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Illuminating Dark Matter in Human DNA Unprecedented Atlas of the Book of Life – SciTechDaily

In an unprecedented atlas, researchers begin to map how genes are turned on or off in different cells, a step toward better understanding the connections between genetics and disease.

Researchers at University of California San Diego have produced a single-cell chromatin atlas for the human genome. Chromatin is a complex of DNA and protein found in eukaryotic cells; regions of chromatin at key gene regulatory elements appear in open configurations within certain cell nuclei. Precisely delineating these accessible chromatin regions in cells of different human tissue types would be a major step toward understanding the role of gene regulatory elements (non-coding DNA) in human health or disease.

The findings are published online in the November 12, 2021, issue of Cell.

For scientists, the human genome, popularly called the book of life, is mostly unwritten. Or at least unread. While science has famously put an (approximate) number to all of the protein-coding genes required to build a human being, approximately 20,000+, that estimation does not really begin to explain how exactly the construction process works or, in the case of disease, it might go awry.

The human genome was sequenced 20 years ago, but interpreting the meaning of this book of life continues to be challenging, said Bing Ren, PhD, director of the Center for Epigenomics, professor of cellular and molecular medicine at UC San Diego School of Medicine and a member of the Ludwig Institute for Cancer Research at UC San Diego.

A major reason is that the majority of the human DNA sequence, more than 98 percent, is non-protein-coding, and we do not yet have a genetic code book to unlock the information embedded in these sequences.

Put another way, its a bit like knowing chapter titles but with the rest of the pages still blank.

Efforts to fill in the blanks are broadly captured in an ongoing international effort called the Encyclopedia of DNA Elements (ENCODE), and include the work of Ren and colleagues. In particular, they have investigated the role and function of chromatin, a complex of DNA and proteins that form chromosomes within the nuclei of eukaryotic cells.

DNA carries the cells genetic instructions. The major proteins in chromatin, called histones, help tightly package the DNA in a compact form that fits within the cell nucleus. (There are roughly six feet of DNA tucked into each cell nucleus and approximately 10 billion miles in each human body.) Changes in how chromatin bundles up DNA are associated with DNA replication and gene expression.

After working with mice, Ren and collaborators turned their attention to a single-cell atlas of chromatin in the human genome.

They applied assays to more than 600,000 human cells sampled from 30 adult human tissue types from multiple donors, then integrated that information with similar data from 15 fetal tissue types to reveal the status of chromatin at approximately 1.2 million candidate cis-regulatory elements in 222 distinct cell types.

One of the initial challenges was identifying the best experimental conditions for such a diverse set of sample types, particularly given each tissues unique makeup and sensitivity to homogenization, said study co-author Sebastian Preissl, PhD, associate director for Single Cell Genomics at UC San Diego Center for Epigenomics, a collaborative research center that carried out the assays.

Cis-regulatory elements are regions of non-coding DNA that regulate transcription (copying a segment of DNA into RNA) of neighboring genes. Transcription is the essential process that converts genetic information into action.

Studies in the last decade have established that sequence variations in non-coding DNA are a key driver in multi-genic traits and diseases in human populations, such as diabetes, Alzheimers disease and autoimmune diseases, said study co-author Kyle J. Gaulton, PhD, assistant professor in the Department of Pediatrics at UC San Diego School of Medicine.

A new paradigm that helps explain how these noncoding variants contribute to diseases posits that these sequence alterations disrupt function of transcriptional regulatory elements and lead to dysregulation of gene expression in disease-relevant cell types, such as neurons, immune cells or epithelial cells, said co-first author Kai Zhang, PhD, a postdoctoral fellow in the Department of Cellular and Molecular Medicine. A major barrier to unlocking the function of noncoding risk variants, however, is the lack of cell-type-specific maps of transcriptional regulatory elements in the human genome.

Ren said the new findings identify disease-trait-relevant cell types for 240 multi-genic traits and diseases, and annotate the risk of noncoding variants.

We believe that this resource will greatly facilitate the study of mechanism across a broad spectrum of human diseases for many years to come.

Preissl said the chromatin atlas will also allow the scientific community to unravel tissue environment-specific differences of cell types that reside in multiple tissues, such as fibroblasts, immune cells or endothelial cells.

