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Inflammation in Gum Disease and Arthritis Linked by Bone Marrow Immune Cells – Genetic Engineering & Biotechnology News

Posted: May 2, 2022 at 2:15 am

Innate immune memory can cause one type of inflammatory conditionfor example, gum diseaseto increase susceptibility to anotherlike arthritis. Now, new findings show that alterations to immune cell precursors in the bone marrow underlie the mechanism that forms the connection.Using a mouse model, the team demonstrated that recipients of a bone marrow transplant were predisposed to more severe arthritis if their donor had inflammatory gum disease.

This work is published in Cell in the article, Maladaptive innate immune training of myelopoiesis links inflammatory comorbidities.

Although we use periodontitis and arthritis as our model, our findings go above and beyond these examples, said George Hajishengalliis, DDS, PhD, professor at the University of Pennsylvania School of Dental Medicine. This is in fact a central mechanism, a unifying principle underlying the association between a variety of comorbidities.

In previous work, Hajishengallis and colleagues explored the role of innate immune memory. Their findings showed that the innate immune systems myeloid cells, such as neutrophils and macrophages, could remember past encounters, becoming more responsive when exposed to a new threat. The work also showed that this trained immunity could be transferred from one organism to another through a bone marrow transplant, protecting recipients from cancer through an innate immune response.

The researchers hypothesized that this trained immunity could be detrimental in the right contexts. The thoughts went like this: We knew the gum disease periodontitis increased the risk of comorbidities like cardiovascular disease, said Hajishengallis. And the reverse is also true: People with the inflammatory disease colitis, for example, have an increased prevalence of periodontal disease. Different mechanisms have been proposed, but no one unifying mechanism could explain this bidirectionality.

The scientists sought the source of the association between comorbidities to the innate immune training they already knew was happening in the bone marrow.

The team showed that, within a week of inducing a mouse to have periodontal disease, the animals myeloid cells and their progenitor cells expanded in the bone marrow. Examining these cells weeks later, after periodontitis was intentionally resolved, the researchers did not notice significant changes in how the cells looked or behaved.

However, these progenitor cells appeared to have memorized the inflammation they were exposed to, as they harbored important epigenetic changes. The researchers found that these alterations, triggered by inflammation, could alter the manner in which the genes would be expressed after a future challenge. The overall pattern of epigenetic changes, the researchers noted, was associated with known signatures of the inflammatory response.

Mice with induced periodontal disease also had more severe responses to a later immune system challenge, evidence of trained immunity.

To put the whole picture together regarding the link between inflammatory conditions, the critical experiment, as Hajishengallis explained, was a bone marrow transplant. Mice that had periodontitis, a severe form of gum disease, served as donors, as did a group of healthy mice serving as controls. Two hundred stem cells from their bone marrow were transplanted into mice that had never had gum disease and which had had their own bone marrow irradiated. A few months later, these mice were exposed to collagen antibodies, which trigger arthritis.

Mice that received the transplant from mice with periodontitis developed more severe arthritis than mice that received a donation of stem cells from periodontally healthy mice, said Hajishengallis. In addition, higher joint inflammation in recipient mice was due to inflammatory cells deriving from the periodontitis-trained stem cells.

Further experiments suggested that the signaling pathway governed by a receptor for IL-1 played a vital role in contributing to this inflammatory memory. Mice that lacked IL-1 receptor signaling could not generate the immune memory that made the recipient mice more susceptible to comorbidities.

The work underscores that blocking IL-1 receptor signaling could be an effective approach to mitigate against these knock-on effects of trained immunity. Weve seen anti-IL-1 antibodies used in clinical trials for atherosclerosis with excellent results, Hajishengallis said. It could be that it was in part because it was blocking this maladaptive trained immunity.

Follow-up projects are examining how other inflammatory conditions, may be linked with periodontal disease, a sign, the researchers said, of how crucial oral health is to overall health.

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Antibodies fighting original virus may be weaker against omicron – The Hub at Johns Hopkins

Posted: May 2, 2022 at 2:15 am

ByMichael Newman

New research may explain why so many vaccinated and boosted individuals experienced breakthrough coronavirus infections caused by the omicron variant. Researchers at Johns Hopkins Medicine and the National Institute of Allergy and Infectious Diseases at the National Institutes of Health have uncovered evidence that while fully vaccinated and boosted people produce a high level of antibodies that work against the original strain of SARS-CoV-2, the same tiny defenders don't do as well in preventing the omicron strain from attacking healthy cells.

The research findings were posted online in the Journal of Clinical Investigation Insight.

"Previous research has shown vaccine-induced antibodies respond to the original strain of SARS-CoV-2 by inhibiting the virus's ability to bind to angiotensin-converting enzyme 2 [commonly known as ACE2], the receptor on a cell's surface through which SARS-CoV-2 gains entry," says study senior author Joel Blankson, professor of medicine at the Johns Hopkins University School of Medicine. "Our study suggests those same antibodies yield less ACE2 inhibition with the omicron strain, opening the door to a breakthrough COVID-19 infection."

Joel Blankson

Professor, Johns Hopkins School of Medicine

To conduct their study, Blankson and his colleagues analyzed two types of immune responses to SARS-CoV-2: the humoral immune response, marked by virus-specific antibodies circulating in the bloodstream and produced by B lymphocytes, or B cells; and the cellular immune response, which is a direct attack on the virus by T lymphocytes, or T cells. Researchers observed these immune responses in 18 healthy and fully vaccinated people, ages 23-62, who experienced breakthrough infections within 14 to 92 days after receiving a booster COVID-19 vaccine. Of the participants, 14 received a booster of the Pfizer-BioNTech mRNA vaccine, one was boosted with the Moderna mRNA vaccine, and the remaining three had an mRNA booster following their initial dose of the Johnson & Johnson viral vector vaccine.

