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Chennai, India

Sri Ramachandra Medical College and Research Institute , now named Sri Ramachandra University , is a deemed university declared under Section 3 of the UGC at 1956, in Porur, Chennai, India. SRU consists of eight constituent colleges with over 45 departments offering about 92 courses in health care and medical studies and research with more than 3500 students.SRU was founded by Sri Ramachandra Education & Health Trust on September 11, 1985 by Shri NPV Ramaswamy Udayar . Originally founded as a medical college, it became a university in September 1994.In 1997, SRU entered into a relationship with Partners Harvard Medical International to pursue curriculum reform, faculty development, and improvements in health care quality and patient safety in the school's affiliated medical centre. One of the results of this collaboration was the achievement of accreditation by Joint Commission International in 2009, the first teaching hospital in India to obtain such accreditation from JCI. The university has been accredited by NAAC with A Grade with a GCPA of 3.52 on a 4-point scale, the highest to be awarded to a private medical university in India. Sri Ramachandra Medical Centre is the associated teaching hospital for the school. Wikipedia.


Shah P.B.,Sri Ramachandra University
The Cochrane database of systematic reviews | Year: 2014

Febrile seizures can be classified as simple or complex. Complex febrile seizures are associated with fever that lasts longer than 15 minutes, occur more than once within 24 hours and are confined to one side of the child's body. It is common in some countries for doctors to recommend an electroencephalograph (EEG) for children with complex febrile seizures. A limited evidence base is available to support the use of EEG and its timing after complex febrile seizures among children. To assess the use of EEG and its timing after complex febrile seizures in children younger than five years of age. We searched the Cochrane Epilepsy Group Specialised Register (17 October 2013), the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 9, 2013), MEDLINE (17 October 2013) and the Clinical Trial Registry (ClinicalTrials.gov (17 October 2013)). We applied no language restrictions. All randomised controlled trials (RCTs) that examined the utility of an EEG and its timing after complex febrile seizures in children. Review authors selected and retrieved the articles and independently assessed which articles should be included. Disagreements were resolved by discussion and by consultation with the Cochrane Epilepsy Group. We applied standard methodological procedures expected by The Cochrane Colloboration. Of 33 potentially eligible studies, no RCTs met the inclusion criteria. We found no RCTs as evidence to support or refute the use of EEG and its timing after complex febrile seizures among children. A randomised controlled trial can be planned in such a way that participants are randomly assigned to the EEG group and to the non-EEG group with sufficient sample size. Source


The present study focuses on the temporal calcium significance in middle cerebral artery occluded (2h ischemia)-reperfused (70h reperfusion) rats treated with nimodipine (NM) through concurrent measurements of excitotoxicity, bioenergetics and neurobehavioural paradigms. Further, the suitable therapeutic time window of calcium channel antagonism in stroke was also ascertained. NM (5mg/kg, i.p.) was administered at pre (30min before the induction of ischemia), during (1h following occlusion of MCA) and post-ischemic (3h after begin of reperfusion) states. The magnitude of neuroprotection in terms of excitotoxicity (glutamate, glutamine synthetase, Na+K+ATPase), bioenergetics (ATP, NAD+) and neurobehavioural paradigms (neurological score and open field exploratory behaviour) were measured and compared to ensure the therapeutic time-window of NM in stroke. Middle cerebral artery occlusion-reperfusion (MCAO/R) was found to elevate glutamate, glutamine synthetase levels and deplete Na+K+ATPase activity in the vehicle treated group (IR group). Significant decrease in bioenergetics such as ATP and NAD+ levels was also observed. Further, IR group demonstrated grievous oxidative stress (increase in lipid peroxidation, protein carbonyl content, nitrite/nitrate levels and decrease in superoxide dismutase and glutathione levels) along with anxiogenic behaviour, neurological deficits and neuronal damage and decreased nuclear to cytoplasm ratio in CA1 hippocampal region. Post-ischemic NM administration reversed the excitotoxicity, neurobehavioural and histopathological alterations significantly, but it restored bioenergetics level in MCAO/R rats only partially.These findings were further confirmed with the combination treatment (CT) of post-ischemic NM and pre-ischemic memantine (MN) administration, since MN showed protective effect in the pre-ischemic administration (Babu and Ramanathan, 2009). The failure of NM to forefend the neurodegeneration on pre- and during-ischemic administration suggests that the initial phase damages in ischemic-reperfusion (IR) might be mediated through other mechanism(s) such as glutamergic overstimulation or reverse operation of glutamate transporters. From the present study, it is concluded that calcium plays a crucial role in post-ischemic status and the suitable therapeutic time window of calcium antagonism is the post-ischemic state. © 2010 ISDN. Source


Balakrishnan K.,Sri Ramachandra University
Research report (Health Effects Institute) | Year: 2011

