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hyperhomocysteinemia/protease
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Hyperhomocysteinaemia and folate deficiency in human immunodeficiency virus-infected children.
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BACKGROUND
Our aim was the detection of possible deficiencies of folate and cobalamin by the measurement of plasma total homocysteine (tHcy) in 69 human immunodeficiency virus (HIV) -infected children on antiretroviral treatment. We studied the relationship of these vitamins and methionine with tHcy
Mitochondrial matrix metalloproteinase activation decreases myocyte contractility in hyperhomocysteinemia.
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Cardiomyocyte N-methyl-d-aspartate receptor-1 (NMDA-R1) activation induces mitochondrial dysfunction. Matrix metalloproteinase protease (MMP) induction is a negative regulator of mitochondrial function. Elevated levels of homocysteine [hyperhomocysteinemia (HHCY)] activate latent MMPs and causes
Influence of folate serum concentration on plasma homocysteine levels in HIV-positive patients exposed to protease inhibitors undergoing HAART.
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BACKGROUND
Homocysteinemia (Hcy) increase and risk factors in HIV-positive patients are not clear yet.
METHODS
HIV-positive patients on stable highly active antiretroviral therapy (HAART) regimens for at least 6 months were enrolled in this cross-sectional study. Among other factors, vitamin B12,
Mitochondrial MMP activation, dysfunction and arrhythmogenesis in hyperhomocysteinemia.
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Chronic volume/pressure overload-induced heart failure augments oxidative stress and activates matrix metalloproteinase which causes endocardial endothelial-myocyte (EM) uncoupling eventually leading to decline in myocardial systolic and diastolic function. The elevated levels of homocysteine (Hcy),
Portal vein thrombosis in a patient with HIV treated with a protease inhibitor-containing regimen.
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We report a case of an HIV seropositive female patient treated with a protease inhibitor-containing regimen who developed recurrent severe life-threathening episodes of haematemesis over time, caused by ruptured oesophageal varices as a consequence of a portal vein thrombosis. Coagulation tests
Increased ER stress as a mechanism of retinal neurovasculopathy in mice with severe hyperhomocysteinemia.
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Hyperhomocysteinemia is implicated in retinal neurovascular diseases including arterial occlusive disease, venous occlusive disease and pseudoexfoliation glaucoma. The mechanism for these diseases is not known. Here we used hyperhomocysteinemic mice lacking the gene encoding
Hyperhomocysteinemia induced by methionine dietary nutritional overload modulates acetylcholinesterase activity in the rat brain.
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Methionine is the only endogenous precursor of homocysteine, sulfur-containing amino acid and well known as risk factor for various brain disorders. Acetylcholinesterase is a serine protease that rapidly hydrolyzes neurotransmitter acetylcholine. It is widely distributed in different brain regions.
Hyperhomocysteinemia causes ER stress and impaired autophagy that is reversed by Vitamin B supplementation.
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Hyperhomocysteinemia (HHcy) is a well-known risk factor for stroke; however, its underlying molecular mechanism remains unclear. Using both mouse and cell culture models, we have provided evidence that impairment of autophagy has a central role in HHcy-induced cellular injury in the mouse brain. We
Relation of Bone Mineral Density with Homocysteine and Cathepsin K levels in Postmenopausal Women.
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UNASSIGNED
Homocysteine (HCY) interferes with collagen cross-linking in bones and stimulates osteoclast activity. The activated osteoclasts secrete cathepsin K (CathK), a cysteine protease, in eminent quantity during bone resorption. Hyperhomocysteinemia may effect bone mineral density (BMD) through
von Willebrand factor multimer composition is modified following oral methionine load in women with thrombosis, but not in healthy women.
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Hyperhomocysteinemia is associated with an increased risk of venous and arterial thrombosis, probably by inducing endothelial damage. Von Willebrand factor (VWF) is an endothelial marker protein. It is a plasma multimeric molecule that plays a thrombophilic role. Our purpose was to investigate VWF
Protein Z, a protein seeking a pathology.
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Protein Z (PZ) is a vitamin K-dependent factor identified in human plasma in 1984 characterized by an homology with other vitamin K-dependent factors (factor VII, IX, X, protein C). In contrast to these factors, PZ does not possess any enzymatic activity but is involved as a cofactor in the
Use of cystatin C determination in clinical diagnostics.
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This paper presents a current view of the possible clinical uses of cystatin C determination. Cystatin C is an inhibitor of cysteine proteases, and relatively stable in the systemic circulation it is comparatively easily determined. Although in clinical practice it is known primarily as a relatively
A Case Series of HIV-Seropositive Patients and Hypercoagulable State-Is It Difficult to Treat Even with Therapeutic Anticoagulation?
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Patients with human immunodeficiency virus (HIV) are at risk of developing thrombosis and are 8 to 10 times more likely to develop thrombosis than the general population. Moreover, if they have hypercoagulable state they can have severe thrombosis and life-threatening thrombotic events. The purpose
Homocysteine induces synthesis of a serine elastase in arterial smooth muscle cells from multi-organ donors.
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OBJECTIVE
In heart transplant recipients with diffuse coronary arteriopathy, we have previously demonstrated the prevalence of elevated homocysteinemia, also known as an independent risk factor for myocardial infarction and stroke. In hyperhomocysteinemic mini-pigs we also observed early detectable
μ-Calpain as a Novel Target for Impairment of Nitric Oxide-Mediated Vascular Relaxation in Diabetes: A Mini Review.
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Diabetes is one of the most prevalent metabolic disorders. In diabetes, incidence of coronary artery diseases and peripheral vascular diseases is increased 2- to 4-fold and 10-fold, respectively, compared to healthy individuals. In spite of extensive studies, the underlying mechanisms of endothelial
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