[Predicting type two diabetes and determination of effectiveness of risk factors applying logistic regression model]

Background and Aim: Diabetes is one of the chronic diseases with no curative treatment; also, it is the most common cause of amputation, blindness and chronic renal failure and the most important risk factor of heart diseases. Logistic regression is one of the statistical analysis models for predicting that can be used to find out the relationship between dependent and predictor independent variables and control of the confounding variables. The aim of this study was to determine the rate of effective variables on diabetes and estimation of the logistic regression model for predicting

Methods: 5357 persons in Kerman city, Iran, were enrolled. Diabetes considered as the response variable and weight, height, body mass index [BMI], waist circumference, hip circumference, waist-to-hip ratio [WHR], age, gender, occupation, education, drugs, drug abuse, activities, systolic and diastolic blood pressure, and levels of total cholesterol, the high-density lipoprotein [HDL], the low-density lipoprotein [LDL], and triglycerides were considered as independent variables in the model. Measures of sensitivity, specificity, accuracy, Kappa measure of agreement and ROC [receiver operating characteristic] curve was applied for determining the power of test

Results: The Sensitivity, specificity, accuracy rate, Kappa measure of agreement and area under the ROC curve for the model were 0.764, 0.725, 0.731, 0.312 and 0.822, respectively. The following variables were significant according to their impact and their importance, respectively: WHR [beta = 2.66, OR=14.32], anti-hypertensive drug [beta =1.279, OR= 3.59], sex [beta =0.707, OR= 2.028], level of education, walking and cycling [beta = 0.136, OR= 1.146], waist circumference [beta =0.12, OR= 1.127], weight [beta = 0.112, OR= 1.118], BMI [beta = 0.053, OR= 1.054], systolic blood pressure [beta =0.052, OR= 1.054], age [beta =0.046, OR= 1.047], diastolic blood pressure [beta =0.043, OR= 1.044], total cholesterol [beta = 0.003, OR= 1.003], triglycerides [beta =0.01, OR= 1.011], LDL [beta = 0.001, OR= 1.001], hip circumference [beta = - 0.025, OR= 1.025], height [beta = -0.071, OR= 0.932], HDL [beta = -0.078, OR= 0.925], an intense 10-minute work activities [beta = -0.507, OR=0.602]

Conclusion: According to the criteria of accuracy and power of prediction, and considering ROC curve value [0.822] which could perform test accuracy as well for the diagnosis of diabetes, the logistic regression model was an appropriate model for the prediction of diabetes in this study

Coronary artery disease risk factors in an urban and peri-urban setting, Kerman, Southeastern Iran [KERCADR study]: methodology and preliminary report

This article was to present the sampling and measurements methods and the main preliminary findings of the KERCADR cohort study [first round] in an urban and peri-urban setting, Kerman, southeastern Iran2009-11. 5900 [3238 female] people aged between 15 to 75 years were recruited in the household survey by non-proportional to size one-stage cluster sampling. Trained internal specialists, general practitioners, clinical psychologists and dentists have assessed the study subjects by person-assisted questionnaires regarding different NCD risk factors including cigarette and opium smoking, physical activity, nutrition habits, anxiety, depression, obesity, hypertension and oral health. Blood samples were also collected for determining FBS, HbA1c, cholesterol and triglyceride. Weighted standardized prevalence estimates were calculated by STATA 10 survey analysis package. The participation rate was more than 95% in all subgroups. Cigarette smoking [18.4% vs. 1.2%], opium use [17.8% vs. 3.0%] and triglyceridemia [16.1% vs. 12.0%] were significantly higher among men than women. In contrast, women were presented with higher level of sever anxiety [29.1% vs. 16.7%], obesity [16.8% vs. 9.2%], low-physical activity [45.1% vs. 39.2%] and uncontrolled diabetes [60.2% vs. 31.0%]. More than 68% of all subjects have presented with moderate to severe gingival index scores. The first round of the KERCADR cohort with sufficient sample size and response rate provided precise estimates for the main clinical and para-clinical NCD risk factors. These evidences need to be translated into public health interventions and monitored in the next rounds of the cohort

effect of co-administration of aquous extract of bunium persicum and endurance training on plasma lipids in hypercholesterolemic male mice

