mustafa mohammadi

The material and spiritual separation of citizens from urban spaces creates an alienation feeling from the city. In this research, an attempt has been made to identify different dimensions of alienation feeling in urban spaces. This research has a practical purpose, and the sequential exploratory mixed method, with the grounded theory approach. In the qualitative phase, the basic components of the alienation feeling were extracted, and a conceptual model of alienation feeling in space was presented. Then, with the hierarchical confirmatory factor analysis, the collected data were fitted with the conceptual structure. Ahvaz citizens was used for the research population, and with stratified sampling, 610 Ahvaz citizens participated. The presented conceptual model is defined by five factors: the attachment to space feeling, the ineffectiveness of space feeling, the liveliness in space feeling, the space insecurity feeling, and the lack of identity in space feeling. Quantitative results showed that the proposed model has a good fit with the experimental data and its structural validity is favourable. The analysis of gender multiple groups showed that structural coefficients and correlation coefficients work differently for women and men. Researchers consider it strategic and useful to conceptualize the alienation feeling in the urban space in a multi-dimensional way, which is based on a lack of identity, insecurity, inefficiency, and lack of vitality, and they advise urban planners to consider this feeling and its causal factors and pay attention to the context of its creation in the urban space design and metropolitan policies.

Diabetic hearts are resistant to cardioprotection by ischemic-postconditioning (IPostC). Protection of diabetic hearts and finding related interfering mechanisms would have clinical benefits. This study investigated the combination effects of vildagliptin (Vilda) and IPostC on cardioprotection and the levels of autophagy and mitochondrial function following myocardial ischemia/reperfusion (I/R) injury in type-II diabetic rats.
Diabetes was established by high fat diet/low dose of streptozotocin and lasted for 12 weeks. The diabetic rats received Vilda (6 mg/kg/day, orally) for one month before I/R. Myocardial regional ischemia was induced through the ligation of left coronary artery, and IPostC was applied immediately at the onset of reperfusion. The infarct size was assessed by a computerised planimetry and left ventricles samples were harvested for cardiac mitochondrial function studies (ROS production, membrane potential and staining) and western blotting was used for determination of autophagy markers.
None of Vilda or IPostC but combination of them could significantly reduce the infarct size of diabetic hearts, comparing to control (P

Excessive apoptosis of the pancreatic beta-cell has been associated with type 2 diabetes. Hyperglycemia significantly stimulates pancreatic islet cell apoptosis. We evaluated the role of crocin and voluntary exercise on apoptosis of pancreas tissue in type2 diabetic rats.
Animals divided into 5 groups as: control (Con), diabetes (Dia), diabetic-crocin (Dia-Cro), diabetic-voluntary exercise (Dia-Exe), diabetic-crocin-voluntary exercise (Dia-Cro-Exe). Type 2 diabetes was induced by high-fat diet (4 weeks) and injection of streptozotocin (STZ) (i.p, 35 mg/kg). Animals received crocin orally (50 mg/kg), voluntary exercise performed alone or together for 8 weeks. At the final of study, blood glucose levels and HbA1c were detected. Also p53 protein levels of pancreas tissue were measured by ELISA.
P53 levels in pancreas tissue of diabetic group were significantly higher than control group. Crocin and exercise significantly decreased the blood glucose, HbA1c levels and p53 expression in treated diabetic groups compared to diabetic group. The glucose, HbA1c and p53 levels were also significantly lower in crocin-voluntary exercise group in comparison to the other experimental groups.
Our results reveal that both crocin and voluntary exercise reduce apoptosis of pancreas through reduction of p53 levels. Moreover, treatments with crocin and voluntary exercise have synergistic anti-apoptotic effects on pancreas tissue of type 2 diabetic rats. Protective effects of these interventions probably perform through the decreasing of glucose and HbA1c levels in blood of rats suffering from diabetes.

