Dogs have been following humans for thousands of years.

Archaeological and genetic data has revealed that dogs accompanied humans when they were migrating to the Americas from East Asia, according to a study published Monday in the Proceedings of the National Academy of Sciences.

Dogs were likely domesticated over 23,000 years ago in Siberia, said lead study author and archaeologist Angela Perri, a research fellow at Durham University's department of archaeology in the United Kingdom. Her team analyzed the genetic makeup of ancient dog remains to estimate when the domestication from wolves to dogs happened.

Archaeological evidence showed that the humans migrated over 15,000 years ago from Northeast Asia across the Bering Land Bridge, a piece of land that connected modern-day Russia to Alaska. The land crossing no longer exists due to rising sea levels.

Perri studied the lineage of American dogs outside the Arctic, which come from a different genetic ancestor than Arctic dogs, and traced it back to ancient Siberian dogs. This lineage has shown that humans brought their dogs with them when they migrated to the Americas, according to the study.

Many people have dogs as pets today and some wonder, "What is this animal and how did it go from a wild predator to curled up next to my bed?" Perri noted.

While there is no definitive answer on why dogs became domesticated, the freezing climactic conditions during this time likely brought wolves and humans closer together for survival, she said.

"Wolves likely learned that scavenging from humans regularly was an easy free meal, while humans allowed this to happen so long as wolves were not aggressive or threatening," Perri said.

The dogs could have also helped humans transport items faster, she said. There is also evidence in the Pacific Northwest of humans using furry creatures as emergency sources of food and fur.

The study is a fascinating example of how canine and human DNA and archaeology can be used to find out more about our past, said Jeffrey Kidd, associate professor of human genetics at the University of Michigan Medical School, who was not involved in the study.

Modern dogs are similar to domesticated dogs from 15,000 years ago, he said, but today there are different furs and colors as a result of breeding.

Kidd is not surprised that humans brought their dogs with them when they migrated to the Americas because of how intertwined dogs are in our society.

"If you and your entire community was going on a journey across the land, wouldn't you bring along your dog?" Kidd said.

The earliest confirmed dog bones were found in Germany over 100 years ago and are about 15,000 years old, Perri said, so her next project is to search for older dog bones in Siberia to aid in her research. She's hoping to gather more evidence to discover how dogs became man's best friend.

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Dogs likely migrated to the Americas with humans over 15,000 years ago, study says - WAAY

Dr. Li has over 30 years of experience in basic and applied biomedical research. She joins Neurophth from the University of Louisville School of Medicine, where she was a professor in the department of Ophthalmology and Visual Sciences for over 14 years. Her research focuses on the role of Hippo/YAP1 signaling pathway on different stages of ocular development, NF-kB/IKK2 inhibition of neovascularization, and gene discovery screening for eye diseases using mouse models.

Throughout her career, Dr. Li has contributed to more than 45 publications in journals including Investigative Ophthalmology & Visual Science (IOVS), Proceedings of the National Academy of Sciences of the United States of America(PNAS), Nature Review Immunology, and Science. She is currently the editorial board member of Scientific Reportsand Source Journal of Ophthalmology. Dr. Li holds a Ph.D. in cell biology from the Washington University in St. Louis and obtained both her Bachelor's and Master of Science degrees in Genetics from Beijing University.

"We are thrilled to have Dr. Li on our team, bringing over 3 decades of her diverse experience in basic and applied biomedical research," said Bin Li, M.D., Ph.D., Founder and Chairman of the Board of Neurophth. "Given her prior experience at Baylor College of Medicine mentored by Dr. Savio Woo, an internationally recognized expert in molecular human genetics and gene therapy, and Dr. Mark Kay, a leading researcher in the fields of AAV gene therapy and the current Head of Division of Human Gene Therapy at the Stanford University School of Medicine, Dr. Li has extensive knowledge in gene therapy for hepatic deficiencies, ocular diseases, and viral vector reconstruction."

"We are excited to have Qiutang join and expand our exceptional research and development team. She brings a wealth of experience in gene therapies for ocular diseases to Neurophth," said Alvin Luk, Ph.D., M.B.A., C.C.R.A., Chief Executive Officer at Neurophth. "Her deep understanding of viral vector design and animal models in the inhibition of neovascularization for ocular diseases, such as age-related macular degeneration and diabetic retinopathy, further bolsters our ability to deliver on our growing pipeline of clinical programs and platform capabilities."

"It has been captivating to watch the scale, scope, and speed with which Neurophth has successfully transformed itself into an innovative and diversified gene therapy company," said Dr. Li. "I look forward to being a part of Neurophth team as the company executes the next stage of its growth strategy and expands its pipeline of gene therapy candidates focused on ocular and non-ocular diseases, building a brighter future for patients worldwide."

About Neurophth

Neurophth is China's first gene therapy company in ophthalmic diseases.Headquartered in Wuhan with subsidiaries in Shanghai, Suzhou, and the U.S., Neurophth, a fully integrated company, is striving to discover and develop gene therapies for patients suffering from blindness and other eye diseases globally. Our AAV validated platform which has been published in Nature - Scientific Reports, Ophthalmology, and EBioMedicine, successfully delivered proof-of-concept data with investigational gene therapies in the retina. Our most advanced investigational candidate, NR082 (rAAV2-ND4), in development for the treatment ofND4-mutated LHON, has received orphan drug designations in theU.S. The pipeline also includesND1-mutated LHON, autosomal dominant optic atrophy, glaucoma, wAMD/DME, and other preclinical candidates. Neurophth has initiated the scaling up in-house process in single-use manufacturing technologies to support future commercial demand at the Suzhou facility. To learn more about us and our growing pipeline, visitwww.neurophth.com.

SOURCE Neurophth Therapeutics, Inc.

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Neurophth Therapeutics Further Expands Ocular Gene Therapy Expertise with Appointment of Qiutang Li, Ph.D., as Chief Scientific Officer - PRNewswire

Researchers at Weill Cornell Medicine and Cornell Universitys Ithaca campus have developed a new computational method for studying genetic and environmental interactions and how they influence disease risk.

Theresearch, in The American Journal of Human Genetics, makes the process of finding these interactions much less difficult and demonstrates their importance in determining body mass index and diabetes risk.

Our study demonstrates that your genes matter and the environment matters and that the interaction of the two can increase risk for disease, said co-senior author,Dr. Olivier Elemento, who is professor of computational genomics in computational biomedicine, professor of physiology and biophysics, associate director of the HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine, and director of the Caryl and Israel Englander Institute for Precision Medicine at Weill Cornell Medicine.