The humoral and cellular immune responses of those participants with breakthrough infections were compared with those from a control group of 31 participants, ages 21-60, who received similar COVID-19 vaccinations and boosters and had no prior infection with SARS-CoV-2.

Although the researchers were not able to document that the breakthrough infections were from the omicron strain, they say it's a strong probability because the omicron variant accounted for more than 90% of the COVID-19 cases treated at the Johns Hopkins Hospital, where the study was conducted, during the time when the study participants became symptomatic.

Coverage of how the COVID-19 pandemic is affecting operations at JHU and how Hopkins experts and scientists are responding to the outbreak

"When we tested antibody-mediated inhibition of SARS-CoV-2 spike protein binding to ACE2, we found that serum from study participants with breakthrough COVID-19most likely the result of omicron infectionhad antibodies that strongly stopped binding by the original strain virus as expected but didn't carry out that function as well when responding to the omicron strain," says Blankson.

The specific reduction in ACE2-inhibiting antibodies responding to omicron, Blankson says, differs from what was seen in previously studied breakthrough infections with the alpha variant. In those cases, infected individuals were found to have lower overall antibody levels to the original virus strain. The levels of antibodies that inhibited the spike protein binding to ACE2high for the original strain of the virus but reduced for omicronwere similar for both the participants with breakthrough infections and those in the control group.

Moreover, the level of cellular immunityas measured by the amount of responding T cells documentedremained strong in the breakthrough and control groups for both the original and omicron strains. This was shown in a second recent study, also co-authored by Blankson, looking at the blood plasma of 15 mRNA vaccine recipients.

"The comparable strong T cell responses for the original and omicron strains in both studies could explain why people, like our study participants, who have breakthrough COVID-19 cases typically experience only mild symptoms during the course of their illness," he explains.

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New drug shows promise slowing tumour growth in some hard-to-treat cancers – University of Toronto

Posted: May 2, 2022 at 2:15 am

Scientists at Sinai Health and the University of Toronto say a new drug designed to block an enzyme essential for the survival of certain cancer cells shows promise in curbing tumour growth.

The preclinical findings,published this month in the journalNature, describe a new drug designed with CRISPR-Cas9 gene-editing technology in the lab ofDaniel Durocher, a senior investigator at Sinai HealthsLunenfeld-Tanenbaum Research Institute(LTRI) and a professor ofmolecular geneticsin U of Ts Temerty Faculty of Medicine.

The researchers identified genes that are essential for the viability of CCNE1 amplified cancer cells, which are characteristic of some hard-to-treat ovarian, endometrial and bladder cancers. They found the enzyme PKMYT1 is essential in CCNE1 amplified cells, but not in otherwise healthy cells. In collaboration with precision oncology companyRepare Therapeutics, the team developed a drug called RP-6306, which blocks PKMYT1 activity and effectively kills the cancer cell.

These cancer cells depend on the PKMYT1 enzyme to survive, said Durocher. Our preclinical data show enormous promise in the drug RP-6306s ability to target these types of tumours and profoundly inhibit tumour growth.

Currently, tumors with CCNE1 amplification have very few therapeutic options.David Gallo, a senior scientist at Repare Therapeutics, said theyve been able to demonstrate that RP-6306 is both potent and selective for oral use in humans.

Gynecological and other solid tumours with amplifications of CCNE1 are notoriously resistant to current standard-of-care treatments, said Gallo, co-first author on theNaturepaper. There is a dire need to find new options for these patients.

The work was a close collaboration between the Durocher lab and Repare Therapeutics. Durocher founded Repare Therapeutics in 2016 alongsideFrank Sicheri, also aLunenfeld-Tanenbaum Research Institute senior investigator who is a professor of molecular genetics andbiochemistryat U of T.

The company is built on the concept of synthetic lethality, a process that incorporates functional genomics to discover genetic vulnerabilities to specific cancer mutations.

This close collaboration between our group and Repare highlights how industry and academia can work together to discover new treatment options for cancer patients,said Durocher. Its rare that a new target is published alongside a launched clinical trial. This speaks volumes about the innovative capacity of the LTRI and its collaborators.

Repare Therapeutics has initiated Phase I clinical trials in patients with CCNE1 amplified solid tumours, with initial results expected in late 2022.

The research was funded by Repare Therapeutics and the Canadian Institutes of Health Research.

This story was originally published at Sinai Health.

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ERC Advanced Grant for cardiac research at the MDC – EurekAlert

Posted: May 2, 2022 at 2:15 am

image:Artificial heart tissue can contract against a resistance and then relax. view more

Credit: Michael Gotthardt, MDC

The contractile and elastic properties of the heart are finely tuned. This is a prerequisite for the cardiac cycle and efficient adaptation. At the MDC, Michael Gotthardt investigates the underlying molecular and biomechanical mechanisms. He is awarded with an ERC Advanced Grant for this work.

MERAS is the acronym on the recently approved project proposal. It stands for: Mechanoregulation of alternative splicing. We would like to understand how the heart responds to environmental factors and adjusts its elastic properties such that it can function at an optimal level, says Michael Gotthardt. He heads the research group Neuromuscular and Cardiovascular Cell Biology at the Max Delbrck Center for Molecular Medicine in the Helmholtz Association (MDC). For his project, he now receives an Advanced Grant of 2.5 million from the European Research Council (ERC).

This ERC Advanced Grant is awarded to scientists with more than ten years of research experience who have already played a prominent role in their field. Out of the 1,735 researchers from across Europe who applied for the grants this year, 253 were successful.

The mechanical work of the heart depends on the sarcomere, the smallest contractile unit. Here, actin and myosin filaments facilitate contraction, while the giant protein titin determines the elastic properties of heart muscle cells. Different titin variants (isoforms) are expressed perfectly adapted to the mechanical needs. The researchers wish to investigate the underlying process alternative splicing in detail.

