053). At 12 months there was no difference between the groups [37]. In the third trial two doses of a bivalent vaccine, containing two “fast killing” isolates, was given 3 weeks apart. One of these was an ocular isolate from Saudi Arabia, and the other from the USA. At 12 and 24 months there was no significant difference in the proportion of children who had acquired active trachoma between the vaccinated and placebo arms. However, at 24 months the proportion of children in the placebo group with conjunctival scarring was higher than in the vaccinated group (18/47 vs 9/55, p = 0.034) [37]. In the Indian trial two doses of a bivalent, formalin inactivated vaccine or placebo were given to children aged less

than 5 years without signs of clinical trachoma [36]. Twelve months www.selleckchem.com/products/DAPT-GSI-IX.html after the second dose 26/182 vaccinated children had developed clinical trachoma (14%), compared to 32/87 in the placebo group (37%) (p < 0.01). Among those who acquired trachoma, there was no difference in severity between vaccinated and control children. These trials showed that whole organism vaccines

can reduce ocular Ct infection and active trachoma, but that protection is short lived and, in some cases, strain-specific. Most encouragingly in The Gambia, where the presence of conjunctival scarring was also recorded, there was evidence that vaccination reduced the incidence of scarring disease. Trials in non-human primates, in particular those in the Taiwan monkey, suggested that vaccination could lead to more severe disease on subsequent exposure; but there was no convincing evidence that vaccination led to more Forskolin datasheet severe disease in humans. Since the 1960s considerable efforts have been made to develop a subunit vaccine against Ct, but only one of these has shown evidence of protection in a NHP [38]. Ct major outer membrane protein (MOMP), when given parenterally in its native form (i.e. maintaining its tertiary structure), reduced the bacterial load in cynomolgus monkeys at the time of

peak shedding following ocular infection (days 3–14). However, it had no impact on the duration of infection or on the progression Metalloexopeptidase of clinical disease. On the other hand, a live attenuated vaccine, consisting of a plasmid-cured (P-) clinical serovar A trachoma isolate (A2497) caused a productive infection, but minimal pathology when inoculated into the eyes of cynomolgus macaques. A2497P-provided a degree of protection from infection and clinical disease on subsequent challenge with the wild type strain [39]. Three of 6 vaccinated monkeys were resistant to challenge ocular infection and, in the 3 which became infected, the bacterial load was lower than in control animals. The 3 monkeys that were protected from infection shared a common MHC class II haplotype. There was no evidence that vaccination led to more severe disease in animals which succumbed to challenge infection [39].

86 to 0.93) using goniometers. In contrast, Bovens et al (1990) reported poor reliability for measurements by physicians of physiological wrist extension using vision. Reliability for measuring physiological thumb abduction was reported to be higher using a pollexograph (ICC 0.59, 95% CI 0.42 to 0.89) than a goniometer (ICC 0.37, 95% CI –0.42 to 0.79). Finally, measuring accessory movements of carpal bones against the capitate bone using a 3-point scale yielded fair to moderate

reliability (weighted Kappa from 0.29 to 0.42) in healthy individuals and fair to almost perfect reliability (weighted Kappa from 0.33 to 0.87) in post-operative patients ( Staes et al 2009). This systematic review included 21 studies investigating inter-rater reliability Selleckchem Antidiabetic Compound Library of measurements of passive movements of upper extremity joints, of which 11 demonstrated acceptable reliability (ICC > 0.75). Reliability varied considerably with the method of measurement and ICC ranged

from 0.26 (95% CI –0.01 to 0.69) for measuring the physiological range of shoulder internal rotation using vision to 0.99 (95% CI 0.98 to 1.0) for the physiological range of finger and thumb flexion/extension using a goniometer. In general, measurements of physiological range of motion using instruments were more reliable than measurements using vision. Furthermore, measurements of physiological range of motion were also more reliable than measurements of end-feel or of accessory range Selleck MAPK inhibitor of motion. Overall, methodological quality of included studies was poor, although two high-quality studies reported almost perfect reliability (Glasgow et al 2003, Nomden et al 2009). In general, Fossariinae reliability for measurements of passive movements of upper extremity joints were substantially higher than for measurements of passive

segmental intervertebral and sacroiliac joints which rarely exceed Kappa 0.40 (Van Trijffel et al 2005, Van der Wurff et al 2000). Seffinger et al (2004) attributed these differences in reliability to differences in size of joints. We think, however, that differences may be more linked to a joint’s potential physiological range of motion. For instance, measurement of large joints with limited range such as the sacroiliac joint is associated with poor reliability, whereas measurement of small joints with greater range, such as the atlantoaxial spinal segment and finger joints, has been shown to be reliable (Cleland et al 2006, Glasgow et al 2003, Ogince et al 2007, Van der Wurff et al 2000). We also found that measuring large physiological ranges of motion, like that in the shoulder and in the wrist, frequently yielded satisfactory levels of reliability and note that these levels were predominantly as a result of using goniometers or inclinometers.

