Lifeboat Foundation: Safeguarding Humanity
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Category: genetics – Page 260

A team of scientists found an unusual trick for growing bigger, heartier crops: inserting a human gene related to obesity and fat mass into plants to supersize their harvest.

Augmenting potatoes with the human gene that encodes a fat-regulating protein called FTO, which essentially alters the genetic code to rapidly mass-produce proteins, made otherwise identical potato plants grow crops that were 50 percent larger, Smithsonian Magazine reports. By growing more food without taking up more space for agriculture, the scientists say their work could help fight global hunger — without adding to its climate impact.

“It [was] really a bold and bizarre idea,” University of Chicago chemist Chuan He, coauthor of a paper published in Nature Biotechnology, told Smithsonian. “To be honest, we were probably expecting some catastrophic effects.”

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Nad plus works for alzheimers.

In June of 2,018 the World Health Organization (WHO) released the 11th edition of its International Classification of Diseases, and for the first time added aging. The classification of aging as a disease paves the way for new research into novel therapeutics to delay or reverse age-related illnesses such as cancer, cardiovascular and metabolic disease, and neurodegeneration., Nutrient sensing systems have been an intense focus of investigation, including mTOR (the mammalian target of rapamycin) for regulating protein synthesis and cell growth; AMPK (activated protein kinase) for sensing low energy states; and sirtuins, a family of seven proteins critical to DNA expression and aging, which can only function in conjunction with NAD+ (nicotinamide adenine dinucleotide), a coenzyme present in all living cells.

Across the kingdom of life, an increase in intracellular levels of NAD+ triggers shifts that enhance survival, including boosting energy production and upregulating cellular repair. In fact, the slow, ineluctable process of aging has been described as a “cascade of robustness breakdown triggered by a decrease in systemic NAD+ biosynthesis and the resultant functional defects in susceptible organs and tissues.” Aging is marked by epigenetic shifts, genomic instability, altered nutrient sensing ability, telomere attrition, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and dysregulated intercellular communication.,

By middle age, our NAD+ levels have plummeted to half that of our youth. Numerous studies have demonstrated that boosting NAD+ levels increases insulin sensitivity, reverses mitochondrial dysfunction, and extends lifespan., NAD+ levels can be increased by activating enzymes that stimulate synthesis of NAD+, by inhibiting an enzyme (CD38) that degrades NAD+, and by supplementing with NAD precursors, including nicotinamide riboside(NR) and nicotinamide mononucleotide (NMN)., A conceptual framework called NAD World, formulated over the last decade by developmental biologist Shin-ichiro Imai, MD, PhD, of Washington University School of Medicine, posits NMN as a critical, systemic signaling molecule that maintains biological robustness of the communication network supporting NAD+..

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Mutations are a part of life. Every time a virus replicates, there is a chance that its genetic code won’t be copied accurately. These typos travel inside new virus particles as they leave one body and move on to infect the next. Some of these mutations die out; others survive and circulate widely. Some mutations are harmless; others increase infectivity or allow a virus to better escape the immune system—that’s when public health bodies might deem that strain a variant of concern.

Swaps or deletions of single amino acids can change the shapes of different proteins. Mutations can happen in any of the proteins of SARS-CoV-2, and these may change the virus’s properties. Many of the worrisome mutations are found on the spike protein, as it is the target of antibody treatments and is mimicked by the currently authorized COVID-19 vaccines. Researchers are especially troubled when typos occur in two parts of the spike protein—the N-terminal domain, which is at the beginning of the protein and which some antibodies target, and the receptor-binding domain (RBD), which grabs hold of ACE2 receptors on human cells and starts the process of infection.

To understand how specific mutations affect the structure and function of the spike protein and what those changes mean for treatments and vaccines, C&EN talked to Priyamvada Acharya, Rory Henderson, and Sophie Gobeil at Duke University. With colleagues, these researchers have combined biochemical assays, cryo-electron microscopy, and modeling to show how the mutations seen in the variants of concern work together to change the stability of the spike protein. The spike is a trimer of three identical protein strands folded and interwoven together. Before the virus has infected a cell, the spike takes on two conformations: a down state, in which the RBD is hidden, and an up state, in which the RBD faces out, ready to bind to ACE2. The team found that different mutations can increase binding in different ways. This process, in which similar features are arrived at independently, is called convergent evolution.

SARS-CoV-2 variants are emerging and gaining traction around the world. What does that mean for our vaccines and treatments for COVID-19?

Continue reading “COVID-19: What you need to know about SARS-CoV-2 variants” | >

Are there vertebrates occupying the planet today whose lifespans extend back to before the founding of the United States? Based on recent research, it seems very likely — and they exist in the form of sharks whose fermented meat are used in a very distinctive Icelandic dish. Scientists have found evidence that Greenland sharks live for hundreds of years — and that there are some whose lifespans extend to 400 or even 500 years.

