Learning Lessons from the COVID-19 Pandemic-A Qualitative Assessment of the Experiences of Pregnant Latinas Infected with COVID-19 and Their Perspectives on Vaccination.

Objectives: To examine the experiences of pregnant Hispanic/Latine people with COVID-19, as well as their perspectives on COVID-19 vaccination in pregnancy.

Methods: We interviewed birthing parents who received care from a teaching hospital in California and tested positive for COVID-19 during pregnancy or delivery. We analyzed transcripts using the constant comparative method for analyzing data to using a phenomological epidemiological approach.

Tricarboxylic acid (TCA) cycle, sphingolipid, and phosphatidylcholine metabolism are dysregulated in infection-induced cachexia.

Cachexia is a life-threatening disease characterized by chronic, inflammatory muscle wasting and systemic metabolic impairment. Despite its high prevalence, there are no efficacious therapies for cachexia. Mice chronically infected with the protozoan parasite represent a novel animal model recapitulating the chronic kinetics of cachexia.

Acute Lymph Node Slices Are a Functional Model System to Study Immunity Ex Vivo.

The lymph node is a highly organized and dynamic structure that is critical for facilitating the intercellular interactions that constitute adaptive immunity. Most ex vivo studies of the lymph node begin by reducing it to a cell suspension, thus losing the spatial organization, or fixing it, thus losing the ability to make repeated measurements. Live murine lymph node tissue slices offer the potential to retain spatial complexity and dynamic accessibility, but their viability, level of immune activation, and retention of antigen-specific functions have not been validated.

T. gondii infection induces IL-1R dependent chronic cachexia and perivascular fibrosis in the liver and skeletal muscle.

Cachexia is a progressive muscle wasting disease that contributes to death in a wide range of chronic diseases. Currently, the cachexia field lacks animal models that recapitulate the long-term kinetics of clinical disease, which would provide insight into the pathophysiology of chronic cachexia and a tool to test therapeutics for disease reversal. Toxoplasma gondii (T.

IL-1R Regulates Disease Tolerance and Cachexia in Infection.

is an obligate intracellular parasite that establishes life-long infection in a wide range of hosts, including humans and rodents. To establish a chronic infection, pathogens often exploit the trade-off between resistance mechanisms, which promote inflammation and kill microbes, and tolerance mechanisms, which mitigate inflammatory stress. Signaling through the type I IL-1R has recently been shown to control disease tolerance pathways in endotoxemia and infection.

Disease Tolerance in Infection.

is a successful protozoan parasite that cycles between definitive felid hosts and a broad range of intermediate hosts, including rodents and humans. Within intermediate hosts, this obligate intracellular parasite invades the small intestine, inducing an inflammatory response. infects infiltrating immune cells, using them to spread systemically and reach tissues amenable to chronic infection.

Toxoplasma gondii infection triggers chronic cachexia and sustained commensal dysbiosis in mice.

Toxoplasma gondii is a protozoan parasite with a predation-mediated transmission cycle between rodents and felines. Intermediate hosts acquire Toxoplasma by eating parasite cysts which invade the small intestine, disseminate systemically and finally establish host life-long chronic infection in brain and muscles. Here we show that Toxoplasma infection can trigger a severe form of sustained cachexia: a disease of progressive lean weight loss that is a causal predictor of mortality in cancer, chronic disease and many infections.

Tuft Cells: New Players in Colitis.

A recent surge of interest in tuft cells, which are chemosensory intestinal epithelial cells, has uncovered new functional roles for these cells in colorectal cancer, metabolic signaling, and type 2 immunity. Here, we explore emerging evidence suggesting that tuft cells are critical for protection during enteric infections and inflammatory responses.

Relationships between membrane water molecules and Patman equilibration kinetics at temperatures far above the phosphatidylcholine melting point.

The naphthalene-based fluorescent probes Patman and Laurdan detect bilayer polarity at the level of the phospholipid glycerol backbone. This polarity increases with temperature in the liquid-crystalline phase of phosphatidylcholines and was observed even 90°C above the melting temperature. This study explores mechanisms associated with this phenomenon.

Regional brain volume differences in symptomatic and presymptomatic carriers of familial Alzheimer's disease mutations.

Background: Mutations in the presenilin (PSEN1, PSEN2) and amyloid precursor protein (APP) genes cause familial Alzheimer's disease (FAD) in a nearly fully penetrant, autosomal dominant manner, providing a unique opportunity to study presymptomatic individuals who can be predicted to develop Alzheimer's disease (AD) with essentially 100% certainty. Using tensor-based morphometry (TBM), we examined brain volume differences between presymptomatic and symptomatic FAD mutation carriers and non-carrier (NC) relatives.

Methods: Twenty-five mutation carriers and 10 NC relatives underwent brain MRI and clinical assessment.

Role of membrane oxidation in controlling the activity of human group IIa secretory phospholipase A(2) toward apoptotic lymphoma cells.

The membranes of healthy lymphocytes normally resist hydrolysis by secretory phospholipase A(2). However, they become susceptible during the process of apoptosis. Previous experiments have demonstrated the importance of certain physical changes to the membrane during cell death such as a reduction in membrane lipid order and exposure of phosphatidylserine on the membrane surface.