Dès la troisième semaine d’interruption de la substitution par an

Dès la troisième semaine d’interruption de la substitution par androgènes de jeunes adultes atteints d’hypogonadisme hypogonadotrope a été observée une réduction de la sensibilité à l’insuline suggérant que le rôle modulateur de la testostérone passe en partie par des mécanismes indépendants des variations de la composition corporelle [37]. Bien que cela n’ait pas été observé au cours de la substitution androgénique d’hypogonadismes hypogonadotropes congénitaux [33], de nombreuses études ont montré que la substitution par androgènes d’hommes adultes hypogonadiques améliorait [4] and [38] ou faisait disparaître les stigmates de SMet [39], [40] and [41].

Un phénotype d’une similitude étroite à celui du SMet est observé

chez l’homme Afatinib in vivo traité par « blocage androgénique » pour carcinome de prostate ne relevant pas d’un geste chirurgical curateur [42]. La profonde hypotestostéronémie ainsi induite s’associe à une élévation significative Nutlin-3a concentration de la glycémie à jeun, du taux des triglycérides et à une surcharge pondérale de type androïde, trois pièces constitutives du puzzle clinico-biologique caractéristique du SMet. Les chiffres de pression artérielle ne sont pas modifiés et le taux de LDL-cholestérol n’est que modestement accru. À l’inverse, l’élévation de la glycémie est une des principales répercussions métaboliques du « blocage androgénique ». Une glycémie à jeun > 7 mmol/L [43] a été retrouvée chez près de la moitié des hommes traités de cette manière. À glycémie égale, l’insulinémie à jeun s’élève significativement trois mois après l’initiation de la thérapeutique chez les deux tiers des hommes traités par « blocage androgénique » [44]. Une réduction de la sensibilité tissulaire à l’insuline apparaît être ainsi une des principales conséquences de l’absence d’androgènes. Parallèlement à la correction de certains paramètres du SMet grâce à la réduction

pondérale chez l’homme s’observe une élévation des taux plasmatique de testostérone et de SHBG [45] and [46]. Ceci fournit un lien de causalité inverse entre SMet et hypotestostéronémie. Les relations entre testostéronémie et SMet Dichloromethane dehalogenase sont à l’évidence bidirectionnelles, vraisemblablement composites et sous-tendues par des mécanismes partagés pour partie par ceux de la déflation androgénique accompagnatrice de l’obésité (voir supra) ou du DT2 (voir infra). Les résultats des études épidémiologiques effectuées chez les hommes et les femmes adultes apportent de plus en plus d’arguments en faveur de l’implication de la SHBG [30] and [47] dans l’émergence d’un SMet. Un abaissement du taux plasmatique de SHBG et/ou un polymorphisme particulier de la molécule pourraient intervenir comme un des facteurs physiopathologiques du SMet ou même du DT2 [48] and [49].

The concentrations

The concentrations www.selleckchem.com/products/at13387.html of sodium and potassium ions were determined by the method of.11 The data obtained from the laboratory results of the tests were

subjected to One Way Analysis of Variance (ANOVA). Significant differences were observed at p ≤ 0.05. The results were expressed as means of five replicates ± standard deviations (SD). This analysis was done using the computer software known as Statistical Package for Social Sciences (SPSS), version 16. The qualitative phytochemical analyses showed, the presence of saponins in very high concentration in both fractions of the chloroform–methanol extract of the leaves of P. americana ( Table 1). Flavonoids were found to be present in very high concentration TSA HDAC mw and moderately high concentration in the chloroform and the methanol fractions respectively. Tannins, terpenoids and steroids were found to be present in moderately high concentrations in both fractions

as shown in Table 1. The phytochemical constituents of the chloroform and the methanol fractions of the chloroform–methanol extract of the leaves of P. americana are summarised in Table 2. The chloroform fraction of the extract contained higher percentages of alkaloids (2.67 ± 0.13%), flavonoids (3.20 ± 0.17%) and steroids (1.36 ± 0.04%) than the methanol fraction while the methanol fraction contained higher percentages of saponins (2.23 ± 0.09%) and tannins (2.73 ± 0.13%) than the chloroform fraction ( Table 2). The charcoal meal (gastro-intestinal motility) test was used to determine the propulsive movement along the gastro-intestinal tract (GIT) of rats. As shown in Fig. 1, the methanol and the chloroform fractions of the extract at the tested doses (100 and 200 mg/kg body weight of each) significantly (p < 0.05) decreased the percentage distance travelled by the charcoal meal along the gastro-intestinal tract of rats in groups 4, 5, 6 and 7 when compared to Bumetanide the value obtained for rats in the charcoal meal-treated control

