Study finds genetic link between driving convictions, accidents and everyday behavior – News-Medical.Net

A new long-term psychological study of drivers has found an association between driving convictions, accidents and everyday behaviour such as eating junk food or alcohol consumption. The researchers have also uncovered evidence that this relationship is associated with genetic variation in serotonin metabolism the same neurotransmitter targeted by many antidepressants. This suggests that risky behaviour in driving and in life may have a common psychological basis.

In an innovative study, researchers from Professor Jaanus Harro's team at the University of Tartu (Estonia) combined psychological, genetic, and biochemical data from the unique Estonian Psychobiological Study of Traffic Behaviour with police and insurance records. 817 drivers (49.2% male, 50.8% female) participated in the study. Over a period of time they completed questionnaires to measure such factors as impulsivity and aggression: in addition, they underwent a series of blood tests and genetic analysis. Linking these results to the police and insurance databases the researchers began to uncover some of the links associated with risky driving. Presenting their findings to the ECNP Conference in Lisbon, they report that 137 drivers who had been cautioned for exceeding the speed limits tended to have faster reaction times, but that they also scored higher on physical and verbal aggression, undertaking more strenuous physical activity, and had higher consumption of junk foods (including energy drinks).

According to lead researcher Tnis Tokko:

"We were able to pick out lots of associations between everyday risk taking and risky driving. For example we found that subjects who drink energy drinks at least once a week were twice as likely to speed as those who didn't drink energy drinks as often. We think the energy drink consumption may be a related to a need for excitement, rather than the drinks themselves being a direct cause of traffic violations; the drivers' underlying psychological makeup may lead them both to speed, and to want to consume more energy drinks or junk food. Similarly, our psychological tests showed us that those with fast decision making skills were 11% more likely to speed, and those with higher excitement seeking were 13% more likely to speed".

He continued:

"Driving history is an excellent platform to study behavioural regulation; most people drive, and driving convictions or accidents are objective records - they remain in databases. We found that significant associations exist between risky traffic behaviour and a range of lifestyle behaviours, such as undertaking strenuous exercise, alcohol consumption, or junk food and energy drink consumption.

The researchers also looked at genetic traits in the volunteer drivers. They found that certain variants of a gene which controls serotonin transport (the 5-HTTLPR polymorphism) were associated with risky driving. Serotonin is the neurotransmitter which is thought to be involved in depression, and which is also regulated by many antidepressant drugs. "We found that certain gene variants are associated with risk-taking behaviour in both driving and in other areas of life; but this is an early finding and still needs to be confirmed" said Tnis Tokko.

The Estonian Psychobiological Study of Traffic Behaviour is a long-term study that started collecting data in 2001 it is believed to be the world's only long-term study to follow drivers while considering psychology, and the related biology. Initially it aimed to identify behaviour patterns of drunk drivers and speeding drivers to try to prevent these behaviours, but it has since expanded to consider other factors.

Tnis Tokko said "We are able to follow various driving-related factors over a period of years, including psychological behaviour, blood tests to understand biological changes, and genetics. We also have a firm idea of which of these drivers have committed traffic violations or have been in accidents. We believe this to be a unique system. This study shows that people who are reckless in traffic also tend to take chances in other areas of life, and our research shows that there may be a biological tendency to this behaviour".

Dr Oliver Grimm, senior psychiatrist at the University Clinic Frankfurt, commented:

"This study is very interesting, as it is already known from large registry studies that ADHD and traffic accidents are more common in adults. This specific study from Estonia now helps to better understand how this accident-prone group is constituted from both the genetic risk and personality traits."

Professor Oliver Howes, Professor of Molecular Psychiatry at King's College, London, said:

"This study adds to other work showing that psychological and biological traits are linked to how people behave in the world. It's important to recognise that the associations don't mean that one leads to the other"

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Study finds genetic link between driving convictions, accidents and everyday behavior - News-Medical.Net

The Multiple System Atrophy Coalition Announces a Groundbreaking Project to Explore the Genetics of MSA – Johnson City Press (subscription)

MCLEAN, Va., Oct. 1, 2021 /PRNewswire-PRWeb/ --The Multiple System Atrophy ("MSA") Coalition announces a ground-breaking million-dollar multi-year collaborative project focused on exploring the genetics of up to 1,200 people with either a diagnosis of probable MSA, in the case of living patients, or postmortem pathological confirmation of multiple system atrophy, aimed at locating commonalities in their genes that might contribute to the development of multiple system atrophy. The aim of this collaborative study is to sequence and organize the genomes of existing genetic samples as well as to organize previously sequenced whole-genome data into a single database that is accessible to researchers worldwide. While many researchers have looked at the genetics of MSA, this will be the first time such a large number of genomes from ethnically diverse populations have been sequenced and organized in such a way as to facilitate thorough analysis and collaborative enterprise.

"MSA is not typically passed from parent to child, except in extremely rare cases. However, there are still important clues about the underlying cause of MSA that can be found by examining the genetic code of a large population of MSA patients and looking for commonalities. Because MSA is a such a rare disease, there is a need for multiple researchers to work together and pool their data. Until now there has not been a concerted effort among genetic labs to combine these rare genetic samples from MSA patients with diverse backgrounds into a large, shared database," said Pam Bower, chair of the MSA Coalition's research committee. "The MSA Coalition is proud to be the driver of this ground-breaking study."

