Category Archives: Transhuman News

Ive been reading the many recent letters regarding the likely reversal of Roe v. Wade. The writer of The case for overturning Roe v Wade has it right by pointing out that there is absolutely nothing in the U.S. Constitution that provides for a right to abortion. The writer however said he was pro-choice, stating that one of the reasons for this was the small size of the unborn baby at the time of most abortions. But of course we were all small during those first several months in our mothers womb, and yet our complete human genetics were already set from the moment of conception.

The writer also said that women should have absolute bodily autonomy, again intentionally ignoring the absolute scientific fact that theres another body involved - that of her not yet born little girl or boy. We keep hearing follow the science, but when the science shows 100% that unique human life begins at conception, abortion supporters pretend science doesnt matter here.

Another writer mistakenly took it upon himself to be able to look into everyone elses hearts and minds and decide that Its about control, not babies . By this he meant people trying to control women. While I dont have the ability to judge others like that writer, I do know from years of working with pro-life that it is about both protecting unborn babies, and offering life-options help to women. Thankfully, I found one point of agreement in his letter, that being that God still loves those who choose abortion. Such merciful love provides forgiveness and restoration for those who repent and receive it.

Several writers blamed the Catholic Church for Roes reversal. While Catholics have been at the forefront working to restore protection for innocent human life in the womb; be assured that there are also tens of millions of other-than-Catholics who are working and praying for this as well.

Also, we keep hearing of the need for abortions to be legal and safe. Well, as pointed out above, legal abortions certainly arent safe for the 50% of the human lives involved who are killed by abortion. In addition, many of the legal abortions arent physically safe for the mother as well. And, they certainly arent safe emotionally, as there is often a lifetime of guilt to deal with.

The bottom line is that intentionally killing innocent human life is most certainly not reproductive health care. Rather, we need to continue to support women who find themselves in an unexpected pregnancy - as is being done with the ever increasing number of pregnancy help centers and homes, church programs and adoption options. Where there is genuine medical need during a pregnancy, there is help available to protect both the life of the mother and her unborn.

Finally, as another writer pointed out, its way past time to stop pretending otherwise - abortion ends the life of a unique and innocent human being! Every human life conceived is a gift of God, created in his image. May we all say no to Roe and yes to life!

Ken Koehler lives in West Fargo.

This letter does not necessarily reflect the opinion of The Forum's editorial board nor Forum ownership.

Originally posted here:
Letter: Why no to Roe and abortion - INFORUM

UPPSALA, Sweden, May 09, 2022 (GLOBE NEWSWIRE) -- Olink Holding AB (publ) (Nasdaq: OLK) today announced that Oxford Genomics at the University of Oxford adopts the Olink technology and becomes the first Olink certified laboratory in the United Kingdom. The partnership will enable novel techniques to unravel mechanisms of disease using the Olink Explore platform.

Oxford Genomics is centered within the Wellcome Centre of Human Genetics which was formed in the founding years of the Human Genome Project; they have been producing cutting edge research for more than two decades. As we move into an age of multi-omic analysis to truly understand the linkage between disease and phenotype, proteomics is an essential tool to complement their other cutting-edge technologies.

With the recent establishment of the Oxford-GSK Institute, Olink Explore will be utilized to build a multiomics approach to mapping molecular mechanisms of complex diseases such as Parkinsons and Alzheimers. Expertise in machine learning and bioinformaticians at Oxfords Big Data Institute will be able to leverage these datasets to pinpoint novel targets and identify signatures to stratify patients.

By utilizing the Olink platform we are interested in discovering biomarkers and early disease signatures in common diseases, because they would provide clues to druggable targets and readouts we can use to test potential therapeutic candidates, said Prof John Todd Director of Wellcome Centre for Human Genetics and Co-Director of Oxford GSK Institute. We are trying to make the drug development process more precise by understanding the heterogeneity in the patients instead of one drug fits all.

The new Olink Explore 3072 platform enables access to an expanded library of carefully curated and validated assays to provide detailed proteomics data to improve understanding of human health. The Olink market-leading proteomics solution measures up to 3,000 proteins per sample using Proximity Extension Assay (PEA) technology combined with next generation (NGS) sequencing readout, providing a highly accurate and reproducible multiplexed method with exceptional specificity.

We are immensely proud to lay the foundation of a long lasting and prosperous partnership with such a prestigious institution as the University of Oxford, utilizing our technology as the first Olink certified laboratory in the United Kingdom. This partnership demonstrates the importance of academic partners in pioneering the establishment of new technologies. It will further democratize the use of the Olink platform in line with our mission to accelerate proteomics together with the scientific community, said Jon Heimer, CEO, Olink Proteomics. The objective is to create a better understanding of the origin of diseases, provide earlier and more accurate diagnoses with individualized treatment and enable more efficient and safer drug development.