group (group 2). The observed effects were dose-dependent with percentage distance travelled by charcoal meal as 62.25 ± 4.57, 57.25 ± 1.50, 58.25 ± 2.22 and 35.25 ± 2.36 for rats in the 100 and 200 mg/kg body weight of the methanol fraction-treated groups (groups 4 and 5), 100 and 200 mg/kg body weight of the chloroform fraction-treated groups (groups 6 and 7) respectively when compared to the value (70.25 ± 3.30) obtained for rats in the charcoal meal-treated control group (group 2). The effects of the methanol and the chloroform fractions of the extract at the tested doses were comparable to that of the standard anti-diarrhoeal agent (hyoscine butylbromide) as shown in Fig. 1. Result of the intestinal fluid sodium ion concentration test as shown in Fig. 2, shows that the rats of the castor oil-treated control group (group 2) had significantly (p < 0.05) increased intestinal fluid sodium ion concentration (227.00 ± 3.46) when compared to the value (192.75 ± 11.

Animal care followed the official governmental guidelines in comp

Animal care followed the official governmental guidelines in compliance with the CPCSEA, New Delhi and experimental protocols were conducted with the approval of the Ethics Committee of Andhra University, Visakhapatnam, India. Cerebral infarction was induced by Bi-lateral

common carotid artery (BCA) occlusion method described by Iwasakhi et al9 briefly; rats were anesthetized with thiopental sodium (30 mg/kg). Cervical vertebrae and the common carotid arteries were then exposed carefully separated from the vagus nerve. These arteries were occluded for 30 min followed by reperfusion for 4 h. The rectal temperature was maintained at 37 ± 0.5 °C with a feedback-controlled heating-pad. Animals which did not lose the righting reflex or convulsed during the ischemic episode were excluded. Aqueous root extract Galunisertib of coleus edulis was administered by 15 days pre-treatment at doses of 150, 250 and 300 mg/kg orally. Rats were randomly divided into groups: Sham control, I/R control (Ischemia/reperfusion) and I/R + ACE (3 doses). Each group contains 6 animals. After predetermined NVP-BKM120 datasheet time point of ischemia/reperfusion, the brains were quickly removed and sliced into coronal sections of 2 mm thickness. Each slice was immersed in a 1.0% solution of 2,3,5-triphenyltetrazolium chloride (TTC) for 30 min. Necrotic infarcted tissue was unstained

and viable tissue was stained dark red, further separated and weighed. Percentage of infarction was calculated.10 In selected group of animals were pre treated with 250 mg/kg po dose, brain

tissues were isolated and used for the estimation of malondialdehyde (MDA),11 superoxide dismutase (SOD),12 and catalase (CAT).13 Data has been represented as mean ± SEM and analyzed by one-way analysis of variance (ANOVA) followed by Tukeys t test (P < 0.05). There was a significant increase in percent cerebral until infarction in I/R group compared to sham control group. A significant dose dependent reduction in percent cerebral infarction was observed with ACE administration. Results were shown in Table 1. MDA levels were significantly increased and SOD, CAT levels were significantly decreased in I/R of rats as compared to sham control group. In ACE treated groups, MDA levels were significantly reduced and SOD and CAT levels were increased significantly. Results were shown in Table 2. After BCA occlusion and reperfusion, several pathological events occur, oxidative stress is one of the most important events to worsen the ischemic condition. Earlier reports suggested that, further increased oxidative stress leads to tissue apoptosis.14 and 7 Free radicals were generated during ischemia and cause oxidative stress and alter the anti oxidative defenses in biological system. All the cells and tissues are equipped with anti oxidative enzymes like superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione reductase (GRD) and substances like reduced glutathione (GSH).