The effect of endurance training on lipid profile and cardiovascular endurance in normal rat after Bunium Persicum Extract [BPE] administration has been previously investigated. In the present study, the effect of co-administration of endurance training and persicum extract on plasma lipid and lipoproteins in hypercholesterolemic male mice was examined. In this experimental study, 60 male mice were, randomly, divided into 4 groups: Vehicle, Endurance Training [ET], Bunium Persicum Extract Administer [BPEA] and ET-BPEA group. The Exercise protocol was performed at a speed of 18 m/min, 40 min/day, 5 day/week for 6-weeks. The Bunium Persicum Extract was also administered in the same period and the desired dose [0.8 mg] was reconstituted in 0.4 ml of distilled water. The amount of Triglyceride [TG], Total Cholesterol [TC], HDL-c, LDL-c and Body Weight were registered at the beginning and also at the end of the 6 weeks. Data were analysed using one-way ANOVA method. The results indicated that the 6-week endurance training accompanied by Bunium Persicum aquous extract administration reduced TC [pretest; 297.7 +/- 37.08, post test; 146.1 +/- 30.8, p=0.019] and LDL-c concentrations [pretest; 151.8 +/- 14.4, post test; 0.12 +/- 8.7, p=0.00l]. On the other hand, Bunium Persicum aquous extract administration increased HDL-c concentration significantly [pretest; 75.9 +/- 12.1, post test; 119.9 +/- 17.9, p=0.003]. Furthermore, the results showed that body weight changes were not significant. These results suggest that co-administration of BPE and ET could significantly affect plasma lipid and lipoproteins. Therfore performing such program maybe useful for preventing cardiovascular diseases

[ effect of enalapril on brain edema and cytokine production following transient focal cerebral ischemia in mice]

Cytokines production as one of the inflammatory pathways in CNS is responsible for most brain damages following ischemia. On the other hand, during inflammation and brain ischemia, most of the renin- angiotensin components [RAS] increase locally. While it is established that blockade of RAS especially AT1 receptors has a protective effect on ischemia, the interaction of cytokines and angiotensin II is not well understood. This study was designed to investigate the effect of angiotensin II inhibitor on cytokine production as well as brain edema. Fifty-four male mice were randomly divided into 5 groups of normal, Sham operated, ischemia, Pretreatment with enalapril [high dose], and Pretreatment with enalapril [low dose] for the measurement of IL-IB and TNF-alpha in the brain and blood serum by ELIZA method. Ischemia caused a significant increase in water content and neurological deficit scores as well as cytokine levels. Treatment with enalapril had paradoxical effect on ischemia. In high dose, 85% of the animals showed convulsion after reperfusion. The IL-1 beta in serum and neurological deficit scores of this group were high, in accordance with clinical signs. In contrast, the low dose of enalapril, had protective effect on ischemia. It caused a significant reduction in brain concentration of both IL-1 beta and TNF- alpha [P<0.05] and improved significantly the neurological deficit scores and brain water content as well. [P<0.05]. Enalapril as an ACE inhibitor, has a dual effect on stroke. At low dose, it has a protective role at least in part by suppressing the local production of pro-inflammatory cytokines while, at high dose, it increases the inflammation by an unknown mechanism

[Role of angiotensin II in reactive oxygen species production and modulatory role of nitric oxide [no] in vessel responses to angII in acute joint inflammation in the rabbit]

