A vaccine against the deadly Ebola virus has led to 100% protection and could transform the way Ebola is tackled, preliminary results suggest.
There were no proven drugs or vaccines against the virus at the start of the largest outbreak of Ebola in history, which began in Guinea in December 2013.
The World Health Organization (WHO) said the findings, being published in the Lancet, could be a “game-changer”.
Experts said the results were “remarkable”.
This trial centred on the VSV-EBOV vaccine, which was started by the Public Health Agency of Canada and then developed by the pharmaceutical company Merck.
Full story at BBC News
Scientists wonder whether they can obtain the resources to test experimental vaccines and treatments in humans.
South Korean officials today announced the end of the country’s recent Middle East respiratory syndrome coronavirus (MERS-CoV) outbreak, butscientists studying the virus and others like it expect more outbreaks to follow.
“We think there will be other coronaviruses in the future that will be important and will need to be dealt with,” said Barney Graham, deputy director of the Vaccine Research Center at the National Institute of Allergy and Infectious Diseases (NIAID). In a paper published today (July 28) in Nature Communications, Graham and his colleagues described the antibody response to a vaccine candidate based on the MERS-CoV spike glycoprotein in mice, and characterized several murine virus-neutralizing monoclonal antibodies. The report follows on another study, published yesterday (July 27) in PNAS, in which researchers from the Institute for Research in Biomedicine (IRB) in Bellinzona, Switzerland, and their colleagues described a MERS-neutralizing monoclonal antibody produced from human B cells that helped prevent and clear MERS-CoV infection in mice.
Graham and his colleagues initiated their study as soon as the MERS-CoV was first sequenced in 2012. “The only thing we had was the sequence of the spike glycoprotein,” he said. But that was enough. Because the spike glycoprotein is required for viral entry into cells, “it’s the obvious target for antibody-mediated protection for a vaccine,” Graham said.
Link to full story at The Scientist
In the last few years, I’ve watched a continuing battle among my friends about which is worse for you: artificial sweeteners or sugar. Unless you want to forgo all beverages that are sweet, you’re going to run into one of these. Rather than rely on anecdote or myth, we can inform this debate with research.
The available evidence points to the fact that there appears to be a correlation between sugar consumption and health problems; none can be detected with artificial sweeteners.
Let’s start with artificial sweeteners. These have, for decades, been attacked as harmful chemicals. But everything is a “chemical,” and not all of them are bad for us. One of the oldest artificial sweeteners is saccharin. Starting in the 1980s, Congress mandated that any product containing it be accompanied by the following: “Use of this product may be hazardous to your health. This product contains saccharin, which has been determined to cause cancer in laboratory animals.”
Very interesting article at the NYT
We just sent out our summer newsletter to everyone. If you didn’t get a copy check it out here!
New research provides a potential pathway to a drug to save people from the progressive damage of severe or repeated concussions
An experimental treatment helps restore normal brain structure and function in mice that have sustained severe concussions, and could lead to a drug that would do the same in humans, according to new research.
The brains of people who suffer from chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease that affects people such as boxers and football players with a history of repetitive hard hits to the head, are characterized by fibrous tangles of a protein called tau. It is not known how traumatic brain injury leads to these tangles, which are also found in the brains of people who suffered from Alzheimer’s disease.
Read full article at MIT Technology Review
A walk in the park may soothe the mind and, in the process, change the workings of our brains in ways that improve our mental health, according to an interesting new study of the physical effects on the brain of visiting nature.
Most of us today live in cities and spend far less time outside in green, natural spaces than people did several generations ago.
City dwellers also have a higher risk for anxiety, depression and other mental illnesses than people living outside urban centers, studies show.
These developments seem to be linked to some extent, according to a growing body of research. Various studies have found that urban dwellers with little access to green spaces have a higher incidence of psychological problems than people living near parks and that city dwellers who visit natural environments have lower levels of stress hormones immediately afterward than people who have not recently been outside.
Link to full article on New York Times
Ethical issues attend the creation of animal-human chimeras.
Late last year, Steve Goldman of the University of Rochester and his colleagues reported that they had transplanted immature glial cells from donated human fetuses into the brains of immunodeficient mouse pups. These human glial cells matured into astrocytes and developed as the primary astrocyte population in the newborn mouse brain. One unexpected outcome of the team’s research, published in the Journal of Neuroscience (34:16153-61), was that these human-mouse chimeras outperformed normal mice almost fourfold in a variety of cognition tests, underscoring the importance of astrocytes in regulating synaptic plasticity and neural connectivity to enhance learning and memory. But the study also raised important ethical considerations—namely, what biological properties differentiate Homo sapiens from other organisms, and when should such “humanized” animals be afforded the rights that people currently enjoy.
Link to full article at The Scientist
Dr Sarah Bond, project Director at Cambridge Biomedical is co-author of paper published in Nature Medicine on
NY-ESO-1–specific TCR–engineered T cells mediate sustained antigen-specific antitumor effects in myeloma
This paper was initially presented at AACR in April 2015
Link to paper on Nature Medicine
Patient-derived organoids reveal autism spectrum disorder–associated anomalies.
An examination of tiny, brain-like organoids generated from the skin cells of patients with autism spectrum disorder (ASD) suggests that the condition may be associated with an overproduction of inhibitory neurons, among other things. The study, published today (July 16) in Cell, reveals that although the patients’ symptoms arose spontaneously, their brain cells behaved similarly in vitro.
“These are patients with idiopathic autism that do not share any genetic causes, and yet the authors find phenotypes shared between their cells. That’s impressive,” said neuroscientist and stem cell biologist Alysson Muotri of the University of California, San Diego, who was not involved in the study. “If someone had asked me, I would have said, ‘You won’t find anything in common, it’s probably going to be a mixed bag.’ But no . . . there seems to be key things that are dysregulated in all of them.” (See “Opinion: New Models for ASD,” The Scientist, May 14.)
Indeed, “one of the most exciting aspects of the work is that it manages to tackle idiopathic neurological disease,” agreed Magdalena Götz of Ludwig-Maximilians-University Munich, who also did not participate in the research.
Link to full article at The Scientist
Measuring the pace of biological aging in young people could someday help prevent age-related diseases
Feel like you’re 40 years old going on 60? Or maybe, 40 going on 21?
Age may be just a number, but medical experts increasingly are saying it might not always be the right number to gauge your health.
Everybody grows older at a different pace, according to a recent study that found the processes of aging can begin fairly early in life. The study calculated the aging rate of 954 men and women—taking various measurements of their bodies’ health—when they were each 26, 32 and 38 in chronological years. By analyzing how these measures changed over time, the researchers were able to see who aged faster and who slower than normal.
The aim of the research is to be able eventually to identify signs of premature aging before it becomes evident years or decades later in chronic diseases such as cardiovascular disease, diabetes or kidney and lung impairment. “Intervention to reverse or delay the march toward age-related diseases must be scheduled while people are still young,” according to the study, published online last week in the Proceedings of the National Academy of Sciences.
Link to full article at WSJ