The Genotoxic Effect of Nasal Steroids on Human Nasal Septal Mucosa and Cartilage Cells In Vitro.

OBJECTIVE: To determine whether budesonide (Bud) and triamcinolone acetate (TA) cause DNA fractures in the nasal mucosa and septal cartilage cells through examinations using the comet assay technique. STUDY DESIGN: Prospective, controlled experimental study. SETTING: University hospital. METHODS: Septal mucosal epithelial and cartilage tissue samples were taken from 9 patients. Cell cultures were prepared from these samples. Then, budesonide and triamcinolone acetate active ingredients at 2 different doses of 0.2 and 10 µM were separately applied to the cell cultures formed from both tissues of each patient, except the control cell culture, for 7 days in one group and 14 days in one group. After the applications, genotoxic damage was scored with the comet assay technique and the groups were compared. RESULTS: In both the budesonide and triamcinolone acetate groups, the comet scores at low and high doses, on the 7th and 14th days were found to be significantly higher in both cartilage and epithelial tissue than in the control group. CONCLUSION: The study results showed that budesonide and triamcinolone acetate lead to a significantly high rate of genotoxic damage in both epithelial tissue and cartilage tissue.

Could radial extracorporeal shock wave therapy have an effect on wound healing in clinical practice by creating genotoxic damage? An in vitro study in mouse fibroblasts.

OBJECTIVES: This study aims to evaluate wound healing effects of in vitro radial extracorporeal shock wave (rESW) application on mouse fibroblasts and whether the cytotoxic effect of extracorporeal shock wave (ESW) was due to a possible genotoxic effect. PATIENTS AND METHODS: After creating an in vitro wound healing model in L929 mouse fibroblast culture, fibroblasts were stimulated with a frequency of 3 Hz, and 100, 250, 500, 1,000 and 1,500 pulses shock waves were applied. Energy flux densities ranging from 0.01 to 0.23 mJ/mm2 (14.3 MPa) at a constant pressure level of 0.5 and 1 bar were applied. Wound healing, cell viability, and genotoxicity were evaluated at 24 and 48 h. RESULTS: All shot numbers for both pressures significantly reduced cell viability (p<0.05). For both 0.5 and 1 bar pressures, in both intervals, the rate of wound healing decreased, regardless of the number of shots (p<0.05). In vitro genotoxic damage was detected at both 0.5 and 1 bar pressures, in both time intervals, regardless of the number of shots. The genotoxic damage increased from 24 to 48 h. CONCLUSION: The study results suggest that, when ESWT is applied in this in vitro experimental setup, cell viability decreases and wound healing is delayed under all conditions. Furthermore, genotoxic damage can be prevented by using shots below 1,000 pulses. Therefore, while investigating the therapeutic effect of ESW therapy in vitro, the upper limit for the number of shots should be 1,000 pulses.

Is cervical swab an efficient method for developing a new noninvasive prenatal diagnostic test for numerical and structural chromosome anomalies?

Background/aim: Prenatal diagnosis is vital to obtain healthy generation for risky pregnancies. There have been several approaches, some of which are routinely applied in clinics to evaluate the possible prenatal deficiencies and/or diseases. In the present study, we aimed to isolate the fetal cells from endocervical samples and try to identify possible anomalies which were proved by Amniocentesis (AS) and chorionic villus sampling (CVS) methods. Materials and methods: Endoservical specimens were collected from 100 pregnant women. Cells were separated in parallel by fluorescence-activated cell sorting (FACS) and magnetic-activated cell sorting (MACS) using human leukocyte antigen (HLA) G233 and placental alkaline phosphatase (PLAP) antibodies. CMA (comprehensive meta-analysis) were carried out and male fetuses were confirmed with Sex determining region Y (SRY) amplification. Results: The percent of HLA G233 and placental and placental alkaline phosphatase (PLAP) positive cells were 4.55% and 84.59%, respectively. The percent of cells positive for both markers was 14.75%. CMA analyses were not informative. (SRY) was amplified in 67% of the samples. Conclusion: However, the success rate of the both cell sorting and scanning of DNA anomalies by aCGH and/or RT-PCR was limited, preventing the applicability of this proposal in the clinics. Still, the success of the proposed method depends on the development of the novel fetal cell-specific antibodies and the improvements in the sorting systems.

