Lifeboat Foundation: Safeguarding Humanity
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Category: biotech/medical – Page 2,480

Hidden in the bones of ancient humans lies evidence of diseases that continue to distress people today. Recently, the examination of two 3,800-year old skeletons revealed the presence of a Yersinia pestis strain, famously the bacterium that causes plague. This strain is now the oldest of its kind sequenced to date, and suggests that the devastation that is the bubonic plague has a Bronze Age origin.

The discovery, published Friday in Nature Communications, pushes back the proposed age of the bubonic plague by 1,000 years. It also adds to the understanding of a disease that is still reported between one and seven times per year in the United States, despite its more ancient reputation: In the U.S. 80 percent of plague cases have been in the bubonic form. Although it’s been present throughout much of recorded history — it was the drive behind some of humanity’s deadliest pandemics including the Justinian Plague and the Black Death — the origin and age of the disease have remained largely a mystery.

“Contrary to previous studies suggesting that Y. pestis was unable to cause disease during that time, we provide evidence that bubonic plague has been affecting humans for at least the last 4,000 years,” study co-author Maria Spyrou tells Inverse.

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A breakthrough stem cell treatment that promises the first effective cure for heart disease will be offered to British patients this year, The Sunday Telegraph can reveal.

Hundreds of thousands stand to benefit after regulators approved a major trial of the regenerative drug capable of shrinking fatal scar tissue which follows a heart attack.

The “off-the-shelf” therapy, which can be harvested for thousands of recipients from one healthy donor, will begin being administered to patients at London’s Royal Brompton Hospital in November.

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A new technique developed by MIT physicists could someday provide a way to custom-design multilayered nanoparticles with desired properties, potentially for use in displays, cloaking systems, or biomedical devices. It may also help physicists tackle a variety of thorny research problems, in ways that could in some cases be orders of magnitude faster than existing methods.

The innovation uses computational neural networks, a form of artificial intelligence, to “learn” how a nanoparticle’s structure affects its behavior, in this case the way it scatters different colors of light, based on thousands of training examples. Then, having learned the relationship, the program can essentially be run backward to design a particle with a desired set of light-scattering properties—a process called inverse design.

The findings are being reported in the journal Science Advances, in a paper by MIT senior John Peurifoy, research affiliate Yichen Shen, graduate student Li Jing, professor of physics Marin Soljacic, and five others.

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Cultural inhibitions also impede the development of end-of-life care. Talking about death has long been taboo. People often feel that it is their filial duty to ensure that sick parents receive curative treatment, even when doctors advise that there is no chance of recovery and the treatment will be painful. Applications to build hospices are sometimes challenged by local residents who resent the presence of death on their doorsteps. Mr Li says neighbours’ objections have forced Songtang Hospice to move six times.

WHEN Li Songtang was 17, officials overseeing Mao’s chaotic Cultural Revolution sent him from Beijing to Inner Mongolia, a northern province where he became a “barefoot doctor”—a medical worker with rudimentary training. His patients included an academic whom the government had expelled in disgrace from the capital, and who had become terminally ill. The patient grew sicker and increasingly troubled by his political black mark. Unable to console him, Mr Li eventually lied that he had persuaded authorities to wipe the slate clean. The patient grabbed his arm with relief and gratitude, recalls Mr Li. “I can still feel it today.”

Mr Li’s experience of caring for the dying man eventually resulted in the hospice he runs in a three-storey building in Beijing’s outskirts. The facility is home to about 300 people, most of them elderly and with late-stage cancer (a patient there is pictured with a nurse). On a weekend the bright corridors are busy with volunteers who have come to chat with patients. Zhang Zhen’e, a smiley 76-year-old who shares her room with six other women, says she tries to stay cheerful because days spent worrying are “days lost”. A nearby ward for dying babies, painted green and decorated with mobiles, is less easy to visit. Eight children snooze there, asleep in mismatched wooden cots.

