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Background: Oxidative stress, has been shown to play an important role in the pathophysiology of cardiac remodelling and heart failure. The aim of study is effect of arginine vasopressin (AVP) on apoptosis of cardiomyocyte via its receptors.Materials and methods: The cell viability effect of AVP in H9C2 cardiomyocytes was assayed using the MTT method. The transcription and translation level of apoptosis genes (Bax, Bcl-2, caspase-3) were discovered with qRT-PCR and western blotting.Results: The results showed that vasopressin could reduce apoptosis in cardiomyocytes cell line through downregulation of caspase-3, BAX and upregulation of Bcl-2 (p < .001). Also, there was a decrease in anti-apoptosis effect of vasopressin when V1A and OTR receptors were blocked with their antagonists.Discussion: These results suggest that activation of V1A and OTR receptors in H9C2 cells mediate protective effect of vasopressin via regulating apoptosis marker that lead to cell survival under conditions of stress oxidative.Key pointAVP may contribute to the improvement of heart ischaemia through its actions on V1A and OTR receptors.

Oxidative stress, has been shown to play an important role in the pathophysiology of cardiac remodelling and heart failure. The aim of study is effect of arginine vasopressin (AVP) on apoptosis of cardiomyocyte via its receptors.The cell viability effect of AVP in H9C2 cardiomyocytes was assayed using the MTT method. The transcription and translation level of apoptosis genes (Bax, Bcl-2, caspase-3) were discovered with qRT-PCR and western blotting.The results showed that vasopressin could reduce apoptosis in cardiomyocytes cell line through downregulation of caspase-3, BAX and upregulation of Bcl-2 (These results suggest that activation of V1A and OTR receptors in H9C2 cells mediate protective effect of vasopressin via regulating apoptosis marker that lead to cell survival under conditions of stress oxidative.Key pointAVP may contribute to the improvement of heart ischaemia through its actions on V1A and OTR receptors.

Background Paraquat poisoning leads to lung injury and pulmonary fibrosis. The effect of paraquat encapsulation by previously described Pectin/Chitosan/Tripolyphosphate nanoparticles on its pulmonary toxicity was investigated in present study in a rat model of poison inhalation. Material and method The rats inhaled nebulized different formulation of paraquat (n = 5) for 30 min in various experimental groups. Lung injury and fibrosis scores, Lung tissue enzymatic activities, apoptosis markers were determined compared among groups. Results Encapsulation of paraquat significantly rescued both lung injury and fibrosis scores. Lung MDA level was reduced by encapsulation. Paraquat poisoning led to lung tissue apoptosis as was evidenced by higher Caspase-3 and Bax/Bcl2 expressions in rats subjected to paraquat inhalation instead of normal saline or free nanoparticles. Again, nanoencapsulation reduced these apoptosis markers significantly. Alpha-SMA expression was also reduced by encapsulation. Nanoparticles per se have no or little toxicity as was evidenced by inflammatory and apoptotic markers and histological scores. Conclusion In a rat model of inhalation toxicity of paraquat, loading of this herbicide on PEC/CS/TPP nanoparticles reduced acute lung injury and fibrosis. The encapsulation also led to lower apoptosis, oxidative stress and alpha-SMA expression in the lung tissue.

As a potent herbicide capable of contaminating water and soil environments, paraquat, which is still widely used worldwide, is toxic to mammals, algae, aquatic animals, etc. Paraquat was loaded on novel nanoparticles composed of pectin, chitosan, and sodium tripolyphosphate (PEC/CS/TPP). The size, polydispersity index, and ζ potential of nanoparticles were characterized. Further assessments were carried out by SEM, AFM, FT-IR, and DSC. The encapsulation was highly efficient, and there was a delayed release pattern of paraquat. The encapsulated herbicide was less toxic to alveolar and mouth cell lines. Moreover, the mutagenicity of the formulation was significantly lower than those of pure or commercial forms of paraquat in a Salmonella typhimurium strain model. The soil sorption of paraquat and the deep soil penetration of the nanoparticle-associated herbicide were also decreased. The herbicidal activity of paraquat for maize or mustard was not only preserved but also enhanced after encapsulation. It was concluded that paraquat encapsulation with PEC/CS/TPP nanoparticles is highly efficient and the formulation has significant herbicide activity. It is less toxic to human environment and cells, as was evidenced by less soil sorption, cytotoxicity, and mutagenicity. Hence, paraquat-loaded PEC/CS/TPP nanoparticles have potential advantages for future use in agriculture.

