Large-scale vibrating coil magnetometer for the magnetic characterization of bulk superconductors.

This work presents the design and validation of a vibrating coil magnetometer for the characterization of the field dependence of the critical current density of centimeter-sized bulk superconductors as an alternative to the destructive methods typically used. The magnetometer is also shown to be capable of measuring the magnetic moment in an applied field of up to 5 T for diverse magnetic materials, such as soft and hard ferromagnets and high-temperature superconducting pellets. The vibrating coil magnetometer was first optimized using finite element simulations and calibrated using a commercial vibrating sample magnetometer. The vibrating coil magnetometer was benchmarked with hysteresis measurements of a Nd2Fe14B disk made with a commercial hysteresisgraph, showing good agreement between the different setups. The magnetic hysteresis of a YBa2Cu3O7-x superconducting pellet was measured at 77 K, showing a penetration field of 1 T and an irreversibility field of 4 T. The field dependent critical current density of the superconductor was then inferred from the magnetic hysteresis measurements and extrapolated at low fields. Finally, the resulting critical current density was used to successfully reproduce the measured magnetization curve of the pellet at 2 T with finite element simulations.

Prospecting potential links between PRRSV infection susceptibility of alveolar macrophages and other respiratory infectious agents present in conventionally reared pigs.

Porcine Reproductive and Respiratory Syndrome virus (PRRSV) is one of the main component of the porcine respiratory disease complex (PRDC), which strongly impact the pig production. Although PRRSV is often considered as a primary infection that eases subsequent respiratory coinfections, the possibility that other PRDC components may facilitate PRRSV infection has been largely overlooked. The main cellular targets of PRRSV are respiratory macrophages among them alveolar macrophages (AM) and pulmonary intravascular macrophages (PIM). AM, contrarily to PIM, are directly exposed to the external respiratory environment, among them co-infectious agents. In order to explore the possibility of a co-infections impact on the capacity of respiratory macrophages to replicate PRRSV, we proceed to in vitro infection of AM and PIM sampled from animals presenting different sanitary status, and tested the presence in the respiratory tract of these animals of the most common porcine respiratory pathogens (PCV2, Actinobacillus pleuropneumoniae, Mycoplasma hyopneumoniae, Mycoplasma hyorhinis, Mycoplasma floculare, Pasteurella multocida, Bordetella bronchiseptica, Streptoccocus suis). In this exploratory study with a limited number of animals, no statistic differences were observed between AM and PIM susceptibility to in vitro PRRSV infection, nor between AM coming from animals presenting very contrasting respiratory coinfection loads.

Improving Methods for Analyzing Antimalarial Drug Efficacy Trials: Molecular Correction Based on Length-Polymorphic Markers msp-1, msp-2, and glurp.

Drug efficacy trials monitor the continued efficacy of front-line drugs against falciparum malaria. Overestimating efficacy results in a country retaining a failing drug as first-line treatment with associated increases in morbidity and mortality, while underestimating drug effectiveness leads to removal of an effective treatment with substantial practical and economic implications. Trials are challenging: they require long durations of follow-up to detect drug failures, and patients are frequently reinfected during that period. Molecular correction based on parasite genotypes distinguishes reinfections from drug failures to ensure the accuracy of failure rate estimates. Several molecular correction "algorithms" have been proposed, but which is most accurate and/or robust remains unknown. We used pharmacological modeling to simulate parasite dynamics and genetic signals that occur in patients enrolled in malaria drug clinical trials. We compared estimates of treatment failure obtained from a selection of proposed molecular correction algorithms against the known "true" failure rate in the model. Our findings are as follows. (i) Molecular correction is essential to avoid substantial overestimates of drug failure rates. (ii) The current WHO-recommended algorithm consistently underestimates the true failure rate. (iii) Newly proposed algorithms produce more accurate failure rate estimates; the most accurate algorithm depends on the choice of drug, trial follow-up length, and transmission intensity. (iv) Long durations of patient follow-up may be counterproductive; large numbers of new infections accumulate and may be misclassified, overestimating drug failure rate. (v) Our model was highly consistent with existing in vivo data. The current WHO-recommended method for molecular correction and analysis of clinical trials should be reevaluated and updated.

[Multiple and successive treatment failures in a patient infected by Plasmodium falciparum in Cambodia and treated by dihydroartemisinin-piperaquine]. / Echecs thérapeutiques multiples et successifs chez un patient infecté par Plasmodium falciparum au Cambodge et traité par dihydroartémisinine-pipéraquine.

