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Meeting the quadruple aim through whole-person care – MedCity News

Posted: July 27, 2022 at 2:51 am

Full customer care service icon. customer vector illustration

The devastation of Covid-19even beyond killing more than one million Americanswas its exposure of the shocking extent of underlying preconditions afflicting our population and our sad failure to treat them. Six of every 10 people in the U.S. suffer from chronic diseases. Roughly 40 million Americans have five or more chronic illnessesaccounting for 41% of all spending in the most expensive health system the world has ever seen. Nonetheless, despite all this spending, 66% of us rate our medical care as low or poor.

Our nation is among the most highly advanced when it comes to treating acute illness by delivering pills and procedures. But the truth is that our system is simply not designed to keep us healthy. Numerous studies show that medical treatment itself accounts for only about 20% of health. Nearly 80% comes from other factors rarely addressed by our system. These are emotional and mental health, behavioral and lifestyle factors, and the social and economic environment in which a person lives.

The good news is that we already have access to a better path to lifelong health and wellbeing. In our new report, The Case for Delivering Whole-Person Care, the Family Medicine Education Consortium and the Samueli Foundation funded the study of numerous real-world examples of health systems, hospitals, and clinics which are currently practicing whole-person care. This approach allows these institutions to achieve the elusive quadruple aim of reducing costs while also improving population health, the patient experience, and even the wellbeing of clinicians.

These are not pie-in-the-sky concepts. For example, the Veterans Administration has documented the remarkable success of a new care model that shifts from a traditional disease-based transactional system to a team-based, person-centered care model that addresses patients physical, emotional, and social wellbeing. In their four-year pilot program with 130,000 veterans at 18 sites, the VA not only reported improved outcomes and patient experience ratings, but also a significant savings of 20 percent, or more than $4,500 annually per veteran.

Whole-person care combines conventional medicine, non-drug treatments, and evidence-based complementary modalities to promote self-care. It uses approaches such as health coaching, group visits, nutritional counseling, acupuncture, yoga, meditation, therapeutic massage, stress reduction, and other non-drug approaches for healing. It explores the social and economic circumstances of the patient and assists them in helping with those. It starts with finding out what matters to the person and then exploring the determinants of health and healing that are most pertinent to them. Thus, the approach goes to the root causes of their ills and seeks to assist them with long-term solutions.

The VAs Whole Health model yielded a reduction of 23% to 38% in opioid use, compared to 11% with conventional care alone. Whole health patients also reported greater improvement in perceptions of care, engagement in care and self-care, life meaning and purpose, pain, and perceived stress. Moreover, VAs own employees reported higher engagement, job satisfaction, and intrinsic motivation, yielding reduced turnover and burnout.

There are large benefits of the whole person care approach:

The heart of these successes is that whole-person health care allows patients to build on and better utilize their own personal healing capacity. We are all familiar with the social determinants of health in which social and economic environments determine health outcomes for an entire zip code. Whole-person care taps into addressing these for the purpose of finding the personal determinants of health those determinants that promote individual healing in any environment.

One practical approach to implementing this type of care is to have practitioners ask the patient to assess their physical, emotional, and spiritual wellbeing through a Personal Health Inventory (PHI). The PHI asks the provocative question: what matters to you in life and what brings you joy? It then goes on to assess how willing you are to make changes in various aspects of your life to achieve that life purpose and enjoy good health. After the PHI, an integrative health visit identifies the patients values and goals for healing. I call this the HOPE Note (Healing-Oriented Practices and Environment) Toolkit.

The HOPE Note builds off of the SOAP Note (subjective, objective, assessment, and plan) that every medical student learns to apply in everyday practice. SOAP asks whats the matter and treats the immediate medical diagnosis or symptoms. HOPE reaches patients on a deeper level by not just asking Whats the matter? Instead, we are asking What really matters to you? It then focuses on addressing the root causes of the malady.

This process builds a stronger relationship with the provider, whose role is to really understand the patients goals for healing and then to provide the evidence and support to help them. This is all not just a feel-good process. Our research has shown that whole-person care yields tangible results supporting the quadruple aim, such as:

In 2021, a study by the National Academy of Sciences, Engineering, and Medicine recognized high-quality whole-person care as the foundation of primary care for a strong U.S. health care system. It recommended system-wide implementation of whole-person, integrated, accessible, and equitable health care by interprofessional teams who are accountable for addressing the majority of an individuals health and wellness needs across settings and through sustained relationships with patients, families, and communities.

We know that this approach works. All we need now is to focus on redesigning our health care system to deliver this type of careand muster the courage to do it.

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Meeting the quadruple aim through whole-person care - MedCity News

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Verve Therapeutics Shares Up 84%; ARKG Offers Exposure – ETFdb.com

Posted: July 27, 2022 at 2:49 am

The biotech sector can offer unique opportunities and strong returns to investors willing to stomach the volatility heightened by the current economic environment.

Shares of Verve Therapeutics (VERV) traded up 22% last Tuesday after the companys recent announcement that it dosed its first human patient with an investigational in vivo base-editing medicine, VERVE-101, as a potential treatment for heterozygous familial hypercholesterolemia, according to recent commentary from ARK Invest.

The treatment from the Cambridge, Massachusetts-headquartered company could offer an alternative for hypercholesterolemia patients who have difficulty managing the side effects of statins and other therapeutic options. Founded by world-renowned experts in cardiovascular medicine, human genetics, and gene editing, Verve Therapeutics develops transformative once-and-done therapies for coronary heart disease, according to ARK.

Shares of Verve Therapeutics are up over 83% over a one-month period, according to YCharts. Over a five-day period, shares are down over 7%, but they are rebounding and up nearly 1% in mid-day trading on Tuesday.

Investors can get exposure to Verve Therapeutics with the ARK Genomic Revolution ETF (ARKG A-). ARKG is an actively managed equity strategy that aims to provide exposure to DNA sequencing technology, gene editing, CRISPR, therapeutics, agricultural biology, and molecular diagnostics.

Companies within ARKG are focused on and are expected to substantially benefit from extending and enhancing the quality of human and other life by incorporating technological and scientific developments and advancements in genomics into their businesses, according to the firm.