Investor Contact Jan Medina, CFAVP Investor Relations & Capital MarketsMobile: +1617802 4157jan.medina@olink.com

Media Contact Andrea PranderCorporate Communications Manager Mobile: +46768775 275andrea.prander@olink.com

About OlinkOlink Holding AB (Nasdaq: OLK) is a company dedicated to accelerating proteomics together with the scientific community, across multiple disease areas to enable new discoveries and improve the lives of patients. Olink provides a platform of products and services which are deployed across major pharmaceutical companies and leading clinical and academic institutions to deepen the understanding of real-time human biology and drive 21st century healthcare through actionable and impactful science. The company was founded in 2016 and is well established across Europe, North America and Asia. Olink is headquartered in Uppsala, Sweden.

About Wellcome Centre for Human GeneticsThe Wellcome Centre for Human Genetics (WCHG) is a research institute of theNuffield Department of Medicineat theUniversity of Oxford, funded by the University,Wellcome,and numerous other sponsors. It is based in purpose-built laboratories on the University of Oxfords Biomedical Research Campus in Headington, one of the largest concentrations of biomedical expertise in the world. Here our researchers are able to work closely with colleagues across University departments including, but not limited to, theDepartment of Psychiatry, theDivision of Cardiovascular Medicineand theBig Data Institute.

With more than 400 active researchers and around 70 employed in administrative and support roles, the Centre is an international leader in genetics, genomics and structural biology. WCHG collaborates with research teams across the world on a number of large-scale studies in these areas. WCHGs researchers expend close to 20m annually in competitively-won grants, and publish around 300 primary papers per year.https://www.well.ox.ac.uk/

About the University of OxfordOxford University has been placed number 1 in the Times Higher Education World University Rankings for the sixth year running, andnumber2 in the QS World Rankings 2022. At the heart of this successare the twin-pillars ofour ground-breaking research and innovationand our distinctive educational offer.

Oxford is world-famous for researchand teachingexcellence and home to some of the most talented people from across the globe.Our work helps the lives of millions, solving real-world problems through a huge network of partnerships and collaborations. The breadth and interdisciplinary nature of our researchalongside our personalised approach to teachingsparks imaginative and inventive insights and solutions.

Through its research commercialisation arm, Oxford University Innovation, Oxford is the highest university patent filer in the UK and is ranked first in the UK for university spinouts, having created more than 200 new companies since 1988. Over a third of these companies have been created in the past three years.The university is a catalyst for prosperity in Oxfordshire and the United Kingdom, contributing15.7 billion to the UK economyin 2018/19, and supports more than 28,000 full time jobs.

Forward-Looking StatementsThis release may contain forward-looking statements within the meaning of applicable securities laws, including the U.S. Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, statements regarding Olinks strategy, business plans and focus. The words may, will, could, would, should, expect, plan, anticipate, intend, believe, estimate, predict, project, potential, continue, target and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements in this press release are based on managements current expectations and beliefs as of the date hereof and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements contained in this press release, including, without limitation, those related to Olinks business, operations, supply chain, strategy, goals and anticipated timelines, including for the delivery of Olink Explore 3072 and the expansion of the Explore platform, competition, and other risks identified in the section entitled Risk Factors in Olinks Registration Statement on Form F-1, as amended (File No. 333-253818) filed with the U.S. Securities and Exchange Commission (SEC) and in the other filings, reports, and documents Olink files with the SEC from time to time. Olink expressly disclaims any obligation to update any forward-looking statements in this release to reflect any change in its expectations with regard thereto or any change in events, conditions or circumstances on which any such statement is based, unless required by law or regulation.

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University of Oxford adopts Olink technology to advance protein biomarker discovery and unravel mechanisms of disease - GlobeNewswire

Health and medicine | Honors and awards | News releases | Science

May 6, 2022

Another lovely day at the University of Washingtons Seattle campus.Pamela Dore/University of Washington

Four faculty members at the University of Washington have been elected to the National Academy of Sciences. The new members from the UW are:

They are among 120 new members and 30 international members to the National Academy of Sciences this year. Election recognizes achievement in science by election to membership, and with the National Academy of Engineering and the National Academy of Medicine provides science, engineering, and health policy advice to the federal government and other organizations, according to an announcement May 3 by the academy.

Buffalo is noted for her research on the neural mechanisms behind learning and remembering. She studies how a system of structures in the brain, including the hippocampus and its surrounding cortical regions, set up new memories and how this system functions during memory retrieval. These structures are the first to be affected in Alzheimers disease. Lesions within these structures are associated with profound memory deficits. Her work may help improve the understanding of what foreshadows the onset Alzheimers and other dementias. She has a particular interest in how the brain maps surroundings, because getting lost in familiar locations is a common early symptom of Alzheimers. Buffalo earned her doctoral degree at the University of California, San Diego and did postdoctoral training in neuropsychology at the National Institute of Mental Health. She received the 2011 Troland Research Award for her innovative studies from the National Academy of Sciences.

