This permitted a comparison between two groups: participants with

This permitted a comparison between two groups: participants with (n = 33) or without shoulder pain (n = 61). Several factors were observed to differ between those with or without pain (Table 1). Those with pain tended to be younger, took longer to be admitted to rehabilitation after their

stroke, and had lower Motor Assessment Scale (Carr et al 1985) scores for the arm. They also tended to have limited passive range of shoulder motion, shoulder subluxation, impaired sensation, and altered muscle tone. For this study, altered muscle tone included both hypotonia and hypertonia (Carr and Shepherd 1998). In contrast, no differences were observed for several variables including the presence of inattention, communication impairment, or area and side of stroke (Table 1). The selleck compound four predictors selected for inclusion in logistic regression were Motor Assessment Scale Upper Arm item, passive range of shoulder flexion, subluxation, and altered sensation. These were selected from the 10 variables that differentiated between people with and without pain (Table 1) for several reasons. The predictors focused on primary and secondary impairments

following the stroke rather than those relating to hospital processes (eg, days between onset and admission to rehabilitation). When two similar variables were moderately related, only one variable was selected. For instance, the Motor Assessment Scale Upper Arm item was selected over the Hand item as it was considered more relevant to the shoulder. Passive range of shoulder flexion was chosen over external rotation as it was ATM Kinase Inhibitor concentration considered easier to measure clinically given the reliance upon retrospective data. Although Nicks and colleagues (2007) suggested that less than 160 degrees shoulder flexion was a predictor for post-stroke shoulder pain, we used ≤ 150 degrees as a predictor due to the distribution

of shoulder ranges observed. Altered tone was not selected as a predictor as it related to several variables including Motor Assessment Scale scores, subluxation and shoulder range of motion. Logistic regression using the four predictors identified shoulder pain as reliably associated with two predictors: Motor Assessment Scale Upper Arm item and passive range of shoulder flexion (Box 1). These findings indicate old that the odds of experiencing shoulder pain are, on average, 14% greater for people with ≥150 degrees passive shoulder flexion relative to those with ≥ 150 degrees. The average odds of shoulder pain increase by 64% for each unit lower on the Motor Assessment Scale Upper Arm item (ie, a score of 5 has a 64% greater chance of shoulder pain than a score of 6). Based on the prediction equation, the mean odds and probabilities for experiencing shoulder pain are estimated for the range of people with stroke admitted to rehabilitation (Table 2). Regression coefficients of predictors Constant = 3.73 PROM shoulder flexion = −1.

For the studies in this report, the sub-confluent passaged 10–87

For the studies in this report, the sub-confluent passaged 10–87 VERO cells were designated as low-density passage 10–87 VERO cells (LD 10–87 VERO cells), while 10–87 VERO cells passaged at confluence were designated as high-density passaged 10–87 VERO cells (HD 10–87 VERO cells). The population doubling times (PDT) for LD 10–87 VERO cells and HD 10–87 VERO cells at p 250 were 26 h for the LD 10–87 VERO cells and 20 h for the HD 10–87 VERO cells. The LD and HD passaged cells used in this study and some of the tumors they formed were confirmed to be of simian origin by karyotyping and by PCR using

primers that recognize simian SINE sequences [28]. These cells have signaling pathway also been found to be free of 26 rodent

viruses and mycoplasma families (Radil, Columbia, MO). Adult (10 mice/dose) and newborn (NB) (3 litters/dose) athymic nude mice were inoculated subcutaneously (107 cells/mouse in 0.1 mL of PBS per cell line) above the scapulae. Tumors were documented to grow progressively by measurements in two dimensions until they were 15–20 mm in size, at which point the animals were euthanized. The tumor incidence in adult and newborn nude mice was recorded at weekly intervals over 12 month observation periods and plotted as survival curves. Wound-healing assays were performed as previously described [29] with some modifications. selleck chemicals Cells were plated 1 × 106 cells/plate in 60-mm culture dishes (Corning, Corning, NY) and allowed to form monolayers. When the cultures reached 90% confluence, they were serum starved for 8 h and the monolayers were wounded with a P200 micropipette

tip, washed with PBS and cultured in DMEM-10. Images of cell migration into the wounded areas were captured at 0, 3, 6, 9, 12 and 15 h. Total RNA from primary (p) African green monkey kidney (AGMK) cells and from cells from LD 10–87 VERO and HD 10–87 VERO cell banks established at every 10 passages from Sitaxentan p140 to p250 was extracted and purified using the miRNeasy mini kit according to the manufacturer (Qiagen Inc., Valencia, CA). The expression of signature miRNAs of these samples was measured using the TaqMan miRNA quantitative PCR assay [30]. Expression values were normalized to a small nucleolar RNA, RNU6 (Applied Biosystems). ΔCt values were calculated using the Ct values of the miRNA and the RNU6 for each corresponding sample. ΔΔCt values are calculated using the ΔCt values of the pAGMK cells and the experimental cell lines for each miRNA. The fold change over pAGMK was calculated.