The funds top holdings as of July 26 include Exact Sciences Corp. (EXAS, 7.42%), Teladoc Health Inc. (TDOC, 5.56%), Ionis Pharmaceuticals Inc. (IONS, 5.30%), CRISPR Therapeutics AG (CRSP, 4.78%), and Signify Health Inc. Class A (SGFY, 4.70%), according to the funds website.

ARKG typically holds between 40 and 60 securities and charges an expense ratio of 75 basis points.

For more news, information, and strategy, visit our Disruptive Technology Channel.

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Double up on the guac? Those avocados are good for your heart health – American Heart Association

Posted: July 27, 2022 at 2:49 am

The American Heart Association says avocados may help reduce your risk for cardiovascular disease, including lowering your cholesterol

DALLAS, July 26, 2022 Adding avocados to a healthy diet could reduce your risk of cardiovascular disease, including lowering your cholesterol, according to research published by the American Heart Association. Thats especially good news because the consumption of avocados in the U.S. has nearly tripled in the past two decades, up to nearly 2.6 billion pounds a year, according to the U.S. Department of Agriculture.

Avocados contain high amounts of fiber, potassium, magnesium, folate, vitamin C and vitamin K. The fruit is a known source of healthy, unsaturated fats and a great replacement for certain fat-containing foods like butter, cheese or processed meats.

A study recently published in the Journal of the American Heart Association found that:

A 2015 study published in the Journal of American Heart Associationfound that eating one avocado a dayas part of a moderate-fat diet resulted in lower "bad" LDL cholesterol.

Although avocados are not a total solution to improving heart health, research shows substantial benefits to adding them to your diet, said Mayra L. Estrella, Ph.D., M.P.H., a member of the American Heart Associations Council on Lifestyle and Cardiometabolic Health and an assistant professor in the Department of Epidemiology, Human Genetics, and Environmental Sciences at the University of Texas Health Science Center School of Public Health in Houston. However, everything in moderation because avocados are not calorie-free. A medium avocado averages about 240 calories and 24 grams of fat, according to the California Avocado Commission. Yet, they are a source of healthy fat that can be eaten in place of "bad" saturated fat in a typical diet. And of course, if youre eating them in guacamole or another types of dip, youll want to be careful not to indulge in too many chips, as well.

The research on avocados aligns with the American Heart Associations guidance to follow the Mediterranean diet a dietary pattern focused on fruits, vegetables, grains, beans, fish and other healthy foods and plant-based fats such as olive, canola, sesame and other non-tropical oils.

The American Heart Association website has a number of heart-healthy recipes using avocados.

Studies published in the American Heart Associations scientific journals are peer-reviewed. The statements and conclusions in each manuscript are solely those of the study authors and do not necessarily reflect the Associations policy or position. The Association makes no representation or guarantee as to their accuracy or reliability. The Association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific Association programs and events. The Association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and biotech companies, device manufacturers and health insurance providers and the Associations overall financial information are availablehere.

Additional Resources:

About the American Heart Association

The American Heart Association is a relentless force for a world of longer, healthier lives.We are dedicated to ensuring equitable health in all communities.Through collaboration with numerous organizations, and powered by millions of volunteers, we fund innovative research, advocate for the public's health and share lifesaving resources.The Dallas-based organization has been a leading source of health information for nearly a century.Connect with us onheart.org,Facebook,Twitteror by calling 1-800-AHA-USA1.

###

For Media Inquiries and AHA/ASA Expert Perspective: 214-706-1173

Cathy Lewis: 214-706-1324, cathy.lewis@heart.org

For Public Inquiries: 1-800-AHA-USA1 (242-8721)

heart.org and stroke.org

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Double up on the guac? Those avocados are good for your heart health - American Heart Association

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Extending the PAX1 spectrum: a dominantly inherited variant causes oculo-auriculo-vertebral syndrome | European Journal of Human Genetics – Nature.com

Posted: July 27, 2022 at 2:49 am

Disorders of the first and second branchial arches include Treacher Collins syndrome (TCS; MIM 154500), auricocondylar syndrome (ACS; MIM 602483), mandibulofacial dysostosis, Guion-Almeida type (MIM 610536), branchio-oto-renal syndrome (BOR; MIM 113650, 610896), Stickler syndrome (MIM 108300) and hemifacial microsomia/oculo-auriculo-vertebral spectrum (HFM/OAVS; MIM 164210). These disorders are thought to result from a combination of inadequate migration and formation of facial mesenchyme during early embryonic life [1]. In TCS, ACS, BOR and Stickler syndrome molecular pathways have been established, however for the spectrum of disease encompassed by OAVS, the full molecular etiology of the condition is the subject of ongoing investigation.

OAVS, also known as Goldenhar syndrome or hemifacial/craniofacial microsomia, is a heterogeneous and complex group of disorders [2]. Craniofacial appearances range from subtle facial asymmetry to HFM or orofacial clefts, preauricular skin tags to microtia and anotia, and epibulbar dermoids to micropthalmia and coloboma [3]. Extracranial defects of the cardiac, renal, vertebral and central nervous systems are reported [3,4,5]. This marked phenotypic variability and a lack of consensus on minimum diagnostic criteria has resulted in considerable discrepancy in reported prevalence, but it is generally now accepted at 1 in 5600 [4].

The etiology of OAVS is still largely unknown and felt to be multifactorial due to both environmental (maternal diabetes, antenatal exposure to vasoactive medications, smoking and twinning) and genetic factors during early embryogenesis [4]. With the widespread adoption of exome or genome sequencing, several genes have now been associated with OAVS [6,7,8,9,10,11], although many have only been identified through segregation in multi-generational single families. Most recently, a large exome/genome sequencing effort of trios identified haploinsufficient variants in SF3B2 in multiple families segregating OAVS [12]. Variants were identified in 3% of sporadic and 25% of familial cases, indicating that while SF3B2 genetic alterations are the most common cause of OAVS identified to date, there is wide genetic heterogeneity for this condition.

The PAX-SIX-EYA-DACH (PSED) network is involved in a variety of developmental processes including roles in morphogenesis of the branchial arches, which acts as the developmental basis for many of the clinical features of OAVS. A proposed mechanism for OAVS is that altered signaling networks cause disrupted migration of cranial neural crest cells, which are essential for normal facial mesenchymal tissue development [4].

