Lifeboat Foundation: Safeguarding Humanity
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Category: genetics

#DigitalTheology #TheologyofDigitalPhysics #PhenomenalConsciousness #CosmicSelf #HolographicPrinciple #DigitalPhysics #theology #pantheism #consciousness

Since we live in a world which isn’t random, but organized at every level, a role for consciousness seems unavoidable. The ‘digital theologian’ shows us compelling evidence from quantum mechanics, mathematics and computer sciences, which not only aligns with a philosophical worldview of the Primacy of Consciousness, but which also assigns a role to information as its modus operandi.

It is quantum mechanics which appears to connect the Universe as a whole to consciousness. A whole, which is more than the sum of its parts and irreducible to mere assumptions deriving from the anatomizing dissection into mental confabulations. Drawing from the holographic principle, perceptroniums and noocentrism, Alex provides crucial keys to unlock the mystery of consciousness to show us how our local consciousness can arise from a non-local cosmic consciousness network.

Carefully building his fortress of arguments, Alex gathers his building bricks from various areas of scientific exploration, ranging from the role of language and tools in the development of our consciousness, the physics of time and epigenetics. Traditional Darwinism and reductive materialism become so challenged, that we become bound to agree with Terence McKenna’s statement that “object fetishism is completely bankrupt.” All these threads are then skillfully woven into the irresistible attractor and only logical conclusion, or Digital Pantheism and Omega Point Cosmology. And with this thus synthesized Apotheosis, Vikoulov brings the architecture of his chef-d’oeuvre to full fruition.

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Summary: PLCG2-P522R, a genetic variant that protects against Alzheimer’s disease, enhances key functions of immune cells.

Source: University of Eastern Finland

A new study conducted by researchers at the University of Eastern Finland found that the PLCG2-P522R genetic variant, which protects against Alzheimer’s disease, enhances several key functions of immune cells. The results obtained in the study highlight the importance of immune cells as a target of future development of new therapies for Alzheimer’s disease.

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11 epigenetic clocks have been published since 2011, but which is best for predicting aging and age-related disease? In this video, I present findings from a recent publication, “Underlying features of epigenetic aging clocks in vitro and in vivo”, that compared data for 11 epigenetic clocks, and derived a new epigenetic clock, the meta-clock.

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Lil bits of info on DNA methylation, clocks.

Breakthrough advances in medicine and better nutrition have dramatically improved the longevity of the average human over the past two centuries. But that’s not to say that some couldn’t go on to live a long life even before the advent of modern medicine. As long as they were spared by disease, wars, and other risks that can bring an untimely death, humans could live to see their 70s, 80s, and even reach 100 years old as far back as ancient Rome.

The longevity of humans is somewhat exceptional among primates. Chimpanzees, our closest living relatives, rarely make it past age 50, despite them sharing over 99% of our DNA. In a new study, researchers think they’ve found our secret: chemical changes along our genome that occurred around 7–8 million years ago when our ancestors branched away from the lineage of chimps.

Slower ticker

There are tens of thousands of genes in the human genome, but that doesn’t mean all of them are active. For instance, through the methylation of DNA across certain sites of the genetic sequence, genes are locked in the “off” position. These modifications, known as epigenetic changes (‘epi’ means ‘above’ in Greek), do not alter the DNA sequence itself but, rather, simply regulate the activity of genes.

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Very interesting!

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“The plan was to scan patients’ genomes—in particular, a set of 13 genes involved in interferon immunity against influenza. In healthy people, interferon molecules act as the body’s security system. They detect invading viruses and bacteria and sound the alarm, which brings other immune defenders to the scene.

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Casanova’s team has previously discovered [genetic mutations](https://medicalxpress.com/tags/genetic+mutations/) that hinder interferon production and function. People with these mutations are more vulnerable to certain pathogens, including those that cause influenza. Finding similar mutations in people with COVID-19, the team thought, could help doctors identify patients at risk of developing severe forms of the disease. It could also point to new directions for treatment, he says.”

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“As the researchers began analyzing patient samples, they started to uncover harmful mutations, in people young and old. The team found that 23 out of 659 patients studied carried errors in genes involved in producing antiviral interferons.”

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“That thought sparked a new idea. Maybe other patients with severe COVID-19 also lacked interferons—but for a different reason. Maybe some patients’ bodies were harming these molecules themselves.”

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“The team’s analysis of 987 patients with life-threatening COVID-19 revealed just that. At least 101 of the patients had auto-antibodies against an assortment of interferon proteins. “We said, ‘bingo’!” Casanova remembers. These antibodies blocked interferon action and were not present in patients with mild COVID-19 cases, the researchers discovered.”

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“. By testing for the presence of these antibodies, she says, “you can almost predict who will become severely ill.”” https://medicalxpress.com/news/2020-09-severe-covid-cases-linked-genetic.html

People infected by the novel coronavirus can have symptoms that range from mild to deadly. Now, two new analyses suggest that some life-threatening cases can be traced to weak spots in patients’ immune systems.

