1, 91.3%) who received PRV exhibited an anti-rotavirus IgA seroresponse (≥3-fold rise from baseline (pD1 to PD3), with a PD3 GMT of 31.3 units/mL. By contrast only 20.0% of placebo recipients (95% CI: 10.0, 33.7%) developed a seroresponse and the PD3 GMT was 3.2 units/mL. SNA response to the human RV serotypes (G1, G2, G3, G4, and P1A [8]) contained in PRV were also measured, as summarized in Table 2. The seroresponses were relatively poor, ranging from 7.0% (for G2) to 33.3% (G4). GMTs were also modest. The SNA

seroresponses detected among the placebo was 0.0% for all serotypes, except P1A [8] (4.0%). Table 3 summarizes the number of person-years of observation by age group, cases of severe RVGE and the incidence density through the first year of life and during the second year of life, according to the ITT and PP analyses. Through the first year of life, there were only 55 RVGE cases detected. Of these 55 RVGE cases, 9 RVGE buy Selinexor cases (3 severe, 6 non-severe) click here occurred prior to 2 weeks after the dose of vaccine; therefore, only 46 RVGE cases (8 severe, 38 non-severe) were part of the PP efficacy analyses. In total, 11 RVGE cases were classified as severe, 4 among PRV vaccinees and 7 among controls, yielding an ITT vaccine efficacy of 42.9% (95% CI: −125.7, 87.7). As 3 RVGE of the cases in the control group

occurred prior to 2 weeks after the third dose of vaccine, the per-protocol efficacy was 1.0% (95% CI: −431.7, 81.6) through the first year of life. Through the first year of life, the efficacy of PRV against RVGE of any severity in the PP population was 9.3% (22 in the PRV group, 24 in the placebo group; 95% CI: −68.9, 51.5). During the second year of follow-up (Table 3), after the surveillance system was modified to adapt 17-DMAG (Alvespimycin) HCl to local customs and heath care seeking practices, there were 96 cases of severe RVGE detected, including 43 among PRV recipients and 53 among placebo subjects; the point estimate of the PP vaccine efficacy was 19.2% (95% CI, −23.1,47.3%) during the second year of follow-up.

The efficacy of PRV against RVGE of any severity on the PP population during the second year of life was also 19.2% (129 cases in the PRV group, 158 cases in the placebo group; 95% CI: −2.7, 36.4). A total of 370 RV isolates from cases of gastroenteritis in vaccinees and controls were submitted to PCR to determine the RV G and P genotypes. Of these, 353 RV isolates (95.4%) contained a G or P type present in PRV. G1 viruses were the most commonly circulating during the course of the study (61%) with a predominance of G1P [8] strains (54.3%) and G1P [6] strains (6.2%). G2 viruses were next most common (27%) with varying P-types—notably G2P [6] (22.2%) and G2P [4] (4.3%) strains. G8 and G9 strains were seen in small numbers (4.6% and 2.4% respectively).

The National Preventative Health Strategy provides an extensive roadmap for preventive actions at all levels (NPHT 2009a) and Box 1 provides some examples of preventive actions physiotherapists could take. Given our knowledge and skill base and our respected status in society, physiotherapists can

be at the forefront of the renewed international prioritising of prevention. For your own health, for the health INCB28060 nmr of your clients and students, and for the health of the human race, I urge you to prioritise prevention. Enhance your own health by maintaining healthy behaviours Model good health habits for family, friends, colleagues, and clients Give flowers or a dance music download voucher rather than alcohol Provide interesting non-al drinks at social gatherings Bring tasty salad/veggie dishes to social gatherings Meet friends for a walk-and-talk rather than cake and coffee Enhance your credibility when discussing with clients by modeling good habits Raise key health issues with clients, in addition

to dealing with their presenting complaint Add standard screening questions about lifestyle factors to your assessment Do some preparation so you are comfortable to raise key health issues with clients Put up prevention posters in clinic waiting room Run monthly themes in your practice highlighting selleck compound a key modifiable health issue Provide a weight, height and BMI calculation station in clinic waiting room Provide pamphlets on resources for clients wishing to address Ketanserin a key health issue once raised Add links from your practice website to resources for clients