The PAX family encode nuclear transcription factors involved in embryogenesis in vertebrates, with five out of the nine PAX genes associated with congenital disorders in humans to date. Biallelic hypomorphic or loss of function variants in PAX1 have been described in several families with otofaciocervical syndrome type 2 (OTFCS2; MIM 615560) [13,14,15,16]. In severe cases, patients can also have severe combined immune deficiency, caused by underdevelopment or absence of the thymus [13].

Here we describe a novel dominant PAX1 variant segregating with full penetrance but variable expressivity in a family with OAVS. All family members are affected with mild but definitive features of OAVS including HFM, misshapen ears and preauricular pits. Imaging on the three available family members did not detect any vertebral anomalies. Our findings suggest a novel cause of OAVS and confirm that heterozygous variants in PAX1 can cause a clinically overt genetic disorder.

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Extending the PAX1 spectrum: a dominantly inherited variant causes oculo-auriculo-vertebral syndrome | European Journal of Human Genetics - Nature.com

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Scientists Unravel the Mystery of Junk Genes That Are Key to Brain Development – SciTechDaily

Posted: July 27, 2022 at 2:49 am

Differentiated cortical neurons expressing the axonal marker Tau (green) and the dendritic marker MAP-2 (red). Credit: Dr. Robert Williams, University of Bath

Scientists are starting to understand the precise workings of a type of gene that, unlike other genes, does not code for proteins the building blocks of life.

New research shows the mechanism by which genes coding for a subset of long non-coding RNA (lncRNA) interact with neighboring genes to regulate the development and function of essential nerve cells. Scientists at the University of Bath led the study.

Despite the prevalence of genes coding for lncRNA in the genome (estimates range from 18,000-60,000 lncRNA genes in the human genome compared to 20,000 protein-coding genes), these segments of DNA were previously written off as junk precisely because the information contained within them does not result in the production of a protein. However, it is now evident that some lncRNAs are anything but trash, and these might end up being crucial in helping those with severe nerve damage regain their physical abilities.

A subset of lncRNA genes are co-expressed in the brain with neighboring genes that code for proteins involved in gene expression regulation, even though the function of the majority of lncRNA genes is still unknown. In other words, genes for these lncRNAs and their protein-coding neighbors work as a pair. Together, they control how vital nerve cells form and function, notably in the brain throughout embryonic development and early life.

The regulatory pathway involved in controlling the levels of one of these gene pairs is described in the new study. Their location and quantity in the genome need to be carefully coordinated, as does the timing of their activity.

We previously defined one of the most profound functions for lncRNA in the brain and our new study identifies an important signaling pathway that acts to coordinate the expression of this lncRNA and the key protein coding gene that it is paired with, explains Dr. Keith Vance, lead author of the study from the Department of Biology & Biochemistry at Bath.

This new research takes us closer to understanding the basic biology of nerve cells and how they are produced. Regenerative medicine is the end-game and with further research we hope to develop a deeper understanding of how lncRNA genes operate in the brain.

This knowledge could be important for scientists looking for ways to replace defective neurons and restore nerve function for instance in people who have had strokes, explains Vance.

Reference: Chromatin interaction maps identify Wnt responsive cis-regulatory elements coordinating Paupar-Pax6 expression in neuronal cells by Ioanna Pavlaki, Michael Shapiro, Giuseppina Pisignano, Stephanie M. E. Jones, Jelena Telenius, Silvia Muoz-Descalzo, Robert J. Williams, Jim R. Hughes and Keith W. Vance, 16 June 2022, PLOS Genetics.DOI: 10.1371/journal.pgen.1010230

The research was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and is published today inPLOS Genetics.

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COVID-19 Can Make the Brain Age by 2 Decades; Here’s 1 Way to Reverse Aging – The Epoch Times

Posted: July 27, 2022 at 2:49 am

A new British study found that the original SARS-CoV-2 virus (i.e. Wuhan strain) can impair cognitive ability in a way equivalent to making the brain age by two decades. Currently, 67 percent of the worlds population has been vaccinated against the COVID-19 pandemic. Is it possible that the vaccines themselves can also cause aging damage?

Nevertheless, theres no need to worry, aging is proven to be a process, and there is a way to help reverse the aging process.

The study was published in the journal EClinicalMedicine. Experts from the University of Cambridge and Imperial College London Medical School evaluated the cognitive effects of the COVID-19 infection in humans.

The research subjects consisted of COVID-19 patients who were hospitalized for severe illness between March and July 2020.

After these patients recovery from acute infection, the researchers conducted follow-up visits for an average of six months to analyze and evaluate their anxiety, depression, and post-traumatic stress. The researchers discovered a significant decline in the patients attention, complex problem solving skills, and memory, along with reduced accuracy, and prolonged reaction time.

These cognitive deficits are similar to the cognitive decline a person would experience between the ages of 50 to 70, which is equivalent to aging by two decades and losing 10 IQ points.

In addition, the recovery of cognitive ability is very slow in patients with COVID-19 infections.

Why does COVID-19 infection cause abnormal aging? Lets first take a look at one concept.

The relationship between genes and epigenetics are like seeds and soil. Genes are like seeds, while epigenetics is like soil. Genes in the human body do not usually change after birth. They are like seeds that lie dormant in the soil, and some will grow, and some will not. What determines whether these seeds will grow or not are the genetic switches, or epigenetics.

Epigenetics is the study of these factors that affect genes being turned on or off. Specifically, one common type of gene switchDNA methylationcan change the expression of genes, shutting them down and making them non-functional. Methylation is a somewhat complex biochemical process in the body, the important thing to remember is that it is one of the ways epigenetic takes place and a process by which genes get turned on and off.

As a result of DNA methylation, there are variations in whether the same genes can be expressed in different organs and at different ages, and the amount of expression.

Cells become senescent as we age. That means they stop dividing and enter a kind of stasis. Instead of dying off as they normally would, they persist, but change shape and size andsecrete inflammatory molecules that cause other nearby cells to become senescent.

In an article published in Nature Reviews Genetics, Steve Horvath, a professor of human genetics and biostatistician at the University of California Los Angeles, concluded that as people age and have more senescent cells, there are characteristic changes in the methylation status of human DNA.

Human beings experience birth, aging, illness, and death, which is now discovered by our scientists to be controlled by our internal epigenetic clock. This is similar to the observations that everything in our universe has its cycle of formation, stasis, degeneration, and destruction.

