MANHASSET, N.Y.--(BUSINESS WIRE)--In an effort to better understand inflammation within the body, researchers at The Feinstein Institutes for Medical Research the global scientific home of bioelectronic medicine successfully controlled the neurons that release molecular proteins and turn on/off inflammation. The preclinical research recently published in the journal Proceedings of the National Academy of Sciences of the United States of America (PNAS). The study points to a new approach to treat diseases such as arthritis, which are characterized by inflammation and pain.

Inflammation is the bodys defense response to injury and infection triggered by molecular proteins, such as high mobility group box 1 protein (HMGB1). These molecules also stimulate sensory neurons, termed nociceptors. Activation of nociceptors controls the inflammation through release of neuropeptides producing neuroinflammation. While important, if unresolved inflammation can be harmful, resulting in autoimmune or autoinflammatory disorders like rheumatoid arthritis or Crohns disease.

Using light or genetic tools, we can turn off and on the switch that controls inflammation in the body, said Sangeeta S. Chavan, PhD, professor in the Institute of Bioelectronic Medicine at the Feinstein Institutes. This preclinical bioelectronic medicine research is paving the way for a variety of new treatment options for people living with serious, chronic health conditions.

The study, led by Dr. Chavan and associate professor Huan Yang, PhD, combines optogenetics, neuronal-specific deletion (or removal) and preclinical models of inflammatory diseases while monitoring inflammation and neuropathic pain. The results show that nociceptor HMGB1 is required for a neuroinflammatory response to injury. These experiments provide direct evidence that nociceptor-related pain can be prevented by targeting HMGB1 a potential therapy of neuroinflammatory diseases.

Our new methodology allows us to develop ways to regulate inflammation mediated by neurons, said Dr. Yang. The optogenetic and neuronal-specific ablation strategies show us the critical role HMGB1 plays in neuroinflammation and pain.

The results show that a new paradigm for nervous system integration of environmental signals to stimulate inflammation is fundamental to spark an immune system defense during infection and injury. The research suggests that targeting HMGB1 may constitute a new therapeutic approach for treating a variety of diseases.

After 30 years of researchers studying how to turn off the immune system, we recently sought a way to turn it on, said Kevin J. Tracey, MD, president and CEO of the Feinstein Institutes. Thanks to this pivot in research, Drs. Yang and Chavan discovered that nerves release a molecule to produce inflammation in the body, which could lead to a new strategy to develop pharmaceutical and bioelectronic therapies.

Dr. Chavan and the Institute of Bioelectronic Medicine continue to advance this emerging field of science which combines molecular medicine, neuroscience and bioengineering to study how to use devices to treat diseases and injury. Dr. Chavan reported in a 2020 study also published in PNAS, the discovery of a small cluster of neurons within the brain that is responsible for controlling the bodys immune response and the release of cytokines, which leads to inflammation in the body.

About the Feinstein Institutes

The Feinstein Institutes for Medical Research is the research arm of Northwell Health, the largest health care provider and private employer in New York State. Home to 50 research labs, 3,000 clinical research studies and 5,000 researchers and staff, the Feinstein Institutes raises the standard of medical innovation through its five institutes of behavioral science, bioelectronic medicine, cancer, health innovations and outcomes, and molecular medicine. We make breakthroughs in genetics, oncology, brain research, mental health, autoimmunity, and are the global scientific leader in bioelectronic medicine a new field of science that has the potential to revolutionize medicine. For more information about how we produce knowledge to cure disease, visit http://feinstein.northwell.edu and follow us on LinkedIn.

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Feinstein Institutes Bioelectronic Medicine Researchers Control Nerve to Turn On/Off Inflammation - Business Wire

The rapid spread of the delta variant of SARS-CoV-2 has put more patients in hospital beds and led to reinstatements of mask mandates in some cities and states. The variant, which is more transmissible than previous variants, also seems more able to cause breakthrough infections in vaccinated people.

Fortunately, vaccines are forming a bulwark against severe disease, hospitalization and death. But with the specter of delta and the potential for new variants to emerge, is it time for booster shots or even a new COVID vaccine?

