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Objective Metabolic abnormalities such as diabetes, dyslipidemia, abdominal obesity, metabolic syndrome, and abnormal levels of plasma adipokines have been observed in patients with schizophrenia. This study aimed to investigate the differences and correlations of plasma vaspin levels with metabolic parameters in patients with schizophrenia and to compare with healthy controls. Method We measured plasma levels of vaspin and metabolic parameters of 100 patients with schizophrenia and 95 healthy controls. Patients with schizophrenia were evaluated with the Positive and Negative Syndrome Scale (PANSS) and The Global Assessment of Functioning. Results Mean levels of body mass index, waist circumference, triglyceride, and low-density lipoprotein cholesterol of the patients were statistically higher than those of the healthy controls (p = 0.002, p Conclusions Our study showed a significant relationship and positive correlation between vaspin and PANSS scores in schizophrenia patients with obesity. Vaspin may play an important role in the metabolic processes of patients with schizophrenia.

Introduction:Multiple sclerosis (MS) is the most common, chronic, inflammatory, demyelinating disease of the central nervous system. We aimed to evaluate the levels of some neurobiochemical markers in order to evaluate their predictive role in MS.Methods:Fifty-one patients with a diagnosis of MS and 37 healthy subjects were included in the study. The patients with MS were diagnosed by a skilled neurologist based on the medical history and physical examination according to revised McDonald criteria. Neuron-specific enolase (NSE) and S100B levels were measured by electrochemiluminescence immunoassay. Glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) were measured by quantitive sandwich enzyme immunoassay technique with a commercially available ELISA kit.Results:There was a significant difference in NSE levels between the patient and the control groups. No significant difference was determined between the patient and the control groups in terms of S100B, MBP, and GFAP levels. S100B levels were positively correlated with Expanded Disability Status scale scores.Conclusion:Our findings indicated that NSE levels are significantly lower in MS patients. However, NSE levels should not be used alone at discriminating the disease. Multifactorial evaluation should be done during the diagnosis and follow-up of MS.

Objective Neonatal sepsis is one of the most important causes of neonatal morbidity and mortality. Symptoms and signs of neonatal sepsis can be silent; therefore, laboratory investigation is necessary in cases of doubt or if there are risk factors. Early diagnosis is important for early intervention and treatment. The most valuable method for diagnosis is blood culture; however, false positivity due to contamination or false negativity despite ongoing fatal bacterial infections can be seen. Pentraxin 3 is a prototype of the long pentraxin family. It has some differences from C-reactive protein (CRP) in terms of gene organization and localization and production site. It is effective in the early phase of inflammation and it is detected as an early marker of sepsis in adults. The aim of this study was to investigate whether pentraxin 3 can be used as a marker in neonatal sepsis. Materials and Methods Thirty newborns with suspected sepsis with antenatal history or the presence of clinical signs of sepsis, such as hypo/hyperthermia, feed intolerance, lethargy, hypotonia, irregular cardiac rhythms, bradycardia, cyanosis, apnea, respiratory distress, or metabolic acidosis, were enrolled in the study as a case group, and 28 healthy newborns were included as a control group. Serum pentraxin 3, procalcitonin, CRP, and hemogram in the study group and serum procalcitonin and pentraxin in the control group were examined. Results Serum pentraxin 3 (pg/mL) and serum procalcitonin (ng/mL) levels were 2,273.82 ± 1,260.75 and 0.86 ± 0.52 in the case group and 957.41 ± 268.00 and 0.19 ± 0.18 in the control group (p Conclusion The present study showed that serum pentraxin 3 levels may be a useful marker in the diagnosis of neonatal sepsis.

Objectives: To evaluate the relationship between the expression level and biologic role of YKL-40 in bipolar disorder (BD). Methods: This case-control study was conducted in the Faculty of Medicine, Canakkale Onsekiz Mart University, Canakkale, Turkey in 2015. One hundred and four patients diagnosed as having bipolar disorder (DSM5 criteria), and 96 participants were included as healthy controls in this study. A human YKL-40 enzyme-linked immunosorbent assay (ELISA) kit was used to measure the serum YKL-40 levels. As independent variables, we collected data on C-reactive protein ( CRP), demographic variables, and medications. Results: The mean YLK-40 levels for the BD was 2723.5±543.8 pg/ml and control groups was 2132.5±576.3 pg/ml (t=7.42, p less than 0.001). The mean CRP levels for the BD was 0.4±0.6 mg/dl and control groups was 0.4±0.7 mg/dl (t=0.02, p =0.985). The receiver operating characteristics (ROC) analysis revealed an area under the curve (AUC) of YKL-40 in the diagnosis of BD as 0.79 (95% confidence interval [CI]: 0.72-0.85) with a sensitivity of 82.7% and specificity of 68.1% at a cutoff level of 2307.1 pg/ml. The use of antidepressants, antipsychotics, mood modifiers, and the presence of any comorbidity was not related to the YKL-40 levels ( p greater than 0.05). Conclusion: With acceptable sensitivity and specificity levels, the YKL-40 can be utilized as a marker in the diagnosis and follow-up of BD. Saudi Med J 2019; 40 (1): 26-32 doi: 10.15537/smj.2019.1.23396 How to cite this article: Sahin B, Inanli I, Caliskan AM, Uysal S. Chitinase-3-like protein 1 levels in bipolar disorder. Saudi Med J 2019; 40: 26-32.

Background Iron deficiency is common in obese children although the underlying mechanism is unclear. Several studies have investigated the relation between iron deficiency and obesity, but studies focusing on children are rare. The aim of this paper is to investigate the associations between iron parameters, pro-hepcidin and soluble transferrin receptor levels in obese children. Methods A total of 110 children aged from 6 to 16, 50 with primary obesity and 60 healthy children and adolescents, were enrolled. Complete blood count, serum iron levels, iron binding capacity, ferritin levels, soluble transferrin receptor, and pro-hepcidin levels were studied. Results Serum iron and transferrin saturation index levels were significantly low, red cell distribution width and ferritin levels were significantly high in obese children compared to control group. No association between soluble transferrin receptor, pro-hepcidin and iron parameters was detected. A positive correlation between ferritin and pro-hepcidin levels was defined. Conclusions Obese children and adolescents were at greater risk for iron deficiency. It should be considered in the diet recommendations.

Objectives: To evaluated Fetuin-A levels of patients admitted in the intensive care unit with a diagnosis of sepsis. Methods : This study was conducted at the Faculty of Medicine, Canakkale Onsekiz Mart University Hospital, Canakkal, Turkey, between February 2015 and October 2015. Forty septic patients were included in the study. Subsequent to clinical suspicion of sepsis, serum levels of C-reactive protein (CRP) and procalcitonin; and white blood cell (WBC) counts were evaluated at 3 time-points: 0 (basal), 24, and 72 hours. Results : The mean Fetuin-A levels at the 3 time-points were 58.5 ± 29.2 ng/mL, 40.9 ± 23.6 ng/mL, and 47.8 ± 25.7 ng/mL, respectively. Fetuin-A levels at 24 hours were significantly lower than the basal level ( p greater than 0.05), where as no significant difference was observed between the basal levels and those at 72 hours ( p greater than 0.05). Correlation between the temporal changes in Fetuin-A levels and the changes in other inflammatory markers (CRP, procalcitonin and WBC) was examined. Fetuin A was found to have only a negative correlation with serum procalcitonin level ( p less than 0.05). Conclusion : In this study, serum Fetuin-A levels in septic patients decreased significantly in the first 24 hours, followed by an insignificant increase at 72 hours. These findings suggest that monitoring of Fetuin-A levels may help predict the time of occurrence of sepsis and prognosis of sepsis. Saudi Med J 2018; Vol. 39 (7): 679-684 doi: 10.15537/smj.2018.7.22418 How to cite this article: Altinisik HB, Altinisik U, Uysal S, Sacar S, Simsek T, Demiraran Y.Are Fetuin-A levels beneficial for estimating timing of sepsis occurrence? Saudi Med J . 2018 Jul;39(7):679-684. doi: 10.15537/smj.2018.7.22418.