Cases of treatment failures following administration of artemisinin-based combination therapies (ACT) remain rare in malaria endemic areas. In Cambodia, however, failures of these treatments are now commonly observed. Usually, these post-treatment recurrences occur only once and a second course of the same treatment is sufficient to cure patients.We describe here an atypical case of a Plasmodium falciparum-infected patient manifesting several malaria recrudescence episodes following dihydroartemisinin-piperaquine (Eurartesim®) treatment. This case report illustrates the current issue of resistance to the latest generation of antimalarial drugs in Southeast Asia and highlights the difficulty in efficaciously fighting malaria in this region if new therapy remains unimplemented.

Transcriptional changes in Crassostrea gigas oyster spat following a parental exposure to the herbicide diuron.

The Pacific oyster Crassostrea gigas is the main oyster species produced in the world, and a key coastal economic resource in France. High mortalities affect Pacific oysters since 2008 in France and Europe. Their origins have been attributed to a combination of biotic and abiotic factors, underlining the importance of environment quality. The impact of water pollution has been pointed out and one of the pollutants, the genotoxic herbicide diuron, occurs at high concentrations all along the French coasts. Previous work has revealed that a parental exposure to diuron had a strong impact on hatching rates and offspring development even if spats were not exposed to diuron themselves. In this study, we explored for the first time the transcriptional changes occurring in oyster spats (non exposed) originating from genitors exposed to an environmentally relevant concentration of diuron during gametogenesis using the RNAseq methodology. We identified a transcriptomic remodeling revealing an effect of the herbicide. Different molecular pathways involved in energy production, translation and cell proliferation are particularly disturbed. This analysis revealed modulated candidate genes putatively involved in response to oxidative stress and mitochondrial damage in offspring of genitors exposed to diuron. Complementary measures of the activity of enzymes involved in these latter processes corroborate the results obtained at the transcriptomic level. In addition, our results suggested an increase in energy production and mitotic activity in 5-month-spats from diuron-exposed genitors. These results could correspond to a "catch-up growth" phenomenon allowing the spats from diuron-exposed genitors, which displayed a growth delay at 3 months, to gain a normal size when they reach the age of 6 months. These results indicate that exposure to a concentration of diuron that is frequently encountered in the field during the oyster's gametogenesis stage can impact the next generation and may result in fitness disturbance.

Effects of an environmentally relevant concentration of diuron on oyster genitors during gametogenesis: responses of early molecular and cellular markers and physiological impacts.

Genitors of the Pacific oyster Crassostrea gigas were submitted during gametogenesis to a short pulse exposure to the herbicide diuron at a realistic environmental concentration. Histological analysis showed no effect of diuron on gametogenesis course, sex ratio and reproductive effort. A non-significant increase in testosterone and progesterone levels was observed in genitors exposed to the herbicide. At cell level, diuron exposure was shown to modulate the phagocytic activity of circulating hemocytes. The results of a transcriptional analysis showed that diuron affected the expression of genes belonging to functions known to play a major role during oyster gametogenesis such as gene transcription regulation, DNA replication and repair, DNA methylation and cytokinesis. Taking into account the results we previously obtained on the same genitors, this study showed a negative effect of diuron on oyster reproduction by inducing both structural and functional modifications of the DNA.

Chronic dietary exposure of zebrafish to PAH mixtures results in carcinogenic but not genotoxic effects.

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants that can be present at high levels as mixtures in polluted aquatic environments. Many PAHs are potent mutagens and several are well-known carcinogens. Despite numerous studies on individual compounds, little is known about the toxicity of PAHs mixtures that are encountered in environmental situations. In the present work, zebrafish were continuously fed from 5 days post-fertilisation to 14 months post-fertilisation (mpf) with a diet spiked with fractions of either pyrolytic (PY), petrogenic light oil (LO), or petrogenic heavy oil (HO) origin at three concentrations. A decrease in survival was identified after 3 mpf in fish fed with the highest concentration of HO or LO, but not for PY. All PAH fractions caused preneoplastic and neoplastic disorders in long-term-exposed animals. Target tissues were almost exclusively of epithelial origin, with the bile duct epithelium being the most susceptible to chronic exposure to all PAH fractions, and with germ cells being the second most responsive cells. Significantly higher incidences of neoplasms were observed with increasing PAH concentration and exposure duration. The most severe carcinogenic effects were induced by dietary exposure to HO compared to exposure to LO or PY (45, 30 and 7 %, respectively, after 9 to 10 months of exposure to an intermediate concentration of PAHs). In contrast, earliest carcinogenic effects were detected as soon as 3 mpf after exposure to LO, including the lowest concentration, or to PY. PAH bioactivation and genotoxicity in blood was assessed by ethoxyresorufin-O-deethylase activity quantification and comet and micronuclei assays, respectively, but none of these were positive. Chronic dietary exposure of zebrafish to PAH mixtures results in carcinogenotoxic events that impair survival and physiology of exposed fish.