Au stade métastatique, les options thérapeutiques sont palliatives. La connaissance précise du ratio bénéfice-risque de chaque modalité thérapeutique reste la base de la prescription en l’absence d’étude randomisée comparative. Le délai d’action et l’efficacité attendue de chaque option thérapeutique sur le contrôle glycémique doivent également être pris en compte mais restent imprécis. L’individualisation des facteurs prédictifs Lonafarnib manufacturer et des marqueurs de substitution de réponse est encore préliminaire. Il doit être mis en place dès la première consultation pour viser la rémission symptomatique complète.

Au moindre doute sur la persistance d’événements hypoglycémiques, de courtes hospitalisations seront proposées dont l’objectif sera de s’assurer de la stricte normalisation glycémique. En l’absence de garantie sur le contrôle glycémique à long terme des thérapies médicales à visée symptomatique pure, une réduction tumorale sera systématiquement discutée. La prise en charge

symptomatique comprend des mesures générales et des traitements anti-sécrétoires. Elles comportent : • des mesures diététiques comprenant une alimentation fractionnée, enrichie en sucres lents, des conseils de « resucrage » en sucres rapides et lents en cas de malaise ; L’interdiction de conduire est à discuter. Le traitement symptomatique fait appel au diazoxide en première ligne, souvent prescrit à la posologie de 50 à 1500 mg par jour. Ce médicament contrôle la sécrétion d’insuline via l’ouverture des canaux potassique

[45]. Son action, rapide mais inconstante, est see more observée dans 50 % des cas d’insulinome. Son efficacité dans l’insulinome malin est mal connue. Cependant, la normalisation glycémique durant plusieurs années voire l’apparition de diabète a été observée chez des patients avec un insulinome métastatique. Des effets indésirables sont constatés chez la moitié des patients : palpitations, nausées, anorexie, hirsutisme, et rétention hydrosodée. Cette dernière peut s’améliorer sous diurétique thiazidique qui potentialise en outre le rôle hyperglycémiant du diazoxide [46] and [47]. Une titration progressive est recommandée en débutant par de faibles whatever doses car le délai d’action peut être court. En cas d’inefficacité, l’arrêt est recommandé en l’absence de preuve du bénéfice de son association aux autres thérapeutiques, d’autant que certains auteurs suggèrent une inhibition de l’effet hyperglycémiant du diazoxide par les analogues de la somatostatine. Ils constituent une alternative au diazoxide en seconde ligne du contrôle symptomatique du fait de leur bonne tolérance et de leur action rapide. Le rationnel de leur utilisation est basé sur l’expression des récepteurs SST2 et SST5 par ces tumeurs, dont l’inhibition entraîne une diminution de la sécrétion d’insuline.

1). The remaining sperms showed abnormalities of different types. The percentage of the abnormal sperm in the extracts-treated rats as 88.1% of group-II (HOCS-M-I), 72.4% of group-IV (HOCS-M-II) and 91.3% of group-V (HOCS-M-III) rats when compared with control group (8.2% of group II) (Table 2 and Fig. 1). However, the percentage of the normal sperm gradually increased to the control by 55 days after cessation of treatment (Table 2). The cauda

epididymal sperm count was significantly reduced in rats treated Selisistat chemical structure with HOCS-I (group-III), HOCS-II (group-IV) and HOCS-III (group-V) showed about 18.5 ± 1.4 × 106, 43.1 ± 1.7 × 106 and 10.2 ± 1.3 × 106 sperm/ml respectively when compared with vehicle control (64.3 ± 2.2 × 106 sperm/ml) (Table 2 and Fig. 2). However, the sperm count gradually increased to the control by 55 days after cessation of treatment (Table 2). In the vehicle control (NHS)-treated rats, cauda epididymal sperm exhibited rapid progressive motility and it was lasted for about 1 h 45 min. But, in the rats treated HOCS-M-II (group-IV) sperm were sluggish for 32 min. On the other hand, in the rats treated with HOCS-M-I (group-III) and HOCS-M-III (group-V) sperm were not at Depsipeptide supplier all motile (Table 2 and Fig. 3). However, the motility recovered gradually to the normal, by

