A Study of Assessing Errors and Completeness of Research Application Forms Submitted to Instituitional Ethics Committee (IEC) of a Tertiary Care Hospital.

INTRODUCTION: Application form of research work is an essential requirement which is required to be submitted along with the research proposal to the Ethics Committee (EC). AIM: To check the completeness and to find the errors in application forms submitted to the EC of a tertiary care hospital. MATERIALS AND METHODS: The application forms of research projects submitted to the Institutional Review Board (IRB), Government Medical College, Bhavnagar, Gujarat, India from January 2014 to June 2015 were analysed for completeness and errors, with respect to the following - type of study, information about study investigators, sample size, study participants, title of the studies, signatures of all investigators, regulatory approval, recruitment procedure, compensation to study participants, informed consent process, information about sponsor, declaration of conflict of interest, plans for storage and maintenance of data, patient information sheet, informed consent forms and study related documents. RESULTS: Total 100 application forms were analysed. Among them, 98 were academic and 2 were industrial studies. Majority of academic studies were of basic science type. In 63.26% studies, type of study was not mentioned in title. Age group of subjects was not mentioned in 8.16% application forms. In 34.6% informed consent, benefits of the study were not mentioned. Signature of investigators/co-investigators/Head of the Department was missing in 3.06% cases. CONCLUSION: Our study recommends that the efficiency and speed of review will increase if investigator will increase vigilance regarding filling of application forms. Regular meetings will be helpful to solve the problems related to content of application forms. The uniformity in functioning of EC can be achieved if common application form for all ECs is there.

Evaluation of cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds on isoprenaline-induced myocardial injury in Wistar albino rats.

In the present study, cardioprotective effect of aqueous extract of Garcinia indica Linn. fruit rinds in isoprenaline-induced myocardial infarction in Wistar albino rats was evaluated. In vitro total phenolic, total flavonoid content and 2, 2'-diphenyl-1-picrylhydrazyl hydrate radical scavenging activity was measured. In vivo effect of aqueous extract of G. indica was evaluated in Wistar albino rats by isoprenaline-induced myocardial injury model. Thirty six rats were randomly divided in 6 groups. Rats were treated with G. indica 250 mg/kg and 500 mg/kg doses for 21 days and myocardial injury was produced by subcutaneous injection of isoprenaline 85 mg/kg on day 20 and 21. Carvedilol 1 mg/kg for 21 days served as active control. Electrocardiogram parameters, cardiac injury markers (serum troponin-I, uric acid, lactate dehydrogenase, creatinine kinase-MB, aspartate aminotransferase and alanine aminotransferase), oxidative stress markers (superoxide dismutase, catalase and malondialdehyde level) and histopathological changes were evaluated in each group and compared using appropriate statistical tests. In vitro evaluation of aqueous extract showed significant antioxidant property. Isoprenaline produced significant myocardial ischemia as compared to normal control group (P<0.05). Administration of G. indica in both the doses did not significantly recover the altered electrocardiogram, cardiac injury markers, oxidative stress markers and histopathological myocardial damage as compared to disease control group (P>0.05). The aqueous extract of G. indica was not found to be cardioprotective against myocardial injury. Further study with more sample size and higher dose range may be required to evaluate its cardioprotective effect.

Interaction between rosuvastatin and rocuronium in rat sciatic-gastrocnemius nerve-muscle preparation.

PURPOSE: Long-term use of rosuvastatin may be associated with myotoxicity. Statins are one of the groups commonly found to be associated with neuromuscular weakness. The present study was designed to investigate the interaction between rosuvastatin and rocuronium in vivo by using a sciatic-gastrocnemius nerve-muscle preparation of rat. METHODS: In our study groups, animals received rosuvastatin 2 mg/kg for 14 and 28 days. Train of four (TOF) stimulation was applied to the sciatic nerve, and gastrocnemius muscle contractions were recorded in Wistar albino rats. Intravenous infusion of rocuronium was given until the twitch responses were abolished. We ultimately compared the effective dose required for a desired effect in 95% of the population (ED95), duration 25%, deep block, recovery index, and time for returning of TOF ratio to 0.9 between the active control and study groups. RESULTS: Chronic administration of rosuvastatin at a dose of 2 mg/kg for 28 days significantly reduced the ED95 of rocuronium as compared to the active control group. Deep block and duration 25% were increased by 3.5 and 2.5 times, respectively, compared to the active control group. The spontaneous recovery of neuromuscular block was delayed, as evidenced by the prolonged recovery index and increase in time required for a return of the TOF ratio to 0.9. CONCLUSION: The neuromuscular blocking potency of rocuronium is increased and recovery is delayed in rats that pre-treated with rosuvastatin.

Nevirapine and/or co-trimoxazole induced Stevens Johnson syndrome in HIV infected patient--a case report.

A 46 years old HIV reactive patient developed Stevens Johnson syndrome (SJS) probably due to nevirapine and/or co-trimoxazole. Patient was on zidovudine + lamivudine + nevirapine along with Co-trimoxazole since last two months. After 15 days, zidovudine was replaced with stavudine due to development of anemia. All these drugs were stopped after development of reaction. Temporal association was found between stavudine, lamivudine, nevirapine, cotrimoxazole and development of the reaction. Nevirapine and Co-trimoxazole were suspected to cause this reaction most probably due to associated hepatotoxicity and their common potential to cause SJS. In our case, patient died despite stopping of all medications.

Central anti-cholinergic syndrome induced by single therapeutic dose of atropine.

A 55 years old male patient, who is planned for bronchoscopy developed central anti-cholinergic syndrome due to therapeutic dose of atropine. Withdrawal of atropine has improved the symptoms. Thereafter, instillation of atropine as eye drops leads to reappearance of symptoms. The reaction was definite according to Naranjo's algorithm. It was severe and definitely preventable according to Modified Hartwig and Siegel's scale and Modified Schumock and Thornton scale respectively. Central anti-cholinergic syndrome may be due to variation in the genetic susceptibility (Idiosyncrasy) to atropine. Idiosyncratic reaction on administration of atropine as a pre-anesthetic medication or eye drops should be kept in mind while prescribing.