OBJECTIVE:Obstructive sleep apnea syndrome (OSAS) has been associated with elevated biochemical markers of inflammation. Although the exact mechanism is unknown, both sleep deprivation and hypoxemia are believed to be important causative factors. YKL-40, also known as chitinase-like protein, has been shown to be related to various inflammatory conditions including atherosclerosis, diabetes, cancer, and asthma. The present study aimed to evaluate the relationship between YKL-40 levels and the Apnea Hypopnea Index (AHI) in patients with obstructive sleep apnea syndrome.PATIENTS AND METHODS:The study was conducted at the Sleep Unit of the Namik Kemal University Research Center. From January 2013 to December 2013, 120 patients diagnosed with OSAS by polysomnography and 40 subjects without OSAS were recruited. Patients in both groups were matched by age, sex, and body mass index (BMI). They were further divided into groups of mild, moderate and severe OSAS based on their AHI value. Serum YKL-40 concentrations were measured by the enzyme-linked immunosorbent assay (ELISA).RESULTS:OSAS patients showed significantly elevated YKL-40 levels compared to the control group; 102,05 (23.14) pg/ml in the control group vs. 144.81 (65.53) pg/ml in the OSAS group. A Spearman correlation analysis showed that serum YKL-40 levels were significantly and positively correlated with AHI (r = 0.434, p < 0.001) and oxygen desaturation index (r = 0.374, p < 0.001).CONCLUSIONS:The study demonstrated that high serum YKL-40 levels correlated with the severity of OSAS and might serve as a nonspecific biomarker for prediction and progression of the disease.

Cadmium (Cd), an environmental and industrial pollutant, generates free radicals responsible for oxidative stress. Cd can also lead to various renal toxic damage such as the proximal tubules and glomerulus dysfunction. Thymoquinone (TQ) is the main constituent of the essential oil obtained from black seeds (Nigella sativa) and has various pharmacological effects. The aim of the present study was to examine the nephroprotective, anti-oxidant, and anti-apoptotic effect of the TQ against Cd-induced nephrotoxicity. A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated, and Cd-treated with TQ; each group contain eight animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the amount of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in TQ-treated groups were given TQ (50 mg/kg body weight) once a day orally together with first Cd injection during the study period. The histopathological studies in the kidney of rats also showed that TQ markedly reduced the toxicity of Cd and preserved the normal histological architecture of the renal tissue. Immunohistochemical analysis revealed that TQ significantly decreased the Cd-induced over expression of nuclear factor-κB in renal tissue. Furthermore, TQ treatment resulted in decreased the number of apoptotic cells. TQ significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses (reduced superoxide dismutase, glutathione peroxidase and catalase activities) in renal tissue resulted from Cd administration. These findings suggest that the nephroprotective potential of TQ in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced nephrotoxicity.

We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

We aimed to investigate the preventive effect of Infliximab (IFX), a tumor necrosis factor (TNF)-α inhibitor, on bleomycin (BLC)-induced lung fibrosis in rats. Rats were assigned into four groups as follows: I—BLC group, a single intra-tracheal BLC (2.5 mg/kg) was installed; II—control group, a single intra-tracheal saline was installed; III—IFX + BLC group, a single-dose IFX (7 mg/kg) was administered intraperitoneally (i.p.), 72 h before the intra-tracheal BLC installation; IV—IFX group, IFX (7 mg/kg) was administered alone i.p. on the same day with IFX + BLC group. All animals were sacrificed on the 14th day of BLC installation. Levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, interleukin (IL)-6, periostin, YKL-40, nitric oxide (NO) in rat serum were measured, as well as, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and reduced glutathione (GSH), hydroxyproline, malondialdehyde (MDA) content in lung homogenates. Lung tissues were stained with hematoxylin and eosin (H&E) for quantitative histological evaluation. The inducible nitric oxide synthase (iNOS) expression and cell apoptosis in the lung tissues were determined quantitatively by immunohistochemical staining (INOS) and by TUNNEL staining, respectively. BLC installation worsened antioxidant status (such as SOD, CAT, GPx, GSH, MPO), while it increased the serum TNF-α, TGF-β, IL-6, periostin, YKL-40, and lipid peroxidation, and collagen deposition, measured by MDA and hydroxyproline, respectively. IFX pretreatment improved antioxidant status as well as BLC-induced lung pathological changes, while it decreased the TNF-α, TGF-β, IL-6, periostin, YKL-40, lipid peroxidation and collagen deposition. Finally, histological, immunohistochemical, and TUNNEL evidence also supported the ability of IFX to prevent BLC-induced lung fibrosis. The results of the present study indicate that IFX pretreatment can attenuate BLC-induced pulmonary fibrosis.

