Relationship between dietary virgin olive oil on brain cholesterol, cholesteryl ester and triglyceride levels and blood brain barrier (BBB) permeability in a rat stroke model

Introduction: Recent studies suggest that dietary virgin olive oil (VOO) reduces hypoxia-re oxygenation injury in rat brain. We have attempted to determine the effect of dietary virgin olive oil on brain lipidomics and its relationship with brain edema in a rat stroke model. Methods: Five groups, each consisting of 6 male Wistar rats, were studied. The first and second groups (control and sham) received distilled water, while three treatment groups received oral VOO for 30 days (0.25, 0.5 and 0.75 ml/kg/day, respectively). Two hours after the last dose, each main group was subdivided into middle cerebral artery occlusion (MCAO)-operated and intact subgroups for assessment of neuropathology (blood brain barrier permeability) and brain lipid analysis. Results: VOO increased the brain cholesteryl ester and cholesterol levels in doses of 0.5 and 0.75 ml/kg/day. VOO in all three doses increased the brain triglyceride levels (p<0.05). Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, after transient MCAO in rats. Conclusion: Although further studies are needed to clarify the mechanisms of ischemic tolerance, VOO is partly associated with increased levels of brain cholesteryl ester, cholesterol and triglyceride in rats

Neuroprotection of Dietary Virgin Olive Oil on Brain Lipidomics During Stroke

Recent studies suggest that dietary virgin olive oil reduces hypoxia-reoxygenation injury in rat brain. This study investigated the effect of pretreatment with different doses of dietary virgin olive oil on brain lipidomics during stroke. In this experimental trial, 60 male Wistar rats were studied in 5 groups of 12 each. The control group received distilled water while three treatment groups received oral virgin olive oil for 30 days (0.25, 0.5 and 0.75 ml/kg/day respectively). Also the sham group received distilled water. Two hours after the last dose, the animals divided two groups. The middle cerebral artery occlusion (MCAO) group subjected to 60 min of middle cerebral artery occlusion (MCAO) and intact groups for brain lipids analysis. The brain phosphatidylcholine, cholesterol ester and cholesterol levels increased significantly in doses of 0.5 and 0.75 ml/kg/day compare with control group. VOO in all three doses increased the brain triglyceride levels. VOO with dose 0.75 ml/kg increased the brain cerebroside levels when compared with control group. VOO pretreatment for 30 days decreased the brain ceramide levels in doses of 0.5 and 0.75 ml/kg/day (p<0.05). Although further studies are needed, the results indicate that the VOO pretreatment improved the injury of ischemia and reperfusion and might be beneficial in patients with these disorders and seems to partly exert their effects via change in brain lipid levels in rat

Investigating the Effect of Pretreatment with Oxygen on Inhibition of Gentamycin-induced Nephrotoxicity in Rats

Introduction: The toxicity of gentamycin in the kidney seems to be related to the generation of reactive oxygen species (ROS). There is evidence that pretreatment with oxygen increases the rate and activity of antioxidant enzymes. Methods: In this experimental study, forty eight female rats (Sprague Dawlley) were divided into 6 groups randomly (8 in each) as follows: group 1 was the control and for other groups different doses of oxygen with Gentamycin was used for 8 days intra-peritoneally (100 mg/kg ). 24-hour urine samples were collected after the final injection. Blood samples were collected and serum was prepared. The left kidney was fixed in formal saline. Serum MDA, creatinin and urea, as well as urine creatinine were measured. 5-micron tissue sections were prepared and stained by Periodic Acid Shift method. Volume density of proximal tubules, necrosis of proximal tubules and lymphocytic infiltration were studied. The data were analyzed by Mann-Whitney test at significant level of p <0.05. Results: Pretreatment with oxygen was effective significantly in two groups of 6 and 4 compared to group 2. The effectiveness was found in inhibition of serum MDA, improving serum, urinary urea and creatinine, preserving tubular volume density, and reducing tubular necrotizing and lymphocyin filtration. Conclusion: Pretreatment with oxygen and its concomitant use can improve renal tissue changes, serum urea and creatinine in gentamycin-induced nephrotoxicity, but cannot preserve them at the same level of control