on preventive issues Include tips for 5 key health issues on specific handouts to clients such as exercise sheets Review course materials to link to key prevention actions were possible Encourage consideration of client’s general health and potential preventive actions by students and junior colleagues Create a ‘fruit club’ at work to encourage 2 fruits a day Walk for meetings of 2–3 people, stand for meetings with more people Advocate for safe active transport routes to school Support good food options at school shop Flash your car lights randomly to encourage safe driving speeds Promote mass media prevention campaigns through your social media network Offer advocacy in this area with local businesses Write to your local council member or community newspaper supporting initiatives like smoke-free public areas or better cycling and walking paths Write or, better still, go to see your local member to support preventive legislation such as speed cameras, cigarette plain packaging, tobacco tax, and food labeling “
“Depression disorders have become a widespread health concern throughout the world. The worldwide prevalence of depression has been estimated at 10.4% (Andrews et al 2000).

68–1.39 (br m, 4H, INK 128 molecular weight 2× –CH2), 1.17 (d, 6H, J = 6.1 Hz, –CH3), 0.81 (s, 9H, 3× –CH3), 0.04 (s, 6H, 2× –CH3); 13C NMR (CDCl3, 75 MHz): δ 167.2, 158.6, 144.6, 128.1, 123.2, 116.8, 113.3, 79.8,

72.2, 66.6, 53.1, 51.6, 35.8, 30.3, 25.6, 23.3, 18.4, −4.7; IR (neat): 2938, 1729, 1608, 1512, 1451, 1379, 1164, 1038 cm−1. The pH of reaction mixture was adjusted to acidic with 1N HCl solution and extracted with ethyl acetate (40 mL). Organic layers were washed with water (15 mL), brine (15 mL), dried (Na2SO4), evaporated under reduced pressure to give 18 (2.28 g, 79%) as a colorless oil, [α]D −12.1 (c 1.2, CHCl3); 1H NMR (CDCl3, 300 MHz): δ 7.20 (d, 2H, J = 8.0 Hz, ArH-PMB), 6.89 (dd, 1H, J = 6.2, 15.7 Hz, olefinic), 6.84 (d, 2H, J = 8.0 Hz, ArH-PMB), 5.71 (d, Quizartinib chemical structure 1H, J = 15.7 Hz, olefinic),

4.31 (d, 1H, J = 11.5 Hz, benzylic), 4.16 (d, 1H, J = 11.5 Hz, benzylic), 3.83 (m, 1H, –OCH), 3.67 (s, 3H, OCH3), 3.47 (m, 1H, –OCH), 1.67–1.52 (m, 2H, –CH2), 1.49 (m, 2H, –CH2), 1.07 (d, 6H, J = 6.1 Hz, –CH3), 0.81 (s, 9H, 3× –CH3), 0.06 (s, 6H, 2× –CH3); 13C NMR (75 MHz, CDCl3): δ 170.1, 158.4, 149.1, 130.1, 128.0, 117.6, 113.8, 76.1, 73.2, 66.2, 55.7, 38.2, 30.3, 26.3, 24.2, 17.5, −4.3; IR (neat): 3449, 3031, 2930, 2857, 1710, 1097 cm−1. To a cooled (0 °C) solution of 18 (1.75 g, 4.27 mmol) in dry THF (15 mL) under nitrogen atmosphere, TBAF (5.13 mL, 5.17 mmol) was added and stirred for 3 h. After completion of reaction, reaction mixture was diluted with water (5 mL) and extracted with ethyl acetate (2 × 40 mL). Organic layers were washed with water (2 × 10 mL), Vasopressin Receptor brine (10 mL), dried (Na2SO4), evaporated to give 8 (1.08 g, 86%)

as a liquid. [α]D +35.4 (c 1.0, CHCl3); δ 7.17 (d, 2H, J = 8.2 Hz, ArH-PMB), 6.88 (dd, 1H, J = 6.1, 15.8 Hz, olefinic), 6.84 (d, 2H, J = 8.2 Hz, ArH-PMB), 5.70 (d, 1H, J = 15.8 Hz, olefinic), 4.31 (d, 1H, J = 11.5 Hz, benzylic), 4.16 (d, 1H, J = 11.5 Hz, benzylic), 4.07–3.89 (m, 1H, –OCH), 3.82 (m, 1H, –OCH), 3.66 (s, 3H, OCH3), 1.67–1.49 (m, 2H, –CH2), 1.47–1.36 (m, 2H, –CH2), 1.07 (d, 6H, J = 6.0 Hz, –CH3), 0.81 (s, 9H, 3× –CH3), 0.01 (s, 6H, 2× –CH3); 13C NMR (CDCl3, 150 MHz): δ 172.3, 158.1, 146.4, 132.6, 128.1, 119.1, 112.8, 78.9, 70.3, 68.6, 56.2, 34.9, 29.8, 23.6; IR (neat): 3451, 2929, 2857, 2102, 1722, 1612, 1514, 1360, 1041, 777 cm−1.