Cadmium (Cd) is a serious environmental and occupational contaminant and may represent a serious health hazard to humans and other animals. Cd is reported to induce the generation of reactive oxygen species, and induces testicular damage in many species of animals. The goal of our study was to examine the anti-apoptotic and anti-oxidant effects of caffeic acid phenethyl ester (CAPE) on Cd-induced oxidative stress, apoptosis, and testicular injury in rats. A total of 40 male Wistar albino rats were divided into four groups: control, CAPE alone, Cd-treated, and Cd-treated with CAPE; each group consisted of 10 animals. To induce toxicity, Cd (1 mg/kg body weight) was dissolved in normal saline and subcutaneously injected into rats for 30 days. The rats in CAPE-treated group were given a daily dose of 10 μmol/kg body weight of CAPE by using intraperitoneal injection. This application was continued daily for a total of 30 days. To date, no examinations of the anti-apoptotic and anti-oxidant properties of CAPE on Cd-induced apoptosis, oxidative damage, and testicular injury in rat testes have been reported. CAPE-treated animals showed an improved histological appearance and serum testosterone levels in Cd-treated group. Our data indicate a significant reduction in the number of apoptotic cells in testis tissues of the Cd-treated group with CAPE treatment. Moreover, CAPE significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses in testes tissue resulted from Cd administration. These findings suggest that the protective potential of CAPE in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced testicular injury.

Objective: In this study, we investigated the relationship between AA and genetic polymorphisms of PON1 R192Q and PON1 L55M. Methods: One hundred and nineteen patients with AA and 104 healthy controls were included in this study. The changes in aminoacid squencies on codon 55 and 192 were analysed by the polymerase chain reaction and restriction enzymes. Results: The frequencies of M, L homozygotes and ML heterozygotes on PON 55 region were 11.8%, 58% and 30.2%, respectively in the patient group while they were 12.5%, 43.3% and 44.2%, respectively in the control group. The frequencies of R, Q homozygotes and RQ heterozygotes on PON1 192 region were 10.9%, 41.2% and 47.9%, respectively in the patient group while they were 9.6%, 42.3% and 48.1%, respectively in the control group. While the frequency of PON 55 L allele was higher in patient group than control group, there were no differences in the frequency of 192 R allel between the groups (p = 0.07, p = 0.947, respectively). Conclusions: There were no statistically significant relations between the AA and the PON1 ML55 and QR192 polymorphism. Although the frequency of PON 55 L allel was higher in the patient group than control group, there were no relation between the AA and both PON1 M/L55 and R/Q192 polymorphism.

OBJECTIVE: To examine the histopathological and biochemical effects of quercetin (QE), which has antioxidant properties, on damaged heart muscle in a lipopolysaccharide (LPS)-induced endotoxemia model in rats. STUDY DESIGN: Rats were divided into 4 groups: Control, QE, LPS, and LPS+QE. Escherichia coli LPS, 10 mg/kg, was administered intravenously to induce endotoxemia in the LPS and LPS+QE groups. A single dose of 50 mg/kg QE was administered intraperitoneally to QE groups 30 minutes prior to administering LPS. The rats were sacrificed at the end of the 6-hour period following LPS application. RESULTS: It was observed in histopathological evaluations that the heart tissue injury and inflammation in the LPS groups were higher than those of the LPS+QE group, and that QE partially prevented damage caused by endotoxemia. Rats in the LPS groups demonstrated significantly increased tissue malondialdehyde levels and significantly decreased enzymatic antioxidants superoxide dismutase and catalase in the cardiac tissue. It was observed that QE treatment increased the superoxide dismutase and catalase enzyme levels that decreased after LPS. CONCLUSION: QE with antioxidant properties prevented heart damage caused by free oxygen radicals that occurred after LPS-induced endotoxemia and increased the antioxidant defense system.