Refined regulatory feedback

Our recent analysis of sarcomeric protein composition not only identified the expected structural proteins, but also proteins that link to cell signalling, metabolism, the regulation of gene expression and alternative splicing. These are proteins you would normally expect in the nucleus but not in the sarcomere, emphasizes Michael Gotthardt. It appears that the sarcomere directly communicates with the nucleus on necessary adaptations. The unexpected feedback from sarcomere to spliceosome could explain how sarcomeres adjust to mechanical stress. This is a new hypothesis that the researchers will explore in depth.

A detailed understanding of the regulatory process could also have therapeutic relevance e.g. for people with heart failure. For most of these patients, the ventricular walls have become so rigid that the chambers are no longer able to fill sufficiently. A drug that interferes with the communication from sarcomere to spliceosome could make a stiff cardiac ventricle more compliant, resulting in more efficient filling.

A second ERC grant

This year, the ERC selection process was not solely based on the submitted proposals, but for the first time included short presentations online of course due to Covid 19. Four slides in eight minutes for a 2.5 million euro project, recounts Michael Gotthardt, who is also Professor of Experimental and translational cardiology at Charit Universittsmedizin Berlin. For the scientist, this is already the second substantial contribution from the EU following his ERC Starting Grant in 2011. It extends over a period of five years. This enables us to build up lasting collaborations and projects with extended time lines. And deep sequencing as a prerequisite to evaluate alternative splicing at scale would otherwise be prohibitively expensive.

Gotthardts team works with genetic mouse models, synthetic heart tissue derived from patient cells and isolated heart muscle cells (cardiomyocytes). Single cell mechanics is precision work. For this, the cardiomyocytes first need to be isolated, secured under a special microscope and electrically stimulated. Then you can derive the active and passive forces, says Michael Gotthardt. This would provide the properties of just one single cell. However, for a convincing study, a large number of these experiments need to be conducted.

The goal: new technologies for single-cell mechanics and multi-omics

Extensive manual work is also required to understand which titin isoforms are expressed in response to stress or disease. Compared to a large piece of tissue, a single cell contains relatively few RNA molecules which means that analysis of gene expression frequently reaches the detection limit.The analysis of alternative splicing is even more difficult for giant titin isoforms with up to 100,000 bases. Here, available short reads need to be assembled like a jigsaw puzzle that misses important pieces, says Michael Gotthardt. With the ERC funding, among other things, he plans to develop technologies for single cell mechanics, -transcriptomics, -proteomics that will facilitate multi-omics approaches and enable higher rates of throughput.

The Max Delbrck Center for Molecular Medicine (MDC)

The Max Delbrck Center for Molecular Medicine in the Helmholtz Association (MDC) is one of the worlds leading biomedical research institutions. Max Delbrck, a Berlin native, was a Nobel laureate and one of the founders of molecular biology. At the MDCs locations in Berlin-Buch and Mitte, researchers from some 60 countries analyze the human system investigating the biological foundations of life from its most elementary building blocks to systems-wide mechanisms. By understanding what regulates or disrupts the dynamic equilibrium in a cell, an organ, or the entire body, we can prevent diseases, diagnose them earlier, and stop their progression with tailored therapies. Patients should benefit as soon as possible from basic research discoveries. The MDC therefore supports spin-off creation and participates in collaborative networks. It works in close partnership with Charit Universittsmedizin Berlin in the jointly run Experimental and Clinical Research Center (ECRC ), the Berlin Institute of Health (BIH) at Charit, and the German Center for Cardiovascular Research (DZHK). Founded in 1992, the MDC today employs 1,600 people and is funded 90 percent by the German federal government and 10 percent by the State of Berlin.www.mdc-berlin.de

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Sen. Orrin Hatch’s legacy tracks the GOP’s evolution on health – NPR

Posted: May 2, 2022 at 2:14 am

Democratic Sen. Ted Kennedy ( left) and Republican Sen. Orrin Hatch teamed up on a series of landmark legislative health care achievements, such as the Ryan White program on AIDS treatment, the Americans with Disabilities Act, and the first major federal child care law. John Duricka/AP hide caption

Democratic Sen. Ted Kennedy ( left) and Republican Sen. Orrin Hatch teamed up on a series of landmark legislative health care achievements, such as the Ryan White program on AIDS treatment, the Americans with Disabilities Act, and the first major federal child care law.

When it comes to health policy, former Utah Republican Sen. Orrin Hatch, who died Saturday at age 88, leaves a complex legacy of major legislative achievements, changing positions, compromises and fierce opposition. In many ways, though, Hatch's evolution and leadership on health policy during his four decades in the U.S. Senate mirror that of the Republican Party.

When he came to Washington as a neophyte politician after an upset victory in 1976, Hatch was a conservative firebrand, one of the early leaders of the "New Right" bent on dismantling the federal welfare state and banning abortion. A former trial lawyer, the new senator had never before held public office.

But the election of Ronald Reagan in 1980 and the Republican takeover of the Senate that made Hatch chairman of the powerful Labor and Human Resources Committee (now the Health, Education, Labor and Pensions Committee) turned him into something of a pragmatist. That pragmatism, it should be noted, was somewhat forced: Even though Hatch was technically the chair, there were enough moderate Republicans on the panel to give the ranking Democrat, Massachusetts' Edward Kennedy, effective control over what could be passed by the committee.

So Hatch learned to compromise and to legislate. In 1984, he negotiated with liberal Rep. Henry Waxman, D-Calif., what is still referred to as the "Hatch-Waxman Act." It's better known as the law that allowed, for the first time, approval of generic copies of brand-name drugs. Although far from a panacea, it is still the single-biggest advance in the fight to rein in high drug prices.