Benzamide and Benzamidine Compounds as New Inhibitors of Urokinasetype Plasminogen Activators.

BACKGROUND & METHOD: In this ongoing research, it is aimed to investigate the synthesis, structure identification and effects on urokinase-type plasminogen activators (uPA) and its receptor levels of 4-(3H-imidazo[4,5-b]pyridin-2-yl)-N-substituted benzamide and benzamidine derivatives. uPA levels obtained from 4b and 7d administration were similar to 5-FU (5-fluorouracil) for colorectal carcinoma cells (p<0.05). 4b and 7d significantly reduced uPAR (urokinase-type plasminogen activator receptor) levels on both cell lines (p<0.05). CONCLUSION: uPAR levels obtaining from 4b and 7d administration were similar to 5-FU for both cell lines colorectal (Colo205, CCL-222) and hepatocellular (HepG2, CCL-23) carcinoma cells (p<0.05).

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, Besançon, 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.

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.

Effect of melatonin on cytokine levels in a hyperthermia-induced febrile seizure model.

Higher serum cytokine levels have been reported in children admitted with febrile seizures and in some experimental models. However, other studies have shown that cytokine levels are influenced by melatonin. In this study, we investigated serum cytokine levels in a hyperthermia-induced febrile rat seizure model and the effect of melatonin. A total of 28 male Sprague-Dawley rats were divided into four groups: the control (C) group, healthy melatonin (MT) group, and hyperthermia-induced febrile seizure groups with (HIFS-MT) and without (HIFS) administration of melatonin. Melatonin (80 mg/kg) was given intraperitoneally 15 min before the seizure. HIFS was induced by placing the rats in 45°C water. The rats were sacrificed under anesthesia after the seizure. Blood samples were drawn by transcardiac puncture to measure serum cytokine and melatonin levels. Serum interleukin (IL)-1ß, IL-6, IL-10, and tumor necrosis factor (TNF)-α levels were lower in the HIFS group than those in the C group (p = 0.005, p = 0.200, p = 0.011, and p = 0.016, respectively). All serum cytokine levels of rats in the MT and HIFS-MT groups were similar to those in the C group. This experimental rat model demonstrated that serum cytokine levels decrease with HIFS and that administering melatonin maintains serum cytokine levels. These results suggest that cytokines may play role in the anticonvulsive activity of melatonin in rats with febrile seizures.

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, 51 patients with ulcerative colitis (UC) and 80 controls were recruited. Genotypes of fractalkine receptorc.745G>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 fractalkine 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.

Effects of silymarin and silymarin-doxorubicin applications on telomerase activity of human hepatocellular carcinoma cell line HepG2.

PURPOSE: Hepatocellular carcinoma (HCC) is resistant to conventional chemotherapeutics such as doxorubicin. Milk thistle extract, or its active constituent silymarin has been used by cancer patients as an alternative and complementary agent. Telomerase activation is one of the initial events of HCC. In this study, we applied doxorubicin and silymarin for 72 hrs in order to test individual and combined effect of the agents on telomerase activity. METHODS: The effects of doxorubicin, silymarin, and their combination on the proliferation of HepG2 cell line were tested by MTT assay, and Checkerboard micro plate method was applied to define the nature of doxorubicin and silymarin interactions on the cells. Lipid peroxidations were assessed by thiobarbituric acid reactive substance (TBARS) level. Telomerase activity was determined according to the telomeric repeat amplification protocol (TRAP). Untreated cells were used as control group. RESULTS: Doxorubicin-silymarin combination had indifferent antiproliferative effects on HepG2 cells. Telomerase activity of the cells incubated with IC50 of doxorubicin and silymarin decreased to 72% (p<0.05). IC50 combinations of doxorubicin and silymarin caused 70% (p<0.05) reduction. All treatments except for the 1/2IC50 of silymarin caused significant increase in lipid peroxidation levels when compared to controls. TBARS levels did not significantly increase when doxorubicin and silymarin were applied in combination, which is in concordance with the indifferent drug interaction. CONCLUSION: IC50 of both doxorubicin and silymarin alone and in combination inhibited telomerase activity. Mechanism of inhibition may be elucidated by further molecular studies.

In vitro effects on biofilm viability and antibacterial and antiadherent activities of silymarin.

