Quantifying our lives is easier than it’s ever been. But a philosopher of games warns that external metrics and data can never capture what’s truly important.
An immune pathway has been discovered that prevents a normally harmless fungus from developing into a fatal infection. The King’s College London study, published in Nature Microbiology, provides the first potential clue as to why only certain patients with weakened immune systems, including those undergoing chemotherapy or living with HIV, are at risk of life-threatening Candida albicans infections.
Candida albicans is a fungus that normally lives harmlessly in areas such as the mouth and gut but can sometimes spread through the body and cause fatal disease.
If the results are confirmed in humans, they could provide a test to identify who is at risk of developing fatal fungal infections and represent a potential therapeutic target to reduce the risk of developing the disease.
et al. used an innovative series of screening and directed evolution steps to produce a new enzyme (CMLase) which can remove a pernicious form of advanced glycation end product (AGE) linkage from proteins. AGEs contribute to biological aging, so CMLase may possess therapeutic potential to combat parts of the aging process.
Advanced glycation end products (AGEs) in proteins, a hallmark of aging, are considered irreversible. Here, authors report the development of CMLase — an enzyme that specifically oxidizes Nε-carboxymethyl-lysine (CML) and restores the native lysine residues in vitro and in human tissue samples.
However, Carpenter was not entirely convinced that hyposalivation drives periodontitis. “I don’t think there’s much evidence for that in…literature about human studies,” he said. Instead, he said that inflammation—which is present in Dp16 salivary glands—could cause hyposalivation. “There’s lots of literature that shows that inflammatory cells can affect salivary secretion,” he noted.
According to Yule, next steps could include looking at whether dysregulated calcium signaling—which is linked with several other diseases—also underlies other Down syndrome-related complications like Alzheimer’s disease. While drugs targeting calcium signaling could potentially help, there is a complexity to it, he noted. “Knowing what the target is [is] good, but the fact that the target is almost universal in cells, then that makes you think about whether it’s something that could be targeted,” explained Yule.
Lacruz agreed that disrupted calcium signaling occurs in other tissues as well. “Understanding why calcium is dysregulated is an important part of what we need to do [next],” he said. More work needs to be done to translate the findings to the clinic, “but we see that as a way forward to potentially impacting the lives of individuals with Down syndrome,” said Lacruz.
Chronic stress significantly influences the pathogenesis of headache disorders, affecting millions worldwide. This review explores the intricate relationship between stress and headaches, focusing on the dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis and autonomic nervous system (ANS). Persistent stress could lead to neuroinflammation, increased pain sensitivity, and vascular changes that could contribute to headache development and progression. The bidirectional nature of this relationship creates a vicious cycle, with recurrent headaches becoming a source of additional stress. Dysregulation of the HPA axis and ANS imbalance could amplify susceptibility to headaches, intensifying their frequency and severity. While pharmacological interventions remain common, non-pharmacological approaches targeting stress reduction, such as cognitive-behavioral therapy, biofeedback, and relaxation techniques, offer promising avenues for comprehensive headache management. By addressing the underlying stress-related mechanisms, these approaches provide a sustainable strategy to reduce headache frequency and improve patients’ quality of life.
Researchers treated male high-fat-fed mice with liraglutide for 14 days, then tracked fecal bacterial communities after a 7-day washout using 16S rRNA sequencing. Liraglutide shifted the microbiome toward Lactobacillus- and Leptogranulimonas-related taxa while reducing several fermentative taxa, but most changes moved back toward baseline after treatment stopped.