University of Florida will perform genetic sequencing under the direction of Matt Farrer, PhD, while storage, analysis and visualization of data will occur at Harvard Medical School in the Clinical Genome Analysis Platform ("CGAP") under the direction of Dana Vuzman, PhD. Additional genomic information will be provided by University College of London, Queen Square Institute of Neurology under the direction of Henry Houlden, MBBS, MRCP, PhD; by Translational Genomics Research Institute (TGen) under the direction of Matt Huentelman, PhD (Funded in part by the Rex Griswold Foundation, a grant from the NIH NINDS (R21-NS093222, PI: Huentelman), and through institutional support of TGen.); and by Seoul National University, under the direction of Beomseok Jeon, MD, PhD and Han-Joon Kim, MD, PhD. The Core G team also plans to coordinate their work with that being done at NIH under the direction of Sonja Scholz, MD, PhD. The group, collectively known as "Core G" (Genetics), will work closely with Vik Khurana, MD, PhD, board member and Scientific Liaison of the Board of Directors of the MSA Coalition and Chief of the Movement Disorders Division at Brigham and Women's Hospital and Harvard Medical School. Dr. Khurana will endeavor to integrate Core G team-member efforts more broadly into the MSA Collaborative Cores Initiative sponsored by the Coalition that will seed fund additional projects over time.

"I am thrilled that after years of planning and deliberation that Core G is funded and ready to go," said Khurana. "This group of terrific researchers, together with their expertise, bring precious patient samples from three continents to establish a foundation upon which other collaborations and initiatives will be built. We are under no illusion that the genetics of MSA will prove challenging, no less than a moonshot. At the same time, genetic insights promise to unlock powerful hypothesis-driven science that can find cures. And so, this moonshot is worth the effort and has been structured to be collaborative, open and sustainable in the long-term."

"We are incredibly proud of assembling this group of world-renowned researchers to collaborate on this project. It has taken almost three years to organize this project and obtain consents from all the institutions involved. Great care has been taken by all contributing institutions to safeguard the privacy of the patients and anonymize the genetic materials, so that patient privacy is protected," said Cynthia Roemer, MSA Coalition board chair. "We are also grateful to our many donors, who have made this project possible, and to the patients we have lost to MSA who generously left bequests to the MSA Coalition to further critical research like this. We quite literally could not do it without them!"

Dana Vuzman, PhD is an Instructor of Medicine at Harvard Medical School and the Director of Genomic Platform Development at DBMI. Dr. Vuzman oversees the implementation of the Clinical Genome Analysis Platform (CGAP) and the Single Cell RNA Platform in the Department. Prior to joining DBMI, she served as Chief Informatics Officer at One Brave Idea, Sr. Director of Biomedical Informatics at KEW, Inc., and Co-Director at Brigham Genomic Medicine. Dr. Vuzman earned her PhD in Computational Biology from the Weizmann Institute of Science in Israel and completed her postdoctoral training in Computational Genetics at Brigham and Women's Hospital and Harvard Medical School.

Matt Farrer, PhD is critically acclaimed for his work in the genetics and neuroscience of Parkinson's disease. His inspiration to apply genetic analysis to complex neurologic disorders came from early work as a care assistant of patients and families with neurologic and psychiatric disorders. Dr. Farrer earned his first degree in Biochemistry with a Doctoral degree in Molecular and Statistical Genetics from St. Mary's Hospital Medical School, UK. He completed a fellowship in Medical Genetics at the Kennedy-Galton Centre, UK and in Neurogenetics at Mayo Clinic. Dr. Farrer became an Assistant Professor of Molecular Neuroscience in 2000 where he opened his first laboratory to predict and prevent Parkinson's disease. Dr. Farrer became a tenured professor in 2006, a Mayo Consultant, and subsequently, a Distinguished Mayo Investigator. In 2010, Dr. Farrer was awarded a Canada Excellence Research Chair to build the Centre for Applied Neurogenetics and Neuroscience at the University of British Columbia, Vancouver, Canada where he became a Professor of Medical Genetics. The Province of British Columbia subsequently awarded him the Don Rix Chair in Precision Medicine, and his team had many notable accomplishments including several new genes and mouse models for Parkinson's disease. The team also implemented high-throughput sequencing in pediatric seizure disorders and neonatology in clinical service. The former was funded through the Medical Services Plan of British Columbia and was a first for Canada.

In 2019, Dr. Farrer accepted an endowed chair at the Norman Fixel Institute for Neurological Diseases (thanks to a generous endowment from the Lauren and Lee Fixel Family Foundation). Dr. Matt Farrer also directs the UF Clinical Genomics Program. As such he currently has appointments and affiliations in the UF College of Medicine's Neurology and Pathology Departments, Clinical and Translational Science Institute, the Evelyn F. and William L. McKnight Brain Institute, the Center for Translational Research in Neurodegenerative Disease, and the Center for Neurogenetic in addition to the Norman Fixel Institute for Neurological Diseases.

Henry Houlden, MBBS, MRCP, PhD: Dr. Houlden is a professor of neurology and neurogenetics in the Department of Neuromuscular Disease, University College, London, Queen Square Institute of Neurology, and undertakes research laboratory works on neurogenetics and movement disorders with a particular interest in rare diseases that are adult or childhood-onset, such as multiple system atrophy (MSA), spinocerebellar ataxia and other movement disorders, inherited neuromuscular conditions, and difficult to diagnose disorders, particularly in diverse and underrepresented populations. He assists with the integration of new gene discovery with exome and genome sequencing identifying disease genes such as CANVAS, NARS1, NKX-6.2, SCA11, SCA15, GRIA2, and GAD1, with functional experimental validation in human tissue and other model systems. Dr. Houlden has clinical expertise in inherited neurological disorders and movement disorders such as multiple system atrophy, ataxia, leukodystrophy, epilepsy and paroxysmal conditions, spastic paraplegia and neuromuscular conditions.

Matt Huentelman, PhD: Dr. Huentelman's research interests center around the investigation of the "-omics" (genomics, transcriptomics, and proteomics) of neurological traits and disease. His laboratory's overarching goal is to leverage findings in these disciplines to better understand, diagnose, and treat human diseases of the nervous system.

Dr. Huentelman joined TGen in July of 2004 after completing his doctoral work at the University of Florida's Department of Physiology and Functional Genomics at the McKnight Brain Institute where he investigated the application of gene therapy in the study and prevention of hypertension. His undergraduate degree is in Biochemistry from Ohio University's Department of Chemistry and Biochemistry at Clippinger Laboratories. Dr. Huentelman's career includes visiting researcher stints in Moscow, Russia at the MV Lomonosov Moscow State University "Biology Faculty" and in the United Kingdom within the University of Bristol's Department of Physiology.