This report describes the results of a time-series analysis of the effect of short-term exposure to particulate matter with an aerodynamic diameter < or = 10 pm (PM10) on mortality in metropolitan Chennai, India (formerly Madras). This was one of three sites in India chosen by HEI as part of its Public Health and Air Pollution in Asia (PAPA) initiative. The study involved integration and analysis of retrospective data for the years 2002 through 2004. The data were obtained from relevant government agencies in charge of routine data collection. Data on meteorologic confounders (including temperature, relative humidity, and dew point) were available on all days of the study period. Data on mortality were also available on all days, but information on cause-of-death (including accidental deaths) could not be reliably ascertained. Hence, only all-cause daily mortality was used as the major outcome for the time-series analyses. Data on PM10, nitrogen dioxide (NO2), and sulfur dioxide (SO2) were limited to a much smaller number of days, but spanned the full study period. Data limitations resulting from low sensitivity of gaseous pollutant measurements led to using only PM10 in the main analysis. Of the eight operational ambient air quality monitor (AQM) stations in the city, seven met the selection criteria set forth in the common protocol developed for the three PAPA studies in India. In addition, all raw data used in the analysis were subjected to additional quality assurance (QA) and quality control (QC) criteria to ensure the validity of the measurements. Two salient features of the PM10 data set in Chennai were a high percentage of missing readings and a low correlation among daily data recorded by the AQMs. The latter resulted partly because each AQM had a small footprint (approximate area over which the air pollutant measurements recorded in the AQM are considered valid), and partly because of differences in source profiles among the 10 zones within the city. The zones were defined by the Chennai Corporation based on population density. Alternative exposure series were developed to control for these data features. We first developed exposure series based on data from single AQMs and multiple AQMs. Because neither was found to satisfactorily represent population exposures, we subsequently developed an exposure series that disaggregated pollutant data to individual zones within the city boundary. The zonal series, despite some uncertainties, was found to best represent population exposures among other available choices. The core model was thus a zonal model developed using disaggregated mortality and pollutant data from individual zones. We used quasi-Poisson generalized additive models (GAMs) with smooth functions of time, temperature, and relative humidity modeled using penalized splines. The degrees of freedom (df) for these confounders were selected to maximize the precision with which the relative risk for PM10 was estimated. This is a deviation from the traditional approaches to degrees of freedom selection, which usually aim to optimize overall model fit. Our approach led to the use of 8 df/year for time, 6 df/year for temperature, and 5 df/year for relative humidity. The core model estimated a 0.44% (95% confidence interval [CI] = 0.17 to 0.71) increase in daily all-cause mortality per 10-pg/m3 increase in daily average PM10 concentrations. Extensive sensitivity analyses compared models constructed using alternative exposure series and contributions of model parameters to the core model with regard to confounder degrees of freedom, alternative lags for exposure and meteorologic confounders, inclusion of outliers, seasonality, inclusion of multiple pollutants, and stratification by sex and age. The sensitivity analyses showed that our estimates were robust to a range of specifications and were also comparable to estimates reported in previous time-series studies: PAPA, the National Morbidity, Mortality, and Air Pollution Study (NMMAPS), Air Pollution and Health: A European Approach (APHEA), and Air Pollution and Health: A European and North American Approach (APHENA). While the approaches developed in previous studies served as the basis for our model development, the present study has new refinements that have allowed us to address specific data limitations (such as missing measurements and small footprints of air pollution monitors). The methods developed in the study may allow better use of routine data for time-series analysis in a broad range of settings where similar exposure and data-related issues prevail. We hope that the estimates derived in this study, although somewhat tentative, will facilitate local environmental management initiatives and spur future studies. Source


Environmental and occupational risk factors contribute to nearly 40% of the national burden of disease in India, with air pollution in the indoor and outdoor environment ranking amongst leading risk factors. It is now recognized that the health burden from air pollution exposures that primarily occur in the rural indoors, from pollutants released during the incomplete combustion of solid fuels in households, may rival or even exceed the burden attributable to urban outdoor exposures. Few environmental epidemiological efforts have been devoted to this setting, however. We provide an overview of important available information on exposures and health effects related to household solid fuel use in India, with a view to inform health research priorities for household air pollution and facilitate being able to address air pollution within an integrated rural-urban framework in the future. Source


Chronic obstructive pulmonary disease (COPD) is the 13th leading cause of burden of disease worldwide and is expected to become 5th by 2020. Biomass fuel combustion significantly contributes to COPD, although smoking is recognized as the most important risk factor. Rural women in developing countries bear the largest share of this burden resulting from chronic exposures to biomass fuel smoke. Although there is considerable strength of evidence for the association between COPD and biomass smoke exposure, limited information is available on the background prevalence of COPD in these populations. This study was conducted to estimate the prevalence of COPD and its associated factors among non-smoking rural women in Tiruvallur district of Tamilnadu in Southern India. This cross-sectional study was conducted among 900 non-smoking women aged above 30 years, from 45 rural villages of Tiruvallur district of Tamilnadu in Southern India in the period between January and May 2007. COPD assessments were done using a combination of clinical examination and spirometry. Logistic regression analysis was performed to examine the association between COPD and use of biomass for cooking. R software was used for statistical analysis. The overall prevalence of COPD in this study was found to be 2.44% (95% CI: 1.43-3.45). COPD prevalence was higher in biomass fuel users than the clean fuel users 2.5 vs. 2%, (OR: 1.24; 95% CI: 0.36-6.64) and it was two times higher (3%) in women who spend >2 hours/day in the kitchen involved in cooking. Use of solid fuel was associated with higher risk for COPD, although no statistically significant results were obtained in this study. The estimates generated in this study will contribute significantly to the growing database of available information on COPD prevalence in rural women. Moreover, with concomitant indoor air pollution measurements, it may be possible to increase the resolution of the association between biomass use and COPD prevalence and refine available attributable burden of disease estimates. Source

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