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Biomedical subjects

Y Gurbuz

Publications and source records attributed to Y Gurbuz.

4 recordsLinked to original sources

Age dependent changes in some immune system parameters and GFAP immunoreactivity in genetically absence epileptic rats.

The present study evaluated the contribution of some peripheral immunological parameters and GFAP immunoreactivity at different ontogenic stages of non convulsive absence epilepsy in WAG/Rij rats. For this, 2- and 6-month-old WAG/Rij rats, and the aged-matched control Wistar-albino rats were used. After collecting blood samples from all rats, the CD3 + (T cells), CD4 + (T helper), CD8 + (T cytotoxic), CD19 + (B cells) and CD25 + (IL-2 receptor, active T cell) cell ratios were determined by indirect immunofluorescence method and, serum IgG, IgA, IgM levels were evaluated by using rat radial immunodiffusion plates. After decapitation, brains were dissected and, GFAP staining was evaluated in the areas of caudate nucleus, thalamus, hippocampus, amygdala and cerebellum by immunohistochemistry. CD3 + cells and IgM levels increased with age in WAG/Rij rats. However, GFAP + astrocytes were decreased with age in caudate nucleus, thalamus, amygdala, and cerebellum of WAG/Rij rats. In the genetically absence epileptic rats, the humoral immunity was found to be affected more and activated by age. Additionally, astrocytes in thalamus and caudate nucleus that are the most important areas in the pathogenesis of absence epilepsy, were found to be decreased with age in WAG/Rij rats. From the results, it can be concluded that peripheral immunological parameters together with astrocytic activity may participate in the etiopathogenesis of absence epilepsy.

Age Factors↗

Stromal microcalcification in prostate.

Prostatic calcification is most commonly encountered as calculus or intraluminal calcifications within atypical small glandular proliferations. This study was undertaken to detect stromal microcalcifications in prostate tissue. All slides from 194 needle biopsies were retrospectively reviewed. Six cases (3.1%) had stromal microcalcifications constantly associated with mononuclear inflammatory infiltrate around the each focus. Association with prostatic glands was not seen in any of the microcalcification foci. Three cases had simultaneous adenocarcinoma and one had high-grade prostatic intraepithelial neoplasia, all of which were apart from the microcalcification foci. In conclusion, stromal microcalcification is a dystrophic, inflammation-mediated, benign process.

Adenocarcinoma↗

Helicobacter pylori status and cell proliferation activity in chronic antral gastritis.

BACKGROUND: Helicobacter pylori is known to cause antral gastritis and multifocal atrophic gastritis. In addition to its inflammatory effect, H. pylori has a direct effect on gastric mucosa. Increased epithelial proliferation, which may be an early biologic change in the development of gastric carcinoma, can be measured using silver stain for nuclear organizer regions (AgNOR). AIM: To detect the relation between H. pylori colonization and AgNOR index. METHODS: One hundred and twenty consecutive antral endoscopic biopsy specimens from patients with dyspepsia were examined for H. pylori colonization, polymorphonuclear infiltrate, mononuclear infiltrate, germinal center formation, mucus depletion and AgNOR index. RESULTS: AgNOR indices were not significantly related to grades of H. pylori colonization and chronic and active inflammation. The index increased significantly (p=0.03; ANOVA) with increasing mucin depletion. CONCLUSION: H. pylori colonization and presence of gastric antral inflammation are not related to cell proliferation activity; the latter is associated with mucin depletion.

Adult↗