Fractalkine receptor polymorphism may not be associated with the development and clinical course of ulcerative colitis

Fractalkine (CX3C), a chemokine expressed by epithelial cells within normal and inflamed colorectal mucosa, induces leukocyte adhesion and migration via fractalkine receptor. The aim of this study was to investigate two single nucleotide polymorphisms of the fractalkine receptor gene as a risk factor both for the development and clinical findings of ulcerative colitis. In this study, si patients with ulcerative colitis (UC) and 8o controls were recruited. Genotypes of fractalkine receptorc.743G>A (V249I) and c.839C>T (T280M) polymorphisms were identified by restriction fragment length polymorphism analyses after polymerase chain reaction.Genotype distribution and allele frequencies of V249I and T280M were not statistically significantly different between UC and control groups (p>0.05). No statistically significant relationship was found between fractalkine receptor polymorphisms and clinical findings of UC. We observed no significant difference in fractalldne receptor polymorphism between patients and control group and no genotype-phenotype relation. Therefore, we concluded that fractalkine receptor polymorphisms may not contribute to the molecular pathogenesis of UC

Frequency of adiponectin gene polymorphisms in polycystic ovary syndrome and the association with serum adiponectin, androgen levels, insulin resistance and clinical parameters

ergun, mehmet ali/0000-0001-9696-0433WOS: 000276624500008PubMed: 20388053Materials and methods. Ninety-six patients with PCOS and 93 healthy control subjects were included in the study. Insulin resistance was estimated via HOMA-IR. Serum adiponectin levels were measured by ELISA. For determination of adiponectin gene polymorphisms, PCR was performed with appropriate primers after genomic DNA was obtained from the peripheral blood of the patients and control subjects. Results. Adiponectin levels were low in patients with PCOS than control subjects. There was no significant statistical difference between the PCOS and control groups with respect to the frequency of polymorphisms and the genotype distribution. Adiponectin gene polymorphisms were not associated with the anthropometric parameters, hyperandrogenism and adiponectin levels in PCOS. However, the fasting insulin level and insulin resistance were significantly higher and more frequent, respectively, in the polymorphic group compared to the other genotypes among patients with PCOS. Conclusion. The risk of PCOS, hyperandrogenism in patients with PCOS and low serum adiponectin levels cannot be directly attributed to T45G adiponectin gene polymorphisms in exon 2, rather these polymorphisms may be associated with insulin resistance and hyperinsulinemia in PCOS

Effect of mometasone furoate nasal spray on the DNA of nasal mucosal cells

Background/aim: Allergic rhinitis (AR) is a respiratory disease caused by inflammation of the nasal mucosa. Intranasal corticosteroids (ICs) are an effective treatment for AR; however, their use has been associated with atrophy in nasal mucosae. Because DNA damage has been linked to several chronic diseases, we hypothesize that use of ICs could cause DNA damage in nasal mucosa cells, leading to mucosal atrophy and septal perforation. Materials and methods: Sixty patients with moderate or severe AR were divided randomly into two groups. Mometasone furoate (MF) and antihistamine tablets (desloratadine) were given to the study (IC) group. Physiologic saline and desloratadine were given to the control ((serum physiologic (SP)) group. Nasal irrigation fluid was taken from patients before study commencement and after 4 weeks of treatment. The comet assay was applied to detect DNA damage in nasal mucosa cells. Results: Nineteen patients were excluded, leaving a study population of 41 patients (IC group: 17 patients; SP group: 24 patients). Genotoxic damage was evaluated by comet assay. Conclusion: Treatment with MF spray for 4 weeks does not cause DNA breaks within cells in the nasal mucosa. These results could form the basis of clinical trials involving treatment with different ICs over longer treatment periods

Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-gamma gene in women with polycystic ovary syndrome

ergun, mehmet ali/0000-0001-9696-0433WOS: 000239396500007PubMed: 16785159Aim. The present study was designed to examine the relationship between Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-gamma gene (PPAR-gamma) and clinical and hormonal characteristics in women with polycystic ovary syndrome (PCOS). Materials and methods. One hundred patients with PCOS and 100 healthy subjects were included in the study. Serum levels of sex steroids were measured. Insulin resistance was evaluated by homeostasis model assessment (HOMA). The responses of glucose and insulin to an oral glucose tolerance test were analyzed by calculating the respective area under the curve (AUC) by the trapezoidal method. We used the restriction fragment length polymorphism technique and polymerase chain reaction to examine Pro12Ala polymorphism in exon 2 of PPAR-gamma. Results. Pro12Ala polymorphism of PPAR-gamma was significantly elevated in control subjects (22%) compared with PCOS subjects (15%). All of the Pro12Ala polymorphisms of PPAR-gamma were heterozygous. When PCOS subjects with the Pro allele and the Ala allele of PPAR-gamma were compared, the latter had lower free testosterone, androstenedione, dehydroepiandrosterone sulfate, insulin and C-peptide levels, as well as lower luteinizing hormone/follicle-stimulating hormone ratio, HOMA insulin resistance index, AUC(insulin), Ferriman-Gallwey score, acne, body mass index and waist-to-hip ratio. Conclusion. We suggest that Pro12Ala polymorphism of the PPAR-gamma gene maybe a modifier of insulin resistance in women with PCOS