Mougous is known for his research on how bacteria interact with each other in the environment and in our bodies. Much of his work focuses on the battles that occur within communities of bacteria. He examines the arsenals they deploy to attack each other and defend themselves. Among his areas of study are antibacterial toxins that disable target cells in a variety of ways, secretion systems that mediate antagonism between bacteria, and the toxins that virulent bacteria secrete to overcome host defense strategies. His laboratory also studies the densely populated mammalian gut microbiome, where conflict rages among microbes as bacteria compete for resources and struggle to survive. His lab is hoping to harness the antimicrobial tactics of bacteria to develop new therapies for infections and other purposes. Mougous earned his doctoral degree from the University of California, Berkeley. He is a Howard Hughes Medical Institute investigator and a researcher at the UW Medicine Institute for Stem Cell and Regenerative Medicine. In 2021, he received the National Institute of Sciences Award in Molecular Biology for his pioneering studies in microbiology.

Dr. Shendures research group has pioneered a variety of genome sequencing and analysis methods, including exome sequencing and its earliest applications to gene discovery for Mendelian disorders and autism; cell-free DNA diagnostics for cancer and reproductive medicine; massively parallel reporter assays; saturation genome editing; whole organism lineage tracing; and massively parallel molecular profiling of single cells. He has received numerous awards, including the 2012 Curt Stern Award from the American Society of Human Genetics, a 2013 National Institutes of Health Directors Pioneer Award and the 2019 Richard Lounsbery Award from the National Academy of Sciences. Dr. Shendure has been an advisor to the NIH Director, the U.S. Precision Medicine Initiative, the National Human Genome Research Institute, the Chan-Zuckerberg Initiative and the Allen Institutes for Cell Science and Immunology. He received his M.D. and Ph.D. degrees in 2007 from Harvard Medical School, where he trained with geneticist and molecular biologist George Church on advancing DNA sequencing techniques. He is currently an investigator with the Howard Hughes Medical Institute, director of the Allen Discovery Center for Cell Lineage Tracing and scientific director of the Brotman Baty Institute for Precision Medicine.

Trumans studies have focused on the genes, hormones and neural architecture underlying insect development and evolution. Early in his career, he identified the key hormone in moths that induces molting, as well as the brain-based circadian rhythms that exert overall control over this process. He later studied regulation of molting in the fruit fly and genes that control metamorphosis in moths. Truman earned a doctoral degree from Harvard University in 1970, where he continued as a Harvard Junior Fellow until joining the UW faculty in 1973. He became a full professor in 1978. He retired from the UW in 2007 and became a Group Leader at the Howard Hughes Medical Institutes Janelia Research Campus, where he studied nervous system metamorphosis in fruit flies. In 2016, Truman returned to the UW as a professor emeritus, and today continues to study the evolution and development of insects and crustaceans at the UWs Friday Harbor Laboratories. In 1970, he received the American Association for the Advancement of Sciences Newcomb Cleveland Research Prize and was a Guggenheim Fellow in 1986. Truman was elected to the American Academy of Arts and Sciences in 2009.

With this years addition, the National Academy of Sciences now has 2,512 active members and 517 nonvoting international members, who hold citizenship outside of the U.S.

Excerpt from:
Four UW researchers elected to the National Academy of Sciences for 2022 - University of Washington

SAN FRANCISCO, CA (IANS) Vineeta Agarwala, the wife of Twitter CEO Parag Agrawal, is now making headlines amid Elon Musks $44 billion takeover deal.

Her role as general partner at Andreessen Horowitz a VC firm which has agreed to pay $400 million as part of Musks new $7.1 billion financing commitments is set to create a conflict of interest.

As a general partner at Andreessen Horowitz, she leads investments for the firms bio and health fund across therapeutics, life sciences tools/diagnostics, and digital health, with a focus on companies leveraging unique datasets to improve drug development and patient care delivery.

Andreessen Horowitz is also one of the biggest backers of Meta.

Prior to joining a16z, Vineeta held many different roles in the healthcare space.

She was a physician, an operator at healthtech startups and investor at the Google Ventures life sciences team.

She was an early data scientist at Kyruus, a management consultant for biotech, pharmaceutical, and medical device clients at McKinsey & Co, and a director of product management at Flatiron Health.

She has collaborated with academic researchers at Cold Spring Harbor Laboratory, Lawrence Livermore National Laboratory, and the Broad Institute, where she did graduate work in computational biology and human genetics.

Vineeta holds a Bachelor of Science in biophysics from Stanford University, and MD and PhD degrees from Harvard Medical School/MIT.

She continues to see patients at Stanford as an adjunct clinical professor in the Division of Primary Care and Population Health.

Vineeta serves on several portfolio company boards, including BigHat Biosciences, GC Therapeutics, Memora Health, Thyme Care, Pearl Health, and Waymark.

Meanwhile, there are doubts over Parags future once Musk takes over, as the Tesla CEO himself can become a temporary CEO of the platform. According to reports, Musk may have also lined up a new Twitter CEO.

Parag is likely to receive nearly $39 million due to a clause in his contract once he leaves Twitter. His total compensation for 2021 was $30.4 million, largely in stocks.

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Parag Agrawal's Wife Vineeta Linked to Musk's Twitter Takeover - India West

When it comes to dog breeds, you may think you know your pups, but a study released this week confirmed what dog trainers and pit bull advocates have known all along: every dogs personality is special and unique!