For now, public health experts say the far bigger emergency is getting first and second doses into people who haven't had a single shot. Most people don't need boosters to prevent severe illness, and it's not clear when or if they will. But companies are already looking into updating their vaccines for coronavirus mutations, and there is a good chance that third shots are coming soon for some people. Already, the Food and Drug Administration (FDA) and Centers for Disease Control and Prevention (CDC) have greenlighted booster shots for immunocompromised individuals.

Related: Coronavirus variants: Here's how the SARS-CoV-2 mutants stack up

"I think we're looking at an inevitable move toward boosters, at least in higher-risk people like those of advanced age and obviously the immunocompromised," said Dr. Eric Topol, a professor of molecular medicine at The Scripps Research Institute in California.

Vaccine developers are working on the question of whether future COVID-19 shots will need to be tweaked for the delta variant, or other new variants. For now though, initial evidence hints that boosters of the original vaccine should add protection against delta.

While all the COVID-19 vaccines in the U.S. are doing a fabulous job of preventing severe disease and death, it's clear that breakthrough infections are more common with this variant. Data on efficacy is still emerging, and efficacy is a moving target depending on a lot of factors. It's hard to make apples-to-apples comparisons between countries or hospital systems, said Jordi Ochando, an immunologist and cancer biologist at the Icahn School of Medicine at Mount Sinai. Different countries have different levels of vaccination, have used different vaccine mixes with different dose scheduling, and have different populations with different age stratification, comorbidities and levels of previous infection.

Still, synthesizing data from different countries suggests the mRNA vaccines by Pfizer-BioNTech and Moderna are probably up to 60% or as low as 50% protective against infection with delta, Topol wrote on Twitter. That's right on the border of efficacy at which the Food and Drug Administration would approve a new COVID-19 vaccine. The J&J vaccine is probably less protective against symptomatic illness than a two-dose mRNA vaccine, based on studies finding that it elicits lower levels of neutralizing antibodies (which block the virus from entering cells).

Data is now emerging that the J&J vaccine likely prevents severe disease from delta as well. Though people with symptomatic breakthrough infections can spread the delta variant, the vaccines do still seem to reduce the likelihood of transmission by making any infection that does occur shorter. A study conducted in Singaporefound that viral load started at similar levels in vaccinated and unvaccinated individuals who were infected with delta, but it dropped much faster in vaccinated individuals, beginning a steeper decline around day 5 or 6 of illness. This could mean that vaccination shortens the infectious period. However, more confirmation is necessary to show whether the Singapore results will hold up. The discovery that vaccinated people can have viable virus in their noses if infected is what made the CDC reverse its recommendation that vaccinated people did not need to wear masks.

It's not clear exactly why delta can break through vaccine-induced protection more frequently, but there may be multiple factors at play. One is that the antibodies that the vaccine elicits may not bind to the virus variant as well. Delta appears to have spike mutation proteins that make original coronavirus antibodies a worse fit, according to research published in Nature in July. This means that previously infected and vaccinated people have antibodies that aren't quite as protective against delta as they were against the original or alpha variants, said Yiska Weisblum, a postdoctoral researcher in retrovirology at The Rockefeller University in New York.

Another possible reason for waning efficacy is that the immune system starts letting down its guard over time. This happens with the pertussis vaccine, which is why expectant parents and other adults who are going to be around unvaccinated newborns should get booster shots.

"Right now, the U.S. is the driver of the world delta wave, and we are the leading force of nurturing new variants, because it's out of control here."

Whether waning immunity is likely to be a problem for COVID-19 vaccines is currently a hot topic among researchers. Israeli health authorities say they've seen an increase in breakthrough infections in people immunized in January versus March and are concerned about an uptick in more severe breakthrough cases in those 60 and older, according to Haaretz.

Data from an Israeli HMO published on the preprint server medRxiv before peer review found that 2% of people who requested a PCR test for any reason post-vaccination received a positive result. People vaccinated more than 146 days before being tested were twice as likely to experience a breakthrough infection. The vast majority of the cases in the study were delta. It's difficult to track waning immunity because you need to revisit the same group of people over time, tracking their infection status, Scripps' Topol told Live Science. That kind of data hasn't really emerged yet. But Topol said he's transitioned from skepticism over waning immunity to belief that it is occurring.

"It does look like there is a substantial interaction with delta finding people who are several months out from when they got fully vaccinated," Topol said. "It's a double hit. If you were six months out, and there is no delta, you're probably fine. The problem is this interaction."