Typically, studying gene-environment interactions creates a huge computational challenge, said lead author Andrew Marderstein, a doctoral candidate in the Weill Cornell Graduate School of Medical Sciences whose research was conducted both in Dr. Elementos lab in New York City andDr. Andrew Clarkslab in Ithaca, enabling him to have immediate access to computational biology and population health expertise.

Genotype-environment interaction can be thought of as the situation where some genotypes are much more sensitive to environmental insults than others, said Dr. Clark, co-senior author and Jacob Gould Schurman Professor of Population Genetics in the Department of Molecular Biology and Genetics in the College of Arts & Sciences and a Nancy and Peter Meinig Family Investigator at Cornell University. These are exactly the cases where changes in the diet or other exposures might have the biggest improvement in health, but only for a subset of individuals.

The millions of genetic variants, or inherited genetic differences found between individuals in a population, and different lifestyle and environmental factors, such as smoking, exercise, different eating habits, can be analyzed for combined effects in numerous ways. When researchers test for gene-environment interactions, they typically analyze millions of data points in a pairwise fashion, meaning they assess one genetic variant and its interaction with one environmental factor at a time. This type of analysis can become quite labor intensive, said Marderstein.

The new computational method prioritizes and assesses a smaller number ofvariantsin the genomeor the complete set of genetic material found in the bodyfor gene-environment interactions.We condensed a problem withanalyzing10 million different geneticvariantsto essentiallyanalyzing only tens ofvariants indifferent regions of the genome, Marderstein said.

While a standard genetic association study might look at whether asinglegeneticvariantcould lead to an average change in body mass index (BMI), this study assessed which geneticvariantswere associated with individuals being more likely to have a higher BMI or lower BMI. The researchers found that looking for sections of DNA associated with the variance in a human characteristic, called a variance quantitative trait locusor vQTL, enabled them to more readily identify gene-environment interactions. Notably, thevQTLs associated with body mass index were also more likely to be associated with diseases that have large environmental influences.

Another area of study where the new computational method might useful is determining how an individual might respond to a specific drug based on gene-environment interactions, said Marderstein. Analysis of social determinants of health, meaning a persons environmental and social conditions, such as poverty level and educational attainment, is a third area that the researchers are interesting in pursuing, according to Dr. Elemento.

Overall, scientists in the precision medicine field are realizing they can sequence a persons DNA, in addition to assessing environmental factors such air quality and physical activity, to better understand whether the individual is at risk of developing a specific disease. The idea down the line is to use these concepts in the clinic, said Dr. Elemento. This is part of the evolution of precision medicine, where we can now sequence somebody's genome very easily and then potentially analyze all of the variants in the genetic landscape that correlate with the risk of developing particular conditions.

Reference: Marderstein AR, Davenport ER, Kulm S, Van Hout CV, Elemento O, Clark AG. Leveraging phenotypic variability to identify genetic interactions in human phenotypes. AJHG. 2021;108(1):49-67. doi:10.1016/j.ajhg.2020.11.016.

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Simplifying the Study of Gene-Environment Interactions - Technology Networks

THOUSAND OAKS, Calif., Jan. 28, 2021 /PRNewswire/ -- Amgen (NASDAQ:AMGN) today announced that it will report its fourth quarter and full year 2020 financial results on Tuesday, Feb. 2, 2021, after the close of the U.S. financial markets. The announcement will be followed by a conference call with the investment community at 5 p.m. EST. Participating in the call from Amgen will be Robert A. Bradway, chairman and chief executive officer, and other members of Amgen's senior management team.

Live audio of the conference call will be simultaneously broadcast over the internet and will be available to members of the news media, investors and the general public.

The webcast, as with other selected presentations regarding developments in Amgen's business given by management at certain investor and medical conferences, can be found on Amgen's website, http://www.amgen.com, under Investors. Information regarding presentation times, webcast availability and webcast links are noted on Amgen's Investor Relations Events Calendar. The webcast will be archived and available for replay for at least 90 days after the event.

About AmgenAmgen is committed to unlocking the potential of biology for patients suffering from serious illnesses by discovering, developing, manufacturing and delivering innovative human therapeutics. This approach begins by using tools like advanced human genetics to unravel the complexities of disease and understand the fundamentals of human biology.

Amgen focuses on areas of high unmet medical need and leverages its expertise to strive for solutions that improve health outcomes and dramatically improve people's lives. A biotechnology pioneer since 1980, Amgen has grown to beone ofthe world'sleadingindependent biotechnology companies, has reached millions of patients around the world and is developing a pipeline of medicines with breakaway potential.

For more information, visitwww.amgen.comand follow us onwww.twitter.com/amgen.

CONTACT: Amgen, Thousand OaksMegan Fox, 805-447-1423 (media)Trish Rowland, 805-447-5631(media)Arvind Sood, 805-447-1060 (investors)

View original content to download multimedia:http://www.prnewswire.com/news-releases/amgen-announces-webcast-of-2020-fourth-quarter-and-full-year-financial-results-301217691.html

SOURCE Amgen

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Amgen Announces Webcast Of 2020 Fourth Quarter And Full Year Financial Results - BioSpace

There are so many different companies that offer genetic analysis to any interested client. One such company, 23andMe, offers some interesting features for those who use itsservices.

It provides insight into a users ethnic history and even breaks down parts of their genetic codes to explain how DNA influenced their appearance or senses. In addition to these easy-to-understand hereditary summaries, it also gives clients a copy of their "raw data."

Here, we'llgo over whattools you can use to interpret your 23andMe raw data, and we'll define what exactly raw data is.

To understand raw data, you need to know a little bit about how DNA works. DNA is something we inherit from both of our parents and, subsequentially, all previous ancestors. Unless you have an identical twin, your genetic code is unique to you. Understanding what your "genetic code" is can help you learn about raw data.

Deoxyribonucleic Acid (DNA) is a molecule that dictates everything that makes us, us. It contains codes for everything from our basic biology to personalized features. While all humans share a majority of the sequence, humans experience small differences in base pairs, which may influence everything, such as our appearance, behavior, and predisposition to diseases.

Base pairs are the "building blocks" of our genetic makeup. When looking at a model of a DNA double helix, they are those little "steps" of the ladder. Each step is comprised of one of four bases: adenine (A), cytosine (C), guanine (G), or thymine (T), and its complementary base pair (A and T or G and C).

When you send your tissue sample over to 23andMe facilities, scientists perform a process called genotyping. As opposed to sequencing, where technicians attempt to calculate the exact sequence of a given length of DNA, genotyping offers an accurate (and cost-effective) shortcut.

Our genetic code is very long, and there are huge chunks of information we cant do anything with yet. Genotyping is a far more effective process for getting useful data for clients.