For some scientists, the lengthy lifespans of certain creatures can also have an impact on research into making humans live longer. That’s true for the immortal jellyfish, and it also applies to the Greenland shark. A recent article by Jonathan Moens at Atlas Obscura explores what scientists have learned from their studies of the long-lived sharks — and what it might mean for humanity.

Greenland sharks’ longevity could be chalked up to genetic or lifestyle factors, or some combination of the two. The University of Manchester’s Holly Shiels suggested that, as Moens writes, “Greenland sharks may have a uniquely sophisticated system to repair damaged DNA.” Other scientists point to the sharks’ habitat — cold Arctic waters — and their ability to live for a long period of time on a relatively small amount of food as signs of a very efficient metabolism.

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Proteins can communicate through DNA, conducting a long-distance dialogue that serves as a kind of genetic “switch,” according to Weizmann Institute of Science researchers. They found that the binding of proteins to one site of a DNA molecule can physically affect another binding site at a distant location, and that this “peer effect” activates certain genes. This effect had previously been observed in artificial systems, but the Weizmann study is the first to show it takes place in the DNA of living organisms.

A team headed by Dr. Hagen Hofmann of the Chemical and Structural Biology Department made this discovery while studying a peculiar phenomenon in the soil bacteria Bacillus subtilis. A small minority of these bacteria demonstrate a unique skill: an ability to enrich their genomes by taking up bacterial gene segments scattered in the soil around them. This ability depends on a protein called ComK, a transcription factor, which binds to the DNA to activate the genes that make the scavenging possible. However, it was unknown how exactly this activation works.

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Because the brain responses in children with different forms of autism overlapped, future therapies that are effective for Phelan-McDermid syndrome could potentially help other autistic children with similar neural patterns, Siper says.

Brain responses to visual stimuli are smaller and weaker in children with Phelan-McDermid syndrome, an autism-linked genetic condition, than in non-autistic children, according to a new study. The difference in response is greater in children with larger genetic mutations.

Mutations or deletions in SHANK3, one of the genes most strongly linked to autism, cause Phelan-McDermid syndrome. More than 80 percent of people with the condition have autism; they also often have intellectual disability, developmental delays and other medical issues, though these traits and their severity can vary widely.

The new study is the first to use electroencephalography (EEG) to measure visual evoked potentials — brain responses that occur shortly after a person views a visual stimulus — in people with Phelan-McDermid syndrome. The team previously identified differences in these responses in people with ‘idiopathic’ autism, or autism with no known genetic cause. Other researchers have linked atypical visual evoked potentials to other single-gene causes of autism, such as Rett syndrome.

Continue reading “Visual response shows promise as biomarker in autism-linked condition” | >

The human body can be genetically inclined to attack its own cells, destroying the beta cells in the pancreas that make insulin, which helps convert sugar into energy. Called Type 1 diabetes, this disorder can occur at any age and can be fatal if not carefully managed with insulin shots or an insulin pump to balance the body’s sugar levels.

But there may be another, personalized option on the horizon, according to Xiaojun “Lance” Lian, associate professor of biomedical engineering and biology at Penn State. For the first time, Lian and his team converted human embryonic stem cells into beta cells capable of producing insulin using only small molecules in the laboratory, making the process more efficient and cost-effective.

Stem cells can become other cell types through signals in their environment, and some mature cells can revert to stem cells—induced pluripotency. The researchers found that their approach worked for human embryonic and induced pluripotent stem cells, both derived from federally approved stem cell lines. According to Lian, the effectiveness of their approach could reduce or eliminate the need for human embryonic stem cells in future work. They published their results today (Aug. 26) in Stem Cell Reports.

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In the fictional links he drew between immortal vampires and bats, Dracula creator Bram Stoker may have had one thing right.

“Maybe it’s all in the blood,” says Emma Teeling, a geneticist studying the exceptional longevity of bats in the hope of discovering benefits for humans.

The University College Dublin researcher works with the charity Bretagne Vivante to study bats living in rural churches and schools in Brittany, western France.

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Studying Novel Plasma Fractions For Age-Related Diseases And Systemic Rejuvenation — Dr. Harold Katcher Ph.D., Chief Scientific Officer, Yuvan Research Inc.

Dr. Harold Katcher is the Chief Scientific Officer at Yuvan Research Inc., a biotech company exploring the development of novel, young plasma fraction rejuvenation treatments in mammals.

Most recently Dr. Katcher was the Academic Director for Natural Sciences for the Asian Division of the University of Maryland Global Campus and throughout his career, Dr. Katcher has been a pioneer in the field of cancer research, and in the development of modern aspects of gene hunting and sequencing (including as one of the discoverers of the breast cancer gene BRCA1) as part of Myriad Genetics, and carries expertise in bioinformatics, chronobiology, and biotechnology.

Continue reading “Dr. Harold Katcher, PhD — Chief Scientific Officer — Yuvan Research — Rejuvenative Plasma Fractions” | >