At least 3.5 percent of study patients with severe COVID-19, the disease caused by the novel coronavirus, have mutations in genes involved in antiviral defense. And at least 10 percent of patients with severe disease create “auto-antibodies” that attack the immune system, instead of fighting the virus. The results, reported in two papers in the journal Science on September 24, 2020, identify some root causes of life-threatening COVID-19, says study leader Jean-Laurent Casanova, a Howard Hughes Medical Institute Investigator at The Rockefeller University.

Seeing these harmful antibodies in so many patients—101 out of 987—was “a stunning observation,” he says. “These two papers provide the first explanation for why COVID-19 can be so severe in some people, while most others infected by the same virus are okay.”

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Toronto scientists have mapped the genes allowing cancer cells to avoid getting killed by the immune system in a finding that paves the way for the development of immunotherapies that would be effective for larger patient populations and across different tumour types.

“Over the last decade, different forms of immunotherapy have emerged as really potent cancer treatments but the reality is that they only generate durable responses in a fraction of patients and not for all tumour types,” says Jason Moffat, a professor of molecular genetics in the Donnelly Centre for Cellular and Biomolecular Research at the University of Toronto who led the work.

The study also revealed the need for to take into account the genetic composition of tumours because of mutations in the cancer cells that can potentially make the disease worse in response to treatment, often referred to as cancer resistance mutations.

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Who are we? Where did we come from? How did we get here? Throughout the ages, humans have sought answers to these questions, pursuing wisdom through religion, philosophy, and eventually science. Evolutionary analyses published by Genome Biology and Evolution (GBE) allow us to peer into the mirror and better understand ourselves as a species, bringing us closer than ever to uncovering the answers to these long-held questions. GBE’s latest virtual issue on human genetics highlights some of the most exciting research published in the journal within the last year and a half, demonstrating the wide variety of evolutionary approaches to this avenue of research as well as a number of fascinating insights into our own biology.

Taking over a decade to complete, the original Human Genome Project cost nearly $3 billion and involved the collective effort of hundreds of scientists. Since then, advances in sequencing technology have resulted in an explosion in and genomics research, with an estimated one million human genomes sequenced to date. While this wealth of data has the potential to answer some of our most fundamental questions, unlocking its mysteries has necessitated the invention of new analytic and computational methods and the integration of techniques and ideas from diverse biological sciences, including physiology, anatomy, medicine, , bioinformatics, and computational, molecular, and evolutionary biology.

A key area of investigation involves identifying ways in which humans differ from other primates—in other words, what makes us human? Several studies published over the last 18 months suggest that part of the answer may be found in transcriptional regulation and changes in gene expression. Edsall et al. (2019) evaluated differences in chromatin accessibility, which impacts access of the transcriptional machinery to the DNA, across five primates including humans. They found high levels of differentiation across species, as well as classes of sites that differed based on selection, genomic location, and cell type specificity. More specifically, Swain-Lenz et al. (2019) found that differences in chromatin accessibility near genes involved in lipid metabolism may provide a mechanistic explanation for the higher levels of body fat observed in humans compared to other primates. Arakawa et al.

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The removal of one gene renders poxviruses—a lethal family of viral infections that are known to spread from animals to humans—harmless, a new study in the journal Science Advances reports.

During this ground-breaking study, scientists from the Spanish National Research Council and the University of Surrey investigated the immune response of cells to poxviruses. Poxviruses, such as cowpox and monkeypox, can spread to humans from infected animals, causing , fever, swollen lymph nodes and even death.

Viruses contain which helps them outsmart host cells, enabling replication and the spread of the . Cells in the body are comprised of molecules that sense the presence of viruses, sometimes via the recognition of their genetic material, and alert the immune system of an upcoming infection. Poxviruses, unlike other viruses, are highly unusual in that they have large DNA genomes that are replicated exclusively in the cell cytosol, an area of the cell full of sensors. How poxviruses manage to stay undetectable has remained unknown.

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In the past decade, researchers have engineered an array of new tools that control the balance of genetic inheritance. Based on CRISPR technology, such gene drives are poised to move from the laboratory into the wild where they are being engineered to suppress devastating diseases such as mosquito-borne malaria, dengue, Zika, chikungunya, yellow fever and West Nile. Gene drives carry the power to immunize mosquitoes against malarial parasites, or act as genetic insecticides that reduce mosquito populations.

Although the newest gene drives have been proven to spread efficiently as designed in laboratory settings, concerns have been raised regarding the safety of releasing such systems into wild populations. Questions have emerged about the predictability and controllability of gene drives and whether, once let loose, they can be recalled in the field if they spread beyond their intended application region.

Now, scientists at the University of California San Diego and their colleagues have developed two new active genetic systems that address such risks by halting or eliminating gene drives in the wild. On Sept.18, 2020 in the journal Molecular Cell, research led by Xiang-Ru Xu, Emily Bulger and Valentino Gantz in the Division of Biological Sciences offers two new solutions based on elements developed in the common fruit fly.

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