Study of genetic damage in the Japanese oyster induced by an environmentally-relevant exposure to diuron: evidence of vertical transmission of DNA damage.

Pesticides represent a major proportion of the chemical pollutants detected in French coastal waters and hence a significant environmental risk with regards to marine organisms. Commercially-raised bivalves are particularly exposed to pollutants, among them pesticides, as shellfish farming zones are subject to considerable pressure from agricultural activities on the mainland. The aims of this study were to determine (1) the genotoxic effects of diuron exposure on oyster genitors and (2) the possible transmission of damaged DNA to offspring and its repercussions on oyster fitness. To investigate these points, oysters were exposed to concentrations of diuron close to those detected in the Marennes-Oleron Basin (two 7-day exposure pulses at 0.4 and 0.6 µg L(-1)) during the gametogenesis period. Genomic abnormalities were characterized using two complementary approaches. The Comet assay was applied for the measurement of early and reversible primary DNA damage, whereas flow cytometry was used to assess the clastogenic and aneugenic effect of diuron exposure. Polar Organic Chemical Integrative Samplers (POCIS) were used in exposed and assay tanks to confirm the waterborne concentration of diuron reached during the experiment. The results obtained by the Comet assay clearly showed a higher level of DNA strand breaks in both the hemocytes and spermatozoa of diuron-exposed genitors. The transmission of damaged genetic material to gamete cells could be responsible for the genetic damage measured in offspring. Indeed, flow cytometry analyses showed the presence of DNA breakage and a significant decrease in DNA content in spat from diuron-exposed genitors. The transmission of DNA damage to the offspring could be involved in the negative effects observed on offspring development (decrease in hatching rate, higher level of larval abnormalities, delay in metamorphosis) and growth. In this study, the vertical transmission of DNA damage was so highlighted by subjecting oyster genitors to short exposures to diuron at medium environmental concentrations. The analysis of POCIS showed that oysters were exposed to integrated concentrations as low as 0.2 and 0.3 µg L(-1), emphasizing the relevance of the results obtained and the risk associated to chemical contamination for oyster recruitment and fitness.

Association between genetic variants in the HNF4A gene and childhood-onset Crohn's disease.

Hepatocyte nuclear 4 alpha (HNF4α), involved in glucose and lipid metabolism, has been linked to intestinal inflammation and abnormal mucosal permeability. Moreover, in a genome-wide association study, the HNF4A locus has been associated with ulcerative colitis. The objective of our study was to evaluate the association between HNF4α genetic variants and Crohn's disease (CD) in two distinct Canadian pediatric cohorts. The sequencing of the HNF4A gene in 40 French Canadian patients led to the identification of 27 single nucleotide polymorphism (SNP)s with a minor allele frequency >5%. To assess the impact of these SNPs on disease susceptibility, we first conducted a case-control discovery study on 358 subjects with CD and 542 controls. We then carried out a replication study in a separate cohort of 416 cases and 1208 controls. In the discovery cohort, the genotyping of the identified SNPs revealed that six were significantly associated with CD. Among them, rs1884613 was replicated in the second CD cohort (odds ratio (OR): 1.33; P<0.012) and this association remained significant when both cohorts were combined and after correction for multiple testing (OR: 1.39; P<0.004). An 8-marker P2 promoter haplotype containing rs1884613 was also found associated with CD (P<2.09 × 10(-4) for combined cohorts). This is the first report showing that the HNF4A locus may be a common genetic determinant of childhood-onset CD. These findings highlight the importance of the intestinal epithelium and oxidative protection in the pathogenesis of CD.