To enable coupling of peptides to streptavidin coated beads for the Luminex system (see below) a separate set of 14-mer MAP Hsp70 peptides, selected based on the first screening with the 14-mer Selleck NVP-BGJ398 peptides, was synthesized using SMPS and modified using amino-terminal biotinylation. A third set of 15-mer peptides consisting of mycobacterial, Bos taurus and E. coli homologues to identified MAP Hsp70 linear epitopes was also synthesized using SMPS and modified using amino-terminal biotinylation. The generation of monoclonal antibodies has been described previously [20]. Briefly, 100 μg of recombinant MAP Hsp70 protein in 80 μL

PBS was mixed with 100 μL Specol [21] (Prionics, the Netherlands) to obtain a water in oil emulsion used for i.p. immunization of Balb/c mice. This immunization was repeated 3 weeks later. Another 3 weeks later, four days prior to hybridoma production the mice were boosted i.v. with 50 μg of the antigen in 50 μL PBS. After 4 days spleen cells were fused with mouse myeloma cells (Sp2/0) using polyethyleneglycol (PEG, Merck, Germany). Antigen specific antibody Pexidartinib purchase producing hybridoma’s were selected by ELISA [22] and subcloned in limiting dilution. The isotype of the monoclonal antibodies was determined using the Mouse Hybridoma Subtyping Kit (Roche, the Netherlands). In general, 96

well EIA plates (Corning Costar Corp., USA) were coated with 100 μL of antigen diluted in sodium bicarbonate buffer (pH 9.6), for 60 min at 37 °C. All subsequent incubations were performed for 30 min at 37 °C, and after each incubation step plates were washed 3 times with PBS containing 0.05% Tween 20. Wells were blocked with 200 μL blocking solution (Roche,

the Netherlands). All antibody fractions were diluted in blocking solution and peroxidase labelled to appropriate antibodies was used as enzyme. Finally, plates were washed extensively, and 100 μL ABTS (2,2′-azinobis (3 ethyl) benzthiazolinsulfonic acid (Roche, the Netherlands) substrate buffer was added to each well. The optical density (OD) was measured after 10 min at 405 nm on a spectrophotometric Elisa reader (Bio-Rad laboratories, USA). Absorbance values were subsequently analyzed. The MAP Hsp70 protein, bovine Hsc70 protein, PPDP, PPDA, and PPDB ELISA to measure antibody responses in cattle sera L-NAME HCl were performed according to methods described previously [6] with minor modifications to detect murine and caprine antibodies as follows. Hybridoma supernatants or sera of immunized/infected goats were used in a predetermined optimal dilution or were serially diluted in blocking buffer as indicated. Secondary antibodies used were polyclonal goat anti-mouse peroxidase (PO) conjugated antibodies (Sigma Aldrich, USA) to detect murine monoclonal antibodies, and rabbit anti-goat IgG-PO (Sigma Aldrich, USA) to detect caprine antibodies. The mycobacterial whole cell ELISA was a modification to the protein ELISA.

Genotypes G1 or G2 were the most common strains across each time period; however, all strains varied over time (Table 4, Fig. 1) and non-G1 or -G2 strains rose to a proportion of ≥10% in only 5 separate seasons. G3 transitioned from the fourth most common strain in the time period before 1994 (9.6%) to the least common (1.2%) in the most recent period. On a relative scale, G4 underwent the most temporal change, decreasing from 31.3% of all strains in the period before