It has been approved that in most tissues NO production increases during acute inflammation and Angiotensin II has a role in production of reactive oxygen species [ROS]. As regulation of joint blood flow [JBF] is important in this situation, this study was performed to investigate the interaction of local Ang II and ROS production and the modulatory role of NO on regulation of JBF during acute inflammation. The study was performed on 24 Newzealand white rabbits divided into three experimental and one control groups. Acute knee joint inflammation was produced by intraarticular injection of 0.5 ml of a 2% solution of carrageenan in knee joint. In the first group after 24 hours animals were anesthetized by thiopental sodium and carotid artery, jugular vein and saphenous artery were cannulated for recording blood pressure, injection of L-NAME and local injection of AngII and losartan respectively. Blood flow was recorded by laser Doppler flow meter. Joint vascular resistance [JVR] was calculated by dividing arterial blood pressure [ABP] by JBF. In the second group, knee joint tissue was used for homogenization and ROS measurement .In the third group, Losartan [10mg/kg] was administrated orally 2 hours before induction of inflammation. L-NAME increased JVR significantly. JVR in response to AngII was significantly increased. This response was significantly potentiated by L-NAME [P<0.01]. Losartan completely blocked the effect of AngII on JVR. Data showed that total amount of antioxidant and catalase activity nonsignificantly increased in inflamed group. Losartan significantly returned the catalase activity of the inflamed joint to the control level [P<0.01]. NO plays a role in the regulation of joint vascular tone and modulates the AT1 receptor response to AngII in acutely inflamed joints. Ang II increased the production of ROS and as a result the amount of antioxidants in acutely inflamed joints and this is via angiotensin II and through AT[1] receptors

[Investigation of response to angiotensin PI [ang PI] and its receptor subtypes in acutely inflamed joint blood vessels in rabbit]

Inflammatory joint diseases are common in elderly, and regulation of joint blood flow [JBF] is important in these conditions. The aim of this study was to investigate the response of inflamed joint blood vessels to angiotensin PI [Ang PI], a vasoconstrictor factor which has been shown to be produced in inflamed joints locally. Identification of Ang PI receptor subtypes in joint blood vessels was the second goal of this study. The present study was performed on 12 Newzland white rabbits. Acute knee joint inflammation was produced by intraarticular injection of 0.5 ml of a 2% of carrageenan solution 24 hours before the experiment. On experiment day, animals were anaesthetized by thiopental sodium [50mg/kg ip] and carotid artery was cannulated for recording blood pressure. JBF was recorded by laser Doppler flow meter. Joint vascular resistance [JVR] was calculated by dividing arterial blood pressure by JBF. Based on Ang PI dose/ response curve of joint blood vessels, the constrictor response was started from 10[-12] M and reached to maximum at 10[-5] M.Losartan completely inhibited this response with no vasodilation left behind, therefore the receptor subtypes are AT[1]. No evidence of presence of AT[2] receptor subtype was observed in joint blood vessels. The comparison of the results of this study with a previous study on normal joints showed that the Ang PI receptor subtypes did not change due to the process of acute inflammation

Effect of betadine on wound healing in rat

Betadine is a disinfectant routinely used in all of the Iranian health centers and many other countries in the world but its effect on wound healing is controversial. The aim of this study was to investigate the effect of betadine on wound healing in rat. In this interventional study, two groups of rats [n=10 each] were randomized as betadine and control groups. Under nesdonal anesthesia, a full thickness skin in an area of 2 cm[2] was excised on dorsal neck of rats and immediately betadine was applied in betadine group. Control group received no treatment. Wound area percentage of recovery and body weight were measured on postoperative days 1, 4, 7 and 10. Number of fibroblasts, collagen fibers, new vessels, lymphocytes, macrophages, neutrophils and thickness of epiderm were determined in three groups by biopsy on day 10. The results showed the percentage of recovery was not significantly different in the 4th, 7th and 10th days. Revascularisation, fibroblasts, lymphocytes, neutrophils, epidermal depth and collagen fibers were not significantly different between two groups. Macrophages in the betadine group were significantly higher than control group. The results propose that betadine not only does not speed up wound healing but also delays the inflammatory phase

