Characterization of Rhesus Macaque Liver-Resident CD49a NK Cells During Retrovirus Infections.

CD49a tissue resident NK cells have been implicated in memory-like NK cell responses, but while this population is well-characterized in mice and in humans, they are poorly described in non-human primates (NHP) which are particularly critical for modeling human viral infections. Others and we have shown that memory-like NK cells are enriched in the liver and because of the importance of NHP in modeling HIV infection, understanding the immunobiology of CD49a NK cells in SIV-infected rhesus macaques is critical to explore the role of this cell type in retroviral infections. In this study mononuclear cells isolated from livers, spleens, and peripheral whole blood were analyzed in acutely and chronically lentivirus-infected and experimentally-naïve Indian rhesus macaques (RM).

Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism.

Microglia adopt numerous fates with homeostatic microglia (HM) and a microglial neurodegenerative phenotype (MGnD) representing two opposite ends. A number of variants in genes selectively expressed in microglia are associated with an increased risk for neurodegenerative diseases such as Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). Among these genes are progranulin () and the triggering receptor expressed on myeloid cells 2 ().

ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy.

APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. ApoE4 increases brain amyloid-β pathology relative to other ApoE isoforms. However, whether APOE independently influences tau pathology, the other major proteinopathy of Alzheimer disease and other tauopathies, or tau-mediated neurodegeneration, is not clear.

The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases.

Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic function during neurodegenerative disorders. We identified a specific apolipoprotein E (APOE)-dependent molecular signature in microglia from models of amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and Alzheimer's disease (AD) and in microglia surrounding neuritic β-amyloid (Aβ)-plaques in the brains of people with AD. The APOE pathway mediated a switch from a homeostatic to a neurodegenerative microglia phenotype after phagocytosis of apoptotic neurons.

Nonsteroidal anti-inflammatory drugs' impact on nonunion and infection rates in long-bone fractures.

Background: There is a dearth of clinical data regarding the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on long-bone fracture (LBF) healing in the acute trauma setting. The orthopedic community believes that the use of NSAIDs in the postoperative period will result in poor healing and increased infectious complications. We hypothesized that, first, NSAID use would not increase nonunion/malunion and infection rates after LBF.

Herd-level prevalence of Mycoplasma spp mastitis and characteristics of infected dairy herds in Utah as determined by a statewide survey.

Objective: To determine herd-level prevalence of Mycoplasma spp mastitis in Utah dairy herds and characterize farms and management practices for positive herds.

Design: Epidemiologic study.

Sample Population: Bulk tank milk samples from 222 of 285 (78%) dairy farms in Utah.