PBMC were plated in duplicate wells at 0 4 million

per we

PBMC were plated in duplicate wells at 0.4 million

per well on MultiScreen 96-well HPVDF filtration plates (MAIPS4510, Millipore) after coating overnight at 4 °C with 10 μg/mL of anti-IFNγ (1-D1K, Mabtech) and blocking with the supplemented medium described above. Cells were incubated (37 °C, 5% CO2) for 18–20 h with positive (phytohaemagglutinin 10 μg/mL, Sigma) or negative (supplemented medium) controls or peptide pools consisting of up to 32 peptides (each 20mers overlapping by 10, final concentration 10 μg/mL/peptide). Plates were developed using biotin–streptavidin–ALP (Mabtech) with the addition of a chromogenic substrate (BioRad). Spots were counted using an ELISPOT reader and associated software (both Autoimmun Diagnostika). Final counts were expressed as sfu/million SB203580 in vitro PBMC after averaging duplicate well counts and subtracting background. For larger proteins, responses from multiple peptide pools were summed to give the response against the whole protein. Data analysis

was carried out using Microsoft Excel®, GraphPad Prism® and STATACorp STATA® with Kaplan-Meier analysis in SPSS®. A total of 34 volunteers passed screening and were enrolled into study groups 1–7 between April and November 2006. Volunteer demographics are shown in Table 1. Fifteen volunteers received VE-822 order one vaccination each in the dose-escalation groups 1–5 (n = 3 per group). Nineteen volunteers

were enrolled into the prime-boost vaccination groups 6 (or ‘FFM’ receiving the vaccine sequence FP9-PP/FP9-PP/MVA-PP, n = 9) and 7 (‘MMF’, n = 10). mafosfamide Three volunteers subsequently withdrew (one from the FFM group due to a pre-existing condition not revealed at screening and two from the MMF group due to unforeseen changes to work and travel plans). All available data has been included in the analysis for these volunteers. Fifteen of the 16 volunteers completing the prime-boost vaccination study subsequently volunteered to enter the separate but linked challenge study. They were joined by six newly-recruited unvaccinated malaria-naïve challenge control volunteers. No serious adverse events (SAEs) occurred during the study. Of 717 adverse events (AEs) recorded during the entire vaccination phase, 577 (81%) were judged probably or definitely related to vaccination (termed ‘vaccine-related’ from here on). Of these, 562 (97%) were AEs anticipated from previous studies of these vaccine vectors about which volunteers were specifically asked at each visit (solicited AEs, Fig. 1). The majority of all AEs reported during the vaccination phase were mild, with only 1 (0.1%) graded severe and 8% moderate in severity. The severe AE was local swelling at the vaccine site.

The randomisation was stratified for lung function (FEV1 > or ≤ 4

The randomisation was stratified for lung function (FEV1 > or ≤ 40% predicted), 6-minute walk distance (> or ≤ 50% predicted) (Troosters et al 1999), and the main limiting symptom in the initial endurance cycle test (ie, dyspnoea, leg fatigue, or a combination of both symptoms). Participants

undertook three sessions per week of supervised group training in their allocated exercise mode for eight weeks. Each participant maintained his/her medication regimen during the intervention period. NVP-BGJ398 nmr An assessor, blinded to group allocation, performed the outcome measures at the end of the intervention period. Participants were included if they had COPD stage I to IV (Global Initiative for COPD classification (GOLD) 2008). Participants were excluded if any of the following criteria applied: acute exacerbation of COPD within the last 4 weeks, significant co-morbidity including malignancy, symptomatic PFI-2 cell line cardiovascular disease, or other systemic or musculoskeletal disease that could hinder the exercise training. As well, participants were excluded if they had a body mass index (weight in kg/height in m2) ≥ 35 kg/m2, required supplemental

