and vervet monkeys in Africa; macaques in Asia might spread the virus among great ape groups, or act as intermediaries, carrying the virus from humans to great apes.

This is something were actively working on, says Gillespie, who is leading a team focused on creating a model of sites across Africa and Asia to guide location-based best practices for ape conservation during the pandemic. Were modeling the different ape species, including variables like demographics, behavioral ecology, and proximity to humans and other susceptible species. This can all influence the dynamics of transmission to wild great apes.

Many protected areas inhabited by wild great apes have quickly developed lockdown measures of their own, such as shutting down tourism, logging and mining operations and extensively testing staff and researchers.

One of the major efforts currently addressing this is led by the Primate Specialist Group and the Wildlife Health Specialist Group, both of the International Union for Conservation of Nature. The two groups released a joint statement in early March, listing ways that humans can minimize risks to wild great apes, including disinfecting their footwear, wearing surgical masks, quarantining when coming from abroad, and immediately leaving an area when feeling the need to cough or sneeze and not returning.

But for local communities who depend on the use of certain forests, current measures might mean theyre left without a livelihood. To this end, the IUCN has created a task force, which includes Gillespie, focused on COVID-19s impacts on areas where wildlife and communities share and depend on the same ecosystems. One component of this effort has been distributing funds to communities that might otherwise be forced to resort to actions that could threaten wildlife.

Melins and Gillespies studies and others like them are proving crucial tools for these conservationists to know where and how to allocate resources to protect species highly vulnerable to the disease, as well as provide scientific backing to policy- and decision-makers about the vulnerability of these species.

Even after the heightened phase of the pandemic has lessened, changes must continue to be made, she says: For primate observational research, we need to continue to be really careful about quarantining ourselves and about our proximities, always using best practices when were interacting with non-human primates. More generally, I hope we can slow and then stop the illegal trade of wildlife, which might help prevent future, different outbreaks.

And then she broadens her thoughts: How will it feel collectively, as humans, if were responsible for the rapid extermination of these species from the Earth?

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What the genetics of COVID-19 mean for the survival of wild great apes - Landscape News

The COVID-19 pandemic has caused supply and manufacturing disruptions in the Healthcare creating uncertainties in every aspect. The change in customer behavior in terms of mobility preferences during this crisis is changing the Healthcare landscape.

This pandemic situation has shut down many production lines owing to the trade restrictions and closed borders, creating a shortage in required parts and limiting the distribution of supplies. Different enforced measures including the closing of workspaces and dismissal of short-time workers have created a depression in the growth rate of the Healthcare Industry.

The growing fear of recession is estimated to decrease overall sales and revenue. A limited supply of parts coupled with a reduced workforce has forced the leading OEMs to shut down their production. A significant drop in demand has restricted the cash inflow which is highly important in payment of salaries to the workforce. With growing uncertainties around the COVID-19 pandemic, the industry leaders are taking measures to adapt to the situation.

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Geographically, the global Automated DNA Extraction Systems Market devices are segmented into viz. North America, Latin America, Europe, Asia-Pacific excluding Japan (APEJ), Japan and the Middle East and Africa (MEA). North America is expected to be the dominant market in the global Automated DNA Extraction Systems Market owing to increasing number of research and development and increasing public-private funding for life science research. Also, the Automated DNA Extraction Systems market in North America will rise due to the advancement in the technology and availability of skilled healthcare professionals. Europe is expected to have the second large share in the global Automated DNA Extraction Systems Market devices market throughout the forecast period. The Automated DNA Extraction Systems Market devices Market in the Asia Pacific excluding Japan is expected to grow at a significant CAGR due to an expansion of product offerings by the key players and increasing biotechnology industries in the region.

Automated DNA Extraction Systems Market: Key Players

The global market for Automated DNA Extraction Systems Market devices is highly fragmented. Examples of some of the key players operating in the global Automated DNA Extraction Systems Market devices are Thermo Fisher Scientific, QIAGEN, Autogen Inc., GeneReach Biotechnology Corp., Genolution Inc., RBC Bioscience Corp., Biosynex SA, Aurora Biomed Inc, bioMrieux SA, ADS Biotec Inc. PerkinElmer Inc., AITbiotech Pte Ltd, Roche Molecular Systems, Inc. Westburg BV among others.

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Sales Revenue of Automated DNA Extraction Systems Market to escalate in the Coming Years Owing to Changes in Market Dynamics During COVID-19 Pandemic...

KUALA LUMPUR, May 18 Three Malaysian students under the sponsorship programme of Public Service Department (PSD) have won the Class of 2020 Departmental Award from the Department of Microbiology and Molecular Genetics, College of Natural Science, Michigan State University, United States.

The PSD, in a statement, said the students Nurul Izzati Mohamed, Nurul Iffa Nazirah Taini Achim and Nuur Aqilah Izzati Othman are currently pursuing a bachelors degree in Microbiology at the university.

Nurul Izzati and Nurul Iffa Nazirah both received the Dietrich C. Bauer Scholarship Award (High Honour Distinction) while Nuur Aqilah Izzati received the Russel Duvall Endowed Scholarship Award (Research).

A total of eight awards were contested and three awards went to Malaysian students. The awards are based on academic excellence throughout the course and the quality and potential of the study conducted, the statement said.

Nuur Aqilah Izzati, 23, the sole recipient of the Russel Duvall Endowed Scholarship, was given the award based on panel assessment on the presentation of a study on Wheat Allergy: Do Wheat Genotypes Differ in Allergenicity.

Born in Batu Pahat, Johor, Nuur Aqilah Izzati was also conducting a joint study with Doctor of Philosophy (PhD) students on a research entitled Transdermal Sensitisation and Oral Elicitation of Anaphylaxis to Salt-Soluble Wheat Protein in An Adjuvant-Free Mouse Model of Wheat Allergy.

The announcement of the award of the three students was published on the official website of the Department of Microbiology and Molecular Genetics, College of Natural Science, Michigan State University, the statement said. Bernama

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Three PSD-sponsored students win awards in the US - Malay Mail

Atlanta music duo the Indigo Girls Amy Ray and Emily Saliers are lifelong friends and have been making music together since the 1980s. They met in elementary school and began performing together in high school in the Decatur area.

Ray says, We started playing back in high school, at Shamrock High School, and it was 1980.

Their work spans a wide variety of genres, from folk, to blues, to country to rock. Their lyrics often focus on social causes and politics and authenticity are themes that are important to them both.

Saliers says of their songwriting process, Its kind of a main agenda if you will for us to encourage people to not worry about conforming in any way. You can probably find examples of that in any song.

Their latest album released this month is Look Long and perfectly weaves together their many different musical influences. Saliers and Ray joined City Lights host Lois Reitzes to talk about the album and their highly successful career.

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The Indigo Girls On Music, Life And Longevity | 90.1 FM WABE - WABE 90.1 FM

What is high-intensity interval training (HIIT)

Nuffield Health explains: HIITtraining stands for High Intensity Interval Training - a form of cardiovascular exercise. HIIT can be further broken down into two main categories SIT (sprint interval training) and HIIT (high intensity interval training).