Genotoxic and enzymatic effects of fluoranthene in microsomes and freshly isolated hepatocytes from sole (Solea solea).

The fluoranthene (Fluo) is one of the most abundant polycyclic aromatic hydrocarbons (PAHs) in human food and in marine compartments. However, the existing data on its genotoxicity is poor and controversial. The aim of this study was to assess in vitro the potential genotoxicity of Fluo in sole and its possible effect on CYP450 modulation. Freshly isolated hepatocytes were exposed for 24 h to a range of Fluo concentrations from 0.5 to 50 µM in both culture flasks and microplate wells. The ethoxyresorufin-O-deethylase (EROD) activity was measured as an indicator of the activity of the cytochrome P450 1A1 (CYP1A1). The genotoxic effects were evaluated by measuring both DNA strand breaks and DNA adducts by the alkaline comet assay and the postlabeling technique respectively. Calf thymus DNA was also exposed to Fluo in the presence of sole liver microsomes in order to check for Fluo DNA adduct formation. In sole hepatocytes, Fluo was shown to induce a decrease in the EROD activity in a concentration-dependent manner. A significant genotoxic effect was observed in terms of DNA strand breakage from an exposure concentration of 5 µM: despite a concentration-dependent effect was observed, it did not follow a linear dose-response. The response was similar whatever the way of exposure in flasks or in wells. One reproducible adduct was detected in the hepatocytes exposed to the highest concentrations of Fluo. The formation of Fluo adducts was confirmed by the detection of one reproducible adduct following in vitro exposure of calf thymus DNA to 100 and 200 µM of Fluo in the presence of sole microsomes. These results demonstrate the potential of sole hepatocytes to metabolize Fluo in 24 h into reactive species, able to induce genotoxicity by DNA strand breakage and DNA adduct formation. Moreover, a miniaturized cell exposure system was validated for further experiments using fewer amounts of hepatocytes and contaminants, and allowing exposure to PAH metabolites.

[Resistance of Plasmodium falciparum to antimalarial drugs: impact on malaria pre-elimination in Madagascar]. / Résistance de Plasmodium falciparum aux antipaludiques: impact sur la pré-élimination du paludisme à Madagascar.

The purpose of this review was to provide up-to-date information on the resistance of Plasmodium falciparum to the main antimalarials used in Madagascar and to assist implementation of the malaria control and elimination program. In 2006, the failure rate for chloroquine treatment was 44% (n = 300) and was comparable to the rate observed in continental Africa. Most treatment failures occurred after the first week of follow-up. P. falciparum resistance to chloroquine appeared to be special in Madagascar with only 3.2% of isolates showing in vitro resistance (n = 372, 7 sentinel sites) and less than 1% harbouring mutant parasites within the Pfcrt gene. Conversely, the Pfmdr1 N86Y point mutation was found in 64.3% (n = 174) of isolates in 2006 and in 51.7% (n = 343) in 2007. Failure of combined sulfadoxine-pyrimethamine therapy, i.e., the recommended intermittent preventive treatment for malaria during pregnancy, and in vitro resistance to pyrimethamine were rare. However, the Pfdhfr 51I/59R/108N allele showed consistently high prevalence levels reaching 33.3% in 2008. Moreover, the single Pfdhfr 164L mutant allele, a haplotype unique to Madagascar, was discovered in 2006 and showed prevalence rates up to 30% in some locations (southeast) in 2008. Up to now, the quadruple mutant allele Pfdhfr 51I/59R/108N/164L has not been observed. Susceptibility to the other antimalarials tested appeared excellent but the number of isolates showing in vitro susceptibility to artemisinin derivatives has been fallen in recent years and this decline may herald a decrease in the efficacy of these drugs.

Plasmodium vivax and the Duffy antigen: a paradigm revisited.

The Duffy blood group antigen is the portal of entry of the Plasmodiumvivax malaria parasite into human red blood cells and the receptor for a number of CXC and CC chemokines. We review here epidemiological data and evidence derived from therapeutic or experimental human infections associating P. vivax and the Duffy glycoprotein and laboratory studies indicating that P. vivax uses the Duffy antigen as a receptor to invade the red cell. We then review recent field observations indicating that the conclusion of the absolute dependence on the presence of Duffy on the red cell for P. vivax infection and development into the red cell no longer holds true and that in some parts of the world, P. vivax infects and causes disease in Duffy-negative people.