Delta's ability to infect the fully vaccinated raises questions about the best strategy going forward. One option would be to give a booster of the same vaccine, raising antibody levels to what scientists hope will be protective levels against delta.

Vaccine manufacturers are also studying versions of the vaccines that update the spike protein targeted by their vaccines.

But trying to play catch-up with delta-specific vaccines might be akin to a game of whack-a-mole, said Dr. Krutika Kuppalli, an infectious disease specialist at the Medical University of South Carolina. There was talk of updating the mRNA vaccines with a spike protein specific to the alpha variant, Kuppalli told Live Science. Now, of course, alpha is vanishing on its own, being replaced by the far more transmissible delta.

"By the time [a new vaccine] might even be ready then we're on to the next one," Kuppalli said.

Related: 14 coronavirus myths busted by science

If delta has taught us anything, it's that ideally, a future SARS-CoV-2 vaccine wouldn't be delta-specific, but rather universal to all potential SARS-CoV lineages, Topol said. A universal vaccine could draw on similarities between the viruses SARS-1, which emerged in 2003, is genetically 95% similar to SARS-CoV-2, after all and be reverse-engineered to produce potent antibodies seen in some people infected with SARS viruses, Topol said.

"We could get there soon," Topol said. "That would hopefully be an enduring solution rather than an 'each Greek letter' solution." (Each new coronavirus variant of concern gets a new Greek letter name.)

Another promising notion is that of a needle-free, nasal spray vaccine against COVID-19. Nasal vaccines deliver directly to the spot where the virus lands and elicit immunity right in the mucous membrane that lines the nose. This mucosal immunity can combat the virus quickly, reducing viral replication in the nose, and thus tamping down viral shedding and transmission, University of Alabama at Birmingham researchers wrote July 23 in the journal Science.

A more immediate option might be to harness the advantages of having multiple approved vaccines, said Mount Sinai's Ochando. Mixing and matching vaccines seems to give an immunological boost over boosters of the same time, Ochando told Live Science, citing several papers published in The Lancet.

But even a booster of the original vaccine is likely to help improve immunity against delta. Weisblum and her colleagues have found that people who were infected with SARS-CoV-2 before delta became predominant and then got fully vaccinated have a broader array of antibodies than those who were only infected or those who were only vaccinated. This suggests that when the body sees some version of SARS-CoV-2 three times, it mounts a broader campaign against the invader strong enough to take down even the delta variant. The researchers even tested these triple-strength antibodies against a spike protein mutated in the lab to resist antibodies from infection or vaccination and found that they conquered this multiple-mutant spike.

"This data suggests that boosting definitely has the potential to increase the breadth of our antibody responses," Weisblum wrote in an email to Live Science. "It also suggests that boosting with the wild type original virus spike could be good enough (since the convalescent vaccinated individuals only saw the original spike), but updating the vaccine to mimic circulating or potentially emerging variants should increase the breadth of the response even more."

One reason the future of COVID-19 vaccines against new variants is hard to understand is that scientists aren't yet sure which immune cells best represent vaccine efficacy in the long term. Most studies now look at neutralizing antibodies. These are a good proxy for protection against infection, said Dr. Zain Chagla, an infectious disease specialist at McMaster University, but may not be as good a representation against protection against severe disease. That's because the immune system recruits a bevy of other cellular protectors such as B cells and T cells to fight once a virus invades. These defenses aren't as quick to the punch as neutralizing antibodies, but they can prevent an infection from turning serious.

Over time, though, antibodies decline (if they didn't, your blood would turn into a sluggish goo of antibodies), while long-term immune cells such as memory B cells and plasma cells persist, ready to mount a new response should the virus reappear again. One challenge for assessing vaccine efficacy going forward will be figuring out which sorts of immune cells to measure to determine how protected someone is from disease after antibody levels decline.

For diseases like hepatitis and measles, researchers have determined a cutoff for an antibody level that provides protection, Chagla said. "As long as you're over that cutoff, it tends to predict success or failure better than just, 'higher is better,'" he said.

There may be a similar cutoff for coronavirus antibodies, but researchers don't know what it is yet.