Beomseok Jeon, MD, PhD: Professor Jeon is the medical director of the Movement Disorder Center, Seoul National University Hospital and is interested in genetics of Parkinsonism and medical and surgical treatment of advanced Parkinson's Disease.

Dr. Jeon earned his undergraduate, MD and PhD degrees from Seoul National University. His clinical interests include Parkinson's disease and other movement disorders including tremor, ataxia, dystonia, and chorea. His research focuses on the role of genetics in movement disorders, especially in the Korean population. He has established a DNA bank of thousands of Korean patients with movement disorders and normal controls. He is also involved in treatment of advanced Parkinson disease, and works with neurosurgical colleagues for various surgical treatment.

Han-Joon Kim, MD, PhD: Dr. Kim is a Professor in the Department of Neurology and the Movement Disorder Center at Seoul National University Hospital, Seoul, Korea. After graduation from the Medical College of Seoul National University in 1997, Dr. Kim took an internship and residency in neurology at Seoul National University Hospital (SNUH) where he became a Movement Disorder Specialist.

Clinically, Dr. Kim has experience with patients with various movement disorders including Parkinson's Disease (PD), Multiple System Atrophy (MSA), other atypical Parkinsonisms, and ataxias. Notably, Dr. Kim has set up a large registry of Korean MSA patients, which will serve as a basis for both observational and interventional studies in this rare disease.

Sonja W. Scholz, MD, PhD: Dr. Scholz is a Neurologist and Neurogeneticist specialized in movement and cognitive disorders. She received her medical degree from the Medical University Innsbruck, Austria. Following graduation, she was a post-doctoral fellow at the Laboratory of Neurogenetics at the NIH's National Institute on Aging (NIA) under the supervision of Drs. Andrew Singleton and John Hardy. She obtained a Ph.D. in Neurogenomics from the University College London, UK in 2010. She then moved to Baltimore to complete her neurology residency training at Johns Hopkins. In 2015, Dr. Scholz received the McFarland Transition to Independence Award for Neurologist-Scientists. She is a Lasker Clinical Research Tenure Track Investigator within the Neurogenetics Branch at the NIH's National Institute of Neurological Disorders and Stroke (NINDS). Her laboratory focuses on identifying genetic causes of neurodegenerative diseases, such as dementia with Lewy bodies, multiple system atrophy, and frontotemporal dementia.

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The Multiple System Atrophy Coalition Announces a Groundbreaking Project to Explore the Genetics of MSA - Johnson City Press (subscription)

Northwesterns SPORE has made advances in understanding the genetic basis of glioblastoma – News-Medical.Net

Glioblastoma is one of the deadliest cancers known to man. While the advent of immunotherapy and other cutting-edge treatments have prolonged life for people afflicted with other types of cancer, the prognosis for glioblastoma has remained relatively constant: just 18 months.

That year-and-a-half can be brutal: bombarding the brain with radiation in an attempt to crush the cancer into submission, often with little success. Glioblastoma is notoriously resistant to therapy, quickly adapting and roaring back with deadly results.

The SPORE is led by Matt Lesniak, MD, chair of Neurological Surgery and the Michael J. Marchese Professor of Neurosurgery, and C. David James, PhD, professor emeritus of Neurological Surgery.

It's not an exaggeration to say that nearly every glioblastoma patient will, unfortunately, succumb to the cancer. It is, in nearly all cases, incurable."

C. David James, PhD, Professor Emeritus of Neurological Surgery

The lethality of glioblastoma and the paucity of effective treatments is what spurred Maciej Lesniak, MD, chair and Michael J. Marchese Professor of Neurosurgery, along with James, to apply for the Specialized Program of Research Excellence (SPORE) grant from the National Cancer Institute, to be awarded to the Robert H. Lurie Comprehensive Cancer of Northwestern University. They didn't do this alone: The 2017 arrival of renowned neuro-oncologist Roger Stupp, MD, the Paul C. Bucy Professor of Neurological Surgery and chief of Neuro-Oncology in the Department of Neurology, bolstered the glioblastoma expertise at Northwestern, and his continued leadership has been a tremendous boon to the program, Lesniak said.

Northwestern's Brain Tumor SPORE part of the Lurie Cancer Center is now three years old, and the bench to bedside process is producing results. Under the leadership of Lesniak and James, the SPORE has made advances in understanding the genetic basis of the disease and developed potential therapies that reduce treatment resistance and clinical trials using immunotherapies. The SPORE philosophy of collaboration and team science under one roof is alive and well.

Since The Cancer Genome Atlas (TCGA) published its landmark 2008 analysis of the genetics of glioblastoma, scientists such as Alexander Stegh, PhD, associate professor in the Ken and Ruth Davee Department of Neurology Division of Neuro-Oncology, have used that roadmap to guide their research.

"The TCGA gave us this 'periodic table' of genes that are deregulated in glioblastoma," said Stegh, who is also an associate professor of Medicine in the Division of Hematology and Oncology.

Alexander Stegh, PhD, associate professor in the Ken and Ruth Davee Department of Neurology Division of Neuro-Oncology, focuses on genetic deregulation that contributes to therapy resistance in glioblastoma.

While some cancers have oncogene activations that are relatively simple to single out, there's an emerging understanding that glioblastoma is caused by variants of many genes. This is why previous attempts at therapies targeting single genes failed, such as those targeting alterations of the EGFR gene, and why Stegh focuses on genetic deregulation that contributes to therapy resistance.

"Rather than going in there with the very ambitious goal of identifying multiple genes and dialing down their expression levels, we take a slightly different approach: How can we specifically downregulate genes that cause therapy resistance, as an adjuvant therapeutic approach," Stegh said.