55 days after cessation of treatment (Table 2). It has been postulated that in multi-herbal formulas, the pharmacological activities of one single herb is either potentiated or prolonged, and/or its adverse effects reduced, due to synergistic or antagonistic effects, by addition of other herbs.7 These types of pharmacological action are called either ‘pharmacological combination effects’ or ‘pharmaceutical

combination effects’. Therefore, in the present study, the authors aimed to evaluate the potential combination effects of herbs in the newly developed oral suspensions for their antifertility activity in mature male rats. (i) In the present investigation, the decrease in the weights of epididymis, medroxyprogesterone seminal vesicle and ventral prostate following oral administration of formulations HOCS-M-I, HOCS-M-II and HOCS-M-III at a single dose for consecutive days for 55 days is similar with effects shown the individual plant drugs in the earlier study. From the overall results, the antigonadal activities of the formulation HOCS-M-III after 55 days of treatment might be due to significant inhibitory effect on pituitary–testicular axis that suppress testicular steroidogenesis and spermatogenesis more effectively than HOCS-M-I and HOCS-M-II treatment. Further, this polyherbal suspension (HOCS-M-III) is more effective which may be explained by the herb–herb interaction13 or due to the synergistic effect of ingredients present in this composite extract.

However, based on the results for the activity monitor, it is unlikely that a larger C646 chemical structure sample

size would have resulted in a positive intervention effect for walking activity. A strength of this study was the location of the program in the children’s homes, in paediatric physiotherapy practices or special schools for children with disabilities. While different characters, motivational skills and training facilities might have influenced the effects of training, this variety increases the generalisability of our results to other paediatric practices. In conclusion, a physical activity stimulation program combining counselling through motivational interviewing, home-based physiotherapy and fitness training was not effective for increasing children’s physical activity, or improving mobility capacity, fitness, fatigue, and attitude towards sports. Further research should be performed to determine the separate contribution of each component of the program for improving physical activity. What is already known

on this topic: Children with cerebral palsy have lower levels of physical activity and fitness compared to their typically developing peers. Physical activity patterns may persist http://www.selleckchem.com/products/Temsirolimus.html into adolescence and adulthood. Exercise programs can improve the fitness of children with cerebral palsy. Studies of interventions to promote physical activity in this population have shown favourable, but non-significant, trends. What this study adds: A physical SB-3CT activity stimulation program consisting of fitness training, counselling and home-based therapy was not effective in children with cerebral palsy. Although the program improved the children’s attitude to sports, the effect was small. Footnotes: a StepWatch™ Activity Monitor 3.0, Orthocare Innovations, Seattle, USA. b MicroFet dynamometer, Biometrics, Almere, The Netherlands. c Corival V2 Lode B.V., Groningen, The Netherlands. d Cosmed, Rome, Italy. eAddenda: Tables 6 and

7 can be found online at doi:10.1016/j.jphys.2013.12.007 The following are the supplementary data to this article: Table 6. Ethics: The Medical Ethical Board of the VU University Medical Center, Amsterdam, approved this study. Parents and children aged 12 years and over gave written informed consent before data collection began. Competing interests: Nil. Grant providers were not involved in the design of the study, data collection, data analysis, manuscript preparation and publication decisions. Source(s) of support: This project is part of the Dutch national LEARN 2 MOVE research program and is supported financially by ZonMw (grant number 89000002), Johanna Kinderfonds, Stichting Rotterdams Kinderrevalidatie Fonds Adriaanstichting, Revalidatiefonds, Phelps Stichting, Revalidatie Nederland, and the Nederlandse Vereniging van Revalidatieartsen.