The trouble with waiting for this data, Ochando said, is that scientists have to study reinfections as they happen. Allowing reinfections opens up the possibility of allowing for more transmission, severe illness and spread. Thus, boosters might be ethically necessary as a precaution, even without rigorous clinical trials delineating their efficacy, Ochando said.

If a third dose of an existing or new formulation of COVID-19 vaccine proves necessary, it doesn't necessarily follow that everyone will need a COVID-19 shot every six months to a year for the rest of their lives. Some vaccines, like the Hepatitis B vaccine, perform best with a 3-dose series, after which there's rarely a need for a booster. It might be that three doses of an mRNA shot at the right spacing will provide strong and long-lasting protection, Cline Gounder, an infectious disease specialist and epidemiologist at the New York University Grossman School of Medicine, said on Twitter.

Whatever the data ultimately shows about the need for boosters, the real bang for the vaccination buck still lies in first shots, not third shots, Kuppalli told Live Science. Facing COVID-19 unvaccinated is much more dangerous than facing it fully vaccinated, and the continued circulation of the virus around the globe just means more opportunity for mutations that could benefit the virus.

"Right now, the U.S. is the driver of the world delta wave, and we are the leading force of nurturing new variants, because it's out of control here," Topol said.

The danger of being unvaccinated is global. Worldwide, only 15.6% of people are fully vaccinated, according to Our World in Data. This has many health experts concerned that high-income countries will be busy handing out booster shots while the rest of the world burns. It's another ethical quandary, Ochando said. Distributing booster shots to the immunocompromised and elderly in wealthy countries makes sense, he told Live Science, but providing third shots to young, healthy people in rich countries is hard to swallow when only 2% of Africa's population has been fully vaccinated, according to the Africa Centres for Disease Control numbers.

Kuppalli agreed.

"I understand countries want to take care of their own, but I think we need leaders to step back and look at the global picture and look at why we are in this continued cycle and look at why these variants keep emerging," Kuppalli told Live Science. "And the reason the variants keep emerging is we are unable to keep the global rate of the virus down."

Originally published on Live Science.

Excerpt from:
Does the explosion of the delta variant mean we need a new COVID-19 vaccine? - Livescience.com

PROVIDENCE, R.I.[Brown University] If youve ever seen a petunia with artfully variegated petals, then youve seen transposons at work. The flowers showy color patterns are due to transposable elements, or DNA sequences that can move locations within a genome. Yet when it comes to transposons effects on humans, the results might not be as lovely or desirable.

As researchers learn more about these so-called mobile genetic elements, theyve found increasing evidence that transposons influence and even promote aging and age-related diseases like cancer as well as neurogenerative and autoimmune disorders, says John Sedivy, a professor of biology and director of the Center on the Biology of Aging at Brown. Sedivy is the corresponding author of a new review article in Nature that discusses the latest thinking and research around transposons.

The splotches and specks of this variety of flower, petunia hybrida W138, are due to the activity of transposons. (Photo: The Petunia Platform, ENS de Lyon)

Lets put it this way: These things can be pretty dangerous, said Sedivy. If they are uncontrolled, and there are many examples of that, transposons can have profound consequences on most forms of life that we know of.

Since the dawn of life, the researchers noted, transposons have coevolved with their host genomes, but its been more of a competitive existence than a peaceful one, earning them the nicknames of junk DNA and molecular parasites. Transposons were first discovered in corn by the Nobel prize-winning geneticist Barbara McClintock in the 1940s, who also found that depending on where they inserted into a chromosome, they could reversibly alter the expression of other genes.

It is now quite apparent that the genomes of virtually all organisms, including humans, contain repetitive sequences generated by the activity of transposons. When these elements move from one chromosome or part of a chromosome to another, they amplify and increase their presence in genomes, sometimes to dramatic levels. According to Sedivy, about half of the human genome is due to the activity of these molecular parasites. Their unregulated activity can have long-term benefits by increasing genetic diversity in organisms, but in most cases the chaos degrades cell function, such as by disrupting useful genes.

Most of what is known about transposons, said Sedivy, comes from genome sequence data that shows their activity in the germline, or throughout successive generations of an organism. However, recent research, including from Sedivy and other scientists at Brown, has revealed a wealth of information on transposon activity during the lifetime of a single individual, as well.