When the Democrats took back the Senate after the 1986 elections, Kennedy became chairman of the committee and Hatch, the ranking Republican. The two teamed up on a series of landmark legislative achievements, from the Ryan White program on AIDS treatment and the Americans with Disabilities Act to the first major federal child care law. And while Hatch was a strong foe of national health insurance, he and Kennedy ultimately pushed through Congress in 1997 the bill to create the Children's Health Insurance Program, which provides low-cost health insurance for low-income families who don't qualify for Medicaid.

The stridently anti-abortion Hatch was outspoken about his support for federal funding for research on embryonic stem cells derived from aborted fetuses. "I think it's the ultimate pro-life position, because I believe being pro-life is not just caring for the unborn but caring for those who are living," he told NPR in 2007.

But like much of the Republican Party in Congress, Hatch returned to his conservative roots after the election of President Barack Obama in 2008. A supporter of the so-called individual mandate requiring people to have health insurance when it was the quasi-official GOP position in the early 1990s, Hatch became an outspoken foe. "Congress has never crossed the line between regulating what people choose to do and ordering them to do it," he said in 2010.

After moderate Utah Republican Sen. Robert Bennett was ousted in a primary in 2010 and replaced by conservative favorite Mike Lee, Hatch grew more conservative to win reelection in 2012. His final term in the Senate was marked by efforts to overturn the Affordable Care Act and further restrict abortion access. The devout Mormon, who in his spare time wrote lyrics for best-selling Christian music, even called the ACA "the stupidest, dumb-a** bill that I've ever seen. Now some of you may have loved it; if you do, you are one of the stupidest dumb-a** people I've ever met." He later apologized for the statement.

A former Kennedy aide, Jim Manley, told The Salt Lake Tribune that "no one epitomizes the rightward lurch of the Republican Party more than Sen. Hatch."

In one final twist, however, Hatch pushed as his successor the 2012 GOP presidential nominee, Mitt Romney. In just his first few years, Romney has become one of the most moderate Republicans in the chamber. That may prove to be Orrin Hatch's final legacy.

KHN (Kaiser Health News) is a national newsroom that produces in-depth journalism about health issues. It is an editorially independent operating program of KFF (Kaiser Family Foundation).

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Genetics goes to the dogs, finds theres not much to breed behavior – Ars Technica

Posted: May 2, 2022 at 2:14 am

Enlarge / In the case of the samoyed, selection for physical characteristics produced a dog that sure looks happy.

Many dog breeds are purely about appearancethink poodles and the Pekingese. But plenty of other breeds,like racing greyhounds, are devoted to specific tasks. For many of these tasks, physical appearance isn't enough; behavior also matters, like herding by sheepdog breeds or fetching by various retrievers.

It's not surprising that many people ascribe these behaviorsand a wide variety of other, less useful onesto their dog's breed and its underlying genetics. Now, a large team of US-based researchers has looked into whether this belief is accurate. And, with a few exceptions, they find that it's not. With a huge panel of volunteer dog owners, they show that the genetics of dog behavior is built from lots of small, weak influences, and every breed seems to have some members that just don't behave as we expect.

The work is based on a citizen science project called Darwin's Ark. Participants were asked to give details about their dog, including whether it belonged to an established breed (either certified or inferred). They were also asked to fill out short surveys that collectively asked about 117 different behaviors. Overall, they obtained data on some 18,000 dogs, about half of them purebreds.

This information was combined with genetic data, including previously published genome sequences from more than 500 purebred dogs. The researchers of the new study added to the previous data by getting complete genome sequences for 27 mixed-breed dogs, collectively termed "Mendel's mutts." Less thorough genome sequencing was also done on 2,000 additional dogs with owners who filled out the behavioral surveys.

The genetic work showed that, as expected, individual breeds are mostly inbred (the significant exception was the Tibetan mastiff, which is distantly related to most modern dog breeds and was left out of these analyses). Despite the inbreeding, however, there was little in the way of genetic variants that are exclusive to a single breed. Out of nearly 17,000 individual variants tested, only 332 were found in just one breed.

The team found that owners generally knew what their dog's breed was (unless it was a mutt). About 90 percent of the dogs that were certified as belonging to a breed appeared to share 85 percent or more of their DNA with purebred members of that breed. For dogs without certified breeding, this dropped to about 60 percent.

Using this data, the researchers confirmed previously published work showing that many physical traits, like leg length and coat properties, had a clear genetic component.

The researchers looked at the genetics of behavior in two different ways. One was to look at the answers to the individual survey questions and determine if they were associated with any genetic variants. This method had the amusing result that the individual behavior with the strongest genetic association was "gets stuck behind objects," which they narrowed down to a small region that contains a gene associated with cognitive capacity in humans. Howling ended up in a region near a gene involved in human language.

They also clustered the survey questions into groups representing general behavioral tendencies, like the willingness and capacity to follow human instructions, sociability toward other dogs, and desire for human contact. Many of these had a significant genetic component, responsible for 25 percent or more of the differences in behavior for human sociability, toy-directed behavior, and ability and interest to respond to commands. But the effects were generally pretty weak, with mutts only showing about 9 percent of their behavioral tendencies that could be explained by genetic factors.

To determine whether any of these behaviors were connected to specific breeds, the researchers compared the breed/behavior linkage of members of a breed to the same linkage in dogs randomly selected from the entire population. In general, there was not a lot there. Only 5 percent of the breed-behavior combinations were significantly linked, compared to about 40 percent for breed-appearance linkages.

There are a few clear connections, such as border collies (a herding dog) being generally good about following human commands. The problem seems to be that there are exceptions for every behavior. Ninety percent of greyhounds, for example, don't seem to bury their toys, but three of themfrequently did. So, even if a trait does tend to be strongly associated with a specific breed, the breed hasn't been bred for it long enough to fix that behavior completely.