Reference: A single-cell atlas of chromatin accessibility in the human genome by Kai Zhang, James D. Hocker, Michael Miller, Xiaomeng Hou, Joshua Chiou, Olivier B. Poirion, Yunjiang Qiu, Yang E. Li, Kyle J. Gaulton, Allen Wang, Sebastian Preissl and Bing Ren, 12 November 2021, Cell.DOI: 10.1016/j.cell.2021.10.024

Co-authors include: James D. Hocker and Yang E. Li, Ludwig Institute for Cancer Research and UC San Diego; Michael Miller, Hiaomeng Hou, Joshua Chiou, Olivier B. Poirion and Allen Wang, all at UC San Diego; and Yunjiang Qiu, Ludwig Institute for Cancer Research, La Jolla.

Funding for this research came, in part, from the Ludwig Institute for Cancer Research, the National Human Genome Research Institute (GRANT 3U54HG006997-04S2), Foundation for the National Institutes of Health (AMP T2D RFP14), the Ruth L. Kirschstein Institutional National Science Research Award from the National Institute of General Medical Sciences (T32 GM008666).

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Illuminating Dark Matter in Human DNA Unprecedented Atlas of the Book of Life - SciTechDaily

Quinton Eriya Has The Genetics To Be A Future Mr. Olympia Threat – Fitness Volt

Canadian bodybuilder Quinton Eriya is set to return for his first bodybuilding contest in more than a year. Ahead of this event, he is looking like he has the potential to be a future star in the sport.

Eriya is just about three years into his bodybuilding career, having just three competitions under his belt so far, with his highest placing being 5th at the 2019 Toronto Pro. However he has a physique that represents what some have called the best genetics the sport has ever seen.

Whether that is true or not is up to interpretation, but one thing that is clear is that he is extremely aesthetic, and has been working to add mass to his impressive frame. He is set to return to action this weekend, for the first time in 2021, at the Romania Muscle Fest Pro, and the updates that he has been posting to his Instagram paint a picture of a severely improved physique.

One of the biggest takeaways from the 2021 Mr. Olympia, was the fact that the new generation of bodybuilders is beginning to make itself known. By all indications, Quinton Eriya is going to be one of the more impressive members of that group.

With competitors like Nick Walker and Hunter Labrada breaking through the top five at the Olympia, there seems to be a shift in the works. Now it seems that the judges are looking for a mix between the mass monsters like Big Ramy and more aesthetic physiques, which is something that Quinton represents well.

To be clear, being huge is still a relevant factor when it comes to judging, and truthfully Eriya still has some filling out to do if he wants to compete with the best in the world. However he has been making serious strides toward that, and if he can keep up the good work, there is little denying that he could be a future Olympia contender in no time.

As much as he seems to have future contender written all over him, the main objective now is for Quinton Eriya to take on the roster at the 2021 Romania Muscle Fest Pro, this weekend. If he is able to get a win or at least a solid placing, at this event, it will be a step in the right direction for this future star.

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Quinton Eriya Has The Genetics To Be A Future Mr. Olympia Threat - Fitness Volt

AncestryDNA vs. 23andMe: Which DNA Kit Delivers the Best Genetic Information? – PCMag.com

DNA kits are useful, popular ways for discovering your roots, as well as identifying potential health conditions. AncestryDNA and 23andMe are the most well-known consumer DNA services, and they cost roughly the same amount of money. So, which DNA kit should you pick to learn more about your family history and genetics? We pit the DNA giants against each other to help you make an informed decision.

OnceAncestryprocesses your DNA sample, your dashboard displays an interactive map of your ethnicity estimate, possible DNA matches, and a map of where your ancestors lived. If you cancel your account, you can download your raw DNA report and take it with you.

Ancestry continually updates your results as the company collects more reference samples and builds better tools. My profile was last updated in September 2021. Subscribers can access an array of historical records, including Census data; create family trees; and contact other Ancestry members.

The company offers three subscription options: AncestryDNA (the original version), AncestryDNA + World Explorer Membership, and AncestryDNA Traits + All Access Membership. The World Explorer Membership opens up access to international records, and the All Access Membership includes access to Fold3 and Newspapers.com. Fold3 has over half a million military records and millions of nonmilitary. A membership to Newspapers.com comes with more than 2 billion articles that go back to the 1700s.

The third-tier plan includes AncestryDNA Traits, which tests for more than 30 traits. These tests reveal many traits, including eye color, vitamin levels, and muscle fatigue. You can view how AncestryDNA determined your results, and learn which factors besides genetics affect those traits, such as diet.