The aim of this study was to identify the potential prognostic roles of the preoperative neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and red cell distribution width (RDW) in patients with laryngeal squamous cell carcinoma (LSCC). 81 patients who underwent surgery for the larynx carcinoma were enrolled in the study. NLR, PLR and RDW were used as outcome measures. Local recurrence was detected in 30 (37.0 %) patients and neck lymph node metastasis was detected 6 (7.4 %) patients during follow-up period. Mortality was seen in 7 (8.6 %) patients. The mean PLR in the T1 and T2 stage tumors were significantly lower than the T4 stage. The mean RDW and PLR were significantly higher in the exitus group than the survivor group. The mean NLR in the patients with local recurrence was significantly higher than the non-recurrent patients. Progression-free survival (PFS) was lower in patients with high NLR. When analyzed by the Cox regression analysis of factors affecting the local recurrence, NLR was found to significantly affect the recurrence. According to ROC analysis for mortality, NLR was not found to be a prognostic factor, although the PLR and RDW were significant prognostic factors. According to Cox regression analysis, a high PLR increases mortality 4.2 times and a high RDW 4.6 times. Although in univariate analysis MCV, RDW and tumor grade were predictors of mortality, RDW and tumor grade independent predictors were found. Further studies involving large patient groups are required.

Objectives We aimed to investigate the effects of hesperetin as a flavanon both histopathologically and immunohistochemically on cochlear apoptosis in a rat model of cisplatin-induced ototoxicity (CIO). The evaluation of the effects of hesperetin on cisplatin-induced hearing loss was performed using distortion product otoacoustic emission (DPOAE). Methods Twenty-eight wistar albino rats were used in the current study. The rats were randomly divided into four groups with seven rats in each group. Group C was exposed to a single dose of cisplatin (12 mg/kg) by intraperitoneal injection. Group CH received intraperitoneally cisplatin (12 mg/kg) and hesperetin (20 mg/kg). Group H was exposed to hesperetin (20 mg/kg) intraperitoneally. The sham group (group S) received normal saline (6 cc) intraperitoneally. The measurements of DPOAE and signal-noise ratios (SNR) were performed before the treatment and again on the first and 6 days after administration of the drugs. Rats were sacrificed and cochleae were dissected 10 days after drug administration. The cochlear tissue was assessed in all groups by histopathologic, immunohistochemical and TUNEL assay. In addition, serum oxidative stress markers and antioxidant parameters were analyzed. Results There was a significant difference between the basal value and the sixth day at frequencies 8.4, 9.6 and 9.96 for group C. We also found a significant difference between the first and sixth day at frequencies 7.2, 8.4, 9.6 and 9.96. On the 6th day, there were significant differences between C and S groups at all frequencies except 2.4. We showed a significant difference between C and H groups at frequencies 4.8, 6.0, 8.4, 9.6 and 9.96. There was also a significant difference between C and CH groups at frequencies 2.4, and 3.6. We found lower levels of oxidants and higher levels of antioxidants in CH group as compared to C group. C group had a significantly greater number of TUNEL-positive cells than did S, H and CH groups. The number of TUNEL-positive cells in CH group was higher than in S and H groups. There was a significant difference between the positive PCNA cells of CH group compared to S and H groups in spiral ganglion and stria vascularis. In addition, there were no positive PCNA cells in C group. Conclusions Hesperetin may prevent ototoxicity by increased antioxidant enzymes and reduced oxidant parameters and protected against apoptosis resulting from a proliferation of cochlear cells in CIO.

Objective: Ankylosing spondylitis (AS) is a chronic inflammatory disease and the increased mortality in these patients is largely caused by cardiovascular diseases. Endothelial cell-specific molecule-1 (ESM-1) is a novel marker to assess endothelial dysfunction and expressed by the vascular endothelium. In this study, the serum ESM-1 levels in patients with AS and the possible association between serum ESM-1 and carotid intima-media thickness (CIMT) as a marker of atherosclerosis was evaluated. Methods: A total of thirty-seven patients with AS and thirty healthy control subjects were included in this study. ESM-1, erythrocyte sedimentation rate(ESR),C-reactive protein (CRP) and CIMT were measured in all subjects. ESM-1 levels were measured by ELISA method. The disease activity of patients with AS were assessed using questionnaires Bath Ankylosing Spondylitis Functional Index (BASFI) and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Results: Serum ESM-1 levels were lower in AS patients than in healthy controls. However, there was no statistically significant difference between ESM-1 levels (304.3±185.2 vs. 373.9±206.9 ng/L, respectively; p=0.064). Patients with AS had significantly higher CIMT levels compared with controls (0.77±0.16 vs. 0.53±0.09 mm, respectively; p Conclusion: The results showed that CIMT values in AS patients were increased when compared to control group. There was no correlation among ESM-1 levels, disease activity and CIMT. In order to reveal the pathological role of the ESM-1 levels in patients with AS need more studies.

Dyslipidemia is one of the most important risk factors for coronary artery disease (CAD), and low-density lipoprotein cholesterol (LDL-C) is used to measure dyslipidemia. Non-high-density lipoprotein cholesterol (non-HDL-C) seems to be an alternative parameter to LDL-C as it is not influenced by triglyceride (TG) levels. The aim of this study is to compare non-HDL-C and LDL-C levels as risk markers in CAD patients. Materials and methods: One hundred and ten CAD patients and 42 individuals with normal coronary angiography results were included in this study. Patients were divided into 2 groups: TG < 200 mg/dL (n = 75) as group 1 and TG > 200 mg/dL (n = 35) as group 2. Total cholesterol (TC), TG, and HDL-C levels were analyzed with a Roche Modular P800 autoanalyzer. LDL-C and non-HDL-C levels were calculated. Results: There were statistically significant differences in TC, TG, HDL-C, and non-HDL-C levels when the groups were compared. Non-HDL-C levels of group 2 were statistically higher than those of group 1 and the control group. There was no significant difference in LDL-C levels between the groups. Conclusion: Non-HDL-C levels are better risk markers than LDL-C levels, especially in patients with TG > 200 mg/dL, and non-HDL-C levels should be taken into consideration when evaluating the risk of CAD.

WOS: 000349619500010 PubMed: 25672430 OBJECTIVES: Prevention of the development of paraplegia during the repair of the damage caused by descending thoracic and thoracoabdominal aneurysms remains an important issue. Therefore, we investigated the protective effect of atorvastatin on ischemia-induced spinal cord injury in a rabbit model. METHOD: Thirty-two rabbits were divided into the following four equally sized groups: group I (control), group II (ischemia-reperfusion), group III (atorvastatin treatment) and group IV (atorvastatin withdrawal). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the iliac bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs of each animal was evaluated according to the Tarlov score. Spinal cord and blood samples were obtained for histopathological and biochemical analyses. RESULTS: All of the rabbits in group II exhibited severe neurological deficits. Atorvastatin treatment (groups III and IV) significantly reduced the level of motor dysfunction. No significant differences were observed between the motor function scores of groups III and IV at the evaluated time points. Light microscopic examination of spinal cord tissue samples obtained at the 72nd hour of reperfusion indicated greater tissue preservation in groups III and IV than in group II. CONCLUSION: This study demonstrates the considerable neuroprotective effect of atorvastatin on the neurological, biochemical and histopathological status of rabbits with ischemia-induced spinal cord injury. Moreover, the acute withdrawal of atorvastatin therapy following the induction of spinal cord ischemia did not increase the neuronal damage in this rabbit model.