3B) and in the hippocampus (F(3–16) = 1.693; p = 0.20; Fig. 2A), there were no alterations in the BDNF levels after chronic treatment. The acute treatment did not alter the NGF protein levels in the prefrontal cortex (F(3–16) = 1.024; p = 0.40 Fig. 2B), in the amygdala (F(3–16) = 3.076; p = 0.58 Fig. 2B) or in the hippocampus (F(3–16) = 0.095; p = 0.96 Fig. 2B). The

chronic treatment increased the NGF levels in the prefrontal cortex with lamotrigine at the dose of 10 and 20 mg/kg (F(3–15) = 8.982; p = 0.01 Fig. 2B), compared with saline, but the NGF protein levels did not alter in the prefrontal cortex with imipramine at the dose of 30 mg/kg (F(3–15) = 8.982; p = 0.57 Fig. 2B). The amygdala (F(3–16) = 0,230; p = 0.87 Fig. 2B) and the hippocampus Entinostat ic50 (F(3–16) = 3.2080; p = 0.51 Fig. 2B) did not have alterations in the BDNF levels after chronic treatment. The acute treatment increased the citrate synthase activity in the amygdala with imipramine at the dose of 30 mg/kg (F(3–10) = 6.474; p = 0.02

Fig. 3A) compared with saline. In the prefrontal cortex and hippocampus there were no alterations in the citrate synthase activity after acute treatment. The chronic treatment did not alter the citrate synthase activity in the prefrontal cortex (F(3–11) = 0.460; p = 0.71 Fig. 3A), amygdala (F(3–12) = 2.676; p = 0.94 Fig. 3A) or hippocampus (F(3–12) = 3.079; SB431542 in vivo p = 0.68 Fig. 3A). The acute treatment increased the creatine kinase activity in the amygdala with imipramine at the dose

of 30 mg/kg (F(3–15) = 5.415; p = 0.01 Fig. 3B), compared with saline. The chronic treatment increased the creatine kinase activity in the hippocampus Dichloromethane dehalogenase with imipramine at the dose of 30 mg/kg and lamotrigine at the dose of 10 mg/kg (F(3–15) = 7.967; p = 0.02 Fig. 3B), compared with control group. The acute treatment decreased the mitochondrial complex I activity in the prefrontal cortex with imipramine at the dose of 30 mg/kg and lamotrigine at the dose of 10 mg/kg (F(3–14) = 10.859; p < 0.001 Fig. 4A) compared with control group. The chronic treatment did not alter the mitochondrial complex I activity in the prefrontal cortex (F(3–14) = 0.570; p = 0.64 Fig. 4A), amygdala (F(3–14) = 2.599; p = 0.09 Fig. 4A) or hippocampus (F(3–12) = 0.875; p = 0.48 Fig. 4A). The acute administration increased the mitochondrial complex II activity in the amygdala with imipramine at the dose of 30 mg/kg and lamotrigine at the dose of 20 mg/kg (F(3–13) = 21.798; p < 0.001 Fig. 4B), and in the hippocampus with lamotrigine at the dose of 10 mg/kg (F(3–11) = 5.643; p = 0,02 Fig. 4B) compared with saline. The chronic treatment increased the mitochondrial complex II activity in the prefrontal cortex (F(3–15) = 19.218; p < 0,001 Fig. 4B) and hippocampus (F(3–12) = 4.471; p = 0,03 Fig.

Socio-economic and geographic disparities in health and intervention selleck kinase inhibitor impact may be highly correlated at the sub-national level, in part due to the geographic clustering of socio-economic characteristics such as wealth and education. In order to explore this, we also estimated the geographical distribution of rotavirus vaccination effects

for one country – India. Esposito et al. developed a national model of rotavirus introduction and estimated the benefit and cost-effectiveness for India. They estimate that rotavirus vaccination could prevent about one-third of rotavirus-associated deaths in India, suggesting that improving current vaccine coverage would significantly increase vaccination impact [28]. This model includes estimates of rotavirus mortality and vaccination coverage by state from DHS data [26] using the same method as described above for wealth quintiles. In order to characterize and compare the distribution of key outcomes at the national level, we developed concentration curves and concentration indices [29]. For a given outcome, the concentration curve graphs the fraction of that outcome that occurs

within different fractions of the population ranked by wealth; for example, the portion of national vaccinations occurring in the bottom 10, 20, and 50 percent of the population ranked by wealth. The concentration index http://www.selleckchem.com/products/jq1.html is a single dimensional number between −1 and 1 that represents the extent to which the concentration curve of an outcome differs from the line of equity where the bottom x percent of the population accounts for x percent