Chronic diabetes impedes cardioprotection in reperfusion injury and hence protecting the diabetic heart would have important outcomes. In this study, we evaluated whether combined postconditioning with ischemia and cyclosporine-A can restore oxidative stress and histopathological changes in reperfusion injury of the diabetic myocardium.
Streptozocin-induced diabetic rats’ hearts and nondiabetic controls in eight subgroups (with or without receiving ischemic-postconditioning (IPostC), cyclosporine-A, an inhibitor of mitochondrial permeability transition, or both of them) suffered from 30 min regional ischemia followed by 45 min reperfusion on an isolated-heart Langendorff system. The levels of lactate dehydrogenase (LDH) in the coronary effluent, and the levels of oxidative stress markers including 8-isoprostane, superoxide dismutase (SOD), glutathione peroxidase (GPX), and total antioxidant capacity (TAC) in myocardial supernatant prepared from the ischemic zone were measured using specific kits, spectrophotometrically. Histopathological studies were performed through the hematoxylin-eosin staining method.
Administration of IPostC and cyclosporine-A (alone or together) in nondiabetic hearts potentially reduced the severity of histological changes and level of LDH release as compared with untreated-controls (P0.1). However, the combined postconditioning with ischemia and CsA exerted significant protective effects in diabetic hearts (P By augmenting the protective effects of IPostC and CsA through their combined application, reperfusion injury and related oxidative stress are reduced in diabetic hearts similar to non-diabetics.

During atherosclerosis process, vasoconstriction phenomenon occurs which in turn leads to tissue hypoxia. A few studies have been performed on the combination of atherosclerosis and hypoxia as stressors that may accelerate secretion of constrictors. The aim of present study was to evaluate the effects of atherosclerosis and hypoxia on serum levels of main vasoconstrictors (epinephrine, norepinephrine and renin).
In this interventional study, 32 New Zealand white rabbits were randomly divided into four groups (n = 8): normal diet (control group), normal diet exposed to hypoxia (11%, 10 days), high-fat diet (cholesterol-2%, 8 weeks), and high-fat diet with hypoxia. Later, serum levels of renin, epinephrine and norepinephrine were measured on second, 56th and 66th days.
High-fat diet and hypoxia caused significant increase in epinephrine and norepinephrine concentrations on days 56 and 66 compared to the control group (P Both high-fat diet and hypoxia increase renin levels in male rabbits. Furthermore, the combination of high-fat diet and hypoxia immensely increases renin levels. Both hypoxia and combined of high-fat diet and hypoxia increase norepinephrine levels. However epinephrine is only increased in the combination of high-fat diet and hypoxia. So the presence of hypoxia in combination with high-fat diet, cause accelerated
and aggravated atherosclerosis.

This study designed to use remote ischemic post conditioning (RIPC) as a protective strategy during percutaneous coronary intervention (PCI) in patients with ST segment elevation myocardial infarction (STEMI) to reduce myocardial cells damage due to reperfusion injury.
Sixty-one patients were divided into test group (32 patients) receiving RIPC and control group (29 patients). Patients were included with first MI who had 20-80 years old. The RIPC protocol was applied on patients arm in three successive episodes during the opening of infarct-related artery (IRA). Whole blood sample were taken from patients after the first episode before IRA opening and after the third episode after IRA opening. The serums were extracted and stored in the freezer -70˚C to determine the levels of glutathione peroxidase (GPX), superoxide dismutase (SOD), total antioxidant capacity (TAC) and malondialdehyde (MDA).
The levels of GPX and SOD after the first episode of RIPC were significantly higher in test group than control group (P The results indicated that RIPC protocol has protective properties in patients with STEMI through enhancing the antioxidant potentials and decreasing lipid peroxidation.

The previous studies have suggested that alteration in oxidative stress and antioxidant defense depends on various factors, such as mode, intensity, frequency and duration of exercise. In this study, we compared the effects of two various durations of resistance exercise (1 month and 4 month) on oxidative stress and antioxidant status in cardiac tissue. Thirty Wistar male rats divided into 3 groups: control (sedentary), exercise-1 (regular exercise for 1 month) and exercise-2 group (regular exercise for 4 months). After the final to the experiment, the rats were anesthetized, and then blood and heart samples were obtained and used to determine glutathione peroxidase (GPX), superoxide dismutase (SOD), malondialdehyde (MDA) and biochemical estimation. MDA levels between control and exercise-2 groups showed no significant difference, hence, MDA level in exercise-1 group was higher compared to control group (P <. 01). The heart GPX activity increased significantly in exercise-2 group regarding other groups (P <. 01). The SOD activities of groups were similar. Creatine kinase (CK) and lactate dehydrogenase (LDH) concentrations increased in the exercise-1 compared to the other groups (P <. 01). Our results indicate that in heart, the adaptation and alteration in oxidative stress and cell injury level depend on duration of exercise.