If you live on this planet, youre likely to have encountered an enthusiastic dog owner oversharing all of the amazing things about their most loyal companion. While were totally on board with the concept that every child is exceptional, this specific breed of enthusiasm got University of Massachusetts geneticist Elinor Karlsson thinking just how much of a dogs personality is actually an inherited trait?

Karlsson and her stacked team of researchers from MIT, Harvard, and the Darwins Ark Foundation interviewed 18,385 dog owners about their canines behavior, including if theyre friendly with strangers, whether theyre possessive, if they enjoy retrieving objects, and even whether they circle before taking a poo.

No Toxic Traits Here!

After comparing the survey results to the DNA of 2,155 purebred and mixed breed dogs, the researchers found that while some breeds may show a greater tendency to howl, retrieve, or respond to human direction, only 9% of all personality traits were directly related to genetics or breed.

Considering there was zero evidence linking any breed with aggression, this study is great news for advocates of breeds like pit bulls and rottweilers, who are often banned by apartments, homeowners associations, and even entire cities.

Its a major advance on how we think about dog behavior, said Elaine Ostrander, who was not involved with the study but is a canine genetics expert at the U.S. National Human Genome Research Institute.

Much like humans, multiple factors come into play to influence a dogs personality, including its environment. So keep on snuggling!

From Wild Animal to Mans Best Friend

The history of dog domestication is lengthy, with evidence placing the beginning of the practice at around 20,000 years ago and some estimates going back more than 100,000 years!

In that time, selective breeding was commonplace with ancient humans breeding dogs for specific tasks, such as hunting, herding, and sitting on their laps. However, it wasnt until the 19th century that people began classifying the animals outside of these generic categories, and tracking their bloodlines.

What began as noblemen and shepherds breeding to improve these individual skills and amplify physical traits like coat color and texture and ear shape ultimately expanded to create the 400-plus designer dog breeds recognized today.

Considering the intentions behind breeding, wed like to submit a request for a part two of this study. If a dogs breed doesnt dictate its personality, does its owners personality dictate the breed of dog they get?

Well be waiting.

By Meghan Yani, contributor for Ripleys.com

FIND AN ATTRACTION NEAR YOU

Source: Research Shows Dog Behaviors Are Largely Unrelated to Breed

by Ripley's Believe It or Not!

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Research Shows Dog Behaviors Are Largely Unrelated to Breed - EverythingGP

Photo: Richard Dawkins, by Anders Hesselbom, Public domain, via Wikimedia Commons.

Editors note: We are delighted to present a series by geologist Casey Luskin on The Positive Case for Intelligent Design. This is the ninth entry in the series, a modified excerpt from the new bookThe Comprehensive Guide to Science and Faith: Exploring the Ultimate Questions About Life and the Cosmos.Find the full series so far here.

One potential objection to the positive case for intelligent design, developed in this series, is that Darwinian evolution might make some of the same predictions as ID, making it difficult to tell which theory has better explanatory power. For example, in systematics, ID predicted reuse of parts in different organisms, but neo-Darwinism also predicts different species may share similar traits either due to inheritance from a common ancestor, convergent evolution, or loss of function. Likewise, in genetics, ID predicted functionality for junk DNA, but evolutionists might argue noncoding DNA could evolve useful functions by mutation and selection. If neo-Darwinism makes the same predictions as ID, can we still make a positive argument for design? The answer is yes, and there are multiple responses to these objections.

First, not all the predictions generated by positive arguments for design are also made by Darwinian theory. For example, Michael Behe explains that irreducible complexity is predicted under design but predictednotto exist by Darwinism:

[I]rreducibly complex systems such as mousetraps and flagella serve both as negative arguments against gradualistic explanations like Darwins and as positive arguments for design. The negative argument is that such interactive systems resist explanation by the tiny steps that a Darwinian path would be expected to take. The positive argument is that their parts appear arranged to serve a purpose, which is exactly how we detect design.1

The same could be said of high-CSI features like protein sequences, which require rare and finely tuned sequences of amino acids to function. These are predicted by ID but are not expected under a blind trial-and-error process of mutation and selection.2

Second, the fact that a different theory can explain some data does not negate IDs ability to successfully make positive predictions. After all, a positive case means that the arguments for design stand on their own and do not depend merely on refuting other theories. While refuting competing hypotheses can certainly help solidify a theorys status as the best explanation, a positive argument must be able to stand on its own. IDs fulfilled predictions show there is positive evidence for design, regardless of what other models may or may not say.

Third, its not clear that in any of these cases neo-Darwinian evolution (or other materialistic models) makesexactlythe same predictions as ID. For example, in systematics, neo-Darwinism may predict the reuse of parts in different organisms, but it predicts that the distribution of parts will generally conform to a treelike pattern (or a nested hierarchy). Intelligent agents are not bound to distribute parts in a tree, and thus reuse of similar parts may be found even among very distantly related organisms. We can test among these different models. A 2018 paper by software engineer Winston Ewert in the journalBIO-Complexityproposed a model of common design called adependency graph, which was based on the technique used by software developers to reuse code among different software projects.3He compared the distribution of gene families reused in different organisms to a treelike pattern predicted by neo-Darwinismversusa dependency graph distribution used by computer programmers and predicted by ID. After analyzing the distribution of gene families in nine diverse types of animals, Ewerts preliminary analysis found that a common design-based dependency graph model fit the data 103000times better than a traditional Darwinian phylogenetic tree.4His ID-based dependency graph model predicted reuse of parts much better than neo-Darwinism.

