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Category: genetics – Page 470

Creating Superman (and woman): Who benefits from human enhancement?

Research involving bowhead whales has suggested that it may one day be possible to extend the human lifespan to 200 years.

From the demigods of Greek mythology to the superheroes of 20th century comic books, we’ve been intrigued by the idea of human enhancement for quite a while, but we’ve also worried about negative consequences. Both in the Greek myths and modern comics and television, each enhanced human has been flawed in some way.

In the area of lifespan enhancement, for instance, Tithonus, though granted eternal life, shrunk and shriveled into a grasshopper, because his immortal girlfriend Eos, forgot to ask Zeus to give him eternal youth. Achilles, while super strong and agile, had a weak spot at the back of his heal, and Superman would lose his power if exposed to “kryptonite”. As for Khan’s people, their physical superiority, both physical and mental, made them overly ambitious, causing a third world war that nearly destroyed humanity in the Star Trek backstory.

Using genetic modification, nanotechnology, bionics, reconstructive surgery, hormones, drugs or any combination of these approaches, real-life human enhancement is looking ever more achievable. As with the fictional examples, the idea of enhancement being a double-edged sword will surely remain part of the discussion. At the same time, though, because enhancement means mastering and manipulating human physiology and the basis of consciousness and self-awareness, the road to enhancement will be paved with advances beneficial to the sick and the disabled. This point must be at center stage when we weigh the pluses and minuses in various enhancement categories, especially physical capability, mental function, and lifespan.

The genetic architecture of the human cerebral cortex

The human cerebral cortex is important for cognition, and it is of interest to see how genetic variants affect its structure. Grasby et al. combined genetic data with brain magnetic resonance imaging from more than 50,000 people to generate a genome-wide analysis of how human genetic variation influences human cortical surface area and thickness. From this analysis, they identified variants associated with cortical structure, some of which affect signaling and gene expression. They observed overlap between genetic loci affecting cortical structure, brain development, and neuropsychiatric disease, and the correlation between these phenotypes is of interest for further study.

Science, this issue p. eaay6690.

Scientists Discover New Neurodegenerative Disorder That May Provide Clues to Alzheimer’s

Dr. Susan White and her genetics team treated two triplets from a family who had an undiagnosed neurodegenerative disorder in 2014. After one year of age, the children’s developmental skills declined. They lost visual coordination. Feeding and swallowing food became impossible. The children developed intractable seizures.

Exactly what led to their neurodegeneration was a mystery.

“As you can imagine, that was just a horrendous experience for their family and we suspected a genetic condition because of that pattern of problems occurring in both children,” White, an associate professor at Murdoch Children’s Research Institute (MCRI) and Victorian Clinical Genetics Services (VCGS), said in an interview with Being Patient.

Our brains as hard drives – could we delete, modify or add memories and skills?

Given the rapid development of virtual reality technology, we may very well be moving toward a time when we’re able to manage the brain’s memories.

Could we develop a similar capability? That may depend heavily upon a handful of ambitious attempts at brain-computer interfacing. But science is moving in baby steps with other tactics in both laboratory animals and humans.

Thus far, there have been some notable achievements in rodent experiments, that haven’t done so well with humans. We don’t have a beam that can go into your mind and give you 60 years worth of new experiences. Nevertheless, the emerging picture is that the physical basis of memory is understandable to the point that we should be able to intervene — both in producing and eliminating specific memories.

At MIT’s Center for Neural Circuit Genetics, for example, scientists have modified memories in mice using an optogenetic interface. This technology involves genetic modification of tissues, in this case within the brain, to express proteins that respond to light. Triggered by implants that deliver laser beams, brain cells can be triggered to be more or less active. In research that has been published in the prestigious journal Nature, the MIT team used the approach in specific brain circuits important to memory consolidation. The researchers were able to enhance the development of negative memories — for instance a shock given to an animal’s leg — and also to convert those negative memories into positive memories. The latter was achieved by letting male mice enjoy some time with females, while nerve cells that usually deliver the negative impulses associated with the former shock were stimulated through the optogenetic interface.

Needle in a haystack: MIPT scientists explain why new dangerous viruses are so hard to identify

In a recently published fundamental review dedicated to the diagnostics of viral infections, a Russian research team featuring MIPT researchers was the first to systematically describe and summarize the cutting-edge technologies in the rapidly developing field of genetics. A number of new effective methods of virus detection have been developed over the past few years, including those targeted at unknown pathogens. The authors described the so-called high-throughput next-generation sequencing as a potent new approach. The method promises to revolutionize the detection and analysis of new pathogenic viruses, but it will be at least several years until it is introduced into mainstream clinical practice.

In response to the rapid spread of the COVID-19 pandemic, an authoritative global scientific journal, aptly named Viruses, published a fundamental review of problems related to identifying and studying emerging pathogens, such as the notorious coronavirus.