Professor Horvath summarized the DNA methylation profiles associated with aging in an epigenetic clock of aging. While our years on Earth are are chronological age, how we live and inherent factors affect how long we will actually live, which is our biological age, or the age of our body. Biological ages can be estimated by using the methylation profiles of aging-related genes. In other words, scientists can focus in on genes linked to aging and then look at how those genes are methylating and from this gauge how far along the person is in that process of degeneration and death. These genetic focal points were carefully selected by scientists, independent of gender, body part, comorbidities, and other factors. And the results have been highly accurate, with a precision of over 95 percent in gauging a persons biological age.

Humans have a normal aging methylation curve. If a persons DNA methylation is above the curve, he or she will age faster than his or her peers; if it is below the curve, he or she will appear younger than his or her peers.

So, what factors can accelerate aging, i.e. epigenetic clock of aging?

A study conducted in Belgium was published in 2018 in the journal Aging. It found that the following factors accelerate epigenetic aging in humans:

This makes us wonder if COVID-19 infection can accelerate the epigenetic aging clock.

A study published in the journal Nature Communications answers this question. The study collected blood samples from 232 healthy individuals, 194 non-severe COVID-19 patients and 213 severe COVID-19 patients for DNA methylation analysis and found that the epigenetic age of COVID-19 patients was significantly accelerated.

In addition, the epigenetic age acceleration in COVID-19 patients is related to the stage of the disease. The age acceleration is fastest during the acute inflammatory phase, when the body and the virus are in intense combat; and it is slightly reversed during the recovery phase.

Even after the infection is over, many people still have symptoms of long COVID. Is this related to the aging caused by COVID-19?

Epigenetic aging is seen in the graying of hair and loosening of teeth. However, on a cellular level, cells in the human body also gradually age.

Cellular senescence refers to a state of cell cycle arrest when cells are stressed, as well as the secretion of various inflammatory cytokines at the same time. In a paper published in Nature Aging, a Japanese research team stated that senescent cells do not die immediately, but instead, they spread inflammatory cytokines to nearby uninfected cells, causing more cells to senesce as well.

So, what are the effects of cellular senescence on our health?

Cellular senescence plays an important role in many age-related diseases, such as degenerative diseases of the nerves, eyes, lungs, and heart.

The aforementioned study was conducted prior to the Omicron variant outbreak, and the Omicron variant is clearly less pathogenic than the old strain. In fact, some of the mutation sites of the Omicron variant counteracted the factors that caused cellular senescence. It is estimated that Omicron causes significantly less accelerated senescence or sequelae than the old strain.

However, the vaccines we are currently administering are still developed using the spike proteins of the old strain of early 2020, so is there a risk of accelerated aging?

The COVID-19 vaccines mainly express spike proteins in the human body. In a study published in the Journal of Virology in 2021, researchers from Saint Louis University in Missouri transfected spike proteins of the old strain into cells in vitro. It was later discovered that a large number of cellular senescence markers (including specific cytokines, interleukins, and specific enzymes, etc) were found in the spike-transfected cells, compared to the control group.

In addition, the spike proteins increase inflammatory factors, cause mitochondrial damage, produce misfolded proteins, and cause genomic instability, all of which accelerate cellular aging.

Reversing aging sounds like a dream come true for everyone. We have already understood so many mechanisms related to aging, so is it possible to find a way to slow down or even reverse aging?

In fact, our daily diet, work habits, and lifestyle all affect the epigenetic aging clock. For instance, during high-temperature cooking, red meat produces glycosylated end products, which are associated with cellular aging; poultry and fish are relatively healthy; and the vitamins in fruits and vegetables help keep cells young, which can help slow down or reverse the aging clock.

In addition, an article published in 2017 in the journal Psychoneuroendocrinology, American and French scholars investigated whether or not sitting in meditation affects the epigenetic aging clock.

The studys subjects were 18 individuals who had been meditating for at least 10 years and meditated for at least 30 minutes a day, and 20 non-meditators. They were divided into two groups: under and over 52 years of age, respectively. The researchers measured the DNA methylation in their blood cells for estimation of their epigenetic aging acceleration.

The results showed that the epigenetic aging acceleration increased in elderly non-meditators, while the acceleration in elderly meditators was more similar to that of younger people and was not affected by the epigenetic aging effect.

Gene expression is also associated with changes in our appearance, so meditators appear younger than their actual age. Furthermore, meditators also have younger brains.

The University of California Los Angeles and the Australian National University jointly published a study in 2016 in the journal NeuroImage. The studys subjects were 250 meditators and 50 non-meditators, both groups with an average age of 51.4 years.

The researchers analyzed and compared the brain ages of the two groups and found that the brain age of the meditators was younger than their actual age. For instance, 50-year-old meditators had the same brain age as a 42.5-year-old non-meditator, while 60-year-old meditators had the same brain age as the 51-year-old non-meditators in the control group.

Interestingly, for the meditators over 50, each additional year of their actual age would make their brain age one month and 22 days younger than their actual age.

In summary, damage caused by SARS-CoV-2 to the human body speeds up the human epigenetic clock of aging and dumbs down the brain. Vaccines based on the old strains in 2020 may also harm the human body in this regard.

At least 67 percent of the worlds people have now been vaccinated; will people in the future get older more quickly? No. It is too early to conclude anything based on cellular data alone rather than human studies. However, the cellular data is a clear reminder for us to take precautions to prevent this.

Meanwhile, it is quite worrisome that when we discussed this topic during a Health 1+1 live broadcast on July 12 2022, quite a few audience members had commented that they themselves or their friends or relatives had become obviously older after receiving the jabs.

The good news is that aging is a long process. During this process, for example, we can develop the habits of healthy living, including eating well, exercising,and daily meditation, which can help slow down or even reverse the aging process, and furthermore bring us various positive health benefits, which will be detailed in future articles.

Views expressed in this article are the opinions of the author and do not necessarily reflect the views of The Epoch Times. Epoch Health welcomes professional discussion and friendly debate. To submit an opinion piece, please follow these guidelines and submit through our form here.

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Mice Model Market Forecast to 2028 – COVID-19 Impact and Global Analysis By Type, Service, Technology, Indication, End User, Application, and Mode -…

Posted: July 27, 2022 at 2:49 am

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The mice model market is expected to grow from US$ 1,705. 70 million in 2022 to US$ 2,340. 90 million by 2028; it is estimated to grow at a CAGR of 5. 4% from 2022 to 2028. The growing usage of mice models in virology and infectious diseases and the rising consumption of personalized medicine are bolstering the growth of the mice model market.