23andMereports cover a few categories: Ancestry Composition, DNA Relatives List, Neanderthal Ancestry, and Maternal and Paternal haplogroups. You unearth more detail by interacting with the map on the ancestry composition page, including the exact heritage percentages. You can also see the last time when that information was updated (our data was refreshed in June 2021).

Based on your mitochondrial (maternal) DNA, the maternal haplogroup section shows which haplogroup you belong to, as well as subgroups. People in the same haplogroup have a common ancestor. For example, the haplogroup T2b shares an ancestor who lived 10,000 years ago; most people in this haplogroup live in Europe. The Y chromosome determines paternal haplogroups.

If you're genetically male (as in, you have an X chromosome and a Y chromosome), you can view both your maternal and paternal lines. People with two X chromosomes can't access this data unless their father or brother submits their DNA.

23andMe offers three options: Ancestry + Traits Service; Health + Ancestry Service; and 23andMe+ membership, including the Health + Ancestry kit. The membership includes more in-depth health information, advanced DNA Relative filters, and access to more than three times the DNA Relatives.

Winner:23andMe

AncestryDNA briefly offered DNA-based health testing starting in 2019, but discontinued the service in winter 2020 to focus on its core products. Members who used this product during its brief lifespan had a chance to download their results in 2020, but they're no longer available in their profiles.

23andMe's Health and Traits reports are available in several categories, such as Health Predisposition, Carrier Status, and Wellness. The company tests for many conditions, including Celiac disease, macular degeneration, and Type-2 diabetes. As mentioned earlier, it also tests for traits like your alcohol flush reaction, muscle composition, and even asparagus odor detection (very likely in our case). The company continues to add new reports.

Even if you've opted out of health testing, you can optionally fill out 23andMe's health questionnaires to help with company research. You can also choose to save your saliva samples at 23andMe's labs for future testing. Otherwise, 23andMe will destroy your sample once it's processed (Ancestry will destroy your sample on request).

Winner:23andMe

AncestryDNA searches its database for matches using the service's DNA Matches feature. Only your username, possible relationship, and genetic ethnicity are visible to other members. AncestryDNA continues to search for matches as its database grows.

Ancestry started as family tree software, and it incorporates your AncestryDNA results into your existing family trees. Aside from that, AncestryDNA has a feature called ThruLines, which uses public Ancestry family trees and your private trees to show common ancestors you share with your matches. It also displays potential ancestors from your grandparents to multiples of great grandparents. If you mouse over a probable ancestor, AncestryDNA shows you how many DNA matches are in its system. You can view as much information about your matches as the matches allow, which can be as little as their relationship to you.

Like AncestryDNA, 23andMe looks for DNA matches among its other members, but only if you opt-in to its DNA Relatives program. You'll get email alerts about possible matches and their relationship with you. You can turn on open sharing to make specific details available for other members, such as your full name. If you leave this off, other users must send you a share request. Depending on profile settings, you can either send a message or an introduction.

Winner:Ancestry

AncestryDNA and 23andMe are both excellent DNA testing services, but they have different focuses. The former is a good choice if youre building a family tree, but the latter has robust health-testing capabilities, and rich reports on maternal/paternal lines and Neanderthal ancestry.In short, 23andMe is the DNA kit you should buy if you're looking for a wide view of your genetics.

Overall Winner:23andMe

Note that it's not just your family's human members whose ancestry might interest you.The best dog DNA test kitscan help you tell a Maltese from a mutt, and we've reviewed the top choices in that category.

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AncestryDNA vs. 23andMe: Which DNA Kit Delivers the Best Genetic Information? - PCMag.com

Sex-specific differences in aging and Alzheimer’s disease may be tied to genetics – National Institute on Aging

When it comes to cognitive aging and Alzheimers disease, the differences between men and women may be related to genetics. According to an NIA-supported study published in JAMA Neurology, August 2021, genes contained in the X chromosome may hold the key to differences between men and women in aging and Alzheimers-related cognitive decline.

Cognitive changes can affect memory, attention, and executive functions such as planning and self-control. These changes can occur as a result of the natural process of aging or dementia such as Alzheimers. Sometimes, cognitive changes are accompanied by changes in the brain such as the formation of neurofibrillary tangles, a hallmark characteristic of the brain tissue associated with Alzheimers. The tangles involve the twisting of tau protein threads of the nerve cells in the brain tissue. The rate and degree of cognitive decline, as well as the extent of neurofibrillary tangles, differ between men and women.