“There are, by various statistical estimations, over 320,000 various viruses infecting mammals,” said Kamil Khafizov, a researcher at MIPT’s Historical Genetics, Radiocarbon Analysis and Applied Physics Lab and one of the review’s authors. “But up to date, less than 1% of this vast multitude has been studied.”

Map shows how eight strains of coronavirus raced around the world

Scientists around the world are tracking at least eight strains of coronavirus around the world, using genetic detective work to show how the virus spreads.

Researchers say the virus appears to mutate very slowly, with only tiny differences between the different strains, and that none of the strains of the virus is more deadly than another.

They also say it does not appear the strains will grow more lethal as they evolve.

Could areas of high Fluoride ingestion be more susceptible to Coronavirus outbreaks?

An interesting opinion:

The US Government Comparative Toxicogenomics database shows that Fluoride can inhibit Human immunity to viruses and pneumonia. Angiotensin I-Converting Enzyme (ACE), 2’-5’-Oligoadenylate Synthetase 1 (OAS1) and Intercellular Adhesion Molecule 1 (ICAM1) are included as susceptible epigenetic targets of the poison.

Read 3 answers by scientists with 1 recommendation from their colleagues to the question asked by Geoff Pain on Feb 4, 2020.

From Bats to Human Lungs, the Evolution of a Coronavirus

There are endless viruses in our midst, made either of RNA or DNA viruses, which exist in much greater abundance around the planet, are capable of causing systemic diseases that are endemic, latent, and persistent—like the herpes viruses (which includes chicken pox), hepatitis B, and the papilloma viruses that cause cancer. “DNA viruses are the ones that live with us and stay with us,” Denison said. “They’re lifelong.” Retroviruses, like H.I.V., have RNA in their genomes but behave like DNA viruses in the host. RNA viruses, on the other hand, have simpler structures and mutate rapidly. “Viruses mutate quickly, and they can retain advantageous traits,” Epstein told me. “A virus that’s more promiscuous, more generalist, that can inhabit and propagate in lots of other hosts ultimately has a better chance of surviving.” They also tend to cause epidemics—such as measles, Ebola, Zika, and a raft of respiratory infections, including influenza and coronaviruses. Paul Turner, a Rachel Carson professor of ecology and evolutionary biology at Yale University, told me, “They’re the ones that surprise us the most and do the most damage.”

Scientists discovered the coronavirus family in the nineteen-fifties, while peering through early electron microscopes at samples taken from chickens suffering from infectious bronchitis. The coronavirus’s RNA, its genetic code, is swathed in three different kinds of proteins, one of which decorates the virus’s surface with mushroom-like spikes, giving the virus the eponymous appearance of a crown. Scientists found other coronaviruses that caused disease in pigs and cows, and then, in the mid-nineteen-sixties, two more that caused a common cold in people. (Later, widespread screening identified two more human coronaviruses, responsible for colds.) These four common-cold viruses might have come, long ago, from animals, but they are now entirely human viruses, responsible for fifteen to thirty per cent of the seasonal colds in a given year. We are their natural reservoir, just as bats are the natural reservoir for hundreds of other coronaviruses. But, since they did not seem to cause severe disease, they were mostly ignored. In 2003, a conference for nidovirales (the taxonomic order under which coronaviruses fall) was nearly cancelled, due to lack of interest. Then SARS emerged, leaping from bats to civets to people. The conference sold out.

SARS is closely related to the new virus we currently face. Whereas common-cold coronaviruses tend to infect only the upper respiratory tract (mainly the nose and throat), making them highly contagious, SARS primarily infects the lower respiratory system (the lungs), and therefore causes a much more lethal disease, with a fatality rate of approximately ten per cent. (MERS, which emerged in Saudi Arabia, in 2012, and was transmitted from bats to camels to people, also caused severe disease in the lower respiratory system, with a thirty-seven per cent fatality rate.) SARS-CoV-2 behaves like a monstrous mutant hybrid of all the human coronaviruses that came before it. It can infect and replicate throughout our airways. “That’s why it is so bad,” Stanley Perlman, a professor of microbiology and immunology who has been studying coronaviruses for more than three decades, told me. “It has the lower-respiratory severity of SARS and MERS coronaviruses, and the transmissibility of cold coronaviruses.”

Scientists Have ‘Reset’ The Cellular Age Of Cells Taken From A 114-Year-Old Woman

For the first time, scientists have reprogrammed cells from a 114-year-old woman into induced pluripotent stem cells (iPS cells), a move which they describe as a significant step toward understanding “the underlying mechanisms of extreme longevity and disease resistance.”

iPS cells are adult cells that have been genetically reprogrammed into an embryonic stem cell-like state and are able to give rise to any of the specialized cell types of the body, whether it’s neurons, blood cells, or heart cells.

Until this new project, researchers weren’t even certain whether they could create viable iPS cells from someone so elderly, let alone a supercentenarian. Now they have shown it’s possible to effectively make these aged cells resemble young pluripotent cells, the researchers believe they might have made a step towards the reversal of cellular aging.

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