Diabetes mellitus as a main risk-factor of ischemic heart disease may interfere with postconditioning’scardioprotective effects. This study aimed to investigate the involvement of glycogen synthase kinase-3β (GSK-3β) and oxidation status in chronic diabetes-induced loss of cardioprotective effect of ischemic-postconditioning (IPostC) in Wistar rats. After 8 weeks of induction of diabetes by streptozotocin (50mg/kg), hearts of control and diabetic rats were isolated and mounted on a constant-pressure Langendorff system. All hearts were subjected to 30min regional ischemia followed by 60min reperfusion (by occluding and re-opening of left anterior descending coronary artery, respectively). IPostC was applied immediately at the onset of reperfusion. At the end of reperfusion, the infarct size of myocardium was measured via computerized planimetry. Myocardial contents of malondealdehyde and glutathione as indices of oxidative status were assayed spectrophotometrically and the total and phosphorylated forms of myocardial GSK- 3β were quantified through western blotting. IPostC reduced the infarct size of control hearts from 41±2.9% to 28±1.9% (P<0.05), whereas it could not induce significant changes in infarct size of diabetic animals (35±1.8% vs. 39±3.1%). IPostC-induced reduction in malondealdehyde and elevation in glutathione contents were significant only in control not in diabetic hearts. The total forms of GSK-3β were similar in all groups; however, the phosphorylation of GSK-3β (at Ser9) by IPostC was greater in control hearts than diabetics (P<0.01). The failure of cardioprotection by IPostC in diabetic hearts may be attributed to the loss of phosphorylation of GSK-3β and thereby increase in oxidative stress in diabetic states.

Oxidative stress plays a key role in the onset and development of diabetes complications. In this study, we evaluated whether voluntary exercise could alleviate oxidative stress in the heart and blood of streptozotocin - induced diabetic rats. 28 male Wistar rats were randomly divided into four groups (n=7): control, exercise, diabetes and exercise + diabetes. Diabetes was induced by injection of streptozotocin in male rats. Rats in the trained groups were subjected to voluntary running wheel exercise for 6 weeks. At the end of six weeks blood and heart tissue samples were collected and used for determination of antioxidant enzymes (including SOD, GPX and CAT activities) and MDA level. Exercise significantly reduced MDA levels both in the heart tissue (p<0.01) and blood samples (p<0.05). In addition, exercise significantly increased SOD (p<0.05), GPX (p<0.001) and CAT (p<0.05) in the heart tissue. Voluntary exercise also significantly increased SOD (p<0.01), GPX (p<0.05) and CAT (p<0.001) in the blood. Voluntary exercise diminishes the MDA level in blood and heart tissue of diabetic rats. It also accentuates activities of SOD, GPX and CAT. Therefore, it may be considered a useful tool for the reduction of oxidative stress in diabetes.