In this study, scientists led by a team at the University of California, San Francisco, analyzed genetic and clinical data from a joint cohort consisting of two long-term studies: the Religious Orders Study and the Rush Memory and Aging Project. The scientists gathered genetic data from the brain tissue of 508 autopsied individuals via RNA sequencing, a technique used to measure how many copies of specific genes are present in a humans cells at a given time.

The scientists also gathered data about participants cognitive function over several years to assess changes in cognition, including memory and attention. Participants did not have dementia at the time of their enrollment in the studies and were monitored periodically until their death. Using genetic and clinical data, the scientists examined associations of cognitive changes and levels of neurofibrillary tangles with genes on the X chromosome.

The X chromosome is one of the two sex chromosomes in humans (the Y chromosome is the other). Women have two X chromosomes, and men have one X and one Y. Unlike the Y chromosome, which contains just 50 to 60 genes, the X chromosome contains hundreds of genes, many of which are related to brain function. However, not much is known about how the expression of X chromosome-linked genes affects brain changes in aging and Alzheimers. Gene expression is the process by which the instructions in our DNA are converted into a functional product, such as a protein.

The scientists found that the expression levels of 19 genes on the X chromosome were linked to changes in cognition and quantity of neurofibrillary tangles. In women, this increased expression was associated with slower cognitive decline. The expression of these genes was not increased in men. This may suggest that specific genes on the X chromosome help protect women from cognitive decline in aging and Alzheimers.

In contrast, the expression of three X chromosome genes associated with neurofibrillary tangles was increased in men. This may suggest that men could be more at risk of developing Alzheimers-related pathological changes than women.

Because this study used a sample population that was 98% white, future studies must be conducted on a more diverse sample. Nonetheless, the expression of X chromosome genes may uncover some of the genetic differences in cognitive aging and Alzheimers between men and women. Research to further examine the role of X chromosome genes in aging and Alzheimers could help advance personalized treatment options for both men and women.

This research was funded in part by NIA grants RF1AG068325, P30AG10161, R01AG15819, R01AG17917, U01AG61356, U01AG46152, R01AG36836, R01AG060393, and R01AG062588.

These activities relate to NIHs AD+ADRD Research Implementation Milestone 2.D, Create programs in basic, translational and clinical research aimed at comprehensive understanding of the impact of sex differences on the trajectories of brain aging and disease, phenotypes of AD and ADRD risk and responsiveness to treatment.

Reference: Davis EJ, et al. Sex-specific association of the X chromosome with cognitive change and tau pathology in aging and Alzheimer Disease. JAMA Neurology. 2021 Aug 23;e212806. doi: 10.1001/jamaneurol.2021.2806.

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Sex-specific differences in aging and Alzheimer's disease may be tied to genetics - National Institute on Aging

Genetic Research Reveals New Clues for the Shared Origins of Irritable Bowel Syndrome and Mental Health Disorders – SciTechDaily

Irritable bowel syndrome. Credit: Scientific Animations

An international study of more than 50,000 people with irritable bowel syndrome (IBS) has revealed that IBS symptoms may be caused by the same biological processes as conditions such as anxiety. The research highlights the close relationship between brain and gut health and paves the way for development of new treatments.

IBS is a common condition world-wide, affecting around 1 in 10 people and causing a wide range of symptoms including abdominal pain, bloating, and bowel dysfunction that can significantly affect peoples lives. Diagnosis is usually made after considering other possible conditions (such as Crohns disease or bowel cancer), with clinical tests coming back normal. The condition often runs in families and is also more common among people who are prone to anxiety. The causes of IBS are not well understood, but an international team of researchers has now identified several genes that provide clues into the origins of IBS.

Although IBS occurs more frequently in those who are prone to anxiety, we dont believe that one causes the other our study shows these conditions have shared genetic origins. Miles Parkes

The research team, including more than 40 institutions and coordinated by scientists in UK and Spain, looked at genetic data from 40,548 people who suffer from IBS from the UK Biobank and 12,852 from the Bellygenes initiative (a world-wide study aiming to identify genes linked to IBS) and compared them to 433,201 people without IBS (controls), focusing on individuals of European ancestry. The findings were repeated with de-identified data from the genomics company 23andMe Inc., provided by customers who have consented to research, by comparing 205,252 people with IBS to 1,384,055 controls.

