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The Gastroenterology Research Laboratory at New York Medical College, New York City, NY, directed by Prof. Dr. George B. Jerzy Glass and after his retirement by Prof. Dr. Bronislaw L. Slomiany and Prof. Dr. Amalia Slomiany served as a lunching pad for successful careers in exploration of mucus for Dr. Andrzej Gindzienski and Dr. Krzysztof Zwierz and Janusz Badurski at the Medical School in Bialystok, Poland as well as Dr. Jerzy Sarosiek at Gastroenterology Research Laboratory, University of Virginia Health Sciences Center, Charlottesville, VA and currently, Gastroenterology Research Laboratory, Kansas University Medical Center, Kansas City, KS, USA. The dynamic and insightful research endeavors implemented at the Medical School of Bialystok revealed new information regarding enzymatic pathways of mucin synthesis especially its carbohydrate components such as hexosamines. These discoveries become instrumental in our understanding of the alimentary tract mucin synthesis and function in health and disease. Similarly innovative mucus research conducted across the Atlantic Ocean uncovered the novelty of mucin elaborated within the esophageal submucosal mucous glands in humans by demonstration that its chemical characteristics are different both from human salivary and gastric mucins. In addition, a novel method for the measurement of the thickness of the gastric mucus layer ex vivo in humans has also been developed. These pioneering works are continued at both mucus exploration centers attracting younger generation of investigators enticed by the mystery of the structure and function of the mucus barrier and its leading role in mucosal protection against injury as well as immediate and unequivocal contribution to mucosal repair and reconstitution process.
The aim of the study was to establish to what degree the 24-week exposure of a rat to 5 and 50 mg Cd/dm³ affects the proliferating activity of cells with PCNA and Ki-67 nuclear immunoreactivity in the submandibular gland cells. The control animals received only redistilled water to drink. The group I rats were given 5 mg Cd/dm³, while the group II animals were given 50 mg Cd/dm³. The highest concentration of cadmium was observed in group II, with a concomitant increase in the number of PCNA-positive cells. In group I, cadmium concentration was significantly less compared to group II, and there were fewer PCNA-positive cells. The reaction for Ki-67 in both experimental groups was negative.
Cholesteatoma is a destructive disease characterized by the progressive expansion of keratinizing squamous epithelium in the middle ear and mastoid, and chronic inflammatory reaction of the subepithelial connective tissue. N-Acetyl-β-d-hexosaminidase (HEX) catalyzes the release of terminal non-reducing N-acetyl-d-hexosamine residues acting on glucosides and galactosides in glycoproteins, GM2-gangliosides and glycosaminoglycans (GAGs). In this study the activities of HEX were measured in cholesteatoma tissue and in normal skin to demonstrate a possible role of HEX in bone resorption in the area adjacent to cholesteatoma. Cholesteatomas (n = 21) and normal adult retroauricular skin (controls, n = 21), were collected from patients during surgery due to chronic otitis media. In 20 of 21 specimens a significantly higher activity of HEX was observed in cholesteatoma tissue compared with that in normal skin. Mean release of HEX from the activated cells was 68.55 ± 30.77 nkat/g wet tissue in cholesteatoma and 31.79 ± 10.02 nkat/g wet tissue in skin specimens. It may explain the process of bone resorption in the area adjacent to cholesteatoma, i.e. ossicles or temporal bone. This study suggests that drugs inhibiting HEX activity, such as iminocyclitols, may be useful in cholesteatoma treatment.
Biological significance, structure and posttranslational processing of N-acetyl-β-hexosaminidase isoenzymes are described. Clinical application of N-acetyl-β-hexosaminidase is also reviewed.
This paper aims to assess the relationship between the urinary activity of N-acetyl-β-D-glucosaminidase (NAG) and its isoenzyme B (NAG-B) and cadmium (Cd) concentration in the urine as well as to evaluate which of these lysosomal enzymes may be a more useful biomarker for the monitoring of Cd-induced tubular damage. For this purpose we have used an experimental model in rats chronically exposed to Cd in which we noted damage to the proximal tubules, including lysosomes. In rats intoxicated with 5 mg Cd/dm3, the urinary activities of NAG and NAG-B increased after 12 weeks of treatment, while at 50 mg Cd/dm3 - activities increased already after the 1st week. The urinary Cd excretion in Cd-exposed rats, but not in the non-exposed ones, positively correlated with the activities of NAG and NAG-B. A positive correlation which was observed between NAG and NAG-B activities was stronger in Cd-exposed animals than in those not exposed. The results of the present and our previous histopathological and histoenzymatic studies, confirm the usefulness of total NAG and NAG-B as sensitive markers of proximal tubular injury for the monitoring of chronic exposure to Cd. Taking into account the strong correlation between the total NAG and its isoenzyme B, similar correlation coefficients between their activities and Cd concentration in urine and simplicity of total NAG determination compared to that of NAG-B, one can conclude that the determination of total NAG is suitable for the monitoring of exposure to Cd. As the urinary activity of total NAG is a sum of activities of several isoenzymes, which may be influenced by various factors, and the intralysosomal localization of NAG-B, we hypothesize that NAG-B should be recommended as a sensitive and useful marker for routine monitoring of chronic exposure to Cd.
Human glycophorin, the major sialoglycoprotein of erythrocyte membranes, was isolated from erythrocytes of healthy individuals and four patients with CDG syndrome. Sugar analysis revealed lower carbohydrate content in three out of four CDG-glycophorin samples. In order to characterize closer the glycosylation differences between glycophorin samples in health and disease, reaction with four biotinylated lectins was performed, using ELISA procedure on polystyrene microplates. Results obtained so far strongly suggest that both N- and O-glycans of glycophorin are affected in CDG syndrome.
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