11 results match your criteria: "Department of Pharmacology and Toxicology. Michigan State University[Affiliation]"
AIDS Res Treat
September 2024
Department of Medicine Trinity Health Grand Rapids Hospital, Grand Rapids, Michigan, USA.
Introduction: Mild cognitive impairment (MCI) is a significant public health concern and a potential precursor to Alzheimer's disease (AD). This study leverages electronic health record (EHR) data to explore rural-urban differences in MCI incidence, risk factors, and healthcare navigation in West Michigan.
Methods: Analysis was conducted on 1,528,464 patients from Corewell Health West, using face-to-face encounters between 1/1/2015 and 7/31/2022.
Integr Environ Assess Manag
November 2024
Department of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA.
Cancer cells produce heterogeneous extracellular vesicles (EVs) as mediators of intercellular communication. This study focuses on a novel method to image EV subtypes and their biodistribution in vivo. A red-shifted bioluminescence resonance energy transfer (BRET) EV reporter is developed, called PalmReNL, which allows for highly sensitive EV tracking in vitro and in vivo.
View Article and Find Full Text PDFChem Biol Interact
August 2021
Department of Pharmacology and Toxicology. Michigan State University, East Lansing, MI, USA. Electronic address:
2,3,7,8-Tetrachlorodibenzo-p-dioxin (dioxin; TCDD) is an environmental contaminant that elicits a variety of toxic effects, many of which are mediated through activation of the aryl hydrocarbon receptor (AhR). Interaction between AhR and the peroxisome proliferator-activated receptor-alpha (PPAR-α), which regulates fatty acid metabolism, has been suggested. Furthermore, with recognition of the prevalence of inflammatory conditions, there is current interest in the potential for inflammatory stress to modulate the response to environmental agents.
View Article and Find Full Text PDFBackground: Blood coagulation protease activity is proposed to drive hepatic fibrosis through activation of protease-activated receptors (PARs). Whole-body PAR-1 deficiency reduces experimental hepatic fibrosis, and studies suggest a potential contribution by PAR-1 expressed by hepatic stellate cells. However, owing to a lack of specific tools, the cell-specific role of PAR-1 in experimental hepatic fibrosis has never been formally investigated.
View Article and Find Full Text PDFThe novel clopidogrel conjugate, DT-678, is an effective inhibitor of platelets and thrombosis in preclinical studies. However, a comparison of the bleeding risk with DT-678 and currently approved P2Y antagonists has yet to be determined. The objective of this study was to evaluate the bleeding tendency of animals treated with clopidogrel, ticagrelor, and DT-678.
View Article and Find Full Text PDFT-type voltage-gated Ca channels (CaV3.2 VGCC) have been hypothesized to control spontaneous transient outward currents (STOCs) through large-conductance Ca-activated K channels (BK), and contribute to the negative-feedback regulation of myogenic tone. We tested this hypothesis in superior epigastric arteries (SEAs) isolated from male C57BL/6 mice.
View Article and Find Full Text PDFHypoxia-inducible factor-1α (HIF-1α) is activated in hepatic stellate cells (HSCs) by hypoxia and regulates genes important for tissue repair. Whether HIF-1α is activated in HSCs after acute injury and contributes to liver regeneration, however, is not known. To investigate this, mice were generated with reduced levels of HIF-1α in HSCs by crossing HIF-1α floxed mice with mice that express Cre recombinase under control of the glial fibrillary acidic protein (GFAP) promoter (i.
View Article and Find Full Text PDFThe purpose of the present study was to determine the effects of quinelorane, a selective D2 receptor agonist, on concentrations of prolactin and alpha-melanocyte-stimulating hormone (alpha-MSH) in plasma of male rats. Quinelorane decreased plasma concentrations of prolactin but not of alpha-MSH, whereas, the D2 receptor antagonist raclopride increased plasma concentrations of both hormones. Quinelorane reversed the effects of raclopride on circulating levels of prolactin, but not alpha-MSH.
View Article and Find Full Text PDFJ Pharmacol Exp Ther
November 1989
Department of Pharmacology and Toxicology Michigan State University, East Lansing.
Effects of the dihydropyridine (DHP) calcium channel agonist Bay K 8644 on spontaneous and neurally evoked release of acetylcholine were measured using conventional intracellular microelectrode recording techniques at rat neuromuscular junctions of preparations that were transected to prevent contraction ("cut muscle preparation"). At concentrations of 0.65 to 2 microM Bay K 8644 caused significant increases in end-plate potential amplitude and mean quantal content in cut muscle preparations, but no effect in uncut preparations in which contractions were blocked by using d-tubocurarine (1 microM).
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