Core and biological motif of self-assembling peptide nanofiber induce a stronger electrostatic interaction than BMP2 with BMP2 receptor 1A

Recent studies suggest that nanotopography can trigger colocalization of integrins and bone morphogenetic protein 2 (BMP2) receptors (e.g., BMPR1A), thereby leading to osteogenesis. In this study, the bone marrow homing peptide 1 (BMHP1) motif was bound to a self-assembling peptide core to form a hydrogel-based nanofiber (R-BMHP1). The docking and molecular dynamic study revealed that the R-BMHP1 sequence induced a stronger electrostatic interaction than BMP2 through arginines in the RADA core sequence and through lysine24 in the BMHP1 motif with BMPR1A. Notably, decrease of polar solvation binding energy will enhance the total binding energy and increases bone regeneration even more than BMP2 The enhanced osteogenesis and bone repair potential of R-BMHP1 nanofiber might be related to its chemical interaction with BMPR1A, which triggered downstream signal transduction through osteogenic genes overexpression in osteo-differentiated mesenchymal stem cells (MSCs), as well as implanted critical-sized bone defects in rats. Following that, calcium deposition occurred by osteoblast-like cells, ALP activity increased in osteodifferentiation MSCs and rat serum, and calcium density improved in bone defects (X-ray). The nanofiber was biocompatible and enhanced the cell viability of MSCs, without multinuclear cell infiltration into the defect site. Taking everything into account, not only does nanotopography induce osteogenesis through colocalization of BMPRs and integrins, but also R-BMHP1 nanofibers (considering their chemical structure) induce cell proliferation, osteogenesis, and bone repair through strong electrostatic interaction with BMPR1A and downstream signaling. The entire outcome of this study manifests the plausibility of R-BMHP1 for spine and spinal cord injury repair. © 201

Effectiveness of meta-cognitive and cognitive-behavioral therapy in patients with major depressive disorder

Objective: The present study aimed to compare the effectiveness of metacognitive therapy (MCT) and cognitive-behavior therapy (CBT) in treating Iranian patients with major depressive disorder (MDD). Methods: Thirty three outpatients meeting DSM-IV-TR criteria for MDD without any other axis I and II disorders were randomly assigned to one of three treatment conditions, i.e. MCT, CBT and pharmacotherapy. The Beck Depression Inventory-II-Second Edition (BDI-II), Beck Anxiety Inventory (BAI), Ruminative Response Scale (RRS) and Dysfunctional Attitude Scale (DAS) were administered for pre-treatment, posttreatment and follow-up. Data were analyzed by repeated measures analysis of variance (ANOVA). Results: Based on repeated measures ANOVA, all the participants demonstrated improvement in depression, anxiety, dysfunctional attitude and ruminative response. Based on percentage results, all the patients in MCT and CBT groups showed significant improvement at post-treatment phase. Conclusions: MCT and CBT were more effective than pharmacotherapy alone In treatment of MDD

Core and biological motif of self-assembling peptide nanofiber induce a stronger electrostatic interaction than BMP2 with BMP2 receptor 1A

Recent studies suggest that nanotopography can trigger colocalization of integrins and bone morphogenetic protein 2 (BMP2) receptors (e.g., BMPR1A), thereby leading to osteogenesis. In this study, the bone marrow homing peptide 1 (BMHP1) motif was bound to a self-assembling peptide core to form a hydrogel-based nanofiber (R-BMHP1). The docking and molecular dynamic study revealed that the R-BMHP1 sequence induced a stronger electrostatic interaction than BMP2 through arginines in the RADA core sequence and through lysine24 in the BMHP1 motif with BMPR1A. Notably, decrease of polar solvation binding energy will enhance the total binding energy and increases bone regeneration even more than BMP2 The enhanced osteogenesis and bone repair potential of R-BMHP1 nanofiber might be related to its chemical interaction with BMPR1A, which triggered downstream signal transduction through osteogenic genes overexpression in osteo-differentiated mesenchymal stem cells (MSCs), as well as implanted critical-sized bone defects in rats. Following that, calcium deposition occurred by osteoblast-like cells, ALP activity increased in osteodifferentiation MSCs and rat serum, and calcium density improved in bone defects (X-ray). The nanofiber was biocompatible and enhanced the cell viability of MSCs, without multinuclear cell infiltration into the defect site. Taking everything into account, not only does nanotopography induce osteogenesis through colocalization of BMPRs and integrins, but also R-BMHP1 nanofibers (considering their chemical structure) induce cell proliferation, osteogenesis, and bone repair through strong electrostatic interaction with BMPR1A and downstream signaling. The entire outcome of this study manifests the plausibility of R-BMHP1 for spine and spinal cord injury repair. © 201

