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Medicated jelly formulations are patient friendly dosage form for pediatric, geriatric and dysphagic patients. These formulations offer rapid dissolution and absorption of drugs through oral mucosa therefore show the early onset of action. The objective of the study was to develop and evaluate oral jelly formulations of vitamin C. Slurry method was adopted using glucose 103gm, sugar 67gm, gelatin 10gm and sorbitol 6.56gm. Preformulation studies were performed including the organoleptic profile, pH, and solubility of both drugs. The medicated jelly of Vitamin C was prepared and evaluated for physical characteristics, weight variation, syneresis, pH, taste and palatability, drug content, release rate characteristics and stability studies. All the jellies were found to have patient welcoming taste and were palatable. All formulations showed more than 50% drug release within 15 minutes, while 93% drug was released in 30 minutes. The results of release kinetics showed that the formulation followed the zero order release kinetics. Thus the drug was released at constant rate independent of the drug concentration involved in the process. All the medicated jellies were found to remain stable stored for 60 days at different temperatures. The present study revealed that medicated jellies of vitamin C could be employed orally in an effective form as an alternative solid oral dosage form for special population such as pediatrics, geriatrics and patients with dysphagia
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Objective: To find the frequency of acute kidney injury in patients undergoing coronary artery bypass grafting
Methodology: The study was conducted in cardiovascular unit Lady Read-ing Hospital Peshawar. It was cross sectional study. Sampling technique was non probability convenient sampling. Data was collected from 20.2.2013 to 20.8.2013. Total 179 patients included in the study. All patients with known coronary artery disease were included in the study whom were planned for revascularization in the form of coronary artery bypass grafting [CABG]. Post-operatively all patients' serum creatinine till 48th post op hour was observed to detect acute kidney injury. Acute Kidney Injury [AKI] was defined as more than 50% or elevation of 0.3 mg/dl of creatinine level from base line
Results: A total of 179 patients undergoing coronary artery bypass grafting were included in the study. Average age of the patients was 46.88 years +/- 9.91 with range 20-60 years. Patients were divided into four groups according to age. The acute kidney injury after coronary artery bypass grafting was observed in 14 [7.82%] patients. Acute kidney injury was more common in old age and it was non significantly more common in male gender
Conclusion: In spite of current highly advance cardiac surgery techniques and post operative care still there is high incidence of acute kidney injury following revascularization and subsequent worst outcomes
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Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Ponte de Artéria Coronária , Estudos Transversais , Doença da Artéria Coronariana , RiscoRESUMO
Arsenic is a major threat to large part of the population due to its carcinogenic nature. The toxicity of Arsenic varies with its chemical form and oxidation states. Glutathione [GSH], a major intra-cellular tripeptide plays a major role in arsenic detoxification. The present study was designed to provide insight into the extent of changes in GSH level by inorganic arsenic in the form of Arsenic trioxide [ATO] and organic arsenic in the form of nitro benzene arsenic acid [NBA]. Lymphocytes [T.cells and B.cells] were investigated for determination of change in GSH metabolic status caused by arsenic. The depletion of GSH level positively correlated with increasing arsenic concentration and time of incubation. The decline in GSH level was consistent with increasing pH and physiological temperature. Our findings show that changes in GSH status produced by Arsenic could be due to adduct [As-[SG][3]] formation. This change in GSH metabolic status provides information regarding mechanism of toxicity of inorganic and organic arsenicals. These findings are important for the rational design of antidote for the prevention of arsenic induced toxicity
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Humanos , Glutationa , Linfócitos T , Linfócitos B , Arsenicais , Óxidos , NitrobenzenosRESUMO
This piece of research work present the toxicological impact of varied concentrations of Palladium Nitrate [Pd [NO[3][2] by changing the chemical status of glutathione and the way how glutathione plays its role in detoxification and conjugation processes of [Pd [NO[3][2] in whole blood components [plasma and Cytosolic fraction]. The impact of different concentration of [Pd [N03]2] on reduced glutathione level in whole blood component [Plasma and Cytosolic fraction] were measured spectrophotometrically following Standard Ellman's method. Compared with control sample, significant decrease in the GSH content in whole blood components [plasma and Cytosolic fraction] was obtained with various concentrations [100microM-1000microM] of Palladium Nitrate. Depleted GSH level was more pronounced with time incubation period [0-90] minutes. These finding shows that changes in the GSH status produced by palladium nitrate could either be due to palladium nitrate and glutathione [Pd-SG] complex formation or by conversion of reduce glutathione [2GSH + Pd[+2] -> GSSG]. This change in the GSH metabolic status provides information regarding the mechanism of palladium, in blood components
Assuntos
PaládioRESUMO