The results showed that overall, heritability of IBS (how much your genes influence the likelihood of developing a particular condition) is quite low, indicating the importance of environmental factors such as diet, stress and patterns of behavior that may also be shared in the family environment.

However, 6 genetic differences (influencing the genes NCAM1, CADM2, PHF2/FAM120A, DOCK9, CKAP2/TPTE2P3 and BAG6) were more common in people with IBS than in controls. As IBS symptoms affect the gut and bowel, it would be expected that genes associated with increased risk of IBS would be expressed there but this is not what the researchers found. Instead, most of the altered genes appear to have more clear-cut roles in the brain and possibly the nerves which supply the gut, rather than the gut itself.

Researchers also looked for overlap between susceptibility to IBS and other physical and mental health conditions. They found that the same genetic make-up that puts people at increased risk of IBS also increases the risk for common mood and anxiety disorders such as anxiety, depression, and neuroticism, as well as insomnia. However, the researchers stress that this doesnt mean that anxiety causes IBS symptoms or vice versa.

Study co-senior investigator and consultant gastroenterologist Professor Miles Parkes from the University of Cambridge explained: IBS is a common problem, and its symptoms are real and debilitating. Although IBS occurs more frequently in those who are prone to anxiety, we dont believe that one causes the other our study shows these conditions have shared genetic origins, with the affected genes possibly leading to physical changes in brain or nerve cells that in turn cause symptoms in the brain and symptoms in the gut.

The study also found that people with both IBS and anxiety were more likely to have been treated frequently with antibiotics during childhood. The study authors hypothesize that repeated use of antibiotics during childhood might increase the risk of IBS (and perhaps anxiety) by altering the normal gut flora (healthy bacteria that normally live in the gut) which in turn influence nerve cell development and mood.

Current treatments for IBS vary widely and include dietary changes, prescription medications targeting the gut or brain, or behavioral interventions. Lead author Chris Eijsbouts from the University of Oxford suggests that discovering genes that contribute to IBS may aid in the development of new treatments in the long term. He said: Even genetic changes that have only subtle effects on IBS can provide clues about pathways to target therapeutically. Unlike the individual genetic changes themselves, drugs targeting the pathways they tell us about may have a considerable impact on the condition, as we know from other disease areas.

Co-senior investigator Dr Luke Jostins from the University Oxford commented: We anticipate that future research will build on our discoveries, both by investigating the target genes identified and exploring the shared genetic risk across conditions to improve understanding of the disordered brain-gut interactions which characterize IBS.

IBS represents a remarkable challenge for genetic studies. These initial findings have been long awaited, and finally tell us this type of research is worth the struggle, added Ikerbasque Professor Mauro DAmato from CIC bioGUNE, co-senior investigator and coordinator of the Bellygenes initiative.

Reference: Genome-wide analysis of 53,400 people with irritable bowel syndrome highlights shared genetic pathways with mood and anxiety disorders by Chris Eijsbouts, Tenghao Zheng, Nicholas A. Kennedy, Ferdinando Bonfiglio, Carl A. Anderson, Loukas Moutsianas, Joanne Holliday, Jingchunzi Shi, Suyash Shringarpure, 23andMe Research Team, Alexandru-Ioan Voda, The Bellygenes Initiative, Gianrico Farrugia, Andre Franke, Matthias Hbenthal, Gonalo Abecasis, Matthew Zawistowski, Anne Heidi Skogholt, Eivind Ness-Jensen, Kristian Hveem, Tnu Esko, Maris Teder-Laving, Alexandra Zhernakova, Michael Camilleri, Guy Boeckxstaens, Peter J. Whorwell, Robin Spiller, Gil McVean, Mauro DAmato, Luke Jostins and Miles Parkes, 5 November 2021, Nature Genetics.DOI: 10.1038/s41588-021-00950-8

This research received funding and support from National Institute for Health Research (NIHR) Biomedical Research Centres in Cambridge, Oxford, Nottingham and Manchester. Further funding and support was received from the Wellcome Trust, the Li Ka Shing Foundation and the Kennedy Trust for Rheumatology Research in the UK, and the Spanish Ministry of Economy and Competitiveness (Instituto Salud Carlos III), the Health Department of the Basque Government and the Swedish Research Council (Vetenskapsradet).