Background: Given the role educational system, it is necessary to most desirable design and implements activities. Internal evaluation is process in which members of the department said the group's objectives and their performance are judged and then reviewed their role and for better performance, essential steps to take.The purpose of this study was the internal evaluation of Physiology Department of Lorestan University of Medical Sciences. Materials and Methods: The study was descriptive and cross sectional conclucted in 2014-2015. Data was collected using questionnaire and was evaluated in 6 areas. Questionnaire was prepared and drafted by some faculty members and Medical Education Development Center. Based on the Likert scale, data was classified favorable, relatively favorable and unfavorable in a range of 0 to 5 points. Results: The results showed that the head of department area (acquired by averaging 4.23), faculty members (3.57), educational courses (3.96) and curriculums of the department of physiology (3.57) are favorable and areas of educational and research requirement and constructions (2.92) and research activities of the faculty members (2.73) are comparatively favorable. Conclusion: According to Likert scale, department of physiology of Lorestan University of Medical Sciences was evaluated and ranked in all mentioned areas (acquired by averaging 3.39), therefore has a satisfactory level.

Background Trauma and ventilator-induced lung injury is often associated with endothelial-epithelial barriers breakdown, which may lead to multiple system organ failure (MSOF) and death in critically ill patients. Although molecular mechanism involved in MSOF is not known, junctional opening is believed to happen. In vitro, thyroid hormones inhibit myosin light chain (MLC) phosphorylation and may, thus, inhibit cellular contraction and junctional opening. Trauma is also associated with tissue hypo-thyroid state. Therefore, we examined the effects of thyroid function on expression of phospho-MLC (pp-MLC) and claudin 4 (Clud4), key proteins involved in regulation of junctional tightness, in lung injury. Methods Rats were rendered hypo-thyroid (Hypo) or hyperthyroid (Hyper) by adding methimazole or levo-thyroxine, respectively, to their drinking water. Untreated euthyroid (Eue) animals were used as control. Lung pp-MLC and Clud4 proteins were assessed by western blotting and in situ immunodetection, respectively. Lung injury was induced by high tidal volume mechanical ventilation. Results Lung injury was significantly enhanced in Hypo animals and attenuated in Hyper animals. Parallel changes in expression of lung pp-MLC were detected. Alterations in lung histomorphology correlated with the level of pp-MLC. Expression of alveolar and bronchiolar Clud4 protein was differentially affected by the state of thyroid gland. Conclusions Our data suggest that thyroid function plays significant role in lung injury perhaps by modulating expression of the proteins involved in junctional tightness. Besides, they strongly support the idea that the tissue hypo-thyroid state may contribute to endothelial-epithelial barriers breakdown associated with trauma.

Introduction: Hereditary nephritis is an umbrella term for a group of congenital childhood diseases including but not limited to Alport syndrome, thin basement membrane disease, and Fabry disease. Objectives: The purpose of this study was a clinicopathologic investigation of Alport syndrome, thin basement membrane disease, and Fabry disease with a focus on the role of electron microscopy and toluidine blue staining in diagnosis. Patients and Methods: In this cross-sectional study, we investigated kidney biopsies with a final diagnosis of either Alport syndrome, thin basement membrane disease or Fabry disease from 2001 to 2016. Electron microscopy and light microscopy were done and the clinical and paraclinical data were extracted from the patients’ medical charts. Electron microscopy role was assessed in terms of necessary, helpful or non-necessary, while correlations between clinical and para-clinical data were determined using appropriate statistical tests. Results: Among the 2865 kidney biopsies, there were 22 patients of hereditary nephritis including 15 (0.52%) Alport syndrome, 5 (0.17%) thin basement membrane disease and 2 (0.07%) Fabry disease diagnosed by electron microscopy. Electron microscopy was essential for the diagnosis of 19 (86.4%) cases, helpful for 3(13.6%) and there was no case for which electron microscopy was non-necessary. The patients’ mean age was 16.1 ± 9.0 years. The most common finding in Alport syndrome was proteinuria (86.7%) followed by hematuria (60.0%). Conclusion: Considering the rate of misdiagnosis of hereditary nephritis using light microscopy and clinical findings alone, electron microscopy study and toluidine blue staining has an essential role in the precise diagnosis in these patients. With regard to the progressive nature of these diseases, prompt diagnosis using electron microscopy is pertinent for therapeutic decisions.

Background: Evidences show that parental morphine addiction impairs CNS development, learning and memory in offsprings. Since long term potentiation (LTP) is a cellular mechanism of learning and memory, in this study the effect of parental morphine addiction on LTP induction in dentate gyrus by high frequency stimulation of perforant path was assessed. Materials and methods: In this experimental study 40 female and 16 male rats (120-140 days old) were addicted by oral administration (32mg/kg, twice daily) of morphine for 5 days. Then male rats were placed with female in 5 groups: 1-test 1 group: addicted female rats (n=20) with non addicted male rats (n=8). 2- test 2 group: non addicted female rats (n=20) with addicted male rats (n=8). 3-test 3 group: addicted female rats (n=20) with addicted male rats (n=8). 4-sham control 1: female received dextrose 5% (n=20) with non addicted male rats (n=8). 5- sham control 2: male received dextrose 5% (n=8) with non addicted female rats (n=20. In pubert offsprings, LTP were induced in dentate gyrus by high frequency stimulation (HFS) of perforant path. The magnitude of potentiation was evaluated as percentage change in population spike (PS) amplitude or excitatory post synaptic potential slope (EPSP) at 5, 30, 60 and 120 minutes after HFS. All values were taken as the mean ±SE. Data were analyzed by two way ANOVA. Results: Amplitude of population spike (PS) and slope of excitatory post synaptic potential(EPSP) 60 and 120 minutes after HFS in offsprings of test 1 and test 2 was less than sham controls (p

