Search

The aim of this study was to evaluate whether the Serum Netrin-1 and Urinary KIM-1 (Kidney Injury Molecule-1) levels are associated with the detection of preeclampsia. A total of 90 patients, including 36 normal pregnant women, 29 patients with nonsevere preeclampsia and 25 patients with severe preeclampsia, were included in this study. Maternal serum Netrin-1 and Urinary KIM-1 levels were measured by using an enzyme-linked immunosorbent assay (ELISA). The results showed that the Levels of Netrin-1 and KIM-1 were statistically higher in women with preeclampsia as compared with normal pregnant women. Furthermore, the Netrin-1 level in women with severe preeclampsia was significantly higher than nonsevere preeclamptic women. inconclusion the current study showed that Maternal serum level of Netrin-1 and Urinary level of KIM-1 can be used as early biomarkers for the detection of preeclampsia.IMPACT STATEMENTWhat is already known on this subject? Preeclampsia is a disorder of widespread vascular endothelial malfunction and vasospasm that occurs after 20 weeks' gestation. Netrin-1 was found to promote angiogenesis. Alteration of placental angiogenesis in early pregnancy is a well-known reason for placental dysfunction such as preeclampsia. Kidney injury with proteinuria is a characteristic feature of preeclampsia. Urine KIM-1 is the most potential biomarker for renal injury in preeclampsia. Due to these facts, we aimed to investigate the role of maternal serum Netrin-1 and Urine KIM-1 levels in preeclampsia presence and severity.What the results of this study add? A significant relationship between Netrin-1 and KIM-1 levels with preeclampsia.What the implications are of these findings for clinical practice and/or further research? Based on these findings, we concluded that increased levels of Netrin-1 and KIM-1 are associated with severe preeclampsia.

The current COVID-19 pandemic is one of the most devastating events in recent history. The respiratory effects of this disease include acute respiratory distress syndrome, systemic inflammation, cytokine storm, and pulmonary fibrosis. Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, is a peptide hormone secreted mainly by the stomach. Interestingly, ghrelin possesses promising antioxidant, anti-and inflammatory effects, making it an attractive agent to reduce the complications of the SARS-CoV-2. In addition, ghrelin exerts a wide range of immunomodulatory and anti-inflammatory effects and can mitigate the uncontrolled cytokine production responsible for acute lung injury by upregulating PPARγ and down-regulating NF-κB expression. Ghrelin has also been reported to enhance Nrf2 expression in inflammatory conditions which led to the suppression of oxidative stress. The current opinion summarizes the evidence for the possible pharmacological benefits of ghrelin in the therapeutic management of SARS-CoV-2 infection.

Summary Introduction Testicular torsion is a common urologic emergency and one of the causes of infertility in males. Hence, prompt diagnosis and treatment are important to prevent testicular damages. It has been reported that memantine, a drug for Alzheimer's disease has anti-oxidative role against cerebral ischemic stroke and cardiac ischemia reperfusion. Objective In this experimental study, the effects of memantine on a testicular torsion injury in adolescent rat testis after ischemia/reperfusion (I/R) were evaluated. Study design Thirty-six adolescent rats were divided into three groups with 12 rats per group including sham-operated, T/D (torsion/detorsion) + vehicle, and T/D + memantine (10 mg/kg). Testicular torsion was induced for 2 h by rotating right testis 7200 in the clockwise direction. In treated group 30 min before detorsion, a single intraperitoneal dose of memantine was administered. After 4 h of reperfusion, orchiectomy was conducted and Histopathological and biochemical evaluations of testicular tissue samples were performed. Results The malondialdehyde level in the T/D group was significantly greater than in the sham operated group. Moreover, the testicular malondialdehyde values in the T/D + memantine group were significantly lower than in the T/D group. Also, significant decreases occurred in catalase and superoxide dismutase activities in the T/D group compared with sham operated group. These values were significantly greater in the memantine group than in the T/D group. Furthermore, after induction of T/D, histopathological evaluations also revealed severe testicular damages which were improved by memantine administration. Discussion Memantine prevented increases in oxidative stress markers and reductions of antioxidants during I/R injury in the current study. Subsequently the histologic injury was reduced in rats treated with memantine. The antioxidant characteristics of memantine and its protective effects have been shown in our study. Conclusion These results suggest that administration of memantine before detorsion prevents I/R cellular damage in testicular torsion. This drug probably acts through reduction of reactive oxygen species and support antioxidant enzyme systems. Download : Download high-res image (308KB) Download : Download full-size image Summary Figure . Administration of memantine before detorsion ameliorates the oxidative stress and decreases the histologic damage that occurs after testicular torsion.

Background Low maternal vitamin D status has been associated with several adverse outcomes during pregnancy. The aim of the study was to evaluate the vitamin D levels in preeclamptic and healthy pregnant women and the role of vitamin D deficiency in the etiology of preeclampsia. Methods In this case-control study, 80 preeclamptic women and 80 healthy pregnant women were selected from Motahari hospital in Urmia, Iran. 2 ml of venous blood sample was collected from each pregnant woman and the serum 25-OH-D level was measured by Enzyme-Linked Immunosorbent Assay (ELISA) and reported in nanograms per milliliter. levels of 25-OH-D less than 10 ng mL−1, between 10 ng mL−1 and 29 ng mL−1 and more than 30 ng mL−1, were considered as deficient, insufficient and normal 25-OH-D concentrations, respectively. Results were analyzed by independent t-test, Mann-Whitney U test, and logistic regression. Results Preeclamptic women (n = 80) were noted to have decreased total 25-OH-D levels relative to healthy control women (n = 80; P = 0.01). This difference in total 25-OH-D remained significant after control for potential confounders [odds ratio (OR) = 4.79, confidence interval (CI) = 1.45–9.87, P = 0.01]. Conclusion These results showed that vitamin D deficiency has a statistically significant relationship with preeclampsia and support the hypothesis that vitamin D deficiency may be a risk factor for preeclampsia.

The study was designed to evaluate the effects of metformin on apoptosis and epididymal sperm quality in a rat testicular ischaemia/reperfusion (I/R) injury model. A total of 72 male rats were divided into four groups (n = 18 for each group): group 1 (sham-operated group), group 2 (metformin group), group 3 (torsion/detorsion [T/D] + saline) and group 4 (T/D + 300 mg kg-1 metformin). Testicular torsion was achieved by rotating the right testis 720° in a clockwise direction for 1 hr. Tissue malondialdehyde (MDA) level and caspase-3 activity increased and the activities of catalase, superoxide dismutase and glutathione peroxidase decreased in comparison with sham-operated group 4 hr after detorsion (p < .001). In six rats of each group 24 hr after detorsion, histopathological changes and germ cell apoptosis were significantly deteriorated by measuring mean of seminiferous tubule diameters (MSTD) and TUNEL test. Moreover, 30 days after T/D, sperm concentration and motility were examined in six animals per group. Metformin pre-treatment reduced MDA and caspase-3 levels and normalised antioxidant enzyme activities 4 hr after detorsion, and germ cell apoptosis was significantly decreased, and the MSTD, as well as sperm functions, was significantly improved. Reduction in oxidative stress and apoptosis may have a major role in cytoprotective effects of metformin.