Pre- and post-treatment of α-Tocopherol on cognitive, synaptic plasticity, and mitochondrial disorders of the hippocampus in icv-streptozotocin-induced sporadic Alzheimer’s-like disease in male Wistar rat

ObjectiveMost dementia cases in the elderly are caused by Alzheimer’s disease (AD), a complex, progressive neurological disease. Intracerebroventricular (ICV) administration of streptozotocin (STZ) in rat’s results in aberrant brain insulin signaling, oxidative stress, and mitochondrial dysfunction that impair cognition change neural plasticity, and eventually lead to neuronal death. The current study aims to define the neuroprotective action of alpha-tocopherol in enhancing mitochondrial function and the function of synapses in memory-impaired rats brought on by icv-STZ.MethodsMale Wistar rats were pre-treated with (α-Tocopherol 150 mg/kg) orally once daily for 7 days before and 14 days after being bilaterally injected with icv-STZ (3 mg/kg), while sham group rats received the same volume of STZ solvent. After 2 weeks of icv-STZ infusion, rats were tested for cognitive performance using a behaviors test and then were prepared electrophysiology recordings or sacrificed for biochemical and histopathological assays.ResultsThe cognitive impairment was significantly minimized in the behavioral paradigms for those who had taken α-Tocopherol. In the hippocampus of icv-STZ rat brains, α-Tocopherol ocopherol effectively prevented the loss of glutathione levels and superoxide dismutase enzyme activity, lowered mitochondrial ROS and mitochondrial membrane potential, and also brought about a decrease in Aβ aggregation and neuronal death.ConclusionOur findings demonstrated that by lowering neurobehavioral impairments caused by icv-STZ, oxidative stress, and mitochondrial dysfunction, α-Tocopherol enhanced intracellular calcium homeostasis and corrected neurodegenerative defects in the brain. These findings examine the available approach for delaying AD connected to mitochondrial malfunction and plasticity issues

Cognitive Impairments Induced by Repeated Sevoflurane Exposure During Pre-adolescence in Adult Male and Female Rats: Involvement of Biochemical, Histological and Neuroplasticity Approaches

Background: In some therapeutic interventions, repeated exposure to pre-adolescence anesthesia is necessary. According to research, exposure to general anesthetics during pre-adolescence can lead to cell death, cognitive and behavioral problems, and neurobehavioral difficulties as an adult. The current study aimed to provide detailed morphological and functional evaluations of the long-term impacts of repeated sevoflurane exposure in male and female rats. Materials and Methods: Seventy-two pre-adolescent rats were randomly divided into male and female control and inhaled sevoflurane groups (concentration of 2%) daily for 15 days. Animals received care for 20-30 days. The influence of repeated exposure to sevoflurane on cognitive functions was tested using the Morris Water Maze, novel object, and social interaction tests. As a measure of oxidative stress, superoxide dismutase (SOD) and glutathione levels were measured. Toluidine blue stain was utilized to evaluate the number of dark neurons in the hippocampus. Effects of sevoflurane on synaptic plasticity were compared in the performant pathway of the CA1 of the hippocampus. Results: Repeated sevoflurane exposure in pre-adolescence led to behavioral disorders in male and female adult rats; there was no significant difference in levels of superoxide dismutase and glutathione. We found a significant quantifiable increase in dark neurons. Electrophysiological recordings indicated impaired long-term potentiation and pair-pulse in adult animals that received repeat sevoflurane exposure. Conclusion: According to our findings, repeated exposure to sevoflurane during pre-adolescence can cause changes in the hippocampus and neuroplasticity in the adult brain. Results from this study may provide a new perspective on how repeated exposure to anesthesia can lead to toxic effects in pre-adolescent rats

A comparison of pre-pregnancy BMI and gestational weight gain on gestational diabetes mellitus in pregnant women referred to Asali hospital in 91-92

