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7-Ketocholesterol is a harmful oxidized byproduct of cholesterol, it is highly toxic with no redeeming qualities and serves no purpose in our bodies aside from allowing heart disease to develop. Check out Underdog Pharma’s recent review at Science Direct to learn more!

Oxidative stress has long been causatively implicated in the aging process [219,220]. As described in section 2, 7KC is the most common stable product of a reaction between cholesterol and a free radical. This is a vicious cycle as 7KC also leads to increased free radical production and release, seemingly by plasma membrane permeabilization. As discussed above, mitochondrial dysfunction and free-radical formation are also strongly implicated in the aging process and so while the precise mechanistic links between mitochondria, 7KC, and aging are still being elucidated they seem likely to be intertwined.

Is 7KC a biomarker of aging? As discussed in section 4, 7KC accumulation is directly implicated in many diseases of aging, including atherosclerosis, heart failure, AMD, NAFLD, and AD. It is thus reasonable to hypothesize that when otherwise unrelated diseases of aging share a common cause, that this cause is likely to be a part of the biological aging process. 7KC is known to accumulate in phagocytic cells such as macrophages (promoting the formation of foam cells), RPE cells, and microglia. It has also been suggested that c. elegans subjected to 7KC could be a good model of 7KC-dependent aging [221]. As 7KC is broadly toxic, and most cells seem to have difficulty metabolizing it, it may be that, with age, 7KC is bioaccumulating and impairing functional activity of the cells and tissue.

As described in Section 3, 7KC is a potent inhibitor of lysosomal function. Lysosomal dysfunction is part of the degenerative aging process and is implicated in the cause of diseases such as AMD, atherosclerosis, and AD in which accumulation of non-degradable biomolecules in the lysosome prevent phagocytic cells from efficiently metabolizing phagocytized biological material [91]. We therefore propose that 7KC plays an important role in the loss of function associated with aging and the lysosomal dysfunction produced by 7KC is a key mediator of this role. Thus, as argued in the previous sections, although diseases of aging present with disparate symptoms, a central element to many of the symptoms could be production and accumulation of 7KC. Despite the fact that the biological effects of 7KC have been studied since at least the 1940s, relatively little has been published quantifying intracellular 7KC levels in vivo with age.

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The Trump administration is proposing new rules to guide future federal regulation of artificial intelligence used in medicine, transportation and other industries.

But the vagueness of the principles announced by the White House is unlikely to satisfy AI watchdogs who have warned of a lack of accountability as computer systems are deployed to take on human roles in high-risk social settings, such as mortgage lending or job recruitment.

The White House said that in deciding regulatory action, U.S. agencies “must consider fairness, non-discrimination, openness, transparency, safety, and security.” But federal agencies must also avoid setting up restrictions that “needlessly hamper AI innovation and growth,” reads a memo being sent to U.S. agency chiefs from Russell Vought, acting director of the Office of Management and Budget.

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It’s common for people to focus on their health at the start of the year.

But few consider the well being of the microbes that live inside the human gut – the microbiome – which are vital to an individual’s good health.

How important are these bacteria? There are as many bacterial cells in us as there are human cells, and they help control everything from inflammation and the development and treatment of cancer to how much energy we get from our foods and perhaps even what foods we crave and our moods.

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For the first time, the agency’s Transiting Exoplanet Survey Satellite (TESS) has discovered a roughly Earth- planet in the habitable zone of its host star, the zone of orbital distances where liquid water could be stable on a world’s surface.

NASA’s TESS Planet Hunter Finds Its 1st Earth-Size World in ‘Habitable Zone’ : Read more

Interesting, perhaps pushing the paradigm limits here. 86% of solar energy is similar to Precambrian earth during the Faint Young Sun, a snow ball earth. Part of the report that is a bit confusing to me is the comment “One of the other planets is a red dwarf about 40% as massive, 40% as wide and 50% as hot as Earth’s sun.” I think this is about the host star being a red dwarf star. Red dwarfs can be flaring stars and cause problems for *habitable* exoplanets. The Sun spins about 2 km/s at the its equator, red dwarf stars can spin faster like 4 km/s or faster, rotation periods 1 day to 10 days so red dwarfs can emit more flares. The report does comment “In 11 months of data, we saw no flares from the star, which improves the chances TOI 700 d is habitable and makes it easier to model its atmospheric and surface conditions,” discovery team leader Emily Gilbert, a graduate student at the University of Chicago, said in the same statement.

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The magnitude of the Great Lisbon Earthquake event, a historic and devastating earthquake and tsunami that struck Portugal on All Saints’ Day in 1755, may not be as high as previously estimated.

In his study published in the Bulletin of the Seismological Society of America, Joao F. B. D. Fonseca at the Universidade de Lisboa used macroseismic data—contemporaneous reports of shaking and damage—from Portugal, Spain and Morocco to calculate the ’s magnitude at 7.7. Previous estimates placed the earthquake at magnitude 8.5 to 9.0.

Fonseca’s analysis also locates the epicenter of the 1755 earthquake offshore of the southwestern Iberian Peninsula, and suggests the rupture was a complicated one that may have involved faulting onshore as well. This re-evaluation could have implications for the seismic hazard map of the region, he said.

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The size of the human brain increased profoundly during evolution. A certain gene that is only found in humans triggers brain stem cells to form a larger pool of stem cells. As a consequence, more neurons can arise, which paves the way to a bigger brain. This brain size gene is called ARHGAP11B and so far, how it works was completely unknown. Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden now uncovered its mode of action. They show that the ARHGAP11B protein is located in the powerhouse of the cell—the mitochondria—and induces a metabolic pathway in the brain stem cells that is characteristic of cancer cells.

The research group of Wieland Huttner, a founding director of the Max Planck Institute of Molecular Cell Biology and Genetics, has been investigating the underlying the expansion of the brain during mammalian evolution for many years. In 2015, the group reported a key role for a gene that is only present in humans and in our closest extinct relatives, the Neanderthals and Denisovans. This gene, named ARHGAP11B, causes the so-called basal brain stem to expand in number and to eventually increase the production of neurons, leading to a bigger and more folded brain in the end. How the gene functions within the basal brain stem cells has been unknown so far.

Takashi Namba, a postdoctoral scientist in the research group of Wieland Huttner, wanted to find the answer to this question, together with colleagues from the Max Planck Institute, the University Hospital Carl Gustav Carus Dresden, and the Department of Medical Biochemistry at the Semmelweis University, Budapest. He found that the ARHGAP11B protein is located in mitochondria, the organelles that generate most of the cell’s source of chemical energy and hence are often referred to as the powerhouse of the cell. Takashi Namba explains the results: We found that ARHGAP11B interacts with a protein in the membrane of mitochondria that regulates a membrane pore. As a consequence of this interaction, the pores in the membrane are closing up, preventing calcium leakage from the mitochondria. The resulting higher calcium concentration causes the mitochondria to generate chemical energy by a metabolic pathway called glutaminolysis.

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