1994 to only 4.0% in 2005–2009 (Fig. 2). The decline in G3 and G4 strains was accompanied by an increase in G9 strains, which demonstrated peak prevalence of ∼15% from 2000 onward but had much lower detection rates in

earlier periods. The presence of G12 typing and detection only emerged at the turn of the century, so now G12 strains constitute about ∼9.0% of these strains PI3K phosphorylation (262/2945), signaling steady transmission in the region. The number of strains with mixed G-types increased linearly over time by 7.2%, but probably reflects more sensitive molecular methods of detection (Table 4). P-types remained more constant with P[4] and P[8] as the top two strains in each time period. P[6] types showed the most variation in prevalence (10.4%; frequency range 8.5–18.9%) and mixed infections also rose >7.4% between the earliest and latest time periods (Table 4). Prior to 1995, 96.3% of all reported rotavirus strains matched KRX-0401 in vitro antigens present in either RotaTeq® or Rotarix™ vaccines (G1–G4). However, by 2005–2009, the proportion of vaccine-matched strains circulating declined to 70.5%. The south (1390 G-samples) and east (3340 G-samples) collectively totaled almost half of the review’s sample size, with north, west, and multiple regional categories each contributing over 1000 G-samples (Table 5). G1 remained

fairly constant until across all regions, with the south identified as the only region in which G1 was not the predominant strain. Non G1- or G2-strains were found in proportions over10% among regions with >10 strains in any one season. G4 proved highly varied regionally, with only 1.7% in the north, 6.5% in the south, 7.0% in the west, and 21.9% in the east. G9 was found in proportions ≥10% in all but the west, while only G12 in the north had a proportion ≥10% (Fig. 2). This review of rotavirus strain diversity in India, Bangladesh, and Pakistan confirms that the Indian subcontinent maintains a more diverse rotavirus genotype portfolio than most regions in the world. Nevertheless, the most common G-types (G1–4) and P-types (P[4], P[8]) globally accounted for three-fourths of all strains over the total time period of almost three decades. Temporal analysis shows G3 and G4 clearly declining in recent years, while G9 and G12 emerge as increasingly dominant circulating strains.

Role of the sponsor: Employees of MedImmune worked collaboratively with the investigators of RTI Health Solutions in the design of the study, in interpretation Y27632 of the results, and reviewed and contributed to the manuscript. Additional contributions: We would like to thank Complete Healthcare Communications, Inc. (Chadds Ford, PA, USA) for editorial assistance in manuscript preparation. “
“Mycobacterium

bovis based Bacille Calmette Guérin (BCG) was originally introduced in the 1930s as an oral vaccine against the human pathogen Mycobacterium tuberculosis, the cause of tuberculosis. In the 1960s, most of the world moved towards intradermal vaccination with lyophilized BCG, but some countries, including Brazil, continued to exploit the oral vaccination route [1] and [2]. BCG, which is still available as a live vaccine, was derived by extensive passage from M. bovis, which naturally infects humans and cattle via the gastrointestinal tract. Live Mycobacteria have the potential to interact strongly with both the innate and adaptive immune system and any vaccine based on them has the potential to be used as a safe clinical probe of p38 MAPK assay human responses [3].

Thus, BCG-based vaccines can potentially provide a safe but effective tool to mimic natural infection and stimulate both innate and acquired immunity under relatively ‘natural’ conditions of gut infection. Further, as BCG is a licensed vaccine many ethical hurdles are consequently reduced for human studies. Immune responses can be both protective and dangerous to the host. For example, many of the symptoms associated with the reactogenicity of vaccines are in fact inappropriately stimulated innate responses. Innate immune responses are difficult to safely monitor in humans as approved methods for stimulating such responses are not generally available and would raise ethical concerns. By delivering oral BCG (which has been given orally to millions of

people with a good record of safety) to healthy volunteers under controlled conditions we aimed to assess if this system had value for monitoring below innate immune activation. The impact of gastrointestinal colonization by BCG was indirectly determined by measuring antigen-specific T-cell and cytokine responses, along with microarray analysis. Further insight was obtained by systematically recording clinical symptoms associated with sequential BCG challenges such as abdominal pain, diarrhoea; upper respiratory tract congestion, secretion; fever and headache. In this way, we sought to build-up an integrated picture of innate and adaptive immune responses at various time points before and after a series of bacterial challenges. We used an oral BCG preparation (BCG Moreau Rio de Janeiro), commercially produced, which has a strong safety record in extensive human testing [4].

