Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Corticosteroids and vitamin D3 analogues inhibit proliferation, enhance normal keratinisation and interfere with cutaneous inflammation in in vitro systems. Both treatments are effective in psoriasis, although several reports suggest that vitamin D3 is less effective in reducing the inflammatory changes compared to its potent effect on keratinocyte growth and differentiation. The aim of the present study was to compare and contrast the effects of the vitamin D3 analogue calcipotriol, clobetasol-17-propionate and a placebo on immunohistochemical markers for epidermal growth, keratinisation and inflammation induced by a standardised single challenge with ultraviolet B (UVB) radiation in normal human skin. Clobetasol proved to inhibit UVB-induced proliferation of epidermal cells, tenascin induction, keratin 16 induction and the accumulation of T lymphocytes and CD1a-positive cells. Epidermal thinning due to clobetasol was also observed. No effect of clobetasol was shown on the enhanced terminal differentiation following UVB challenge. In contrast, calcipotriol reduced the member of transglutaminase-positive cells following UVB challenge but increased the thickness of the epidermis without a significant effect on other markers for keratinisation, epidermal proliferation and inflammation. The present study reconfirms the potent effect of topical corticosteroids on various aspects of UVB-challenged skin. In contrast, calcipotriol interfered especially with one differentiation pathway (transglutaminase) without modulation of other UVB-induced changes.
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PMID:Effects of calcipotriol and clobetasol-17-propionate on UVB-irradiated human skin: an immunohistochemical study. 905 56

Dilated cardiomyopathy (DCM) is a disorder of unknown aetiology characterized by the left ventricular cavity enlargement and wall thinning associated with reduced left ventricular wall motion. DCM in chronic alcoholics is supposed to be caused by alcohol induced myocardial damage (alcoholic cardiomyopathy). Nevertheless, cardiotropic viruses, such as enteroviruses have long been suspected as causative agents for at least some forms of DCM. In the present study, 13 cases of DCM in chronic alcoholics were investigated with qualification and quantification of infiltrating leucocytes using immunohistological antibodies against leucocyte common antigen (LCA), T-lymphocytes (CD3) and macrophages (CD68). In addition, the expression of tenascin, playing a role in the initiation of fibrotic changes, was examined. All antigens were known to be possibly enhanced in cases of chronic myocarditis. Using these immunohistological techniques, 2 out of 13 cases had evidence for chronic inflammatory myocardial alterations in the sense of lymphocytic infiltrates (>2.0 CD3 T-lymphocytes/visual field at 400 x (HPF); >7 CD3 T-lymphocytes per mm(2)). These cases were diagnosed as having inflammatory cardiomyopathy. The other cases without myocardial inflammation were diagnosed as idiopathic/alcoholic DCM.
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PMID:Alcoholic cardiomyopathy versus chronic myocarditis--immunohistological investigations with LCA, CD3, CD68 and tenascin. 1195 34

After onset of myocardial infarction (MI), the left ventricle (LV) undergoes a continuum of molecular, cellular, and extracellular responses that result in LV wall thinning, dilatation, and dysfunction. These dynamic changes in LV shape, size, and function are termed cardiac remodeling. If the cardiac healing after MI does not proceed properly, it could lead to cardiac rupture or maladaptive cardiac remodeling, such as further LV dilatation and dysfunction, and ultimately death. Although the precise molecular mechanisms in this cardiac healing process have not been fully elucidated, this process is strictly coordinated by the interaction of cells with their surrounding extracellular matrix (ECM) proteins. The components of ECM include basic structural proteins such as collagen, elastin and specialized proteins such as fibronectin, proteoglycans and matricellular proteins. Matricellular proteins are a class of non-structural and secreted proteins that probably exert regulatory functions through direct binding to cell surface receptors, other matrix proteins, and soluble extracellular factors such as growth factors and cytokines. This small group of proteins, which includes osteopontin, thrombospondin-1/2, tenascin, periostin, and secreted protein, acidic and rich in cysteine, shows a low level of expression in normal adult tissue, but is markedly upregulated during wound healing and tissue remodeling, including MI. In this review, we focus on the regulatory functions of matricellular proteins during cardiac tissue healing and remodeling after MI.
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PMID:Role of matricellular proteins in cardiac tissue remodeling after myocardial infarction. 2154 Sep 92