Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inappropriate expression of major histocompatibility complex (MHC) molecules on epithelial and endothelial cells is a recognized marker of autoimmune disease. An autoimmune pathogenesis has been suspected in dilated cardiomyopathy (DCM). In the normal heart, MHC products are usually not detectable on myocytes using immunochemical techniques. MHC molecule expression has not, however, been assessed on cardiac endothelial cells. The aim of this study was to investigate possible autoimmune phenomena and MHC molecule expression in fresh endomyocardial biopsies from 29 patients with DCM. These were compared with those observed in surgical specimens from 63 patients with other acquired cardiac disease and from 22 with congenital heart disease (CHD) as normal controls. Conventional immunofluorescence (IFL) with monoclonal antibodies (MoAbs) to lymphocyte and macrophage markers and to MHC molecules was employed, and double IFL with antiserum to human Factor VIII was used for the identification of endothelial cells. Myocytes did not express MHC molecules in either DCM or controls. In normal hearts, Class II molecules were detected on endothelial and endocardial cells in only a few cases (3/22 and 2/22 respectively). By contrast, endothelial and endocardial cells inappropriately expressed Class II in a high proportion of DCM patients (28/29 and 22/29) but less frequently in other acquired cardiac diseases (19/63, P less than 0.001 and 11/63, P less than 0.001 respectively). In all the DCM biopsies examined there was a hierarchy of Class II subloci product expression (DR greater than DP greater than DQ); lymphocytic infiltration was a rare finding and macrophages/dendritic cells were not prominent. The finding of inappropriate MHC Class II molecule expression on cardiac endothelial and on endocardial cells suggests a possible pathogenic role for these cells in the initiation and/or perpetuation of DCM.
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PMID:Inappropriate major histocompatibility complex expression on cardiac tissue in dilated cardiomyopathy. Relevance for autoimmunity? 218 52

The effects of environmental hyperthermia (exposure to a hot, dry microclimate) on the human body were investigated with particular reference to certain clotting parameters in healthy subjects and patients at risk of thrombosis. The study covered 70 volunteers, 10 of them clinically healthy (6 males and 4 females) aged 37.7 +/- 9.7 and 60 patients at risk of thrombosis aged 18-60 and divided according to pathology as follows: 26 with ischaemic cardiopathy, 22 with metabolic disorders (12 diabetics, 8 with dyslipidaemia, 2 with hyperuricaemia) and 12 with obliterating arteriopathies of the lower extremities (Fontaine stage 2 and 3). The following standardised protocol was adopted: 2 hours exposure in a controlled climate chamber (40 degrees C, 40-50% humidity, standard air speed 4 m/min, barometric pressure 760 mmHg) for a total of 8 exposures (2 per week for 1 month). This approach was adopted in order to assess not only the effect of each single exposure but also the role of any adaptation to heat. Three blood samples were taken from each subject for each session: the first in basal conditions in a comfortable environment, the second at the end of the 2 hour exposure; the third 30 minutes after the end of the session. Simultaneously samples of arterial blood were taken for pH assays and a spleen echography was performed in basal conditions and at the end of the session for each subject. Each blood sample was tested for several parameters essentially attributable to blood concentration for a broader view of the biological effects of exposure to heart (Ht, blood protein, Nat, K+). The clotting factors under specific study were also assessed (platelet count and volume, beta-thromboglobulin, PF4, von Willebrand Factor VIII, thromboxane B2, fibronectin). Body weight, blood pressure and oral temperature were also measured in all subjects before and after each session. In all subjects both healthy and at risk of thrombosis oral temperature increased (1 +/- 0.4 degrees); on average blood pressure was already higher in basal conditions in the patient group; body weight fell by 900 +/- 120 G in both groups. Ht and blood protein increased significantly in both groups while electrolyte changes were insignificant and blood pH showed a tendency towards acidosis. Clotting parameters revealed a tendency towards thrombophilia in all subjects: platelet count and volume were already higher in the patient group in basal conditions and increased after exposure to hyperthermia. Beta-thromboglobulin, FP4, Factor VIII, thromboxane B2 and fibronectin all increased.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Influence of high environmental temperature on various parameters of blood coagulation in healthy subjects and in thrombosis risk patients]. 369 44

A precordial tumor of the pericardium was radiologically diagnosed as the cause of an untypical clinical picture of heart disease in a 41-year-old soldier. As the patient had an increased asbestos exposure due to his profession, he was admitted to operation under the tentative diagnosis of a pericardial mesothelioma and the question of an occupational disease (BK 4105). Microscopic and immunohistochemical findings are compatible with the diagnosis of a synovial sarcoma of the pericardium. The present immunohistochemical marker spectrum allowed a reliable differentiation between synovial sarcoma and pericardial mesothelioma, which is more frequent than synovial sarcoma. The epithelioid component was determined using the following antibodies: MNF 116, CK 19, CK 7, EMA and Ber EP-4 were positive while Factor VIII, Calretinin, S100, Vimentin, CEA, CD 31, bcl-2 and HBA-71 were negative. The sarcomatous component was determined with antibodies to Vimentin, bcl-2 and HBA-71 which were positive, and to MNF 116, CK 19, CK 7, Factor VIII, Calretinin, S100, EMA, CEA, Ber EP-4 and CD 31 which were negative. Synovial sarcomas of the pericardium in the lower anterior mediastinum or the myocardium are exceedingly rare. A causal relationship between tumor formation and an increased asbestos exposure--similar to the epidemiologically based experiences with pericardial mesothelioma--is not likely. Primary extrapericardial synovial sarcoma could be excluded.
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PMID:[Synovial sarcoma of the pericardium]. 988 9