In an interview, Sedivy discussed the mechanisms driving transposons, how their activity influences and promotes age-related tissue degeneration and disease and what can be done to fight back.

There are two main groups: 'DNA transposons' move using a DNA intermediate in a 'cut and paste' mechanism, and retrotransposons move using a 'copy and paste' mechanism that involves an RNA intermediate. Thirty five percent of the human genome is comprised of retrotransposon DNA sequences. The reason they move is to survive; it allows them to relocate to and increase their presence in their hosts. You can think of transposons as viruses there are some viruses that are, in fact, transposable elements. HIV (human immunodeficiency virus) is a perfect example because it uses the retrotransposition mechanism to insert itself into the genome, and then lets the host cell do the replication for it. This means that unless you kill all the cells that HIV has infected, you cant get rid of it. Thats what retrotransposons do, too. They live in the genome, including the germline so that eggs and sperm carry these genetic elements and pass them along to future generations.

Transposons have been studied quite extensively, one important impact in medicine being their role in propagating antibiotic-resistance genes in bacteria. The level of activity in an individual human body, over a single lifetime, was thought to be quite low and of minimal consequence. Its now become quite obvious thats not the full story.

First of all, its important to realize that aging is not an active process. While it might seem that youre programmed to deteriorate, aging is in fact a successive sequence of failures. Cellular processes and mechanisms become more error-prone over time. Cancer, for example, is a disease of aging because at some point, a fatal error is committed which then propagates and leads to disease. As biologists who study aging, we applied the error and failure theory to retrotransposable elements and discovered thats exactly what was happening. Its now widely appreciated that over a lifespan, these elements become more active in somatic tissues theres very good evidence that this is happening. There are multiple surveillance mechanisms that our cells use to keep these elements under control and suppress their activity; several layers of active defense that are necessary to keep the retrotransposons under wraps, so to speak. It appears that aging, or senescent, cells lose some of their ability to control the activity of retrotransposons. The defense mechanisms no longer work as well.

The aging brain of a person with Alzheimer's already shows a significant amount of damage. There's also reasonably good evidence that the brain, for some reason, is a particularly permissive site for retrotransposon activity, so the retrotransposons can basically have a field day in that tissue because theres very little that can stop them. So they promote further damage. This is a major topic in our recent review article in Nature. The question becomes: What can be done to limit the activity of these elements?

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Beware the 'molecular parasites' involved in aging and disease - Brown University

Multiple classes of drugs exist for treating rheumatoid arthritis (RA) patients. But close to 90% of patients failing methotrexate are prescribed the worlds largest selling drug class, tumor necrosis factor- inhibitor (TNFi) therapies even though the majority dont respond adequately.

A new study published in Rheumatologyand Therapy demonstrates that PrismRA, a molecular signature test using a simple tube of blood, can predict the likelihood of not achieving a clinically meaningful response of at least a 50% improvement in symptoms in targeted therapy-nave patients and now, those patients already exposed to the TNF-inhibitor class or currently on an anti-TNF agent.

Erin Connolly-Strong, PhD, Head of Medical Affairs at Scipher Medicine, co-author of the study explains the results and science behind PrismRA.

The objective was to prospectively demonstrate that PrismRA can predict the likelihood of not achieving response, low disease activity, or remission with TNFi therapy across multiple clinical outcome measures at 3 and 6 months, including ACR50, ACR70, DAS28-CRP, and CDAI.

This was a prospective multi-center trial, which is important when we think about the objectives around the study, since a main goal was predicting the likelihood of not achieving response to the TNF-inhibitor class of medications, which are commonly prescribed for RA. We wanted to do that prospectively, but also challenge ourselves by looking at multiple disease activity measures. Our previous study had been retrospective, and we defined treatment response primarily with the ACR50 measure.

In this new study we really wanted to push the envelope, so the results could be very actionable for physicians. We demonstrated that by using the standard clinical measures, we can predict response accurately at 3 and 6 months.

Our previous study validated the PrismRA molecular signature in samples from the CorEvitas registrys CERTAIN study cohort. In this earlier study we prospectively collected both the patients molecular and clinical data.

One of the positive things about RA therapeutics is choice. There are multiple classes of drugs approved for the disease. But the American College of Rheumatology (ACR) guidelines can be a challenge when it comes to selecting targeted therapy, since the professional society doesnt rank one therapy over another or suggest an ideal prescribing order.