Background: In addition to adequate nutrition and balance of nutrients in the pregnant mother's diet, maternal weight gain during pregnancy has a major impact on maternal health and fetal well-being. The purpose of this study was to compare pre-gestational BMI and gestational weight gain on GDM according to the new definition of GDM. Materials and Methods: This descriptive cross-sectional study was carried out on 18 to 35 years old pregnant women with no underlying disease using convenience sampling method In the first months of pregnancy, women's height, weight and blood pressure as well as FBS were measured.The second assessment was done in the 24th-28th weeks of gestation using repeated measurements of weight, blood pressure, and gestational diabetes screening test (GCT). The third evaluation was conducted at the end of pregnancy to measure mother and infant weight.The data was analyzed by SPSS, version 16, t-test and Mann-Whitney test. Results: In this study, 600pregnant women were evaluated.Mean BMI befor pregnancy in the women with GDM was significantly higher than in the women without the above-mentioned problems(P=0.0001). The mean weight gained during pregnancy in the women with these symptoms was significantly higher than that in the women without the above –mentioned problems(P=0.039)(P=0.0001). Compared to pre-pregnancy BMI, weight gain during pregnancy had a higher with GDM(0.278 vs 0.077). Conclusion: Pre-pregnancy BMI in comparison with weight gain during pregnancy, had a higher correlation with GDM and macrosomi

Frequency of positive results of vibroacoustic stimulation test in evaluating fetus health of pregnant women with non-reactive NST

Background : Non-Stress Test (NST) is one of the most common methods used to evaluat fetus health, which its results are presented as reactive and non-reactive. One of the limitations of this test is the high number of false non-reactive cases. Different studies have suggested a combination of vibroacoustic stimulation and NST to reduce the number of non-reactive cases and duration of the test. Materials and Methods: The present study examined a group of tests, and used simple randomized sampling. The number of the sample was 55 individuals and the data collection tools were NST, sonography instruments, NST result paper, a tooth brusher, a watch, a demographic questionnaire, and a checklist. Vibroacoustic stimulation with an electronic brush was performed on fetus head situated on mother’s abdomen for 3 seconds and then NST was continued for a further 20 minutes. Then the results were recorded. The obtained data were gathered by SPSS 19 software, and analyzed using descriptive statistics. Results: In this study, 85.5% of the non-reactive cases changed into reactive through vibroacoustic stimulation. The amount of false positive was lower with vibroacoustic stimulation in comparison with NST. Conclusion: Vibroacoustic stimulation, as a technique for evaluating fetus health, makes it possible to save time, costs and personnel. It is also leads to sooner and better diagnosis of fetus health

Opioid Use Disorder Induces Oxidative Stress and Inflammation: The Attenuating Effect of Methadone Maintenance Treatment

Objective: Frequent use of opioids produces reactive oxygen species, upregulates inflammatory factors, and contributes to opiate dependence. In this study, we examined perturbations of plasma oxidative and inflammatory markers in patients with opioid use disorder in two phases. In the first phase, we compared the oxidative status in patients with opioid use disorders and in healthy controls; and in the second phase, we examined oxidative changes before and after methadone maintenance treatment. Method: To explore whether oxidative changes were associated with opioid use disorder, we compared plasma oxidative and inflammatory markers in patients with opioid use disorder and in smoking and non-smoking healthy participants. All participants completed measures of catalase (CAT), glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), matrix metalloproteinase (MMP-9), and TNF-α at baseline. Baseline measures were compared using Kruskal-Wallis test. In the second phase, to explore oxidative changes during transition from opium use to methadone, blood and urine samples of patients with opioid use disorder were re-evaluated on Days 3, 7, and 14 after methadone therapy. Repeated measures analysis was used to determine the relative contribution of intervention to changes in CAT, GSH, MDA, SOD, MMP-9, and TNF-α level over time. Results: We observed lower SOD and catalase activities, and higher TNF-α and MMP-9 level in patients compared to the two comparison groups. Opioids exacerbated the oxidative imbalance and superimposed the underlying oxidative injury in smoker comparison group. Methadone therapy was associated with lower MMP-9 and TNF-α level, and higher SOD and catalase activities two weeks after therapy; showing an improvement in oxidative profile. Conclusion: This was an investigation indicating an oxidative imbalance before methadone therapy and during early days of transition from opium use to methadone. Being aware of redox status is crucial for determining an appropriate antioxidant therapy in opioid use disorder