The process scans genetic code to look for specific gene variants that are very popular or ones that we already know about. 23andMe takes these datasets and transforms them into an easy-to-understand infographic.

What you'll see is a neat little printout letting you know where your ancestors originated from. What the scientists behind the scenes see is a printout containing various locations and a whole bunch of As, Gs, Ts, and Cs. This printout is your raw data that 23andMe sends you with your results.

Related:The Best Ancestry Tracing Sites

Your raw data may seem like a jumbled mess of characters, but its incredibly useful information. Although 23andMe offers some insight into the genetic information it analyzes, it doesn'texplain everything.

The raw data offers tons of surprise information that you can use. This information isnt just interesting from ahistoricalperspective; the information also offers insight into your health and can be a useful genealogy tool for you and your loved ones.

To access this information, you need to find how to "read" this information. Luckily, you dont need to be a renowned geneticist to take that raw data and do something with it.

While you could theoretically search through journals and try to analyze your raw data yourself, there are a couple hundred thousand markers to sift through. The best way to make the most out of your raw data is to utilize one of the many available tools online.

With countless platforms to chose from, it may be challenging to pick out the best one for you. Consider what information you want to learn from your raw data before you choose an analysis tool.

Xcode Life offers a variety of packages, so you can order exactly what you want. With many different reports to chose from, you can customize the information you want, as well as find options to fit your budget. It displays its findings in an easy-to-read format for everyone to enjoy.

There are over 15 options to choose from, including Gene Sleep, Traits and Personality,Gene Allergy, and more.There are also different bundles available so you can save money. Its packages start at $20.

If you are interested in finding extended ancestry information and basic health information, DNA Land offers free assessment packages.

Although it doesn'tgo into as much detail as some of the paid contenders, it offers great added insight at no extra charge. DNA Land will even use your anonymous submissions to further scientific research.

Nutrahacker takes gene analysis one step further. It designs your reports so that you can "empower yourself" with the newfound information.

Its specialized assessments determine an optimized list of supplements and fitness information for you, in addition to general health data. While its packages start at $25, it also offers some free basic assessments.

If you are on a tighter budget, Promethease offers more inexpensive health reports. It anonymously cross-references your raw data with SNPedia, a human genetics wiki. While it gives you a lot of information for the price, the process is not as straightforward as other options.

You dont need to be an expert, but many find the platform a bit more technical. However, having a super basic background in statistics should suffice. Health reports start at $12.

Research continues to advance every day, and Genomelink makes a point to keep its dynamic options updated by the week. It offers over 200 analysis options to investigate everything from your personality and career strengths to your health vulnerabilities and longevity.

If you're on a budget, Genomelink also has over 20 free analyses. These come with the option to order premium reports delivered via straightforward infographics.

There is so much information to learn from your genetic makeup. With so many easy and accessible tools to further explore the data you already paid for, why not make the most of what you have? It only takes a few clicks of a button to receive a comprehensive health report that is both interesting and informative.

Considering online DNA testing? Several options are available, but 23andMe and ancestryDNA are the top dogs.

Brittni is a neuroscience graduate student who writes for MakeUseOf on the side of her studies. Shes a seasoned writer who began her freelance writing career back in 2012. While shes mainly focused on technology and medicine shes also spent time writing about animals, pop culture, video game recommendations, and comic book reviews.

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Turn 23andMe Raw Data Into Meaningful Results With These Websites and Tools - MakeUseOf

January 29, 2021 I COVID-19 may become seasonal, severe infection associated with myeloid immune cells, potential Achilles heel of coronaviruses identified, melatonin synthesized in lungs could have protective effect, and plitidepsin outperforms remdesivir in preclinical trials. Plus: NSAID use during COVID-19 is time-dependent on its harm or benefit and NAU to test Allarity drug against Coronavirus Variant B117.

Research News

COVID-19 may be seasonal, like the flu, suggests a new paper published in Evolutionary Bioinformatics. Authors of the paper show that COVID-19 cases and mortality rates, among other epidemiological metrics, are significantly correlated with temperature and latitude across 221 countries. They also explain that our own immune systems could be partially responsible for the pattern of seasonality. For example, our immune response to the flu can be influenced by temperature and nutritional status, including vitamin D, a critical nutrient to our immune defenses. The researchers add that it is, however, too soon to say how seasonality and our immune systems interact in the case of COVID-19. DOI:10.1177/1176934321989695

SARS-CoV-2 independently entered Russia at least 67 times, primarily at the end of February and beginning of March 2020, according to a new study published in Nature Communications. Researchers of the study used 211 virus genomes, which were sequenced at Smorodintsev Research Institute of Influenza, and all genomes had been obtained from patients from 25 Russian regions during mid-March to April 2020. They determined that the vast majority of introductions came from European countries, and no cases of introduction from China were registered, which they attribute to the timely closure of borders with the country. Currently, nine local virus lineages are circulating in Russia, which are not present elsewhere in the world. DOI:10.1038/s41467-020-20880-z

Research led at Vanderbilt University Medical Center has discovered a proofreading exoribonuclease, called nsp14-ExoN, which can correct errors in the RNA sequence that occur during replication, when copies of a virus are generated. They believe that this may be the Achilles heel of the coronavirus, a finding that could help close the door on COVID-19 and possibly head off future pandemics. Using cutting-edge technologies and novel bioinformatics approaches, the researchers discovered that this ExoN also regulates the rate of recombination, which is the ability of the coronavirus to shuffle parts of its genome and even pull genetic material from other viral strains while it replicates in order to gain evolutionary advantage. These patterns of recombination are conserved across multiple coronaviruses, including SARS-CoV-2. They believe that the coronavirus ExoN is therefore a conserved, important target for inhibition and attenuation in the ongoing pandemic. This research is published in PLOS Pathogens. DOI:10.1371/journal.ppat.1009226

Also at Vanderbilt University Medical Center (VUMC), researchers have identified genetic factors that increase the risk for developing pneumonia to help identify patients with COVID-19 at greatest risk for this life-threatening complication. The researchers conducted genome-wide association studies (GWAS) of more than 85,000 patients whose genetic information is stored in VUMCs BioVU biobank. They identified nearly 9,000 cases of pneumonia in patients of European ancestry and 1,710 cases in patients of African ancestry. After further analysis, the research team linked the gene that causes cystic fibrosis (CF) and European ancestry and the mutation that causes sickle cell disease (SCD) in patients of African ancestry as the strongest pneumonia associations. After removing patients with CF and SCD, they then pinpointed a pneumonia-associated variation in a gene called R3HCC1L in patients of European ancestry, and one near a gene called UQCRFS1 in patients of African ancestry. They believe these findings could be applied to identifying patients with high risk of severe pneumonia to enable early interventions. They have published this work in the American Journal of Human Genetics. DOI:10.1016/j.ajhg.2020.12.010