Because of the loss of pigs after the OURT88/1 boost, only four p

Because of the loss of pigs after the OURT88/1 boost, only four pigs were subsequently challenged with virulent Uganda

1965. Two of these developed transient pyrexia and low viraemia. Pig 1834 had a temperature at day 6 of 40.3 °C, and the virus genome was detected at 227 copies/ml and virus at 1.75 HAD50/ml; pig 1845 had a temperature at day 7 of 40.6 °C and the virus genome was detected at 633 copies/ml; and virus at 2 HAD50/ml. The other two pigs challenged with virulent Uganda 1965 isolate showed no clinical signs and no virus was detected in blood by qPCR or HAD assay. Five pigs were challenged with Benin 97/1, two pigs (1811, 1844) developed typical ASF (Fig. 3C and D) and were terminated at days 6 and 7 respectively before developing severe disease. The remaining pigs (1809, 1829, 1837) did not develop pyrexia or other ASF clinical signs but occasionally virus genome was detected Fulvestrant by qPCR at concentrations up to 323 copies/ml but virus was not detected by HAD assay. The two groups of naïve pigs challenged with either virulent Uganda 1965 or Benin 97/1 all developed severe clinical signs of ASF with VE-821 cell line high viraemia (up to 5.37 × 107 genome copies/ml; virus up to 7.25 HAD50), and either died or were terminated within 8 days of challenge (Fig. 3). Post-mortem

examination confirmed severe ASF in these control pigs (see summary in Supplementary Table 2). In the third experiment, 7 immune pigs were

generated and 6 of these were challenged with Benin 97/1. One pig (474) showed pyrexia from 2 weeks after the first immunisation (Supplementary Fig. 1C). This pig was euthanised before the OURT88/1 boost. Post-mortem examination of this pig revealed a dark enlarged spleen characteristic of ASFV infection and Montelukast Sodium virus DNA was detected from the spleen and retropharyngeal lymph node (RLN) by qPCR (8790 and 41000 virus genome copies/mg tissue respectively) and by cytopathic effect in cultures of porcine macrophages. HAD was not observed in these cultures, indicating that the replicating virus was non-HAD, as expected for the OURT88/3 isolate. Six pigs each of the immune and non-immune groups were challenged with Benin 97/1. All of the immunised pigs were protected from challenge without showing any clinical signs or development of viraemia (Fig. 2C and D). Low copy numbers of the virus genome were detected by qPCR, but not HAD, in spleen and RLN of pig 55 at the termination of the experiment but not in any other lymphoid tissues and blood in this pig, or in any tissues from the other immunised and challenged pigs. In contrast, high copy numbers of virus genome and of virus were detected in blood (up to 5.62 × 108 virus genome copies/ml; virus up to 8.3 HAD50/ml) and tissues (virus ∼7 HAD50/mg of tissue) were detected from all lymphoid tissues in all of the non-immune pigs challenged (see summary in Supplementary Table 2).

First trimester

First trimester Kinase Inhibitor Library chemical structure uterine artery Doppler, shows promise but needs further ‘real life’ evaluation [200]. Markers of preeclampsia risk that become available in the second and third trimesters include measures of: placental

perfusion, vascular resistance, and morphology (e.g., mean maternal second trimester BP, 24-h ABPM, Doppler); maternal cardiac output and systemic vascular resistance; fetoplacental unit endocrinology [e.g., pregnancy-associated plasma protein-A (PAPP-A) in the first trimester, and alpha-fetoprotein, hCG, and inhibin-A in the early second trimester]; maternal renal function (e.g., serum uric acid or microalbuminuria); maternal endothelial function and endothelial–platelet interaction (e.g., platelet count, antiphospholipid antibodies, or homocysteine); oxidative stress (e.g., serum lipids); and circulating angiogenic factors [201], [202] and [203]. Systematic reviews of primary studies have evaluated clinically available this website biomarkers [163], [164] and [204] and no single clinical test reaches the ideal of ⩾90% sensitivity for preeclampsia prediction. Only uterine artery Doppler

at 20–24 weeks has sensitivity >60% for detection of preeclampsia, particularly when testing is performed: (i) in women at increased risk of preeclampsia; (ii) during the second trimester, and/or (iii) when predicting severe and early preeclampsia. Women with abnormal velocimetry could be considered for increased surveillance to detect preeclampsia or other adverse placental outcomes. Uterine artery Doppler should not be used in low risk women [162] and [205]. It is unclear whether markers used for Down syndrome screening are useful in isolation (or with uterine artery Doppler) for preeclampsia prediction

