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PubMed ID: 24589963 Purpose. Polycystic ovary syndrome (PCOS) is a common endocrine disorder which is associated with multiple risk factors for atherosclerosis. The aim of this study was to investigate the CIMT which is used in the early diagnosis of atherosclerosis and visceral obesity by ultrasound in newly diagnosed polycystic ovary syndrome with normal body mass index. Materials and Methods. A case-control study was conducted on 25 PCOS women (18-30 years of age) and 25 controls. BMI was matched volunteer controls. Carotid intima media thickness (CIMT) and fat distribution as visceral fat thickness (VFT) with subcutaneous fat thickness (SFT) were measured by ultrasound. After, visceral fat ratio (VFR) fat ratio (VFR) was calculated using VFT divided by SFT. The variables were compared using the ?2-test and Student's t test. Results. Comparing women with PCOS to the control group showed that CIMT was similar in both groups (p=0.84). The VFT in the PCOS group was higher than the control group (p=0.048). Whereas, the SFT was higher in the control group when compared to women with PCOS (p=0.007). The VFR was significantly higher in women with PCOS when compared to the control group (1.12 ± 0.38 vs. 0.81 ± 0.34; p=0.005). Conclusions. CIMT which used as early atherosclerosis predictors have not increased in newly diagnosed PCOS women. Body fat distribution was observed in visceral area in the newly diagnosed PCOS women. VFR follow up may provide benefit as a quantitative method for the assessment and follow up of visceral obesity in women with PCOS. © Società Editrice Universo (SEU).

Yellow rust resistance locus Yr10 located on chromosome 1B in Moro and originated from the Turkish line PI178383 was investigated in terms of polymorphism in seven winter type bread wheat cvs. ( Triticum aestivum ssp. Aestivum) Altay2000, izgi2001, Sonmez2001 (yellow rust resistant), Aytin98, ES14, Harmankaya99 ( yellow rust susceptible) and PI178383 as control. Exon 1 (1 - 833 bp) and Exon 2 ( 1989 - 3630 bp) parts of Yr10 were amplified with three primers. Amplification was not observed with E2A primers in Harmankaya99, izgi2001 and Sonmez2001 cvs, while amplification products were observable at all tested varieties with the other primers. PCR results showed that E2A reverse primer is not able to anneal to the three varieties mentioned above. Sequence analysis and bioinformatics analysis proved that there has been single nucleotide changes especially in the second exon. The most similar sequences to the first exon of Harmankaya99, izgi01 and Sonmez2001 are AF509535 (Aegilops tauschii NBS-LRR-like gene), AF509534 (A. tauschii NBS-LRR-like gene sequence) and AF509534, respectively. These results could be helpful in revealing divergence between resistant and susceptible varieties.

WOS: 000273144300011 Background. Drug induced thrombocytopenia is mostly related with nonsteroidal anti-inflammatory drugs (NSAID), anticonvulsants, sulfonamides, diuretics, cinchona alkaloid derivatives, penicillamine and gold salts. Oral sulfonylureas such as glibenclamide, chlorpropamide and glimepiride are known to induce thrombocytopenia. Case report. We report a 42 year old female admitted to emergency department with a complaint of hematochesia. She has been using oral gliclazide for three years. Laboratory results revealed bicytopenia: haemoglobin=8.9 g/dL (N=12.3-15.3), white blood count (WBC)=12100/mu L (N=4400-11300). platelet count=4000/mu L (N=150000-450000). All examinations to etiology of thrombocytopenia were negative including, autoimmune, infectious (viral-bacterial) and haematological diseases. Colonoscopic examination showed 50% construction of the lumen ill the first 15 cm segment of the colon by all ulcerovegetant mass. Pathological examination was reported as adenocarcinoma. Thrombocyte levels increased oil the 4(th) day after stopping gliclazid treatment. Conclusions. It is the first case of gliclazid induced thrombocytopenia in literature. So we recommended that platelet count should be regularly checked ill all patients receiving sulfontylurea drugs including gliclazid.