SIT is a form of very intense interval training that shouldonly be performed by already well-conditioned people who have no contrary health conditions.

You perform 3-5 intervals of very short maximal-intensity exercise working until you can't sustain the intensity, followed by a prolonged recovery period.

This would typically be 20-30 seconds of work followed by a three to five-minute rest interval."

HIIT involves exercising from 30 seconds to three minutes, working between 80-100 percent of your maximum heart rate, with shorter recovery periods than SIT.

Nuffield Health continues: There is no specific formula to HIIT but as a rule of thumb I would recommend your recovery period should be at least the same as your work interval and can become shorter as you get fitter.

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How to live longer: The best exercise for increasing life longevity - what is it? - Express

FROM 1960 till 2020, there has been a 28-fold increase in the number of centenarians. The path to longevity is strewn with false promises of expensive elixirs, exotic supplements, and stem cell rejuvenation. Human longevity is a complex interplay between the genes, the environment and lifestyle.

Genes and longevity

The study of human longevity genes is a developing science. Scientists estimate that between 15 and 30 per cent of the variation in human life span is determined by genes, but it is not clearly understood which genes are relevant, and how they contribute to longevity. In 2015, Ancestry, a genealogy and genetics company, partnered Calico, a Google spinoff, to study data from more than 54 million families and their family trees representing six billion ancestors, and were able to tease out a set of pedigrees that included over 400 million people. These individuals were connected to one another by either a parent-child or a spouse-spouse relationship.

In 2018, they published their results in Genetics, a journal of the Genetics Society of America. The study found that the lifespan of spouses were more similar and better correlated than in siblings of opposite gender. The study concluded that life span heritability is likely 7 per cent or less, and hence the contribution of genes to longevity is even lower.

Although genes seem to have only a small influence on lifespan, they appear to play a larger role in centenarians. Hence, there are a few genetic factors that do give you a headstart in the journey to longevity.

Being a first-degree relative of a centenarian makes it more likely for you to remain healthy longer and to live to an older age than your peers. First-degree relatives are less likely at age 70 years to have the age-related diseases that are common among older adults.

Women generally live longer than men , and the number of female centenarians is more than fourfold higher than that of male centenarians. It is thought that this is due to a combination of social and biological factors. Studies on mammals and Korean eunuchs has shown that the removal of testosterone at a young age was correlated with an increase in lifespan.

Genetic studies show that centenarians have a lower genetic risk of having heart disease, stroke , high blood pressure, high cholesterol, Alzheimer's disease and decreased bone mineral density. A study on Chinese centenarians published in 2013 showed that 55 per cent have normal systolic blood pressure, 82 per cent had normal diastolic blood pressure and less than 20 per cent were on long term medication. Hence, centenarians appear to have genes that reduce that risk of age-related chronic illnesses.

Biological clock

Epigenetics is the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself. One of the major mechanisms in which epigenetics manifest itself is by the process of DNA methylation, which involves the chemical modification of the DNA, thereby modifying the gene function and expression.

Through this process, certain genes can be silenced or activated and potentially impact age-related diseases such as cancer, osteoarthritis, and neurodegeneration. The biological or epigenetic clock in centenarians show a decrease in DNA methylation age, indicating that they are biologically younger than their chronological age. There is also data to suggest that although circadian rhythms deteriorate during ageing, they seem to be well preserved in centenarians, including preserved sleep quality.

Environment and longevity

Environmental factors have a large impact on longevity. Better living environment, clean food, clean water, good sanitation, reduction of infectious diseases, and access to better healthcare have resulted in significant improvement in human longevity.

Using Italy as an example of the impact of a better living environment, the average life expectancy went up from 29 years in 1861 to 84 years in 2020. The number of centenarians in Italy increased from 165 in 1951 to more than 15,000 in 2011, and the incidence of deaths occurring in those less than 60 years of age, decreased from 74 per cent in 1872 to less than 10 per cent in 2011 .

The continuous increase in lifespan in recent decades is mainly due to the advances in medical science. It is estimated that medical advances have allowed an increase in lifespan of five years in the last two decades and additional two years in the last decade.

When comparing two countries at different stages of development in 1950, the average life expectancy increase of 11 years from 68 years in 1950 to 79 years in 2020 in the USA, which was more developed in 1950, was much less remarkable than the increase of 3114 years in average life expectancy from 43 years in 1950 to 77 years in 2020 in China, which was less developed in 1950. The significant improvement in the living environment in China has contributed to the narrowing in the average life expectancy between those living in the US and China.

Lifestyle and longevity

In addition to environmental factors, lifestyle factors have an important impact on longevity. A study of more than 300,000 individuals over 7.5 years showed that individuals with social relationships have more than 50 per cent greater probability of survival compared with those with few and poor social interactions.

A study on centenarians in Utah in the US between 2008 and 2015 suggested that sleep, life satisfaction and social attachment were significant predictors of days lived. There is an extricable linkage between lifestyle and socioeconomic status. The term socioeconomic status as used in longevity studies encompass all the factors that can impact longevity including wealth, geography, education, occupation, ethnicity, cultural environment, neighbourhood environment, quality of healthcare and quality of diet. It is well established that the socioeconomic status of an individual will have a major impact on health and longevity.

A study on more than 120, 000 individuals by researchers from Harvard, published in the Circulation journal in April 2018, identified five low-risk lifestyle factors for increased life expectancy. They were: no smoking, non obese ( body mass index of 18.5 to 24.9 kg/m2), exercise (at least 30 minutes per day of moderate to vigorous physical activity, including brisk walking), low-risk alcohol consumption (5 to 15 gm/day for women and 5 to 30 gm/day for men), and a high score for healthy diet.

In this study, the projected life expectancy at age 50 years was on average 14.0 years longer among female Americans with five low-risk factors compared with those with zero low-risk factors; for men, the difference was 12.2 years.

These findings are consistent with a study on Chinese centenarians in which less than 20 per cent were smokers and less than 40 per cent drank alcohol. Hence, in general, most centenarians do not smoke, do not drink alcohol or are low-risk alcohol drinkers, are sociable, friendly, cope well with stress, are satisfied with life, have healthy diets and sleep well.

In summary, the main drivers of longevity in the first eight decades of life are the socioeconomic environment and lifestyle choices. Beyond the eighties, the inheritance of genes that defer age-related chronic diseases and a younger biological clock will help to propel these individuals beyond a hundred years.

This series is produced on alternate Saturdays in collaboration with Singapore Medical Specialists Centre

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How to live to 100 - Business Times

This Sunday, Tiger Woods and Peyton Manning will tee it up, and play a golf match for charity against Phil Mickelson and Tom Brady.

The event, played at the Medalist Golf Club in Hobe Sound, FL., has been named The Match: Champions for Charity, and is expected to raise more than $10 million for Covid-19 relief.

A live sporting event, featuring four of the greatest in their respective sports, will surely garner a large television audience.

In terms of longevity in their sport, Manning and Brady defied the odds. Manning, age 44, played quarterback in the NFL for 18 seasons before retiring in 2016.

