6 results match your criteria: "University of Kentucky Lexington 40536[Affiliation]"

Background: The comparative outcomes with immediate, staged in-hospital, and staged out-of-hospital complete revascularization for patients with ST-segment-elevation myocardial infarction and multivessel disease remain unclear.

Methods And Results: An electronic search of MEDLINE, SCOPUS, and Cochrane databases was performed through August 2023 for randomized trials evaluating immediate, staged in-hospital, and staged out-of-hospital complete revascularization for patients with ST-segment-elevation myocardial infarction and multivessel disease. The primary outcome was major adverse cardiac events (MACEs).

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Background And Objectives: Diabetes mellitus, a global health problem, is associated with metabolic complications such as hyperglycemia, hyperlipidemia, hypertension, cardiovascular diseases, and loss of vision. The present study evaluated the antidiabetic and antihyperlipidemic effects of ethanol extract of (L.) N.

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Integrin-associated CD151 is a suppressor of prostate cancer progression.

Am J Transl Res

April 2020

Department of Pharmacology and Nutritional Sciences, Department of Molecular and Cellular Biochemistry, and Markey Cancer Center, University of Kentucky Lexington 40536, KY, USA.

Owing to the complexity of interacting molecular networks on the cell surface, integrin-associated tetraspanin CD151 remains controversial regarding its clinical importance and functional impact in prostate cancer. The current study evaluated dynamics and clinical importance of CD151 expression and its function in prostate cancer by IHC analysis of two independent patient cohorts (n=80, 181), bioinformatic interrogation of the TCGA database, and evaluation of gene knockdown effect at the cellular level. Our data showed that aside from high mRNA expression, CD151 was primarily localized to intercellular junctions at the plasma membrane in normal prostate glands or benign tissues, regardless of nature of antibodies used.

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In the past, purification of choline acetyltransferase (ChAT, EC 2.3.1.

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Increasing evidence suggests heterogeneity in the molecular pathogenesis of cystic fibrosis (CF). Mutations such as deletion of phenylalanine at position 508 (delta F508) within the cystic fibrosis transmembrane conductance regulator (CFTR), for example, appear to cause disease by abrogating normal biosynthetic processing, a mechanism which results in retention and degradation of the mutant protein within the endoplasmic reticulum. Other mutations, such as the relatively common glycine-->aspartic acid replacement at CFTR position 551 (G551D) appear to be normally processed, and therefore must cause disease through some other mechanism.

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