Objective. Acute mercury intoxication among children can occur through unintentional exposure, and neurotoxicity is one of the main findings in acute exposures. In this study, we aimed to study the central nerve system markers, namely neuron-specific enolase (NSE), S100B, and glutamate receptor (GRIA 1) levels and discuss the mechanisms of central nerve system damage and whether these parameters could be used as markers of acute elemental mercury intoxication neurotoxicity. Materials and methods. This is a case-control study which includes 169 children with acute elemental mercury intoxication, who were exposed to mercury in the school laboratory from a broken jar, and 45 sex- and age-matched controls without mercury exposure. Patient group were divided into three subgroups according to the neurological examination performed during the admission. Neuropathy Group included the children with neurological symptoms including peripheral neuropathy and decreased muscle strength (n = 39) (with or without dilated...

Objective: Ischemic stroke is defined as acute neurological disorder according to cerebral vascular damage and reduced blood flow to a particular region of the brain. Ischemic stroke is a major cause of morbidity and mortality and placed 3rd among the causes of death. About 80% of all strokes depend on ischemic cause. Atherosclerotic plaque rupture or addition of a thrombus on plaque is the most common cause of ischemic stroke. Atherosclerosis is associated with the level of blood lipids from the first stages of the formation process. In our study, we aimed to investigate non-HDL, total cholesterol / HDL-cholesterol and LDL-cholesterol levels in patients with acute ischemic stroke. Methods: This study was performed in 52 patients who were admitted at Ankara Numune Hospital for Education and Investigation, Division of Neurology between December 2009- May 2010 with a diagnosis of acute ischemic stroke in the first 24 hours and 48 healthy individuals matched for age and gender, who was admitted at the hospital during the same period. Total cholesterol, triglycerides and HDL cholesterol levels were measured by DXC 800 autoanalyzer (Beckmann-Coulter, USA). LDL cholesterol, total cholesterol / HDL-cholesterol and non-HDL cholesterol levels were calculated according to the formulas. Results: Patient group had significantly lower HDL-C levels than the control group (p=0.009), whereas the triglyceride and total cholesterol / HDL-C levels were significantly higher (p=0.013, p=0.018). Total cholesterol, LDL cholesterol and non-HDL cholesterol levels did not differ significantly between groups. There were significant correlations between non-HDL-cholesterol levels and triglycerides, total cholesterol, LDL cholesterol (respectively r=0.468, r=0.964, r=0.851) (respectively p

The slow coronary flow (SCF) phenomenon is characterized by slow progression of angiographic contrast medium in the coronary arteries in the absence of stenosis in the epicardial vessels. The pathophysiological mechanisms of SCF phenomenon remain uncertain. Several hypotheses, however, have been suggested for SCF phenomenon, including an early form of atherosclerosis, small vessel dysfunction, dilatation of coronary vessels, imbalance between vasoconstrictor and vasodilatory factors, platelet function disorder, and inflammation. Atherosclerosis and inflammation are the most accepted mechanisms for the pathogenesis of SCF. Thrombin activatable fibrinolysis inhibitor (TAFI) was described as a new inhibitor of fibrinolysis recently and plays an important role in coagulation and fibrinolysis. In previous studies, the role of TAFI was associated with inflammation and evolution of atherosclerosis in coronary artery disease. There are no data available about TAFI levels in patients with SCF phenomenon investigated by angiography. Our goal was to evaluate TAFI antigen (Ag) levels in patients with SCF and to determine the association of the TAFI Ag level with traditional cardiovascular risk factors in our study. The study group constituted 41 patients with angiographically confirmed SCF and 46 patients with normal coronary flow as the control group. The TAFI Ag levels of each patient were determined. Between the control and study group, a statistical difference in the levels of TAFI Ag (p

Background International Council for Standardization in Haematology suggested Westergren method as the reference method to analyze erythrocyte sedimentation rate (ESR). However, in recent years closed automated systems that measure ESR directly from a capped EDTA blood sample tube have been developed. We evaluated the analytic performance of one of these new methods, the Ves-Matic Cube 200. Methods K2EDTA and citrated blood samples were taken from 101 randomly selected outpatients in Ankara Numune Education and Research Hospital. The ESR results using Ves-Matic Cube 200 and Westergren as reference method from 101 patients were compared and interference studies were performed. Results We found the mean difference between the two methods as 0.19 ± 15.85 mm/hr (−3.317 to 2.940 mm/hr, 95% confidence interval). Regression analysis yielded the equation “y = −2.59 + 1.15x” between the two methods (r = 0.82). Conclusions Ves-Matic Cube 200 should be monitored carefully for good quality control. Temperature correction should be applied to study control material as recommended by the manufacturer. Ves-Matic Cube 200 device should be monitored carefully, performance studies should be performed, and the results should be checked in order to eliminate the random errors during the routine studies.

The increasing prevalence of both asthma and obesity are major health problems. Recent studies established a possible link between obesity and asthma; however, the underlying mechanism is not clear. The aim of the study was to analyze the prevalence of metabolic syndrome in postmenopausal subjects with asthma and search the interactions between adipokines, metabolic syndrome, and asthma. A total of 45 female patients (57.5 ± 13.9 years) with asthma and 30 healthy subjects (59.6 ± 12.8 years) in postmenopausal status were enrolled in this study. For the diagnosis of metabolic syndrome, modified World Health Organization diagnostic criteria were used. Blood levels of glucose, lipid profile, HbA1c, insulin, CRP, leptin, adiponectin, tumor necrosis factor-alpha, interleukin (IL)-6, IL-8 and plasminogen activator inhibitor-1 (PAI-1) were measured. The mean body mass index was 29.6 ± 5.4 for asthma patients and 28.2 ± 5.3 for the control group. The incidence of metabolic syndrome was found as 26 % for both groups. Insulin resistance as calculated by homeostasis model assessment (HOMA-IR) and fasting insulin levels were significantly higher in asthma patients (p < 0.001 for both parameters). Leptin levels were significantly higher (p = 0.001) and adiponectin levels were lower (p = 0.029) in asthma patients compared to controls. We concluded that although incidence of obesity and metabolic syndrome was not higher in postmenopausal asthma patients than controls, there was an impairment of glucose metabolism and altered adipokine levels in asthma patients.

Hepcidin is considered a major regulator of iron metabolism. Despite previous studies showing elevated ferritin and hepcidin levels in type 2 diabetes mellitus (DM), no study has investigated hepcidin levels in pregnant women with gestational DM (GDM).A case-control study was conducted in 30 cases of GDM, 47 pregnant women with impaired glucose tolerance (IGT) and 72 pregnant women with normal glucose tolerance (control) between April 2009 and July 2011. Serum hepcidin and other iron metabolism parameters were analyzed in all groups.Serum ferritin and serum iron were significantly elevated in the GDM group compared to controls (p = 0.014, p = 0.018, respectively) and to the IGT group (p = 0.021, p = 0.008, respectively). Hepcidin levels were elevated significantly in the diabetic patients compared to the IGT group (p = 0.011) and controls (p = 0.002). We found no correlation between hepcidin and other iron metabolism parameters (Hb, serum iron and ferritin), whereas positive correlations were found between hepcidin and parameters of glucose metabolism (fasting blood glucose, fasting insulin level and glucose value response to glucose challenge test).Serum hepcidin concentrations were increased in pregnant women with IGT and GDM and this was not related to inflammation parameters.