New York, July 20, 2022 (GLOBE NEWSWIRE) -- Reportlinker.com announces the release of the report "Mice Model Market Forecast to 2028 - COVID-19 Impact and Global Analysis By Type, Service, Technology, Indication, End User, Application, and Mode" - https://www.reportlinker.com/p06295682/?utm_source=GNW Moreover, the rising advancements in gene editing tools are likely to emerge as a significant future trend in the mice model market during the forecast period.

However, various regulations and laws for the ethical use of animals in research are hampering the overall market growth.Scientists have used animals to model human diseases for over a hundred years.Mice are particularly useful for this because they share many of the same biological traits as humans and have over 80% identical genetic components to humans.

A mice model is a laboratory mouse used to study some aspect of human physiology or disease.Various model organisms are used in this regard, but mice are particularly useful because they share mammalian traits with humans and suffer from many of the same diseases as humans.

Many mice models have been created to target specific human diseases using selective breeding and genetic engineering.The use of mice models in disease research programs has contributed to significant medical breakthroughs.

Mice are the model of choice because they are strikingly similar to humans at the genomic level and the disease pathophysiology in mice is similar to humans. Mice models are an inexpensive and efficient tool to speed up research and drug testing. These features provide researchers with a powerful tool for understanding the mechanisms of human disease and for testing novel drug therapies.Mice models are essential tools to study the pathogenesis of infectious diseases and for the preclinical evaluation of vaccines and therapies against various human pathogens.The use of genetically defined inbred mouse strains, humanized mice, and gene knockout mice has enabled the research community to study the process of the way pathogens cause diseases, the role of specific host genes in controlling or promoting disease, and potential targets for prevention or identification of treatment for a variety of infectious agents.

With the emergence of new infectious diseases, the animal model has become a vital tool for studying disease mechanisms and developing therapeutics.Mice with xenografted human immune systems have been used to study the pathogenesis of various infectious agents, including Plasmodium falciparum (malaria), Mycobacterium tuberculosis, dengue virus, and influenza virus.

These models have been beneficial for studying HIV, including analyzing viral and host factors that promote viral replication, HIV interactions with the hosts immune response, and as platforms for testing therapeutic approaches to control or cure HIV infection.Mice models are an essential resource for studying the mechanisms underlying infectious disease pathogenesis and as platforms for testing potential vaccines and therapies.

Mice models are necessary for learning about infections from many human pathogens. They are widely used for preclinical screening of vaccines/therapies because of their high reproducibility, low cost, and ease of experimental manipulation.

Over the past century, advances in the development of vaccines, antibiotics/antivirals, and infection control measures have significantly reduced the public health burden of infectious diseases.However, there has been an increase in contagious viral diseases over the years.

In the past two decades, there have been three outbreaks of COVID-19SARS-CoV in 2002, MERS-CoV in 2012, and SARS-CoV-2 in 2019.However, the current SARS-CoV-2 is much more severe than the SARS-CoV in 2002 and has spread to more than 213 countries, affecting millions of people.

The emergence of the COVID-19 pandemic in 2019 has prompted animal models to study its pathology and develop an effective treatment.Aside from coronavirus studies, mice models are considered the best small animal models for hepatitis B virus (HBV), hepatitis C virus (HCV), Zika virus, and cytomegalovirus (CMV).

According to the WHO, over 17 million people die from infectious diseases yearly. Over the past two decades, over 30 new infectious diseases have emerged. As per the UNAIDS, 38 million people were affected by HIV at the end of 2019. Mice models have been widely used for various viral studies due to their small size, low cost, ease of use, and high reproducibility. Thus, the growing number of infectious disease is driving the mice model market.The mice model market is segmented into type, service, technology, indication, end user, application, and mode.Based on type, the market is segmented into inbred mice, outbred mice, genetically engineered mice, hybrid mice, surgically modified mice, and spontaneous mutant mice.

The inbred mice segment is estimated to account for the largest market share from 2022 to 2028.Mice Model Market OpportunitiesBasic research, safety assessment for large molecule therapeutics, simulation of a few human-specific infectious diseases, and efficacy testing of immunotherapy approaches all use humanized mice models.The human protein is expressed in cells and tissues while the mouse protein shows a different variability.

Humanized mice models are generally used to study cancer genetics, autoimmune diseases, regenerative medicine, human hematopoiesis, infectious diseases, transplantation, and autoimmunity.They enhance the translational value of preclinical research by enabling researchers to understand disease pathways in a better manner.

Both mice and human genes & proteins are examined for fidelity and structure to determine the optimal expression and functionality of the human protein in a mouse.Recent models also reflect hematopoiesis, natural immunity, neurobiology, and molecular signaling pathways that influence disease pathobiology.

These mice models also enable studies of human pathobiology, natural disease processes, and therapeutic efficacy across a broad spectrum of human diseases. Overall, humanized mice models offer low-cost, high-throughput studies of infection or degeneration in natural pathogen-host cells and the opportunity to test disease transmission and eradication.Humanized mice models have been xenografted with human cells or engineered to express human genes.These mice are used extensively to elucidate and understand human physiology and the etiology of human-specific infections.

Humanized mice models are used in biomedical research to develop therapeutics due to their numerous advantages, such as small size, high reproductive cycle, ease of handling, and increased genomic similarity to humans.These humanized mice models are essential in preclinical research studies because they mimic several human-specific diseases and can be used to study the efficacy and safety of immunotherapy approaches.

Humanized mice models have also been essential in designing and developing vaccines and antibody-based therapies for COVID-19.These models have developed since the onset of the COVID-19 outbreak, which further helped in providing a more profound and better understanding of the infection and the effectiveness of antiviral therapeutics and supported the development of efficient drugs and therapies to treat COVID-19 patients.

Due to the aforementioned factors, the humanized mice models will continue to be widely used in the coming years, thereby contributing to the mice model market growth.The World Health Organization (WHO), Centers for Disease Control and Prevention (CDC), Indian Council of Medical Research (ICMR), Occupational Safety and Health Administration (OSHA), Mutant Mouse Regional Resource Center (MMRRC), Food and Drug Administration (FDA), Canadian Council on Animal Care (CCAC), Centers for Personalized Medicine (CPM), and Organizations for Economic Co-operation and Development (OECD), are among the primary and secondary sources referred to while preparing the report on the mice model market.Read the full report: https://www.reportlinker.com/p06295682/?utm_source=GNW

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Mice Model Market Forecast to 2028 - COVID-19 Impact and Global Analysis By Type, Service, Technology, Indication, End User, Application, and Mode -...

