effect of neem [Azadirachta indica] leaf extract and neem compound nimolicine on gastric acidity

This study has been conducted to look at the and acid effect of Neem and to compare the effect of leaf extract with the pure compound nimolicine on the gastric acidity. Nimolicine has been studied for its anti acid effect for the first time. Experimental study. This study was conducted in the department of Physiology, Baqai Medical College and the Department of Pharmacology in Baqai Institute of Pharmaceutical Sciences, Karachi. Ethanol induced gastric ulcers in albino rats were treated with methanolic neem leaf extract [800mg/day for 5 days] and nimolicine [1%/day for 3 days] and the gastric acid secretion was estimated. The control of the treated group was given peanut oil 1 ml/day for 5 days. The effect on gastric secretion was compared with the effect of anti-ulcer drugs cimetidine [50 mg/kg for 7-10 days] and omeperazole [2.5 mg/kg/day for 7-14 days]. Neem leaf extract is a better suppressor of H-ion secretion compared to nimolicine but both neem leaf extract and nimolicine did not show a significant suppression of acid compared to ranitidine and omeperazole. The comparison between control and ranitidine in suppression of acid was significant. Methanolic NLE and neem compound nimolicine do not decrease gastric acidity and their role as anti-ulcer agents may be because of other mechanisms which need to be studied

Nitric oxide measurement from blood to lungs, is there a link?

Endothelium-derived nitric oxide [NO] is a key molecule in regulation of vascular tone and its association with vascular disease has long been recognized. NO inhibits many processes known to be involved in the formation of atherosclerotic plaque, including monocyte adhesion, platelet aggregation and vascular smooth muscle cell proliferation. Another important role of endothelial NO is the protection of the vascular wall from the oxidative stress induced by its own metabolic products and by the oxidation products of lipids and lipoproteins. Endothelial dysfunction, occurs at very early stages of atherosclerosis. It is therefore possible that deficiency in local NO availability could be a final common pathway that accelerates atherogenesis in humans. In addition to its role in the vascular endothelium, NO availability has been shown to modulate metabolism of lipoproteins. Negative correlation has been reported between plasma concentrations of NO metabolic products and plasma total and Low Density Lipoprotein [LDL] cholesterol levels while High Density Lipoprotein [HDL] improves vascular function in hypercholesterolaemic subjects. The loss of NO has considerable effect on the development of the disease. In the early stages of the disease reduced NO would leave the endothelium vulnerable to increased leukocyte diapedesis and increase the possibility of LDL oxidation. Oxidative stress and endothelial dysfunction are major contributors to development and progression of atherosclerosis in Diabetes Mellitus. Moreover, reports show that diabetics have impaired lung functions. It has been proposed that insulin resistance leads to airway inflammation. Exhaled nitric oxide [ExNO] is a recently introduced non invasive marker to measure inflammation and oxidative stress in the lung. So far no work has been done on exhaled NO levels in patients with DM. There are also no studies correlating exhaled NO to blood NO levels. We are also aiming to see if there is any relationship between exhaled NO with serum NO levels in diabetics as well as healthy individuals

How do the intercept and the gain of the dyspnea-heart rate relationship respond to exercise in cardiac patients?

To study the dyspnea-heart rate relationship in patients with a positive exercise tolerance testing [ETT] and to compare it with normal healthy controls who had a negative ETT. This was a matched case-control study, in which all patients and their controls underwent an ETT [Bruce protocol] at the Cardiopulmonary Diagnostics Laboratory of a tertiary health care facility. Twenty two male patients, who tested positive on an ETT, were taken as cases and their dyspnea profile was measured during the ETT using the Borg scale. Age, sex and body mass index matched healthy subjects who tested negative on the ETT were recruited as controls and underwent similar dyspnea assessment. Regression analysis of the dyspnea/heart rate relationship was performed to calculate the slope and intercept for every patient and these were compared with the values of the respective controls. The dyspnea/heart rate relationship in patients was found to be linear. The mean intercept [ +/- SEM] was significantly lower in patients when compared with controls; 100.68 +/- 5.25 beats min-1 in patients compared with 113.14 +/- 3.51 beats min-1 in controls [p=0.005]. However, the slope did not show any significant difference between patients and controls. Changes in dyspnea, in this group of patients, is translated via modulation of the intercept [threshold] of the dyspnea/heart rate relationship