The hydrogenated nanocrystalline silicon (nc-Si:H) thin films were produced by capacitively-coupled plasma enhanced chemical vapor deposition (PECVD) technique at low substrate temperatures ( T s ≈ 40–200 °C). Firstly, for particular growth parameters, the lowest stable T s was determined to avoid temperature fluctuations during the film deposition. The influence of the T s on the structural and optical properties of the films was investigated by the Fourier transform infrared (FTIR), UV–visible transmittance/reflectance and X-ray diffraction (XRD) spectroscopies. Also, the films deposited at the center of the PECVD electrode and those around the edge of the PECVD electrode were compared within each deposition cycle. The XRD and UV–visible reflectance analyses reveal the nanocrystalline phase for the films grown at the edge at all T s and for the center films only at 200 °C. The crystallinity fraction and lateral dark conductivity decrease with lowered T s . FTIR analyses were used to track the hydrogen content, void fraction and amorphous matrix volume fraction within the films. The optical constants obtained from the UV–visible transmittance spectroscopy were correlated well with the FTIR results. Finally, the optimal T s was concluded for the application of the produced nc-Si:H in silicon-based thin film devices on plastic substrates.

Antecedentes Se cree que la lesion pulmonar inducida por el oxigeno conduce al desarrollo de una displasia broncopulmonar en los recien nacidos prematuros. Hemos evaluado los efectos favorables del aceite de Nigella sativa (NSO) en ratas con lesion pulmonar inducida por hiperoxia. Metodos Se utilizaron 30 ratas Sprague-Dawley recien nacidas a las que se dividio aleatoriamente en 3 grupos para aplicarles hiperoxia (O2 al 95%), hiperoxia+NSO o el grupo de control (O2 al 21%). A las crias del grupo de hiperoxia+NSO se les administro NSO a una dosis de 4ml/kg al dia por via intraperitoneal durante el periodo de estudio. Se realizo una evaluacion histopatologica, inmunoquimica y bioquimica (superoxido dismutasa [SOD], glutation peroxidasa [GSH-Px], malonilaldehido [MDA] y mieloperoxidasa [MPO]). Resultados En la evaluacion histopatologica e inmunoquimica, la gravedad de la lesion pulmonar fue significativamente inferior en el grupo de hiperoxia+NOS (p

Oxygen-induced lung injury is believed to lead to the development of bronchopulmonary dysplasia in premature infants. We have evaluated the beneficial effects of Nigella sativa oil (NSO) on rats with hyperoxia-induced lung injury.Thirty newborn Sprague-Dawley rats were randomly divided into 3 groups as hyperoxia (95% O(2)), hyperoxia+NSO and control (21% O(2)). Pups in the hyperoxia+NSO group were administered intraperitoneal NSO at a dose of 4ml/kg daily during the study period. Histopathologic, immunochemical, and biochemical evaluations (superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], malonaldehyde [MDA] and myeloperoxidase [MPO]) were performed.In the histopathologic and immunochemical evaluation, severity of lung damage was significantly lower in the hyperoxia+NOS group (P.05). Tissue GSH-Px and SOD levels were significantly preserved, and MDA, MPO levels were significantly lower in the hyperoxia+NSO group (P.05).NSO significantly reduced the severity of lung damage due to hyperoxia.

Background/Aims: Visfatin is a novel adipokine with insulinomimetic properties that increases in diabetes. However, for gestational diabetes mellitus (GDM) there are conflicting reports. Recent studies have reported a positive association of serum ferritin concentrations with insulin resistance. Thus, we assessed serum levels of visfatin in pregnant women with varying degrees of glucose tolerance and investigated the possible interaction of visfatin with parameters of iron metabolism. Methods: Visfatin levels were measured at 24-28 weeks of gestation in 88 women who were divided into three groups according to their response to a 50-gram glucose challenge test and a 100-gram oral glucose tolerance test: control group (n = 28), impaired glucose tolerance (IGT) group (n = 30) and GDM group (n = 30). Results: Visfatin levels were significantly higher in the GDM and IGT group than in control (p < 0.001 for GDM vs. control, and p = 0.004 for IGT vs. control). Serum visfatin was significantly associated with serum ferritin, insulin, age, gravidity, and body mass index. In a linear regression model, the covariates explained only 17% of variability of serum visfatin concentration. Body mass index (p < 0.001) contributed independently to visfatin variance. Conclusion: Serum visfatin concentration is significantly higher in GDM and is correlated with ferritin levels.

Objectives: The study demonstrates a gel problem sourced from the internal heat of centrifuges without temperature control. It was planned to investigate the internal temperatures of temperature controlled centrifuges and the centrifuges without temperature control and the effect of centrifuge temperature on enzymes and thyroid panel. Design and Methods: Internal heat of the centrifuges were monitored in the most busy working hours. Blood samples were obtained from 42 patients to two separate biochemistry tubes. One sample of the same patient was centrifuged with a temperature-controlled centrifuge (Group 1) and the other was centrifuged with a centrifuge without temperature control (Group 2). AST, ALT, GGT, LDH, total protein, albumin, TSH, fT3 and fT4 levels were determined in the same run of the analyzer. Results: ALT and TSH values in Group 2 were significantly lower, fT4 values were significantly higher than Group 1. Conclusions: Laboratories should be aware of a possible internal heat production in centrifuges without temperature control and gel tubes should be centrifuged in temperature controlled centrifuges especially in centrifuge units with high working load.

BACKGROUND The aim of the study was to investigate oxidant/antioxidant status by determining serum ischemia-modified albumin (IMA) levels with oxidative/antioxidant parameters in patients with ankylosing spondylitis (AS) compared to the controls. METHODS The serum concentrations of IMA, IMA/albumin ratio (IMAR), malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were measured in 40 AS patients and 35 healthy controls. RESULTS Mean serum IMA, IMAR, MDA, TOS, and OSI levels were increased in patients with AS when compared to the control group (p < 0.05 for all). Serum levels of SOD and GPx were significantly lower in the patient group than in the healthy subjects (p < 0.001 for both). Serum TAC levels were decreased in patients with AS compared to the controls but the statistical difference was not significant. Serum IMA levels were found to be positively correlated with BASDAI, BASFI, BASMI, and ASDAS-CRP (r = 0.356, r = 0.370, r = 0.412, r = 0.353, respectively, and p < 0.05 for all). IMAR values showed significant correlations with BASFI, BASMI, and ASDAS-CRP (r = 0.351, p = 0.026; r = 0.400, p = 0.010; and r = 0.379, p = 0.016, respectively). CONCLUSIONS Depletion in antioxidant systems and overproduction of free radicals leading to formation of the oxidative stress may play a role in the development of AS. Increased levels of IMA might provide important contributions to the underlying oxidative stress in AS.