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Flow Cytometry Market is expected to reach a value of USD 11467.80 Million by 2027, at a CAGR of 8.88% over the forecast period (2021 2027) – Digital…

Posted: July 27, 2022 at 2:48 am

Flow cytometry is a well-known method for identifying cells in solution, and it is most commonly used to examine peripheral blood, bone marrow, and other body fluids. Flow cytometry is used to identify and quantify immune cells, as well as to characterize haematological tumours. Increasing global incidence and prevalence of HIV/AIDS and cancer, increasing adoption of flow cytometry techniques in research and academia, expanding public-private initiatives in the fields of immunology and immuno-oncology research, technological advancements, and the increasing incorporation of AI platforms in flow cytometry workflows, and advancements in flow cytometry software are driving the flow cytometry markets growth. Flow cytometry has emerged as a critical tool for drug discovery and development safety and exploratory purposes. This tool is used throughout the research process, from pre-clinical trials to target identification and screening.

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Flow cytometry can analyze a large number of particles in a short amount of time and provide statistically reliable information about cell populations. These capabilities, combined with its multi-parametric approach, make flow cytometry more suitable for use in drug discovery and development processes in the pharmaceutical and biopharmaceutical industries. Furthermore, biomarker research has become an essential component of drug discovery and development. It provides valuable evidence to guide clinical decisions, evaluates drug pharmacodynamics, and assists with drug filings with regulatory bodies. This also boosts a drugs market value and accelerates the development process. Flow cytometry is widely used in biomarker research to monitor cell population development and differentiation, assess target engagement and biomarker expression in cells, and evaluate cell functions and signaling events. Furthermore, biomarker research has become an essential component of drug discovery and development. It provides valuable evidence to guide clinical decisions, evaluates drug pharmacodynamics, and assists with drug filings with regulatory bodies.

Read market research report, Global Flow Cytometry Market Segmented By Product (Instruments (Cell Analyzers, Cell Sorters), Reagents & Consumables, Software, Accessories, Services) By Technology (Cell-based, Bead-based) By Application (Research (Pharmaceutical (Drug Discovery, Stem Cell, In Vitro Toxicity), Apoptosis, Cell Sorting, Cell Cycle Analysis, Immunology, Cell Viability), Industrial, Clinical (Cancer, Organ Transplantation, Immunodeficiency, Hematology), By End-use (Commercial Organizations, Hospitals, Academic Institutes, Clinical Testing Labs) & By Region Forecast And Analysis 2021-2027 by SkyQuest

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Developing a novel effective reagent is a complex process that includes a variety of challenges such as variations in fluorochrome brightness and marker expression levels, issues with the stability of some fluorochromes, and optical background issues (due to significant emission spill over from non-primary fluorescent reagents) (Source: Becton, Dickinson, and Company White Paper). Provided this, it is reasonable to conclude that one of the major challenges that manufacturers face in the flow cytometry reagents market is the development of reagents (that have multicolour capabilities and provide high speed, sensitivity, and ease of use in flow cytometry processes).Maintenance costs and a variety of other indirect expenses increase the total cost of ownership of these instruments. As a result, high product installation costs and other related expenses impede optimal adoption of flow cytometry instruments in clinical and research applications, particularly in developing countries. Moreover, flow cytometry instruments are equipped with advanced features and functionalities, making them expensive. Countries such as China, Japan, India, and South Korea provide significant growth opportunities for major players in the global flow cytometry market. These opportunities for growth can be attributed to increased research initiatives across key countries, low regulatory barriers, continuous improvements in healthcare infrastructures, a growing patient population, rising healthcare expenditures, and the strengthening distribution networks of market leaders in these regions. To leverage on the growth opportunities in these countries, players in the flow cytometry market are increasingly focused on expanding their regional product offerings and enhancing their presence in emerging markets through various growth strategies such as expansions, partnerships, and collaborations, among others.

The prominent players in the flow cytometry market are Becton, Dickinson and Company, Danaher Corporation, Thermo Fisher Scientific, Inc., Agilent Technologies, Inc., and Luminex Corporation. These companies have adopted both organic and inorganic growth strategies, such as product launches and acquisitions, to maintain their leading positions in the flow cytometry market.The report published by SkyQuest Technology Consulting provides in-depth qualitative insights, historical data, and verifiable projections about market size. The projections featured in the report have been derived using proven research methodologies and assumptions.

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SkyQuest has segmented the Global Flow Cytometry Market based on Product, Technology, Application, End-Use and Region: Flow Cytometry Market By Product (Revenue, USD Million, 2021 2027)o Instruments Cell Analyzers Cell Sorterso Reagents & Consumableso Softwareo Accessorieso Services Flow Cytometry Market By Technology (Revenue, USD Million, 2021 2027)o Cell-basedo Bead-based Flow Cytometry Market By Application (Revenue, USD Million, 2021 2027)o Research Pharmaceutical Drug Discovery Stem Cell In Vitro Toxicity Apoptosis Cell Sorting Cell Cycle Analysis Immunology Cell Viabilityo Industrialo Clinical Cancer Organ Transplantation Immunodeficiency Hematology Flow Cytometry Market By End-use (Revenue, USD Million, 2021 2027)o Commercial Organizationso Hospitalso Academic Instituteso Clinical Testing Labs Flow Cytometry Market Regional Outlook (Revenue, USD Million, 2021 2027)o North America U.S. Canadao Europe Germany France UK Italy Spain Rest of Europeo Asia Pacific China India Japan Rest of Asia Pacifico Central & South America Brazil Rest of CSAo Middle East & Africa GCC Countries South Africa Rest of MEA

List of Key Players of Flow Cytometry Market

Becton, Dickinson and Company (US) Danaher Corporation (US) Thermo Fisher Scientific, Inc. (US) Luminex Corporation (US) Agilent Technologies, Inc. (US) Sony Group Corporation (Japan) Bio-Rad Laboratories, Inc. (US) Miltenyi Biotec GmbH (Germany) Enzo Biochem, Inc. (US) Sysmex Corporation (Japan) bioMrieux S.A. (France) Cytonome/ ST, LLC (US) Sartorius AG (Germany) Cytek Biosciences, Inc. (US) Union Biometrica, Inc. (US)About Us-

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Flow Cytometry Market is expected to reach a value of USD 11467.80 Million by 2027, at a CAGR of 8.88% over the forecast period (2021 2027) - Digital...