Tom Brady, winner of six Super Bowls, is still an active player, who will turn 43 in August as he directs the offense of the Tampa Bay Bucs.

Tiger Woods, age 44, and Phil Mickelson, age 49, continue to play golf at a very high level. Between the two, they have 126 PGA victories. If they can stay healthy, they both may win again, and add to their Hall of Fame careers.

However, in terms of career length and success, they still have to go some to match Old Man River, the incomparable Sam Snead. I dont like to quote statistics, but it is necessary to illustrate the incredible durability of his golfing life.

Born in the Virginia hills in 1912, he was caddying at age seven, and an assistant club pro at age 17.

Turning pro in 1934, he won enough money to play golf full time.

He won the Greater Greensboro Open in 1938, played here in North Carolina, the first of eight times he would win that event.

The last time was in 1965, when he was age 52 and 10 months, the record for the oldest player to win a regular PGA tournament.

Sam won the L.A. Open in 1945, and finished second in the same tournament, on the same course in 1974 when he was age 62. That same year he finished 3rd in the PGA Championship.

In 1979, he shot his age, 67, at the Quad Cities Open; then went out and shot a 66 in the final round of the tournament. He just kept rolling along, playing competitive golf, and often out driving players that were as much as 50 years younger. At age 85, he shot a 78 at the Greenbrier Club in White Sulphur Springs, West Virginia.

I first met Sam Snead in the sporting goods department of K-Mart in Delray Beach, FL in 1984.

He was in the fishing aisle looking for rubber worms, and wearing his customary straw palmetto hat. That meeting led him to do a signing of memorabilia at our sports auction house. On that day, I was able to talk with Sam about his remarkable career, and how he was able to sustain his performance.

First there was the swing, described by Jack Nicklaus and Ben Hogan as the best ever in golf history. He was known to hit the ball long and straight, not with a draw or fade, and he had no peer at hitting the long irons. The swing was fluid and rhythmical, as he would sometimes hum a waltz to keep his timing.

They said my swing was natural, but I worked very hard at it, said Sam, who was self taught. I practiced and played all day, and then practiced some more at night with the car headlights.

Sam was loose jointed, extremely flexible, and demonstrated that for us when he stood in a doorway, and kicked the door jam 7 1/2 feet up. I tried that at home, and it didnt work out so well. By his early teens, he was hitting the ball further than any adults.

There is the story, repeated by Snead, that at age 14, he hit his ball onto the green into the foursome of Mr. Alva Bradley, President of the Chesapeake and Ohio Railroad. Bradley was furious and yelled at the young Snead, Son, dont you know better than to hit a fairway shot into an occupied green? Snead replied, Mr. Bradley, that wasnt no fairway shot, that was my tee shot. Since the railroad president had never seen a 345 yard tee shot, he made him do it again. Sam did it.

Another secret to Sneads success was his competitiveness, and will to win at all times. Growing up poor he learned a respect for money, and that was naturally on his mind his whole life. He recalled that, the biggest Christmas he ever had as a kid was when he found 15 cents and a pair of socks under his breakfast plate.

Snead only played in the British Open once. The year was 1946, and he won the title, but he lost money on the trip, because the winning purse was less than his expenses. He never gambled in a casino, but he loved to have a few bucks on a golf game. He knew how to set the odds, With golf it wasnt gambling.

Samuel Jackson Snead passed away from complications from a stroke in 2002, just a few days shy of his 90th birthday. Too bad he isnt still around for this weekends exhibition. He would be about 108, but I think he would still want a piece of the action.

I feel fortunate. I got to see Ted Williams and Mickey Mantle at the bat, Jim Brown run the football, and Bob Cousy dribbling down on the fast break. And I got to see Sam Snead swing the golf club. An American legend.

Mike Wood is a sports correspondent for The Daily Advance.

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Wood: Sam Snead, the king of golf longevity - The Daily Advance

TOKYO -- The coronavirus pandemic has made the issue of longevity even more relevant given that the damage to financial markets could force people into longer working lives, Lynda Gratton, a leading expert on human resources and organizational behavior, told Nikkei.

She also expects more flexible work patterns to emerge now that people have brokenthe norm of working eight hours a day, five days a week, by adoptingteleworking.

"Executives should be preparing now to experiment with four-day working weeks," she said.

Gratton, a professor of business management at London Business School, serves as a member of Japanese Prime Minister Shinzo Abe's council on social change. Her 2016 book "The 100-Year Life," co-authored with Andrew Scott, examines the question of how social systems and the structure of life need to evolve in an era of growing longevity.

Edited excerpts from the interview follow.

Q: The global spread of the coronavirus is expected to affect life expectancy. Do you think that the premise of "The 100-Year Life" needs to be changed?

A: It is unlikely that decades of progress in terms of increasing life expectancy will be washed away by the coronavirus.

The longevity agenda we described at the heart of "The 100 Year Life" remains. We pointed to the significant gap between social structures and work practices and individuals' life expectancy that has accumulated over the decades. That gap is still there between how we each plan our life and how we long we now have to live.

In fact, the likely impact of coronavirus on the current and future performance of financial markets and rates of return means that many more people now face the prospect of even longer working lives.

Q: When we look at the impact of the coronavirus on elderly people, we can't help but think about the negative aspects of aging, not only for individuals but also for society. How can we switch our mindset to a positive one?

A: Coronavirus is accelerating many issues of an aging society and longevity.It is also revealing deep confusions about "aging" and "old." The danger is that because the fatality rates of coronavirus are so much greater for older people, this will reinforce negative stereotypes. However, it is possible that this is the start of a new debate that updates our concepts of aging.

Key to the longevity agenda is the idea that age is "malleable" -- in the sense that it can be affected by individual actions and environment and by government policy. As a result, how old you are in years may not be a good measure of how old you are biologically. So whilst the coronavirus is most dangerous for the elderly, the link between age and morbidity is heavily affected by underlying health conditions.

What is ever more apparent is that the more you take steps to improve how you age, the better your resilience in the face of future shocks.

It would also be wise to shift the debate beyond a simple distinction of "young" and "old" and recognize that as life lengthens, this distinction becomes less important.

As an illustration, in 1947 a 20-year-old in Japan could expect to live to the age of 63. By 2018, under conservative assumptions, that expectation is now 85 years. That means that a "young" 20-year-old today has a much greater chance of being "old." Therefore, they should be much more interested in how society treats older people in response to a once-in-50-year pandemic.

Q: How will the coronavirus change how the way people work?

A: The coronavirus will accelerate some latent trends in how, where and why we work. It is clear that we are all a great deal more confident in virtual working.

As one Chinese businessman saidto us in early March over a video link: "In the pre-pandemic world," he noted, "I used to travel between Hong Kong and Beijing once a week for a couple of meetings. Now I find I can do 4 or 5 meetings a day -- my productivity has significantly increased." After China gets back to normal will he still fly every week? I doubt it.

