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Objective Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine and metabolic disorder characterized by hyperandrogenism, hyperinsulinemia, and insulin resistance. The prevalence of PCOS is increasing worldwide. Although the etiology of this disease is currently unknown, it is thought to be closely related to inflammation and oxidative stress. Our study aimed to compare patients have PCOS to healthy volunteers and assess the changes in oxidative stress and inflammatory parameters in these patients. Methods Thirty patients between the ages of 18-45 diagnosed with PCOS and 30 healthy volunteers with the same demographic characteristics were included in this study. Clinical parameters were measured using immunoassays. Oxidative stress biomarkers, total oxidant (TOS), total antioxidant (TAS), total thiol (TT), and native thiol (NT) levels were measured using photometric methods according to Erel’s method. The dynamic disulfide level (DIS) and oxidative stress index (OSI) were calculated using mathematical equations. Among the inflammatory parameters, values for interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) were measured photometrically using commercially purchased kits. Results Moreover, TT and NT levels were lower in patients with PCOS compared to those in the healthy group statistically significantly (P

Abstract Major depressive disorder (MDD) is a debilitating illness that includes depressive mood. Repetitive Transcranial Magnetic Stimulation (rTMS) is a therapy method used in the treatment of MDD. The purpose of this study was to assess neurotrophic factors, and oxidative stress levels in MDD patients and evaluate the changes in these parameters as a result of rTMS therapy. Twenty-five patients with MDD and twenty-six healthy volunteers with the same demographic characteristics were included in the study. Brain-derived neurotrophic factors were measured photometrically with commercial kits. Oxidative stress parameters were measured by the photometric method. Oxidative stress index (OSI) and disulfide (DIS) levels were calculated with mathematical formulas. In this study, total antioxidant status (TAS), total thiol (TT), and native thiol (NT) antioxidant parameters and brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and allopregnanolone (ALLO) levels were reduced in pre-rTMS with regard to the healthy control group; TOS, OSI, DIS, and S100 calcium-binding protein B (S100B) levels were increased statistically significantly (p

Background: Rosacea is a chronic progressive inflammatory disease and characterized by facial erythema, telangiectasias, papules, and pustules. The disease is more common in women than in men while affecting 2%-10% of the population. Though the pathogenesis of rosacea is not fully understood, oxidative stress is one of the asserted pathogenic factors. In this study, we purposed to assess the oxidative stress and thiol-disulfide homeostasis (TDH) in rosacea disease. Materials and Methods: Forty patients with rosacea and 40 healthy people as a control group, both in ages of 18-70 years, with the same demographic characteristics were included, who were applied to the Istanbul Training and Research Hospital Dermatology Clinic. Serum total antioxidant status (TAS), total oxidant status (TOS), total thiol (TT), and native thiol (NT) levels were evaluated by using the automated and spectrophotometric method according to Erel and Neselioglu. Oxidative stress index (OSI), disulfide (DIS) levels, and NT/TT, DIS/TT and DIS/NT percentages were calculated mathematically. Results: TAS, TT, and NT levels were decreased in rosacea patients compared with the healthy group, whereas TOS, OSI, and DIS levels were increased. Additionally, although DIS/TT and DIS/NT percentages were higher in patients, NT/TT ratio was lower than the healthy group, and these findings were statistically significant (p < 0.001). Conclusion: The results showed that oxidative stress levels were increased in rosacea patients and TDH shifted toward DIS formation. It has been thought that oxidative stress is a parameter that may be utilized in the clinical evaluation of the disease. [ABSTRACT FROM AUTHOR]

We seek to demonstrate the variations in the exchange rate pass-through (ERPT) and identify the shift in the price-setting behavior by placing the emphasis on the implemented exchange rate and monetary policy regimes. Having a history of several distinct monetary regimes, Turkey exhibits a genuine laboratory in this respect. Our empirical results reveal that the pass-through from exchange rates to domestic prices has changed dramatically. We detect breaks in the pass-through coefficients at three episodes, all of which coincide with a shift in monetary/exchange rate regime, lending support to the view that monetary and exchange rate regimes might be among the major determinants of the ERPT process. (JEL C51, E31, E58), I. INTRODUCTION Understanding and quantifying the impact of exchange rate shocks on the domestic prices has always been of interest to both academicians and the central banks. The fact that [...]

The correlation between the success of Turkish football team Fenerbahce and the country's industrial performance is discussed. The success of the football team has a positive effect on the mood and morale of the workers resulting in increased productivity.