Most ordinary public health activity, such as routine immunisation, or health and safety inspections of restaurants, would count as rescuing those unidentifiable individuals who would then not contract disease. It would seem better to acknowledge that the eradication campaign does not rescue the people who do not get polio in the future. Rather it permanently removes a health risk of a certain kind from their environment, and so makes it the case that no one will in the future have to be rescued from this health risk. This is an important benefit, and as the next

section explores, is the ground for a more successful argument in favour of eradication policies. Malaria currently creates a burden of disease of over 82 million DALYs per year [16]. If an effective vaccine becomes available, and a successful eradication campaign then reduced learn more to zero the burden of disease from malaria for the remainder of human existence, this would provide an extraordinarily large health benefit [17]. Whilst we have found no special reason to opt for eradication policies just as such, eradicating disease is clearly one way of meeting more general desiderata of public health policy BIBW2992 research buy – reducing the burden of disease equitably and efficiently. Eradication policies

will sometimes have a more favourable balance of burdens and benefits than other competing health interventions – and in such cases they should be chosen. Standard cost effectiveness tools struggle to accurately account for the benefits of ordinary national vaccination campaigns [18]. Accounting for the benefits of eradication campaigns Oxalosuccinic acid is significantly more difficult. In

what follows, I shall aim to sketch some of these additional problems, and argue that they should not stand in the way of eradication campaigns. The first difficulty relates to uncertainty. It is extremely difficult to globally eradicate a disease. Only one such attempt has so far succeeded in humans, so it would be unrealistic to think that any given eradication campaign could be guaranteed success. Where an eradication campaign fails it can fail more or less gracefully. It can fail gracefully where, despite not leading to global eradication of a disease, it leads to a significant and sustained reduction in prevalence of the disease, or it can fail less gracefully, leaving no sustained reduction in the prevalence of the disease, and a trail of negative associations that makes it more difficult to mount eradication campaigns in the future. Constructing a model for the prospective cost effectiveness of eradication campaigns is thus very challenging, though progress is being made here [19]. Second, there are both ethical and cost effectiveness reasons for thinking that eradication campaigns should aim to go big and go fast [20].

“
“La stratégie thérapeutique au long cours dans la bronchopneumopathie chronique obstructive (BPCO) est détaillée par la Société de pneumologie de langue française (SPLF) dans ses recommandations publiées en 2010 [1], auxquelles

s’ajoutent un guide « Parcours de soins » décrivant la prise en charge des patients souffrant de BPCO publié le 11 juin 2014 par le collège de la Haute Autorité de santé (HAS), comportant trois documents : le guide parcours de soins BPCO, les points critiques du parcours de soins BPCO et le schéma parcours de soins BPCO [2], [3] and [4]. À ces documents BLU9931 concentration qui témoignent de la multiplicité et de la complémentarité des approches de cette pathologie, du patient et de sa prise en charge thérapeutique, on peut ajouter les dernières recommandations de la HAS sur les bonnes pratiques du sevrage tabagique publiées fin 2013 [5], ainsi que la fiche « points clés et solutions » sur la mise en œuvre de click here la réhabilitation respiratoire publiée en mai 2014 [6]. Tous ces documents attestent de l’intérêt du corps médical et des autorités de santé pour le fardeau de santé publique que représente la BPCO, source majeure de mortalité, de handicap et de dépenses

de santé. Le texte qui suit est fondé sur les recommandations de la SPLF, les many documents des autorités de santé (HAS, ANSM et Agence européenne du médicament [EMA]) et sur l’analyse de références bibliographiques complémentaires. La BPCO est une maladie hétérogène dont il est nécessaire d’évaluer la sévérité avant de décider et d’initier une stratégie thérapeutique (encadré 1). VEMS : quatre stades de sévérité de l’obstruction. MRC : Medical Research Council ; VEMS : volume expiratoire maximal seconde. La vérification d’une obstruction bronchique (rapport VEMS/CVF < 70 %) est indispensable au diagnostic. Les stades de sévérité (I à IV) sont définis sur le niveau

de l’obstruction bronchique mesuré par le volume expiratoire maximal seconde (VEMS), exprimé en pourcentage de la valeur théorique. Au stade I (VEMS ≥ 80 %), les patients sont pas ou peu dyspnéiques. Au stade II (50 % ≤ VEMS < 80 %), une dyspnée d’effort est fréquente. Au stade III (30 % ≤ VEMS < 50 %), la dyspnée se traduit souvent par une diminution de la capacité d’exercice et une fatigue. Au stade IV (VEMS < 30 %), la qualité de vie est très altérée par une dyspnée survenant pour des efforts minimes de la vie courante, voire au repos. Cependant, l’intensité de la dyspnée est non seulement mal corrélée avec ces stades de sévérité mais aussi fréquemment sous-évaluée.

