120 research outputs found
Strategy for systematic review of observational studies and meta-analysis modelling of risk factors for sporadic foodborne diseases
In order to design effective public health strategies, and, in particular, effective food safety interventions to
reduce the burden of foodborne disease, the most important sources of enteric illnesses should be identified. Both
case-control and cohort observational studies have for long been powerful approaches among epidemiologists to
investigate the association of exposure and illness. In the literature, there are numerous case-control and cohort
studies reporting results on risk factors and routes of transmission of sporadic foodborne infections. The objective
of this article is to describe, in depth, the strategies implemented for systematic review and meta-analysis
of the associations between multiple risk factors and eleven food and waterborne diseases, namely, non-typhoidal
salmonellosis, campylobacteriosis, Shiga-toxin E. coli infection, listeriosis, yersiniosis, toxoplasmosis,
norovirus infection, hepatitis A, hepatitis E, cryptosporidiosis and giardiasis. First, this article describes the
procedures of systematic searches in five bibliographic engines, screening of relevance and assessment of
methodological quality according to pre-set criteria. It proceeds with the explanation of a broad data categorisation
scheme established to hierarchically group the risk factors into travel, host-specific factors and pathways
of exposure (i.e., person-to-person, animal, environment and food routes), with views to harmonising and
supporting the integration of outcomes from studies investigating a variety of potential determinants of disease.
Next, the article describes the four meta-analysis models that were devised in order to calculate: (i) overall oddsratios
of acquiring the disease due to a specific risk factor by geographical region; (ii) overall odds-ratios of
acquiring the disease from the different risk factors; (iii) overall risks of disease from consumption of ready-toeat
and barbecued foods; and (iv) overall effects of food handling (i.e., consuming food in raw, undercooked or
unwashed state) and food preparation setting (i.e., eating food prepared outside the home) on risk of disease.
The procedures for sensitivity analysis and removal of any influential and potentially-biased odds-ratio; and two
methods for publication bias assessment are outlined. Finally, details are given on deviations from the standard
risk categorisation scheme for specific foodborne hazards.info:eu-repo/semantics/publishedVersio
Infections in Infants during the First 12 Months of Life: Role of Placental Malaria and Environmental Factors
Background: The association between placental malaria (PM) and first peripheral parasitaemias in early infancy was assessed in Tori Bossito, a rural area of Benin with a careful attention on transmission factors at an individual level. Methodology: Statistical analysis was performed on 550 infants followed weekly from birth to 12 months. Malaria transmission was assessed by anopheles human landing catches every 6 weeks in 36 sampling houses and season defined by rainfall. Each child was located by GPS and assigned to the closest anopheles sampling house. Data were analysed by survival Cox models, stratified on the possession of insecticide-treated mosquito nets (ITNs) at enrolment. Principal Findings: Among infants sleeping in a house with an ITN, PM was found to be highly associated to first malaria infections, after adjusting on season, number of anopheles, antenatal care (ANC) visits and maternal severe anaemia. Infants born from a malaria infected placenta had a 2.13 fold increased risk to present a first malaria infection than those born from a non infected placenta ([1.24-3.67], p<0.01) when sleeping in a house with an ITN. The risk to present a first malaria infection was increased by 3.2 to 6.5, according to the level of anopheles exposure (moderate or high levels, compared to the absence of anopheles). Conclusions: First malaria infections in early childhood can be attributed simultaneously to both PM and high levels of exposure to infected anopheles. Protective measures as Intermittent Preventive Treatment during pregnancy (IPTp) and ITNs, targeted on both mothers and infants should be reinforced, as well as the research on new drugs and insecticides. In parallel, investigations on placental malaria have to be strengthened to better understand the mechanisms involved, and thus to protect adequately the infants high risk group
Activation of natural regulatory T cells by IgG Fc-derived peptide Tregitopes
We have identified at least 2 highly promiscuous major histocompatibility complex class II T-cell epitopes in the Fc fragment of IgG that are capable of specifically activating CD4+CD25HiFoxP3+ natural regulatory T cells (nTRegs). Coincubation of these regulatory T-cell epitopes or “Tregitopes” and antigens with peripheral blood mononuclear cells led to a suppression of effector cytokine secretion, reduced proliferation of effector T cells, and caused an increase in cell surface markers associated with TRegs such as FoxP3. In vivo administration of the murine homologue of the Fc region Tregitope resulted in suppression of immune response to a known immunogen. These data suggest that one mechanism for the immunosuppressive activity of IgG, such as with IVIG, may be related to the activity of regulatory T cells. In this model, regulatory T-cell epitopes in IgG activate a subset of nTRegs that tips the resulting immune response toward tolerance rather than immunogenicity
Significant Reduction of Antibiotic Use in the Community after a Nationwide Campaign in France, 2002–2007
Didier Guillemot and colleagues describe the evaluation of a nationwide programme in France aimed at decreasing unnecessary outpatient prescriptions for antibiotics. The campaign was successful, particularly in reducing prescriptions for children
Genome wide linkage study, using a 250K SNP map, of Plasmodium falciparum infection and mild malaria attack in a Senegalese population
Multiple factors are involved in the variability of host's response to P. falciparum infection, like the intensity and seasonality of malaria transmission, the virulence of parasite and host characteristics like age or genetic make-up. Although admitted nowadays, the involvement of host genetic factors remains unclear. Discordant results exist, even concerning the best-known malaria resistance genes that determine the structure or function of red blood cells. Here we report on a genomewide linkage and association study for P. falciparum infection intensity and mild malaria attack among a Senegalese population of children and young adults from 2 to 18 years old. A high density single nucleotide polymorphisms (SNP) genome scan (Affimetrix GeneChip Human Mapping 250K-nsp) was performed for 626 individuals: i.e. 249 parents and 377 children out of the 504 ones included in the follow-up. The population belongs to a unique ethnic group and was closely followed-up during 3 years. Genome-wide linkage analyses were performed on four clinical and parasitological phenotypes and association analyses using the family based association tests (FBAT) method were carried out in regions previously linked to malaria phenotypes in literature and in the regions for which we identified a linkage peak. Analyses revealed three strongly suggestive evidences for linkage: between mild malaria attack and both the 6p25.1 and the 12q22 regions (empirical p-value = 5 x 10(-5) and 96 x 10(-5) respectively), and between the 20p11q11 region and the prevalence of parasite density in asymptomatic children (empirical p-value = 1.5 x 10(-4)). Family based association analysis pointed out one significant association between the intensity of plasmodial infection and a polymorphism located in ARHGAP26 gene in the 5q31-q33 region (p-value = 3.7 x 10(-5)). This study identified three candidate regions, two of them containing genes that could point out new pathways implicated in the response to malaria infection. Furthermore, we detected one gene associated with malaria infection in the 5q31-q33 region
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