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Could Genetics Be the Key to Never Getting the Coronavirus? – The Atlantic

Posted: July 27, 2022 at 2:47 am

Last Christmas, as the Omicron variant was ricocheting around the United States, Mary Carrington unknowingly found herself at a superspreader eventan indoor party, packed with more than 20 people, at least one of whom ended up transmitting the virus to most of the gatherings guests.

After two years of avoiding the coronavirus, Carrington felt sure that her time had come: Shed been holding her great-niece, who tested positive soon after, and she was giving me kisses, Carrington told me. But she never caught the bug. And I just thought, Wow, I might really be resistant here. She wasnt thinking about immunity, which she had thanks to multiple doses of a COVID vaccine. Rather, perhaps via some inborn genetic quirk, her cells had found a way to naturally repel the pathogens assaults instead.

Carrington, of all people, understood what that would mean. An expert in immunogenetics at the National Cancer Institute, she was one of several scientists who, beginning in the 1990s, helped uncover a mutation that makes it impossible for most strains of HIV to enter human cells, rendering certain people essentially impervious to the pathogens effects. Maybe something analogous could be safeguarding some rare individuals from SARS-CoV-2 as well.

Read: America is running out of COVID virgins

The idea of coronaviral resistance is beguiling enough that scientists around the world are now scouring peoples genomes for any hint that it exists. If it does, they could use that knowledge to understand whom the virus most affects, or leverage it to develop better COVID-taming drugs. For individuals who have yet to catch the contagiona fast-dwindling proportion of the populationresistance dangles like a superpower that people cant help but think they must have, says Paula Cannon, a geneticist and virologist at the University of Southern California.

As with any superpower, though, bona fide resistance to SARS-CoV-2 infection would likely be very rare, says Helen Su, an immunologist at the National Institutes of Allergy and Infectious Disease. Carringtons original hunch, for one, eventually proved wrong: She recently returned from a trip to Switzerland and found herself entwined with the virus at last. Like most people who remained unscathed until recently, Carrington had done so for two and a half years through a probable combination of vaccination, cautious behavior, socioeconomic privilege, and luck. Its entirely possible that inborn coronavirus resistance may not even existor that it may come with such enormous costs that its not worth the protection it theoretically affords.

Of the 1,400 or so viruses, bacteria, parasites, and fungi known to cause disease in humans, Jean-Laurent Casanova, a geneticist and an immunologist at Rockefeller University, is certain of only three that can be shut out by bodies with one-off genetic tweaks: HIV, norovirus, and a malaria parasite.

The HIV-blocking mutation is maybe the most famous. About three decades ago, researchers, Carrington among them, began looking into a small number of people who we felt almost certainly had been exposed to the virus multiple times, and almost certainly should have been infected, and yet had not, she told me. Their superpower was simple: They lacked functional copies of a gene called CCR5, which builds a cell-surface protein that HIV needs in order to hack its way into T cells, the viruss preferred human prey. Just 1 percent of people of European descent harbor this mutation, called CCR5-32, in two copies; in other populations, the trait is rarer still. Even so, researchers have leveraged its discovery to cook up a powerful class of antiretroviral drugs, and purged the virus from two people with the help of 32-based bone-marrow transplantsthe closest that medicine has come to developing a functional HIV cure.

The stories with those two other pathogens are similar. Genetic errors in a gene called FUT2, which pastes sugars onto the outsides of gut cells, can render people resistant to norovirus; a genomic tweak erases a protein called Duffy from the walls of red blood cells, stopping Plasmodium vivax, one of several parasites that causes malaria, from wresting its way inside. The Duffy mutation, which affects a gene called DARC/ACKR1, is so common in parts of sub-Saharan Africa that those regions have driven rates of P. vivax infection way down.

In recent years, as genetic technologies have advanced, researchers have begun to investigate a handful of other infection-resistance mutations against other pathogens, among them hepatitis B virus and rotavirus. But the links are tough to definitively nail down, thanks to the number of people these sorts of studies must enroll, and to the thorniness of defining and detecting infection at all; the case with SARS-CoV-2 will likely be the same. For months, Casanova and a global team of collaborators have been in contact with thousands of people from around the world who believe they harbor resistance to the coronavirus in their genes. The best candidates have had intense exposures to the virussay, via a symptomatic person in their homeand continuously tested negative for both the pathogen and immune responses to it. But respiratory transmission is often muddied by pure chance; the coronavirus can infiltrate people silently, and doesnt always leave antibodies behind. (The team will be testing for less fickle T-cell responses as well.) People without clear-cut symptoms may not test at all, or may not test properly. And all on its own, the immune system can guard people against infection, especially in the period shortly after vaccination or illness. With HIV, a virus that causes chronic infections, lacks a vaccine, and spreads through clear-cut routes in concentrated social networks, it was easier to identify those individuals whom the virus had visited but not put down permanent roots within, says Ravindra Gupta, a virologist at the University of Cambridge. SARS-CoV-2 wont afford science the same ease of study.

Read: Is BA.5 the reinfection wave?

A full analogue to the HIV, malaria, and norovirus stories may not be possible. Genuine resistance can manifest in only so many ways, and tends to be born out of mutations that block a pathogens ability to force its way into a cell, or xerox itself once its inside. CCR5, Duffy, and the sugars dropped by FUT2, for instance, all act as microbial landing pads; mutations rob the bugs of those perches. If an equivalent mutation exists to counteract SARS-CoV-2, it might logically be found in, say, ACE2, the receptor that the coronavirus needs in order to break into cells, or TMPRSS2, a scissors-like protein that, for at least some variants, speeds the invasive process along. Already, researchers have found that certain genetic variations can dial down ACE2s presence on cells, or pump out junkier versions of TMPRSS2hints that there could be tweaks that further strip away the molecules. But ACE2 is very important to blood-pressure regulation and the maintenance of lung-tissue health, said Su, of NIAID, whos one of many scientists collaborating with Casanova to find SARS-CoV-2 resistance genes. A mutation that keeps the coronavirus out might very well muck around with other aspects of a persons physiology. That could make the genetic tweak vanishingly rare, debilitating, or even, as Gupta put it, not compatible with life. People with the CCR5-32 mutation, which halts HIV, are basically completely normal, Cannon told me, which means HIV kind of messed up in choosing CCR5. The coronavirus, by contrast, has figured out how to exploit something vital to its hostan ingenious invasive move.