We also expect the patterns of work to become a great deal more flexible. We've learned to manage our new daily routines by coordinating closely with colleagues and building in time flexibility. We've eased the stress of managing multiple boundaries between home and work with short-term tactics like creating blocks of time. These new capabilities to manage time and resources are fast morphing into the foundation for crafting new ways of working.

In doing so, we've inevitably broken the norm of working eight hours a day, five days a week. Will we move swiftly back to this traditional time model? We doubt it, and executives should be preparing now to experiment with four-day working weeks and to accommodate more employees who ask to work late in the evening (or very early in the morning) instead of 9-5.

The economic shock of coronavirus will inevitably lead to a surge in unemployment and accelerate automation. Not all those jobs will come back as whole sectors and specific jobs disappear for a long period of time. So the new agenda will be about upskilling, particularly in digital skill,but also importantly about reskilling -- investing in new skills to shift into jobs with better prospects.

Q: Do you think it makes more sense now than ever to have a buffer for financial preparedness? Are liquidity and efforts to maintain employment the right way to think about resilience?

A: Financial liquidity is an important way in which companies and individuals can buy themselves time in the face of negative shocks such as the coronavirus. However, it is important to realize that liquidity simply acts as a buffer and helps provide a short-term window of support. In the longer term, ultimately it is resilience that is crucial.

Resilience is built through flexibility -- both in corporate actions and resources, and in individual skills and priorities. The capacity to respond to shocks by adjusting individual plans, focusing on new markets or learning valuable new skills is the foundation of resilience.

And looking ahead, the coronavirus is not the only exponential curve that threatens the performance of firms and or the livelihood of people. In the coming years we will all be faced with significant challenges in the form of the impact of technologies such as [artificial intelligence] and robotics, the issues of an aging society and the concerns about climate change.

What we can learn from this crisis is the need to be prepared, to anticipate ahead, and to be flexible in our response.

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Time to experiment with 4-day working weeks: Lynda Gratton - Nikkei Asian Review

Talbert Manufacturing, Rensselaer, Indiana, a leader in specialized heavy-haul solutions, received a Longevity Award from the Specialized Carriers & Rigging Association. The SC&RA is an international organization representing members from more than 46 countries. Every year, it presents Longevity Awards to member companies for their longtime support and dedication to the association and its mission of monitoring and affecting pending legislation and regulatory policies as well as staying up to date on safety concerns and best business practices in the industry. Talbert was recognized with the 70 Years award.

It is important that Talbert continues our membership with SC&RA as they are very strong in advocacy, education and networking for many of the industries we serve, says Troy Geisler, vice president of sales and marketing for Talbert Manufacturing. They are vital to our customers as they continue to help shape and influence the regulations and industry-wide policies that affect heavy haul moves not only in North America but across the globe. We want to be more than just a manufacturer. We want to be part of the drive for industry change to help push for safe and legal work practices and policies.

For more than eight decades, Talbert Manufacturing has been providing innovative and reliable transport solutions customized to client specifications. Throughout that time, Talbert has built thousands of custom units and prides itself not only on the relationships that it has nurtured along the way, but also on the trailers durability and longevity; 92% of the Talbert trailers built since 1985 are still on the road today. Over the years, the company has stayed true to the mission Austin Talbert had in 1938 when he set out to change the heavy-haul industry: to design and build safety, quality and durability into every last detail of its trailers. That mission aligns with the SC&RAs dedication to advocate and educate on safety and industry best practices.

Talbert has long been dedicated to producing safe, durable and custom-built solutions to our customers specific transportation needs, says Geisler. A part of our legacy has been the many relationships that have been built over the years by our customers, suppliers and associations such as the SC&RA. We are honored to receive this Longevity Award and we want to continue our commitment to be the company customers can count on for the long haul.

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Talbert Manufacturing recognized for 70 years of industry support and dedication - Irrigation & Green Industry magazine

COVID-19 has caught everyone by surprise. Theres no vaccine or defense, other than the one offered by nature right now your immune system. The world is worried about their health. Knowing how your immune system works at a genetic level may give you some answers you need to improve your odds of recovering from or even avoiding being infected with a virus like COVID-19.

Dr. Yael Joffe, is the Chief Science Officer at 3X4 Genetics. She says COVID-19 can be damaging and may be fatal. The virus triggers the hosts immune system and causes the body to react. Understanding your genes can help. Heres what you need to know.

The problem is that this immune response, in certain cases, can overreact. In order to kill the virus, the immune system floods the body with its in-built cellular defense system. However, when left unchecked the response may cause damage to your own cells, and with COVID-19, particularly the cells in your respiratory system. This being said, these responses differ widely amongst individuals. Partly because of how their genes respond.

Knowing how prepared your immune system is to defend yourself against the virus is a must. Youre gifted with a complex immune system, or cellular defense mechanisms. It springs into action when a toxin or pathogen (viruses and bacteria) overwhelms the body. Dr. Joffe explains: The way these mechanisms act can differ from person-to-person because of your genes. By taking a genetic test you will then be able to tell how ready your immune system is, and whether your cellular defense processes work optimally.

Genes are switches. When a protein or enzyme is needed by the body, the gene is switched on to make that protein. This is true for how the cellular defense system responds.

A number of genes switch on when the virus is detected to mobilize against it and switch off when the virus is killed off and flushed out. The problem with a virus-like COVID-19 is that the response is so powerful, cellular defense mechanisms like inflammation and oxidative stress are turned up so high that the body can be flooded and overwhelmed by the defense mechanisms themselves, causing damage to the cells. How efficiently these on and off processes work differs between individuals. Its partly due to their own genetic makeup. Once you know how optimally your cellular defense processes are working, you can understand better how resilient your immune system is. Then you can take steps to address shortfall.

Dr. Christine Houghton, Founder and Chief Science Officer at Cell-Logic is an expert on the relationship of genes with nutrition. She says knowing more about your genes can help your healthcare practitioner make positive changes through nutrition to improve and optimize these metabolic processes.

While many will be reaching for mega doses of supplements, your system is unique, nuanced, and very complex. A single nutrient like vitamin C, by itself, is nothing compared to the many small, calculated tweaks required at a molecular level to have your immune system work at its prime.

Your bodys core cellular defense processes such as inflammation, oxidative stress, detoxification, and methylation are required to fight off COVID-19. They are activated and switched off via genes. Their reaction time and how efficiently they respond can be adjusted using a personalized, wholesome, and healthy diet, together with targeted nutrigenomic supplements.

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master switch that is responsible for switching on (and off) hundreds of genes involved in cellular defense. It responds to the presence of any pro-oxidant molecule in the body that then activates many of the genes involved in the cellular defense processes. If it switches on quickly, you can flush the coronavirus out better. Although there are Ts and Cs to this process. Complications can occur with underlying chronic health conditions.

Houghton says that one way in which we can optimize the function of Nrf2s is by the ingestion of a nutrigenomically active molecule called Sulforaphane. The precursor to Sulforaphane is found abundantly in raw, calciferous vegetables such as broccoli, broccoli sprouts, cauliflower, and cabbage. Unfortunately, its destroyed during cooking, and a quality broccoli sprout supplement may be required.

