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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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MRSA bacterium captured by a hybrid cell membrane-coated nanorobot (colored scanning electron microscope image and black and white image below) (credit: Esteban-Fernández de Ávila/Science Robotics)

Engineers at the University of California San Diego have developed tiny ultrasound-powered nanorobots that can swim through blood, removing harmful bacteria and the toxins they produce.

These proof-of-concept nanorobots could one day offer a safe and efficient way to detoxify and decontaminate biological threat agents — providing an fast alternative to the multiple, broad-spectrum antibiotics currently used to treat life-threatening pathogens like MRSA bacteria (an antibiotic-resistant staph strain). MRSA is considered a serious worldwide threat to public health.

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The secret to longevity may lie in the microbiome and the gut, according to researchers from McGill University, Canada.

lifespan fruit flies future timeline

It is already known that the bacteria living in our intestinal tract could have an influence on how well we age. Building on this knowledge, McGill University scientists fed fruit flies with a combination of probiotics and a herbal supplement called Triphala. These experiments were able to prolong the insects’ longevity by 65% and protect them against chronic diseases associated with aging.

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Aged population is increasing worldwide due to the aging process that is inevitable. Accordingly, longevity and healthy aging have been spotlighted to promote social contribution of aged population. Many studies in the past few decades have reported the process of aging and longevity, emphasizing the importance of maintaining genomic stability in exceptionally long-lived population. Underlying reason of longevity remains unclear due to its complexity involving multiple factors. With advances in sequencing technology and human genome-associated approaches, studies based on population-based genomic studies are increasing. In this review, we summarize recent longevity and healthy aging studies of human population focusing on DNA repair as a major factor in maintaining genome integrity. To keep pace with recent growth in genomic research, aging- and longevity-associated genomic databases are also briefly introduced. To suggest novel approaches to investigate longevity-associated genetic variants related to DNA repair using genomic databases, gene set analysis was conducted, focusing on DNA repair- and longevity-associated genes. Their biological networks were additionally analyzed to grasp major factors containing genetic variants of human longevity and healthy aging in DNA repair mechanisms. In summary, this review emphasizes DNA repair activity in human longevity and suggests approach to conduct DNA repair-associated genomic study on human healthy aging.

Aging is an inevitable process in human life. Many countries are rapidly transitioning to an aging society due to increasing life expectancy and advanced medical supports [1–3]. Over the last few decades, the advent of aging society is considered a crucial issue that may cause future decline in productivity of community [1, 4]. Many researchers have recently warned that urban environmental pollutants can cause physiological weakness and increase the risk of premature aging or chronic diseases in the elderly population [5–9]. Thus, interest in antiaging and healthy longevity is constantly increasing. “Active aging” or “successful aging” has been spotlighted as a strategy to promote social contribution of the elderly [10]. The definition of successful aging remains controversial.

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A journalist, a soup exec, and an imam walk into a room. There’s no joke here. It’s just another day at CrisprCon.

On Monday and Tuesday, hundreds of scientists, industry folk, and public health officials from all over the world filled the amphitheater at the Boston World Trade Center to reckon with the power of biology’s favorite new DNA-tinkering tool: Crispr. The topics were thorny—from the ethics of self-experimenting biohackers to the feasibility of pan-global governance structures. And more than once you could feel the air rush right out of the room. But that was kind of the point. CrisprCon is designed to make people uncomfortable.

“I’m going to talk about the monkey in the room,” said Antonio Cosme, an urban farmer and community organizer in Detroit who appeared on a panel at the second annual conference devoted to Crispr’s big ethical questions to talk about equitable access to gene editing technologies. He referred to the results of an audience poll that had appeared moments before in a word cloud behind him, with one bigger than all the others: “eugenics.”

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Johnson and Johnson recently announced that it was halting a clinical trial for a new Alzheimer’s drug after safety issues emerged. This latest failure adds to the dozens of large, costly clinical trials that have shown no effect in treating this devastating disease.

The growing list of failures should give us pause for thought – have we got the causes of Alzheimer’s all wrong?

In the first analysis of the disease, the German physician, Alois Alzheimer, noted odd changes in the brain of a patient who died of the condition. Alzheimer identified two kinds of protein aggregates that are not found in younger brains: plaques that are found between brain cells and tangles that are found inside brain cells.

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Very promising since “Identifying what changes are happening in the brain when interventions successfully reduce depressive symptoms could allow us to create more effective, pharmaceutical-free approaches to help alleviate depression in people who experience chronic traumatic brain injury symptoms,” said study author Dr. Sandra Bond Chapman, founder and chief director of the Center for BrainHealth.


Images show prefrontal connectivity patterns after cognitive training in individuals who suffered traumatic brain injury. Kihwan Han et al (2018) _____ Cognitive training reduces depression, rebuilds injured brain structure & connectivity after traumatic brain injury (UT-Dallas release): “New research from the Center.

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