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Heart Warriors: ‘Genetics is the future of medicine’ according to U of A researcher, who uses it to help with muscular dystrophy – The Gateway Online

Posted: May 2, 2022 at 2:14 am

A University of Alberta researcher researching muscular dystrophy was one of five researchers at the institution to receive a grant from the Heart & Stroke Foundation of Canada.

Toshi Yokota, a professor in the department of medical genetics and current The Friends of Garrett Cumming Research Chair, was a recipient of the 2021-2022 Grant-In-Aid program. This provides funding for important, pertinent, and novel research in the area of heart disease and stroke over three years.

The project funded by the Heart & Stroke Foundation of Canada involves using peptides, short chains of amino acids, to deliver antisense oligonucleotides-shorts, DNA-like molecules, to help with heart failure in patients suffering with muscular dystrophy.

Duchenne muscular dystrophy (DMD), the most common type of muscular dystrophy, is most commonly seen in males, with one in 3,500 males born worldwide suffering from this condition. A person with muscular dystrophy would see progressive weakening of their muscles, such as in their arms and legs and eventually their torso as well.

These patients often do not die from issues with the muscles of their limbs since they can still survive without them; what causes many patients to die in their 20s and 30s is heart failure. Previous methods which have been developed are unable to enter the heart to help with heart failure. Yokota and their team are studying a new molecule which may help with this.

We started this project a couple of years ago and in collaboration with Dr. Hong Moulton, at the Oregon State University, Yokota said. She discovered a new peptide called the DG-9 [and] I found that it works very well in the heart; it penetrates the membrane and we can deliver antisense oligos to the heart muscle.

Yokotas love of research started back when they were a child.

From my elementary school or secondary school I always liked science and I read lots of books about science and I like, for example, watching stars and insects or animals, they said. It sounded quite natural to me. I like science and I like research.

Yokota began diving more into genetics during their undergraduate degree at the University of Tokyo. In graduate school, one of their professors, Dr. Shinichi Takeda, had just started a new lab researching muscular dystrophy and was looking for new students.

I thought genetics was the future of medicine and thats very fascinating I think its quite natural to me to join his lab, they said.

Something that Yokota wants students to remember is to focus on what you can do and what interests you, not what you cannot do.

When I was a high school student I was more interested in astrophysics and read many books written by Stephen Hawking and other scientists, they said. But it turned out I am better at biology and I changed my focus to biology at my university, which worked out very well.

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Is osteoarthritis hereditary? Genetics, causes, and more – Medical News Today

Posted: May 2, 2022 at 2:14 am

Osteoarthritis (OA) is a degenerative joint disease that causes pain and stiffness and decreases mobility. While OA is not always hereditary, experts believe that there may be a genetic component that increases the risk of developing this condition.

Around 32.5 million adults in the United States have OA. Various factors contribute to individuals developing OA, including increasing age, obesity, joint injuries, and a persons sex.

While genetics play a role in increasing the risk of someone developing OA, this condition is not hereditary.

This article explores how genetics contribute to OA and discusses other risk factors.

There are over 100 different types of arthritis, and OA is one of the most common. OA is a degenerative joint disease that worsens over time. Currently, there is no cure for this condition.

When a person has OA, their cartilage breaks down. Cartilage is a protective, fibrous connective tissue that cushions the ends of bones and allows them to move easily over each other.

When cartilage begins to break down, the bones rub against one another. In addition, bony spurs, or osteophytes, might form as the bone attempts to heal itself.

People with OA may experience pain, stiffness, and swelling in the joints.

Autoimmune forms of arthritis, such as rheumatoid arthritis, result from the immune system attacking the bodys healthy tissue.

However, doctors usually consider OA a wear and tear disease, as it is more common in people over the age of 50 and is more likely to affect weight-bearing joints, such as the knees and hips. Injuries or genetic predisposition can also increase the risk of OA.

While OA is not always heredity, in some cases, a person can inherit an increased risk of developing this condition. Experts do not currently know how the predisposition of an increased risk of developing OA passes between family members.

Experts estimate that around 4070% of OA cases have a genetic component, with a stronger link for the hip, hand, and spine. The hereditary forms of OA arise from mutations in genes that help form and maintain bone and cartilage. This type of OA may appear at a young age and rapidly progress.

There is not a single specific gene that increases the risk of developing OA. Multiple genes and other risk factors, such as obesity, injuries, and joint anatomy, also contribute to OA.

Research suggests that several groups of genes may increase the risk of developing OA, including:

While scientists have identified different gene variations that may contribute to OA, they do not yet know precisely what part genetics play in developing this condition.

Additionally, people with certain genetic traits or inheritable conditions, such as Ehlers-Danlos syndrome (EDS), may have an increase in the risk of developing OA.

People with EDS have low collagen levels, which can reduce their ability to support muscles and joints. This can lead to unstable and hypermobile joints that may contribute to OA.

More research is necessary to understand the complex interplay between genetic factors and OA.

The cause of OA is wear and tear at the joints.

A range of factors can contribute to individuals developing OA:

Typically, OA risk increases with age and appears most often in individuals over the age of 50. However, it can appear in younger individuals, particularly after a bone fracture or a cartilage or ligament tear.

OA usually worsens over time and can develop in several joints. It often begins in a single large joint, such as a hip or knee, but it may also involve a smaller joint, such as an ankle.

Some people may have OA in a single joint, but it may progress to involve other joints, such as the spine, neck, and wrists.

While doctors do not fully understand why this happens, it is possible that the pain from OA causes the individual to move differently, which then forces the joints out of alignment.

OA is a degenerative condition with no cure. This condition worsens over time and can cause significant difficulty in mobility.

If a person has individuals in their family with OA, it does not mean they will also develop the condition. Experts estimate that the heritability of OA is around:

Researchers do not fully understand the link between OA and life expectancy. In some cases, OA of the knee or hip may negatively affect an individuals life expectancy, but this is potentially due to pain, difficulty in mobility, and other health conditions.