As there are many variables, it is important to consult a specialist who can help you prepare your immune system to be strong and resilient. This is especially true in times when there is an unchecked virus on the loose.

Can you prepare your immune system now? Dr. Joffe says the short answer is yes. You can start to optimize your immune system response for COVID-19-like threats through a tailored nutrigenomic dietary plan.

Make an appointment with an accredited nutrigenomic health practitioner and get a nutrigenetic test done to learn about the variability of your genes and your response to diet and lifestyle choices. This will inform them what cellular processes require the most attention. They will then recommend a nutrigenomic plan. They will also let you know what foods to eat to bolster your immune system to fight off a virus. This might also require some nutrigenomic supplements which mimic and optimize natural processes in your body.

Having a healthy immune system supported by an optimally functioning cellular defense mechanism could not only give you the edge in the fight against COVID-19, but will help you live a better, healthier, and longer life.

WATCH Longevitys Q&A with Dr Yael Joffe on genes and COVID-19. CLICK HERE.

As a dietitian who was both disappointed and disillusioned with the dietetics profession, Dr. Joffe was fortunate enough to start working in the field of nutrigenomics in 2000. She obtained my PhD from the University of Cape Town. She explored the genetics and nutrition of obesity in South African women. Today Dr. Joffe regularly speaks at conferences and workshops. She was also part of the team that built the first Nutrigenomic genetic test in 2000 in the United Kingdom. This was three years before the mapping of the human genome.

Dr. Joffe co-authored Its Not Just Your Genes, The SNP Journal, and Genes to Plate. The first gene-based recipe book. She has also published in peer-reviewed journals and been involved in the development and supervision of nutrigenomics courses around the world. Dr. Joffe is currently an Adjunct Professor, teaching Nutrigenomics at Rutgers University and at Maryland University of Integrative Health. She went on to establish Manuka Science in 2014, an online Translational Nutrigenomics training course for health practitioners. More recently she launched the 3X4 Clinic in Cape Town, and 3X4 Genetics. The company brings together expert nutrigenomic practitioners with the best genetic test and user experience. When not working to disrupt health care, she seeks equal parts discomfort and inspiration in open water swimming.

Dr. Christine Houghton Founder Director Senior Scientist Cell Logic has enjoyed a fulfilling and varied career in Nutritional Medicine spanning more than 30 years. Her work continues to stay at the forefront of this rapidly evolving profession. As a clinician, author, and educator, she is dedicated to promoting a model of health care that closely reflects diet and lifestyle choices. She holds a BSc in Biochemistry from The University of Queensland. As well as a Graduate Diploma in Human Nutrition from Deakin University in Victoria. Dr. Houghton is an Adjunct Lecturer in the School of Human Movement and Nutrition Science at The University of Queensland.

Want to read more about building your immunity? Click here.

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Is Your Immune System Ready to Fight COVID-19? The Answer is in Your Genes - Longevity LIVE

One of the finest coaches in the history of the National Basketball Association died on Friday at the age of 78. What Jerry Sloan will be remembered for the most is one characteristic. That is simply his longevity.

We live in an era where general managers press the panic button whenever a team goes through a four of five game losing streak. To think that Jerry Sloan lasted 22 seasons as the head coach of Utah is quite simply unthinkable. However for 1809 regular season games, it was Sloan behind the Utah bench, and the Jazz went on to win 1127 of them.

The passing of Sloan comes at a time when his Jazz squad has recently generated some degree of fame. It was Sloan who led the Jazz attack while on the sidelines, as he tried mightily to beat the powerful Chicago Bulls led by Michael Jordan and Scottie Pippen. For basketball fans who have been born since 2000, and did not get to see Sloan in his prime as a head coach, you might have had your opportunity to do so in recent weeks through the ESPN Documentary The Last Dance.

Yes, Sloan had great talent himself. He had the opportunity to coach hall of famers John Stockton and Karl Malone. Just how good were this duo? Malone is second all-time in points behind Kareem Abdul-Jabbar and Stockton is the NBA all-time leader in assists and steals.

However what might be shocking to NBA fans of past and present is that Sloan never once was named the head coach of the year. Even though he had a career winning percentage of .603, and .623 with the Jazz.

Sloan will go down in history as one of the finest basketball coaches of all-time. The only coaches with more wins are Don Nelson, Lenny Wilkens, and Gregg Popovich. That is the kind of company Sloan is a part of and deserves to be.

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Jerry Sloan will be remembered for his longevity - The Sports Daily

It is time countries start paying attention to bio-security needs to protect their people and economies from potential risks

Genetic engineering is the frontier science of the 21st century and Chinahas been one of the leaders of the game. We already know of genetically-modified babies born in Macao, China. We also know of an US engineer Juan Carlos claiming that he had created the worlds first human-monkey hybrid embryo in a lab in China, because it was impossible to carry out such pioneering research in his home country due to legal regulations. China is fast becoming the worlds capital for controversial science, with marked ethical lapses in medical research, including genetic modification of life forms. The same wealth of knowledge has been applied on microorganisms as well, to enable better therapeutic drugs and other proteins for treatment modalities as well as for capacity-building in the field of potential biological warfare.

How zoonotic viruses infect humans has been a major focus of modern virology. We know that SARS and MERS came from bats but that doesnt convince one that the COVID-19 is of similar origin. US Intelligence says the Coronavirus is not genetically modified nor did an organism escape the lab. Professor Shan-Lu Liu at the Ohio State University says there is no credible evidence of gene tweaking. The virus genome sequence is available and had it been altered, we would have seen signs of gene alteration, insertion, deletion, or changes at the nucleotide bases. He added that the salient points in the sequence that differ from bat viruses appear natural, as the genes at those sites are scattered randomly like they would be, in nature. However, scientists say they cannot rule out genetic work by a proficient team of bio-technologists taking appropriate measures to cover up. Also, outcomes of such research to diagnose genomic intervention cannot be arrived at quickly as they would be very elaborate.

It has been observed that genetic changes to a virus usually result in attenuation, which had earlier led to the belief that the risks of viral bio-attacks were low. Most suspected agents for bio-terrorism have been toxin-releasing bacteria like Anthrax. But scientists have now identified certain viruses as potential candidates for bio-terrorism like the Pox virus, Dengue virus, Ebola virus, Lassa fever virus and a few more.

A report in October 2003 said that a US Government-funded project had created an extremely virulent form of mousepox that kills all mice even if they have been on anti-viral drugs or vaccinated. The research brings forth the prospect of pox viruses being turned into lethal organisms even for people who have been vaccinated. Scientists say such research is risky as pox viruses have been known to cross species. But further work has not stopped as scientists say their work is necessary to explore what bio-terrorists might do.

Research found many of the modified viruses were not contagious and if they escaped from a lab they could not cause ecological chaos by wiping out a species. However, such discovery also meant that bio-terrorists might attempt to use the same trick to modify a virus with the motive of using it only on targeted person/s and not rebounding on the attackers, hence meeting the main criterion of a bio-weapon.

