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Singla M.,Jawaharlal Institute of Postgraduate Medical Education & Research | Prabhakar S.,Jawaharlal Institute of Postgraduate Medical Education & Research | Modi M.,Jawaharlal Institute of Postgraduate Medical Education & Research | Medhi B.,Pharmacology | And 2 more authors.
Epilepsia | Year: 2011

Purpose: To determine the effect of administration of a short course of prednisolone on seizure and radiologic outcome in patients with solitary cysticercus granuloma (SCG). Methods: One hundred forty-eight subjects presenting with new-onset seizures (<15 days duration) and with SCG demonstrated on imaging studies were randomly allocated to either treatment with prednisolone (40-60 mg/day for 2 weeks) or placebo in addition to standard antiepileptic drug therapy. The subjects were followed up for seizure recurrence for 9 months. Repeat computed tomography (CT, at 3 months) and magnetic resonance imaging (MRI, at 6 months) to evaluate resolution and calcification of the lesion. Key Findings: There was no difference in the proportion of subjects with seizure recurrence during the follow-up period in the treatment (n = 16, 21.9%) and control (n = 19, 25.33%) groups (p = 0.7). However, generalized seizures occurred in a significantly lesser proportion of subjects in the treatment group (n = 3, 15.79%) in comparison to the control group (n = 12, 60.00%) (p = 0.015). There were no significant differences in the proportion of subjects with complete resolution of the SCG on repeat CT at 3 months [treatment group (27, 46.7%) and control group (23, 39.8%); p = 0.453] and repeat MRI at 6 months [treatment group (28, 46.7%) and control group (21, 38.9%); p = 0.402]. Significance: The administration of a short course of prednisolone does not offer significant improvement in seizure control, although a benefit in terms of reducing the likelihood of generalized seizures is possible. Furthermore, it does not improve the chances of resolution of the SCG on follow-up imaging studies. © 2011 International League Against Epilepsy.

Moeen-ud-din H.,Allama Iqbal Medical College | Murad S.,Pharmacology | Fatima A.,LM and DC
Pakistan Journal of Medical and Health Sciences | Year: 2014

To get good compliance of therapeutic goal of hypolipidemic agents by cardiologist and patient, some herbal drugs have had been used by some expert cardiologists. Among those herbal medicines Kalonji is most important drug used as hypolipidemic agent. In this research work hypolipidemic effects of kalonji are compared with hypolipidemic effects of Niacin. It was single blind placebo-controlled comparative study, conducted at Jinnah Hospital, Lahore from September 2013 to December 2013. Ninety hyperlipidemic patients were enrolled after written and well explained consent. Ninety patients were divided in three groups, one group as placebo and other two groups for Niacin and kalonji. After six weeks of therapy by 2 medicines, research proved highly significant changes in LDL-cholesterol, but significant changes in HDL-cholesterol in hyperlipidemic patients.

Tseng C.-L.,National Yang Ming University | Wei J.-W.,Pharmacology
Journal of the Chinese Medical Association | Year: 2012

Background: Information related to histamine-induced cellular responses in C6 glioma cells through second messenger pathways has not been fully studied, especially the involvement of arachidonic acid (AA) metabolism. In addition, specific labeled ligand binding to histamine receptor sites still needs to be clarified. Methods: Labeled mepyramine ligand was used to study its binding sites; [ 3H] inositol was used to detect inositol 4-phosphate (IP 1) formation, and fura-2/AM was used to detect intracellular free calcium ion ([Ca 2+]i) level activated by the phosphatidylinositol-phospholipase C (PI-PLC) pathway. Also, labeled AA was used to detect the metabolism of AA and its metabolites release via the activation of phospholipase A2 in the presence of histamine. Results: C6 glioma cells incubated with histamine in the presence of 10 mM LiCl for 60 minutes induced an increase of IP 1 and glycerophosphoric-inositol (GPI) accumulation. In addition, histamine caused an increase of extracellular AA with its metabolite release, eliciting a transient and sustained increase of free [Ca 2+]i. The sustained increase of [Ca 2+]i was almost or completely blocked by La 3+ and excess ethylene diamine tetraacetic acid. The calcium ion influx associated with the sustained phase required the presence of histamine on the receptor sites, and could be blocked by a H 1 antagonist, chlorpheniramine. Conclusion: C6 glioma cells possess histamine H 1 receptors that have affinity towards [ 3H]mepyramine binding, and are coupled to PI-PLC to generate inositol phosphates and to increase [Ca 2+]i, and they are coupled to phospholipase A2 (PLA2) to generate GPI and AA with its metabolite release. The transient increase in [Ca 2+]i can be attributed to Ca 2+ release from intracellular stores, whereas the sustained increase in [Ca 2+]i is due to influx of extracellular calcium ions. The sustained increase in [Ca 2+]i plays a role in the activation of histamine receptor-coupled PLA2. © 2012.

