Biomedical subjects

T Cagatay

Publications and source records attributed to T Cagatay.

4 recordsLinked to original sources

PubMed2004

Hashimoto thyroiditis and obstructive sleep apnea syndrome: is there any relation between them?

Hashimoto thyroiditis (HT), which is an autoimmune disease of thyroid gland, has been declared to present with concomitant several systemic diseases. In this study, the coexistence of the Hashimoto disease with the sleep apnea syndrome has been examined. Seven female patients (33-66 year of age) with Hashimoto thyroiditis were evaluated for sleep apnea syndrome. The diagnosis of Hashimoto disease was based on the high titers of anti-thyroid antibodies and histological findings. None of the patients had any complaints of sleep disturbances. Seven healthy subjects with similar age and sex characteristics were taken as the control group. All the patients and the control subjects were undertaken a full polysomnography (PSG). Five patients with HT showed the characteristics of obstructive sleep apnea syndrome (one severe, one moderate and three mild OSAS), whereas no sleep breathing disturbance was found in the control group. These findings suggest that sleep related breathing problems may develop in the patients with autoimmune thyroiditis even if they are euthyroid.

Adult↗

PubMed2003

Sarcoidosis after use of interferon for chronic hepatitis C: report of a case and review of the literature.

Although interferon has not been classified in the pathogenesis of sarcoidosis, it may rarely lead to this disease during treatment of chronic hepatitis C. The case of a 36-year-old woman with chronic hepatitis C who developed sarcoidosis within 10 weeks of treatment with recombinant interferon-alpha2a and ribavirin is described and all seven similar cases published in English from 1989 to 2001 are discussed.

Adult↗

PubMed2000

P53 but not p16INK4a induces growth arrest in retinoblastoma-deficient hepatocellular carcinoma cells.

BACKGROUND/AIM: Both p16INK4a and p53 proteins are negative regulators of the cell cycle. In human hepatocellular carcinomas (HCC), the loss of function of p53, retinoblastoma (pRb) and pl6INK4a genes by different mechanisms has been largely documented, but their hepatocellular effects are poorly known. We compared the growth-inhibitory effects of p16INK4a and p53 proteins in Hep3B cell line-derived clones. METHODS: Cells were transfected with inducible p16INK4a and p53 expression vectors, and stable clones were analyzed for transgene expression by Western blotting and immunoperoxidase staining. Effects on cell growth were analyzed by in vitro growth assay, thymidine incorporation and flow cytometry. Biochemical effects of p53 were tested by Northern blotting of p21Cip1 transcripts and by Western blotting of p21Cip1, mdm-2, bax, cyclin-dependent kinase 2 and cyclin E proteins. The pRb protein was studied by Western blotting and immunoprecipitation assays. RESULTS: The induction of p16INK4a protein expression did not affect in vitro growth of cells. In contrast, p53 protein in its wild-type conformation provoked a growth arrest accompanied by transactivation of p21Cip1 gene and accumulation of p21Cip1, bax and mdm-2 proteins. p53-induced growth arrest was due to a cell cycle arrest at the G1/S transition, probably mediated by p21Cip1 protein, which inhibits cyclin-dependent kinase 2/cyclin E complexes. CONCLUSIONS: The lack of detectable pRb protein and resistance of cells to p16TNK4a strongly suggest that p53 is able to arrest the growth of HCC cells by a mechanism independent of "p53-retinoblastoma pathway". These findings are applicable to HCC with abberrations of both p53 and pRb genes, and may not represent the universal effects of p53 in hepatic cells.

Carcinoma, Hepatocellular↗

PubMedDate not supplied

Right heart haemodynamic values and respiratory function test parameters in chronic smokers.

During coronary angiography in 24 chronic smokers with coronary heart disease, cardiac function measurements were taken and correlated with respiratory function tests. Fourteen patients had evidence of chronic obstructive pulmonary disease. Cardiac output had a direct correlation with vital capacity, forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), and velocity at 25% of FVC (V(max)25). Pulmonary artery resistance was inversely correlated with FEV1/FVC, while pulmonary artery oxygen saturation weakly correlated with FEV1 and V(max)25. The pulmonary artery pressure had a weak correlation with the pulmonary artery resistance and an intermediate correlation with the right atrium and the right ventricular pressures. Early diagnosis and therapy of chronic obstructive pulmonary disease in smokers may be possible without using invasive methods.

Aged↗