[206]. Thrombophilia screening is not recommended for investigation of prior preeclampsia or other placental complications, except if the woman satisfies the clinical MycoClean Mycoplasma Removal Kit criteria for the antiphospholipid antibody syndrome [207] and [208]. As no single test predicts preeclampsia with sufficient accuracy to be clinically useful [209], interest has grown in researching multivariable models that include clinical and laboratory predictors available at booking and thereafter [166], [209] and [210]. Clinicians should support clinics conducting relevant prospective longitudinal studies. We have based our recommendations on both prevention of preeclampsia and/or its associated complications. Pregnant women have been classified as being at ‘low’ or ‘increased’ risk of preeclampsia, usually by the presence of one or more risk markers as shown in Table 5 [see Prediction].

apec org uk/), Australian Action on Pre-eclampsia (AAPEC) www aap

apec.org.uk/), Australian Action on Pre-eclampsia (AAPEC) www.aapec.org.au), New Zealand Action on Pre-eclampsia (NZ APEC) (www.nzapec.com/), and Association de Prevention et d’Actions contre la pre-eclampsie (APAPE) (www.eclampsie.moonfruit.fr/) [515]. The Preeclampsia Foundation advocates for: better patient (and health care provider) Bosutinib cell line education about the antenatal, early postnatal and long-term maternal implications of preeclampsia; an emphasis on early maternal signs

and symptoms of preeclampsia; better doctor–patient communication about preeclampsia; and evidence-based guidelines for pre-eclampsia screening, detection; and management [515]. There is growing evidence that women may experience post-traumatic stress disorder up to seven years postpartum [516], [517], [518], [519], [520], [521], [522], [523] and [524], the prevalence of symptoms being highly variable, ranging from the minority to the majority of women, and higher after: maternal hospitalization >7 days, HDP onset/delivery preterm, NICU admission, adverse neonatal outcomes, and uncertainty about the child’s long-term health [519]. Symptoms are not specific to the HDP, and follow preterm delivery for other indications GDC-0449 concentration [520]. Although post-traumatic stress symptoms do not have an impact on infant cognitive or psychomotor development at one year of age, maternal symptoms are amenable

to clinical psychological therapy, and earlier referral may abbreviate treatment [523]. Women and their maternity care providers seem to view experiences of preeclampsia differently. For health-care professionals, preeclampsia represented the 3-mercaptopyruvate sulfurtransferase care that must be delivered,

primarily responding to the biology of preeclampsia. For women, generally lacking knowledge and understanding about pre-eclampsia, preeclampsia represented fear and risk [525]. In a survey of women who had experienced preeclampsia, eclampsia and/or HELLP, preeclampsia was viewed as very important to all and traumatic to many respondents, women, their partners, close relatives, or friends. The provision of information and support was valued prior to, and at the time of, diagnosis as well as being revisited during ongoing care [526]. Women are not knowledgeable about the HDP, even with pre-existing hypertension, and are not satisfied with the medical information they receive, suggesting that clinicians should both place more value on informing women about their disease and its potential course, and check that women have understood the information [527] and [528]. Although limited health literacy may complicate risk communication, tools have been developed for such purposes [527] and [528]. Women enjoy participating in aspects of their care, be it receiving information as study participants [529], or participating in management of their BP [530]. They do not object to being randomized [380]. Women have expressed a preference for home or day care [531] and self (rather than 24-h ambulatory) BP monitoring [532].

Efficacy against incident HPV-16/18 associated CIN2+ was 89 8% (9

Efficacy against incident HPV-16/18 associated CIN2+ was 89.8% (95% CI = 39.5–99.5; rate reduction = 3.4/1000 women) using our a priori algorithm for HPV type attribution and 88.7% (95% CI = 31.3–99.5; rate reduction = 3.0/1000

women) using the alternative (exploratory) definition that considers viral persistence when making HPV type attribution. A total of 11 HPV-16/18 associated CIN2+ events were observed using our a priori definition; 10 were CIN2 and one was a CIN3. The single HPV-16/18 CIN2+ event in the HPV arm occurred in a participant who at entry had antibodies against both HPV-16 and HPV-18, and evidence (by DNA test) of infection with a non-oncogenic HPV type (HPV-66), and who was