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Genetic Research Reveals New Clues for the Shared Origins of Irritable Bowel Syndrome and Mental Health Disorders - SciTechDaily

Genetics, History, and the Mystery of Jewish Resilience Mosaic – Mosaic

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Is COVID-19 here to stay? A team of biologists explains what it means for a virus to become endemic – The Apopka Voice

By Sara Sawyer, Professor of Molecular, Cellular and Developmental Biology, University of Colorado Boulder; Arturo Barbachano-Guerrero, Postdoctoral Researcher in Virology, University of Colorado Boulder, and Cody Warren, Postdoctoral Fellow in Virology a

Now that kids ages 5 to 11 are eligible for COVID-19 vaccination and the number of fully vaccinated people in the U.S. is rising, many people may be wondering what the endgame is for COVID-19.

Early on in the pandemic, it wasnt unreasonable to expect that SARS-CoV-2 (the virus that causes COVID-19) might just go away, since historically some pandemic viruses have simply disappeared.

For instance, SARS-CoV, the coronavirus responsible for the first SARS pandemic in 2003, spread to 29 countries and regions, infecting more than 8,000 people from November 2002 to July 2003. But thanks to quick and effective public health interventions, SARS-CoV hasnt been observed in humans in almost 20 years and is now considered extinct.

On the other hand, pandemic viruses may also gradually settle into a relatively stable rate of occurrence, maintaining a constant pool of infected hosts capable of spreading the virus to others. These viruses are said to be endemic.

Examples of endemic viruses in the United States include those that cause the common cold and the seasonal flu that appear year after year. Much like these, the virus that causes COVID-19 likely wont die out, and most experts now expect it to become endemic.

We are a team of virologists and immunologists from the University of Colorado Boulder studying animal viruses that infect humans. An essential focus of our research is to identify and describe the key adaptations that animal viruses require to persist in the human population.

So why did the first SARS virus from 2003 (SARS-CoV) go extinct while this one (SARS-CoV-2) may become endemic?

The ultimate fate of a virus depends on how well it maintains its transmission. Generally speaking, viruses that are highly contagious, meaning that they spread really well from one person to the next, may never die out on their own because they are so good at finding new people to infect.

When a virus first enters a population with no immunity, its contagiousness is defined by scientists using a simple mathematical term, called R0, which is pronounced R-naught. This is also referred to as the reproduction number. The reproduction number of a virus represents how many people, on average, are infected by each infected person. For example, the first SARS-CoV had an R0 of about 2, meaning that each infected person passes the virus to two people on average. For the delta variant strain of SARS-CoV-2, the R0 is between 6 and 7.

The goal for public health authorities is to slow the rate by which viruses spread. Universal masking, social distancing, contact tracing and quarantines are all effective tools to reduce the spread of respiratory viruses. Since SARS-CoV was poorly transmissible, it just took a little bit of public health intervention to drive the virus to extinction. Given the highly transmissible nature of the delta variant, the challenge for eliminating the virus will be much greater, meaning that the virus is more likely to become endemic.

Its clear that SARS-CoV-2 is very successful at finding new people to infect, and that people can get infected after vaccination. For these reasons, the transmission of this virus is not expected to end. Its important that we consider why SARS-CoV-2 moves so easily from one person to the next, and how human behavior plays into that virus transmission.

SARS-CoV-2 is a respiratory virus that is spread through the air and is efficiently transmitted when people congregate. Critical public health interventions, like mask use and social distancing, have been key in slowing the spread of disease. However, any lapse in these public health measures can have dire consequences. For instance, a 2020 motorcycle rally brought together nearly 500,000 people in Sturgis, South Dakota, during the early phases of the pandemic. Most of the attendees were unmasked and not practicing social distancing. That event was directly responsible for an increase in COVID-19 cases in the state of South Dakota and nationwide. This shows how easily the virus can spread when people let their guard down.

The virus that causes COVID-19 is often associated with superspreading events, in which many people are infected all at once, typically by a single infected individual. In fact, our own work has shown that just 2% of the people infected with COVID-19 carry 90% of the virus that is circulating in a community. These important supercarriers have a disproportionately large impact on infecting others, and if they arent tracked down before they spread the virus to the next person, they will continue to sustain the epidemic. We currently dont have a nationwide screening program geared toward identifying these individuals.

