CNN’s Nick Paton Walsh takes us inside of an ICU in Sao Paulo, Brazil, where medical personnel are struggling to meet the needs of those infected with coronavirus.
Category: biotech/medical – Page 1,902
“I do believe there’s great potential to bring in artificial intelligence to provide early warning of future problems” such as disease outbreaks, Air Force Lt. Gen. John N.T. “Jack” Shanahan, director of the Pentagon’s Joint Artificial Intelligence Center, said in an interview.
Artificial intelligence could spot and track earlier outbreaks of disease around the world, the Pentagon’s AI chief says as he retires from service.
In order to find and treat cancerous tumors, a team of scientists is working on an aggressive new approach that involves a swarm of tiny, cancer-killing robots.
The idea is to inject the nanobots, which are engineered to look and travel like white blood cells, into a patient’s veins and move them around inside the body with powerful magnets.
“Our vision was to create the next-generation vehicle for minimally invasive targeted drug delivery that can reach even deeper tissues inside the body with even more difficult access routes than what was previously possible,” Metin Sitti, Director of Physical Intelligence at the Max Planck Society, said in a press release.
BENGALURU/LONDON (Reuters) — The United States has secured almost a third of the first 1 billion doses planned for AstraZeneca’s experimental COVID-19 vaccine by pledging up to $1.2 billion, as world powers scramble for medicines to get their economies back to work.
While not yet proven to be effective against the coronavirus, vaccines are seen by world leaders as the only real way to restart their stalled economies, and even to get an edge over global competitors.
Humans are living longer than ever before. But alongside these increases in life expectancy are an increase in the occurrence of age-related diseases such as cancer and dementia.
But understanding the biology of ageing, and knowing the genes and proteins involved in these processes, will help us increase our “healthspan”—the period that people can live in a healthy and productive state, without age-related diseases.
In a recent study, our team identified a novel anti-ageing protein, called Gaf1. We found that Gaf1 controls protein metabolism, a process that has been implicated in ageing and disease. We also found that without Gaf1, cells have a shorter lifespan.
The lessons from his presidency show that a quick retreat to the past can be just a mirage.
A study published in Current Biology reports on one of the first comprehensive characterizations of poorly formed memories, and may offer a framework to explore different therapeutic approaches to fear, memory and anxiety disorders. It may also have implications for accuracy of some witness testimony.
Senior author Professor Bryce Vissel, from the UTS Centre for Neuroscience & Regenerative Medicine, said his team used novel behavioral, molecular and computational techniques to investigate memories that have not been well-formed, and how the brain deals with them. “For memories to be useful, they have to have been well-formed during an event—that is, they have to accurately reflect what actually happened.
”However, in the real world many memories are likely to be inaccurate—especially in situations where the experience was brief, sudden or highly emotional, as can often occur during trauma. Inaccurate memories can also occur when the memory is poorly encoded, potentially as a result of subtle differences in how each person processes memory or because of disease like Alzheimer’s or dementia.”
The feds have ordered 300 million doses of a potential coronavirus vaccine from British drugmaker AstraZeneca, officials said Thursday.
The company will get up to $1.2 billion from the US Department of Health and Human Services to speed the development and production of the vaccine with the goal of delivering the first doses as early as October, according to officials.
The deal between AstraZeneca and HHS’s Biomedical Advanced Research and Development Authority includes clinical studies that will start this summer with about 30,000 US volunteers, officials said.
A research study in mice by investigators at the University of Rochester Medical Center (URMC) suggests it would be possible to repair the brain cell damage caused by multiple sclerosis (MS). The research was published in the journal Cell Reports.
The research, led by Steve Goldman, professor of Neurology and Neuroscience at URMC and co-director of the Center for Translational Neuromedicine, manipulated embryonic and induced pluripotent stem cells to create glia, a type of brain cell. Glial progenitor cells, a subtype of these cells, eventually form the primary support cells of the brain, astrocytes and oligodendrocytes, which play essential roles in the health and signaling behavior of nerve cells.
MS is an autoimmune disorder where the body’s immune system attacks oligodendrocytes. Oligodendrocytes manufacture myelin, which makes the insulation that allows nerve cells to communicate with each other. As myelin decreases in MS, the signaling between nerve cells is interrupted, which causes the loss of function that leads to problems with sensation, motor function and cognitive problems.
The factors mediating fatal SARS-CoV-2 infections are poorly understood. Here, we show that cigarette smoke causes a dose-dependent upregulation of Angiotensin Converting Enzyme 2 (ACE2), the SARS-CoV-2 receptor, in rodent and human lungs. Using single-cell sequencing data, we demonstrate that ACE2 is expressed in a subset of secretory cells in the respiratory tract. Chronic smoke exposure triggers the expansion of this cell population and a concomitant increase in ACE2 expression. In contrast, quitting smoking decreases the abundance of these secretory cells and reduces ACE2 levels. Finally, we demonstrate that ACE2 expression is responsive to inflammatory signaling and can be upregulated by viral infections or interferon treatment. Taken together, these results may partially explain why smokers are particularly susceptible to severe SARS-CoV-2 infections. Furthermore, our work identifies ACE2 as an interferon-stimulated gene in lung cells, suggesting that SARS-CoV-2 infections could create positive-feedback loops that increase ACE2 levels and facilitate viral dissemination.