of the outcomes. We estimated the health cost due to disparities in vaccination between wealth quintiles within each country by modeling a scenario in which vaccination rates in all quintiles are equal to that of the quintile with the highest coverage. Detailed information is presented for Methisazone the 8 countries with the highest rotavirus mortality estimates and available distributional data from DHS. Fig. 1 shows the estimated co-distribution of under-5 rotavirus mortality and vaccination coverage by wealth quintile for 8 countries. Each line represents a different country and each point in the line represents one wealth quintile in that country. In general coverage was highest and mortality lowest in the richest quintile. However countries varied in the relative disparities for each of the variables. Fig. 2 shows the benefits (under-5 rotavirus deaths averted per 1000 births) and cost-effectiveness ratio (CER, $/DALY) associated with rotavirus vaccination for each wealth quintile within the 8 countries. Each point in the figure represents a different quintile. In most countries, the CER is highest (least cost-effective) for the richest quintile and the benefit is the lowest, primarily due to lower estimated mortality rates.

Pain intensity was measured using the mean of three 0–10 numerical rating scales for least and usual LBP over the previous 2 weeks, and current LBP intensity; scores of five or more were defined as high pain intensity (Dunn et al., 2010). Functional disability was measured using the modified 23-item RMDQ (Patrick et al., 1995) with high functional disability defined as a score CX-5461 nmr greater than 14 (Cherkin et al., 1998). Bothersome LBP was defined if people rated their pain during the previous 2 weeks as very much or extremely bothersome

(Dunn and Croft, 2005). Information on previous LBP, and presence or absence of leg pain, distal leg pain and upper body pain (shoulder, arm, neck or head) over the previous 2 weeks was also collected. Probable cases of clinical anxiety or depression were defined as scores of eleven or more on the HADS (Zigmond and

Snaith, 1983). People were classified as catastrophisers if they felt that the pain was terrible and was never going to get any better based on a modified item from the Coping Strategies Questionnaire (Rosenstiel and Keefe, 1983). The use of single items to measure this construct has since been validated (Jensen et al., 2003), and the construct validity of this particular question has been established (Hill et al., 2008). Fear-avoidance beliefs were recorded if people stated http://www.selleckchem.com/products/GDC-0941.html that they could not do all the things normal people do because it is too easy for them to get injured, an item modified from the Tampa Scale for Kinesiophobia (Kori et al., 1990) and recommended for use as a single item (Vlaeyen et al., 2001). Self-reported health status was measured as reporting fair or poor on the general health perceptions question, and vitality was measured using with the vitality

sub-scale, from the Short Form-36 questionnaire (Ware, 2000). For vitality, people below the bottom tertile (with scores less than 25) were defined as having low vitality. Outcome 12-months after baseline was measured using the Chronic Pain Grade (CPG; Von Korff et al., 1992). This classifies individuals into grades of chronic LBP: 0 (pain free), I (low disability, low intensity), II (low disability, high intensity), III (high disability, moderately limiting) and IV (high disability, Cell press severely limiting). A poor outcome is defined here as CPG IV (highly disabling and severely limiting LBP). This measure was chosen as the outcome as it was not included as a prognostic indicator in the current analysis. Participants who returned the complete baseline and 12-month questionnaires were included in this analysis. Crude RRs with 95% confidence intervals (CI) were calculated for the associations between all potential prognostic indicators at baseline and 12-month outcome. Indicators that had a statistically significant association with outcome were then adjusted for potential confounders using Cox regression models with a constant time variable (Thompson et al., 1998).

, Blainville, Canada) was approved by the FDA in April 2013.2 The withdrawal of Bendectin from the US left American women without an FDA-approved drug for NVP and was associated with a 3-fold increased risk of hospitalization of women check details for the severe forms of this condition.3 Presently, 97.7% of prescriptions for the treatment of NVP in the US are with medications

not labeled for use in pregnancy, not indicated for NVP, and not classified as safe in pregnancy (FDA category A). The use of ondansetron for the treatment of NVP has steadily increased from 50,000 prescriptions per month in 2008 to 110,000 at the end of 2013 (Figure). This means that around 1 million pregnant American women are exposed to ondansetron out selleck kinase inhibitor of 4 million pregnancies a year. Ondansetron (GlaxoSmithKlein Inc, Philadelphia, PA) is a serotonin 5-HT3 receptor antagonist, originally introduced to prevent nausea and vomiting induced by cancer chemotherapy, radiation therapy, and surgery. The fact that ondansetron became generic in 2007, and hence its price dropped, might have been an important cause for this increase,