Diabetes is associated with micro- and macro-vascular complications affecting several organs. Oxidative stress plays a crucial role in the etiology of vascular disease in diabetes.. The present study aimed to investigate the beneficial effect of troxerutin on diabetes-induced histopathological damages in rat aorta with focusing on its antioxidative actions.. Male Wistar rats were randomly divided into four groups (n = 8/each): control, control plus troxerutin, diabetic and diabetic plus troxerutin. Diabetes was induced in rats by a single intraperitoneal injection of streptozotocin (50 mg/kg) and lasted for 10 weeks. Troxerutin was administered orally in concentration of 150 mg/kg/daily for one month before killing rats. At the end of treatment period, thoracic aorta was isolated and divided into two parts; one part was immersed in 10% formalin for histopathological evaluations and the other was frozen by liquid nitrogen for assessment of malondialdehyde (MDA, the main product of lipid peroxidation), activity of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX).. Lipid deposition in tunica intimae and media, thickening and structural deformity of vascular tissues as well as the level of plasma glucose and aortic tissue levels of lipid peroxidation were significantly increased in diabetic rats compared to control ones (P < 0.05). Troxerutin significantly reduced the severity of all vascular histopathological damages in treated versus untreated diabetic rats. In addition, treatment of diabetic rats with troxerutin significantly decreased the levels of MDA (5.1 ± 0.3 vs. 9.3 ± 1.2 nmol/mL) (P < 0.01) and increased the activity of antioxidant enzyme GPX compared to untreated-diabetic groups.. Troxerutin may reduce the vascular complications and tissue injuries induced by chronic diabetes in rat aorta through increasing the activity of tissue antioxidant system and reducing the level of lipid peroxidation..

Regular training is suggested to offer a host of benefits especially on cardiovascular system. In addition, medicinal plants can attenuate oxidative stress-mediated damages induced by stressor insults. In this study, we investigated the concomitant effect of cinnamon extract and long-term aerobic training on cardiac function, biochemical alterations and lipid profile following exhaustive exercise. Male Wistar rats (250-300 g) were divided into five groups depending on receiving regular training, cinnamon bark extraction, none or both of them, and then encountered with an exhausted exercise in last session. An 8-week endurance training program was designed with a progressive increase in training speed and time. Myocardial hemodynamics was monitored using a balloon-tipped catheter inserted into left ventricles. Blood samples were collected for analyzing biochemical markers, lipid profiles and lipid-peroxidation marker, malondealdehyde (MDA). Trained animals showed an enhanced cardiac force and contractility similar to cinnamon-treated rats. Co-application of regular training and cinnamon had additive effect in cardiac hemodynamic (P<0.05). Both regular training and supplementation with cinnamon significantly decreased serum levels of total cholesterol, low-density lipoprotein (LDL), and increased high-density lipoprotein (HDL) level and HDL/LDL ratio as compared to control group (P<0.01). Furthermore, pre-treatment with cinnamon extract and/or regular training significantly reduced MDA level elevation induced by exhausted exercise (P<0.01). Long-term treatment of rats with cinnamon and regular training improved cardiac hemodynamic through an additive effect. The positive effects of cinnamon and regular training on cardiac function were associated with a reduced serum MDA level and an improved blood lipid profile.

Myocardial infarction (MI) is the acute condition of necrosis in myocardium which occurs as a result of imbalance between coronary blood supply and myocardial demand. The resultant oxidative stress excess leads to worsen the condition. The aim of this study was to investigate the effect of mebudipine, a new dihydropyridine calcium channel blocker, on lipid peroxidation and antioxidant enzymes in myocardial ischemia-reperfusion injury. Male Wistar rats (250-300g) were randomly divided to Control-ischemic, mebudipine-ischemic and vehicle (ethanol-ischemic) groups. The hearts of anaesthetized rats were removed and mounted on Langendorff apparatus and perfused by Krebs-Henseleit solution under constant pressure of 75mmHg at 37°C. Ischemic groups were received 30 min global ischemia and 120min reperfusion and the mebudipine and vehicle groups received mebudipine (0.1nM) or ethanol (0.01%)-enriched solution 25min before global ischemia. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase levels of heart tissue samples were determined by commercial specific Kits. Mebudipine significantly reduced the MDA level (2.3±0.07 nmol/mg protein) as the biochemical indicator of oxidative damage and lipid peroxidation product as compared with those of vehicle (4.6± 0.01 nmol/mg protein) and control groups (4.8 ± 0.09 nmol/mg protein). Furthermore, antioxidant enzymes SOD (0.1±0.006 in drug vs. 0.037±0.009 U/mg Protein in control), GPX (16±0.009 in drug vs. 0.068±0.01 U/mg Protein in control) and catalase activities (0.075±0.006 in drug vs. 0.028±0.002 U/mg Protein in control), activities of myocardium were significantly increased by mebudipine (P<0.01). Our results showed that mebudipine may have antioxidant activity against myocardial ischemia-reperfusion injury, since it decreased oxidative stress by enhancing the enzymatic antioxidant defense and inhibiting the lipid peroxidation. Thus, this drug can reduce the intensity of cardiac ischemic insults.