In recent years, asymmetric dimethyl arginine (ADMA) has emerged as an early marker and/or mediator of endothelial dysfunction and it has been proved to be a novel, independent risk factor of cardiovascular and metabolic diseases. Our aim in this study was to compare the ADMA concentrations among patients with a history of gestational diabetes mellitus (GDM) with controls. Thirty women with a history of GDM and 40 age-matched and BMI-matched healthy controls were enrolled in this study. ADMA concentrations, fasting blood glucose levels, 75-g oral glucose tolerance test (OGTT) second hour plasma glucose levels, and insulin levels were compared between two groups. The fasting blood glucose levels were also significantly higher in patients with GDM history. Although second hour values of 75-g OGTT were higher in patients with GDM history, the difference between groups was not statistically significant. However, the insulin and homeostatic model assessment insulin resistance levels were statistically significantly higher in patients with a history of GDM. The concentrations of ADMA were found to be statistically higher in patients with a history of GDM (0.45 ± 0.11 vs. 0.31 ± 0.13 μmol/l, respectively; P = 0.01). This study shows that women who had a history of GDM are under risk for cardiovascular diseases, although they seem to be healthy and have normal blood biochemical levels, because of elevated serum ADMA levels. Clinicians should be aware of this increased cardiovascular disease risk among patients with a history of GDM.

Objectives The relation between nonalcoholic steatohepatitis and iron metabolism is still controversial. Free fatty acids, iron, and other sources of oxidative stress probably result in cell damage, and necroinflammation mediated by various cytokines. Design and methods Sixty patients were diagnosed with NASH were included in the study, and the patient group was divided into three subgroups. Iron metabolism markers, inflammatory cytokines, including TNF-α, IL-6 and IL-8, MDA and nitric oxide levels were measured. Results Serum ferritin, inflammatory cytokines, and oxidative stress markers were significantly higher in the patient group. Among three patient groups, divided according to the results of ultrasonic examination, there were significant changes with regard to these parameters. Conclusion The study results suggest that liver iron and fat accumulation, oxidant stres, and inflammatory cytokines are closely related. Therefore, levels of serum ferritin, MDA, IL-6, TNF-α and IL-8 could represent the indices of activity and progression of NASH.

Pseudothrombocytopenia (PTCP) is a laboratory event of platelet clustering related to drugs used for anticoagulation. This condition is engendered by autoantibodies against platelets in usually EDTA-anticoagulated blood. Pseudothrombocytopenia has no clinical significance but when evaluated as true thrombocytopenia, this misconception may lead to unnecessary diagnostic procedures. Heparin-induced thrombocytopenia with thrombosis (HITT) is a complication of heparin treatment caused by heparin platelet factor 4 (HPF-4) antibodies, leading to platelet activation and hypercoagulability. In our study, 48 patients with PTCP and 36 healthy volunteers were included. Heparin platelet factor 4 antibody positivity was detected in 12 patients from PTCP group; nobody from control group had. Citrated serum samples and peripheral blood smears showed normal platelet count. Of the 4 patients using heparin derivative, 1 (2.1%) had antibody positivity but without any bleeding symptoms. In conclusion, HPF-4 antibody positivity might be a risk factor for PTCP. Clinicians should be aware of this kind of condition.

WOS: 000290313300006, PubMed: 21389698, Background and Objectives: Cardiovascular disease is prevalent in chronic kidney disease (CKD). Uric acid is increased in subjects with CKD and has been linked with cardiovascular mortality in this population. However, no study has evaluated the relationship of uric acid with angiographically proven coronary artery disease (CAD) in this population. We therefore investigated the link between serum uric acid (SUA) levels and (i) extent of CAD assessed by the Gensini score and (ii) inflammatory parameters, including C-reactive protein (CRP) and pentraxin-3, in patients with mild-to-moderate CKD. Material and Methods: In an unselected population of 130 patients with estimated glomerular filtration rate (eGFR) between 90 and 30 ml/min/1.73 m(2), we measured SUA, serum pentraxin-3, CRP, urinary protein-to-creatinine ratio, lipid parameters and the severity of CAD as assessed by coronary angiography and quantified by the Gensini lesion severity score. Results: The mean serum values for SUA, pentraxin-3 and CRP in the entire study population were 5.5 +/- 1.5 mg/dl, 6.4 +/- 3.4 ng/ml and 3.5 +/- 2.6 mg/dl, respectively. The Gensini scores significantly correlated in univariate analysis with gender (R = -0.379, p = 0.02), uric acid (R = 0.42, p = 0.001), pentraxin-3 (R = 0.54, p = 0.001), CRP (R = 0.29, p = 0.006) levels, eGFR (R = -0.33, p = 0.02), proteinuria (R = 0.21, p = 0.01), and presence of hypertension (R = 0.37, p = 0.001), but not with smoking status, diabetes mellitus, and lipid parameters. After adjustments for traditional cardiovascular risk factors, only uric acid (R = 0.21, p = 0.02) and pentraxin-3 (R = 0.28, p = 0.01) remained significant predictors of the Gensini score. Conclusions: SUA and pentraxin-3 levels are independent determinants of severity of CAD in patients with mild-to-moderate CKD. We recommend a clinical trial to determine whether lowering uric acid could prevent progression of CAD in patients with CKD. Copyright (C) 2011 S. Karger AG, Basel, NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [HL-68607], R.J.J. is supported by NIH grant HL-68607.

Purpose The prevalence of obesity has significantly increased among children and adolescents worldwide and is becoming an important health care problem in parallel with the increased prevalence of obesity pediatric non-alcoholic fatty liver disease. Betatrophin is a newly define hormone that is commonly secreted by liver and plays role in glucose tolerance. This study aimed to investigate the relationship between serum betatrophin levels and non-alcoholic fatty liver disease in obese children. Methods The study included 40 obese children with a body mass index (BMI) above 95th centile, and 35 non-obese subjects with a BMI 3-85th centile, whose age and gender were similar to those of the patient group. For the evaluation of metabolic parameters fasting serum glucose, insulin, alanine aminotransferase, aspartate aminotransferase, lipid profile and serum betatrophin levels were measured. Total cholesterol: high-density lipoprotein cholesterol and low-density lipoprotein cholesterol: high-density lipoprotein cholesterol ratios were calculated as “atherogenic indices.” Results Serum betatrophin levels of the obese subjects were similar to that of non-obese subjects (p=0.90). Betatrophin levels were not correlated with the metabolic parameters. Conclusion In the present study, levels of betatrophin are not different between obese and insulin resistant children and non-obese subjects, and they are not correlated with atherogenic indices. To elucidate the exact role of betatrophin in obesity, further studies are required to identify the betatrophin receptor and/or other possible cofactors.

Nonalcoholic fatty liver disease (NAFLD) is an important cause of liver failure. Whatever its cause, the liver failure is accompanied by multiple changes in the hemostatic system. The objective of the current report was to study several homeostasis parameters such as protein C, protein S, factor 7, factor 8 levels, platelet counts, prothrombin time and activated partial thromboplastin time, and plasminogen activator inhibitor in patients with fatty liver. A total of 28 consecutive patients with ultrasound proven NAFLD and 33 healthy volunteers were included in the study. Plasma prothrombin time and activated partial thromboplastin time were within normal ranges in both NAFLD and control groups. Plasma factor 7, factor 8, protein S, and protein C levels were decreased in NAFLD patients but the difference was not statistically significant, whereas plasminogen activator inhibitor 1 levels were significantly increased in patients with NAFLD compared to controls. In conclusion, in all types of liver disease, some alterations in hemostatic parameters are awaited. As fatty liver disease is very common in clinical practice, clinicians should be aware of this kind of alterations.