Stegh has published several papers identifying important genes implicated in glioblastoma therapy resistance, but one gene, called Bcl2L12, was found to be especially amenable to therapeutic delivery.

Combining his genetic expertise with the nanotechnology expertise of Chad Mirkin, PhD, professor of Medicine in the Division of Hematology and Oncology; and the clinical trial expertise of Priya Kumthekar, MD, '08 '11 '12 GME, associate professor of Neurology in the Division of Neuro-oncology, the investigators designed a spherical nucleic acid drug that crossed the blood-brain barrier and primed tumor cells for death.

The trial, published in Science Translational Medicine, was the first of its kind to show that a nano-therapeutic crossed the blood-brain barrier and into brain tumor cells in patients.

"This unique 3D design has the ability to infiltrate tumor cells to correct the genes inside and make them susceptible for therapy-induced killing," Stegh said.

Bcl2L12 was initially identified as a treatment target by Stegh in 2007. "To go from identifying this gene during my postdoctoral work, to get to the point of actually targeting it and establishing proof-of-concept in patients, it's very gratifying," Stegh said. "We are looking forward to building on this success."

A recurrent obstacle in glioblastoma treatment is the blood-brain barrier. Efforts to develop treatments beyond simple chemotherapy are often stymied by the selective permeability of the barrier, but projects in the SPORE are using emerging technologies to break through. Beyond the project using SNA's, a group of investigators led by Lesniak used stem cell "shuttles" to deliver immunotherapy directly to the tumor site.

Neural stem cells have an affinity for the brain, often traveling to areas of injury. Taking advantage of this travel pattern, investigators modified neural stem cells to produce an oncolytic virus, which targets cancer cells and jump-starts the body's immune response.

The phase I clinical trial, published in The Lancet Oncology, found that this approach was safe and tolerable for patients, and even showed signs that the treatment may improve progression-free and overall survival.

"This is the first-in-human clinical trial to test the neural stem cell delivery of an engineered oncolytic adenovirus," Lesniak said.

Roger Stupp, MD, the Paul C. Bucy Professor of Neurological Surgery, and Priya Kumthekar, MD, '11 '12 GME, associate professor in the Ken and Ruth Davee Department of Neurology Division of Neuro-Oncology, were co-authors of the study published in Brain. Atique Ahmed, PhD, associate professor of Neurological Surgery, was senior author.

This emphasis on results or clinical trials testing therapies is what unites all members of the Brain Tumor SPORE. Kumthekar, who has a hand in nearly all clinical trials coming out of the SPORE, chalks up their success to two things: planning and people.

"When we are testing drugs in the pre-clinical phase, we are planning the early clinical phase I. When we are in phase I, we are planning phases II and III," Kumthekar said. "We are always planning the next phase with the goal to get drugs that work to patients as fast as possible."

Further, the wealth of bright minds within the Lurie Cancer Center have made collaboration seamless and stimulating for participating faculty. From her work with Stegh and Mirkin, to pre-clinical work with Atique Ahmed, PhD, associate professor of Neurological Surgery, the greatest resource of the Brain Tumor SPORE has been its people, Kumthekar said.

One collaborative project between Kumthekar, Ahmed and Stupp, found that a drug currently used to prevent organ rejection in transplant patients could also reduce chemotherapy resistance in glioblastoma. Published in Brain, investigators found this drug blocks one molecular synthesis pathway used by cancer cells being treated with radiation therapy; when unable to create molecules essential for DNA synthesis, the cancerous cells are more likely to succumb to the therapy and die.

Back-and-forth collaboration between Kumthekar and Ahmed bringing clinical trial and laboratory expertise together is part of why this drug was selected by the Alliance for Clinical Trials in Oncology, part of the National Clinical Trials Network (NCTN). As a lead academic participating site, Lurie Cancer Center provides scientific leadership in the development and conduct of clinical research within the NCTN, and planning for the phase I trial at Northwestern is already in full swing. A potential phase III trial could be at several alliance network locations around the U.S., according to Kumthekar.

"The field is very interested in drug repurposing right now, and this helps us speed availability of drugs to patients," Kumthekar said.

The end goal of patient care is what unites all members of the SPORE from laboratory-based scientists to clinical trial experts and as these therapies march forward through the lengthy process of clinical trial evaluation, some scientists are hopeful that better treatments are just around the corner.

"Over the last ten to fifteen years, our body of knowledge about the molecular characteristics of glioblastoma has increased tremendously," James said. "As we take the information generated by dozens, if not hundreds of labs and analyze individual patient tumors to determine characteristics that can be targeted with specific therapies, I think we will begin to see more rapid progress in effective treatment of this cancer."

Lesniak, James, Stupp, Stegh, Mirkin, Kumthekar and Ahmed are members of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University and part of the Lou and Jean Malnati Brain Tumor Institute at the Lurie Cancer Center. Lesniak is director of neuro-oncology at the Lurie Cancer Center. Lesniak and James are principal investigators of Lurie Cancer Center's Brain Tumor SPORE.

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Opportunities in the Animal Genetics Market to 2026: Asia Pacific Set to Witness Rapid Growth in – GlobeNewswire

Dublin, Sept. 30, 2021 (GLOBE NEWSWIRE) -- The "Global Animal Genetics Market Research Report: Forecast (2021-2026)" report has been added to ResearchAndMarkets.com's offering.

The global animal genetics market is likely to grow at a CAGR of 6.4% in the forecast period of 2021-26 due to the surging advancements in continuous genetic alteration practices resulting in the growing production of animals with modified breeds and massive investments by numerous end-user industries. Animal producers are gaining huge milk & meat production by leveraging the technology of animal genetic alterations. With the help of strategic breeding, farmers can yield more substantial gains, which shall expand the end-user base and the overall market growth.

Based on the Animal Type, the Poultry segment registered the fastest market growth. It accounted for higher than USD 1.4 billion in recent years and is likely to continue the pace. The prominent factors for the market growth are the rise in the requirement for better quality food products, like meat, eggs & milk, and the flooding population & urbanization across regions. Hence, it shall continue to propel the demand and attain the fastest market growth in the forecast period.