Diabetes mellitus results in wide disorders in central and peripheral nervous systems. Prevalence of cognitive disorders in diabetic patients is more compared to that in non-diabetic patients. Brain-derived neurotrophic factor (BDNF) prevents cell death by stimulating synthesis of antiapoptic factors in cell cultures. The present study aimed at investigating the effects of experimental diabetes on programmed cell death in hippocampus and its relation with the amount of BDNF and the related gene expression. Twenty male Wistar rats (200+20 g) were divided into two groups: control and diabetic. Diabetes was induced by injection of streptozotocin (single dose, 50mg/kg). Duration of the study was 8 weeks. At the end of the experiment, the rats were anesthetized by thiopental sodium and then brain was removed. Immediately, the hippocampus was removed on ice and kept frozen by liquid nitrogen and kept in freezer -800C until detection. Hippocampus tissue was homogenized in prepared buffer and after centrifugation supernatant was used for determination of apoptosis, level of BDNF protein and its gene expression. An increase in the amount of apoptosis following induction of diabetes was observed. Furthermore, diabetes induction increased the level of BDNF protein and its gene expression compared to the control group (P<0.05). Induction of diabetes increased the amount of apoptosis in the hippocampus of diabetic rats. As a defense mechanism, the level of BDNF protein and the related gene expression increases to prevent the apoptosis in the hippocampus.

Objective(s)Several studies have reported improved response of exercised hearts to myocardial infarction (MI). This study was aimed to evaluate the preventive role of treadmill exercise and diosgenin on cardiac marker enzymes, thiobarbituric acid reactive substances (TBARS), total antioxidant status (TAS), lipids, and electrocardiographic (ECG) patterns in isoproterenol (ISO)-induced myocardial infarction (MI) in male Wistar rats. Materials and MethodsOne hundred Wistar rats were divided into ten groups: Control rats (C), saline (S), L-cremephor (LC), exercise (E), diosgenin dissolved in L-cremephor (15 mg/kg/day) (D), exercise+ diosgenin (E+D), ISO injected (150 mg/kg) (ISO), exercise + ISO (E+ISO), diosgenin + ISO (D+ISO) and exercise+ diosgenin+ ISO (E+D+ISO). At the end of the experiment all animals anesthetized and blood samples were collected for biochemical estimation and also the ECG patterns were recorded. ResultsExercise and diosgenin pretreatment significantly decreased the lactate dehydrogenase (LDH) and TBARS level in ISO injected animals. Exercise and diosgenin pretreatment significantly decreased serum total cholesterol and increased high density lipoprotein (HDL-C). ISO-treated rats showed pathological Q waves along with elevated ST segments. The altered electrocardiograms (ECG) of ISO-treated rats were also restored to near normal by diosgenin and exercise, but exercise and diosgenin had synergistic effects. Conclusion The present investigation demonstrates that combination of diosgenin and exercise exhibited significant protection against ISO induced electrocardiographical and biochemical changes. The cadioprotective mechanism(s) appear to be through changing lipid metabolism.

There are controversial reports about the exact mechanisms of lead-induced hypertension, but many factors such as alteration in the responsiveness of cardiovascular system to endogenous substances including catecholamines could be one of the mechanisms involved. In present study, the effect of exposure to 100 ppm lead acetate by drinking water (in the periods of 4, 8 and 12 weeks) on the responsiveness of rat isolated beating heart to β-adrenergics was investigated, using Langendorff isolated heart setup. The isolated hearts were perfused with Krebs-Henseleit solution at 37˚C and pH=7.4 and gassed with 95% O2 + 5% CO2. The rate (chronotropic) and contractile (inotropic) responses of the heart to β-adrenergics (isoproterenol and dobutamine) were recorded by adding these agents at multiple concentrations to the perfusion solution. The blood pressure in 8- and 12-week lead-treated groups was significantly increased compared with those of the control group (P<0.01). The chronotropic response to many doses of isoproterenol (as β1,2-adrenergic) in only 12-, but not in 4- and 8-week lead-treated groups was significantly increased, as compared with those of control (P<0.05). The inotropic response to this drug was also significantly increased in both 8- and 12-week lead-treated rats (P<0.05, P<0.01). Similar findings were observed in the dobutamine (as selective β1-adrenergic) treated groups, but the contractile response of the latter agent was greater than the isoproterenol. Low-level of lead increases blood pressure and both chronotropic and inotropic effects of β-adrenergics. These effects could imply an important role in the pathogenesis of lead-induced hypertension.