Limited treatment options in infectious diseases caused by resistant microorganisms created the need to search new approaches. Several herbal extracts are studied for their enormous therapeutic potential. Silymarin extract, from Silybum marianum (milk thistle), is an old and a new remedy for this goal. The purpose of this study is to evaluate the antibacterial and antiadherent effects of silymarin besides biofilm viability activity on standard bacterial strains. Minimal inhibitory concentration (MIC), minimal bactericidal concentration (MBC), antiadherent/antibiofilm activity, and effects on biofilm viability of silymarin were evaluated against standard bacterial strains. MIC values were observed between 60 and >241 µg/mL (0.25->1 mmol/L). Gram-positive bacteria were inhibited at concentrations between 60 and 120 µg/mL. Gram-negative bacteria were not inhibited by the silymarin concentrations included in this study. MBC values for Gram-positive bacteria were greater than 241 µg/mL. Adherence/biofilm formations were decreased to 15 µg/mL silymarin concentration when compared with silymarin-untreated group. Silymarin reduced the biofilm viabilities to 13 and 46 % at 1 and 0.5 mmol/L concentrations, respectively. We demonstrated that silymarin shows antibacterial and antiadherent/antibiofilm activity against certain standard bacterial strains which may be beneficial when used as a dietary supplement or a drug.

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

CONTEXT: Propranolol, atenolol, and ICI118,551 are non-selective ß-adrenergic receptor (AR), ß1-AR, and ß2-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: ß-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 ß-ARs. ICI118,551 was the most cytotoxic, whereas atenolol was the least effective ß-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: Beta2-AR antagonist seemed to be the most cytotoxic ß-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, ß2-selective blockage seemed to be more effective for non-stimulated cells. Effect of the selective ß-AR antagonists showed variation depending on the concentration, incubation time, and histological origin of cells.

Corchorus olitorius (jute) extract induced cytotoxicity and genotoxicity on human multiple myeloma cells (ARH-77).

CONTEXT: Corchorus olitorius L. (Malvaceae) has industrial importance in world jute production and is a widely cultivated and consumed crop in Cyprus and in some Arabic countries. OBJECTIVE: The present study investigated cytotoxic and genotoxic effects of leaf extracts (LE) and seed extracts (SE) of the C. olitorius on the multiple myeloma-derived ARH-77 cells. The extracts were also evaluated for their total phenol content (TPC) and free radical scavenging activity (FRSA). MATERIALS AND METHODS: C. olitorius was collected from Nicosia, Cyprus. TPC and FRSA were measured by Folin-Ciocalteu and DPPH free radical methods, respectively. Cytotoxicity was evaluated by the MTT assay (4-2048 µg/mL range), and DNA damage (at IC50 and ½IC50) was measured by the comet assay. RESULTS AND DISCUSSION: The LE had significantly higher total phenol (78 mg GAE/g extract) than the SE (2 mg GAE/g extract) with significantly higher FRSA (IC50 LE: 23 µg/mL and IC50 SE: 10 401 µg/mL). Both LE and SE exerted cytotoxic effects on cells after 48 h. The IC50 of SE (17 µg/mL) was lower than LE (151 µg/mL), which demonstrates its higher cytotoxicity on cells. The extracts were applied at 150 and 75 µg/mL for LE and at 17 and 8.5 µg/mL for SE, and the results of the comet assay revealed that the extracts induced genotoxic damage on ARH-77 cells. In both 48 h leaf and seed extract treatments, genotoxic damage significantly increased with increasing concentrations at relevant cytotoxic concentrations. CONCLUSION: To our knowledge, this is the first report demonstrating the high cytotoxic potential of C. olitorius SE and the genotoxic potential of LE and SE.

Identification of promoter region methylation patterns of MGMT, CDKN2A, GSTP1, and THBS1 genes in intracranial meningioma patients.