Nesfatin-1 is a recently discovered neuropeptide derived from its precursor nucleobindin-2 (NUCB2) and has been implicated in the regulation of feeding and energy metabolism. It is located in the brain and also produced at the periphery and present in the plasma. However, its pathophysiological role in humans remains unknown. Polycystic ovary syndrome (PCOS) is commonly presented with obesity, insulin resistance, hyperandrogenemia and hirsutism. To characterize serum nesfatin-1 levels in PCOS women and determine association of nesfatin-1 with metabolic parameters. It is a cross-sectional study of 55 PCOS and 28 healthy women matched in age, in a university hospital setting. Anthropometric, hormonal, metabolic parameters and nesfatin-1 blood levels were determined. Nesfatin-1 levels were significantly higher in PCOS group compared with the controls 371.43 ± 2.50 versus 275.55 ± 1.74 pg/mL. Multivariate logistic regression analysis that contains: nesfatin-1, body mass index and homeostasis model assessment index revealed significant correlation of nesfatin-1 with the existence of PCOS (p

Insulin resistance is a well-documented risk factor for the development of endometrial cancer. Adiponectin and vaspin are insulin-sensitizing proteins that are secreted from adipose tissue. A clear association between serum levels of adipokines and endometrial cancer has yet to be established. The study group consisted of postmenopausal women with confirmed endometrial cancer, whereas patients with benign endometrial conditions constituted the control group. The two groups were compared in terms of insulin resistance and serum levels of adiponectin and vaspin. A total of 60 patients with confirmed endometrial cancer and 70 controls with benign endometrial conditions (polyps and atrophy) were enrolled. Median homeostasis model assessment of insulin resistance value was significantly higher in the study group compared with the control group (2.93 vs 1.27, PPPPP=0.001) and 13.23 (2.94–59.64; P=0.001). Our results show that lower levels of circulating adiponectin and vaspin levels are associated with an increased risk of developing endometrial cancer.

Long-term organic solvent exposure may cause toxic effects in central nervous system . Trichloroethylene (TCE) is known to be one of the neurotoxic chlorinated organic solvents. Trichloroacetic acid (TCA) is an oxidative pathway metabolite of TCE. S100B, a calcium-binding protein in glial cells, and neuron specific enolase (NSE) in neuron cytoplasma are protein markers of astrocyte and neuron damage, respectively.Clinical and laboratory assesments were performed in 25 participants with organic solvent exposure history. Control group included 25 healthy age and sex-matched individuals. Measurements of serum S100B and NSE were performed using Roche Cobas E 601 compatible kits and elechtrochemiluminescence immunoassay. The levels of TCA in urine were measured by the headspace GC technique, after methyl esterification by methanol.Median value of urine TCA in solvent-exposed group was 12.30 mg/L with 10.20 mg/L and 35.00 mg/L minimum and maximum values, respectively. The difference between serum S100B levels of solvent-exposed group (0.064 μg/L) and control group (0.049 μg/L) was statistically significant (p0.05). Serum NSE levels of control group (15.61 ng/ml) were higher than solvent-exposed group (13.90 ng/ml) but difference was not statistically significant (p0.05).Serum S100B levels were found to be higher in solvent-exposed group when compared with control group. NSE levels were comparable between two groups. Increased Serum S100B levels in organic solvent exposure may indicate a preventive response to neuronal damage caused by reactive oxygen species (ROS) produced through oxidative metabolic pathways of organic solvents.

PURPOSE: To investigate hepcidin levels in each trimester and their association with other haematological variables and inflammation markers during normal pregnancy among low-risk pregnant women in rural Turkey. METHOD: The series comprised 103 healthy Turkish primigravida women with a normal pregnancy. Blood samples were obtained at 11-14, 24-28 and 30-34 weeks of gestation. Haemoglobin, hematocrit, red cell indices, white blood cell count, platelet count, iron status indicators (plasma iron, transferrin, ferritin levels and iron binding capacity), serum hepcidin, interleukin-6 and C-reactive protein levels were analysed. The proportions were compared using Pearson's ?2 test or Friedman's test. RESULTS: The mean serum hepcidin concentrations at 11-14, 24-28 and 30-34 weeks of gestation were as follows: 7.8 ± 3.4 ng/mL, 8.6 ± 3.1 ng/mL and 7.3 ± 3.0 ng/mL, respectively. The mean serum ferritin concentrations with median values at each trimester were 14.2 (11.5), 9.5 (8.8) and 11.2 (9.3), respectively. The mean serum CRP values at each trimester were 5.1 (4.0), 5.5 (4.6) and 6.0 (5.5), respectively. The serum hepcidin levels were not related to iron status or the haemoglobin, IL-6 or C-reactive protein levels. CONCLUSIONS: There was no association between serum hepcidin and serum ferritin, IL-6 or CRP concentrations in each trimester among low-risk pregnant women.

Liver biopsy, which is considered the gold standard for the evaluation of hepatic fibrosis in patients with chronic hepatitis B (CHB), has certain limitations. The aim of this study was to investigate the diagnostic performance of non-invasive markers of hepatic fibrosis as potential alternatives to liver biopsy.The medical records of 221 patients with a diagnosis of CHB who underwent a liver biopsy were reviewed. Indirect indicators of fibrosis were calculated for each patient based on previously described formulas [Aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio (AAR), age-platelet index (API), cirrhosis discriminant score (CDS), AST-platelet ratio index (APRI), Forns index, FIB-4, Pohl score, AAR-platelet score (AARP), fibro-quotient (FibroQ), AST/platelet/Gammaglutamyl transpeptidase (GGT)/Alphafetoprotein (AFP) (APGA) index, Platelet/Age/Phosphatase (ALP)/AFP/AST (PAPAS) index, Lok's model, Goteborg University Cirrhosis Index (GUCI)]. Diagnostic adequacy of these indices was evaluated by receiver operating characteristic curve analysis.Area under the receiver operating characteristic curves for the FIB-4, Forns, GUCI, APRI, PAPAS, APGA and FibroQ indices were 0.701, 0.680, 0.670, 0.670, 0.639, 0.638 and 0.588, respectively. The AAR, API, CDS and AARP indices, Pohl score and Lok's model were all deemed diagnostically inadequate. FIB-4 had the best diagnostic adequacy whereas AAR had the worst.Our results suggest that out of the 13 indices evaluated, only FIB-4 index may be useful in estimating the extent of fibrosis in patients with CHB. There is a need for more comprehensive prospective studies to help determine the diagnostic value of non-invasive tests for liver fibrosis.

The exposure of gastric mucosa to damaging factors, such as ethanol and some therapeutic drugs, produces pathological changes: inflammatory process, hemorrhagic erosions and even acute ulcers. Ankaferd blood stopper (ABS) comprises a standardized mixture of five different plant extracts. The purpose of our present investigations is to explain the participation of reactive oxygen species in acute gastric mucosal damage by acetylsalicylic acid (ASA) and the effects of new hemostatic agent ABS. Experiments were carried out on 23 male Wistar rats. To assess gastric mucosal damage, biochemical and histopathological data were used. The colorimetric assays were used to determine the malondialdehyde (MDA) and superoxide dismutase (SOD) activity. The level of myeloperoxidase (MPO) activity, the level of nitric oxide (NO) and the proinflammatory cytokine tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay technique. We demonstrated that the biological effects of ROS were estimated by measuring the tissue and plasma levels of MDA, the products of lipid peroxidation, as well as the activity of SOD and the scavenger of ROS produced by ASA in the experiment group. Moreover, it was found that MPO activity as well as NO and TNF-α levels also demonstrated significant improvement by ABS treatment. The pathogenesis of experimental ASA-induced mucosal damage in rat stomach includes the generation of ROS that seems to play an important role, due to the generation of lipid peroxides, accompanied by the impairment of antioxidative enzyme activity of cells. ABS appeared to attenuate the oxidative and inflammatory changes caused by ASA-induced gastric mucosal damage in rats.