This study was designed to elucidate the protective effects of ferulic acid (FA) on formaldehyde-induced hepatotoxicity by measuring some routine biochemical parameters, cytokine levels, and oxidative stress-related parameters in addition to YKL-40 in male Wistar albino rats. Tissue superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities, and tissue malondialdehyde (MDA) levels were measured. Also, serum YKL-40, TNF-α, IL-6, IL-1β, IL-8, total protein, albumin, total bilirubin concentrations, and AST, ALT, ALP, and LDH activities were measured. Histological specimens were examined in light microscopy. Formaldehyde significantly increased tissue MDA, and serum cytokine levels and also decreased activities of antioxidant enzymes. FA treatment decreased MDA and cytokine levels and increased activities of antioxidant enzymes. FA also alleviated degeneration due to formaldehyde toxicity. We suggested that FA can be used as a promising hepatoprotective agent against formaldehyde toxicity because of the obvious beneficial effects on oxidative stress parameters.

In this study, it was aimed to examine the effects of Urtica dioica L. (UD) that has antioxidant feature in the experimental testicular I/R model in rats in terms of anti-apoptotic and antioxidative effects. In our study, 24 male rats were divided into three groups: control group, I/R group and I/R+UD (2mgkg(-1)) group. Seminiferous tubule calibre measurement, Johnson score, haematoxylin-eosin staining, proliferative cell nucleus antigen (PCNA) immunohistochemical staining and TUNEL as histopathological have been conducted. The structural deterioration in the testicular on I/R group has reduced after the treatment of UD. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end labelling (TUNEL), and there was a rise in the expression of proliferating cell nuclear antigen (PCNA) in testis tissues of UD-treated rats in the I/R group. The I/R+UD group showed a decrease in malondialdehyde levels and an increase in the activities of superoxide dismutase, catalase and glutathione peroxidase in comparison with the I/R group. It could be concluded that protective effects of UD on the I/R testicles are via reduction of histological damage, apoptosis, oxidative stress and lipid peroxidation.

OBJECTIVE Cancer-related inflammation affects many aspects of malignancy, including proliferation and survival of malignant cells, angiogenesis, and therapeutic response. Some biomarkers representing the degree of systemic inflammation, such as the Glasgow prognostic score, NLR and PLR, have been shown to have prognostic value in many kinds of cancer patients. Aim of this study to investigate to compare neutrophil/leukocyte (NLR) and platelet/lymphocyte (PLR) ratios of the patients with colorectal neoplastic polyps and colorectal cancer (CRC) and tried to determine whether this could be used as a biomarker in follow up of the patients with neoplastic polyps. PATIENTS AND METHODS A total of 100 colorectal polyps, 113 colorectal cancers and 124 healthy controls were included in the study. Exculusion criteria were endocrinologic or metabolic diseases, acute or chronic diseases, hypertension and atherosclerotic heart diseases, renal diseases. Blood count parameters of the patients were measured. The NLR was calculated as a simple ratio between the absolute neutrophil and the absolute lymphocyte counts. The PLR was defined as the platelet counts to lymphocyte ratio. RESULTS A statistically significant difference was not detected between Group A and C with regard to NLR and PLR. NLR and PLR were found statistically significantly high in Group B (CRC), Group A (colorectal polyp) and Group C (healthy individuals) (p < 0.001 and p < 0.001). Our study showed that the optimum NLR cut-off point for neoplastic polyps was 2.28 (sensitivity: 68.7%, specificity: 42.3%). When the sensitivity and specificity levels of the PLR were assessed, they were 68.7% and 46.5% for neoplastic polyps, 80% and 68.9% for colorectal cancer. CONCLUSIONS NLR and PLR may be used for follow up conversion of colonic and rectal neoplastic polyps to invasive tumor.