Ewert tested the data against common descent. But even convergent evolution struggles to explain reuse of parts. Richard Dawkins acknowledges it is vanishingly improbable that exactly the same evolutionary pathway should ever be traveled twice,5yet we often find striking similarities across distantly related organisms, such as the camera-like structure of the vertebrate eye and the octopus (cephalopod) eye. What evolutionary biology calls extreme convergence is better explained by common design.

With junk DNA, its true that neo-Darwinian evolution predicts that functionality could sometimes evolve for noncoding DNA, and that finding function in a given case does not necessarily refute that model. Yet a major prediction of modern evolutionary theory is that neutral (neither harmful nor beneficial) mutations occur frequently and accumulate as useless genetic junk in genomes. For example, in 1972 the pioneering molecular evolutionary biologist Susumu Ohno published an article titled So much junk DNA in our genome. Writing in a volume titledEvolution of Genetic Systems,he argued that at the most, only 6% of our DNA is functional genes, with the rest being untranscribable and/or untranslatable DNA representing extinct genes or natures experiments which failed akin to fossil remains of extinct species.6

Biologists soon envisioned additional evolutionary mechanisms for filling our genomes with junk. In his influential 1976 bookThe Selfish Gene,Richard Dawkins predicted that a large fraction of our genomes has no function, because, The true purpose of DNA is to survive, no more and no less. The simplest way to explain the surplus DNA is to suppose that it is a parasite, or at best a harmless but useless passenger, hitching a ride in the survival machines created by the other DNA.7In 1980,Naturepublished two papers by influential biologists furthering the concept of selfish junk DNA. The first article, Selfish Genes, the Phenotype Paradigm and Genome Evolution, by W. Ford Doolittle and Carmen Sapienza, maintained, Natural selection operating within genomes will inevitably result in the appearance of DNAs with no phenotypic expression whose only function is survival within genomes.8A second paper, Selfish DNA: the ultimate parasite, was by Francis Crick, who won the Nobel Prize for determining the structure of DNA, and the eminent origin-of-life theorist Leslie Orgel. They concluded that much DNA in higher organisms is little better than junk, and it would be folly in such cases to hunt obsessively for its function.9Since that time, Darwinian thinkers have been seduced by the idea that parasitic DNA and random mutations will spread junk throughout our genomes. In 1994,Kenneth Miller published an article claiming that the human genome is littered with pseudogenes, gene fragments, orphaned genes, junk DNA, and so many repeated copies of pointless DNA sequences that it cannot be attributed to anything that resembles intelligent design.10Many similar quotes could be given showing that the idea of junk DNA was born, bred, and flourished from within an evolutionary paradigm.

As might be expected from such statements, the literature admits that evolutionary thinking has hindered research into functions for junk DNA.A 2003 article inScientific Americannoted that introns, a type of noncoding DNA found within genes, were immediately assumed to be evolutionary junk a view that the article later called one of the biggest mistakes in the history of molecular biology.11That same year, a paper in the journalScience observed that [a]lthough catchy, the term junk DNA for many years repelled mainstream researchers from studying noncoding DNA.12A striking admission came in a 2020 paper inNature Reviews Geneticstitled Overcoming challenges and dogmas to understand the functions of pseudogenes, which argues that dogma in biology causes demotivation into exploring pseudogene function by the a priori assumption that they are functionless. According to the paper, [t]he dominant limitation in advancing the investigation of pseudogenes now lies in the trappings of the prevailing mindset that pseudogenic regions are intrinsically non-functional and there is an emerging risk that these regions of the genome areprematurely dismissedas pseudogenic and therefore regarded as void of function.13

The ID communitys view of junk DNA stands in stark contrast to the typical evolutionary view. Going back to some of ID theorys early days in the 1990s, ID theorists have been predicting that noncoding DNA would turn out to have functions. In 1994, pro-ID scientist Forrest Mims submitted a letter toSciencethat warned against assuming that junk DNA was useless.14In 1998,William Dembski wrote that on an evolutionary view we expect a lot of useless DNA. If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit functionDesign encourages scientists to look for function where evolution discourages it.15Many other ID theorists have made similar predictions over the years. What might have happened if their predictions had been heeded?

In 2021, the journalNatureacknowledged that prior to the Human Genome Project (HGP), which was completed in 2003, there was great debate over whether it was worth mapping the vast non-coding regions of genome that were called junk DNA, or the dark matter of the genome. The article noted that over 130,000 genomic elements, previously called junk DNA have now been discovered, and highlighted how important these junk segments have turned out to be:

[I]t is now appreciated that the majority of functional sequences in the human genome do not encode proteins. Rather, elements such as long non-coding RNAs, promoters, enhancers and countless gene-regulatory motifs work together to bring the genome to life. Variation in these regions does not alter proteins, but it can perturb the networks governing protein expression With the HGP draft in hand, the discovery of non-protein-coding elements exploded. So far, that growth has outstripped the discovery of protein-coding genes by a factor of five, and shows no signs of slowing. Likewise, the number of publications about such elements also grew in the period covered by our data set. For example, there are thousands of papers on non-coding RNAs, which regulate gene expression.