[Comparison of the effect of infrared [IR] and Phenytoin cream on skin wound healing in rat]

Background and Objective: Infrared [IR] is one of the modalities in electrotherapy that indicates for treatment of some diseases with minimal side effects, but there is different ideas about its effects on wound healing. The aim of this study was to investigate effects of IR on skin wound healing in rat and its comparison with phenytoin's effect

Methods: This interventional and experimental study was done on three groups of rats. After inducing general anesthesia in rats, skin wound was made on dorsal neck about 2 cm[2]. Then from third day after operation, IR and phenytoin cream [1%] were indicated in two groups. No treatment was administered for control group. Wound surface area, percentage of recovery and rat weight change post operation at 1[st], 4[th], 7[th] and 10[th] day were measured. Number of fibroblasts, collagen fibers, new vessels, lymphocytes, macrophages, neutrophils and thickness of epiderm were determined in three groups by biopsy at 10[th] day

Findings: The results showed that percentage of recovery was not significantly different in three groups at 4[th] day. But, percentage of recovery at 7[th] day in IR, control and phenytoin group were 51.5+/-17.7, 38.8+/-17.9 and 55.3+/-10.1, respectively [P<0.04] and at 10[th] day in IR, control and phenytoin group were 68.4+/-17.5, 57+/-18.4 and 78.9+/-8.2, respectively [P<0.01]. Number of new vessels, fibroblasts, macrophages, lymphocytes, neutrophils and thickness of epiderm were not significantly different in three groups after 10[th] days. Number of collagen fibers was significantly different in three groups [P<0.01]

Conclusion: Findings suggest that infrared accelerates wound healing from 7[th] day that this effect is the same as phenytoin's healing effect

[ effect of chronic inflammation on knee joint vascular beta-adrenoceptors in rabbit]

It has been shown that inflammation reduces the effectiveness of sympathetic nerves in the regulation of knee joint blood flow, and the joint vascular-beta adrenoceptors are changed due to acute inflammation from a majority of beta-1 to an equality of beta-1 and beta -2 receptors. To investigate the role of sympathetic nerves in nerve induced vasoconstriction and changes in joint vascular beta-adrenoceptors due to chronic inflammation, in 21 NZW rabbits, chronic inflammation of the knee joint was induced by Antigen induced arthritis method, In experiment day animals were anesthetized and the caudal femoral artery, a branch of tibia1 artery, was cannulated to inject the beta -agonists intra-arterially close to the joint. Posterior articular nerve [PAN] was dissected pee for electrical stimulation. Electrical stimulation of PAN resulted in 18.1 +/- 6.2% reduction of blood flow measured by laser Doppler flowmetry technique. Phentolamine completely blocked the constrictor response and reversed it to vasodilation [+8+/- 2.2 %]. Propranolol [nonselective beta-adrenoceptor antagonist] completely blocked this vasodilation response and reverse it to a vasoconstriction. Atenolol [beta l antagonist] no significantly reduced the dilator response but ICI 118551 [beta2 antagonist] reduced 50% of this response. Close intra-arterial injection of different doses of beta-agonists, Isoprinosine [nonselective beta agonist], Dobutamine [beta <1 agonist] and Salbutamol [beta <2 agonist] increased the joint blood flow by the potency rank order of " Isoprenaline > Salbutamole > Dobutamine " .The isoprenaline dose response curve was shifted to the right by J adrenoceptor antagonists by the potency rank order of propranolol> ICI> atenolol. Overall, this study showed that beta 2-adrenoceptor response is stronger and suggested that the shift porn beta l- to beta 2-adrenoceptor subtype started by acute inflammation continued in chronic inflammation and the sympathetic vasoconstrictor response was nearly recovered toward normal compared to acute inflammation

Role of nitric oxide and ATP-sensitive K+ channels in regulation of basal blood flow and hypercapnic vasodilatation of cerebral blood vessels in rabbit