The purpose of this study was to evaluate the effects of cerebral hypoperfusion on cognitive ability, TNFα, IL1β and PGE2 levels in both hippocampi in a modified two-vessel occlusion model. Both common carotid arteries of adult male Wistar rats were permanently occluded with an interval of 1 week between occlusions. Learning and memory were significantly decreased after 1 month. This reduction was not significant after 2 months, which may be attributed to blood flow compensation. The TNFα level was significantly increased after 3 h and 1 day. IL1β was significantly increased after 1 day. After a week there was no significant difference in pro-inflammatory levels. Furthermore, there was no difference between right and left hippocampi. It is possible that TNFα and IL1β elevation initiates pathologic processes that contribute to memory impairment.

Background: Drug abuse is associated with numerous complications including hormonal disorders of hypothalamic-pituitary-gonadal axis and spermatogenic disorders. We have compared the hormone concentration of pituitary-gonadal axis and the semen analysis in opioid-dependent and non-opioid-dependent men.Materials and Methods: In this case-control study, serum concentration of pituitary- gonadal axis hormones and semen analysis in 48 opioid-dependent men as eligible to participate in the study were compared with those in 12 non-dependent men.Results: Free testosterone concentration in all test groups was significantly less than that in control group. Furthermore, the concentration of Dihydrotestosterone (DHT) and Dehydroepiandrosterone Sulfate (DHEAS) in all test groups except those addicted to heroin was less than in those in control group. Concentrations of LH, FSH, prolactin, SHBG, progesterone and estradiol, normal and abnormal sperm count in test groups were significantly different from control group. However, in all test groups, sperm motility rate was less than control group. No significant relationship was found between the concentration of sex hormones and the status of sperms motility. Conclusion: Chronic use of opioids will affect testosterone hormone and sperm, and it will cause hypogonadism and impairment of sperm motility.

Introduction: Evidences show that parental morphine addiction impairs CNS development, learning and memory in offsprings. Regarding the role of glutamate in dentate gyrus on learning and memory, in this study the effect of parental morphine addiction on extracellular glutamate concentration of dentate gyrus was assessed. Materials and methods: In this study 20 female and 8 male rats were addicted by oral administration (32mg/kg twice daily) of morphine for 5 days . Then the animals were exposed to20 non addicted female, and 8 non addicted male rats In pubert offsprigs. Basal and electrical stimulated (700µA and 10Hz frequency) of extracellular glutamate concentration of dentate gyrus were collected by in vivo microdialysis technique and measured using flurometric HPLC. Findings: In male offsprings of sham control1, sham control2, test1 and test2 basal and electrical stimulated of extracellular glutamate concentration of dentate gyrus were: 0.67±0.04, 1.11±0.1, and in female offsprings were 0.47±0.06, 0.88±0.05 (n=5). The basal and stimulated extra cellular glutamate concentration of dentate gyrus was decreased in both test1 and test2 offsprings. It was less in test1 than test2 offsprings. The glutamate concentration of dentate gyrus in female offsprings of test1 group was less than that of the male offsprings. conclusion: The results suggest that parental morphine addiction may cause learning deficiency through reduction of extracellular glutamate concentration in dentate gyrus so the side effects of parental morphine addiction in offsprings must be considered.

Trauma and ventilator-induced lung injury is often associated with endothelial-epithelial barriers breakdown, which may lead to multiple system organ failure (MSOF) and death in critically ill patients. Although molecular mechanism involved in MSOF is not known, junctional opening is believed to happen. In vitro, thyroid hormones inhibit myosin light chain (MLC) phosphorylation and may, thus, inhibit cellular contraction and junctional opening. Trauma is also associated with tissue hypo-thyroid state. Therefore, we examined the effects of thyroid function on expression of phospho-MLC (pp-MLC) and claudin 4 (Clud4), key proteins involved in regulation of junctional tightness, in lung injury.Rats were rendered hypo-thyroid (Hypo) or hyperthyroid (Hyper) by adding methimazole or levo-thyroxine, respectively, to their drinking water. Untreated euthyroid (Eue) animals were used as control. Lung pp-MLC and Clud4 proteins were assessed by western blotting and in situ immunodetection, respectively. Lung injury was induced by high tidal volume mechanical ventilation.Lung injury was significantly enhanced in Hypo animals and attenuated in Hyper animals. Parallel changes in expression of lung pp-MLC were detected. Alterations in lung histomorphology correlated with the level of pp-MLC. Expression of alveolar and bronchiolar Clud4 protein was differentially affected by the state of thyroid gland.Our data suggest that thyroid function plays significant role in lung injury perhaps by modulating expression of the proteins involved in junctional tightness. Besides, they strongly support the idea that the tissue hypo-thyroid state may contribute to endothelial-epithelial barriers breakdown associated with trauma.