The dilemma for physicians is having to work through that, as well as the challenge of formularies. So, really when we think about a major problem that needs solving in RA, its that despite having all of these choices, anti-TNF therapy is the go-to.

Two out of 3 targeted treatment-nave patients will also not have an adequate response to anti-TNF medications. We need to get patients to the right therapy as quickly as possible, so that they can start to experience symptom improvement, a better quality of life, and hopefully remission.

The big question is who should not get TNF inhibitor therapy? Thats why we designed a molecular signature response classifier to rule out anti-TNF agents for those patients who are unlikely to respond to them so they can go on an alternative FDA-approved therapy faster and avoid unnecessary delays, dose escalations, or cycling.

Examining the problem more closely, there are 2 main types of patients for whom PrismRA can help inform treatment decisions first, the targeted therapy-nave patient and then second, all of the other patients who have already been exposed to the TNF-inhibitor class or are currently on an anti-TNF agent.

Providers need to know if TNF is the right pathway, as well, so thats part of what we were looking to solve in this trial to expand our intended use beyond just that nave population, but also to really be able to provide accurate predictions in that targeted therapy population as a whole.

This is one of the most fascinating areas of our research. When you go to scientific meetings, theres always a new biomarker being presented, but they rarely come to fruition. Thats because identifying individual biomarkers often doesnt consider a patients full biology, since theyre usually just a genomic or protein marker.

Were unique in that we have what we call our "molecular signature."We find a set of biological markers that capture individuals genetic makeups and their disease behavior. The molecular signature does this by including RNA, protein, and other features that reflect a patients biology.

For PrismRA specifically we include protein expression, RNA expression, patient and provider-reported outcomes, and patient characteristics. So, its all of those things together that give us the complete biology of that patient. That signature has components that are important in RA and that help us predict the patients likely response to anti-TNF treatment.

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In RA, new molecular signature test confirms who won't respond to anti-TNF therapy during any point in therapeutic journey - BioPharma Dive

Neeta L. Vora, MD, Assistant Professor and Director of Reproductive Genetics in the Department of Obstetrics & Gynecology, has been awarded $3.4 million for a Research Project Grant (R01) from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) toward studying the identification of genes critical to human brain development with validation in a zebrafish model.

Neeta L. Vora, MD, a Maternal Fetal Medicine-Geneticist from the Department of Obstetrics and Gynecology, has been awarded a Research Project Grant (R01) from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) toward studying the identification of genes critical to human brain development with validation in a zebrafish model. The grant, funded at $3.4 million, was submitted through the UNC Center for Womens Health Research in October, 2020.

Fetal brain abnormalities (FBA) are one of the most common prenatal sonographic abnormalities detected and account for approximately 20 percent of birth defects, posing a substantial burden on the health care system.

The project proposed by Dr. Vora will identify genes critical to human brain development by applying exome sequencing in pregnancies with FBA. Novel candidate genes will then be targeted in zebrafish using gene editing technology (CRISPR). This work will shed light on the molecular underpinnings of human brain development to improve the diagnosis, prevention, and treatment of FBA, leading to novel preventive and therapeutic strategies that can be applied in the perinatal period.

The work is significant because understanding the etiology of fetal brain abnormalities will inform parents regarding recurrence risk in future pregnancies as well as inform care in the newborn period which has the potential to improve neonatal outcomes, says Vora.

Dr. Vora is triple boarded in Obstetrics and Gynecology, Maternal Fetal Medicine, and Clinical Genetics. She completed her residency and fellowship at Tufts Medical Center in Boston, MA, and joined UNC OB-GYNs Division of Maternal-Fetal Medicine in 2012. She is now an associate professor and serves as the Director of Reproductive Genetics at UNC where she supervises six prenatal genetic counselors.

She has authored more than 55 articles on prenatal genetics, ranging from cell free DNA to whole exome and genome sequencing. She had a K23 from the NICHD to study use of new genomic technologies in obstetrics and has an R21 to study novel genes critical to human brain development in a zebrafish model. She is a co-investigator on both a multicenter prenatal whole genome sequencing grant and a grant on how parents prepare for a prenatal diagnosis of a genetic condition.