[Acquired copper deficiency myelopathy]. / Myélopathie postérieure par carence en cuivre acquise.

INTRODUCTION: The hematological manifestations of acquired copper deficiency are well known. But the neurological manifestations have only been recognised in the past few years. The most common neurological manifestation in adults is a myeloneuropathy with prominent sensory ataxia and spastic gait. Electrophysiological tests reveal an axonal sensorimotor peripheral neuropathy. Spinal MRI shows an augmented T2 signal involving the dorsal column. The causes of acquired copper deficiency include gastric surgery, excessive zinc ingestion, and malabsorption but in most cases, the cause remains unclear. Early recognition and treatment may prevent neurological deterioration but improvement seems to be slight and inconstant. OBSERVATION: We report two new cases of acquired copper deficiency myeloneuropathy associated with a nephrotic syndrome and, in one case, with a major iron overload syndrome. Biological abnormalities disappeared under copper supplementation. A significant neurological improvement with disappearance of ataxia occurred in one patient who received copper supplementation eight months after symptom onset. CONCLUSIONS: Nephrotic syndrome might be another complication of acquired copper deficiency. Delayed treatment is not necessarily associated with a deleterious neurological prognosis. Significant neurological improvement under copper supplementation is possible.

Relationship between PAH biotransformation as measured by biliary metabolites and EROD activity, and genotoxicity in juveniles of sole (Solea solea).

Polycylic aromatic hydrocarbons (PAHs) are ubiquitous contaminants in the marine environment. Their toxicity is mainly linked to the ability of marine species to biotransform them into reactive metabolites. PAHs are thus often detected at trace levels in animal tissues. For biomonitoring purposes, this findings have two main consequences, (i) the determination of the PAH tissue concentration is not suitable for the evaluation of individual exposure to PAHs (ii) it can explain sometimes the lack of correlations obtained with relevant markers of toxicity such as genotoxicity biomarkers. The aim of the present study was to better investigate the link between PAH exposure and genotoxicity in marine flatfish. During a laboratory experiment, juvenile soles were exposed for four weeks to a mixture of three PAHs, namely benzo[a]pyrene, fluoranthene and pyrene, followed by one week of depuration. Fish were exposed via the trophic route to a daily PAH concentration of 120 µg/g food. Fish were sampled at different time points. The bioavailability and the biotransformation of PAHs were assessed by the measurement of biliary metabolites using a sensitive UPLC MS/MS method. The 7-ethoxyresorufine-O-deethylase was also measured in liver subcellular fractions as a biomarker of phase I biotransformation activities. Genotoxicity was assessed in parallel by the measurement of DNA strand breaks in fish erythrocytes by the alkaline comet assay. During this study, the high amount of PAH metabolites produced in sole demonstrated the bioavailability of PAHs and their biotransformation by fish enzymes. A positive correlation was observed between the level of hydroxylated PAH metabolites and genotoxicity as measured by the alkaline comet assay.

Anderson's disease (chylomicron retention disease): a new mutation in the SARA2 gene associated with muscular and cardiac abnormalities.

Anderson's disease (AD) or chylomicron retention disease (CMRD) is a rare hereditary lipid malabsorption syndrome linked to SARA2 gene mutations. We report in this study a novel mutation in two sisters for which the Sar1b protein is predicted to be truncated by 32 amino acids at its carboxyl-terminus. Because the SARA2 gene is also expressed in the muscle, heart, liver and placenta, extraintestinal clinical manifestations may exist. For the first time, we describe in this study in the two sisters muscular as well as cardiac abnormalities that could be related to the reported expression of SARA2 in these tissues. We also evaluated six other patients for potential manifestations of the SARA2 mutation. The creatine phosphokinase levels were increased in all patients [1.5-9.4 x normal (N)] and transaminases were moderately elevated in five of the eight patients (1.2-2.6 x N), probably related to muscle disease rather than to liver dysfunction. A decreased ejection fraction occurred in one patient (40%, N: 60%). The muscle, liver and placental tissues that were examined had no specific abnormalities and, in particular, no lipid accumulation. These results suggest that myolysis and other extraintestinal abnormalities can occur in AD/CMRD and that the clinical evaluation of patients should reflect this.

Magnetostatic interactions and coercivities of ferromagnetic soft nanowires in uniform length arrays.