With the availability of complete genetic sequences of various organisms, theres increasing concern about abuse of such data. The possibilities of mixing and matching traits from different organisms and combining these with insights drawn from human genomics to target some ethnic groups are very real. It is known that certain ethnic groups are more susceptible to some pathogens than others and genetic variations in some people manifest as varied disease susceptibility to microorganisms and even their response to medicines.

DNA shuffling, yet another technology with potential for bio-weapon development was used by scientist Stemmer to develop a new strain of E.coli that had reduced sensitivity to the antibiotic Cefotaxime. Such a scenario has the potential of leaving a patient resistant to treatment.

The genetic modification of life forms has been a controversial practice. There should be stringent regulations in place for genetic research work where permissions are granted only when the positives outweigh the negatives. The current pandemic is a stark reminder of the threat bio-weaponised micro-organisms can pose and the possibility of misuse of research laboratories, with instances of human survival threats breaking upon us. There is dire need for biotechnology regulations to be firmed up and an international regulatory body being formed with stringent ethical mandates. The current pandemic brings to light the necessity to revisit the Biological Weapons Convention (BWC) formed in 1975 and reset the rules according to the current context. It is time countries start paying attention to bio-security needs to protect their people and economies from potential risks. There should be due strength-weakness analysis of our animal and public health systems and appropriate bio-security protocols must be put in place. This is an area that has been overlooked for decades and must now be revived for the health and survival of our nation/s and species.

(The writer is an author and a doctor by profession)

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Beware the bugs of war - Daily Pioneer

SILVER SPRING, Md., May 20, 2020 /PRNewswire/ -- You have probably heard of GMOs or genetically modified organisms, but how much do you know about them? GMO is a common term used by consumers to describe foods that have been created through genetic engineering. While GMOs have been available to consumers since the early 1990s and are a common part of today's food supply, research shows consumers have limited knowledge and understanding about what GMOs are, why they are used, and how they are made.

The U.S. Food and Drug Administration (FDA), with the U.S. Department of Agriculture (USDA) and U.S. Environmental Protection Agency (EPA), launched Feed Your Mind, a new Agricultural Biotechnology Education and Outreach Initiative. The Initiative aims to increase consumer awareness and understanding of genetically engineered foods or GMOs. Find answers to your questions and help educate others with Feed Your Mind's science-based educational resources, like web pages, fact sheets, infographics, and videos.

What are GMOs? "GMO" is a common term used to describe a plant, animal, or microorganism that has had its DNA changed through a process scientists call genetic engineering. Most of the GMO crops grown today were developed to help farmers prevent crop loss. There are ten GMO crops currently grown and sold in the U.S.: alfalfa, apples, corn, cotton, papayas, potatoes, soybeans, summer squash, and sugar beets.

Are GMOs safe to eat? Many federal agencies play an important role in ensuring the safety of GMOs. FDA, USDA, and EPA work together to ensure that crops produced through genetic engineering are safe for people, animals, and the environment. Collaboration and coordination among these agencies help make sure food developers understand the importance of a safe food supply and the rules they need to follow when creating new plants through genetic engineering.

Look for "Bioengineered food" on food labels Soon, you may see the term "bioengineered food" on certain food packaging. Congress used "bioengineered food" to describe certain types of GMOs when it passed the National Bioengineered Food Disclosure Standard. The Standard establishes requirements for labeling foods people eat that are bioengineered or may have bioengineered ingredients. It also defines bioengineered foods as those that contain detectable genetic material that has been modified through certain lab techniques and cannot be created through conventional breeding or found in nature.

To learn more about the Feed Your Mind Initiative, visit http://www.fda.gov/feedyourmind.

Contact: Media: 1-301-796-4540 Consumers: 1-888-SAFEFOOD (toll free)

View original content to download multimedia:http://www.prnewswire.com/news-releases/feed-your-mind-with-fdas-new-education-initiative-on-genetically-engineered-foods-301062642.html

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Feed Your Mind with FDA's New Education Initiative on Genetically Engineered Foods - Stockhouse

When I talk to my students aboutthe tempestuous relationship between science and religion, I like to bring up the case of Francis Collins. Early in his career, Collins was a successful gene-hunter, who helped identify genes associated with cystic fibrosis and other disorders. He went on to become one of the worlds most powerful scientists. Since 2009, he has directed the National Institutes of Health, which this year has a budget of over $40 billion. Before that he oversaw the Human Genome Project, one of historys biggest research projects. Collins was an atheist until 1978, when he underwent a conversion experience while hiking in the mountains and became a devout Christian. In his 2006 bestselling bookThe Language of God, Collins declares that he sees no incompatibility between science and religion. The God of the Bible is also the God of the genome, he wrote. He can be worshipped in the cathedral or in the laboratory. Collins just won the$1.3 million Templeton Prize, created in 1972 to promote reconciliation of science and spirituality. (See my posts on the Templeton Foundationhereandhere). This news gives me an excuse to post an interview I carried out with Collins forNational Geographicin 2006, a time whenRichard Dawkins, Daniel Dennett and others were vigorously attacking religion. Below is an edited transcript of my conversation with Collins, which took place in Washington, D.C. I liked Collins, whom I found to be surprisingly unassuming for a man of such high stature. But I was disturbed by our final exchanges, in which he revealed a fatalistic outlook on humanitys future. Collins, it seems, haslots of faith in God but not much in humanity. John Horgan

Horgan:How does it feel to be at the white-hot center of the current debate between science and religion?

Collins:This increasing polarization between extremists on both ends of the atheism and belief spectrum has been heartbreaking to me. If my suggestion that there is a harmonious middle ground puts me at the white-hot center of debate--Hooray! Its maybe a bit overdue.

Horgan:The danger in trying to appeal to people on both sides of a polarized debate is--

Collins:Bombs thrown at you from both directions!

Horgan:Has that happened?

Collins[sighs]: The majority have responded in very encouraging ways. But some of my scientific colleagues argue that its totally inappropriate for a scientist to write about religion, and we already have too much faith in public life in this country. And then I get someverystrongly worded messages from fundamentalists who feel that I have compromised the literal interpretation of Genesis 1 and call me a false prophet. Im diluting the truth and doing damage to the faith.

Horgan:Why do you think the debate has become so polarized?

Collins:It starts with an extreme articulation of a viewpoint on one side of the issue and that then results in a response that is also a little bit too extreme, and the whole thing escalates. Every action demands an equal and opposite reaction. This is one of Newtons laws playing out in an unfortunate public scenario.

Horgan:I must admit that Ive become more concerned lately about the harmful effects of religion because of religious terrorism like 9/11 and the growing power of the religious right in the United States.

Collins:What faith hasnotbeen used by demagogues as a club over somebodys head? Whether it was the Inquisition or the Crusades on the one hand or the World Trade Center on the other? But we shouldnt judge the pure truths of faith by the way they are applied any more than we should judge the pure truth of love by an abusive marriage. We as children of God have been given by God this knowledge of right and wrong, this Moral Law, which I see as a particularly compelling signpost to His existence. But we also have this thing called free will which we exercise all the time to break that law. We shouldnt blame faith for the ways people distort it and misuse it.

