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Category: biotech/medical – Page 1306

These club cell-secreted factors are able to nullify immune suppressor cells that otherwise help tumors escape an effective antitumor response,” said co-senior author Dr. Vivek Mittal, director of research at the Neuberger Berman Lung Cancer Center and the Ford-Isom Research Professor of Cardiothoracic Surgery at Weill Cornell Medicine. “We’re excited by the possibility of developing these club cell factors into a cancer treatment.

Malignant tumors can enhance their ability to survive and spread by suppressing antitumor immune cells in their vicinity, but a study led by researchers at Weill Cornell Medicine and NewYork-Presbyterian has uncovered a new way to counter this immunosuppressive effect.

In the study, published Sept. 20 in Nature Cancer, the researchers identified a set of anti-immunosuppressive factors that can be secreted by called cells that line airways in the lungs. They showed in a mouse model of lung cancer that these club cell factors inhibit highly potent immunosuppressive cells called myeloid-derived suppressor cells (MDSCs), which tumors often recruit to help them evade antitumor immune responses.

The inhibition of the MDSCs led to an increase in the number of antitumor T cells at the tumor site, and greatly improved the effectiveness of FDA approved PD1 immunotherapy.

Continue reading “Scientists find a new way to reverse immune suppression in tumors” | >

As this is the first report of neuro-inflammation in Kleefstra syndrome, the next step is to find out if it also occurs in the human condition. Shinkai believes the chances are high and says he would not be surprised if other neurological diseases caused by epigenetic dysregulation were also related to abnormal inflammation in the brain.

Researchers at the RIKEN Cluster for Pioneering Research (CPR) in Japan report that Kleefstra syndrome, a genetic disorder that leads to intellectual disability, can be reversed after birth in a mouse model of the disease. Published in the scientific journal iScience, the series of experiments led by Yoichi Shinkai showed that postnatal treatment resulted in improved symptoms, both in the brain and in behavior.

Normally, we get two good copies of most genes, one from each parent. In Kleefstra , one copy of the EHMT1 gene is mutated or missing. This leads to half the normal amount of GLP, a protein whose job is to control genes related to brain development through a process called H3K9 methylation. Without enough GLP, H3K9 methylation is also reduced, and the connections between neurons in the brain do not develop normally. The result is and autistic-like symptoms. “We still don’t know if Kleefstra syndrome is a curable disease after birth or how this epigenetic dysregulation leads to the ,” says Shinkai. “Our studies in have provided new information about what causes the behavioral abnormalities associated with the syndrome and have shown that a cure is a real possibility in the future.”

Reasoning that extra GLP might be an , the researchers performed a series of experiments in mice that were engineered to have only one good copy of the EHMT1 gene. The brains of these mice show characteristics of the human condition, including 40% less GLP and 30% less H3K9 methylation. The mice also display several behaviors seen in humans with Kleefstra syndrome, such as reduced locomotion and greater anxiety. After each experiment, the researchers measured these factors and compared them to normal mice to see if the treatment had been effective.

Continue reading “A genetic brain disease reversed after birth” | >

Science is examining the brain’s neural activity for applications ranging from innovative therapies for brain-related injuries and disease to computational learning architectures for artificial intelligence and deep neural networks.

A research team has developed a tool that lets researchers see more of a live mouse’s brain, to make discoveries that can advance research into the neural circuit mechanisms that form the underlying behavior of the human brain. The tool overcomes the drawback of traditional brain probes—the small amount of tissue they can access, which limits their ability to image neurons of interest.

The innovation is to insert an imaging probe with side-viewing capabilities into a previously inserted optically matched channel—an ultrathin-wall glass capillary—to convert deep brain imaging into endoscopic imaging. The operator can freely rotate the probe to image different , getting a 360-degree view for imaging along the entire length of the inserted probe. This large-volume imaging enables an increase of about 1,000 times in access volume, compared with what is available for imaging at the tip of typical miniature imaging probes.

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The pharmaceuticals firm GSK has struck a five-year partnership with King’s College London to use artificial intelligence to develop personalised treatments for cancer by investigating the role played by genetics in the disease.

The tie-up, which involves 10 of the drug maker’s artificial intelligence experts working with 10 oncology specialists from King’s across their labs, will use computing to “play chess with cancer”, working out why only a fifth of patients respond well to immuno-oncology treatments.

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Merck, known as MSD outside the US and Canada, and Ridgeback Biotherapeutics have announced that its MOV-e-AHEAD study has started to enrol its first participants to test antiviral molnupiravir in post-exposure prophylaxis of COVID-19 infection.

The global study will include approximately 1,332 participants who are 18 years or over and reside in the same household as someone with laboratory-confirmed SARS-CoV-2 infection, has at least one sign or symptom of COVID-19 and has not had those signs and symptoms for more than five days.

Participants will be randomised onto molnupiravir, an investigational oral antiviral therapeutic, or placebo every 12 hours for 5 days. The trial will not look at vaccinated people, those who have had COVID-19 before or anyone showing signs or symptoms of infection.

The MOVe-AHEAD trial will test whether the drug prevents infection in those living in the same household as someone with confirmed COVID-19.

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Red blood cells are the most abundant cell type in blood, carrying oxygen throughout the human body. In blood circulation, they repetitively encounter various levels of oxygen tension. Hypoxia, a low oxygen tension condition, is a very common micro-environmental factor in physiological processes of blood circulation and various pathological processes such as cancer, chronic inflammation, heart attacks and stroke. In addition, an interplay between poor cellular deformability and impaired oxygen delivery is found in various pathological processes such as sickle cell disease. Sickle red blood cells simultaneously undergo drastic mechanical deformation during the sickling and unsickling process.

The interactions between hypoxia and cell biomechanics and the underlying biochemical mechanisms of the accelerated damage in diseased are well understood, however, the exact biomechanical consequences of hypoxia contributing to red cell degradation (aging) remains elusive.

Researchers from Florida Atlantic University’s College of Engineering and Computer Science, in collaboration with the Massachusetts Institute of Technology (MIT), sought to identify the role of hypoxia on red blood cell aging via the biomechanical pathways. In particular, they examined hypoxia-induced impairment of red blood cell deformability at the single cell level, compared the differences between non-cyclic hypoxia and cyclic hypoxia, and documented any cumulative effect vs. hypoxia cycles, such as aspects that have not been studied quantitatively. Red blood cell deformability is an important biomarker of its functionality.

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