Under an ID paradigm, debates over whether to investigate junk DNA would have ended much sooner with an emphatic Yes!, furthering our knowledge of genetics and medicine. When it comes to junk DNA, ID has made superior predictions.

Next, Does Intelligent Design Make Predictions or Retrodictions?

Originally posted here:
Does Darwinism Make the Same Predictions as ID? - Discovery Institute

It could be in their genes, posits Tangye. Genetic influences are either making people vulnerable to really severe disease but may also contribute to resistance there are populations of people who probably should have been infected and sick but werent.

Exactly which genes have a protective effect is part of an international research project called the COVID Human Genetic Effort, that Christodoulou is involved with.

We are collecting information and DNA from individuals who have been hyperexposed to COVID but who dont seem to contract COVID for example, living in a household where multiple family members were infected, but one member of the household wasnt to see if genetic factors can be identified that might offer protection against COVID infection, says Christodoulou, who is also the chair of Genomic Medicine at the University of Melbourne.

While researchers keep searching for the genetic clues, a new study published at the end of April, found booster shots can increase the range of immune cells, called memory B cells, making them more effective at neutralising COVID.

With any infection or vaccination, our body responds and then forgets the virus, explains Tangye, but becomes better at responding with repeated exposure. The first and second doses are like the training, getting your immune system into good shape and ready to take off and the third really gives you the protection you are primed and ready to go.

So if someone who has recently been vaccinated is exposed to COVID, they may be protected. If they have been boosted, this may provide even more protection, at least for a time.

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The degree of exposure how long we were in contact with someone and whether we were inside or out will also make a difference, as will our behaviour.

People have become much more cognisant of social distancing and washing their hands and wearing masks. There are those non-pharmaceutical interventions people have embraced, Tangye says.

As for how healthy you are generally, that unfortunately wont make us resistant to catching COVID.

We regularly hear of otherwise young, fit and healthy individuals contracting very severe COVID, says Christodoulou. For those otherwise healthy people we know that there are some factors that are associated with this, e.g., having so-called auto-antibodies to type 1 interferons (type 1 interferons are the first line of defence against COVID) or having mutations in genes that are involved in production and function of type 1 interferons.

Being healthy is good. But healthy people are still getting sick. Its not a panacea.

Interestingly, Tangye adds that there are people who naturally have this type 1 interferon pathway turned up a little bit: That can be pathogenic they can get these inflammatory diseases that dont have a defined triggerthese non-infectious, spontaneous flares for no good reason but people with those conditions may well have some resistance to COVID just because they have that innate immune response primed.

These people account for only a fraction of never COVIDs. For the rest, it seems to come down to a combination of immunity, genetics, environment and luck.

Being healthy all round puts you in better shape against infectious diseases and lifestyle disease, says Tangye. Being healthy is good. But healthy people are still getting sick. Its not a panacea.

Most of us may not be able to do much to avoid the virus, but we can still look to never COVIDs for some answers.

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If we can identify genetic reasons why people dont get COVID, it may help inform ways by which SARS COV2 enters or attacks our cells remember viruses are hopeless on their own. They need all the machinery of our cells to be disease-causing, explains Tangye.

So if we can disrupt the human cell processes without too many adverse events we could be better at stopping viral infection.

Make the most of your health, relationships, fitness and nutrition with our Live Well newsletter. Get it in your inbox every Monday.

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Havent had COVID yet? Its got to do with more than your T cells - Sydney Morning Herald

Barsh, G. S. The genetics of pigmentation: From fancy genes to complex traits. Trends Genet. 12, 299305 (1996).

CAS PubMed Article Google Scholar

Robbins, L. S. et al. Pigmentation phenotypes of variant extension locus alleles result from point mutations that alter MSH receptor function. Cell 72, 827834 (1993).

CAS PubMed Article Google Scholar

Donatien, P. D. et al. The expression of functional MSH receptors on cultured human melanocytes. Arch. Dermatol. Res. 284, 424426 (1992).

CAS PubMed Article Google Scholar

Klungland, H., Vage, D. I., Gomez-Raya, L., Adalsteinsson, S. & Lien, S. The role of melanocyte-stimulating hormone (MSH) receptor in bovine coat color determination. Mamm. Genome 6, 636639 (1995).

CAS PubMed Article Google Scholar

Melin, A. D. et al. The relationship between MC1R mutation and plumage color variation in pigeons. Nature 17, 211214 (2008).

Google Scholar

Manceau, M., Domingues, V. S., Linnen, C. R., Rosenblum, E. B. & Hoekstra, H. E. Convergence in pigmentation at multiple levels: Mutations, genes and function. Philos. Trans. R. Soc. B Biol. Sci. 365, 24392450 (2010).