Based on the Animal Type, the Canine segment in the animal genetics market shall attain the largest market share in the forecast years. It owes to the rapidly increasing research for high-quality breeding among dogs. Furthermore, the genetic research on canines is expanding the discovery of diverse genes implicating in the size, personality traits, and fur color. These factors are leading to the exponential demand for animal genetics to enhance the overall market share., states the author in their research report, "Global Animal Genetics Market Analysis, 2021."

Various microeconomic and macroeconomic characters are burgeoning exponential extensions for the APAC market. Factors like high population density and urban sprawl are enduring the demands of food producers to satisfy nutritional needs by increasing livestock production. Moreover, the animal healthcare ecosystem has been on a constant development path and is creating several opportunities for market leaders to bring effective testing procedures.

The Global Animal Genetics Market has a vast opportunity due to the constant launches and developments of new products and strategies. Various companies adopt these practices to extend their brand and product globally in the animal genetics industry.

With the swiftly surging population, their main objective is to meet the growing demands of different people. Moreover, producers operating in the market adopted different approaches of product innovation to cater to the rapidly changing customer demands.

Key Questions Answered in the Market Research Report:1. What are the overall market statistics or market estimates (Market Overview, Market Size- By Value, Forecast Numbers, Market Segmentation, Market Shares) of the Global Animal Genetics Market?2. What is the region-wise industry size, growth drivers, and challenges?3. What are the key innovations, opportunities, current & future trends, and regulations in the Global Animal Genetics Market?4. Who are the key competitors, their key strengths & weaknesses, and how do they perform in the Global Animal Genetics Market based on the competitive benchmarking matrix?5. What are the key results derived from the market surveys conducted during the Global Animal Genetics Market study?

Key Topics Covered:

1. Introduction

2. Preface

3. Executive Summary

4. Impact of COVID-19 on Global Animal Genetics Market

5. Global Animal Genetics Market Trends & Insights

6. Global Animal Genetics Market Dynamics

7. Global Animal Genetics Market Hotspots & Opportunities

8. Global Animal Genetics Market Regulations & Policy

9. Global Animal Genetics Market Outlook, 2016- 2026F

10. North America Animal Genetics Market Outlook, 2016-2026F

11. South America Animal Genetics Market Outlook, 2016-2026F

12. Europe Animal Genetics Market Outlook, 2016-2026F

13. Middle East & Africa Animal Genetics Market Outlook, 2016-2026F

14. Asia Pacific Animal Genetics Market Outlook, 2016-2026F

15. Key Strategic Imperatives for Success and Growth

16. Competition Outlook

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/sjxkme

About ResearchAndMarkets.comResearchAndMarkets.com is the world's leading source for international market research reports and market data. We provide you with the latest data on international and regional markets, key industries, the top companies, new products and the latest trends.

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Opportunities in the Animal Genetics Market to 2026: Asia Pacific Set to Witness Rapid Growth in - GlobeNewswire

The Jackson Laboratory appoints Dr. Lon Cardon as its next president and chief executive officer – Yahoo Finance

Lon Cardon, Ph.D., FMedSci

The Jackson Laboratory, an independent, nonprofit biomedical research institution, today announced the appointment of Lon Cardon, Ph.D., FMedSci, a pioneer in human genetics and drug discovery, as its next president and chief executive officer.

Bar Harbor, Maine, Oct. 04, 2021 (GLOBE NEWSWIRE) -- The Jackson Laboratory, an independent, nonprofit biomedical research institution, today announced the appointment of Lon Cardon, Ph.D., FMedSci, a pioneer in human genetics and drug discovery, as its next president and chief executive officer. Effective on November 29, Cardon will succeed current President and CEO Edison Liu, M.D., who will step down after a decade of leadership. Liu will continue to serve as a JAX professor studying the functional genomics of cancer with a focus on breast cancer.

After ten years of steering JAX through impressive expansion, dramatic change and remarkable achievements, Ed has made an indelible impact at JAX as a leader, researcher, and oncologist in our local communities and within the global biomedical research field, said David Roux, chairman of The Jackson Laboratory Board of Trustees. We are now thrilled to appoint Lon as the next president and CEO of JAX. Under his leadership, Lon will guide the Laboratory as it propels into its next intense period of growth.

Timothy Dattels, vice chairman of The Jackson Laboratory Board of Trustees and chair of the Presidential Search Committee added, As both an accomplished academic researcher as well as a demonstrated successful leader in both pharma and biotech, Lon is extremely well-suited to shape the vision, impact and strategic direction of The Jackson Laboratory over the next decade.

In his new role, Cardon will develop and drive a clear, integrated strategy for the Laboratorys continued long-term success, leveraging the unique and powerful interplay of JAXs deep expertise in mammalian genetics and human genomics combined with the latest advances in digital technologies such as artificial intelligence, machine learning and new computation platforms as well as its research, educational and business strengths.

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For many years there has been immense promise to translate human genetics and genomics discoveries into new diagnostics, prognostics and treatments for both common and rare diseases, said Cardon. Many of the foundational pieces are finally coming into place. The next step is to put them together to begin to realize this promise.

The Jackson Laboratory has a unique combination of critical components to finally approach the long-awaited potential of genetics for translation, coupling deep understanding of mouse models of human disease with extensive genetic and genomics expertise, large-scale research capacity, and computational and data analytics to bring it all together. I am excited to lead the organization to help shape a new era for human health where understanding all of our unique genomes will help to predict, treat and modify the course of disease.