Other types of OA, such as OA of the hand, do not appear to have an effect on life expectancy.

OA is a degenerative joint disease that worsens over time, causing difficulty in mobility and pain. Age is the primary factor that increases OA risk, but other causes include injury, obesity, sex, and genetics.

The heritability of OA is around 4070%. However, having family members with OA does not mean that a person will develop the condition.

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Preimplantation Genetics Diagnosis (PGD) Market Future Growth with Technology and Current Trends 2021 to 2030 Queen Anne and Mangolia News – Queen…

Posted: May 2, 2022 at 2:14 am

Preimplantation genetic diagnosis (PGD) also referred as embryo screening, is a branch of genetics involves in genetic testing of embryo through in-vitro fertilization (IVF). PGD eliminates risk of selective pregnancy termination for couples who are at substantial risk of transferring serious genetic, chromosomal, or hereditary disorders such as spinal muscular atrophy and cystic fibrosis.

The global PGD market size is estimated to be $79.5 million in 2015 and expected to reach $121.5 million registering a CAGR of 6.14% from 2016 to 2022. The global PGD market is expected to witness notable growth in the near future owing to the rise in prevalence of genetic, hereditary, and chromosomal diseases.

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Market Statistics:

The file offers market sizing and forecast throughout 5 primary currencies USD, EUR GBP, JPY, and AUD. It helps corporation leaders make higher choices when foreign money change records are available with ease. In this report, the years 2020 and 2021 are regarded as historic years, 2020 as the base year, 2021 as the estimated year, and years from 2022 to 2030 are viewed as the forecast period.

The Centers for Medicare and Medicaid Services report that US healthcare expenditures grew by 4.6% to US$ 3.8 trillion in 2019, or US$ 11,582 per person, and accounted for 17.7% of GDP. Also, the federal government accounted for 29.0% of the total health expenditures, followed by households (28.4%). State and local governments accounted for 16.1% of total health care expenditures, while other private revenues accounted for 7.5%.

This study aims to define market sizes and forecast the values for different segments and countries in the coming eight years. The study aims to include qualitative and quantitative perspectives about the industry within the regions and countries covered in the report. The report also outlines the significant factors, such as driving factors and challenges, that will determine the markets future growth.

Moreover, PGD have high chances of conceiving healthy embryos. However, the high costs incurred in the PGD technologies hamper the market growth. Moreover, stringent government regulations and ethical concerns also obstruct the market growth. In the near future, increase is expected in adoption of PGD worldwide owing to its various applications for development of healthy embryo.

The global PGD market is segmented based on the test type and geography. Based on type, the market can be segmented into aneuploidy, chromosomal abnormalities, gender selection, HLA typing, single gene disorder, X-linked diseases, and others (disability, and adult onset disease). Geographically, the market is segmented into North America, Europe, Asia-Pacific and LAMEA.

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The key market players areReprogenetics, LLC, Genea Limited, Illumina, Inc., Laboratory Corporation of America Holdings, Natera, Inc., PerkinElmer, Inc., Quest Diagnostics Incorporated, Genesis Genetics Ltd., and Reproductive Genetics Innovations LLC.

KEY MARKET BENEFITS:

In-depth study of the global preimplantation genetic diagnostic market was conducted based on current testing trends of genetic test and based on the preferences for designer babiesPotential analysis of opportunities was evaluated for understanding different aspects of preimplantation genetic test that are currently under various phases of clinical trials along with the variants that would gain prominence in the futureA deep analysis of key market dynamics that influence the adoption of PGD tests in the forecast periodAnalysis of volume and vale share analysis of PGD testing at a global and regional levelKey market players are profiled and their strategies are analyzed thoroughly for understanding the various technologies adopted by them for development and production of diagnostic tests for PGD testing

KEY MARKET SEGMENT:

By Test Type

Chromosomal abnormalitiesGender selectionX-linked diseasesAneuploidySingle gene disordersOthers

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By Region

North AmericaEuropeAsia-PacificLAMEA

Table of Content:

Key Questions Answered in the Market Report

How did the COVID-19 pandemic impact the adoption of by various pharmaceutical and life sciences companies? What is the outlook for the impact market during the forecast period 2021-2030? What are the key trends influencing the impact market? How will they influence the market in short-, mid-, and long-term duration? What is the end user perception toward? How is the patent landscape for pharmaceutical quality? Which country/cluster witnessed the highest patent filing from January 2014-June 2021? What are the key factors impacting the impact market? What will be their impact in short-, mid-, and long-term duration? What are the key opportunities areas in the impact market? What is their potential in short-, mid-, and long-term duration? What are the key strategies adopted by companies in the impact market? What are the key application areas of the impact market? Which application is expected to hold the highest growth potential during the forecast period 2021-2030? What is the preferred deployment model for the impact? What is the growth potential of various deployment models present in the market? Who are the key end users of pharmaceutical quality? What is their respective share in the impact market? Which regional market is expected to hold the highest growth potential in the impact market during the forecast period 2021-2030? Which are the key players in the impact market?

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Excerpt from:
Preimplantation Genetics Diagnosis (PGD) Market Future Growth with Technology and Current Trends 2021 to 2030 Queen Anne and Mangolia News - Queen...

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Madjid Bougherra interview: Its part of the genetics to be a Rangers player that you never give up until the end – The Athletic

Posted: May 2, 2022 at 2:14 am

In the unusually muted build-up to the final Old Firm derby of this season, there has been the temptation to bill the meeting as incidental or even inconsequential. There are two reasons for this: with just four games remaining of the Premiership season, Celtic are six points clear of Rangers with a vastly superior goal difference, and Rangers have the small matter of being 90 minutes away from a European final, before RB Leipzigs visit on Thursday.