The mechanisms underlying cerebral hypercapnic vasodilatation are not fully understood. To investigate the role of nitric oxide [NO] and ATPsensitive potassium [KATP] channels in basal blood flow regulation and hypercapnia-induced vasodilatation in rabbit cerebral blood vessels. The change in cerebral blood flow was measured by a laser Doppler flowmeter in 18 New Zealand white rabbits, in two groups, under general anesthesia with sodium pentobarbital. Nomega- nitro-L-arginine methyl ester [L-NAME] and glibenclamide were administered locally and systemically before and during induction of hypercapnia. The change in cerebral blood flow was not significant following local and systemic L-NAME administration, showing a nonsignificant role of local and systemic NO in regulation of rabbit basal cerebral blood flow. Hypercapnia increased cerebral blood flow by 17.3 +/- 4.4% before and 17.3 +/- 5.8% after local, and 5.8 +/- 3.2% [p<0.05] after systemic L-NAME administration. The change in cerebral blood flow was not significant after local and systemic administration of glibenclamide indicating a lack of KATP channel role in basal blood flow regulation. Hypercapnia increased cerebral blood flow by 27.2 +/- 8.7% before and 24.7 +/- 6.4% after local, and 49.3 +/- 9.7% after systemic administration of glibenclamide [p: NS in both cases]. Regional NO production had no role in basal cortical blood flow regulation and systemic NO contributed to 66% increment in cerebral blood flow during hypercapnia. Also, the KATP channels did not mediate the effect of NO or other vasodilators responsible for increasing cerebral blood flow during hypercapnia

Role of local nerves and prostaglandins in regulation of basal blood flow and hypercapnic vasodilatation of cerebral blood vessels in the rabbit

The mechanisms underlying cerebral vasodilatation during hypercapnia are not fully understood. To examine the role of nerves and prostaglandins in the regulation of basal blood flow and in hypercapnia-induced vasodilatation in the cerebral blood vessels of rabbit. Cerebral blood flow was measured by laser Doppler flowmeter in 18 NZW rabbits anesthetized with sodium pentobarbital. Tetrodetoxin was administered locally and indomethacin [a prostaglandin inhibitor] both locally and systemically before and during induction of hypercapnia. Basal cerebral blood flow did not change significantly in response to local tetrodetoxin, and also after local and systemic administration of indomethacin. Hypercapnia increased cerebral blood flow by 25.9 +/- 3.9% before and by 24.3 +/- 6.5% after administration of TTX and by 22.1 +/- 7.1% before and by 18.2 +/- 6.3% after administration of indomethacin. In the rabbit, prostaglandin and regional nerves had no role in regulation of basal cerebral blood flow, nor did they contribute to cerebral vascular dilatation during hypercapnia

Metabolic acidosis and severe hypotension: influence on survival time and shock period during hemorrhage in the cat

Metabolic acidosis and severe hypotension are the main causes of irreversibility during hemorrhagic shock. The influence of these two factors on durations of shock period and survival time were studied in four groups of anesthetized cats. In group I the animals were made hypotensive by reducing mean arterial blood pressure [Pa] to 45 mmHg with concurrent metabolic acidosis. In group II the same level of hypotension was produced, along with an intravenous infusion of 12% sodium bicarbonate solution [0.25 ml/kg/min.]; thus metabolic acidosis was prevented and arterial blood pH [pHa] was kept within its normal range- In group III the Pa was kept at 50 mmHg in the presence of metabolic acidosis, and in group IV, the Pa was kept at 50 mmHg [the same as group III] but acidosis was prevented. Durations of shock period and survival times of all groups were compared. The results of this study show that 1] preventing metabolic acidosis increased survival time by 400%, 2] keeping the Pa at 50 mmHg increased survival time by 800%, and 3] prevention of metabolic acidosis at a Pa of 50 mmHg still augmented survival time by more than 250%. We therefore conclude that control of pHa and prevention of severe hypotension may increase survival rates in patients suffering from hemorrhage