The superpowers of genetic resistance can have other forms of kryptonite. A few strains of HIV have figured out a way to skirt around CCR5, and glom on to another molecule, called CXCR4; against this version of the virus, even people with the 32 mutation are not safe. A similar situation has arisen with Plasmodium vivax, which we do see in some Duffy-negative individuals, suggesting that the parasite has found a back door, says Dyann Wirth, a malaria researcher at Harvards School of Public Health. Evolution is a powerful strategyand with SARS-CoV-2 spewing out variants at such a blistering clip, I wouldnt necessarily expect resistance to be a checkmate move, Cannon told me. BA.1, for instance, conjured mutations that made it less dependent on TMPRSS2 than Delta was.

Read: The BA.5 wave is what COVID normal looks like

Still, protection doesnt have to be all or nothing to be a perk. Partial genetic resistance, too, can reshape someones course of disease. With HIV, researchers have pinpointed changes in groups of so-called HLA genes that, through their impact on assassin-like T cells, can ratchet down peoples risk of progressing to AIDS. And a whole menagerie of mutations that affect red-blood-cell function can mostly keep malaria-causing parasites at baythough many of these changes come with a huge human cost, Wirth told me, saddling people with serious clotting disorders that can sometimes turn lethal themselves.

With COVID-19, too, researchers have started to home in on some trends. Casanova, at Rockefeller, is one of several scientists who has led efforts unveiling the importance of an alarm-like immune molecule called interferon in early control of infection. People who rapidly pump out gobs of the protein in the hours after infection often fare just fine against the virus. But those whose interferon responses are weak or laggy are more prone to getting seriously sick; the same goes for people whose bodies manufacture maladaptive antibodies that attack interferon as it passes messages between cells. Other factors could toggle the risk of severe disease up or down as well: cells ability to sense the virus early on; the amount of coordination between different branches of defense; the brakes the immune system puts on itself, so it does not put the hosts own tissues at risk. Casanova and his colleagues are also on the hunt for mutations that might alter peoples risk of developing long COVID and other coronaviral consequences. None of these searches will be easy. But they should be at least simpler than the one for resistance to infection, Casanova told me, because the outcomes theyre measuringserious and chronic forms of diseaseare that much more straightforward to detect.

If resistance doesnt pan out, that doesnt have to be a letdown. People dont need total blockades to triumph over microbesjust a defense thats good enough. And the protection were born with isnt all the leverage weve got. Unlike genetics, immunity can be easily built, modified, and strengthened over time, particularly with the aid of vaccines. Those DIY defenses are probably what kept Carringtons case of COVID down to a mild course, she told me. Immune protection is also a far surer bet than putting a wager on what we may or may not inherit at birth. Better to count on the protections we know we can cook up ourselves, now that the coronavirus is clearly with us for good.

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Could Genetics Be the Key to Never Getting the Coronavirus? - The Atlantic

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Noonan appointed Kent Professor of Genetics and Professor of Neuroscience – Yale News

Posted: July 27, 2022 at 2:47 am

James Noonan

James Noonan, who has made critical and novel contributions to the fields of human evolutionary genetics and neurodevelopment, was recently appointed the Albert E. Kent Professor of Genetics and Professor of Neuroscience, effective immediately.

Noonan received his B.S. in biology and English literature from the State University of New York at Binghamton in 1997, and his Ph.D. in genetics from Stanford University School of Medicine in 2004. He completed a postdoctoral fellowship in the Genomics Division at Lawrence Berkeley National Laboratory from 2004 to 2007. In 2007, he was recruited to Yale as assistant professor and was promoted to associate professor in 2013, and professor in 2021. He has a secondary appointment in Yales Department of Neuroscience.

Noonans research program is focused on deciphering the role of gene regulatory changes in the evolution of uniquely human traits. This work addresses a central hypothesis in human evolution, proposed more than 40 years ago: that changes in the level, timing, and location of gene expression account for biological differences between humans and other primates. Noonan has discovered thousands of human-specific genetic changes that alter gene expression and regulation, and by pioneering novel genetic models, his lab has begun to reveal how human-specific regulatory changes alter developmental traits. His work has provided key insights into the genetic origins of human biological uniqueness and has driven the rise of a new field: human evolutionary developmental biology.

Noonans seminal research discovered two classes of gene regulatory elements implicated in human evolution. The first are Human Accelerated Regions (HARs), which encode transcriptional enhances which are highly conserved across species and show many human-specific sequence changes (Science 2006, Science 2008). Using humanized mouse models, he has shown that HARs alter developmental gene expression and drive the evolution of novel phenotypes. As an example, he recently showed that one HAR altered expression of a transcription factor that has a role in limb development, possibly contributing to changes in skeletal patterning in human limb evolution (Nature Communications, 2022). These findings provide mechanistic insight into how HARs modified gene expression in human evolution. Using massively parallel assays, he has also comprehensively characterized the effect of thousands of human-specific sequence changes in HARs on their activity during neurodevelopment (Proceedings of the National Academy of Sciences, 2021)

He also identified thousands of human-specific changes in enhancer activity by direct analysis of developing human and nonhuman tissues. These loci, termed Human Gain Enhancers (HGEs), have gained activity in the developing human limb (Cell, 2013) and cerebral cortex (Science, 2015). These studies identified the biological pathways in limb and cortical development likely altered by human-specific regulatory changes, providing the basis for understanding their effects using genetic and experimental models.

Noonan has also contributed substantially to the educational programs of Yale School of Medicine, revolutionizing its graduate training landscape and empowering experimental genetics research across many labs at Yale. He designed the first course in genomics in the medical school more than 12 years ago, serving hundreds of students and faculty with the skills required to excel at the frontier of modern biomedical science. His training efforts have helped to set the standards of genomic research at Yale and ensured that the university remains a world leader in genomics.

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Noonan appointed Kent Professor of Genetics and Professor of Neuroscience - Yale News

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