The primary objective of this in vitro study was to prevent the risk of toxicity associated with bupivacaine, widely used in clinical practice, by using magnesium (Mg), a readily available and cost-effective element, as an adjuvant. We hypothesized that Mg might exhibit a protective effect against cytotoxicity in a colon cell culture model under conditions of bupivacaine-induced LAST. Our secondary aim was to investigate its effect on genotoxicity, apoptosis, and iROS. CCD-18Co cells were used in our study. Control group (group C), Bupivacaine group (group B), Magnesium group (group M), and Bupivacaine+Mg group (group BM) were created. The viability of CCD-18Co cells incubated for 24 h in group C was determined to be 100%. These cells were evenly divided, and bupivacaine was administered to group B at concentrations of 5 to 300 μM. In group M, doses of Mg at 0.625 to 320 mEq were added. It was determined that the maximum viability was observed at a Mg dose of 40 mEq (p < 0.05). In group BM, bupivacaine was administered at the same concentrations in combination with Mg (40 mEq), and cell viability was measured. DNA damage, apoptosis, and iROS were assessed at concentrations of bupivacaine by administering 40 mEq Mg. In group B, viability decreased dose-dependently in CCD-18Co (p < 0.05, p < 0.01, p < 0.001). In group BM, the viability decreased in cells at increasing concentrations compared to group C (p < 0.05, p < 0.01, p < 0.001), but the viability was affected positively compared to group B (p < 0.05). In group B, DNA damage increased (p < 0.05, p < 0.001). In group BM, DNA damage increased (p < 0.05, p < 0.001). However, in group BM, DNA damage levels were reduced compared to group B (p < 0.05, p < 0.01). In group B, apoptosis increased (p < 0.05, p < 0.001); in group BM, apoptosis increased (p < 0.001) compared to group C. However, in group BM, apoptosis decreased compared to group B (p< 0.05). iROS increased in group B (p < 0.05, p < 0.01, p < 0.01) and group BM (p < 0.05, p < 0.01, p < 0.001) compared to the group C. However, in group BM, iROS decreased in comparison to group B (p < 0.05). In conclusion, Mg exhibits a protective effect against bupivacaine-induced toxicity.

Objective:Breast cancer (BC) remains to be one of the most diagnosed cancer types among women around the world. Drug repurposing is suggested to be a convenient alternative for drug development in cancer treatment. Ivermectin, the antiparasitic agent produced by the bacterium Streptomyces avermitilis, is currently being examined thoroughly in oncology and has begun to be seen as a potential drug candidate for BC therapy. However, studies are limited, and the exact anti-tumorigenic mechanism is not yet clarified in breast cancer.Methods:For elucidating the molecular mechanisms of Ivermectin’s potential anticancer effects, we have examined its in vitro effects on BC cells in terms of cell viability, intracellular ROS levels, glutathione levels, mitochondrial membrane potential, apoptosis, and DNA damage.Results:Ivermectin induces apoptosis via oxidative stress and DNA damage in BC cells.Conclusion:The in vitro mechanistic studies of promising anticancer agents for repurposing are essential guides for drug developers. For this purpose, ivermectin should be further studied as a drug candidate for its potential in the treatment of breast cancer.

Atherosclerosis is a chronic vascular inflammatory disease associated to oxidative stress and endothelial dysfunction. It is characterized by lipid accumulation in the arterial wall, increased hyperlipidemia, oxidative stress, lipid peroxidation, and protein oxidation. Our study included 45 patients ages of 40–60 and 45 healthy volunteers with similar demographic characteristics without any chronic disease as well. Fasting plasma glucose, BUN, creatinine, LDL-cholesterol, HDL-cholesterol, triglyceride, total cholesterol, HbA1c, and C-reactive protein (CRP) levels were measured using commercial kits by autoanalyzer. The oxidative stress biomarkers total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), native thiol (NT), catalase (CAT), paraoxonase (PON1), and arylesterase (ARES) enzyme activities were measured using photometric methods. The inflammatory biomarkers interleukin 1 beta (IL-1β), tumor necrosis factor-α (TNF-α), presepsin (PSPN), and raftlin (RFTN1) levels were measured with ELISA Kits. Oxidative stress index (OSI) and disulfide (DIS) were calculated. The clinical, biochemical biomarkers such as BUN, creatinine, HDL, LDL, total cholesterol, triglyceride, and CRP levels were found to be higher than the control group and lower post-treatment compared to the pre-treatment group (p