Celtic can virtually crown themselves champions if they win at Celtic Park today (Sunday) but Rangers could add a bit of pressure to the run-in if they cut the gap to three points.

It would still take a minor miracle for them to retain the title as they would need to take a maximum 12 points from here while hoping Celtic earn five or less in their final three games (Hearts and Motherwell at home, either side of a trip to Dundee United), but out in Dubai there is one man with good reason not to give up hope.

Former Rangers centre-back Madjid Bougherra won the championship in all three of his three seasons at Ibrox between 2008 and 2011, with Rangers twice coming from behind Celtic in the title race to clinch the trophy.

Like many foreign players who immerse themselves in Glasgows footballing tombola after signing for one of the clubs, Bougherra knows what the rivalry means and what the fixture can do to those involved.

He experienced just about every emotion possible from putting four past Celtic, to losing by three, being acrimoniously sent off, involved in heated battles and scoring a crucial winner well, almost.

But when searching for a reason why Giovanni van Bronckhorsts side should not concede defeat in their attempts to retain their domestic crown, he refers back to his 2008-09 debut season, when Gordon Strachans Celtic side looked destined to make it four in a row.

A season that had began with great momentum, including a 4-2 win away to their rivals, had gone off the rails for Rangers after losing against Inverness Caledonian Thistle and then drawing with Hearts in consecutive games. It left Walter Smiths side six point behind Celtic in April; they had a game in hand, but it seemed like they had lost their grip.

Its part of the genetics to be a Glasgow Rangers player that you never give up until the end, says Bougherra, who is now manager of Algeria A the national team compromised of home-based players.

The mentality is to win and win and win. Anything is possible in football, so they need to give everything as the fans will remember that, even if the result doesnt work out.

In that first season, I still believed. We knew it would not come easily but Steven Davis scored (the only goal of a May derby at Ibrox), which meant we won the last derby of the season, and we never looked back.

Davis may well have a part to play this afternoon too, 13 years later. The midfielder, now 37, was a key part of that period along with Bougherra, as Rangers won two of those three titles on the last game of the season away to Dundee United in 2009 and then Kilmarnock two years later.

Maurice Edus stoppage-time winner in a February 2010 derby helped seal their second title, but it was a rebound from Bougherras initial shot. I gave him a kick once we got inside, he laughs.

If Rangers are to pull off a minor miracle in the coming weeks, it will require an even greater Houdini act than when they lost 3-0 to Celtic in February 2011 to fall eight points behind in the race before clawing back the deficit, culminating in an exhilarating 5-1 final day victory away to Kilmarnock.

To win in the last game gave it more charm, more flavour to winning the trophy. When we won against Dundee United (in 2009), I remember the helicopter waiting for us.

You are focused on the game, so you dont hear the helicopter. Sometimes you dont even hear the fans either. The second year we won, it was good as we won with games to spare but it was not as good as the first and third seasons.

In what turned out to be Bougherras final season at the club, the two Glasgow teams played each other no fewer than seven times across the three domestic competitions as the rivalry reached boiling point in March.

Rangers had three men sent off in a 1-0 Scottish Cup last-16 loss at Celtic Park. Bougherra admits the red mist descended as referee Calum Murray gave him a second yellow card in the 93rd minute, and saw him grab the officials wrist to try to prevent Murray ordering him off.

I made a tackle (on Kris Commons) when I was already booked. Ally (McCoist, then Smiths No 2) had been shouting to me to calm down and be careful. I just gave him a wink to say, Its OK, no worries.

It is part of the derby that sometimes you need to be strong and your emotions go up and down with the referee. I was controlling it but the tackle was a very good tackle as I took the ball, not the player. We were losing 1-0 and had a few minutes left so I was not happy to have a second card, as in the derby that tackle is good.

After I was a little nervous, as I didnt want him to give me another yellow. When you are in the game you can lose control, so I went to see him and apologise.

The crazy thing (about Rangers-Celtic matches) is you can play six times, seven times or 10 times and all the players have the same spirit and desire to win. You are never fed up with this game, it is special and you feel the hatred.

I call this a real, real derby. The people are too passionate. The spirit, the noise and the intensity of the game is unique in Europe.

Steven Whittaker was also sent off for two yellows in the first half, as was El Hadji Diouf who spent the season on loan from Blackburn Rovers in a melee after full time.

Diouf and Bougherra produced something of an iconic image as they left Hampden in the week that followed, having had additional bans for their behaviour quashed. So did McCoist for his touchline fracas with Celtic manager Neil Lennon, an incident the Scottish government saw fit to hold a national summit over.

It was a special season as Diouf signed and had some fights with Scott Brown, so there were things that pushed the atmosphere more, Bougherra says. Among these was Diouf mocking Browns celebrations a couple of weeks later after Rangers beat Celtic in the League Cup final.

He just did it himself, laughs Bougherra. Hes a unique player but people dont know him outside of football. I didnt know him before but hes a funny guy and amazing to know. He has a big personality but he is one of those players that when he goes on the pitch he is a different person as he is a winner.

He had a lot of respect for the coaches but I would see Walter smile at him many times in training and its not easy to get a smile from Walter!

This was the type of intensity that Bougherra quickly realised he had to live with if he was to be a success in Glasgow. But only two and a half years before he joined Rangers from Charlton Athletic of the English Championship for 2.5 million it would have seemed far-fetched.

It was a dream to be a footballer, but I was concentrated on my studies in Dijon which was about programming software on computers, Bougherra says of a football journey that began in France in 2002. I was playing in the amateur league on a Sunday mornings but (second-tier club) Gueugnon came to watch me as they were just an hour away.

The first year, it was very hard training every day. I had pain everywhere but my body started changing over time. The second year I was with the first team, and the third year I was playing all the time. But in the fourth year a new coach came in and didnt want me.