Cardon joined BioMarin in September 2017 as chief scientific officer and senior vice president and was promoted in 2019 to chief scientific strategy officer to enrich BioMarins pipeline. Before joining BioMarin, he was a senior vice president at GlaxoSmithKline, leading departments and divisions spanning genetics, molecular biology, computational biology, statistics and epidemiology, and ultimately leading an early-to-late pipeline division called Alternative Discovery and Development. Prior to Cardons 14-year tenure in industry, he spent the first half of his career as a senior academic in the United Kingdom and United States, initially as professor of Bioinformatics at the University of Oxford and then as professor of Biostatistics at the University of Washington and co-chair of the Herbold Bioinformatics Program at the Fred Hutchinson Cancer Research Center.

Cardon received his Ph.D. from the University of Colorado and conducted his postdoctoral research in the Department of Mathematics at Stanford University. He has been awarded a Wellcome Trust Principal Fellowship and is an elected Fellow of the U.K.s Academy of Medical Sciences and the American Association for the Advancement of Science.

Cardon has authored more than 225 scientific publications and 15 books and chapters, mainly focused on genetics methodology, applications and discoveries for rare and common diseases, ranging from Huntingtons disease to dyslexia. He is an elected Fellow of the UKs Academy of Medical Sciences and the American Association for the Advancement of Science.

About The Jackson Laboratory

The Jackson Laboratory is an independent, nonprofit biomedical research institution with more than 2,400 employees. Headquartered in Bar Harbor, Maine, it has a National Cancer Institute-designated Cancer Center, a genomic medicine institute in Farmington, Conn., and facilities in Ellsworth and Augusta, Maine, in Sacramento, Calif., and Shanghai, China and a joint venture in Beijing. Its mission is to discover precise genomic solutions for disease and empower the global biomedical community in the shared quest to improve human health.

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Researchers discover how a genetic mutation in mice and monkeys interferes with viruses – News-Medical.net

A nationwide team of researchers, led by scientists at University of Utah Health and The Rockefeller University, has determined how a genetic mutation found in mice and monkeys interferes with viruses such as HIV and Ebola. They say the finding could eventually lead to the development of medical interventions in humans

The gene, called retroCHMP3, encodes an altered protein that disrupts the ability of certain viruses to exit an infected cell and prevents it from going on to infect other cells.

Normally, some viruses encase themselves in cell membranes and then make an exit by budding off from the host cell. RetroCHMP3 delays that process long enough that the virus can no longer escape.

This was an unexpected discovery. We were surprised that slowing down our cell biology just a little bit throws virus replication off its game.

Nels Elde, Ph.D., senior author of the study and evolutionary geneticist, Department of Human Genetics at U of U Health

The study appears online Sept. 30 in advance of the Oct. 14 issue of Cell.

RetroCHMP3 originated as a duplicated copy of a gene called charged multivesicular body protein 3, or CHMP3. While some monkeys, mice, and other animals have retroCHMP3 or other variants, humans only have the original CHMP3.

In humans and other creatures, CHMP3 is well known for playing a key part of a role in cellular processes that are vital for maintaining cellular membrane integrity, intercellular signaling, and cell division.

HIV and certain other viruses hijack this pathway to bud off from the cellular membrane and infect other cells. Based on their research, Elde and his colleagues suspected that the duplications of CHMP3 they discovered in primates and mice blocked this from happening as protection against viruses like HIV and other viral diseases.

Building on this notion, Elde and other scientists began exploring whether variants of retroCHMP3 might work as an antiviral. In laboratory experiments conducted elsewhere, a shorter, altered version of human CHMP3 successfully prevented HIV from budding off cells. But there was a glitch: the modified protein also disrupted important cellular functions, causing the cells to die.

Unlike the other researchers, Elde and his colleagues at U of U Health had naturally occurring variants of CHMP3 from other animals in hand. So, working in collaboration with researchers Sanford Simon at The Rockefeller University, along with Phuong Tieu Schmitt and Anthony Schmitt at Pennsylvania State University, they tried a different approach.

Using genetic tools, they coaxed human cells to produce the version of retroCHMP3 found in squirrel monkeys. Then, they infected the cells with HIV and found that the virus had difficulty budding off from the cells, essentially stopping them in their tracks. And this occurred without disrupting metabolic signaling or related cellular functions that can cause cell death.

Were excited about the work because we showed some time ago that many different enveloped viruses use this pathway, called the ESCRT pathway, to escape cells, says Wes Sundquist, Ph.D., a co-corresponding author of the study and chair of the Department of Biochemistry at the University of Utah. We always thought that this might be a point at which cells could defend themselves against such viruses, but we didnt see how that could happen without interfering with other very important cellular functions.

From an evolutionary perspective, Elde believes this represents a new type of immunity that can arise quickly to protect against short-lived threats.

We thought the ESCRT pathway was an Achilles heel that viruses like HIV and Ebola could always exploit as they bud off and infect new cells, Elde says. RetroCHMP3 flipped the script, making the viruses vulnerable. Moving forward, we hope to learn from this lesson and use it to counter viral diseases.

More specifically, that lesson raises the possibility that an intervention that slows down the process may be inconsequential for the host, but provide us with a new anti-retroviral, says Sanford Simon, Ph.D, a study co-author and a professor of Cellular Biophysics at The Rockefeller University.

Source:

Journal reference:

Rheinemann, L., et al. (2021) RetroCHMP3 Blocks Budding of Enveloped Viruses Without Blocking Cytokinesis. Cell. doi.org/10.1016/j.cell.2021.09.008.

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Researchers discover how a genetic mutation in mice and monkeys interferes with viruses - News-Medical.net

Supreme Court issues notice to government on admission to Medical Genetics courses – The Hindu

The Supreme Court on Friday sought a response from the government on a plea challenging a notification for NEET-Super Specialities (NEET-SS) 2021 in August allowing postgraduates from a broad spectrum of medical disciplines to apply for Doctorate of Medicine (Medical Genetics) and Doctorate of National Board in Medical Genetics courses.

A Bench of Justices D.Y. Chandrachud and B.V. Nagarathna issued notice and listed the case for hearing after two weeks.

The order was passed on a petition filed by the Society of Indian Academy of Medical Genetics, which challenged the validity of the information bulletin published by the National Board of Examinations on August 31.