CAS Article Google Scholar

Rmpler, H. et al. Nuclear gene indicates coat-color polymorphism in mammoths. Science 313, 62 (2006).

PubMed Article Google Scholar

Kerje, S., Lind, J., Schtz, K., Jensen, P. & Andersson, L. Melanocortin 1-receptor (MC1R) mutations are associated with plumage colour in chicken. Anim. Genet. 34, 241248 (2003).

CAS PubMed Article Google Scholar

Kijas, J. M. H. et al. Melanocortin receptor 1 (MC1R) mutations and coat color in pigs. Genetics 150, 11771185 (1998).

CAS PubMed PubMed Central Article Google Scholar

Vge, D. I., Klungland, H., Dongsi, L. & Cone, R. D. Molecular and pharmacological characterization of dominant black coat color in sheep. Mamm. Genome 10, 3943 (1999).

PubMed Article Google Scholar

Beaumont, K. A. et al. Altered cell surface expression of human MC1R variant receptor alleles associated with red hair and skin cancer risk. Hum. Mol. Genet. 14, 21452154 (2005).

CAS PubMed Article Google Scholar

Bastiaens, M. T. et al. Melanocortin-1 receptor gene variants determine the risk of nonmelanoma skin cancer independently of fair skin and red hair. Am. J. Hum. Genet. 68, 884894 (2001).

CAS PubMed PubMed Central Article Google Scholar

Bree, E., Rmpler, H., Schneberg, T. & Hoekstra, H. E. Molecular and functional basis of phenotypic convergence in white lizards at White Sands. Proc. Natl. Acad. Sci. U.S.A. 107, 21132117 (2010).

ADS Article Google Scholar

Haitina, T., Ringholm, A., Kelly, J., Mundy, N. I. & Schith, H. B. High diversity in functional properties of melanocortin 1 receptor (MC1R) in divergent primate species is more strongly associated with phylogeny than coat color. Mol. Biol. Evol. 24, 20012008 (2007).

CAS PubMed Article Google Scholar

Nakayama, K., Shotake, T., Takeneka, O. & Ishida, T. Variation of the melanocortin 1 receptor gene in the macaques. Am. J. Primatol. 70, 778785 (2008).

CAS PubMed Article Google Scholar

Hamada, Y., Watanabe, T., Takenaka, O., Suryobroto, B. & Kawamoto, Y. Morphological studies on the Sulawesi macaques I: Phyletic analysis of body color. Primates 29, 6580 (1988).

Article Google Scholar

Evans, B. J. et al. Mitogenomics of macaques (Macaca) across Wallaces Line in the context of modern human dispersals. J. Hum. Evol. 146, 102852 (2020).

PubMed Article Google Scholar

Takenaka, O. et al. Origin and evolution of the Sulawesi macaques 1. Electrophoretic analysis of hemoglobins. Primates 28, 8798 (1987).

Article Google Scholar

Evans, B. J. et al. Speciation over the edge: Gene flow among non-human primate species across a formidable biogeographic barrier. R. Soc. Open Sci. 4, 170351 (2017).

ADS PubMed PubMed Central Article CAS Google Scholar

Evans, B. J., Supriatna, J., Andayani, N. & Melnick, D. J. Diversification of sulawesi macaque monkeys: Decoupled evolution of mitochondrial and autosomal DNA. Evolution 57, 19311946 (2003).

PubMed Article Google Scholar

Harding, R. M. et al. Evidence for variable selective pressures at MC1R. Am. J. Hum. Genet. 66, 13511361 (2000).

CAS PubMed PubMed Central Article Google Scholar

Mundy, N. I. & Kelly, J. Evolution of a pigmentation gene, the melanocortin-1 receptor, in primates. Am. J. Phys. Anthropol. 121, 67 (2003).

CAS PubMed Article Google Scholar

Valverde, P., Healy, E., Jackson, I., Rees, J. L. & Thody, A. J. Variants of the melanocyte-stimulating hormone receptor gene are associated with red hair and fair skin in humans. Nat. Genet. 11, 328330 (1995).

CAS PubMed Article Google Scholar

Wolf Horrell, E. M., Boulanger, M. C. & DOrazio, J. A. Melanocortin 1 receptor: Structure, function, and regulation. Front. Genet. 7, 116 (2016).

Article CAS Google Scholar

Frndberg, P. A., Doufexis, M., Kapas, S. & Chhajlani, V. Cysteine residues are involved in structure and function of melanocortin 1 receptor: Substitution of a cysteine residue in transmembrane segment two converts an agonist to antagonist. Biochem. Biophys. Res. Commun. 281, 851857 (2001).

PubMed Article CAS Google Scholar

Catania, A., Airaghi, L., Colombo, G. & Lipton, J. M. Alpha-melanocyte-stimulating hormone in normal human physiology and disease states. Trends Endocrinol. Metab. 11, 304308 (2000).

CAS PubMed Article Google Scholar

McRobie, H. R., King, L. M., Fanutti, C., Symmons, M. F. & Coussons, P. J. Agouti signalling protein is an inverse agonist to the wildtype and agonist to the melanic variant of the melanocortin-1 receptor in the grey squirrel (Sciurus carolinensis). FEBS Lett. 588, 23352343 (2014).