positive (by DNA test) for SB431542 clinical trial HPV-16 and -45 11 months after enrollment and diagnosed with CIN3 15 months after enrollment. Efficacy estimates against CIN2+ associated with non-HPV-16/18 oncogenic HPV types were 59.9% (a priori definition) and 78.7% (exploratory definition). The breakdown of HPV types detected by arm is summarized in Fig. 2a (a learn more priori definition) and b (exploratory definition). Efficacy estimates irrespective of HPV type were 61.4% (95% CI = 29.5–79.8; rate reduction = 8.4/1000 women; N = 37 in control arm and 14 in HPV arm) by our a priori and 75.3% (95% CI = 48.1–89.3; rate reduction = 9.2/1000 women; N = 33 in control arm and 8 in HPV arm) by our exploratory definition of incident outcomes. Results for individual oncogenic HPV types are summarized in Supplemental Tables 2a and 2b. Supplementary Table 2a.   Vaccine efficacy against CIN2+ outcomes (by individual HPV types; a priori definition) – ATP cohort for efficacy – Costa Rica HPV-16/18 vaccine new trial (CVT). Efficacy against incident HPV-16/18 infections during the study was 79.5% (95% CI = 74.0–84.0; rate reduction = 115/1000 women) (Table 2). Efficacy in this group of young adults was lowest in the first year of follow-up (57.1%; 95% CI = 33.2–73.0) and higher in subsequent years (82.6% in year 4+; 95% CI = 73.0–89.2).

Safety findings are summarized in Table 3. Rates of solicited local and general AEs were comparable in the two arms in the hour following vaccination. The rate of local solicited AEs within 3–6 days following any vaccination was higher among those in the HPV arm (53.7% for all; 1.8% for grade 3 AEs) compared to the control arm (19.9% for all; 0.0% for grade 3 AEs). Unsolicited AEs reported in the month following any vaccination were comparable between arms. The proportion of participants with SAEs, SAEs possibly related to vaccination, medically significant conditions, new-onset chronic diseases, autoimmune AEs, neurological AEs, and deaths were comparable between arms. All but 12 SAEs possibly related to vaccination were pregnancy related [18].

, 2012) Like other CPPW communities, the SNHD used a portion of

, 2012). Like other CPPW communities, the SNHD used a portion of their grant funds to support PA. The SNHD’s strategies to

increase PA included selleck compound the promotion and improvement of local trails. We have previously reported on the characteristics and effect of its media campaign promoting trail use, where we observed a 52% increase in mean users per hour over six months (Clark et al., in press). This portion of the project involves the same trails but a longer time period and also includes an alteration to the trail environment. A recent review of trails and PA completed by Starnes et al. (2011) reports that trail use has been both positively and negatively associated with age, racial and ethnic minority status, and gender. The reviewers

also reported mixed results from studies investigating access to trails and levels of PA, and called for further click here research to investigate the relationship between trails and PA. Price et al. (2013) recently studied correlates of trail use in Michigan and reported higher levels of use among males, those with higher levels of education, and White race/ethnicity. Most previously published studies of trail usage are cross-sectional and rely on self-reported behaviors (Starnes et al., 2011). Few studies have reported on objective measures of trail use or changes in trail usage over time. Evenson et al. (2005) analyzed PA among those living near a new trail, before and after construction, but their study showed no significant increase in PA. Another study of the promotion of a newly constructed trail in Australia aminophylline used data from telephone surveys and objective counts to assess PA changes among people living nearby (Merom et al., 2003). The authors reported both an increase in cycling traffic and an increase in PA among one subgroup (Merom et al., 2003). Fitzhugh et al.

(2010) reported a positive effect on PA in adults when trail access was improved, but they did not report on the effect of signage. Price et al. (2012) studied seasonal variations in trail use among older adults, but they did not assess the effect of changing the trail environment. Although the presence of trail signage is noted in trail environment assessment tools (Troped et al., 2006), to our knowledge there are no published articles on the effect of trail signage on trail usage. Accordingly, the purpose of our study was to assess the longer term effects of the marketing campaign and to compare usage on trails which were altered by adding way-finding and incremental distance signage to usage on control trails which were not altered, using longitudinal data obtained from objective measures of trail use. We employed a quasi-experimental design with a comparison group to assess the effect of signage additions on trail use in Southern Nevada.