Horgan:Isnt the problem when religions say,Thisis the only way to truth? Isnt that what turns religious faith from something beautiful into something intolerant and hateful?

Collins:There is a sad truth there. I think we Christians have been way too ready to define ourselves as members of an exclusive club. I found truth, I found joy, I found peace in that particular conclusion, but I am not in any way suggesting that that is the conclusion everybody else should find. To have anyone say, My truth is purer than yours, that is both inconsistent with what I see in the person of Christ andincrediblyoff-putting. And quick to start arguments and fights and even wars! Look at the story of the Good Samaritan, which is a parable from Jesus himself. Jews would have considered the Samaritan to be a heretic, and yet clearly Christs message is:Thatis the person who did right and was justified in Gods eyes.

Horgan:How can you, as a scientist who looks for natural explanations of things and demands evidence, also believe in miracles, like the resurrection?

Collins:My first struggle was to believe in God. Not a pantheist God who is entirely enclosed within nature, or a Deist God who started the whole thing and then just lost interest, but a supernatural God who is interested in what is happening in our world and might at times choose to intervene. My second struggle was to believe that Christ was divine as He claimed to be. As soon as I got there, the idea that He might rise from the dead became a non-problem. I dont have a problem with the concept that miracles might occasionally occur at moments ofgreatsignificance where there is a message being transmitted to us by God Almighty. But as a scientist I set my standards for miracles very high. And I dont think we should try to convince agnostics or atheists about the reality of faith with claims about miracles that they can easily poke holes in.

Horgan:The problem I have with miracles is not just that they violate what science tells us about how the world works. They also make God seem too capricious. For example, many people believe that if they pray hard enough God will intercede to heal them or a loved one. But does that mean that all those who dont get better arent worthy?

Collins:In my own experience as a physician, I have not seen a miraculous healing, and I dont expect to see one. Also, prayer for me is not a way to manipulate God into doing what we want Him to do. Prayer for me is much more a sense of trying to get into fellowship with God. Im trying to figure out what I should be doing rather than telling Almighty God whatHeshould be doing. Look at the Lords Prayer. It says, Thywill be done. It wasnt, Our Father who are in Heaven, please get me a parking space.

Horgan:Many people have a hard time believing in God because of the problem of evil. If God loves us, why is life filled with so much suffering?

Collins:That isthemost fundamental question that all seekers have to wrestle with. First of all, if our ultimate goal is to grow, learn, discover things about ourselves and things about God, then unfortunately a life of ease is probably not the way to get there. I know I have learned very little about myself or God when everything is going well. Also, a lot of the pain and suffering in the world we cannot lay at Gods feet. God gave us free will, and we may choose to exercise it in ways that end up hurting other people.

Horgan:The physicist Steven Weinberg, who is an atheist, has written about this topic. He asks why six million Jews, including his relatives, had to die in the Holocaust so that the Nazis could exercise their free will.

Collins:If God had to intervene miraculously every time one of us chose to do something evil, it would be a very strange, chaotic, unpredictable world. Free will leads to people doing terrible things to each other. Innocent people die as a result. You cant blame anyone except the evildoers for that. So thats not Gods fault. The harder question is when suffering seems to have come about through no human ill action. A child with cancer, a natural disaster, a tornado or tsunami. Why would God not prevent those things from happening?

Horgan:Some theologians, such as Charles Hartshorne, have suggested that maybe God isnt fully in control of His creation. The poet Annie Dillard expresses this idea in her phrase God the semi-competent.

Collins:Thats delightful--and probably blasphemous! An alternative is the notion of God being outside of nature and of time and having a perspective of our blink-of-an-eye existence that goes both far back and far forward. In some admittedly metaphysical way, that allows me to say that the meaning of suffering may not always be apparent to me. There can be reasons for terrible things happening that I cannot know.

Horgan:I think youre an agnostic.

Collins:No!

Horgan:You say that, to a certain extent, Gods ways are inscrutable. That sounds like agnosticism.

Collins:Im agnostic about Gods ways. Im not agnostic about God Himself. Thomas Huxley defined agnosticism as not knowing whether God exists or not. Im a believer! I have doubts. As I quote Paul Tillich: Doubt is not the opposite of faith. Its a part of faith. But my fundamental stance is that God is real, God is true.

Horgan:Im an agnostic, and I was bothered when in your book you called agnosticism a copout. Agnosticism doesnt mean youre lazy or dont care. It means you arent satisfied with any answers for what after all are ultimate mysteries.

Collins:That was a putdown that should not apply to earnest agnostics who have considered the evidence and still dont find an answer. I was reacting to the agnosticism I see in the scientific community, which has not been arrived at by a careful examination of the evidence. I went through a phase when I was a casual agnostic, and I am perhaps too quick to assume that others have no more depth than I did.

Horgan:Free will is a very important concept to me, as it is to you. Its the basis for our morality and search for meaning. Dont you worry that science in general and genetics in particularand your work as head of the Genome Project--are undermining belief in free will?

Collins:Youre talking about genetic determinism, which implies that we are helpless marionettes being controlled by strings made of double helices. That is so far away from what we know scientifically! Heredity does have an influence not only over medical risks but also over certain behaviors and personality traits. But look at identical twins, who have exactly the same DNA but often dont behave alike or think alike. They show the importance of learning and experience--and free will. I think we all, whether we are religious or not, recognize that free will is a reality. There are some fringe elements that say, No, its all an illusion, were just pawns in some computer model. But I dont think that carries you very far.

Horgan:What do you think of Darwinian explanations of altruism, or what you callagape, totally selfless love and compassion for someone not directly related to you?

Collins:Its been a little of a just-so story so far. Many would argue that altruism has been supported by evolution because it helps the group survive. But some people sacrifically give of themselves to those who are outside their group and with whom they have absolutely nothing in common. Like Mother Teresa, Oscar Schindler, many others. That is the nobility of humankind in its purist form. That doesnt seem like it can be explained by a Darwinian model, but Im not hanging my faith on this.

Horgan:If only selflessness were more common.

Collins:Well, there you get free will again. It gets in the way.

Horgan:What do you think about the field of neurotheology, which attempts to identify the neural basis of religious experiences?

Collins:I think its fascinating but not particularly surprising. We humans are flesh and blood. So it wouldnt trouble me--if I were to have some mystical experience myself--to discover that my temporal lobe was lit up. Id say, Wow! Thats okay! That doesnt mean that this doesnt have genuine spiritual significance. Those who come at this issue with the presumption that there is nothing outside the natural world will look at this data and say, Ya see? Whereas those who come with the presumption that we are spiritual creatures will go, Cool! There is a natural correlate to this mystical experience! How about that! I think our spiritual nature is truly God-given, and may not be completely limited by natural descriptors.

Horgan:What if this research leads to drugs or devices for artificially inducing religious experiences? Would you consider those experiences to be authentic? You probably heard about the recent report from Johns Hopkins that the psychedelic drug psilocybin triggered spiritual experiences.