with easier access to Medicaid and health maintenance organizations. Prescribing ondansetron as a first line option is not consistent with American Professors in Gynecology and Obstetrics and American College of Obstetricians and Gynecologists evidence-based recommendations for the management of NVP.4 and 5 It should be remembered that most drugs used in pregnancy, including steroids for the through prevention of respiratory distress syndrome, all tocolytic agents, and magnesium sulfate for the prevention of cerebral palsy,

to mention a few, have not been approved by the FDA. Yet, they are standard of care. In contrast, in the case of ondansetron there are unresolved issues surrounding the fetal and maternal safety, including recent warnings by the FDA on its potential to cause serious dysrhythmias.6 The fetal safety of the ondansetron was first investigated in humans by Einarson et al7 in 2004 through a prospective controlled cohort study of 176 women, in whom we could not detect an increased teratogenic risk. However, this sample size had the statistical power to rule out only a 5-fold increased risk of major malformations, and not any specific malformation. In February 2013, Pasternak et al8 reported that ondansetron was not associated with increased malformation rates when used for morning sickness. This was based on retrospective analysis of data from the Danish Birth Registry, collected between 2004 and 2011 and linked to the National Prescription Register. Each of the 1970 women exposed to ondansetron was matched to 4 unexposed controls.

The electropherograms obtained were analyzed using the sequencing analysis software (Sequence Navigator, version 1.01, Applied Biosystems). The nt and deduced aa sequences were compared with sequences available in the NCBI (National Center for Biotechnology Information) GenBank database using the BLAST (Basic Local Alignment Search Tool) program. Phylogenetic and molecular Cisplatin ic50 evolutionary analyses were conducted using MEGA version 4.0 [36]. Dendrograms constructed were confirmed by two different methods,

neighbor joining and maximum parsimony. The data were analyzed using Epi Info 2002 and Stata 10.0. Chi square and Mann Whitney U tests were performed to determine the significance of differences observed between groups. Partial nucleotide SCH727965 chemical structure sequences of VP1, VP2, VP3, VP4, VP6, VP7, NSP1, NSP2, NSP3, NSP4 and NSP5 of the G10P[15] strains were submitted to the GenBank database and their accession numbers are HQ660637, HQ660638, HQ660639, FJ798615, FJ798616, FJ798617, HQ660640, HQ660641, HQ660642, FJ798618, HQ660643 respectively. The median (interquartile range [IQR]) age of the 394 children enrolled in the study was 10 (7) months, with >90% of children less than 2 years of age. The median Vesikari score of diarrheal severity was 11.0 and the children required

admission for a mean duration of 2.8 days. Of 394 children screened, we found that 158 children were infected with rotavirus (40%). The common G types identified in order of frequency were G1 (47/158, 29.7%), G2 (43/158, 27.2%), G9 (22/158, 13.9%), G10 (2/158, 1.2%), G12 (1/158, 0.6%) and mixed infections (27/158, 17.8%). The common P types were P[4] accounting for 57/158 (36%) samples, P[8] 57/158 (36%), P[11] 3/158 (1.8%) and P[6] 2/158 (1.2%). Mixed infections with varied P types were seen in 5 (3.2%). G typing alone was possible in 23 samples below (14.4%), only P typing in 5 samples (3.6%) and 11 samples were completely untypeable (6.9%). The common G:P combinations seen

in children were, G2P[4] in 39/158 (24.6%) samples, G1P[8] in 29/158 (18.3%) samples, G9P[8] in 21/158 (13.2%) samples, G1P[4] in 4/158 (2.5%) samples and G10P[11] in 1/158 sample (0.6%) (Fig. 1a). We collected total of 627 samples from animals with diarrhea, including 589 cows (25 were calves), 2 buffaloes, 11 bullocks and 25 goats (11 were kids). The mean duration of diarrhea was 4.5 days for adult animals, 4 days for calves and 3 days for goat kids. Out of 627 animals we found 35 (1 bullock, 2 goats, 32 cows) infected with rotavirus (5.5%). The common G types identified in order of frequency were G6 (17/35, 48.5%), G2 (10/35, 28%), G10 (4/35, 11%), G8 (2/35, 5.7%) and mixed infections (2/35, 5.7%).