The impairment of skin integrity derived from derangement of the orthorhombic lateral organization is mainly caused by dysregulation of ceramide amounts in the skin barrier. Ceramides, fatty acids, and cholesterol-containing nano-based formulations have been used to impair the skin barrier. However, there is still a challenge to formulate novel formulations consisting of ceramides due to their chemical structure, poor aqueous solubility, and high molecular weight. In this study, the design and optimization of Ceramide 3 (CER-NP)-loaded liposomes are implemented based on response surface methodology (RSM). The optimum CER-NP-loaded liposome was selected based on its particle size (PS) and polydispersity index (PDI). The optimum CER-NP-loaded liposome was imagined by observing the encapsulation by using a confocal laser scanning microscope (CLSM) within fluorescently labeled CER-NP. The characteristic liquid crystalline phase and lipid chain conformation of CER-NP-loaded liposomes were determined using attenuated total reflectance infrared spectroscopy (ATR-IR). The CER-NP-loaded liposomes were imagined using a field emission scanning electron microscope (FE-SEM). Finally, the in vitro release of CER-NP from liposomes was examined using modified Franz Cells. The experimental and predicted results were well correlated. The CLSM images of optimized liposomes were conformable with the other studies, and the encapsulation efficiency of CER-NP was 93.84 ± 0.87%. ATR-IR analysis supported the characteristics of the CER-NP-loaded liposome. In addition, the lipid chain conformation shows similarity with skin barrier lipid organization. The release pattern of CER-NP liposomes was fitted with the Korsmeyer–Peppas model. The cytotoxicity studies carried out on HaCaT keratinocytes supported the idea that the liposomes for topical administration of CER-NP could be considered relatively safe. In conclusion, the optimized CER-NP-loaded liposomes could have the potential to restore the skin barrier function.

Objective: Hypertension is a multi-factorial process prevalent in developed as well as in developing countries. Urotensin-II, different antioxidants, free radicals, and inflammatory biomarkers play an essential role in the cardiovascular system. The aim of this study is to investigate Urotensin-II, oxidative stress, and inflammation markers in normotensive, hypertensive, and resistant hypertensive patients. Methods: Fifty resistance hypertensive (rHT) patients, 50 hypertensive patients, and 50 age gender matched normotensive controls (NT-control) were enrolled. Urotensin-II (UII), total oxidant status (TOS), total antioxidant status (TAS), native thiol (NT), total thiol (TT), disulfide (DIS), interleukin 1 beta (IL1β), interleukin 6 (IL6), tumor necrosis factor-alpha (TNFα), high sensitive c reactive protein (hsCRP), high-density lipoprotein (HDL) low-density lipoprotein (LDL), and total cholesterol (TC) were evaluated. Results: Serum levels of UII, IL1β, IL6, TNFα, DIS, TOS, and OSI were found higher in rHT and HT as compared to NT-control (p

Glioblastoma, as an invasive tumor, is one of the most common primary malignant brain tumors. Despite maximum aggressive treatment, patients with glioblastoma have a dismal prognosis. Thymoquinone (TQ) has been found to show anti-cancer effects on different types of cancer. There are a few in vitro studies on the effect of TQ on glial tumors. However, the molecular mechanism of TQ's anti-cancer effect has not been fully elucidated. In the present study, we aimed to investigate the genotoxic, apoptotic, and cytotoxic effects of TQ on C6 rat glioma cells.C6 glioma cells were analyzed after 24 h of exposure to different concentrations of TQ by the ATP cell viability assay for cytotoxicity, comet assay for genotoxicity, 2′,7′dichlorodihydrofluorescein diacetate (H2DCF-DA) for intracellular reactive oxygen species (iROS) generation, 3.3′dihexyloxacarbocyanine iodide (DiOC6(3)) for mitochondrial membrane potential, GSH/GSSG-Glo Assay for glutathione level and Fura-2AM for intracellular calcium levels. Apoptosis induction was studied by acridine orange/ethidium bromide double staining, flow cytometry, and western blotting analyses. Caspase-3, Caspase-9, Bax, Bcl-2, and pSTAT3 protein levels were determined by the western blotting method.Cytotoxicity was enhanced by TQ in C6 glioma cells in a concentration-dependent manner. TQ also induced DNA damage, apoptosis, and increased iROS. Also, MMP and GSH levels were decreased by TQ. It inhibited pSTAT3, resulting in apoptosis induction through the regulation of anti-apoptotic and pro-apoptotic proteins.Our results suggest that TQ would be an effective treatment in glioma. Further studies should support these findings.