Objective(s)In addition to antihypertensive effects, amlodipine may exhibit cardiovascular protective effects in heart tissue. The aim of this study was to evaluate the effects of amlodipine and/or high cholesterol diet on blood, heart tissue concentration and mRNA expression of endothelin-1 (ET-1) in male New Zealand white rabbits.Materials and MethodsA total of 40 male New Zealand rabbits were divided into four groups: the normal control group, normal group receiving amlodipine, high-cholesterol diet group and high-cholesterol diet with amlodipine group. After 8 weeks, all the animals anesthetized and blood or tissues samples were collected.ResultsAfter 8 weeks of a high cholesterol diet, the group with such a diet had a significantly higher ratio of left ventricle(LV) weight to body weight than the control group (P= 0.0001). After treatment with amlodipine for 8 weeks, ET-1 level was reduced considerably in comparison with the control (P= 0.01) and high-cholesterol diet groupes (P= 0.01). Amlodipine consumption caused significant reduction (P= 0.01) in the level of ET-1 in heart tissues of high-cholesterol diet group but it had no remarkable effect on the reduction of heart tissue ET-1 in amlodipine group compared with the control group. ConclusionThe present study demonstrates that ventricular prepro-ET-1 mRNA quantitatively increases in the high-cholesterol diet rabbits which results in development of ventricular hypertrophy. It seems that the treatment with amlodipine retards the progression of LV hypertrophy through attenuation of ET-1 levels independent of lipid changes.

A lumbar epidural catheter inserted in a 17 year-old man for applying anesthesia for internal fixation of femur fracture and subsequent postoperative epidural analgesia. In the third postoperative day, during unsuccessful attempt for removing the catheter, it was broken and was retained in his back. A CT-scan was performed and shows a fragment of catheter in the sub-laminar ligament between L3 and L4 without any connection with epidural space. As the patient had no complaint the fractured fragment was left in site and he was just followed up in the clinic. The knowledge of practical method in locating the retained epidural catheter

Reperfusion is essential for the survival of ischemic myocardium. However reperfusion itself leads to latter complications include decreasing cardiac contractile function and myocardial tissue injury. The purpose of this study is to evaluate the effect of mebudipine against injuries due to Ischemia-reperfusion in isolated rat heart. 28 male Wistar rats (250-300g) divided in four groups (n=7): sham group, control group, vehicle group and drug group. The animals anesthetized by sodium pentobarbital (60mg/kg –ip). The hearts were removed quickly and mounted on Longendorff apparatus and perfused by Krebs-Henseleit solution under constant pressure at 37 ºC. Ischemic groups after 20 minutes stabilization received 30 global ischemia and 120 minutes reperfusion. In drug group the hearts before ischemia were perfused 25 minutes with mebudipine-enriched Krebs-Henseleit(0.1×10-3 μM). At the end of experiment tissue heart samples were prepared. Mebudipine prevented from increasing of left ventricular end diastolic pressure (LVEDP) and enhanced significantly the left ventricular developed pressure (LVDP) and strength of heart contractility (p<0.05). Also mebudipine decreased remarkable the rate of edema, inflammatory cells infiltration and heart tissue necrosis compared to control group. Results of this study indicate that mebudipine by improving the strength of heart contractility in ischemia-reperfusion period and also by decreasing of myocardial injury can have important protective effects against ischemia-reperfusion injuries in heart.