Finally, asymptomatically infected people account for roughly half of all infections of COVID-19. This, when coupled with a broad range of time in which people can be infectious two days before and 10 days after symptoms appear affords many opportunities for virus transmission, since people who dont know they are sick generally take few measures to isolate from others.

The contagious nature of SARS-CoV-2 and our highly interconnected society constitute a perfect storm that will likely contribute to sustained virus spread.

Given the considerations discussed above and what we know about COVID-19 so far, many scientists believe that the virus that causes COVID-19 will likely settle into endemic patterns of transmission. But our inability to eradicate the virus does not mean that all hope is lost.

Our post-pandemic future will heavily depend on how the virus evolves over the coming years. SARS-CoV-2 is a completely new human virus that is still adapting to its new host. Over time, we may see the virus become less pathogenic, similar to the four coronaviruses that cause the common cold, which represent little more than a seasonal nuisance.

Global vaccination programs will have the greatest impact on curbing new cases of the disease. However, the SARS-CoV-2 vaccine campaign so far has touched only a small percentage of people on the planet. In addition, breakthrough infections in vaccinated people still occur because no vaccine is 100% effective. This means that booster shots will likely be needed to maximize vaccine-induced protection against infection.

With global virus surveillance and the speed at which safe and effective vaccines have been developed, we are well poised to tackle the ever-evolving target that is SARS-CoV-2. Influenza is endemic and evolves quickly, but seasonal vaccination enables life to go on as normal. We can expect the same for SARS-CoV-2 eventually.

Four seasonal coronaviruses circulate in humans endemically already. They tend to recur annually, usually during the winter months, and affect children more than adults. The virus that causes COVID-19 has not yet settled down into these predictable patterns and instead is flaring up unpredictably around the globe in ways that are sometimes difficult to predict.

Once rates of SARS-CoV-2 stabilize, we can call it endemic. But this transition may look different based on where you are in the world. For instance, countries with high vaccine coverage and plentiful boosters may soon settle into predictable spikes of COVID-19 during the winter months when the environmental conditions are more favorable to virus transmission. In contrast, unpredictable epidemics may persist in regions with lower vaccination rates.

This article is republished from The Conversation under a Creative Commons license.

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Is COVID-19 here to stay? A team of biologists explains what it means for a virus to become endemic - The Apopka Voice

Scientist Camilla Pang On Being Neurodivergent And The Power Of Science : Short Wave – NPR

Scientist and author Camilla Pang turns her memoir into an instruction manual for life. Greg Barker/Penguin Books hide caption

Scientist and author Camilla Pang turns her memoir into an instruction manual for life.

Camilla Pang is a postdoctoral scientist and writer. When she was five years old, she asked her mother a vexing question: "Is there an instruction manual for humans - like a guidebook - something that explains why people behave the way they do?"

Years later, Pang was diagnosed with autism spectrum disorder, attention-deficit/hyperactivity disorder, and generalized anxiety disorder. At the time, she simply felt like an outsider.

"No, Millie," her mother told her.

Pang did find answers and connection in her uncle's science textbooks. She began scribbling facts and figures in notebooks and reading about all kinds of science. She went on to obtain a Ph.D. in bioinformatics from University College London and she reached a place in her life where she had enough material to write the instruction manual she wished she'd had as a kid.

Short Wave host Emily Kwong talks with Pang about her memoir, An Outsiders Guide to Humans: What Science Taught Me About What We Do And Who We Are.

She says it is a guidebook for anyone searching for a blueprint to the human condition, pairing scientific principles with the more befuddling aspects of human behavior and daily life. In making tough decisions, Pang deploys lessons from machine learning. In seeking harmony in relationships, she turns to wave theory. Her writing is both prescriptive and reassuring and she ultimately wants to help people feel less alone.

"I think there's no greater empathy than enabling people to feel that they can do something, and be assuring them that what they feel is valid," Pang says.

The British version of the book, Explaining Humans: What Science Can Teach Us About Love, Life and Relationships, won the Royal Society Science Book Prize in 2020. A paperback version of An Outsider's Guide to Humans will be available December 7, 2021 from Penguin Books.

This episode was produced by Rebecca Ramirez, edited by Gisele Grayson and fact-checked by Margaret Cirino. The audio engineer was Leo Del Aguila.

