The aim of this study was to assess retrospectively the hemostatic efficacy and safety of the topical use of Ankaferd Blood Stopper (ABS) in the setting of dental surgery. Following the approval from of the Local Research Ethics Committee ABS as a hemostatic agent in Dentistry, ABS was topically applied by homogeneously spraying to the 25 patients during dental interventions. Based on this retrospective evaluation; Tissue healing was evaluated at the 48th hour. The patients received 1 to 5 mL of ABS; the median dose was 2 mL. Bleeding stopped in median 1.8 seconds (1 to 3 seconds) in the first ABS application in 20 patients. Five patients needed a second dose of ABS; four of them were given 5 mL ABS totally. No patient had wound infection and the healing process appeared to be normal. ABS is useful for the local hemostasis and wound healing in periodontal surgeries.

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In recent years, the role of free radical damage consequent to oxidative stress is widely discussed in diabetic complications. In this aspect, the protection of cell integrity by trace elements is a topic to be investigated. Vanadium is a trace element believed to be important for normal cell function and development. The aim of the present study was to investigate the effect of vanadyl sulfate supplementation on the antioxidant system in the muscle tissue of diabetic rats. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg body weight) to male Swiss albino rats. The rats were randomly divided into 4 groups: Group I, control; Group II, vanadyl sulfate control; Group III, STZ-diabetic untreated; Group IV, STZ-diabetic treated with vanadyl sulfate. Vanadyl sulfate (100 mg/kg) was given daily by gavage for 60 days. At the last day of the experiment, rats were killed, muscle tissues were taken, homogenized in cold saline to make a 10% (w/v) homogenate. Body weights and blood glucose levels were estimated at 0, 30 and 60th days. Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), as well as carbonic anhydrase (CA), myeloperoxidase (MPO) activities and protein carbonyl content (PCC) were determined in muscle tissue. Vanadyl sulfate administration improved the loss in body weight due to STZ-induced diabetes and decreased the rise in blood glucose levels. It was shown that vanadium supplementation to diabetic rats significantly decrease serum antioxidant enzyme levels, which were significantly raised by diabetes in muscle tissue showing that this trace element could be used as preventive for diabetic complications.

We investigated whether PPAR-γ2 gene polymorphisms are associated with serum lipids and the occurrence of coronary heart disease (CHD) prospectively characterised for the presence or absence of Type 2 diabetes in a Turkish population. Our study included 202 patients with CHD (102 with diabetes, 100 without diabetes) and 105 controls. PPARγ genotypes were determined by PCR-RFLP technique. The PPARγ-C161T CC homozygote genotype was associated with significantly increased CHD risk when compared with the T allele carriers (CT+TT) in CHD patients with diabetes (OR:1.951, 95%CI: 1.115-3.415, P = 0.019), whereas PPARγ-P12A polymorphism was not associated with CHD risk (P > 0.05). Serum HDL-C levels were significantly lower in controls with the P12A heterozygote when compared with the P12P homozygote (P = 0.002). In the CHD patients with diabetes, CT heterozygote genotype showed higher serum triglyceride than the CC homozygote genotype (CT:2.42 ± 1.89 vs. CC:1.61 ± 0.21, P = 0.015). Our findings shows the association of these two polymorphisms with serum triglyceride levels, which was increased in the order of P12P-CC < P12P-CT < P12A-CC < P12A-CT in the CHD patients with diabetes. Furthermore, we observed that the increasing effects of the CT genotype on serum triglyceride levels could be modified by PPARγ P12A polymorphism (P12A-CT:2.30 ± 1.75 vs. P12P-CC:1.79 ± 1.14, P = 0.028). We suggested that homozygote CC genotype of the PPARγ C161T polymorphism might be associated with an increased CHD risk especially in patients with diabetes. We observed that the C161T CT heterozygote genotype shows an unfavorable effect on serum lipid profile in CHD patients with diabetes and this effect was weaken with the presence of P12P homozygote genotype.

It has been suggested that the estrogen receptor alpha (ERα) and vitamin D receptor (VDR) genes as possibly implicated in reduced bone mineral density (BMD) in osteoporosis. The present study investigated the relation of ERα PvuII/XbaI polymorphisms and VDR FokI/TaqI polymorphisms with BMD in Turkish postmenopausal women. Eighty-one osteoporotic and 122 osteopenic postmenopausal women were recruited. For detection of the polymorphisms, polymerase chain reaction-restriction fragment lenght polymorphism techniques have been used. BMD was measured at the lumbar spine and hip by dual-energy X-ray absorptiometry. Distributions of ERα (PvuII dbSNP: rs2234693, XbaI dbSNP: rs9340799) and VDR genotypes (FokI dbSNP rs10735810, TaqI dbSNP: rs731236) were similar in study population. Although overall prevalence of osteoporosis had no association with these genotypes, the prevalence of decreased femoral neck BMD values were higher in the subjects with ERα PvuII "PP" and ERα XbaI "XX" genotypes than in those with "Pp/pp" genotypes and "xx" genotype, respectively (P < 0.05). Furthermore, subjects with VDR FokI "FF" genotype had lower BMD values of femoral neck and total hip compared to those with "Ff" genotype (P < 0.05). In the logistic regression analysis, we confirmed the presence of relationships between the VDR FokI "FF" genotypes, BMI ≤ 27.5, age ≥ 55 and the increased risk of femoral neck BMD below 0.8 value in postmenopausal women. The present data suggests that the ERα PvuII/XbaI and VDR FokI polymorphisms may contribute to the determination of bone mineral density in Turkish postmenopausal women.

Objective: The aim was to investigate the factors affecting the quitting smoking success of the patients followed in the smoking cessation outpatient clinic and the rate of quitting smoking in this clinic. Methods:From the 320 cases who applied to the smoking cessation clinic, 241 cases with a 12 month follow-up completed between June 2011 and June 2012 were included in the study. Routine biochemical and hematological tests, respiratory function test, electrocardiography, and posteroanterior chest radiography were requested from the cases. Moreover, the cases were requested to complete the Fagerstrom nicotine dependence test, anxiety and depression assessment scale and the outpatient clinic's form, including demographic data. The medicines taken and the duration of use were recorded. The quitting smoking success of the patients and the factors affecting this success were evaluated.Results: Generally, at the end of the first year, the rate of quitting smoking was 37.3%. The demographic characteristics of the groups who quit smoking and who failed to quit smoking were similar. Fagerstrom dependence degree (p<0.001) and the number of cigarettes smoked at the workplace (p<0.001) were higher. The individuals included in the group who quit smoking put on more weight. Overall, 27.4% of the patients received behavioural education (BE), 56% of them received behavioural education and nicotine replacement therapy (BE+NRT), 9.5% of them received BE+Bupropion, 2.5% of them received BE+Varenicline, and 4.6% of them received BE+Bupropion+NRT treatments. The rates of quitting smoking were 15.2%, 43.7%, 52.2%, 66.7% and 45.5%, respectively. With the administration of pharmacological treatment for a sufficient time, the rates of quitting smoking rose meaningfully (p<0.001). Conclusion:Quitting smoking is a difficult process that has to be evaluated individually for every case. In this process, the administration of sufficient behavioural education and pharmacological treatment with sufficient time for appropriate individuals will increase the success rate.

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