Aim It has been shown that heart rate recovery index is an independent risk factor for cardiovascular mortality. It has been reported in most epidomiologic studies that an elevated associated with cardiovascular diseases. The aim of this study was to investigate whether there is a relationship between heart rate recovery index and neutrophillymphocyte ratio. Materials and Methods A total of 238 patients who underwent coronary angiography due to abnormal treadmill exercise test results and who admitted to Cardiology Department of Faculty of Medicine at Namik Kemal University were evaluated retrospectively. heart rate recovery index was

INTRODUCTION:Asymmetric dimethylarginine (ADMA) and nitric oxide (NO) show their mechanism of action reciprocally, the balance between these molecules contributes to the tight regulation of airways tone and function.OBJECTIVES:The aim of this study to determine the serum levels of ADMA and NO in patients with chronic obstructive pulmonary disease (COPD) and establish whether their level vary in relation to forced expiratory volume in 1s (FEV1 ), to assess their role in pathophysiology of COPD.MATERIALS AND METHODS:This study consisted of 58 patients with COPD and 30 healthy subjects. Serum ADMA and NO levels were measured using enzyme-linked immunosorbent assay and the colorimetric method, respectively.RESULTS:Serum ADMA levels were significantly higher, however, NO levels were lower in patients with COPD compared with controls. ADMA levels were inversely correlated with NO levels. Serum ADMA and NO were significantly correlated with FEV1 . Multivariable logistic regression analysis revealed that serum ADMA and NO were independently and significantly associated with the presence of COPD. Multiple linear regression analysis showed that COPD was positively associated with ADMA, additionally COPD and ADMA were independently and inversely associated with NO. NO levels were decreased, ADMA levels were increased compliant with progression of COPD stages.CONCLUSION:While circulating ADMA is higher, NO is lower in COPD and both show a strong correlation to the degree of airflow limitation. ADMA seems to be a possible new marker of prognosis of COPD and can be a novel therapeutic target for the treatment of COPD.

Objective: Obesity has recently become one of the most important health problems throughout the world. This fact led to the controversies on the clinical use of insulin sensitivity indices. Indices previously described or introduced in this study have been evaluated to choose one, which is capable of exhibiting significant distinctions between healthy children and those involved in the classes of childhood obesity. Materials and Methods: A total of 179 girls; 81 morbidly obese(MO), 42 obese(O), 16 overweight(OW) and 40 normal(N) participated in the study. Groups were constituted based upon age- and sex-specific body mass index percentiles tabulated by World Health Organization. Homeostasis Model Assessment of Insulin Resistance(HOMA-IR), HOMA-IR/BMI, log HOMA-IR, fasting glucose/fasting insulin ratio(FGIR), quantitative insulin sensitivity check index(QUICKI), Raynaud, reciprocal insulin indices and also new indices HOMA-IR*BMI, HOMA-IR*fat mass index(FMI), QUICKI*BMI, QUICKI*FMI were calculated. The cut-offs 3.16 and 2.5 for HOMA-IR, 7 and 6 for FGIR, 0.357 and 0.328 for QUICKI were evaluated to estimate insulin resistance. Statistical analyses were performed with Predictive Analytics SoftWare(PASW) Statistics 18. Results and Conclusion: QUICKI*FMI was able to make a clear-cut separation between the groups. A new trilogy for cut-offs (HOMA>2.5, FGIR<7, QUICKI<0.328); each giving the similar results, has been suggested. Multifaceted character of QUICKI was also introduced. QUICKI was capable of discriminating MO from O when 0.328 cut-off was used, and O from OW when 0.357 cut-off was used. QUICKI*FMI index, a new one, was unique in detecting the advanced level of differences(p≤0.005) between N-OW, OW-O and O-MO groups during childhood obesity. Key words Obesity, childhood, insulin sensitivity index