BACKGROUND: Cytogenetic, molecular and epigenetic changes are all known to take place in the pathogenesis of meningiomas. In this study, we aimed at investing methylation of MGMT (DNA repair), CDKN2A (cell cycle control), GSTP1 (detoxification), and THBS1 (angiogenesis inhibitor) genes, which are known to be unmethylated in normal tissue, in meningioma samples. MATERIALS AND METHODS: Methylation specific polymerase chain reaction was used to study promoter regions methylation of genes in 36 patient samples. RESULTS: Methylation in promoter regions of MGMT, CDKN2A, GSTP1, and THBS1 genes were found in 11.1%, 8.3%, 2.8%, and 0% of the cases, respectively. About 19.4% of cases revealed promoter methylation of at least a single gene, whereas only 2.8% of cases revealed methylation of more than one gene. Based on their World Health Organization 2007 grade; 6.3% of grade I cases, 35.3% of grade II cases, and 33.3% of grade III cases showed hypermethylation in the promoter regions of the genes studied. No statistically significant relation was found between promoter zone methylation and factors such as age, sex, histopathology, grade, or recurrence. CONCLUSIONS: Further research on promoter zone methylation will help expose the methylation profile and pathogenesis of meningiomas, which will consequently guide to a deeper understanding of the pathogenesis of the disease, thus ensuring a better understanding of the prognosis and considering novel treatment options.

Lack of association between eotaxin-1 gene polymorphisms and nasal polyposis.

OBJECTIVE: To examine whether there is an association of eotaxin-1 gene polymorphisms with nasal polyposis (NP). STUDY DESIGN: Cross-sectional study. SETTING: Tertiary referral center. SUBJECTS AND METHODS: The study group included 85 patients with NP and 93 controls without sinonasal disease. Genotypes of eotaxin-1 (-384 A>G and +67 G>A) were identified by restriction fragment length polymorphism analyses after polymerase chain reaction. RESULTS: The -384 A>G and +67 G>A single nucleotide polymorphisms were higher in patients with NP than in controls (P = .044 and P = .019, respectively). However, their relation was statistically poor (association coefficient = 0.18). Consistent with this result, comparisons of allele frequencies for both single nucleotide polymorphisms were not significantly different (-384 A>G, P = .164; +67 G>A, P = .144). CONCLUSION: In this study, eotaxin-1 -384 A>G or 67 G>A genotypes were not associated with susceptibility to NP.

Copper-induced oxidative damage, antioxidant response and genotoxicity in Lycopersicum esculentum Mill. and Cucumis sativus L.

Adequate copper (Cu(2+)) concentrations are required for plants; however, at higher concentrations it can also cause multiple toxic effects. In the present study, lipid peroxidation, hydrogen peroxide levels as well as ascorbate peroxidase (APX: EC 1/11/1/11) and catalase (CAT: EC 1.11.1.6) activities were determined in Lycopersicum esculentum Mill. and Cucumis sativus L. seedlings after 7-day exposure to copper sulfate. In addition, DNA damage in these two crops was assessed by measuring micronucleus (MN) frequency and tail moments (TM) as determined by Comet assay. Inhibitory copper concentrations (EC(50): 30 and 5.5 ppm for L. esculentum and C. sativus, respectively) were determined according to dose-dependent root inhibition curves, and EC(50) and 2×EC(50) were applied. Malondialdehyde (MDA) and H(2)O(2) levels significantly increased in all groups studied. CAT activity increased in treatment groups of C. sativus. APX activity increased in L. esculentum seedlings due to 2×EC(50) treatment. Reductions in mitotic indices (MI) represented Cu(2+)dependent root growth inhibition in all treatment groups studied. According to TMs and MN frequencies, copper exposure induced significant DNA damage (p < 0.05) in all study groups, whereas the DNA damage induced was dose dependent in C. sativus roots. In conclusion, Cu(2+)induced oxidative damage, elevations in H(2)O(2) levels and alterations in APX and CAT activities, as well as significant DNA damage in nuclei of both study groups. To our knowledge, this is the first comparative and comprehensive study demonstrating the effects of copper on two different plant species at relevant cytotoxic concentrations at both biochemical and genotoxicity levels with multiple end points.

Effects of ascorbic acid and ß-carotene on HepG2 human hepatocellular carcinoma cell line.