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Chemically induced pluripotent stem cells (CiPSCs) may provide an alternative and attractive source for stem cell-based therapy. Sufficient telomere lengths are critical for unlimited self-renewal and genomic stability of pluripotent stem cells. Dynamics and mechanisms of telomere reprogramming of CiPSCs remain elusive. We show that CiPSCs acquire telomere lengthening with increasing passages after clonal formation. Both telomerase activity and recombination-based mechanisms are involved in the telomere elongation. Telomere lengths strongly indicate the degree of reprogramming, pluripotency, and differentiation capacity of CiPSCs. Nevertheless, telomere damage and shortening occur at a late stage of lengthy induction, limiting CiPSC formation. We find that histone crotonylation induced by crotonic acid can activate two-cell genes, including Zscan4; maintain telomeres; and promote CiPSC generation. Crotonylation decreases the abundance of heterochromatic H3K9me3 and HP1α at subtelomeres and Zscan4 loci. Taken together, telomere rejuvenation links to reprogramming and pluripotency of CiPSCs. Crotonylation facilitates telomere maintenance and enhances chemically induced reprogramming to pluripotency.

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It was a great pleasure to share latest data and insights with a fantastic community of researchers, engineers, innovators and investors last week, hosted by the Imperial College Centre for Neurotechnology in London. Hope you enjoy the overview slides!

Presentation by Alvaro Fernandez hosted by the Imperial College Centre for Neurotechnology in London.

Description: As seen in patent and investment trends, research findings and consumer/patient behaviors, Mental Health and Brain Enhancement are rapidly evolving in transformational ways which some call “empowering” and some “controversial.” Alvaro Fernandez, Editor-in-Chief of independent market research firm SharpBrains, will present and discuss the latest market data and forecasts on how digital platforms are poised to revolutionize brain & mental health diagnostics, monitoring, therapies and enhancement.

Programme:

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A new class of patients could soon be treated for breast cancer, no chemotherapy required. That’s because they don’t really benefit from it, according to a study published Sunday in the New England Journal of Medicine.

Those patients: those diagnosed with early-stage, invasive, hormone-receptor-positive breast cancer who scored in a specific range of a genetic test. They benefit just as much from chemotherapy, which many don’t tolerate well and can have long-term consequences, as they do from hormone treatments, which have many fewer side effects.

But before this study came out, many people in this group were prescribed chemotherapy because doctors had, based on the best information available, assumed it would help them. For those people, the side effects of chemotherapy could have been avoided, without making the treatment any less effective.

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Today, we will be taking a look at a new study showing that an NAD+ precursor was able to improve mitochondrial function in cells and flies with a model of Parkinson’s disease.

Summary

While mitochondrial dysfunction is emerging as key in Parkinson’s disease (PD), a central question remains whether mitochondria are actual disease drivers and whether boosting mitochondrial biogenesis and function ameliorates pathology. We address these questions using patient-derived induced pluripotent stem cells and Drosophila models of GBA-related PD (GBA-PD), the most common PD genetic risk. Patient neurons display stress responses, mitochondrial demise, and changes in NAD+ metabolism. NAD+ precursors have been proposed to ameliorate agerelated metabolic decline and disease. We report that increasing NAD+ via the NAD+ precursor nicotinamide riboside (NR) significantly ameliorates mitochondrial function in patient neurons. Human neurons require nicotinamide phosphoribosyltransferase (NAMPT) to maintain the NAD+ pool and utilize NRK1 to synthesize NAD+ from NAD+ precursors. Remarkably, NR prevents the age-related dopaminergic neuronal loss and motor decline in fly models of GBA-PD.

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Researchers at the University of California San Diego School of Medicine have shown that they can block inflammation in mice, thereby protecting them from liver disease and hardening of the arteries while increasing their healthy lifespan.

The study, published in the journal Nature, shows that inflammation can be blocked using a naturally occurring antibody that binds with oxidized phospholipids (OxPL), molecules that are located on the cell surface and are modified by inflammation [1]. This is the first time in a living animal that OxPL has been shown to trigger inflammation that leads to the formation of arterial plaques, the foundation of heart disease.

The mice were given a high-fat diet and treated with the antibody, which prevented artery-hardening arterial plaques from forming, prevented liver disease, and increased their lifespan. The study results also highlight a potential new approach to preventing or reversing a variety of inflammatory diseases.

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By Andy Coghlan

Many people with cancer die not from their original tumour, but from secondary tumours that grow elsewhere around the body. Now we’re a step closer to understanding how cancers are able to spread.

Sakari Vanharanta of the Medical Research Council Cancer Unit at the University of Cambridge and his colleagues have been studying kidney cancer cells. They found that to spread, these cells tap into the same genetic “travel” machinery normally used by healthy white blood cells to roam around the body.

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