First-order reversal curve diagrams have been used to investigate magnetostatic interactions and average coercivity of individual wires in soft ferromagnetic uniform length nanowire arrays. We present a method for identifying these physical parameters on the out-of-plane first-order reversal curve diagrams: the position of the irreversible part on the critical axis is a good approximation to the average value of the nanowire coercivity and the maximum interaction field is equal to the interaction field at saturation. Their dependence upon material (CoFeB and Ni) and nanowire length are presented. The magnetostatic interactions increase linearly with length, in agreement with a model developed previously. The global array coercivity, obtained from magnetization curves, is generally lower than the apparent average coercivity for individual nanowires. This coercivity reduction increases linearly with the magnetostatic interactions. The general shape of the out-of-plane first-order reversal curve diagrams is compared with those obtained from a theoretical moving Preisach model.

Electroluminescence from single-wall carbon nanotube network transistors.

The electroluminescence (EL) properties from single-wall carbon nanotube network field-effect transistors (NNFETs) and small bundle carbon nanotube field effect transistors (CNFETs) are studied using spectroscopy and imaging in the near-infrared (NIR). At room temperature, NNFETs produce broad (approximately 180 meV) and structured NIR spectra, while they are narrower (approximately 80 meV) for CNFETs. EL emission from NNFETs is located in the vicinity of the minority carrier injecting contact (drain) and the spectrum of the emission is red shifted with respect to the corresponding absorption spectrum. A phenomenological model based on a Fermi-Dirac distribution of carriers in the nanotube network reproduces the spectral features observed. This work supports bipolar (electron-hole) current recombination as the main mechanism of emission and highlights the drastic influence of carrier distribution on the optoelectronic properties of carbon nanotube films.

First order reversal curves (FORC) diagrams of Co nanowire arrays.

Nanowire arrays of Co and Ni have been obtained by current pulse electrodeposition into nanoporous alumina templates. By adjusting the pH of the bath, the microstructure of the Co wires was tailored, resulting in two types of arrays of crystalline Co--hcp, with c-axis nominally parallel (Co (c parallel)), or nominally perpendicular (Co (c perpendicular)) to the wire. First-order reversal curve (FORC) diagrams provide information on average coercivity of the individual nanowire and the factors influencing the field created in the saturated array by the magnetostatic interactions. The dependences of this field on array geometry (wire length and diameter) and saturation magnetization were found to be in excellent agreement with theoretical predictions from a micromagnetic model. For arrays with lower wire diameter, the average coercivity of the individual wires is systematically higher than the coercivity of the array. The most important difference between the two Co series is in the dependence of the FORC diagrams on the wire diameter, with the Co (cl) showing significant pattern changes at large diameters. Two possible sources of those changes are discussed.

Exciton formation and annihilation during 1D impact excitation of carbon nanotubes.

Near-infrared electroluminescence was recorded from unipolar single-wall carbon nanotube field-effect transistors at high drain-source voltages. High resolution spectra reveal resonant light emission originating from the radiative relaxation of excitons rather than heat dissipation. The electroluminescence is induced by only one carrier type and ascribed to 1D impact excitation. An emission quenching is also observed at high field and attributed to an exciton-exciton annihilation process and free carrier generation. The excitons' binding energy in the order of 270 meV for 1.4 nm SWNTs is inferred from the spectral features.

Efficacy of chloroquine-proguanil malaria prophylaxis in a non-immune population in Bangui, Central African Republic: a case-control study.

A case-control study was conducted to evaluate the efficacy of the combination of chloroquine plus proguanil as malaria prophylaxis in a non-immune population living in the Central African Republic. Cases were patients presenting with a malaria attack confirmed by a positive blood film and/or an HRP2 positive antigen test at the Pasteur Institute of Bangui. Two control subjects were included per case: one was a relative or close friend and the other was matched to the patient with respect to the length of stay. A questionnaire assessing malaria prophylaxis habits and malarial risk factors over the 2-month period prior to inclusion in the study was given to 48 cases and 96 controls. A conditional logistic regression was used to identify risk factors. The efficacy of the chloroquine plus proguanil regimen was found to be high (95.5%, 95% CI 74.0-99.2%) in this country known for high chloroquine resistance. Our data lend some support to the use of chloroquine plus proguanil in Bangui, and the protective efficacy of chloroquine plus proguanil should now be studied prospectively as part of a randomised controlled trial of various prophylactic drugs.