Melanocortin-4 Receptor Gene Polymorphisms in Obese Patients

YILMAZ, AKIN/0000-0002-4368-0777; ergun, mehmet ali/0000-0001-9696-0433WOS: 000264260500013PubMed: 19184404Obesity is a complex disease caused by both genetics and environmental factors. Melanocortin-4 receptor (MC4R) (MIM 155541) gene polymorphisms were reported to be the cause of monogenic obesity in humans. We studied three polymorphisms (Val50Met, Val103Ile, and Ser58Cys) and a mutation (Asn274Ser) of the MC4R gene in 203 obese patients and in 110 healthy subjects in the Turkish population. A high incidence of Val103Ile and Val50Met polymorphisms as well as the Asn274Ser mutation was found in the obese patients, whereas no significant correlation was found regarding the Ser58Cys polymorphism. We conclude that there is a concordance between the polymorphisms (Val103Ile, Val50Met, Ser58Cys) that were first studied in the Turkish population with obesity

beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration

Context: Propranolol, atenolol, and ICI118,551 are non-selective beta-adrenergic receptor (AR), beta(1)-AR, and beta(2)-AR antagonists, respectively. Objective: We investigated the efficacy of propranolol, atenolol, and ICI118,551 on proliferation, migration, and invasion of non-stimulated breast (MCF7), colon (HT-29), and hepatocellular (HepG2) cancer cells. Materials and methods: beta-AR expression profiling of cells was performed by real time PCR. Cell proliferation was determined by MTT. Boyden chamber and scratch assays were performed to evaluate invasion and migration. Results and discussion: All cell lines expressed beta-ARs. ICI118,551 was the most cytotoxic, whereas atenolol was the least effective beta-AR antagonist for 24, 48, and 72 h. Cell invasion was inhibited by ICI118,551 (45, 46, and 50% for MCF7, HT29, and HepG2, respectively) and propranolol (72, 65, and 90% for MCF7, HT29, and HepG2, respectively). Propranolol, atenolol, and ICI118,551 reduced migration of MCF7, HT-29, and HepG2 cells to varying extents depending on the application concentration and duration. Propranolol and atenolol reduced migration of MCF7 and HT-29 in a concentration-dependent manner, whereas migration of these cells decreased after 48 and 72 h of ICI118,551 applications. Conclusion: Beta(2)-AR antagonist seemed to be the most cytotoxic beta-blocker on non-stimulated cancer cells. Propranolol and ICI118,551 were more effective than atenolol in inhibiting invasion and migration of non-stimulated MCF7 and HT-29 cells; ICI118,551 being the most potent. Concordantly, beta(2)-selective blockage seemed to be more effective for non-stimulated cells. Effect of the selective beta-AR antagonists showed variation depending on the concentration, incubation time, and histological origin of cells

Odontogenic effects of two calcium silicate-based biomaterials in human dental pulp cells

Background. The goal of treating exposed pulp with an appropriate pulp capping material is to promote the dentinogenic potential of the pulpal cells. There have been recent attempts to develop more effective pulp-capping materials. Objectives. The aim of this study was to evaluate the effect of newly developed calcium silicate-based material on odontogenic differentiation of primary human dental pulp cells (HDPCs), in comparison with a contemporary calcium silicate-based material. Material and methods. Human dental pulp cells isolated from dental pulps were cultured in standard culture conditions in Dulbecco's Modified Eagle's Medium (DMEM) and then the effects of Micro-Mega mineral trioxide aggregate (MM-MTA) (Micro-Mega, Besancon, France) and ProRoot MTA (MTA) (Dentsply Sirona, Tulsa, USA) (positive control) were evaluated on HDPCs at 1, 7 and 14 days. Untreated cells were used as a negative control. Odontoblastic differentiation was assessed by alkaline phosphatase (ALP) activity. Runtrelated transcription factor 2 (RUNX2), alkaline phosphatase liver/bone/kidney (ALPL), bone morphogenetic protein 2 (BMP2), dentin sialophosphoprotein (DSPP), and Distal-less homeobox 3 (DLX3), as odontoblastic/ osteoblastic expression markers, were evaluated by semi-quantitative real-time polymerase chain reaction (RT-PCR) analysis. Calcium levels of culture media were also determined. Results. The MM-MTA group significantly increased the expression of BMP2 compared with that of the MTA group at 3 different time periods (p < 0.05). The up-regulation of ALPL between day 1 and 14 and the up-regulation of DSPP between day 7 and 14 were significant in both groups (p < 0.05). Micro-Mega MTA and MTA exhibited similar messenger RNA (mRNA) expression levels of ALPL, DSPP, RUNX2, DLX3, and ALP activities, as well as calcium levels. Conclusions. Based on the cell responses observed in this study, MM-MTA might be used efficiently in dental pulp therapy as a potential alternative to MTA

Does Theobromine Increase the Apoptotic Effect of STI571?

Objective: STI571, a selective tyrosine kinase inhibitor is used in CML chemotherapy. It has limited effects in some cases due to drug resistance and intoxication as other chemotherapeutic agents. Thus, many cancer patients use dietary supplements and herbal extracts for increasing the effectiveness of chemotherapeutic agents. Theobromine, a metabolite of cacao has prooxidant effects and regulates intercellular signaling pathways. The aim of the study is to determine the potential apoptotic effects of STI571 and theobromine on K562 cells, when used alone and in combination. Methods: Inhibitory concentrations of STI571 and theobromine were determined by MTT method. Both agents were applied to the cells at 48 h time period alone and in combination. Caspase activities were assessed colorimetrically. Apoptosis and necrosis were evaluated by using acridine orange/ethidium bromide staining. p<0.05 was considered as statistically significant. Results: Caspase activities increased when both agents administrated alone. Theobromine increased effects of STI571 on caspase activities in time and type dependent manner (p<0.05). Apoptotic cell rates also increased when two agents applied in combination (p<0.05) in time dependent manner. Theobromine also reduced necrotic cell rates. Conclusion: Although there are limited data about the intracellular effects of theobromine, we showed that theobromine has effects on the caspase pathway related apoptotic response carried out by STI571. We believe that this in vitro study will shed light for further researches