An intriguing new study from researchers at Stockholm University and Karolinska Institutet has described a mechanism by which virus particles can interact with proteins in biological fluids and become more infectious, while also accelerating the formation of plaques often associated with neurodegenerative diseases such as Alzheimer’s.
It’s comforting to think of the body as a machine we can trick out. It helps us ignore the strange fleshy aches that come with having a meat cage. It makes a fickle system—one we truly don’t understand—feel conquerable. To admit that the body (and mind that sits within it) might be far more complex than our most delicate, intricate inventions endangers all kinds of things: the medical industrial complex, the wellness industry, countless startups. But it might also open up new doors for better relationships with our bodies too: Disability scholars have long argued that the way we see bodies as “fixable” ultimately serves to further marginalize people who will never have the “standard operating system,” no matter how many times their parts are replaced or tinkered with.
Tech gurus are obsessed with treating bodies like machines—something a 30-year-old cartoon about a tricked-out detective suggests won’t work.
Helicobacter pylori, a globally distributed gastric bacterium, is genetically highly adaptable. Microbiologists at LMU have now characterized its population structure in individual patients, demonstrating an important role of antibiotics for its within-patient evolution.
The cosmopolitan bacterium Helicobacter pylori is responsible for one of the most prevalent chronic infections found in humans. Although the infection often provokes no definable symptoms, it can result in a range of gastrointestinal tract pathologies, ranging from inflammation of the lining of the stomach to gastric and duodenal tumors. Approximately 1 percent of all those infected eventually develop stomach cancer, and the World Health Organization has classified H. pylori as a carcinogen. One of Helicobacter pylori’s most striking traits is its genetic diversity and adaptability. Researchers led by microbiologist Sebastian Suerbaum (Chair of Medical Microbiology and Hospital Epidemiology at LMU’s Max von Pettenkofer Institute have now examined the genetic diversity of the species in the stomachs of 16 patients, and identified specific adaptations that enable the bacterium to colonize particular regions of the stomach.
Many mutations in DNA that contribute to disease are not in actual genes but instead lie in the 99% of the genome once considered “junk.” Even though scientists have recently come to understand that these vast stretches of DNA do in fact play critical roles, deciphering these effects on a wide scale has been impossible until now.
Using artificial intelligence, a Princeton University-led team has decoded the functional impact of such mutations in people with autism. The researchers believe this powerful method is generally applicable to discovering such genetic contributions to any disease.
Publishing May 27 in the journal Nature Genetics, the researchers analyzed the genomes of 1,790 families in which one child has autism spectrum disorder but other members do not. The method sorted among 120,000 mutations to find those that affect the behavior of genes in people with autism. Although the results do not reveal exact causes of cases of autism, they reveal thousands of possible contributors for researchers to study.
The role that the gut microbiome plays in aging is increasingly being appreciated in the research world as more evidence arrives to support it. A new publication reviews the various supporting evidence and takes a look at the gut microbiome in the context of nutrient-rich diets and how they facilitate the progression of dysbiosis and disease [1].
What is the microbiome?
The microbiome is the varied community of bacteria, archaea, eukarya, and viruses that inhabit our guts. The four bacterial phyla of Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria comprise 98% of the intestinal microbiome.
Humans may not be able to burp properly in space, but we can now edit a genome. For the first time, astronauts aboard the International Space Station (ISS) have used CRISPR-Cas9 to edit the DNA of brewer’s yeast.
The goal wasn’t to create super space yeast. The astronauts were studying how DNA repair mechanisms work in space, so they snipped through strands of the fungus’s genetic code in a number of places to mimic radiation damage.
“The damage actually happens on the space station and the analysis also happens in space,” said Emily Gleason of miniPCR Bio, the company that designed the DNA lab aboard the ISS. “We want to understand if DNA repair methods are different in space than on Earth.”
Microorganisms like bacteria and fungi are increasingly becoming resistant to our best drugs, which is hurtling us towards a terrifying future where once-easily-treated infections become potentially life-threatening again. In a new approach to this problem, researchers from the University at Buffalo and Temple University have tested an alternative to antibiotics that uses existing drugs to starve a fungal infection of vital nutrients.