CAS PubMed Article Google Scholar

Eizirik, E. et al. Molecular genetics and evolution of melanism in the cat family. Curr. Biol. 13, 448453 (2003).

CAS PubMed Article Google Scholar

Miao, Y. W. et al. The role of MC1R gene in buffalo coat color. Sci. China Life Sci. 53, 267272 (2010).

CAS PubMed Article Google Scholar

Monti, D. M. et al. Physiological change in an insular lizard population confirms the reversed island syndrome. Biol. J. Linn. Soc. 108, 144150 (2013).

Article Google Scholar

Bradley, B. J., Gerald, M. S., Widdig, A. & Mundy, N. I. Coat color variation and pigmentation gene expression in rhesus macaques (Macaca mulatta). J. Mamm. Evol. 20, 263270 (2013).

Article Google Scholar

Mundy, N. I. & Kelly, J. Investigation of the role of the agouti signaling protein gene (ASIP) in coat color evolution in primates. Mamm. Genome 17, 12051213 (2006).

CAS PubMed Article Google Scholar

Manceau, M., Domingues, V. S., Mallarino, R. & Hoekstra, H. E. The developmental role of agouti in color pattern evolution. Science 331, 10621065 (2011).

ADS CAS PubMed Article Google Scholar

Watanabe, K. & Matsumura, S. The borderlands and possible hybrids between three species of macaques, M. nigra, M. nigrescens, and M. hecki, in the northern peninsula of Sulawesi. Primates 32, 365370 (1991).

Article Google Scholar

Watanabe, K., Matsumura, S., Watanabe, T. & Hamada, Y. Distribution and possible intergradation between Macaca tonkeana and M. ochreata at the borderland of the species in Sulawesi. Primates 32, 385389 (1991).

Article Google Scholar

Riley, E. P., Suryobroto, B. & Maestripieri, D. Distribution of Macaca ochreata and identification of mixed Ochreata-Tonkeana groups in South Sulawesi, Indonesia. Primate Conserv. 22, 129133 (2007).

Article Google Scholar

Riley, E. P. The endemic seven: Four decades of research on the: Sulawesi macaques. Evol. Anthropol. 19, 2236 (2010).

Article Google Scholar

Schillaci, M. A., Froehlich, J. W., Supriatna, J. & Jones-Engel, L. The effects of hybridization on growth allometry and craniofacial form in Sulawesi macaques. J. Hum. Evol. 49, 335369 (2005).

PubMed Article Google Scholar

Evans, B. J., Supriatna, J. & Melnick, D. J. Hybridization and population genetics of two macaque species in Sulawesi, Indonesia. Evolution 55, 16861702 (2001).

CAS PubMed Article Google Scholar

Widayati, K. A. et al. Functional divergence of the bitter receptor TAS2R38 in Sulawesi macaques. Ecol. Evol. 9, 1038710403 (2019).

PubMed PubMed Central Article Google Scholar

Supriatna, J. Macaca ochreata. The IUCN Red List of Threatened Species, Vol. 8235. https://doi.org/10.2305/IUCN.UK.2008.RLTS.T12557 (2008).

Longmire, J. L. et al. Use of Lysis Buffer in DNA Isolation and Its Implication for Museum Collections (Museum of Texas Tech University, 1997).

Book Google Scholar

Rozas, J. et al. DnaSP 6: DNA sequence polymorphism analysis of large data sets. Mol. Biol. Evol. 34, 3299. https://doi.org/10.1093/molbev/msx248 (2017).

CAS Article PubMed Google Scholar

Leigh, J. W. & Bryant, D. POPART: Full-feature software for haplotype network construction. Methods Ecol. Evol. 6, 11101116 (2015).

Article Google Scholar

Yang, Z. PAML 4: Phylogenetic analysis by maximum likelihood. Mol. Biol. Evol. 24, 15861591 (2007).

CAS PubMed Article Google Scholar

Choi, Y. & Chan, A. P. PROVEAN web server: A tool to predict the functional effect of amino acid substitutions and indels. Bioinformatics 31, 27452747 (2015).

CAS PubMed PubMed Central Article Google Scholar

Lu, D., Vage, D. I. & Cone, R. D. A ligand-mimetic model for constitutive activation of the melanocortin-1 receptor. Mol. Endocrinol. 12, 592604 (1998).

CAS PubMed Article Google Scholar

Damian, M. et al. High constitutive activity is an intrinsic feature of ghrelin receptor protein: A study with a functional monomeric GHS-R1a receptor reconstituted in lipid discs. J. Biol. Chem. 287, 36303641 (2012).

CAS PubMed Article Google Scholar

Ritz, C., Baty, F., Streibig, J. C. & Gerhard, D. Dose-response analysis using R. PLoS ONE 10, 113 (2015).

Article CAS Google Scholar

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Functional divergence of the pigmentation gene melanocortin-1 receptor (MC1R) in six endemic Macaca species on Sulawesi Island | Scientific Reports -...