Melatonin produced in the lungs acts as a barrier against SARS-CoV-2, blocking the expression of genes that encode proteins in cells serving as viral entry points, finds researchers at the University of So Paulo (USP). The hormone, therefore, prevents infection of these cells by the virus and inhibits the immune response so that the virus remains in the respiratory tract for a few days and then leaves the host, say the researchers. They used RNA sequencing data to quantify the level of expression of 212 COVID-19 signature genes in 288 samples from healthy human lungs. The researchers correlated these gene expression levels with a gene index that estimated the capacity of the lungs to synthesize melatonin (MEL-index). They then were able to determine that when the MEL-index was high, the entry points for the virus in the lungs were closed, and vice-versa. The research team suggests the potential for nasal administration of melatonin to prevent disease from developing in pre-symptomatic COVID-19 patients. This study is published in Melatonin Research. DOI:10.32794/mr11250090

In a new study, published in Cell Reports Medicine, La Jolla Institute for Immunology (LJI) researchers suggest that T cells can mount attacks against many SARS-CoV-2 targets, beyond the key sites on the viruss spike protein. They believe that by attacking the virus from many angles, the body is equipped to potentially recognize different SARS-CoV-2 variants. The researchers examined T cells from 100 people who had recovered from COVID-19 to take a closer look at the genetic sequence of the virus to separate the potential epitopes from the epitopes that these T cells would recognize. Their analysis revealed that not all parts of the virus induce the same strong immune response in everyone, and T cells can recognize dozens of epitopes on SARS-CoV-2 that vary from person to person. They determined that each study participant had the ability to recognize about 17 CD8+ T cell epitopes and 19 CD4+ T cell epitopes. DOI:10.1016/j.xcrm/2021/100202

John Hopkins Medicine researchers, in collaboration with Immunoscape, have published a complete profile of the response of T cells in people who have recovered from SARS-CoV-2 infection. The paper, published in The Journal of Clinical Investigation, better defines which T cells interact with which specific portion of the SARS-CoV-2 virus and how those interactions can provide long-lasting immunity against COVID-19. The researchers collected blood samples from 30 convalescent patients who had recovered from mild cases of COVID-19 and the Immunoscape team, a U.S.-Singapore biotechnology company, used its highly sensitive human leukocyte antigen (HLA)-SARS-CoV-2 tetramers to tag and identify the types of virus-recognizing CD8+ T cells. The researchers found that as levels of neutralizing antibodies increased in the convalescent plasma, so did the number of memory CD8+ T cells that recognized SARS-CoV-2 epitopes. They believe this means lasting protection against reinfection, and this knowledge will guide COVID-19 vaccine design to produce a strong immune response that could provide years of protection. DOI:10.1172/JCI145476

Severe COVID-19 patients have significantly elevated levels of a certain type of immune cell in their blood, call monocytic myeloid-derived suppressor cells (M-MDSC), according to a new study published in the Journal of Clinical Investigation. Karolinska Institutet researchers studied 147 patients with mild to fatal COVID-19 who were sampled repeatedly from blood and respiratory tract. These samples were then compared with patients who had influenza and healthy individuals. They found that the patients with severe COVID-19 had significantly higher levels of M-MDSCs in their blood when compared to milder cases and healthy participants. COVID-19 patients also had fewer T cells in their blood than healthy individuals that showed signs of impaired function. Additionally, their analysis revealed that the levels of M-MDSCs early in the course of infection seemed to reflect subsequent disease severity. DOI:10.1172/JCI44734

Researchers have engineered an antibody that effectively neutralizes SARS-CoV-2 and that also acts against multiple SARS-like viruses. Their antibody, ADG-2, was studied in mice. To engineer this broadly neutralizing antibody (bnAb), the researchers started with antibodies from the memory B cells of a 2003 SARS survivor that cross-neutralized multiple SARS-related viruses with modest potency. They then selectively engineered the binding affinities of several of these bnAbs, creating improvements in their abilities to bind the virus. The researchers then studied the engineered antibodies for SARS-CoV-2 neutralizing activity in mouse cell lines. ADG-2 was particularly effective. It showed broad binding activity to more than a dozen SARS-related coronaviruses. This research is published in Science. DOI:10.1126/science.abf4830

Plitidepsin has shown a potent efficacy against SARS-CoV-2 in preclinical trials, outperforming the antiviral remdesivir. These results, published in Science, show that in studies in human cells, plitidepsin demonstrated potent anti-SARS-CoV-2 activity: 27.5-fold more so than remdesivir as tested in the same cell line. In a model of human lung cells, plitidepsin greatly reduced viral replication. In further experiments involving both plitidepsin and remdesivir in vitro, the researchers suggest that plitidepsin has an additive effect with the approved drug and would be a potential candidate for a combined therapy. Authors of the research article believe that this promising treatment, which has limited clinical approval for the treatment of multiple myeloma, should be strongly considered for expanded clinical trials for the treatment of COVID-19. DOI:10.1126/science.abf4058

Oregon Health & Science University (OHSU) researchers have demonstrated that antibodies generated by the SARS-CoV-2 virus react to other strains of coronavirus and vice-versa. They determined, however, that antibodies generated by the 2003 SARS outbreak had only limited effectiveness in neutralizing SARS-CoV-2. The researchers believe that these findings have implications on both vaccine effectiveness and diagnosis of COVID-19. They believe that more work needs to be done to determine the lasting effectiveness of COVID-19 vaccine, given the speed of mutations. The team believes their study also suggests that efforts to accurately discern a previous COVID-19 infection, by analyzing antibodies in the blood, may be complicated by the presence of antibodies reacting to other strains of coronavirus including the common cold. This study is published in Cell Reports. DOI:10.1016/j.celrep.2021.108737

A new method to mapping viral mutations that escape leading clinical antibodies against COVID-19 has revealed mutations in the SARS-CoV-2 virus that allow it to evade treatments, including a single amino-acid mutation that fully escapes Regenerons antibody cocktail. University of Washington researchers and colleagues developed this scanning method to map how mutations to the receptor-binding domain (RBD) affect its recognition by antibodies. Their maps identified mutations that escape antibody binding, including a single mutation that escapes both antibodies in the Regeneron antibody cocktail. To further investigate, the team examined deep sequencing data from a persistently infected patient who was treated with the antibody cocktail at day 145 after diagnosis with COVID-19, and their analysis identified resistance mutations that arose in the patient. Furthermore, after they examined all human-derived SARS-CoV-2 sequences available as of mid-January 2021, the researchers report a substantial number of RBD mutations that escaped one or more of the antibodies that are in circulation. This paper is published in Science. DOI:10.1126/science.abf9302