Recent studies have demonstrated that vegetable rich diets have protective effects on the occurrence and prognosis of various cancers. In addition to dietary intakes, ascorbic acid and ß-carotene are also taken as supplements. The aim of this study was to assess effects of ascorbic acid, ß-carotene and their combinations on human hepatocellular carcinoma cell line HepG2. Ascorbic acid and ß-carotene were applied to cells as plasma peak concentrations (70 and 8 µM, respectively) and their half concentrations (35 and 4 µM, respectively) for 24 and 48 h. Genotoxic and cytotoxic effects of ascorbic acid and ß-carotene were evaluated by alkali single cell gel electrophoresis (SCGE), acridine orange/ethidium bromide staining patterns of cells (apoptosis and necrosis) and lipid peroxidation (thiobarbituric acid reactive substances, TBARS). Results of the SCGE demonstrated that both ascorbic acid and ß-carotene caused DNA damage on HepG2 which were also concordant to increased apoptosis and necrosis of cells. Increased TBARS values also demonstrated increased lipid peroxidation in these cells. Results of the present study demonstrates that when dietary intakes of ascorbic acid and ß-carotene and their relevant achievable plasma level concentrations were considered, both ascorbic acid and ß-carotene induce genotoxic and cytotoxic damage on HepG2 together with increased oxidative damage in contrast to their protective effect on healthy cells. This may be correlated to oxidative status and balance of ROS in hepatocellular carcinoma cells.

PON1 55 and 192 gene polymorphisms in type 2 diabetes mellitus patients in a Turkish population.

Diabetes mellitus is a multifactorial metabolic disease, caused by the complete or relative absence of insulin hormone, which results in the deterioration of carbohydrate, protein, and lipid metabolism. The PON1 55 and 192 polymorphisms have been reported to be associated with type 2 diabetes and its complications. In this study, the involvement of the PON1 55 and 192 polymorphisms and paraoxonase enzyme activity in diabetic complications was assessed. The MM and QQ genotypes were the most frequent in complications of type 2 diabetes in both of the polymorphisms. PON enzyme activity was lower in the type 2 diabetes group with respect to the control group. Regarding both genotypes and enzyme activity, correlations were found between the PON1 55 and 192 genotypes and diabetic complications. This study thus helps to outline a genotype-phenotype relation for the PON1 gene in a Turkish population.

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

AIM: Although the association between adiponectin gene polymorphisms and insulin resistance has been investigated in many studies, there are only a few studies, which have investigated adiponectin gene polymorphisms in patients with polycystic ovary syndrome (PCOS). The objectives of this study were to determine the frequency of T45G polymorphisms localised in exon 2 of the adiponectin gene in a Turkish population with PCOS and to determine the association of T45G polymorphisms with insulin resistance and serum adiponectin levels in PCOS. MATERIALS 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.

Matrix metalloproteinase-9 promoter gene polymorphism (-1562C>T) in nasal polyposis.

BACKGROUND: Expression of matrix metalloproteinase (MMP)-9 increases in nasal polyp tissues. However, the impact of MMP-9 genotypes on the development of nasal polyposis (NP) is unknown. The aim of this study was to examine a potential association of MMP-9 promoter gene polymorphism with the development of NP. METHODS: A prospective and case-control study was performed on 93 patients with NP and 115 controls without sinonasal disease. Genotypes of MMP-9 (-1562C>T) were identified by restriction fragment length polymorphism analyses after polymerase chain reaction. RESULTS: The frequency of -1562CT genotype of MMP-9 was significantly high in NP patients with aspirin-induced asthma (p = 0.014). Distribution of T allele was significantly high in NP patients with aspirin-induced asthma (p = 0.013). MMP-9 genotypes were not associated with gender or the presence of atopy. CONCLUSION: In this study, MMP-9 -1562CT genotype was associated with susceptibility to NP in aspirin-induced asthmatic patients. Because this report is a population-based study, further research should be performed on larger study subjects to reveal the precise role of MMP-9 promoter gene polymorphism in the development of NP.

Detection of MEFV gene mutations in patients with inflammatory bowel disease.

Inflammatory bowel disease (IBD) with ulcerative colitis (UC) and Crohn's disease (CD) as the most common forms is an inflammation of the gastrointestinal tract. Familial Mediterranean fever (FMF) is another inflammatory disease as well. In the current study we studied FMF gene mutations in 47 patients with IBD and 25 healthy individuals to investigate the effects of these mutations on the clinical status of IBD. Twelve mutations were analyzed by reverse hybridization after multiplex PCR amplification of DNA samples. We did not find an association between FMF gene mutations and IBD phenotypic characteristics. However, in patients without Mediterranean fever (MEFV) mutations, extraintestinal disease frequencies were higher (p<0.05). IBD has a genetic basis with multiple genes probably playing a role via several pathways during disease progression. Studying other genes interacting with FMF gene in a larger group of patients will add to the knowledge of disease pathogenesis.