I was looking for a loan and had an opportunity in Greece but at the last moment (in the January 2006 window) Crewe Alexandra came in, as they were looking for a centre-back. I was playing for the Algeria Under-23s and an agent was talking about me. We played Port Vale and I played well so I signed and had a fantastic three months (playing 11 games in the Championship).

I had gone from a No 10 to a No 5, so it was easy for me to become a defender as the game was in front of me now, not behind.

His loan at Crewe brought a move to Sheffield Wednesday, also in the Championship, that summer. Six months later, then-Premier League Charlton bought him, but he suffered an injury on his debut against Manchester United at Old Trafford that meant he didnt start again until the final day of the season, by which time the south London club had been relegated.

After a season back in the Championship, Bougherra was all set to join Premier League-bound West Bromwich Albion in the summer of 2008 when he received an 11th-hour phone call from a familiar voice.

My fitness coach at Sheffield Wednesday, Adam Owen (by then working at Ibrox), phoned me and told me to sign for Rangers, he says.

I took a flight during the night and signed in Glasgow the next day. They had just sold Carlos Cuellar (to Aston Villa) for big money so he showed my profile to Walter Smith and decided to take me.

Ally McCoist came to meet me. I felt very comfortable with him. He talks to you as a friend and a brother, so I felt I had signed for a family club.

It had taken until the age of 25 for Bougherra to reach that level but countryman Riyad Mahrez, who he rates as the best he has ever played with, almost joined him in Scottish football after he went on trial to St Mirren the following year as an unknown teenager. Despite scoring seven goals in his trial games, a deal wasnt offered, and the rest is history.

He had a long story before Leicester and Man City, a little bit like me, as it is hard to find a club who trusts you, says Bougherra.

Thats the difficulty, as it sometimes takes time to find the coach who sees something in you. I have many friends who never found that coach to push them higher, so that is the bad side. Football is a little bit like Jenga. You need to survive and never give up.

Bougherra found that coach in Smith, who passed away in November at the age of 73.

Hes a legend. People love him and all the players loved him. In the UK, and especially Glasgow, they respect the people who do good things for the club. Not many places do, so it is amazing. I have no words other than: we miss him.

Smiths impact on Bougherra can be felt in the emotion of the 39-year-olds voice when he speaks.

Walter was very calm due to his experience and he had a big character. Without talking, you respected him and were afraid to miss something, Bougherra says. Ally had our mentality, because he was young he was close to us. So Walter was the big boss and it was the perfect mix.

The first time I saw him very sad, he started shouting in the changing room. Trust me, no one in the dressing room was speaking.

I experienced it too as I had a habit of being five minutes late for training and he put me on the bench after I qualified for the World Cup (in 2010) and came back late.

It was the first time we had qualified in my life, so the atmosphere was amazing and I wanted to stay two days more to enjoy it. I lost my French passport. I had my Algerian one but they needed it for the visa or something.

He was not happy at all. I said sorry and that was the good thing about Walter as when you tell him you are wrong and are sorry, he turns very quickly although he still put me on the bench! I made an assist in the next game, though, so he put me back on the pitch.

Bougherra, whose sturdy physique made him instantly recognisable, says he used to give Rangers kit man Jimmy Bell a headache as he would ask for bigger shorts and shirts, particularly when, one season, the supplied shirts came in a skin-tight fit.

That may have been easier to sell to him during Ramadan, which he is currently observing as he takes a break in Dubai, but Smith was always accommodating when it came to his fasting, and that compassion is what stood out to Bougherra as his greatest quality.

When I had the space, I had the habit to go forward (from centre-back). I gave him a headache! It was my need to run every game. I cannot stay in my position but when I went forward, I came back very fast!

You can find some coaches who change you and the way you play but he used what I have and tried to improve on it, not to take things away from my game. There are too many coaches who try to change a player, but he was different. Tactically, he gave me things to follow every game but he was different.

This is why I felt comfortable with him and why I gave everything for him. He told me, As long as everything you do is for the team and not for yourself, it will be OK.

He gave me that confidence and sometimes I liked to go straight forward or other times I gave the ball to the attacker and keep going to offer a cross. I never remember him saying to stay back once.

Although Bougherras defensive qualities were what helped build a solid foundation alongside David Weir, the freedom he was given in possession is what helped produce two memorable goals, against Dundee United and Stuttgart, as he went on mazy runs before finishing off what were solo strikes any striker would have been proud of.

I was waiting for this one for a long time after about 200 runs, I finally succeeded, he says.

The Stuttgart one was good but I went really far by myself against Dundee United, so that is the best one Ive ever scored.

Bougherra had fellow Algerians Brahim Hemdani and Salim Kerkar as team-mates at Ibrox and the latters role as a cult figure in his two seasons at the club between 2010 and 2012 is what proves his love of the club.

I played with his brother, who was a very good player. Salim was at Gueugnon too when he was young, so I knew him from there, Bougherra says. The club couldnt sign many players as the finances were controlled, so I brought him to the coach for a trial.

Kerkar was signed and, despite only making a handful of starts in cup competitions, was regularly cheered like a hero while warming up.

This is why I love the fans in Glasgow, as small things can be turned into funny or lovely things. I was happy as he helped us in some situations and was like my smaller brother.

Bougherra left Rangers the season before the club imploded to join the Lekhwiya club in Qatar, but says if hed had his way, he would have stayed longer.

I was close to signing for four more years, but the financial situation meant that the offer from Qatar gave them (Rangers) money, he says.

Rangers was the highlight of my career there and I could not have found better anywhere. I didnt know what the competitive mentality was before I joined Rangers but I learned how to win not just one game but to become a winner.

(Top photo: Craig Halkett/PA Images via Getty Images)

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Madjid Bougherra interview: Its part of the genetics to be a Rangers player that you never give up until the end - The Athletic

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