Monash University researchers have discovered two new molecules that provide profound protection in experimental models of asthma, as well as protection from acute respiratory distress syndrome (ARDS) that is seen in some patients with severe COVID-19. In their study, originally designed to investigate how the immune system impacts gut bacteria, the researchers found that p-cresol sulfate (PCS), a gut bacteria by-product, led to a striking protection against asthma. They then determined that PCS was produced by enhanced bacterial metabolism of L-tyrosine, a well-known amino acid found in dietary supplements. The researchers saw significant protection against lung inflammation in mice given either L-tyrosine or PCS, as well as protection from ARDS. The researchers now aim to test one of the molecules in a clinical trial in asthmatics this year. These new findings are published in Nature Immunology. DOI:10.1038/s41590-020-00856-3

Non-steroidal anti-inflammatory drugs (NSAIDs) reduced both antibody and inflammatory responses to SARS-CoV-2 infection in mice, a new study finds that is published in the Journal of Virology. The authors of the study highlight that the timing of NSAID use during COVID-19 is important. They explain that NSAIDs anti-inflammatory activity could be detrimental early in SARS-CoV-2 infection because inflammation is usually helpful during this stage. This changes at later stages of COVID-19, particularly if the patient experiences intense inflammation known as cytokine storm. The researchers also note that a reduction in neutralizing antibodies caused by NSAIDs could be benign, or it might hinder the immune systems ability to fight the infection in its early stages. It could also reduce the magnitude or duration of protection from either natural infection or vaccination. DOI:10.1128/JVI.00014-21

Rhesus macaque monkeys infected with SARS-CoV-2 developed protective immune responses that could be reproduced with a vaccine, according to University of California, Davis (UC Davis) researchers. The team infected eight rhesus macaques at the California National Primate Research Center (CNPRC) with SARS-CoV-2 virus isolated from the first human patient treated at UC Davis, and they followed the immune responses in the monkeys over two weeks. The animals showed signs of lasting immunity and, most importantly, structures called germinal centers developed in the lymph nodes near the lungs. These germinal centers contained cells call T follicular helper (Tfh) cells. Germinal centers and Tfh cells are associated with generating plasma cells that remain in the body for many years to produce antibodies against pathogens the immune system has seen before, the researchers explain. They believe these results suggest that vaccines that induce this response will support immunity against COVID-19. This study is published in Nature Communications. DOI:10.1038/s41467-020-20642-x

Patients who have recovered from severe COVID-19 infection could be left with more protective T cells needed to fight reinfection, finds a team of researchers led at La Jolla Institute for Immunology (LJI). For their study, published in Science Immunology, the team analyzed CD8+ T cells from 39 COVID-19 patients and 10 individuals who had never been exposed to the virus. Of the COVID-19 patients, 17 had a mild case that did not require hospitalization, 13 had been hospitalized, and nine needed intensive care support. Surprisingly, the researchers saw weaker CD8+ T cell responses in patients with milder COVID-19 cases and saw the strongest CD8+ T cell responses in the patients who required hospitalization or intensive care. The team now hopes to study how T cells in tissues hit hardest by SARS-CoV-2, such as the lungs, react to the virus. They explain the importance of this as the memory T cells that provide long-term immunity need to live in the tissues. DOI:10.11260/sciimmunol.abe4782

In a new study published in Science Signaling, scientists discovered that SARS-CoV-2 may enter and replicate in human cells by exploiting newly identified sequences within cell receptors. They also suggest that these sequences could potentially serve as targets for new therapies against COVID-19. After analyzing the Eukaryotic Linear Motif database, the team of scientists discovered that ACE2 and various receptors contained several short linear motifs (SLiMs), or small amino acid sequences, that they predict plays a role in endocytosis and autophagy, or the entering of human cells and cellular housekeeping. The team determined that two SLiMs in ACE2 bound to endocytosis-related proteins, and one SLiM in the integrin beta-3 (3) bound to two proteins involved in autophagy. They believe that their prediction models could help identify similar SLiMs that assist with the replication of not only SARS-CoV-2, but other viruses that cause disease. DOI:10.1126/scisignal.abd0334

Ohio University researchers have published the first structural biology analysis of a section of the COVID-19 viral RNA called the stem-loop II motif, which they believe could be a potential target for anti-viral drugs to combat the virus. The research team identified this non-coding section of the RNA that is likely key to SARS-CoV-2 replication. Interestingly, they determined that the structural flexibility of this noncoding RNA motif differs by only a single nucleotide when compared to that in the early 2000s SARS-CoV outbreak, and the team also identified FDA-approved drugs that bind to the RNA motif and alter its flexibility. Since the structure and flexibility of noncoding RNA affects its function, the researchers suggest that it may be possible to develop antiviral drugs that specifically target this RNA motif to battle the virus. This research is published in Biochemical and Biophysical Research Communications. DOI:10.1016/j.bbrc.2021.01.013

Innate immunity may play a larger role in controlling SARS-CoV-2 viral load than adaptive immunity, according to a new study published in ACS Pharmacology & Translational Science. Researchers of the study developed a mathematical model that predicts viral load over time in organs that express the ACE2 receptor, which allows SARS-CoV-2 entry into human cells. They then used this model to simulate different conditions to determine this key role for innate immunity in controlling viral load. The researchers suggest the importance of starting antiviral or interferon therapy as soon as possible after the onset of COVID-19 symptoms. DOI:10.1021/acsptsci.0c00183

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Clear Labs announced the availability of the Clear Dx Whole Genome Sequencing (WGS), the first automated WGS solution that determines the complete RNA sequence of the SARS-CoV-2 genome in less than 24-hours with only minutes of hands-on time. The Clear Dx platform is powered by next generation sequencing (NGS), robotics and cloud-based analytics, and as a result, their WGS can more easily determine the nature of virus transmission by differentiating virus strains and monitoring mutations that lead to variants. In addition to WGS, the platform also features the Clear Dx SARS-CoV-2 Diagnostic Assay, which has received EUA, that allows labs to perform diagnostic screening and genomic surveillance simultaneously. Press Release

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Profile of T Cells, Broadly Neutralizing Antibodies, Anti-Viral Targets: COVID-19 Updates - Bio-IT World

Introduction

Calcium channel blockers (CCBs) are widely used in the treatment of hypertension. In addition to their antihypertensive effects, CCBs may also lead to many adverse reactions, including peripheral edema, dizziness, flushing, fatigue, headache, palpitations, and gingival enlargement.14 Peripheral edema, particularly of lower limbs, is the most common side effect of CCBs. CCBs-induced peripheral edema is more common in women and is related to age, upright posture and duration of CCBs therapy.2,5 Although it has been known for decades that CCBs could cause peripheral edema, there are still very few genetic markers that could be used in clinical treatment.