Investigation of Vestibular Aqueduct in High-Resolution CT Scan in Patients with Otosclerosis

Background and Objective: Otosclerosis is caused by abnormal bone remodeling in the middle ear, which is associated with dizziness and lightheadedness. An underlying cause of dizziness in this disease can be the presence of an enlarged vestibular aqueduct. In this study, the prevalence of enlarged vestibular aqueduct in these patients compared to the normal population has been investigated. Methods: In this cross-sectional study, 26 people with bilateral otosclerosis and 26 people with at least one healthy ear requiring a CT scan were compared. Vestibular aqueduct was tested by evaluating the two factors of the midpoint width between the external diaphragm and the common crus, and its width in the external diaphragm region and comparing the two groups. Bone conduction, speech detection threshold, and gap between bone conduction and air conduction were calculated and compared in otosclerosis patients with enlarged versus normal vestibular duct. Findings: The median width of the vestibular aqueduct in the area of the external aperture in patients with otosclerosis (1.2 mm) was significantly greater than that of healthy subjects (1 mm) (p=0.046). Regarding the size of the vestibular aqueduct in otosclerosis patients, 5 patients (9.6%) were found with enlarged vestibular aqueduct in radiological findings. However, this difference was not statistically significant. In otosclerosis patients, bone conduction threshold in all frequencies was significantly higher in people with enlarged vestibular aqueduct compared to other patients (p<0.001). Conclusion: Based on the results of this study, the prevalence of enlarged vestibular aqueduct in patients with otosclerosis is considerable, and it is better to pay enough attention to the CT scan of patients before surgery to prevent possible complications

The Effects of Pretreatment with Various Doses of L-Arginine on Cisplatin-Induced Nephropathy of Male Rats

Introduction: Cisplatin is a widely used anti-cancer drug, which its application is limited by nephrotoxicity. In this study, the effect of pretreatment with different l-arginine doses on Cisplatin-induced renal functional injury was investigated. Methods: 63 male rats were divided into 7 groups: In groups 3, 4, 5 and 6, 60 min before the Cisplatin injection (5mg/kg); L-Arginine with doses of 50,100,200 or 400mg/kg was injected, respectively. In group7, normal saline was injected before Cisplatin administration. In groups 1 and 2, normal saline was injected instead of Cisplatin. In group 2, 60min before normal saline injection, 400mg/kg L-Arginine was administered and in group1, instead of L-arginine, normal saline was injected too. Injections were intraperitoneal. 72h after Cisplatin injection, blood sampling and plasma separation were done. Urine sample was collected 24 hours before blood sampling by metabolic cage. The mean of plasma urea and creatinine levels and creatinine clearance (ml/day.kg) and fractional excretion of Na (FENa, %) were compared among different groups as renal functional parameters. Results: In comparison to group 7, L-arginine injection in a dose of 400mg/kg led to significant amelioration of all parameters. 200 mg/kg L-arginine administration led to significant decrease in plasma urea level and FENa. 100mg/kg L-arginine caused significant improvement in fractional excretion of sodium. L-arginine injection with 50mg/kg dose, significantly ameliorate all renal function tests instead of creatinine clearance. Conclusion: Pretreatment with L-arginine administration with 400 or 50 mg/kg doses, respectively, had the highest effect on reducing Cisplatin-induced nephropathy. L-arginine injection with intermediate doses i.e. 200 or 100 mg/kg had less effect in reducing Cisplatin-induced nephropathy and it needs more investigations