peptidase/infarction

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Collagen peptidase in serum of patients with myocardial infarction.

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Activity of collagen peptidase was measured in patients with myocardial infarction. Determinations were carried out 1, 3, 6, 9, 14 and 21 days after admission to the hospital. A decrease of activity was observed between the 6th-21st day of the disease. A low correlation with serum aminotransferases

Streptokinase promotes development of dipeptidyl peptidase IV (CD26) autoantibodies after fibrinolytic therapy in myocardial infarction patients.

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Dipeptidyl peptidase IV (DPP IV) (CD26) plays a critical role in the modulation and expression of autoimmune and inflammatory diseases. We recently reported that sera from patients with rheumatoid arthritis and systemic lupus erythematosus contained low levels of DPP IV and high titers of anti-DPP

Plasma dipeptidyl-peptidase-4 activity is associated with left ventricular systolic function in patients with ST-segment elevation myocardial infarction.

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Plasma dipeptidyl-peptidase-4 activity (DPP4a) is inversely associated with left ventricular function in patients with heart failure (HF) or diabetes. However, the association between DPP4a and left ventricular function in ST-segment elevation myocardial infarction (STEMI) patients has not been

Dipeptidyl peptidase-4 inhibitor improves cardiac function by attenuating adverse cardiac remodelling in rats with chronic myocardial infarction.

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UNASSIGNED What is the central question of this study? Although cardioprotective effects of dipeptidyl peptidase-4 (DPP-4) inhibitors have been demonstrated, their cardiac effects in chronic myocardial infarction (MI) are unclear. We determined the effects of a DPP-4 inhibitor on cardiac function

A novel mutation of the high-temperature requirement A serine peptidase 1 (HTRA1) gene in a Chinese family with cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL).

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OBJECTIVE Mutations in the high-temperature requirement A serine peptidase 1 (HTRA1) gene were studied in a Chinese family with cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL). METHODS Exons 1-9 of the HTRA1 gene were amplified and

Effects of dipeptidyl peptidase-4 inhibitor in insulin-resistant rats with myocardial infarction.

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Adverse cardiac remodeling after myocardial infarction (MI) leads to progressive heart failure. Obese-insulin resistance increases risks of MI and heart failure. Although dipeptidyl peptidase-4 (DPP4) inhibitor is known to exert cardioprotection, its effects on adverse remodeling after MI in

Myocardial infarction in type 2 diabetes using sodium-glucose cotransporter-2 inhibitors, dipeptidyl peptidase-4 inhibitors, or glucagon-like peptide-1 receptor agonists: proportional hazards analysis by deep neural network-based machine learning.

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Aims: Some hypoglycemic therapies were associated with lower risk of cardiovascular outcomes. We investigated the incidence of cardiovascular disease among patients with type 2 diabetes using antidiabetic drugs from three classes, which were sodium-glucose co-transporter-2 inhibitors

Dipeptidyl peptidase-4 inhibitors and GLP-1 reduce myocardial infarct size in a glucose-dependent manner.

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BACKGROUND The dipeptidyl peptidase-4 (DPP-4) inhibitors Sitagliptin and Vildagliptin lower blood glucose by augmenting endogenous levels of glucagon-like peptide-1 (GLP-1), an incretin which also confers cardioprotection. As such, we hypothesized that treatment with DPP-4 inhibitors are also

Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart.

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OBJECTIVE We hypothesized that dipeptidyl peptidase (DPP)-4 inhibitor (vildagliptin) reduces fatal arrhythmias, cardiac dysfunction and infarct size caused by ischaemia-reperfusion (I/R) injury via its attenuation of cardiac mitochondrial dysfunction. METHODS In total, 26 rats were randomized to

Dipeptidyl peptidase-4 inhibitors are associated with improved left ventricular diastolic function after acute myocardial infarction in diabetic patients.

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Dipeptidyl peptidase-4 (DPP4) is an integral membrane glycoprotein that modulates the pathological state of diabetes mellitus (DM), and DPP4 inhibitors are a new class of anti-type-2 DM drugs. Recent preclinical studies have associated DPP4 inhibition with improved myocardial systolic and diastolic

A dipeptidyl peptidase-4 (DPP-4) inhibitor, linagliptin, attenuates cardiac dysfunction after myocardial infarction independently of DPP-4.

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Dipeptidyl peptidase-4 (DPP-4) inhibitors not only improve impaired glucose tolerance in diabetes, but also have pleiotropic extra-pancreatic effects such as preconditioning effect for myocardial ischemia-reperfusion injury. Here, we investigated the anti-remodeling effects of linagliptin, a DPP-4

Polymorphisms in dipeptidyl peptidase IV gene are associated with the risk of myocardial infarction in patients with atherosclerosis.

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BACKGROUND Dipeptidyl peptidase IV (DPP-IV) is not only important in pancreatic β-cell regulation but also has proinflammatory actions that can contribute to atherosclerosis progression. Previously, we showed that DPP-IV is co-localized with CD31 (an endothelial cell marker) in the neovessels within

Genetic deletion or pharmacological inhibition of dipeptidyl peptidase-4 improves cardiovascular outcomes after myocardial infarction in mice.

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OBJECTIVE Glucagon-like peptide-1 (7-36)amide (GLP-1) is cleaved by dipeptidyl peptidase-4 (DPP-4) to GLP-1 (9-36)amide. We examined whether chemical inhibition or genetic elimination of DPP-4 activity affects cardiovascular function in normoglycemic and diabetic mice after experimental myocardial

Dipeptidyl peptidase-4 inhibition improves cardiac function in experimental myocardial infarction: Role of stromal cell-derived factor-1α.

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BACKGROUND In addition to degrading glucagon-like peptide-1 (GLP-1), dipeptidyl peptidase-4 (DPP-4) inactivates several chemokines, including stromal cell-derived factor-1α (SDF-1α), a pro-angiogenic and cardiomyocyte protective protein. We hypothesized that DPP-4 inhibition may confer benefit

[Clinical experiences in the determination of transaminases, aldolases, dehydrogenases, isomerases, peptidases and other modern serum enzyme reactions with special reference to liver diseases and heart infarct].

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