Myosin light chain kinase (MLCK) may play a key role in cellular contraction, paracellular permeability and lung water homeostasis. In vitro, thyroid hormones (THs) potently inhibit MLCK activation and, hence, MLC phosphorylation. Whether similar effect is exerted by THs in in vivo systems is not known. Therefore, we investigated the effects of hypothyroid (HO) and hyperthyroid (HR) states on the level of phospho-MLC, aquaporin 5 (AQP5) protein expression, and water holding capacity in the rat lung. Alterations in thyroid state were induced by adding methimazole or levothyroxine (L-T4) to animals’ drinking water. Serum TH concentration and thyroid gland histomorphology were assessed to verify the onset of the thyroid state. Lung phospho-MLC and AQP5 proteins were assessed by Western blotting and immunohistochemistry. Lung extravascular water content was estimated by the tissue wet weight-to-dry weight (W/D) ratio. The HO state induced significant increases in the expression of lung phospho-MLC and AQP5 proteins. In contrast, the HR state caused moderate decreases in lung phospho-MLC and AQP5 proteins. While lung water holding capacity was significantly increased in HO animals, it was significantly reduced in HR animals. The data of this study show that THs are able to modulate MLC phosphorylation in in vivo systems. Besides, they suggest that the circulating level of THs may alter lung fluid balance not only through expression of water channels but also through regulation of cellular contraction and paracellular permeability.

This work analyzes the effects of Satureja khuzestanica essential oil (SKEO) on the thyroid and antioxidant system, assessed by measuring levels of tri-iodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPx) activity. Forty adult male Sprague Dawley rats (225 ± 25 g) were divided into five equal groups: one control and four hyperthyroid groups that received placebo, 200 mg kg(-1) body weight of vitamin (Vit.) E, 225 mg kg(-1) body weight of SKEO, 200 and 225 mg kg(-1) body weight of Vit. E and SKEO together, respectively. Hyperthyroidism was induced by administering of L-thyroxin in drinking water. After 30 days of L-thyroxin consumption, serum T3 and T4 levels, TSH, and oxidative stress indices were determined. Significant increase in serum T3, T4 and MDA concentrations with a simultaneous significant decrease in TSH, GSH level and GPx activity were observed in hyperthyroid group (p0.05). In the treatment groups, SKEO and/or Vit. E can compensate serum MDA elevation and GPx activity reduction. Only, SKEO + Vit. E could compensate the decline of GSH levels in response to hyperthyroidism. Supplementation of SKEO, plus Vit. E as antioxidants is useful in attenuating lipid peroxidation and may potentially benefit hyperthyroid patients.

Attention to addiction of women alone for fetus and infant's health has caused the possible role of father's status was less considered, while some developmental impairments including decrease of liter size, weight loss, congenital deficiencies, behavioral disorders, and learning and memory impairments in offspring with addicted father have been reported. In this study the effects of addiction of one or both parents to morphine on male and female offspring hippocampal long-term potentiation (LTP), were assessed. One hundred twenty female and 48 male rats (4-5 months, 250-270 g) were used. Forty females and 16 males were addicted by oral administration of morphine (32 mg/kg twice daily) for 5 days before mating. Then each two males with five females were housed (coupled) per cage as five groups for coupling: (A) addicted females+5% dextrose males (add.F); (B) addicted males+5% dextrose females (add.M); (C) addicted females+addicted males (add.MF); (D) 5% dextrose females+intact males (dex.F); (E) 5% dextrose males+intact females (dex.M). In puberty offspring LTP was induced in hippocampal dentate gyrus by stimulation of perforant path (pp). Changes of population spikes (PS) amplitude and LTP slope at 0, 5, 30, 60 and 120 min were evaluated. Slope of LTP at 30, 60 and 120 min, and amplitude of PS at 60 and 120 min in add.F and add.M offspring were significantly lower than dextrose groups (P0.01). LTP slope and PS amplitude of male and female offspring did not different between add.F and add.M groups. Our results suggest that both parental and paternal addiction to morphine may cause memory deficiency through reduction of LTP in hippocampus.