Sandozi T.,Pharmacology
Research Journal of Pharmaceutical, Biological and Chemical Sciences | Year: 2013

To compare the cost analysis of H2 antagonists and proton pump inhibitors (PPIs) prescribed in a tertiary care hospital.A prospective cross sectional study was done for three months. All hospitalized patients prescribed H2 antagonists and PPIs in the medical and surgical wards of the hospital were included in the study. The total number of patients prescribed H2 antagonists and PPIs, their subtypes and the indication for their prescription was noted. The cost analysis of these two groups of anti-secretory (ASD) drugs was determined and compared. 112 patients were prescribed H2 antagonists and PPIs during their hospitalization. PPIs were prescribed more frequently than H2 antagonists. An indication for prescription was present in only 45% of the patients. The cost analysis showed a vast difference in the cost of treatment between (PPIs) and H2 antagonists. This study showed inappropriate prescription of PPIs.

Tseng C.-L.,National Yang Ming University | Wei J.-W.,Pharmacology
Chinese Journal of Physiology | Year: 2013

Molecular events involved in the homologous desensitization of histamine-mediated signal transduction system in glioma cells are not well understood. The aim of this study was designed to gain further insight into possible events in the process using the C6 glioma cells. Incubation of histamine caused increases in inositol phosphate (IP1) formation and intracellular free-calcium concentration [Ca2+]i in C6 glioma cells via the activation of a G-protein-coupled phospholipase C (PI-PLC). Histamine also caused an increase in extracellular release of arachidonic acid (AA) and formation of glycerophosphoinositol (GPI). These effects are likely to be mediated through the activation of receptor-coupled phospholipase A2 (PLA2). Pretreatment of C6 cells with histamine, from 0.1 μM to 1 mM concentrations, for 10 to 60 min significantly reduced the histamine-induced IP1 production, [Ca2+]i accumulation, AA release and GPI formation, despite repeated wash of the cells with buffer solution. Staurosporine (10 nM), a protein kinase C inhibitor, reversed almost completely IP1 production, or partially for [Ca2+]i, GPI formation and AA release of this homologous desensitization effect of histamine. Pretreatment of C6 cells with phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, at 0.1 nM to 0.1 μM for 2 to 15 min caused a reduction of histamine-induced IP1 formation and [Ca2+]i accumulation, but enhanced histamine-induced AA release and GPI formation. 10 nM staurosporine completely reversed the effect of PMA on histamine-induced IP1 formation and partially on [Ca2+]i accumulation. However, staurosporine potentiated the effect of PMA on histamine-induced AA release and GPI formation, but the effect could be blocked by H7, a calcium-dependent protein kinase C inhibitor. Our results indicate that activation of protein kinase C by histamine in the signal transduction system is involved in the histamine-induced homologous desensitization event. Since PMA pretreatment could not mimic histamine-induced homologues desensitization event in AA release and GPI formation, it is likely due to the dual actions of this protein kinase activator: on calcium independently, and also on calcium dependent via influx of calcium ion through the plasma membrane. The calcium flux effect of PMA is related to the difference between PMA and histamine on the effects of AA release and GPI formation via activation on phospholipase A2. The results of this study provided strong evidence that protein kinase C is involved in this homologous desensitization caused by continuous histamine receptor activation. © 2013 by The Chinese Physiological Society and Airiti Press Inc.

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