Amlodipine is a first-line antihypertensive drug and a long-acting 1,4-dihydropyridine calcium channel blocker.6 It became the fifth most prescribed medication in the United States in 2018.7 However, therapy trials report that the incidence of amlodipine-induced peripheral edema is about 19%, which also probably serves as the main reason behind the limited use of this drug.8,9 To our knowledge, factors that increase the serum concentration of drugs may also increase the risk of side effect. Accordingly, genetic factors affecting the metabolism of amlodipine will consequently influence its clearance, thus possibly resulting in peripheral edema. In recent years, numerous studies have focused on identifying genetic factors determining the responses to amlodipine therapy, including aspects of efficacy and safety.1012 Nevertheless, the genetic predisposition to amlodipine-induced peripheral edema remains unclear. However, some studies shine light on CYP genes, which are involved in the metabolism of amlodipine.13,14

CYP3A is a subfamily of cytochrome P450 and is involved in the metabolism of many compounds.10,1517 CYP3A4 and CYP3A5 are the two major enzymes of CYP3A family and play important roles in the dehydrogenation of amlodipine.18 However, it has been reported that CYP3A4, rather than CYP3A5, plays a more important role in amlodipine clearance in vivo.16 However, according to our observations, almost all SNPs of CYP3A4 are very rare in Chinese Han or East Asian.1921 A recent study evaluated the influence of CYP3A polymorphisms on the pharmacokinetic (PK) parameters of 10 CYP3A substrates including amlodipine, and it turned out CYP3A4 polymorphisms did not show a pronounced influence on PK of amlodipine.22 So, as far as we know, CYP3A4 does not suffice as an explanation towards the incidence of amlodipine-induced adverse responses. Additionally, the contribution of CYP3A5 in amlodipine metabolism is still controversial. CYP3A5 expression varies among individuals due to gene polymorphisms that result in non-productive mRNA splicing and lower or undetectable expression of the protein.14,23,24 Pharmacogenomics studies have found that CYP3A5 gene polymorphisms have significant impact on drug metabolism, efficacy, and toxicity.25,26 Recent studies have reported a possible relationship between CYP3A5 and amlodipine. CYP3A5*3/*3 genotypes might be associated with blood pressure response to amlodipine,27 and CYP3A5*3 may affect the disposition of amlodipine.13 In Chinese hypertensive patients who underwent renal transplantation, researchers have demonstrated that CYP3A5*3 polymorphism affects the antihypertensive efficacy of amlodipine. In such patients with CYP3A5*3/*3, the reduction in diastolic blood pressure (DBP) was significantly higher than those with other genotypes.28 Additionally, compared with CYP3A5*1/*1, CYP3A5*1/*3 patients exhibit a lower metabolic ratio of amlodipine in vivo and hypertensive patients with CYP3A5*1/*3 genotypes show a higher decrease in blood pressure.14 These findings suggest that CYP3A5 genetic variants are really involved in amlodipine response, having an impact on treatment effectivity of amlodipine.

Although studies have identified that CYP3A5 polymorphisms do play a role in blood pressure control and treatment responses of amlodipine, the effect of a particular genotype in amlodipine-induced peripheral edema remains unclear. Here, we aim to test whether any genetic variants associate with amlodipine-induced peripheral edema. For this, we used the targeted region sequencing method to genotype the SNPs in all known haplotypes of CYP3A5, and evaluated their effect on amlodipine-induced peripheral edema in Chinese Han hypertensive patients.

We recruited a total of 240 patients with essential hypertension who have ever been treated with amlodipine or L-amlodipine for more than 4 weeks. The participants were outpatients from Beijing Chaoyang Hospital of Capital Medical University and the Second Hospital of Jilin University. The demographic characteristics and baseline data were collected, including gender, age, body mass index (BMI), smoking and drinking status, blood pressure, heart rate and use of medications. Participants were also questioned about peripheral edema symptoms (leg or ankle edema). Two trained physicians evaluated the adverse drug reactions caused by the amlodipine or L-amlodipine based on the WHO-UMC scale.29 We classified the participant as a peripheral edema case if WHO-UMC causality categories were certain, probable, or possible. The others were grouped as controls.

The DNA Sampling Swabs (Taitong Gene Testing Equipments Co., Ltd., Suzhou, China) were used for collecting oral buccal mucosa cells. Genomic DNA was isolated from the swabs, using Hi-Swab DNA kit (TIANGEN, Beijing, China) according to the manufacturers instructions. Quantification of the DNA concentration was performed using the manufacturers protocol with the Qubit dsDNA HS Assay Kit (Yeasen, Shanghai, China). Methods for targeted region capture and NGS have been reported previously.30 Illumina HiSeq X was used to sequence the captured DNA with paired-end reads of 150 bp length. Table S1 lists the targeted regions of sequencing and the 24 SNPs of CYP3A5.

High-quality sequencing reads were obtained from the raw data by removing reads that contained adapters, were with unknown bases, or had a low-quality using the Trimmomatic (v0.36)31 program. The high-quality reads were aligned to human reference genome hg19 using the Burrows-Wheeler Aligner (BWA, v0.7.15)32 using the default parameters. The Genome Analysis ToolKit (GATK, v3.8)33 was used for indels realignment, quality score recalibration, variant calling, and genotyping (using Haplotype Caller).

Demographic and clinical characteristics of different groups were compared by t-test or Chi-square (2) test according to the data category. The associations between gene polymorphisms and the risk of peripheral edema were assessed by codominant model, dominant model, recessive model and allele model by calculating the odds ratios (ORs) and 95% confidence intervals (CIs) using logistic regression with or without adjustment by gender and alcohol status. Stratification was done by gender. Analyses above were carried out on R-4.03. PLINK 1.934 was used to calculate the minor allele frequency and assess HardyWeinberg equilibrium (HWE) for each SNP. Additionally, linkage disequilibrium (LD) block and haplotype were assessed by Haploview35 software. The D and r2 values for all pairs of SNPs were calculated. P value<0.05 was considered as the significant level.