Background: In the present study, the protective and therapeutic effects of quercetin (QE) on renal injury induced by methotrexate (MTX) have been examined. Materials and methods: A total of 24 male rats were divided into the following three groups: control group, MTX group, and MTX+QE group. Rats in MTX group received 20mg/kg of single dose of MTX, while those in MTX+QE group received 20mg/kg of single dose MTX, in addition to 15mg/kg of QE administered 30min prior to MTX and in the following 5-day period as a single daily dose. At the end of the experimental period, renal tissues were removed for histopathological and biochemical assessments. Results: Light microscopic examination showed a disruption of the renal structure in rats in MTX group in the form of tubular degeneration and dilation, with shedding of the tubular epithelial cells into the lumen. QE treatment was associated with less marked degenerative changes, with a similar histological appearance to that of controls. Furthermore, QE treatment resulted in decreased the number of apoptotic cells. Biochemical assessments showed significantly higher malondialdehyde (MDA) levels in MTX group as compared to control and MTX+QE groups. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) levels showed a significant decrease in MTX group as compared to controls. However, QE significantly suppressed MDA level, compensated deficits in the anti-oxidant defenses [reduced SOD, GSH-Px, and CAT levels] in kidney tissue resulted from MTX administration. Conclusions: In conclusion, renal toxic effects of MTX may be alleviated by QE.

Exacerbations in chronic obstructive pulmonary disease (COPD) reduce quality of life and are associated with a more rapid deterioration of the disease. Growth differentiation factor-15 (GDF-15) is a novel candidate exacerbation biomarker. In this study, we aimed to assess GDF-15 as a biomarker of acute exacerbation of COPD (AE-COPD). Lung function parameters, arterial blood gas analysis, and circulating levels of GDF-15, C-reactive protein (CRP), and fibrinogen were assessed in 29 patients on admission to the hospital for AE-COPD, in 29 age-, gender-, and body mass index (BMI)-matched patients with stable COPD, and 29 matched controls with normal lung function. Patients with AE-COPD had higher circulating concentrations of GDF-15 (p < 0.001), CRP (p < 0.001), and fibrinogen (p < 0.002) compared with patients with stable COPD and healthy controls. GDF-15 levels correlated with systemic inflammatory marker CRP in patients with AE-COPD (r = 0.677, p < 0.001) and with stable COPD (r = 0.417, p = 0.024). Multivariate logistic regression analysis revealed GDF-15 (odds ratio 18.16, 95 % confidence interval (CI) 2.51–134.32; p = 0.005) as an independent predictor of AE-COPD. In receiver operating characteristic analysis, GDF-15 achieved an area under the curve of 0.78 for the identification of AE-COPD. In conclusion, GDF-15 is a novel blood biomarker of AE-COPD that is more sensitive than that of CRP. GDF-15 may offer new insights into the pathogenesis of AE-COPD.

Objective: To explore the protective effects of curcumin against renal injury induced by formaldehyde in rats. Methods: A total of 21 male Sprague-Dawley rats were included. The animals were divided into three groups. The control group received 10 ml/kg of physiological saline intragastrically and intraperitoneally on a daily basis. The formaldehyde group were given 10 ml/kg of physiological saline intragastrically plus 10 mg/kg of formaldehyde intraperitoneally. The formaldehyde + curcumin group received 10 mg/kg of intraperitoneal formaldehyde daily as well as 100 mg/kg of curcumin intragastrically. After the completion of 14 days, the kidneys were removed. Tissue microscopic examination was performed with haematoxylin-eosin and periodic acid-Schiff staining. Also, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and xanthine oxidase (XO) activities, and malondialdehyde (MDA) and nitric oxide (NO) levels were measured in tissue samples. Results: Formaldehyde induced renal injury. The degenerative tissue changes in the formaldehyde + curcumin group seemed to regress, exhibiting similar characteristics to those of the controls. MDA, XO and NO were significantly higher in formaldehyde group than in controls, while a significant reduction occurred in SOD, CAT and GSH-Px activities in the formaldehyde group. Also, renal tissue MDA, XO and NO were significantly lower in the formaldehyde + curcumin group than in the formaldehyde group, while tissue SOD, CAT and GSH-Px activities were significantly higher. Conclusion: Curcumin improved the formaldehyde-induced renal degeneration. Also, curcumin was found to prevent the reduction in SOD, CAT and GSH-Px activities, while preventing MDA, XO and NO levels, exhibiting a protective effect against the formaldehyde-induced oxidative renal injury.