oxygen during exercise training, or used a walking aid. The study participants underwent pulmonary function testing including spirometry, lung volumes, and carbon monoxide transfer factor, and the six-minute walk test. Pulmonary function tests were performed according to the recommended standards (ATS/ERS Task Force 2005a, 2005b, 2005c) and results were compared with predicted normal values (Quanjer et al 1993). In the walk group, participants trained on a 26-m circular indoor track with the

initial training speed set at 75% of the participant’s peak walking speed, achieved in the incremental shuttle walk test (Hernandez et al 2000). Each participant was given a goal of completing a set number of laps in each five-minute period. All participants used a lap counter to monitor the number of laps walked during the prescribed duration. In the cycle group, participants were trained on an upright cycle ergometer with the initial training intensity set at 60% of the peak work capacity achieved in the incremental cycle test (Maltais et al 1997). The initial training intensities were chosen based on previous studies that reported that these training intensities were tolerated by participants Astemizole with COPD (Hernandez et al 2000, Maltais et al 1997). The training intensities for both groups were progressed as symptoms permitted so that the dose of training was maximised, with participants in the walk group walking at a faster pace and those in the cycle group cycling at a higher work rate. In the walk group, if walking speed became limited by stride length, further progress of training intensity was achieved by adding weights in 2 kg increments to a backpack. The duration of training for both groups was 30 minutes in the first week and increased by five minutes every two weeks to a maximum of 45 minutes by Week 6.

5 and 67 9 showed inhibition; neither 67 11 nor 67 13 could inhib

5 and 67.9 showed inhibition; neither 67.11 nor 67.13 could inhibit this activity (Fig. 3A). Essentially similar results were obtained for inhibition of C4b cofactor activity by the monoclonal antibodies. Only 67.5 and 67.9 showed inhibition, SCR7 in vivo while 67.11 and 67.13 failed to inhibit the C4b cofactor activity (Fig. 3B). These data therefore revealed that CCP domain 3 and/or linker between CCPs 3 and 4 of VCP play an essential role in imparting the cofactor activities. Besides acting as a cofactor for C3b and C4b inactivation, VCP is also an efficient

decay accelerator of the classical/lectin pathway C3-convertase C4b,2a. Thus, to examine the effect of mAbs on VCP-mediated decay of the convertase, we utilized a hemolytic assay. In this assay, C4b,2a was formed on antibody sensitized sheep erythrocytes using purified complement components and then the enzyme was allowed to decay in the presence of rVCP or rVCP pre-incubated with each of

the mAbs. The activity of the remaining enzyme was assayed by adding EDTA-sera (a source of C3-C9) and measuring hemolysis. Interestingly, the antibodies that inhibited the C3b and C4b cofactor activities (67.5 and 67.9) also inhibited the decay-accelerating activity of VCP, albeit with 67.5 having much less effect compared to 67.9. Among the remaining two antibodies 67.11 and 67.13, which bound to CCP 4 domain, only the former had moderate inhibitory activity while the latter did not AT13387 order inhibit the decay activity. until The C3-convertase decay inhibition efficiency of the monoclonals followed the order 67.9 ≈ 67.11 > 67.5 with 67.13 having negligible inhibitory potential (Fig. 4). Since mAbs differentially inhibited the VCP functions it was intriguing to know if blocking VCP function in vivo with these mAbs would translate into differences in viral pathogenesis. For in vivo disabling of VCP using mAbs, a prerequisite is that they should be retained at the site of injection until VCP is secreted by the infected cells. To verify this, we determined their half-life. The mAbs (67.5 and 67.9) were labeled with 131I, injected intradermally on either

flanks of New Zealand White rabbits and imaging was carried out with a γ-ray camera. The results showed that the labeled antibodies were retained at the site of injection even after 72 h. The half-life was found to be 8 h for both the antibodies (Fig. 5; data not shown for 67.9). Next, in order to determine whether disabling of VCP using neutralizing mAb affects VACV pathogenicity, we used a rabbit skin lesion model. In these experiments, VACV-WR was injected intradermally (104 pfu) either alone or in combination with mAbs and the lesion size was measured over a period of time. Initially, the two blocking antibodies (67.5 and 67.9) were titrated with VACV-WR to identify the optimal concentration required for reduction in lesion response. When varying concentrations of 67.5 (Fig. 6A) or 67.