Activity interference was also recorded in the diaries daily using Item 5 from the 12-Item Short-Form Health Survey (Ware et al 1996), a 5-point scale anchored by ‘not at all’ through to ‘extreme interference’. To ensure completeness of follow-up, data from the diaries were collected by telephone interview at weekly intervals for the first four weeks, then monthly or until recovery for the subsequent eight GSK1349572 research buy weeks (84 days in total). At

three months, a telephone exit interview was conducted at which the Neck Disability Index (Vernon and Mior 1991) was administered and pain scores were collected. Primary outcome: The primary outcome was the time taken from commencement of treatment to recovery from the episode of neck pain. The day of recovery from the episode of neck pain was defined as the first day of seven consecutive days on which the patient rated the intensity of their average daily neck pain as < 1 on the numerical rating scale from 0 to 10. Secondary outcomes: Secondary outcomes included time to recovery of normal activity as well as pain (numerical rating scale 0–10) and disability Selinexor (Neck Disability Index scale 0–50) scores at

three months. Time to recovery of normal activity was defined as the first day of seven consecutive days in which the participant rated the degree of interference ‘not at all’. We examined 22 putative prognostic factors. Eight demographic variables were examined: age, gender, level of education, employment status, change of employment status due to neck pain, smoking habit, whether a compensation claim for neck pain had been lodged, and self-rated general health. Level of education was determined using items from the Australian Census 2001 (Trewin 2000). Employment status was determined using categories described by

Kenny et al (2000). Self-rated general health was measured using Item 1 of the 12-Item Short-Form Health Survey (SF-12). The 14 clinical variables examined were: pain intensity on the 0–10 numerical rating scale, duration of neck pain, disability measured by the Neck Disability Index from 0 (none) to 50 (worst), the physical (PCS) and mental health (MCS) component summary scales of the SF-12, presence of concomitant symptoms (upper limb pain, headache, upper back pain, lower back pain, dizziness and nausea), past history of neck pain, previous sick leave for also neck pain, and use of analgesics. The clinical course of the episode of neck pain was described using Kaplan-Meier survival curves and using descriptive statistics. Prognostic factors were evaluated using separate prognostic models for recovery from the episode of neck pain and disability at 3 months. The first stage involved examination of the univariate relationship between the outcome and each prognostic variable, using Cox regression (for time to recovery), and linear regression (for disability at 3 months). Variables with significant associations (p < 0.

[17]) with 50% case-fatality, ∼65 deaths would occur by chance alone within a week of vaccination. Applying valid estimates of intussusception case-fatality AG-014699 mouse from Africa will be useful for future benefit risk deliberations with regard to rotavirus vaccines. In summary, the recently published data on efficacy and impact of rotavirus vaccines from resource poor settings coupled with the high mortality of rotavirus disease in these settings provides stark

evidence of the need for rotavirus vaccines to improve child health in Africa. Emerging data from early introducer countries have also identified the possibility of a low level intussusception risk in some settings highlighting the need for scientifically sound safety monitoring data to better understand the benefit risk

ratio of rotavirus vaccination in developing countries. Thus, as these countries begin planning preparations for vaccine Selleckchem Gefitinib introduction, the WHO recommended that countries consider establishing disease surveillance systems to monitor the safety and effectiveness of these vaccines for measuring the full impact of rotavirus vaccines. However, the quality of post-marketing vaccine safety surveillance systems in African countries appears inadequate for detecting very rare adverse events such as intussusception. In addition, there is insufficient baseline data on the epidemiology and management of intussusception in Africa which is crucially needed for implementing surveillance systems. The lessons learned from this

Intussusception workshop address several of these gaps relevant for establishing intussusception surveillance. Attention should be directed towards larger “sentinel” paediatric hospitals with surgical services when implementing many surveillance systems for intussusception in Africa. Addressing confounding effects of age will be crucial for reliably determining whether a causal link exists between events identified through surveillance and rotavirus vaccine. And lastly, to make reliable interpretations of causality between rotavirus vaccine and intussusception, cases of intussusception presenting to the sentinel sites must be identified independent of the child’s vaccination status. If these conditions can be met and active sentinel surveillance for intussusception is established, the prospects are good for generating robust postlicensure safety monitoring data for rotavirus vaccines in Africa, thus allowing these countries to confidently undertake the WHO recommendations while ensuring the safety of rotavirus vaccines.