Collins:Yes. If you are talking about the ingestion of an exogenous psychoactive substance or some kind of brain-stimulating contraption, that would smack of not being an authentic, justifiable, trust-worthy experience. So that would be a boundary I would want to establish between the authentic and the counterfeit.

Horgan:Some scientists have predicted that genetic engineering may give us superhuman intelligence and greatly extended life spans, and possibly even immortality. We might even engineer our brains so that we dont fear pain or grief anymore. These are possible long-term consequences of the Human Genome Project and other lines of research. If these things happen, what do you think would be the consequences for religious traditions?

Collins:That outcome would trouble me. But were so far away from that reality that its hard to spend a lot of time worrying about it when you consider all the truly benevolent things we could do in the near term. If you get too hung up on the hypotheticals of what night happen in the next several hundred years, then you become paralyzed and you fail to live up to the opportunities to reach out and help people now. That seems to be the most unethical stance we could take.

Horgan:Im really asking, Does religion requires suffering? Could we reduce suffering to the point where we just wont need religion?

Collins:In spite of the fact that we have achieved all of these wonderful medical advances and made it possible to live longer and eradicate diseases, we will probably still figure out ways to argue with each other and sometimes to kill each other, out of our self-righteousness and our determination that we have to be on top. So the death rate will continue to be one per person by one means or another. We may understand a lot about biology, we may understand a lot about how to prevent illness, and we may understand the life span. But I dont think we will figure out how to stop humans from doing bad things to each other. That will always be our greatest and most distressing experience here on this planet, and that will make us long the most, perhaps, for something more.

Further Reading:

In Defense of Disbelief: An Anti-Creed

Can Faith and Science Coexist?

Richard Dawkins Offers Advice for Donald Trump, and Other Wisdom

What Should We Do With Our Visions of Heaven and Hell?

Mind-Body Problems(free online book, also available asKindle e-bookandpaperback).

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One of the World's Most Powerful Scientists Believes in Miracles - Scientific American

NEW HAVEN, Conn., May 21, 2020 (GLOBE NEWSWIRE) -- Kleo Pharmaceuticals, Inc., a leading company in the field of developing next-generation, fully synthetic bispecific compounds designed to emulate or enhance the activity of biologics, and Celularity, Inc., a leading developer of allogeneic, or off-the-shelf, natural killer (NK) cell therapies, today announced a preclinical research collaboration to rapidly advance synergistic combinations of each companys technology platform as potential treatments for COVID-19 and multiple myeloma.

The collaboration comes at an opportune time for both companies. Earlier this year, Kleo received IND authorization from the U.S. Food and Drug Administration (FDA) to test its CD38-targeting antibody recruiting molecule (ARMTM) in combination with autologous NK cells in a clinical study. In early April, Celularity received FDA authorization to evaluate one of its allogeneic NK cell products, CYNK-001, in COVID-19 infected adults. CYNK-001 is the only cryopreserved allogeneic, off-the-shelf Natural Killer (NK) cell therapy being developed from placental hematopoietic stem cells. It also is being investigated as a treatment for acute myeloid leukemia (AML), multiple myeloma (MM), and glioblastoma multiforme (GBM).

We look forward to working with Celularity to advance the ARMTM technology platform across multiple drug programs, said Doug Manion, MD, CEO of Kleo Pharmaceuticals. Celularitys cryopreserved allogeneic NK cells easily combine with the ARMTM platform, which is expected to facilitate NK cell targeting toward cancerous tumors or sites of viral infection. Celularitys CEO Robert Hariri, MD, PhD added, We quickly realized the advantages of Kleos synthetic bifunctional technology, and the synergistic potential between ARMTM molecules and our allogeneic NK cells. The speed and modularity of the Kleo platform allow for the development of ARMTM-allogeneic NK cell combination therapies across a wide variety of indications.

When used in combination with NK cells, ARMTM molecules behave similarly to chimeric antigen receptors, though their synthetic nature eliminates the need for genetic engineering. ARMTM molecules associate with NK cells via IgG antibodies bound to a first moiety, while also containing an interchangeable and customizable second moiety. Selection of the second moiety can be used to confer affinity of an ARMTM-NK cell complex against a biological target, such as the spike protein of COVID-19 particles or CD38 expressed on the surface of multiple myeloma hematologic tumors, ultimately facilitating NK-cell mediated destruction of target cells. This modular design allows ARMTM molecules to be broadly applicable across a range of drug programs.

About Kleo Pharmaceuticals, Inc.

Kleo Pharmaceuticals is a unique biotechnology company developing next-generation, bispecific compounds designed to emulate or enhance the activity of biologics based on the groundbreaking research of its scientific founder Dr. David Spiegel at Yale University. Kleos compounds are designed to direct the immune system to destroy cancerous or virally infected cells and are currently in development for the treatment of various diseases, including multiple myeloma and COVID-19. Compared to biologics, Kleos compounds are smaller and more versatile, leading to potentially improved safety and efficacy. They are also much faster and more efficient to design and produce, particularly against novel targets. Kleo develops drug candidates based on its proprietary technology platforms, all of which are modular in design and enable rapid generation of novel immunotherapies that can be optimized against specified biological targets and combined with existing cell- or antibody-based therapies. These include Antibody Recruiting Molecules (ARMs) and Monoclonal Antibody Therapy Enhancers (MATEs). Biohaven Pharmaceutical Holding Company (NYSE:BHVN) and PeptiDream Inc. (Nikkei:PPTDF) are investors in Kleo Pharmaceuticals. For more information visit http://kleopharmaceuticals.com.

About Celularity

Celularity, headquartered in Warren, N.J., is a clinical-stage cell therapeutics company delivering transformative allogeneic cellular therapies derived from the postpartum human placenta. Using proprietary technology in combination with its IMPACT platform, Celularity is the only company harnessing the purity and versatility of placental-derived cells to develop and manufacture innovative and highly scalable off-the-shelf treatments for patients with cancer, inflammatory and age-related diseases. To learn more, please visit http://www.celularity.com.

Forward-Looking Statements

This news release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements involve substantial risks and uncertainties, including statements that are based on the current expectations and assumptions of the Company's management. All statements, other than statements of historical facts, included in this press release regarding the Company's plans and objectives, expectations and assumptions of management are forward-looking statements. The use of certain words, including the words "estimate," "project," "intend," "expect," "believe," "anticipate," "will, "plan," "could," "may" and similar expressions are intended to identify forward-looking statements. The forward-looking statements are made as of this date and the Company does not undertake any obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise.

CONTACT INFORMATION

LifeSci Advisors (Investors)

Irina Koffler

646-970-4681

ikoffler@lifesciadvisors.com

Kleo Pharmaceuticals (Media)

Brian Dowd

(203) 643-9172

bdowd@kleopharmaceuticals.com

Celularity Inc. Media Contact:

Dani Frank

Factory PR

celularity@factorypr.com

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Kleo Pharmaceuticals and Celularity Enter into Research Collaboration to Rapidly Develop Allogeneic NK Cell Combination Therapies for COVID-19 and...