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In this study, we seek to determine the association between the polymorphism of the ADIPOQ (rs1501299) gene and adiponectin levels in gestational diabetes mellitus (GDM) patients.

Objective: Cadmium (Cd) is a well-known widespread environmental pollutant and is not rapidly excreted by the kidneys; instead, it accumulates and causes kidney damage. This study aimed to compare the effects of antioxidant curcumin and resveratrol on antioxidant defense in Cd-induced rat kidney tissue. Methods: In the study, 36 (200-250 gr) Wistar albino rats were divided into 6 (n=6) groups. Group 1: control; group 2: CdCl2; group 3: curcumin; group 4: CdCl2 + curcumin; group 5: resveratrol; group 6: CdCl2 + resveratrol. At the end of the experiment, malondialdehyde (MDA), total oxidant capacity (TOC), and total antioxidant capacity (TAC) activities were measured in kidney tissues. Results: In the CdCl2-treated group, oxidative stress index (OSI), TOC, and MDA levels increased compared with the control group, and TAC values decreased (p<0.05). In the case of resveratrol or curcumin administered with Cd, TAC levels increased, MDA levels, and OSI values decreased compared with the group administered only Cd (p<0.05). Conclusion: Both resveratrol and curcumin may have protective effects in the kidneys against CdCl2-induced oxidative damage. [ABSTRACT FROM AUTHOR]

Several studies have reported differences in radiation toxicity between the sexes, but these differences have not been tested with respect to histopathology and genes. This animal study aimed to show an association between histopathological findings of radiation-induced lung toxicity and the genes ATM, SOD2, TGF-β1, XRCC1, XRCC3 and HHR2. In all, 120 animals were randomly divided into 2 control groups (male and female) and experimental groups comprising fifteen rats stratified by sex, radiotherapy (0 Gy vs. 10 Gy), and time to sacrifice (6, 12, and 24 weeks postirradiation). Histopathological evaluations for lung injury, namely, intra-alveolar edema, alveolar neutrophils, intra-alveolar erythrocytes, activated macrophages, intra-alveolar fibrosis, hyaline arteriosclerosis, and collapse were performed under a light microscope using a grid system; the evaluations were semi quantitatively scored. Then, the alveolar wall thickness was measured. Real-time quantitative reverse transcription PCR (RT-qPCR) was used to determine gene expression differences in ATM, TGF-β1, XRCC1, XRCC3, SOD2 and HHR2L among the groups. Histopathological data showed that radiation-induced acute, subacute, and chronic lung toxicity were worse in male rats. The expression levels of the evaluated genes were significantly higher in females than males in the control group, but this difference was lost over time after radiotherapy. Less toxicity in females may be attributable to the fact that the expression of the evaluated genes was higher in normal lung tissue in females than in males and the changes in gene expression patterns in the postradiotherapy period played a protective role in females. Additional data related to pulmonary function, lung weights, imaging, or outcomes are needed to support this data that is based on histopathology alone. [ABSTRACT FROM AUTHOR]

In this study, the aim was to determine the production of Cu/Zn SOD (SODl) enzyme in the heart, liver, and pancreas of rats administered Homalothecium sericeum extract. The effect of the use of moss extract has not been studied for Cu/Zn SOD enzyme production in different tissues ofrats or for the cytotoxic effects on these tissues. In our study, 50 mg/kg (Group I, n: 6), 100 mg/kg (Group II, n: 6), 300 mg/kg (Group III, n: 6) and 500 mg/kg (Group N, n: 6) doses of moss extract and 1 ml of distilled water (Group V, n: 6) were administered by gavage to 30 female rats for 30 days. Cu/Zn SOD enzyme immunoreactivity was investigated in liver, heart and pancreas tissues depending on the increase in moss extract dose. To determine Cu/Zn SOD immunoreactivity, after the application of Cu/Zn SOD primary antibodies using immunohistochemical staining methods, DAP was used as coloring and hematoxylin was used as inverse dye. The stained tissue samples were evaluated with an image analysis system under the research microscope and the study used the Kruskal-Wallis Test, one of the nonparametric tests, to detect the differences between the groups statistically. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to investigate the frequency of ACE insertion/deletion (I/D) and AT1R (A1166C) gene polymorphisms in ischemic stroke patients in Trakya region and the relation between these gene polymorphisms and stroke subtypes and vascular risk factors. Patients and Methods: The study involved 162 patients with ischemic stroke and 146 control subjects. Ischemic stroke patients were divided into large and small vessel disease subgroups according to ORG 10172 in Acute Stroke Treatment TOAST criteria. The ACE I/D polymorphism was investigated using polymerase chain reaction (PCR), and the AT1R (A1166C) polymorphism was identified using PCR and restriction fragment length polymorphism (RFLP) assay. Results: The ACE I/D genotype distribution in patients (DD=34.0%, ID=50.0%, II=16.0%) did not differ from those in controls (DD=34.3%, ID=49.7%, II=16.1%). The AT1R A1166C genotype distribution in patients (AA=58.0%, CA=34.6%, CC=7.4%) did not significantly differ from those in controls (AA=60.1%, CA=35.7%, CC=4.2%). There was also no difference among the stroke subgroups regarding the distribution of ACE I/D and AT1R (A1166C) polymorphisms. Conclusion: Our results show that ACE I/D and AT1R (A1166C) gene polymorphisms were not genetic risk factors for ischemic stroke in subjects in Trakya region. [ABSTRACT FROM AUTHOR]

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The roles of many genes in the pathophysiology of lung cancer have been investigated in different studies. Cyclin D1 (CCND1) gene plays a significant role in the transition from G1 to S phase of the cell cycle and in the phosphorylation of retinoblastoma tumor suppressor protein. In this study, we aimed to identify the relationship between CCND1 A870G gene polymorphism with lung cancer. CCND1 A870G genotypes were determined in 75 patients with lung cancer and in 65 control subjects. DNA was isolated from blood samples and then CCND1 A870G gene polymorphism was identified using PCR and RFLP assay. The distribution of CCND1 A870G polymorphism did not show any significant differences in all lung cancer patients and controls. There was no correlation between CCND1 A870G polymorphism and histopathological findings. However, the AA + AG genotype was significantly higher in metastatic patients, when compared with non-metastatic patients. Thus, the results show that CCND1 gene polymorphism may be a predictor for detecting patients with poor survival who having metastatic disease.