Indeed, during the second year of follow-up, 96 cases of severe R

Indeed, during the second year of follow-up, 96 cases of severe RVGE were detected. During the second year of follow-up the point estimate of vaccine

efficacy was 19.2%. We surmise that if a similarly intense and culturally compatible surveillance selleckchem system had also been utilized through the first year of follow-up, the number of cases of severe RVGE detected would have been greatly increased due to the higher burden of severe rotavirus GE in the first year of life. Thus, the estimate of vaccine efficacy may have been higher. The composite of experiences in poorer developing countries in Africa and Asia now provides convincing evidence that the level of efficacy of oral RV vaccines measured in individual subject-randomized,

double-blind, controlled field trials (approximately 50–65% efficacy) is lower [7], [8] and [24] than the efficacy of vaccine documented in controlled field trials in industrialized LEE011 purchase and transitional countries [3] and [4]. The reduced immunogenicity and efficacy of both live and non-living oral vaccines in populations in developing countries has been previously described with multiple vaccines, such as oral polio vaccine, cholera vaccine and Shigella vaccines [25], [26], [27], [28], [29], [30], [31], [32], [33] and [34] and is the subject of much discussion and research to understand the basis of this phenomenon. Possibilities include potential vaccine factors, such as restricted immunogenicity or host factors such as gut enteropathy, and co-morbidities as described elsewhere [35], [36] and [37] This has led some to become discouraged about what live oral RV vaccines can accomplish in the world’s least developed countries (where RV vaccines are most needed) and to propose

starting afresh on new vaccine strategies such as parenterally administered inactivated Etomidate vaccines [38] and [39]. On the other hand, there are also clear reasons for optimism. The immunogenicity in Mali was comparable to that in Ghana and Kenya, where sufficient numbers of cases were captured to yield site-specific efficacies of 65.0% and 83.4%, respectively, through the first year of life [4] and [40]. Moreover, it is likely that the actual impact of widespread immunization of infants in Mali with live oral RV vaccine would result in an impact far greater than anticipated based just on the estimate of vaccine efficacy because of indirect protection and a herd immunity effect. Experiences in the U.S.A. [41], [42], [43] and [44], Australia [45], [46] and [47], and Latin America [48] show an unequivocal herd immunity effect wherein the observed fall in rotavirus disease far exceeds the expectation based just on estimates of direct vaccine efficacy and immunization coverage.

The increase in availability and use of

The increase in availability and use of click here rotavirus vaccines in the

future underlines the importance of surveillance networks to investigate the post-vaccine introduction epidemiology of rotavirus in terms of disease burden and effect on strain types. Sudhir Babji was supported by the Global Infectious Disease Research Training Grant (D43TW007392; PI – GK). None of the authors report a conflict of interest. “
“Rotavirus infection, mostly caused by Group A viruses, is prevalent in human populations worldwide. Although the virus infects older individuals, the disease can be severe in immunologically naïve infants and young children. The burden of severe rotavirus illness and deaths falls heavily upon children in low and middle-income countries: more than 80% of rotavirus-related deaths are estimated to occur in lower income countries of Asia and sub-Saharan Africa [1]. India has an especially large population at risk of clinically significant rotavirus gastroenteritis (GE); of the 1.2 billion people, 11% are <5 years old. Worldwide in 2008, diarrhea attributable to rotavirus infection resulted in 453,000 deaths (95% CI 420,000–494,000) in children younger than 5 years representing Palbociclib mouse 37% of deaths attributable to

diarrhea and 5% of all deaths in children younger than 5 years. Five countries accounted for more than half of all deaths attributable to rotavirus infection: Democratic Republic of the Congo, Ethiopia, India, Nigeria, and Pakistan with India alone accounting for 22% of deaths (98,621 deaths) [2]. Typical clinical signs of infection include fever, projectile vomiting, and profuse watery diarrhea, which may significantly dehydrate the infected child. Moderate to severe dehydration in young children is more often associated Dipeptidyl peptidase with rotavirus infection than other enteropathogens. There are no specific medications for rotavirus GE, but rehydration with oral rehydration salts (ORS) has long been a standard therapy for acute infantile diarrhea. Severe dehydration can be life threatening and requires treatment in a clinic or hospital where the child

can receive intravenous (IV) fluids and appropriate case management. The purpose of this observational study was to carry out a hospital-based surveillance of rotavirus gastroenteritis in children ≤59 months of age and develop estimates of disease burden in the population under surveillance. A prospective hospital-based surveillance was conducted at 12 medical centers attached to Medical Schools across India. From North India subjects were enrolled from Dayanand Medical College & Hospital, Ludhiana; Chhatrapati Shahuji Maharaj Medical University, Lucknow; Kalawati Saran Children Hospital, New Delhi; Post Graduate Institute of Medical Education and Research, Chandigarh and Sawai Man Singh Medical College, Jaipur.