We gained rich data on local context from the stakeholder FGs, pa

We gained rich data on local context from the stakeholder FGs, particularly relating to the cultural and religious practices of the communities within the study population, which shaped the intervention design. The importance of understanding the cultural and religious

context in minority ethnic communities has been highlighted in other studies. In a childhood obesity prevention study targeting minority ethnic communities in London, Verteporfin Rawlins reported child and parent perceptions of healthy eating and physical activity. The findings relating to South Asian communities resonate strongly with our data, for example the influence of places of worship and the role of extended family members on healthy lifestyles (Rawlins et al., 2013). A recent comprehensive evidence synthesis review on adapting health promotion programmes (including diet and physical

activity) for minority ethnic groups also draws attention to the importance of tailoring to particular contexts. The authors concluded that such adaptation Epigenetic inhibitor increased intervention relevance and acceptability, although whether this results in increased effectiveness is undetermined (Liu et al., 2012). The need for considering local context brings up the question of intervention transferability to different settings. Hawe and colleagues argue that a complex intervention can be standardised and transferable if it is the function and process of the intervention (e.g. mechanisms to increase children’s physical activity in school) that are standardised rather than the components (e.g. a specific curricular activity). This enables the delivery of interventions to take into account

local context (Hawe et al., 2004). This approach necessitates a theoretical understanding of the change mechanisms of local context at each intervention site. We would argue that this is a viable approach. An understanding mafosfamide of the contextual factors is essential for tailoring intervention components and thus determining their success. For example, barriers to childhood obesity prevention interventions, such as lack of parental time repeatedly emerge in the literature (O’Dea, 2003, Pocock et al., 2010, Power et al., 2010 and Sonneville et al., 2009). However, this barrier can only be addressed if the precise nature of the constraints on parental time is understood. In this study mothers were likely to be constrained through obligations such as looking after extended families or attendance at places of worship (Pallan et al., 2012), whereas in a North American study of white middle class children, perceived time constraints related to parents’ work commitments (Power et al., 2010). Different approaches to intervention would be required to overcome this barrier in these two communities. The iterative development process enabled us to implicitly gain a theoretical understanding of change pathways, and use this to drive intervention development.

The DASS-Depression focuses on reports of low mood, motivation, a

The DASS-Depression focuses on reports of low mood, motivation, and self-esteem, DASS-anxiety on physiological arousal, perceived panic, and fear, and DASS-stress on tension Selleckchem Bafilomycin A1 and irritability. Instructions to client and scoring: A respondent indicates on a 4-point scale the extent to which each of 42 statements applied over the past week. A printed overlay is used to obtain total scores for each subscale. Higher scores on each subscale

indicate increasing severity of depression, anxiety, or stress. Completion takes 10 to 20 minutes. A shorter, 21-item version of the DASS (DASS-21), which takes 5 to 10 minutes to complete, is also available. Subscale scores from the shorter ABT263 questionnaire are converted to the DASS normative data by multiplying the total scores by 2. Individual patient scores on the DASS subscales can be interpreted by converting them to z-scores and comparing to the normative values contained within the DASS manual. A z-score < 0.5 is considered to be within the normal range, a z-score of 0.5 to 1.0 is mild, 1.0 to 2.0 is moderate, 2.0 to 3.0 is considered severe, and z-scores > 3 are considered to be extremely severe depression/anxiety/stress.

Although it has been suggested that a composite measure of negative mood can be obtained by taking a mean of the 3 subscales, interpretation of this score is problematic as normative data or cut-off scores are not currently available. Clinimetrics: Internal consistency for each of the subscales of the 42-item

and the 21-item versions of the questionnaire are typically high (eg Cronbach’s α of 0.96 to 0.97 for DASS-Depression, 0.84 to 0.92 for DASS-Anxiety, and 0.90 to 0.95 for DASS-Stress ( Lovibond 1995, Brown et al 1997, Antony et al 1998, Clara 2001, Page 2007). There is good evidence that the scales are stable over time ( Brown et al 1997) and responsive to treatment directed at mood problems ( Ng 2007). Evidence has been found for construct ( Lovibond 1995) and convergent ( Crawford and Henry 2003) validity for the anxiety and depression subscales of both the long and short versions L-NAME HCl of the DASS. The clinimetric properties of the questionnaire have been examined in general and clinical populations Including chronic pain ( Taylor 2005), post myocardial infarction ( Lovibond 1995), psychiatric inpatients ( Ng 2007) and out-patients ( Lovibond 1995). Patients who present for physiotherapy care may also have low or disturbed mood, particularly clinically relevant symptoms of depression and anxiety. Co-morbid mood disturbance is likely to influence patients’ symptoms (including reporting of symptoms), complicate management, and slow recovery from the primary presenting condition. Accurate evaluation of mood is therefore an essential element of a comprehensive physiotherapy assessment.


