A strain of the dysentery-causing bacterium isolated in 1915 tells the story of a young soldier who died of the disease in the early days of World War I.
In early 1915, less than a year into the First World War, Private Ernest Cable, a 28-year-old British soldier serving in the 2nd Battalion of the East Surrey Regiment, stumbled into No. 14 Stationary Hospital in Wimereux, France. He was suffering from severe abdominal cramping and bloody diarrhea. Doctors diagnosed him with dysentery. Not long after, Cable was dead.
Nicholas Thomson, a genomicist at the Wellcome Trust Sanger Institute, first came to know of Cable’s lethal infection at a conference in October 2011. At the meeting, he met a woman named Philippa “Pippa” Bracegirdle, who worked in the archives of the UK National Collection of Type Cultures (NCTC), the oldest collection of bacterial cultures in the world. Over a drink, Bracegirdle mentioned that the collection contained an isolate of Shigella, the dysentery-causing kin of E. coli that had killed Cable. Later identified as Shigella flexneri serotype 2a, it was the first bacterial isolate deposited in NCTC’s now 5,000-sample-strong biobank.
With the 100-year anniversary of the start of “the war to end all wars” coming up in just a few years, Thomson was inspired to take a closer look at the isolate. Having studied the genetics of Shigella and other pathogens, he decided to sequence the bacterium. But as Thomson learned more from Bracegirdle about the isolate, he realized he had a rare opportunity to find out more about the patient who died from it a century ago.
Researchers uncover a previously unknown way UV light can act on melanin, spurring cancer-causing mutations hours after sun exposure.
In 1971, Angelo Lamola—who was then at Bell Laboratories—used an unusual chemical, trimethyldioxetane, to produce DNA lesions in a test tube. Decades later, the same lesions, produced by sunlight, were linked to melanoma, an aggressive type of skin cancer. Now, researchers at Yale University and their colleagues have found that this reaction occurs in the skin cells of mice hours after ultraviolet (UV) light exposure. The team’s results are published today (February 19) in Science.
“The study is really interesting and provocative,” said David Fisher, a cancer biologist focusing on melanoma at Massachusetts General Hospital in Boston who was not involved in the work. “It underlines even more than what we knew previously: that melanin biochemistry is a two-edged sword—there are benefits and liabilities.”
UV light acts directly on DNA to form cyclobutane pyrimidine dimers (CPDs) within picoseconds, which, if not repaired, subsequently result in a mutation—a cytosine-to-thymine change. Most melanomas stem from these fast-forming CPDs that linger and lead to mutations.
Yale biophysicist Douglas Brash and his colleagues were doing time course experiments after irradiating murine melanocytes—the cells in the skin that produce melanin pigments and in which most melanomas arise—and stumbled onto an unusual observation: the melanocytes continued to produce CPDs four hours after exposure to either UVA or UVB light. “To a photochemist, this is totally preposterous. The difference between four hours and a millionth of a million of a second is as if something that should have taken one second at the time of the dinosaurs was just finishing up now,” said Brash.
A new compound has blocked H.I.V.infection so well in monkeys that it may be able to function as a vaccine against AIDS, the scientists who designed it reported Wednesday.
H.I.V. has defied more than 30 years of conventional efforts to fashion a vaccine. The new method stimulates muscle cells to produce proteins that somewhat resemble normalantibodies, which have Y-shaped heads. These proteins have both a head and a tail, and they use them to simultaneously block two sites on each “spike” that the virus uses to attach itself to a cell.
If both sites can be blocked on every spike, the virus becomes helpless and drifts off unattached into eventual oblivion by the immune system.
A National Institutes of Health-funded consortium publishes 111 reference maps of DNA and histone marks.
n a culmination of a multiyear project to identify the chemical modifications of DNA and its associated proteins that regulate gene expression, members of the Roadmap Epigenome Consortium today (February 18) published their analysis of 111 different human epigenomes in Nature. The National Institutes of Health (NIH)-funded team’s analysis—comparing histone and DNA methylation, DNA availability, and other marks such as histone acetylation among the 111 genomes as well as 16 previously released annotated epigenomes from theEncyclopedia of DNA Elements (ENCODE) project—was accompanied by articles examining the patterns of chemical markers and chromatin structure in stem cells, Alzheimer’s disease, and cancer.
“It is definitely a milestone,” said Kristian Helin of the University of Copenhagen, who was not involved in the research. “It should mostly be credited for the enormous amount of work . . . that hopefully will serve as a very good guide for epigenome studies in the future.”
Human skin from cadavers that have had their cells removed can help treat wounds, researchers say.
This new treatment could prove especially helpful for chronic skin wounds, which are a growing threat to public health, scientists added. According to the National Institutes of Health, treating such wounds costs the United States more than $25 billion annually.
About 1 in 100 people in the United States will suffer from chronic leg ulcers during their lifetime. With an aging population and increasing rates of diseases linked to ulcers and other skin wounds, such as diabetes, obesity and heart disease, the prevalence and costs of such wounds are likely to rise in the future, said study senior author Ardeshir Bayat, a bioengineer and clinician-scientist at the University of Manchester in England.
Researchers uncover one way capsaicin—the spicy compound found in chili peppers—provides pain relief.
Capsaicin—a substance in chili pepper plants that makes them spicy hot—exerts its pain- attenuating effects by triggering a signaling cascade that results in the inactivation of mechano-sensitive transmembrane channels in neurons, according to a study published this week (February 10) in Science Signaling.
Initially causing a burning hot sensation, the compound is used as a topical pain medication because, when applied regularly, results in numbness to local tissue. Despite being widely used, researchers have previously not known how capsaicin exerts its pain-killing effects.