Mercury is harmless in an insoluble form, such as mercuric sulfide, but it is poisonous in soluble forms such as mercuric chloride or methylmercury. Mercury is a neurotoxin. Outbreaks of mercuric chloride poisonings have made it clear that adults, children, and developing fetuses are at risk from ingestion exposure to mercury. It is very important and interesting to study the reaction of mercuric chloride and Glutathione as biomarker of Glutathione role in detoxification and conjugation in components [Plasma and Cytosolic Fraction]. The effect of mercuric chloride's different concentrations was examined on GSH present in plasma and cytosolic fraction. Decrease in GSH level was dependant on mercuric chloride concentration. The decrease in GSH level of blood components was more prominent with the time of incubation of mercuric chloride. Decrease in the concentration of reduced state Glutathione may be due the interaction of reduced state Glutathione [GSH] and mercuric chloride to form oxidized Glutathione [GSSG] or mercuric-glutathione complex. This change in GSH metabolic status provides information regarding the role of GSH in detoxification of mercuric chloride. The effect of mercury metal on Glutathione in blood components has been discussed in this paper in vitro condition as a model for in Vivo condition
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Humanos , Intoxicação por Mercúrio/prevenção & controle , Mercúrio/toxicidade , Compostos de Mercúrio/toxicidade , Ácido DitionitrobenzoicoRESUMO
Metallo-elements including Vanadium [V] have strong affinity for sulfhydryl [-SH] groups in biological molecules including Glutathione [GSH] in tissues. Because of this fact it was of interest to further investigate the interaction of Ammonium Vanadate [NH[4]VO[3]] with Glutathione as a biomarker of toxicity and the role of Glutathione in the detoxification and conjugation processes in whole blood components including plasma and cytosolic fraction. Effects of different concentrations of Ammonium Vanadate [NH[4]VO[3]] on the level of reduced Glutathione in whole blood components [Plasma and Cytosolic fraction] were examined. GSH depletion in plasma and cytosolic fraction was Ammonium Vanadate's concentration-dependent. Depleted GSH level was more pronounced with more incubation time period. These findings show that changes in the GSH status produced by Ammonium Vanadate could be due to either by adduct formation of Vanadium and glutathione i.e. [V-SG] or by increased production of oxidized Glutathione [2GSH +V[+5] - GSSG]. This change in GSH metabolic status provides some information regarding the mechanism of toxicity by Ammonium Vanadate and the protective role of glutathione
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Humanos , Glutationa/sangue , Vanadatos/metabolismo , Dissulfeto de Glutationa/metabolismo , Biomarcadores/sangue , Citosol/metabolismo , Relação Dose-Resposta a DrogaRESUMO
Aluminium is being used in the medicines in the form of antacids. The Aluminium metal can be leached from our utensils and can harm the body for its side effects, if become available to the systemic circulation. So it is important to check the effect of Aluminum on the Glutathione in vivo condition. Ellman method was used to determine the effect of Aluminum on GSH level in whole blood spectrophotometerically. 5,5-Dithiobis, 2-Nitrobenzoic Acid, Glutathione, Aluminium sulphate, phosphate buffer, HC1 [Hydrochloric acid] and other laboratory instruments were used to conduct the research work. Time dependent effect of Aluminum on Glutathione level in whole blood was also checked and decrease was observed. This study also shows the effect of Aluminum as helping agent for the Glutathione to enhance the antioxidant system of the body or a cause for depletion of reduced Glutathione
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Humanos , Glutationa/sangue , Sangue , Antiácidos , Ácido Ditionitrobenzoico , Ácido Clorídrico , AntioxidantesRESUMO
To evaluate the protective role of vitamin-E [alpha-tocopherol] on caecal ulcerogenicity of diclofenac sodium administration in albino rats. An animal study carried on experimental albino rats. The study was carried out in the department of Anatomy, Basic Medical Sciences Institute, Jinnah Postgraduate Medical Centre, Karachi, from 2001 to 2002. Diclofenac sodium and vitamin-E were administered to male albino rats separately and simultaneously at a dose of 2 mg/kg/body weight [for each drug] orally once daily for two weeks. These animals were sacrificed. Caeca were identified and removed, opened along mesenteric border, stretched and examined under dissecting microscope. The severity of erosions and ulcers was rated according to an arbitrary scale of Bonta. The caecum was then fixed in 10% formalin, embedded in paraplast. 4 micro m thick sections were cut on rotary microtome and stained with haematoxylin and eosin [H and E]. The histomorphological features of caecal mucosa were compared with those in the control animals and analyzed statistically. The study revealed that diclofenac sodium administration in albino rats produced ulcerative changes in caecal mucosa and simultaneously vitamin-E protected caecal ulcerogenicity. These results suggest that diclofenac sodium causes severe caecal mucosal damage in albino rats, however, could be protected by simultaneous administration of vitamin-E in albino rats
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Animais de Laboratório , Ceco/efeitos dos fármacos , Úlcera/prevenção & controle , Antioxidantes , Vitamina E , RatosRESUMO
Based on World Health Organization statistics, the worldwide prevalence of diabetes is expected to increased from an estimated 155 million in the year 2000 to 300 million in 2025. Diabetic nephropathy is an important cause of morbidity and mortality and is now among the most common causes of end stage renal failure [ESRF] in the developed countries. Renin angiotensin system has been implicated in the pathophysiology of diabetic nephropathy and associated complications due to its specific effects on intra-glomerular blood flow, resistance and general effects. In this clinical trial we have used antitypertensive agent i.e., Losartan [AT-1 receptor blocker] and found it to be effective both in delaying the development of renal damage secondary to diabetes and avoidance of other major complications associated to diabetic nephropathy