was little evidence of cross-protection against HPV


was little evidence of cross-protection against HPV types 52 and 58 [51] and [52]. Efficacy of the bivalent vaccine against incident infection with HPV31 up to 6.4 years was 59.8% (95% CI: 20.5–80.7); and 77.7% (39.3–93.4) against HPV45. Vaccine selleck chemicals llc efficacy was also observed after 3.3 years of follow-up against CIN2+ associated with HPV31. No cases associated with HPV45 were observed in the vaccine group, while few cases were observed in the placebo group (PATRICIA trial). End-of-study results found vaccine efficacy of 100% (95% CI: 41.7–100) against CIN2+ associated with HPV45 in the TVC-naïve. As HPV45 is common in adenocarcinoma, this might add to the overall SB203580 order protection of the vaccine [24], [53] and [54]. Vaccination with HPV vaccines is expected to reduce the prevalence of the HPV vaccine types. There might, however, be concern how this would affect the distribution of other oncogenic HPV types. Human papillomaviruses are genetically very stable DNA viruses. Escape mutants or new HPV types are therefore unlikely to develop [55] and [56]. HPV type replacement after

vaccination depends whether there is natural competition between HPV types, and if this competition is stronger than the cross-protection afforded by the vaccine [55] and [56]. As vaccine-induced cross-protection against HPV31, 33 and 45 is much higher than that induced after natural infection, it is unlikely that type replacement will take place for these types [56]. But even if type replacement would occur, it remains to be seen if it would have implications on public health. The risk of developing cancer due to HPV16 or 18 is much higher than the risk of developing

cancer by other HPV types [56]. A study conducted Suplatast tosilate in the US showed that 4 years after vaccination with the quadrivalent vaccine, the HPV vaccine types decreased in vaccinated (31.8%), as well as non-vaccinated (30.2%) individuals. The prevalence of non-vaccine type HPV increased 14% for all participants [57]; however, it was not mentioned which types did increase. Reducing the number of doses of the HPV vaccine could have important public health implications, as adherence to the schedule and thus coverage might increase with reduced number of vaccine doses. In the Costa Rica Vaccine Trial, in which many women missed one or more of the three doses of a randomly assigned bivalent HPV vaccine or control (hepatitis A) vaccine, the efficacy of fewer than three doses was evaluated up to 4.2 years after vaccination. Vaccine efficacy against 12-month persistent HPV16/18 infection was 80.9% (95%CI = 71.1–87.7%) for three doses of the HPV vaccine, and 84.1% (95%CI = 50.2–96.3%) for two doses. No cross-protection against HPV31, HPV33 and HPV45 was observed after administering two doses [58].

All 198 cited references are listed at the end of the document “

All 198 cited references are listed at the end of the document. “
“Latest update: July 2010. Next update: Not indicated. Patient group: Adults and children presenting with non-cystic fibrosis bronchiectasis. These are patients with symptoms of persistent or recurrent bronchial sepsis related to irreversibly damaged and dilated bronchi. Intended audience: Clinicians who manage patients with non-CF bronchiectasis.

Additional versions: Nil. Expert working group: The guideline group consisted of 21 experts, including adult physicians, paediatricians, specialist nurses, ABT-263 manufacturer physiotherapists, microbiologists, a general practitioner, surgeon, immunologist, radiologist, and a patient representative. Funded by: Not indicated. Consultation with: External peer reviewers were consulted. Approved by: British Thoracic Society. Location: Pasteur MC, Bilton D, Hill AT (2010) Guidelines for non-CF bronchiectasis. Thorax 65(S1): 1-64. Description:This 64 page document presents evidence-based clinical practice guidelines on the background, potential causes, clinical assessments, investigations, and management of adults and children with non-CF bronchiectasis. It begins with a 6-page summary of all recommendations. The guidelines then provide information on the potential underlying causes of bronchiectasis, and its associations