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Scientist Camilla Pang On Being Neurodivergent And The Power Of Science : Short Wave - NPR

Opinion | You Are the Object of Facebooks Secret Extraction Operation – The New York Times

As we move into the third decade of the 21st century, surveillance capitalism is the dominant economic institution of our time. In the absence of countervailing law, this system successfully mediates nearly every aspect of human engagement with digital information. The promise of the surveillance dividend now draws surveillance economics into the normal economy, from insurance, retail, banking and finance to agriculture, automobiles, education, health care and more. Today all apps and software, no matter how benign they appear, are designed to maximize data collection.

Historically, great concentrations of corporate power were associated with economic harms. But when human data are the raw material and predictions of human behavior are the product, then the harms are social rather than economic. The difficulty is that these novel harms are typically understood as separate, even unrelated, problems, which makes them impossible to solve. Instead, each new stage of harm creates the conditions for the next stage.

All of it begins with extraction. An economic order founded on the secret massive-scale extraction of human data assumes the destruction of privacy as a nonnegotiable condition of its business operations. With privacy out of the way, ill-gotten human data are concentrated within private corporations, where they are claimed as corporate assets to be deployed at will.

The social effect is a new form of inequality, reflected in the colossal asymmetry between what these companies know about us and what we know about them. The sheer size of this knowledge gap is conveyed in a leaked 2018 Facebook document, which described its artificial intelligence hub, ingesting trillions of behavioral data points every day and producing six million behavioral predictions each second.

Next, these human data are weaponized as targeting algorithms, engineered to maximize extraction and aimed back at their unsuspecting human sources to increase engagement. Targeting mechanisms change real life, sometimes with grave consequences. For example, the Facebook Files depict Mr. Zuckerberg using his algorithms to reinforce or disrupt the behavior of billions of people. Anger is rewarded or ignored. News stories become more trustworthy or unhinged. Publishers prosper or wither. Political discourse turns uglier or more moderate. People live or die.

Occasionally the fog clears to reveal the ultimate harm: the growing power of tech giants willing to use their control over critical information infrastructure to compete with democratically elected lawmakers for societal dominance. Early in the pandemic, for example, Apple and Google refused to adapt their operating systems to host contact-tracing apps developed by public health authorities and supported by elected officials. In February, Facebook shut down many of its pages in Australia as a signal of refusal to negotiate with the Australian Parliament over fees for news content.

Thats why, when it comes to the triumph of surveillance capitalisms revolution, it is the lawmakers of every liberal democracy, especially in the United States, who bear the greatest burden of responsibility. They allowed private capital to rule our information spaces during two decades of spectacular growth, with no laws to stop it.

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Opinion | You Are the Object of Facebooks Secret Extraction Operation - The New York Times

How Would Your Prayer Life Change If You Saw It As An Opportunity For Fellowship, Rather Than An Obligation? – WFMZ Allentown

LANDENBERG, Pa., Nov. 15, 2021 /PRNewswire-PRWeb/ -- Author Barbara A. Richmond shares to enlighten the purpose and benefits of prayer as well as the effects of prayerlessness in Men Ought Always to Pray: God Wants an Intimate Relationship ($58.99, paperback, 9781662834011; $9.99, e-book, 9781662834028).

Even though He had no sins to confess and knew the Father better than anyone, Jesus spent a good chunk of His earthly life praying. He encouraged His followers to pray as well, providing them with a model prayer to get them started. Richmond takes His example and other Biblical teachings and helps readers see the true purpose behind prayer and how to achieve the sweet fellowship God offers.

"Prayer is the most earnest way we exemplify our love to God. During prayer, we are most conscious of God's presence, and this is the time that we can give all of our being to Him," said Richmond.

Dr. Barbara A. Richmond is a highly educated, anointed woman of God who loves to pray. She is an ordained minister, pastor and evangelist with a Ph.D. in Human Behavior, a Master's in Psychology and a Certificate in Biblical Studies.

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Xulon Press, a division of Salem Media Group, is the world's largest Christian self-publisher, with more than 15,000 titles published to date. Men Ought Always to Pray is available online through xulonpress.com/bookstore, amazon.com, and barnesandnoble.com.

Media Contact

Dr. Barbara A. Richmond, Salem Author Services, 484-751-7551, Barbyalobruc2@gmail.com

SOURCE Xulon Press

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How Would Your Prayer Life Change If You Saw It As An Opportunity For Fellowship, Rather Than An Obligation? - WFMZ Allentown