The pathways involved in the regulation of a disintegrin and metalloproteinase with thrombospondin motifs 9 (ADAMTS9) expression have not yet been elucidated. Therefore, the aim of this study was to investigate the involvement of nuclear factor-κB (NF-κB), mitogen activated protein kinases (MAPK) and Phosphatidylinositol 3-kinase (PI3 kinase) in ADAMTS9 gene regulation, with special focus on the involvement of NF-κB in IL-1β-induced ADAMTS9 expression. The OUMS-27 chondrosarcoma cells were exposed to IL-1β. They were pretreated with 20 μM PD98059 (specific inhibitor of p44/42 kinase), 10 μM SB203580 (specific inhibitor of p38 kinase), 20 μM SB600125 (MAPK inhibitor), and 1 μM Wortmannin and 10 μM LY294002 (specific inhibitors of PI3 kinase) for 30 min and subsequently incubated with IL-1β. For the effects of NF-κB and IκB inhibitors, cells were pretreated with curcumin or BAY117085 for 30 min and subsequently incubated with IL-1β. BAY117085 and different concentrations of curcumin were applied to the cells just after the first experiment to determine their concentration effect on ADAMTS9 gene expression. After total RNA was extracted, they were reversely transcribed with random primers and then real-time polymerase chain reaction (PCR) was performed on cDNA samples. There was a significant difference between control and stimulated cells in terms of ADAMTS9/β-actin ratio. Wortmannin and LY294002 did not have any repressive effect on the OUMS-27 whereas SB203580 and SP600125 were found to decrease the expression of ADAMTS9 gene. BAY 117085 and curcumin, which are two NF-κB inhibitors, led to a decrease in the ratio of ADAMTS9/β-actin. As a conclusion, the pathways MAPK and NF-κB were thought to be responsible pathways for the induction of ADAMTS9 gene.

The aim of this study was to compare cord blood S100B levels and cord blood gas parameters of term infants with meconium-stained amniotic fluid (MSAF) to those infants with clear amniotic fluid.Term pregnant women at an active phase of labor and having MSAF were defined as the study group (n = 35) and pregnant women with clear amniotic fluid, and matched for age, parity, and gestational age were defined as the control group (n = 35). Cord blood S100B levels and gas parameters were measured.LogS100B values of study and control groups were 2.40 ± 0.21 and 2.43 ± 0.29 pg/ml, respectively. The difference was not statistically significant (p = 0.675). LogS100B levels slightly increased as meconium thickened. (2.32 ± 0.16, 2.41 ± 0.17, and 2.44 ± 0.28 pg/ml, respectively). However, no difference was found between groups (p = 0.438). Moreover, the study group had a statistically lower HCO(3) level (21.80 vs 23.60 mmol/l) and a higher rate of base deficit (4.85 vs 3.25 mmol/l) than the control group. However, median HCO(3) and base deficit values were within normal limits in both groups.The present study showed that cord blood S100B levels of infants born through MSAF were not different from those with clear amniotic fluid. This finding suggests that MSAF, regardless of its thickness, may not be related to brain damage in low risk term pregnancies.

Background Necrotizing enterocolitis (NEC) is one of the most common gastrointestinal emergencies in newborn infants but up to now there is no completely effective treatment for it. Objective In order to show that a combination of melatonin and prostaglandins may be useful to save lives, we use newborn rat as a model of necrotizing enterocolitis to test the hypothesis of using the combination therapy might have more potential effect on mucosal cytoprotection and healing. Patients and methods A total of 60 newborn pups from 5 time-mated Sprague–Dawley pregnant rats were divided equally into 5 groups as follows: NEC (subjected to NEC), NEC + Melatonin, NEC + Prostaglandin, NEC + Prostaglandin + Melatonin and control. These animals were fed with hyperosmolar formula 3 times daily and subjected to 100% CO2 inhalation for 10 min, + 4 °C cold exposure for 5 min, and 97% O2 for 5 min twice daily to induce NEC. This procedure was applied to the pups for 3 days. Results The macroscopic scoring, intestinal injury scoring and apoptosis index scoring were all found to be significantly lower in NEC + Prostaglandin + Melatonin group compared with NEC group. Anti-oxidant enzyme activities were significantly higher, whereas lipid peroxidation was significantly lower in NEC + Prostaglandin + Melatonin group compared with NEC group. Conclusion This combination therapy showed cytoprotective and healing effects on mucosa in the intestinal tissue of rat pups in necrotizing enterocolitis model. Therefore, this therapy might also show benefit in preterm infants with NEC. After confirmation of this data by other clinical and experimental studies, it may be a novel therapeutic option for the prevention of NEC in preterm infants.

The pathways involved in the regulation of a disintegrin and metalloproteinase with thrombospondin motifs 9 (ADAMTS9) expression have not yet been elucidated. Therefore, the aim of this study was to investigate the involvement of nuclear factor-κB (NF-κB), mitogen activated protein kinases (MAPK) and Phosphatidylinositol 3-kinase (PI3 kinase) in ADAMTS9 gene regulation, with special focus on the involvement of NF-κB in IL-1β-induced ADAMTS9 expression. The OUMS-27 chondrosarcoma cells were exposed to IL-1β. They were pretreated with 20 μM PD98059 (specific inhibitor of p44/42 kinase), 10 μM SB203580 (specific inhibitor of p38 kinase), 20 μM SB600125 (MAPK inhibitor), and 1 μM Wortmannin and 10 μM LY294002 (specific inhibitors of PI3 kinase) for 30 min and subsequently incubated with IL-1β. For the effects of NF-κB and IκB inhibitors, cells were pretreated with curcumin or BAY117085 for 30 min and subsequently incubated with IL-1β. BAY117085 and different concentrations of curcumin were applied to the cells just after the first experiment to determine their concentration effect on ADAMTS9 gene expression. After total RNA was extracted, they were reversely transcribed with random primers and then real-time polymerase chain reaction (PCR) was performed on cDNA samples. There was a significant difference between control and stimulated cells in terms of ADAMTS9/β-actin ratio. Wortmannin and LY294002 did not have any repressive effect on the OUMS-27 whereas SB203580 and SP600125 were found to decrease the expression of ADAMTS9 gene. BAY 117085 and curcumin, which are two NF-κB inhibitors, led to a decrease in the ratio of ADAMTS9/β-actin. As a conclusion, the pathways MAPK and NF-κB were thought to be responsible pathways for the induction of ADAMTS9 gene.

Resveratrol has a preventive potential on bleomycin-induced pulmonary fibrosis in prophylactic use; however, it was not studied in the treatment of the fibrosis. This study investigated the role of resveratrol on the treatment of bleomycin-induced pulmonary fibrosis. Intratracheal bleomycin (2.5 mg/kg) was given in fibrosis groups and saline in controls. First dose of resveratrol was given 14 days after bleomycin and continued until sacrifice. On 29th day, fibrosis in lung was estimated by Aschoft’s criteria and hydroxyproline content. Bleomycine increased the fibrosis score (3.70 ± 1.04) and hydroxyproline levels (4.99 ± 0.90 mg/g tissue) as compared to control rats (1.02 ± 0.61 and 1.88 ± 0.59 mg/g), respectively. These were reduced to 3.16 ± 1.58 (P = 0.0001) and 3.08 ± 0.73 (P > 0.05), respectively, by resveratrol. Tissue malondialdehyde levels in the bleomycin-treated rats were higher (0.55 ± 0.22 nmol/mg protein) than that of control rats (0.16 ± 0.07; P = 0.0001) and this was reduced to 0.16 ± 0.06 by resveratrol (P = 0.0001). Tissue total antioxidant capacity is reduced (0.027 ± 0.01) by bleomycine administration when compared control rats (0.055 ± 0.012 mmol Trolox Equiv/mg protein; P = 0.0001) and increased to 0.041 ± 0.008 (P = 0.001) by resveratrol. We concluded that resveratrol has some promising potential on the treatment of bleomycin-induced pulmonary fibrosis in rats. However, different doses of the drug should be further studied.