with other pathologies. The clinical presentation in both adults and children is detailed, and evidence for diagnostic investigations is provided, such Pexidartinib mouse as immunological tests, radiological investigations, sputum microbiology, and lung function tests. General principles of management are indicated, followed by evidence for physiotherapy in this condition. This includes interventions such as airway clearance techniques, active cycle of breathing techniques, manual techniques, positive expiratory

pressure, autogenic drainage, high frequency chest wall oscillation, and exercise. The evidence for the use of airway pharmacotherapy such as mucolytics, hyperosmolar agents, bronchodilators, inhaled corticosteroids and leukotriene receptor antagonists are detailed, followed by evidence for SB-3CT management using antibiotics. Recommendations are given for assessments needed in patients with acute exacerbations in the outpatient and inpatient sector, with criteria provided to determine when inpatient treatment of an acute exacerbation is required. Finally, evidence for surgery, complications and management of the advanced disease is provided. All 549 cited references are provided. “
“This textbook primarily offers clinicians a multidisciplinary approach to the diagnosis and management of headache. Because fewer chapters are devoted to the diagnosis and management of orofacial pain and bruxism, this appears to be a secondary but related focus taken by the book’s editors.

2812 ± 265 mg/ml, P < 0 01; 4248 ± 279 mg/ml

vs 2403 ± 2

2812 ± 265 mg/ml, P < 0.01; 4248 ± 279 mg/ml

vs. 2403 ± 208 mg/ml, P < 0.05; Fig. 3E). To determine the extent to which undernutrition influences protection from EDIM infection and viral replication in immunized vs. unimmunized and nourished vs. undernourished mice, we challenged all 4 experimental groups with murine rotavirus (EDIM) by oral gavage at 6 weeks of age and collected stool for 7 days immediately post-challenge. Rotavirus vaccine was highly efficacious in both nourished and undernourished mice. As shown in Fig. 4, we observed a significant reduction in virus AZD9291 in vitro shedding in RRV-immunized RBD and CD mice compared to unimmunized controls. In unimmunized mice, peak intensity of infection occurred 1 day earlier in the RBD group (Fig. 4). Day 2 after EDIM challenge, viral shedding was 1917 ± 487 ng/ml for control mice and 5018 ± 622 ng/ml for RBD mice (P < 0.001) while on Day 3, viral shedding was 4708 ± 580 ng/ml for control mice and 2361 ± 374/ml for RBD mice (P < 0.01). We detected no differences in titers of anti-RV serum IgG, anti-RV stool IgA, total serum IgG and total serum IgA following EDIM challenge in unvaccinated RBD and CD mice (Fig. 5A, C, D, and F). Moreover, we found no differences in levels of anti-RV serum IgG and anti-RV stool IgA between vaccinated RBD and CD mice (Fig. 5A and C). In contrast, both immunized and unimmunized

RBD mice exhibited significantly higher mean anti-RV serum IgA relative to nourished controls (P < .0001 PI3 kinase pathway by ANOVA, Fig. 5B). Unvaccinated RBD mice showed significant increases in total serum IgA ( Fig. 5E, P < 0.01). Furthermore, in immunized RBD mice a higher percentage of rotavirus stool IgA was specific for RV following EDIM challenge relative to nourished controls (mean of 23% vs. 9%; P < 0.001 by ANOVA corrected for total IgA). In this first ever study of effects of weanling undernutrition on immune responses to both rotavirus immunization (RRV) and challenge (EDIM) we find that oral rotavirus

Dichloromethane dehalogenase vaccination adequately protects mice against EDIM despite altered antibody responses to vaccination and challenge. In addition, we show that serum anti-rotavirus IgA levels are elevated in both immunized and unimmunized undernourished mice following EDIM infection. We further demonstrate that unimmunized, undernourished mice shed rotavirus more rapidly than unimmunized, nourished mice. Strikingly, we find that in immunized RBD mice anti-RV stool IgA makes up a higher percentage of the total stool IgA compared to CD mice, both pre- and post-EDIM challenge. Similar to secondary analyses of clinical trial data conducted by Parez-Schael et al., we found that malnutrition alone does not impair the efficacy of rotavirus immunization [30]. The strengths of our laboratory study design allowed us to examine undernutrition, rotavirus immunization, and rotavirus infection, alone and in combination, with appropriate controls for age and diet.