Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method of apheresis of plasma euglobulin fraction, cryoglobulins and Willebrand factor was developed. In one session of plasmapheresis 1500-1700 ml of patient's plasma were removed, fractionated and returned. The method was used in 2 patients with immune complex vasculitides. In one of them the disease developed against a background of chronic active hepatitis, in the other patient it manifested itself in cryoglobulin- and cryofibrinogenemia. Clinical improvement was noted in both cases: the absence of myalgia, arthralgia, hemorrhagic eruption, and ulcerative-necrotic skin changes. The normalization of increased ristomycin-cofactor activity of Willebrand factor and CIC levels was noted in one case. A decrease in the content of plasma cryoglobulins, cryofibrinogen, and urine protein concentration (from 1.5 up to 0.03%) was noted in the other case. A possibility of the use of the method in other pathological conditions (DIC-syndrome, unstable angina, atherosclerotic angiopathy) accompanied by endothelial damage, was discussed. Willebrand factor multimers form complexes with low density lipoproteins therefore the removal of these complexes may be useful in the treatment of hypercholesteremia and atherosclerosis.
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PMID:[Apheresis of euglobulins, cryoglobulins and the von Willebrand factor in vasculitis]. 295 14

The clinical and pathologic findings are reported in seven consecutive patients with progressive and fatal pulmonary hypertension which was not explained by predisposing cardiac or pulmonary diseases. Pulmonary arterial lesions consisted of atherosclerosis of the elastic pulmonary arteries, and medial hypertrophy and concentric laminar fibrosis of the muscular pulmonary arteries in seven patients, plexiform lesions in six patients and necrotizing vasculitis in one patient. Pulmonary emboli were not identified. Five patients had manifestations of autoimmune disease, including laboratory abnormalities (positive antinuclear antibody, positive latex agglutination for rheumatoid factor, hypergammaglobulinemia or antimitochondrial antibody) in four, necrotizing vasculitis in one, Raynaud's phenomenon in two and clinical evidence of multisystem collagen vascular disease in two. Five patients had liver disease which developed prior to or concomitant with the onset of pulmonary hypertension. At autopsy, one patient had prominent periportal fibrosis and four had macronodular (postnecrotic) cirrhosis (active in three and inactive in one). Four of these five patients with liver disease and pulmonary hypertension had evidence of autoimmune phenomena. The findings in the seven patients suggest an association between autoimmune disease, plexogenic pulmonary hypertension and liver disease of the chronic active hepatitis-postnecrotic cirrhosis type.
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PMID:Severe pulmonary hypertension associated with macronodular (postnecrotic) cirrhosis and autoimmune phenomena. 742 41

The Tibetan herbal remedy PADMA 28 revealed promising results to support treatment of atherosclerosis, Charot syndrome (intermittent claudication), chronic active hepatitis and infection of the respiratory tract. The remedy was confirmed to be closely linked with anti- and pro-oxidative properties in vitro. In this study, apoptogenic and survival effects of PADMA 28 were investigated in the T cell-derived lymphocytic leukaemia cell line CEM-C7H2. PADMA 28 led to a concentration-dependent inhibition of cell proliferation accompanied by the accumulation of CEM-C7H2 cells in subG1 phase, fragmentation of poly (ADP-ribose) polymerase (PARP) and nuclear body formation. Treatment with PADMA 28 rescued to some extent cells over-expressing Bcl-2 from apoptosis. This finding suggests that the mechanism of action of PADMA 28 may be via interference with Bcl-2 triggered survival pathways.
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PMID:Apoptosis induced by the Tibetan herbal remedy PADMA 28 in the T cell-derived lymphocytic leukaemia cell line CEM-C7H2. 1613 18