The society argued that the bulletin contradicted the guidelines prescribed by the National Medical Commission that only aspirants from Medicine, Paediatrics and Obstetrics could apply for the Medical Genetics courses concerned.

The petition noted that elite medical institutes such as the AIIMS restricted admissions to the Medical Genetics courses to these three streams.

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Supreme Court issues notice to government on admission to Medical Genetics courses - The Hindu

‘Forest Genetics and the Tree of Life’: Local forester to speak at Weldon Baptist about God, living things – The Daily Herald

Forester Bradley W. Antill will be a guest speaker at Weldon Baptist Church on Wednesday to discuss the subject Forest Genetics and the Tree of Life.

Born in Norton, Ohio, Antill said he moved to Shallotte to take up a forestry job with the Federal Paperboard. He then moved to Henrico in 1997 for a job with the Coastal Lumber Company in Weldon, which has since changed its name in 2004 to Coastal Timberlands Company.

According to a press release, Antill will discuss how trees are the lifeblood of the local forest industries.

Actually, our very life depends on a specific tree and what we do with it, Antill wrote as an excerpt in the press release. The forest industry has always been at the forefront of genetic research, including cloning; trying to get the best tree to grow. But only one specific tree can claim to be the source of eternal life, the Tree of Life.

The Rev. Francis Kyle, the new pastor at Weldon Baptist, said they are excited to hear Antill speak on the interlaced topics he is knowledgeable and passionate about.

Those intertwining topics are land, trees, people and the God of the Bible who created the land and trees on the third day of creation by merely speaking them into existence Genesis 1:9-13, and created male and female in His image on the sixth day Genesis 1:26-27, Kyle said. And, of course, the Lord Jesus Christ, the financially poor Jewish carpenter from Nazareth yet who simultaneously and supernaturally was also the unselfish and sinless Son of God who lovingly sacrificed Himself for us selfish sinners on an old rugged wooden cross at Calvary in Jerusalem. Brad is a shining and inspiring example of intentionally living to the glory of God in ones workplace.

When asked if his discussion will combine science and religion, Antill disagreed.

I use Creation, the things I see every day in the outdoors, to relate to the Creator, he said. Romans Chapter 1, clearly states that Gods creation is one of the ways God reveals himself, to teach us about who he is. The Bible is his guidebook.

Many in the modern world may prefer to separate science from religion, while others consider creation science instead, which is the teaching and research based upon the belief that biblical accounts of the creation of the world and universe are scientific facts.

Antill also disagreed that science and faith are polar opposites since science only exists because God created the universe and placed physical laws upon which science rests.

What I do is take various elements of forestry, trapping, hunting, fishing and history to illustrate a biblical truth, he said. Man has been searching for a special tree since he was kicked out of the Garden of Eden. So, maybe we can understand that search better by seeing how it is done in forestry.

When asked what people can expect to hear on Wednesday, Antill said his devotions and talks show that the words of the Bible can be understood by seeing the fingerprints left by God surrounding everybody.

Often it involves illustrations parables, similar to what Jesus used when he taught, he said. These everyday examples illustrate a spiritual truth or application found in the Bible. My audience may learn a little bit about forestry, but I hope they learn more about the Creator and his love for us.

Antill said he is passionate about this topic because the Creator desires everyone to understand that their lives have meaning and they were not accidents.

The first decision of consequence man had to make involved a tree, he said. The last decision of consequence a man will make will involve a tree. Lets get together and talk about both.

According to the press release, the presentation is part of Weldon Baptists new Uncommon Christian Speaker Series with a free lunch provided by the churchs Hospitality Committee. Antills outdoor-themed Christian devotional books will also be for sale at a discounted price of $7.

The event will be held from 11:30 a.m. to 1 p.m. inside the Daniel Fellowship Hall at Weldon Baptist Church, 609 Washington Ave. A question and answer session will follow at the presentation.

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'Forest Genetics and the Tree of Life': Local forester to speak at Weldon Baptist about God, living things - The Daily Herald

Genetic discrimination: The next great health battle likely to wash up on NZ shores – Newstalk ZB

Theres growing concern about genetic discrimination in New Zealand and the lack of Government intervention in this fast-moving field.

As genetictesting becomes more accessible than ever before, there are calls for a line in the sand to be drawn and a final answer toaquestionnot yet canvassed: should insurers be able to use our geneticinformation?

Genetic discrimination is using someones genetic information to discriminate against them to treat them in a way thats different to someone else because we know something about their genetics.

Currently,lifeand health insurance companies in New Zealand are allowed to use thisdatain determining coverand premiumsfor applicants something experts sayanecdotalevidence suggest hasledto increased premiums, or no cover at all.

While insurers may argue it's their right to know a person's medical history researchers say genetics is, in fact, not a part of one's history, but a part of their future.

There are a lot of complexities in determining someone's genetic makeup and whether they are prone to getting a disease later in life.

There are also ways to mitigate and change the outcome of a patient's health once becoming privy to this information. For example, getting a mastectomywill drastically limit the chances of getting breast cancer, but there are fears an insurer may refuse cover based on a positive BRCA gene test regardless.

University ofOtago law and bioethics lecturerDr Jeanne Snellingsaysif people do have the test,and its positive, they can do things tominimisedevelopment of the disease.

They can undergo surveillance, get prophylactic preventative treatment and their risk could be quite similar to someone elses in the end. But, the insurance company is taking this absolutist approach saying that a positive test disqualifies you from obtaining life insurance cover.

There aredoubts about whether an insurance company would have staff with the expertise on hand to dissect someones genetic information.

University of Aucklands Faculty of Medical and Health Sciences Professor Andrew Shelling says it usually takes acastofspecialists to trawl through the data of an entire persons genome.

Good luck to the insurance company if they can find something, let us know. Because we have an entire team of experts from the clinicians to thebioinformaticiansto the geneticists who sit in a multi-disciplinary clinic each week trying to discuss the outcomes of what theyre looking at.