Her research team includes, but is not limited to, Kelly Gilmore (study coordinator and prenatal genetic counselor), Karen Dorman (Director of Perinatal Research), Amber Ivins (research assistant), and Erica Davis (zebrafish collaborator at Northwestern). Dr. Vora is grateful to the MFM division for their support, the Center for Womens Health Research, the NICHD, and NC TraCS and the Program for Precision Medicine in Health.

For more information on Dr. Voras research, publications, and lab team, visit her research website.

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Vora Awarded $3.4 million for Identification of Genes Critical to Human Brain Development | Newsroom - UNC Health and UNC School of Medicine

The partnership brings an integrated diagnostic approach to advance the early detection of pancreatic cancer.

ALISO VIEJO, Calif., Aug. 17, 2021 /PRNewswire/ -- The PRECEDE Consortium (PRECEDE) and Konica Minolta Precision Medicine, Inc. (KMPM) announced today that KMPM and its subsidiaries, Ambry Genetics and Invicro, have joined as partners to bring a novel integrated diagnostic approach to support PRECEDE's mission for increasing survival rates for pancreatic cancer patients through early detection.

According to the American Cancer Society, pancreatic cancer is one of the deadliest cancers, with a 5-year survival rate of just 10 percent[1]. The PRECEDE Consortium is a highly collaborative international effort comprised of over 35 leading academic medical centers across the globe to transform the early detection and prevention of pancreatic cancer, with the aim of increasing the 5-year survival rate from 10 percent to 50 percent within the next 10 years.

Together, KMPM and PRECEDE Consortium will bring their expertise and resources in genetic testing, pathology, and imaging to determine who is at an elevated risk for developing pancreatic cancer, define that risk, and invite those at elevated risk into state-of-the art clinical screening programs. The coordinated plan by KMPM and the PRECEDE Consortium is to analyze and standardize data curated through LATTICE, an integrated diagnostics platform, that runs on Amazon Web Services, Inc. (AWS). LATTICE uses Amazon HealthLake, a HIPAA-eligible service that helps organizations store, transform, query, and analyze health data, and will help researchers and clinicians gain new genomic insights for detecting and preventing pancreatic cancer.

One of the most significant challenges in determining who is at an elevated risk for pancreatic cancer has been the lack of infrastructure and protocols to support the translation of molecular imaging data, sequencing data, and diagnostics technology data. The analysis of this data is critical for informing disease detection, prevention, and treatment. KMPM's focus on multi-omics and multimodal data has spurred their development of LATTICE, which they plan to use to securely aggregate diagnostics, imaging, and informatics data from the PRECEDE study in one seamless, standardized platform to better derive new insights for preventive and managed care.

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"As a surgeon and scientist who has spent my entire career taking care of pancreatic cancer patients and trying to improve survival for this intractable disease, it is clear that early detection is likely to have the greatest impact in changing outcomes," said Dr. Diane M. Simeone, Principal Investigator of PRECEDE and Director of the Pancreatic Cancer Center at NYU Langone Health. "Through this innovative partnership we expect to curate and analyze large amounts of data in an unprecedented way to optimize early detection methods for pancreatic cancer."

"Machine learning may offer healthcare and life sciences organizations the opportunity to normalize, index, structure, and aggregate data in a way that makes it easier for clinicians to understand relationships in data and support better patient care," said Dr. Taha Kass Hout, Director of Machine Learning at AWS. "We are excited to support the PRECEDE Consortium as they work to predict and prevent pancreatic cancer using LATTICE."

"Early identification can have a life-changing impact for patients at a high risk for pancreatic cancer," said Aaron Elliott, KMPM CEO. "By leveraging the LATTICE platform, PRECEDE will be able to help more healthcare providers, researchers, and scientists harness the power of diagnostics, imaging, and informatics to find novel associations and biomarkers for the early detection of pancreatic cancer."