Two hundred and forty enrolled patients were separated into 64 cases and 176 controls. The general characteristics of the study population are summarized in Table 1. In agreement with previous reports, a higher incidence of CCB-induced peripheral edema was observed in women. A significant difference was found in the sex ratio between cases and controls (P=0.00048). In addition, the frequency of drinkers was 29.69% in the case group and 46.02% in the control group (P=0.034). There was no significant difference between the two groups regarding other characteristics.

Table 1 Characteristics of the Study Population

All the observed SNPs and the minor allele frequencies (MAF) in two groups are listed in Table 2. Except rs15524, rs4646453 and rs776746, the other SNPs were rare or not detected in the studied population. Therefore, we focused on these three SNPs (MAF>0.05) for further studies. Distributions of genotype frequencies of the SNPs did not show any deviation in HardyWeinberg equilibrium (P>0.05).

Table 2 Observed CYP3A5 Variations and Frequencies

The genotype and allele allocations of the test polymorphisms differed considerably between cases and controls (Table 3). In more detail, the frequencies of alleles rs15524 G, rs4646453 A, and rs776746 T were significantly lower in cases than those in the control group (G vs A: OR=0.53, P=0.011; A vs C: OR=0.54, P=0.019; T vs C: OR=0.58, P=0.03; respectively). Furthermore, there was a statistically significant difference in genotype of the rs15524 and rs4646453 between the two groups in dominant model with or without adjustment by gender and alcohol status (GG+AA vs AA: OR=0.5, P=0.021; AA+AC vs CC: OR=0.54, P=0.04). As for rs776746, the presence of TT+CT genotype demonstrated a significantly lower risk after gender and alcohol status adjustment (TT+CT vs CC: OR=0.57, adjusted P=0.044).

Table 3 Genotype Frequencies of Study SNPs in Case and Control Groups

Stratified analyses were performed to access the differential effect of gender on the association between amlodipine-induced edema and the polymorphisms. No significant differences were identified, but the relevant genotypes still showed lower risk in all subgroups. The details are presented in Table 4.

Table 4 Stratified Analyses Between SNPs and Risk of Amlodipine-Induced Peripheral Edema

We employed Haploview program to assess the Linkage disequilibrium (LD) block and haplotype of the three SNPs of CYP3A5. The LD analysis indicated that these SNPs were in strong LD with each other (Figure 1, rs15524 and rs4646453 D=0.965, r2=0.821; rs15524 and rs776746 D=0.979, r2=0.919; rs776746 and rs4646453 D=0.989, r2=0.898). Frequencies of four haplotypes were found to be more than 1% in the haplotype analysis (Table 5). The most represented haplotype in the whole cohort of controls and cases was ACC, followed by GAT, GCC and GCT. Two haplotypes (ACC and GAT) were significantly associated with the risk of amlodipine-induced peripheral edema. The frequency of the ACC haplotype was higher in the cases than controls (79.7% vs 67.9%, P=0.012), whereas the frequency of the GAT haplotype was lower in the cases (17.2% vs 28.1%, P=0.015).

Figure 1 Linkage disequilibrium coefficients (|D|) and LD block among the three polymorphisms of CYP3A5.

Table 5 Haplotype Frequencies of CYP3A5 Gene and the Association with the Amlodipine-Induced Peripheral Edema Risk

Studies have demonstrated that genetic polymorphisms may influence the gene function, thus causing alterations in the pharmacokinetics (PK) and pharmacodynamics (PD) of the gene-associated drugs. Moreover, genetic variants have been confirmed for their association with appearance of adverse reactions to drugs, such as ACE inhibitors-induced cough36 and rosuvastatin-induced myotoxicity.37 To our knowledge, this is the first study to investigate the relationships of CYP3A5 polymorphisms and amlodipine-induced peripheral edema by using a casecontrol retrospective study in the Chinese population. Our study reveals that amlodipine-induced peripheral edema may associate with genetic polymorphisms in CYP3A5 gene. We find that the distribution of allele and genotype frequencies of the three SNPs are significantly different between cases and controls. Specifically, the alleles rs15524 G, rs4646453 A, and rs776746 T reduce the risk of amlodipine-induced peripheral edema. On the other hand, A, C, and C increase the risk and haplotype analysis also confirms this. These findings support the hypothesis that genetic variation in CYP3A5 is involved in the development of amlodipine-induced peripheral edema.

CYP3A5 is highly polymorphic with significant inter-individual variation in the enzyme activity contributing to the absorption, metabolism and tissue distribution of drugs.24,38 Genetic polymorphisms of CYP3A5 may potentially alter its proteins expression and function, and subsequently influence the clearance of any drugs metabolized by CYP3A5.38 The most studied SNP related to CYP3A5 functional variation is rs776746 (also known as CYP3A5*3 or CYP3A5*3C). Homozygous carriers of this SNP (*3/*3 or CC) lack functional CYP3A5 protein because of the frameshift mutation and truncation of the translated protein.39 Previous studies have confirmed that CYP3A5*3 is associated with drug metabolism, and CYP3A5*3/*3 carriers have decreased metabolism of nifedipine40 and tacrolimus,41 compared to CYP3A5*1/*1 and CYP3A5*1/*3 carriers. Patients with CYP3A5*3/*3 who are treated with tacrolimus may have an increased risk of nephrotoxicity as compared to patients without it.25,26 These findings suggest that the CYP3A5 *3/*3 carriers have low activity of CYP3A5 enzyme and decreased metabolism for certain drugs dependent on it, resulting in the appearance of an adverse reaction to the drug. Conforming to these findings, our study also indicates that there is an association between CYP3A5*3 and the occurrence of amlodipine-induced peripheral edema and that *3/*3 (CC) carriers have a higher risk of peripheral edema.

CYP3A5*1D (rs15524) is another frequently studied SNP in CYP3A5, which is in the 3-untranslated region (UTR). CYP3A5*1D is differentially distributed among populations ranging from 77.5% in Americans to 71.4% in East Asians, 40.6% in Africans, and even rarer in Europeans (less than 8%) (GnomAD).21 SNPs in UTRs may influence the stability of mRNA, thus affecting the expression and activity of the enzyme.42,43 According to a study identifying the potential SNPs related to miRNA, rs15524 may influence the hsa-miR-500a-5p that targets CYP3A5, affecting its expression.44 In addition, studies have found that CYP3A5*1D influences the pharmacokinetics of many drugs, including tacrolimus45 and carbamazepine.46 Therefore, rs15524 may act as a genetic marker and should be considered while studying or prescribing drugs metabolized by CYP3A5. Here, we find that the frequencies of rs15524 G allele and GA+GG genotypes in cases are lower than controls, which indicates that this SNP is associated with reduced risk of incidence of amlodipine-induced peripheral edema. In other words, CYP3A5*1D/*1D carriers may have an increased risk than others.