Based on the increased complexity of genetic testing nowadays, there is also a risk of getting it wrong if you dont have the right expertise. Hesaid.

There'salsoconcernpeople will not opt for undergoing genetic testing purely based on the fact it could be used by insurers -- and thus, miss out on the opportunity to decreasefuturehealth risks.

Despite the life-saving prevention available through genetic testing, experts say people avoiditand research because they are afraid of insurance discrimination.

This not only limits what a person can do to better their health in future -- but stunts medical research, particularly in minority groups like Mori and Pasifika, whose genetics are an even greater enigma to researchers than Pakeha.

Professor Shelling says we know that Mori have been discriminated against for years and this may be another form of it.

We base a lot of our genetics on European DNA, so for our Mori and Pasific people we dont always know what their results mean in a clinical setting.

We have an extra responsibility as genomic scientists to support Mori and Pasific getting genetic testing and make sure they dont get further discriminated against.

In a lot of our research studies around New Zealand, we are trying to increase the number of Mori and Pasific participants.

He fears if they have any concerns about insurance, theyllturn away from being part of these studies.

It's a conflict Jane Tiller anethical, legal and social advisor for Public Health Genomics at Melbournes Monash University --has battled for five years in Australia where a moratorium's been put in place to try and curb the issue.

Now, in Australia, you can get life insurance up to $500,000. If you try and take out more, you have to then disclose your genetic test results. she said.

She says the moratoriums a good step towards consumer protection but its a fraught approach.

"It goes up to certain financial limits and is only five years. So, we dont know what will happen in 2024 when it ends.

We are still gathering data about how its [the moratorium]working. Were remaining concerned about the lack of Government regulations on this issue.We would like to see a complete ban, like in Canada.

The moratorium isalso self-regulated by the insurance industry.

Self-regulation has been shown to be conflicted and problematic, both in Australia and New Zealand.

Theres very little transparency on how insurance companies use this data.Because this is self-regulated, theres a lot of questions around how decisions are made and what data is relied on.

The newly formed AGenDA (Against Genomic Discrimination Aotearoa) group, is lobbying for Government attention on this issue.

AGenDasmessage is that genetic discrimination is not only aconsumer protection issue, but a human rights issue.

Theysay itsnot just about making sure insurers get the information they need todiscriminate; its about stopping them from discriminatingaltogether. Its about ensuring consumers can make decisions about healthcare and learn empowering information without fear of discrimination for themselves or their family members.

They say thesectorhas come to presume divulgence -- an expectation thats been born of our insurance industry over many years.

The Financial Services Councils Richard Kiplin says its not something companies will ask for but if a client has information, it's only fair that they disclose it.

Within the New Zealand sector organisation by organisation will make their own calls. he said.

Whats important for New Zealand consumers to understand is that this is a complex area, and life companies need to assess risk and theyll do that in an appropriate way.

Genetic testing,at this point of time, is not a standard part of that -- but thats obviously evolving and moving very fast.

I think if people have had a genetic test and have information then they know information that a life and health company would want to understand. And so thats a part of the disclosure process.

Kiplin says hes open to working with researchers and other parties in future to solidify guidelines around genetic testing.

We have a robust committee structure thats been looking at some of these issues and reviewing guidelines.

The sector is never static, theres always stuff you can change and this is one of the big areas of the future.Hesaid.

AGenDAis alsoconcerned at the lack of Government intervention.

The Minister of Commerce and Consumer Affairs David Clark points towards the Ministry of Business, Innovation and Employment's Insurance Law Review.

"Insurer use of genetic testing results is one of many issues raised with MBIE during the course of the review, but it was not highlighted as a significant issue in the submissions (it was mentioned in two out of around 500 submissions received). Hesaid.

Clark mirrors the industrys openness to work with experts to understand the situation better.

Im told, the industryhavepreviously told my officials they are not seeing high levels of genetic testing, but I am open to further briefings on the matter.

The MBIEreview was promptedto ensure New Zealands insurance contract law is facilitating insurance markets that work well and enable individuals and businesses to effectively protect themselves against risk.

In November 2019 the Government agreed tothereform which includesmaking sure insurers ask consumers the right questions, the requirement for policies to be written and presented clearly, strengthening protection for consumers against unfair terms and extending powers to the Financial Markets Authority to monitor and enforce compliance.

Next steps for the review include release of an exposure draft Bill for consultation in late-2021.

Genetic testing has been described asa quantum leap for healthcare. A new kind ofapparatuswe can use to decode our future health.

In July 2021,the World Health Organization (WHO) provided the first global recommendations to help establish human genome editing as a tool for public health, with an emphasis on safety, effectiveness and ethics.

While their concerns are mainly based around the use of genetics to edit our DNA --WHO Director-General,Dr Tedros Adhanom Ghebreyesus, recognisedgenome editing and testing as a potential to advance our ability to treat and cure disease.

"But the full impact will only be realized if we deploy it for the benefit of all people, instead of fueling more health inequity between and within countries,Hesaid.

In September, the WHOrecommended DNA testing as a first-choice screening method for cervical cancer prevention.

It recognised DNA-based testing for human papillomavirus (HPV) has been shown to be more effective than todays commonly used screening methods aimed at detecting and preventing cervical cancer, a major cause of death among women worldwide.

Asgenetictestingbecomesmore mainstream,as the technologies mature,and as testsbecome moreprecise and affordable-- it evolves from being aniche offering tobecomingilluminatedon healthcarescentrestage.

And whilegenetictesting is applauded for its potential to become a part of our everyday health toolbox one question remains:should insurers be able to use our genetic information?

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Genetic discrimination: The next great health battle likely to wash up on NZ shores - Newstalk ZB

Obesity and genetics: Researchers have found 14 genes that cause weight gain and three that help prevent it, opening door to new treatments – Genetic…

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Obesity and genetics: Researchers have found 14 genes that cause weight gain and three that help prevent it, opening door to new treatments - Genetic...