The widespread usage of blood count autoanalyzers has led to a major improvement in cellular hematology because of quick and accurate results found in most instances. However, spurious test results also can be observed like pseudothrombocytopenia (PTCP). In our study, we aimed to evaluate the clinical and laboratory factors associated with PTCP. Forty-six patients with PTCP and 69 healthy volunteers were enrolled in the study. Sex distribution was similar between the groups. Hospitalization, infection, the use of low-molecular-weight heparin and pregnancy increased the incidence of PTCP. Atherosclerosis and some drugs such as warfarin and calcium channel blockers were associated with PTCP, but the coincidence was not statistically significant. Antinuclear antibody positivity was higher in PTCP group (18.8% vs 7.2%; P=0.033) but anticardiolipin positivity rates were similar when compared to controls. Pseudothrombocytopenia was frequently misdiagnosed, which led to inappropiate treatments. Therefore, this situation should be kept in mind.

The aim of this study was to evaluate mean platelet volume (MPV), thrombopoietin (TPO), and platelet levels in patients with ischemic stroke and compare this with healthy controls.We prospectively studied 50 patients with ischemic stroke and compared them with 37 control participants who have evaluated in internal medicine polyclinic and had no history of cerebrovascular events. All patients were within 24 hours after stroke; MPV and TPO were measured on admission.Both TPO and MPV values were significantly higher in patients with stroke (P = .00; P = .001).Increased TPO levels may increase both platelet count and platelet size, resulting in more hemostatic tendency, which may contribute to the progression of ischemic stroke.

To observe thrombopoietin (TPO) levels in patients with non-alcoholic fatty liver disease (NAFLD).The study was performed between November 2010 and March 2011 at the Department of Internal Medicine, Faculty of Medicine, Fatih University, Ankara, Turkey. A total of 60 consecutive patients with ultrasound proven NAFLD (study group), and 28 healthy volunteers (control study) were included in the study. The patient group was divided into 3 subgroups according to the ultrasonographic images as follows: minimal, intermediate, and marked hepatosteatosis. The TPO levels of the patient subgroups were compared with the healthy controls. All the data were collected prospectively, and recorded in FUHIS data collecting system, which is produced by our data-knowledge team. Quantitative measurements of thrombopoietin level were carried out by using the Human Thrombopoietin Quantikine ELISA Kit (RD Systems, Minneapolis, Minnesota, USA).Thrombopoietin levels were significantly increased in the patient subgroups compared with the controls. The TPO levels were also higher in the patient subgroup of grade 1-nonalcoholic fatty liver disease (grade 1- NAFLD) compared with the control group.The TPO increased in patients with NAFLD possibly as an acute phase reactant to decreased inflammation. In clinical practice, physicians should be alerted to increased TPO levels in patients.

Aim The aim of this study is to investigate the effect of formoterol (β2 adrenergic receptor agonist) on peritoneal VEGF levels in rats with endometriosis. Materials and methods Experimental endometriosis was constituted with implantation of endometrial tissue. The implants were examined by second laparatomy and rats were divided randomly into four groups. One cc saline was applied ip to the control (C) group ( n = 8) daily, 22.5 μg/kg/day ip formoterol was applied to the second (F) group ( n = 10) daily, 22.5 μg/kg/day ip formoterol and 10 mg/kg/day ip propranolol were applied to the third (FP) group ( n = 10) daily, 45 μg/kg/day ip formoterol was applied to the fourth (FF) group ( n = 9). Before treatment and after 30 days treatment period, peritoneal VEGF levels, the volumes and histopathological properties of the implants were evaluated. Results There were significant differences in between the peritoneal VEGF levels before and after treatment in group 2(F) and group 4(FF) ( p (a): 0.01, 0.01 respectively). But there were no significant changes in between the volumes of implants before and after treatment among the groups ( p > 0.05). There were no significant differences among the groups in histopathological parameters ( p > 0.05). Conclusion Formoterol treatment was seen to have no effect on the volumes and histopathological structure of endometriotic implants in our study. On the other hand, based on the group 2(F) and 4’s (FF) VEGF levels after the treatment, low dose or high dose formoterol may be effective with long term therapy. Formoterol may reduce the development of endometriosis.

Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail. We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 m² who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium × phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD. The mean serum calcitonin was 11.5 ± 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (β = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not. Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.

Necrotizing enterocolitis (NEC) is the most common neonatal gastrointestinal emergency, predominantly affecting low-birth weight, premature infants. Early clinical signs of NEC are nonspecific and the laboratory findings are not fully reliable. Its severe morbidities and rapid progression require the application of new biomarkers for early diagnosis and intervention. The complement activation product, C5a (anaphylatoxin) has been reported to be a contributing factor leading to mesenteric ischemia/reperfusion injury which is a predisposing factor in the pathogenesis of NEC. Therefore, our aim was to evaluate the efficacy of serial C5a measurements in the diagnosis and follow-up of NEC. Preterm infants, whose gestational age and weight matched each other, were grouped as controls (n = 23) and NEC (n = 22). Serum levels of C5a, serum amyloid-A (SAA), C-reactive protein (CRP), and interleukin-6 (IL-6) levels were measured on the third day of life for the control group and on the day of diagnosis (1st day), 3rd and 7th days of the NEC group. C5a, SSA, CRP, and IL-6 levels were significantly higher in the NEC patients compared to the control group (P < 0.05) in the follow-up. Additionally, serum levels of C5a were found to be more accurate than the other parameters for the prediction of death and requirement for surgery at the time of diagnosis (P < 0.05). In conclusion, C5a may be useful as a new marker for both diagnosis and follow-up of infants with NEC in combination with clinical and radiographical findings.

The aim of this study was to evaluate the preventive effect of N-acetylcysteine (NAC) on the development of necrotizing enterocolitis (NEC) in an experimental rat model.Thirty newborn Sprague-Dawley rats were randomly divided into 3 groups: NEC, NEC + NAC, and control. Necrotizing enterocolitis was induced by enteral formula feeding, exposure to hypoxia-hyperoxia, and cold stress. Pups in the NEC + NAC group were administered NAC at a dose of 150 mg/kg daily by intraperitoneal route from the first day until the last day of the study. All pups were killed on the fifth day. Proximal colon and ileum were excised for histopathologic, immunohistochemical (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling and caspase-3, caspase-8, caspase-9), and biochemical evaluation, including xanthine oxidase, total antioxidant status, total oxidant status, malondialdehyde, and myeloperoxidase activities.The pups in the NEC + NAC group had better clinical sickness scores compared with those in the NEC group (P.05). In histopathologic and apoptosis evaluations (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling and immunohistochemical evaluation for caspase-3 and caspase-9), the severity of bowel damage was significantly less in the NEC + NAC group compared with the NEC group (P.01). Tissue malondialdehyde, myeloperoxidase, xanthine oxidase levels, and total oxidant status were significantly decreased in the NEC + NAC group, whereas total antioxidant status (TAS) was significantly increased in the NEC + NAC group (P.01).N-acetylcysteine therapy significantly reduced the severity of intestinal damage in NEC.