As for CYP3A5*1E (rs4646453), it is associated with a decreasing risk of amlodipine-induced peripheral edema. However, there is litter information about the function of the rs4646453. To some extent, this is possible because the SNP locates in the intron region. Studies have revealed that CYP3A5 rs4646453 is in LD with rs776746,47 and there is a strong LD between rs15524 and rs776746.39,46 Our findings are consistent with these studies and further promote that the presence of LDs with rs776746 may partly explain the role of rs15524 and rs4646453 in amlodipine-induced peripheral edema.

Given all these findings, there are some limitations in our present study that we would like to acknowledge. First, the population in our study is Chinese Han, and it is known that the frequency of mutations differs among ethnic groups. Hence, our results may apply well to Chinese population but are probably not suitable for populations of other ethnic groups. Second, we have performed a retrospective study and not a prospective one. The study is also limited by the smaller number of samples. The third limitation is not involving other genes contributing to amlodipine metabolism, such as CYP3A4. As we mentioned before, polymorphisms of CYP3A4 are rare in Chinese, and the evidence so far that CYP3A4 polymorphisms influence amlodipine metabolism is scarce. So, we took no account of them currently. But it would be better for future studies to include these related genes to better explain the connection between genetic factors and amlodipine-induced peripheral edema. Hence, more casecontrol studies with large number of polyethnic samples and involvement of diversified factors are necessary.

None the less, our study does investigate the novel relationship between the genetic variants and amlodipine-induced peripheral edema. In conclusion, we provide evidence that CYP3A5 polymorphisms are involved in the occurrence of amlodipine-induced peripheral edema, and the three genetic variants of CYP3A5 have the potential to serve as novel biomarkers for amlodipine-induced adverse reactions. Our findings thus provide new insights into amlodipine-induced peripheral edema and are of importance in developing and prescribing personalized and precise medicine for hypertension.

The raw data are available on reasonable request to the correspondence author Songnian Hu.

All the participants have signed the written informed consent, and approval was obtained from the Research Ethics Board of Beijing Chaoyang Hospital of Capital Medical University and the Research Ethics Board of the Second Hospital of Jilin University. This study has been conducted in accordance with the World Medical Association Declaration of Helsinki.

We thank all the participants included in this study.

All authors declare that they have no conflicts of interest for this work.

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[Full text] Association of CYP3A5 Gene Polymorphisms and Amlodipine-Induced Periph | PGPM - Dove Medical Press

By the time I am 60 years old in 2050, our global population will have increased to 9.7 billionpeople. Thats an additional ~2 billion human beings that will need to be fed. With over275 million hectares(680 million acres) of irrigated land globally, researchers note that to grow enough food for our projected population increase, we will need crops to produce more output on existing land.

Experts estimate that to provide for the 2050 population forecast, annual cereal production will need to rise by 50% to about3 billion tonnes. To do this, we must implement plant breeding technologies as one part of a comprehensive solution for global hunger.

The big news, as reported in the journalNature, is that researchers have sequenced new variations of genomes in barley and wheat. The international team includes scientists from the University of Adelaides Waite Research Institute, along with the10+ Genome Project, spearheaded by Curtis Pozniak, a professor at the University of Saskatchewan, Canada. Pozniak is in collaboration with the International Barley Pan Genome Sequencing Consortium, led by Nils Stein, professor at theLeibniz Institute of Plant Genetics and Crop Plant Research.

What does that mean for society today? Because barley and wheat are staple crops on a global level, scientists may have found a way to produce the high yield necessary to feed more mouths within our lifetime. And its not just a boon to cereal production; these discoveries bring us one step closer to unlocking the entire gene set, otherwise known aspan-genome,in wheat and barley, which has ramifications for all future research in plant genomics and cereal farming.

Heres how the research unfolded: Scientists conducting field tests in Chile found a way to increase the amount of protein (expansin) in the plants, which controls growth rate.The result: grains that were up to 12% larger than usual with higher yields as well. In the past, there had always been a tradeoff between grain size and number.

This is especially good news because wheat provides about 20% of the calories consumed by humans, and the current yield is increasing at only about 1% annually a far cry from the 50% needed to supply the population by 2050. Field results were a critical component, as they helped prove the effectiveness of these variations, by showing that the plants could perform under typical agricultural conditions. The teams of researchers are now working to make this research available to farmers and the greater food industry to help inform their decisions on crop production.

Currently, more than 800 million peopleworldwideare chronically hungry, and about 2 billion are nutritionally deficient. This is ahugepublic health concern. Whats more, fertile land and water supply are becoming scarcer, and production increases are falling off amplifying the need for more productive land.

Gene-editing technologies can only address global hunger and land and water availability if theyve gained consumer trust.GMOsand gene-editing are some of the most studied plant technologies. They also have the capacity to increase yield and lower chemical fertilizer and pesticide use, provide crops with better resilience to poor climate conditions, ward off pests, reduce post-harvest loss, and produce more nutrient-dense foods.

And yet, even with 30 years of research and countless commercial applications proving that gene-edited or GMO crops are as safe as conventionally grown crops, there is still hesitation from mainstream culture.

What if you were to wake up at 60, 70 or 80 years old, and instead of looking at flourishing families youre looking at 900 million people going hungry,landonce used for playgrounds now dedicated to growing food, and the population still multiplying? While this may seem like a stretch, if we dont accept plant breeding technology and realize its fundamental impact on food security, we may not meet increasing global food demands. More and more people will go hungry.

It seems like a luxury to even discuss consumer food production preference when people in developing countries are dying of starvation. With COVID running rampant, Africa is unable to make use of new plant technology, including GMOs, due to bottlenecks caused by the pandemic. This, asRuramiso Mashumba, an African smallholder farmer shared with us, is not a matter of preference but truly, a matter of life and death.

So, while our issue here in the United States remains a social challenge of widespread consumer adoption,developing countries are struggling with political barriers, preventing them from using lifesaving technology.

We hope to see more plant technologies such as this emerge and we hope that consumers do their research and come to understand the safety and vital nature of these developments.

What will 2050 look like? Your decisions today have an impact. Understanding the safety of new plant technologies, and the good they can do, is of chief importance to feeding generations to come.

Hayley N. Philip is a writer and researcher for Dirt to Dinner with a focus in health and nutrition.

A version of this article was originally posted at Dirt To Dinner and has been reposted here with permission. Dirt To Dinner can be found on Twitter @Dirt_To_Dinner

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With fertile land and water growing scarce, high-yield wheat and barley could help save millions from hunger - Genetic Literacy Project