Histology and histopathology Vol.17, nº 4 (2002)
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- PublicationOpen AccessThe possible role of the gut neuroendocrine system in diabetes gastroenteropathy(Murcia : F. Hernández, 2002) El-Salhy, M.Gastrointestinal symptoms such as nausea and vomiting, heartburn, abdominal pain, diarrhoea, constipation and faecal incontinence are common in patients with diabetes. Diabetes gastroenteropathy is a clinically relevant problem. In addition to the increased morbidity it causes, it results in severely impaired metabolic control, which in turn increases the risk of hyper-/hypoglycaemia. Moreover, the poorly controlled blood glucose level increases the risk of secondary diabetes complications, namely, retinopathy, nephropathy, neuropathy and cardiovascular affection. Gastrointestinal symptoms may also cause malnutrition in patients with diabetes, which, together with the disturbed immune defence in diabetes, may cause intercurrent infections. Gastrointestinal symptoms in patients with diabetes are attributed to disturbed gastrointestinal motility. Gastrointestinal dysmotility in diabetes is believed to be caused by autonomic neuropathy and/or hyperglycaemia. The neuroendocrine system of the gut secretes peptides/amines that play an important role in regulating gastrointestinal motility. It is conceivable, therefore, to assume that a disturbance in this regulatory system may contribute to the pathogenesis of gastrointestinal complications in diabetes. The present review gives an updated overview of the abnormalities in the gastrointestinal neuroendocrine system in diabetes, speculates upon the possible role of these abnormalities in the pathogenesis of diabetes gastroenteropathy and, finally, predicts the possible clinical implications of these findings.
- PublicationOpen AccessModulation of pulmonary neuroendocrine cells in idiopathic interstitial pneumonia(Murcia : F. Hernández, 2002) Ito, T.; Ogura, T.; Ogawa, N.; Udaka, N.; Hayashi, H.; Inayama, Y.; Yazawa, T.; Kitamura, H.In order to reveal modulation of the number of pulmonary neuroendocrine cells (PNEC) in interstitial lung diseases and to clarify significance of cell proliferation activity in occurrence of PNEC, we counted airway PNEC of the patients of idiopathic interstitial pneumonia, secondary interstitial pneumonia and control lungs, and compared the number of PNEC with airway Ki-67 labeling. The lung tissue samples were obtained by video-assisted thoracoscopic surgery from 22 patients with usual interstitial pneumonia (UIP), 7 with nonspecific interstitial pneumonia (NSIP), 8 with chronic hypersensitivity pneumonia (CHP), 13 with collagen vascular disease (CVD), and were compared with agematched control lungs. The tissues were immunostained for chromogranin A and for Ki-67. Average incidence of bronchiolar PNEC in normal, UIP, NSIP, CHP, CVD lungs was 0.169%, 0.348%, 0.326%, 0.175% and 0.201%, respectively, and average Ki-67 labeling index in them was 0.241%, 1.186%, 1.605%, 1.058%, and 2.353%, respectively. And, in UIP lungs, PNEC incidence or Ki-67 labeling index was different according to pathological lesions. Thus, PNEC increase in the bronchiole of UIP, and the incidence of PNEC varies according to degree of activity of epithelial cell proliferation probably related to epithelial cell injury. Moreover, enhanced expression of human homolog of achaete-scute complex (hASH1) mRNA in UIP lungs suggests that hASH1 could play roles in the regulation of PNEC.
- PublicationOpen AccessFocal adhesion kinase: Protein interactions and cellular functions(Murcia : F. Hernández, 2002) Abbi, S.; Guan, J.L.Integrin-mediated cell adhesion to extracellular matrix (ECM) plays important roles in a variety of biological processes. Recent studies suggested that integrins mediate signal transduction across the plasma membrane via activating several intracellular signaling pathways. Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that has been shown to be a major mediator of integrin signal transduction pathways. Upon activation by integrins, FAK undergoes autophosphorylation as well as associations with several other intracellular signaling molecules. These interactions in the signaling pathways have been shown to regulation a variety of cellular functions such as cell spreading, migration, cell proliferation, apoptosis and cell survival. Recent progress in the understanding of FAK interactions with other proteins in the regulation of these cellular functions will be discussed in this review
- PublicationOpen AccessEnhanced accumulation of the isoprostane, 8-epi-PGF2a, in human aortic and pulmonary valves of patients with coronary heart disease(Murcia : F. Hernández, 2002) Mehrabi, M.R.; Serbecic, N.; Ekmekcioglu, C.; Tamaddon, F.; Wild, T.; Plesch, K.; Sinzinger, H.; Glogar, H.D.The aim of the present study was to investigate whether the isoprostane 8-epi-PGF2a differently accumulates in semilunar valves of patients suffering from coronary heart disease (CHD, n=19) as compared to valves from healthy heart donors (controls, n=6). Sections from isolated aortic and pulmonary valves were analyzed by semiquantitative immunohistochemistry. The 8-epi-PGF2a-content was determined by using a specific radioimmunoassay. The accumulation of 8-epi-PGF2a in both valves was higher in CHD-patients in comparison to controls (Aortic valves: 36.49±11.26 % vs. 15.78±3.04 %; pulmonary valves: 46.79±9.80 % vs. 14.99±3.57 %). The results from the radioimmunoassay revealed comparable findings in both groups (CHD vs. controls: 395.95±86.09 vs. 139.50±47.46 pg/mg protein in the aortic valves and 430.47±76.30 vs. 147.33±53.84 pg/mg protein in pulmonary valves). Pulmonary valves seem to be more susceptible to oxidative stress than aortic valves as evidenced by a higher accumulation of 8-epi-PGF2a in CHD patients. Considering the data presented in this study, we suggest that 8-epi-PGF2a is a valuable indicator of oxidative injury in human semilunar valve
- PublicationOpen AccessProtective role of the complement regulatory protein human CD-55 in cardiac xenograft: a descriptive study and a revision of the literature(Murcia : F. Hernández, 2002) Cappello, F.; Bellafiore, M.; Palma, A.; Marcianò, V.; Licata, L.; Cannino, G.; Gentile, C.; Zummo, G.; Farina, F.; Bucchieri, F.The limited and inadequate availability of organs from human donors has resulted in the utilisation of xenografts as an alternative tool. Nevertheless, hyperacute rejection (HAR) following xenograft determines the loss of the transplanted organ. The “primum movens” is the activation of the complement pathway mediated by the binding of natural xenogenic antibodies to the endothelium of the graft, followed by the lysis of the endothelial cells with subsequent oedema, thrombosis and necrosis of the transplanted organ. In this work we describe morphological and biomolecular observations of isolated human-decay accelerating factor (h-DAF, CD55) transgenic pig hearts, after perfusion for four hours with human blood. H-DAF is a membrane glycoprotein inhibiting the complement activation in humans. We describe considerably reduced damages in transgenic hearts, compared to controls. The cardiac function resulted preserved. Our data are in agreement with what was already shown by other groups using different experimental models. In conclusion, we encourage the use of new sources of transgenic animals, pointing out the importance of morphological analysis in evaluation of xenograft.