The PRECEDE Consortium is currently providing clinical care to high-risk patients at designated academic medical institutions and enrolling eligible patients into its observational longitudinal prospective cohort study. The PRECEDE study plans to grow to include over a hundred institutional partnerships and expand the cohort to over 10,000 high risk individuals for this important study. For more information on PRECEDE and its Consortium members please visit, precedestudy.org

About PRECEDE Founded in 2018, The PRECEDE Consortium is a highly collaborative international effort to improve survival for pancreatic cancer by improving early detection, screening, risk modeling, and prevention for those with a heritable risk for pancreatic cancer. PRECEDE's mission is to increase the survival of patients diagnosed with pancreatic cancer from 10% to 50% in the next ten years by partnering with top researchers, industry, academic institutions, survivors, and families dedicated to preventing and ending pancreatic cancer. The largest effort of its kind, PRECEDE utilizes a novel collaboration and data-sharing model to evaluate at-risk individuals for pancreatic cancer. Working collaboratively, PRECEDE aims to better define who is at risk, determine the level of risk, and enroll those at elevated risk into state-of-the-art screening programs to help put an end to pancreatic cancer.

About KONICA MINOLTA PRECISION MEDICINE, Inc.Konica Minolta Precision Medicine, Inc. (KMPM) is a comprehensive precision diagnostics company dedicated to advancing technologies that accurately predict, detect and treat disease. Powered by proprietary software platforms, best-in-class genomics technology from Ambry Genetics Corporation, and industry-leading radiology and pathology services from Invicro, LLC, KMPM is uniquely equipped to collect, analyze, and report on multi-modal precision diagnostic data sets. This comprehensive approach will drive clinical access to novel diagnostic assays through the company's extensive network of healthcare providers and pharmaceutical partners. LATTICE is a trademark of Ambry Genetics.

Media Contact:Simone Jackenthal Email: sjackenthal@tridentdmg.com

[1] American Cancer Society. Cancer Facts & Figures 2021. Atlanta, Ga: American Cancer Society; 2021.

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SAN FRANCISCO, Aug. 12, 2021 /PRNewswire/ --The global regenerative medicine marketsize is expectedto reach USD 57.08 billion by 2027, growing at a CAGR of 11.27% over the forecast period, according to a new report by Grand View Research, Inc. Recent advancements in biological therapies have resulted in a gradual shift in preference toward personalized medicinal strategies over the conventional treatment approach. This has resulted in rising R&D activities in the regenerative medicine arena for the development of novel regenerative therapies.

Key Insights & Findings:

Read 273 page research report, "Regenerative Medicine Market Size, Share & Trends Analysis Report By Product (Cell-based Immunotherapies, Gene Therapies), By Therapeutic Category (Cardiovascular, Oncology), And Segment Forecasts, 2021 - 2027", by Grand View Research

Furthermore,advancements in cell biology, genomics research, and gene-editing technology are anticipated to fuel the growth of the industry. Stem cell-based regenerative therapies are in clinical trials, which may help restore damaged specialized cells in many serious and fatal diseases, such as cancer, Alzheimer's, neurodegenerative diseases, and spinal cord injuries. For instance, various research institutes have adopted Human Embryonic Stem Cells (hESCs) to develop a treatment for Age-related Macular Degeneration (AMD).

Constant advancements in molecular medicines have led to the development of gene-based therapy, which utilizes targeted delivery of DNA as a medicine to fight against various disorders. Gene therapy developments are high in oncology due to the rising prevalence and genetically driven pathophysiology of cancer. The steady commercial success of gene therapies is expected to accelerate the growth of the global market over the forecast period.

Grand View Research has segmented the global regenerative medicine market on the basis of product, therapeutic category, and region:

List of Key Players of Regenerative Medicine Market

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About Grand View Research

Grand View Research, U.S.-based market research and consulting company, provides syndicated as well as customized research reports and consulting services. Registered in California and headquartered in San Francisco, the company comprises over 425 analysts and consultants, adding more than 1200 market research reports to its vast database each year. These reports offer in-depth analysis on 46 industries across 25 major countries worldwide. With the help of an interactive market intelligence platform, Grand View Research helps Fortune 500 companies and renowned academic institutes understand the global and regional business environment and gauge the opportunities that lie ahead.

Contact:Sherry JamesCorporate Sales Specialist, USAGrand View Research, Inc.Phone: 1-415-349-0058Toll Free: 1-888-202-9519Email: [emailprotected]Web: https://www.grandviewresearch.comFollow Us: LinkedIn| Twitter

SOURCE Grand View Research, Inc.

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Regenerative Medicine Market Size Worth $57.08 Billion By 2027: Grand View Research, Inc. - PRNewswire