Does sucralfate affect the normal gastric mucosa? Histologic, ultrastructural, and functional assessment in the rat

Although the action of sucralfate on ulcerated mucosa has been demonstrated, its effect on the histology, ultrastructure, and function of normal gastric mucosa is unknown. We investigated the effect of acute administration of sucralfate on the gastric mucosal history, ultrastructure, mucosal potential difference, and luminal release of prostaglandin E2. At 15 min, 1 h, and 3 h after intragastric instillation of sucralfate, whitish incrustations of the drug were firmly adhering to the glandular mucosa. Mucosal histology after sucralfate administration demonstrated the following: disruption and exfoliation of some of the surface epithelial cells, mucosal hyperemia, prominent release of mucus from the surface epithelial cells, and edema of lamina propria and submucosa. These changes were most prominent in the areas where sucralfate was in contact with the mucosal surface. Scanning and transmission electron microscopy confirmed the above changes. Sucralfate produced a drop in gastric mucosal potential difference and a significant increase in luminal release of prostaglandin E2. Sucralfate produces distinct morphologic and functional changes in the normal gastric mucosa, which may account for its preventive and therapeutic efficacy.     

Molecular mechanism of troponin-C function

Conclusions There is now a large body of evidence in support of the view that Ca²⁺ binding to the low affinity sites of TnC induces a movement of helices B and C away from helices A and D, thus opening a hydrophobic cavity, the site of interaction with TnI. Another site of similar structure is formed by the helical segments in the C-terminal domain. Both sites appear to interact with the inhibitory segment of TnI. Whereas the interactions at both sites are necessary for the full regulatory activity of TnC, the interaction at the C-terminal domain stabilizes the complex and that involving the N-terminal domain is directly linked to the release of inhibition. In the absence of Ca²⁺ the inhibitory region of TnI would preferentially bind to actin and on Ca²⁺ binding to sites I and II it would switch to the site in the N-terminal domain of TnC. Detachment of TnI from actin gives rise to further events in thin filament regulation.     

Detection of citrate synthase-reacting autoantibodies after heart transplantation: an epitope mapping study

Abstract Autoimmune mechanisms play an important role in the pathogenesis of allograft vasculopathy following heart transplantation, but the autoantigens involved have been only sparsely studied. Citrate synthase (CS) enzyme is a conserved molecule, and, as an important mitochondrial autoantigen, it is protected by the "immunological homunculus". Tissue destruction and alteration of the immune regulatory mechanisms can induce pathological immune response against CS in other autoimmune diseases. In our present study we aimed to detect CS-specific autoantibodies in heart transplant patients, therefore, prospective, randomised clinical tests were conducted on 33 heart transplant patients and compared with 130 healthy blood donors. The level and isotype of CS antibodies were detected by simple binding indirect enzyme-linked immunosorbent assay (ELISA). The epitope specificities of the autoantibodies were measured on synthetic overlapping peptide sequences of CS enzyme by an indirect multi-pin ELISA method. Mainly IgM isotype CS autoantibodies were found in healthy controls, while IgG was found at higher levels and frequency (four-times higher) in heart transplant patients. Autoantibodies of IgG isotype recognise different epitopes than do autoantibodies of IgM isotype, even within the same group and individual. New epitope-specific IgG and IgM isotype autoantibodies appeared in heart transplant patients when compared with the controls. Our findings suggest a possible role of CS-specific autoantibodies in the pathomechanism of allograft vasculopathy.     

The interleukins

Immune response is regulated by a number of soluble mediators. Interleukins belong to these mediators, as a well defined group of regulatory molecules. Interleukins are necessary for the differentiation and activation a T and B lymphocytes and other cells. They play an important role in inflammation: they cause fever, leukocytosis etc. Some interleukins are being used as therapeutic agents.     

Malignant histiocytosis associated with chronic hepatitis

A case of malignant histiocytosis successfully treated with splenectomy and chemotherapy is presented. 33 months after surgery the patient's overall condition is satisfactory. The result is attributed to the fact, that in the time of the operation there was no systemic proliferation. The concomitantly present chronic viral hepatitis was worsened by the treatment.