Publications by authors named "Rodier P"

Background: From 2008 to the end of 2011, Europe experienced a major outbreak of measles. The outbreak hit France especially hard, with measles hotspots in the South-East of France. It is known that people living in precarious socio-economic conditions are more exposed to infectious diseases.

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Objectives: The aim was to present the diagnosis and treatment of a case of unilateral idiopathic gingival fibromatosis (IGF) in a geriatric patient.

Background: IGF is a rare condition characterised by an enlargement of the attached and marginal gingivae with no obvious association to any causative factor. Gingival overgrowth causes inaesthetic changes and clinical symptoms such as speech disturbances, tooth movement, and occlusal problems.

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In order to apply the recommendations of the French High Council on Public Health (CSHPF), the association "Médecins du Monde" and the departmental centre for the fight against tuberculosis led; in 2010-2011, two campaigns for on-site screening, in Marseille, with Roma families in situations of precariousness. These campaigns came up against a number of difficulties which must be addressed in order to make them more effective.

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Unlabelled: Poor children are more susceptible to infectious diseases. Routine medical follow-up is infrequent in these patients, sometimes resulting in immunization delays. The aim of this study was to correlate a number of socioeconomic factors related to poverty with vaccination coverage in children visiting a pediatric emergency ward.

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The target of this study is the adaptation of the ferrozine method to flow injection analysis (FIA) to perform iron analysis in situ using an in situ chemical analyser in hydrothermal environments. The adaptation of the method to FIA was followed by its optimisation using an experimental design screening method. The goals of the optimisation steps were to decrease the detection limit and to increase the measuring range to cope with the constraints of in situ analysis.

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Objective: To replicate the factor structure and predictive validity of revised Autism Diagnostic Observation Schedule algorithms in an independent dataset (N = 1,282).

Method: Algorithm revisions were replicated using data from children ages 18 months to 16 years collected at 11 North American sites participating in the Collaborative Programs for Excellence in Autism and the Studies to Advance Autism Research and Treatment.

Results: Sensitivities and specificities approximated or exceeded those of the old algorithms except for young children with phrase speech and a clinical diagnosis of pervasive developmental disorders not otherwise specified.

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Autism is a neurodevelopmental disorder characterized by an early onset of abnormal social, communicative, and repetitive behavior. Engrailed-2 (EN2) was identified as an autism candidate gene because its influence on cerebellar development in mice parallels neurodevelopmental abnormalities seen in individuals with autism. Studies investigating association between markers at EN2 (chr7q36), a location associated with language disorders, and autism reveal mixed findings.

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Autism spectrum disorders (ASDs) are common, heritable neurodevelopmental conditions. The genetic architecture of ASDs is complex, requiring large samples to overcome heterogeneity. Here we broaden coverage and sample size relative to other studies of ASDs by using Affymetrix 10K SNP arrays and 1,181 [corrected] families with at least two affected individuals, performing the largest linkage scan to date while also analyzing copy number variation in these families.

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Offspring of rats exposed to valproic acid (VPA) on gestational day (GD) 12 have been advocated as a rodent model of autism because they show neuron loss in brainstem nuclei and the cerebellum resembling that seen in human autistic cases . Studies of autistic children have reported alterations in acquisition of classical eyeblink conditioning and in reversal of instrumental discrimination learning . Acquisition of discriminative eyeblink conditioning depends on known brainstem-cerebellar circuitry whereas reversal depends on interactions of this circuitry with the hippocampus and prefrontal cortex.

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Data from 10 sites of the NICHD/NIDCD Collaborative Programs of Excellence in Autism were combined to study the distribution of head circumference and relationship to demographic and clinical variables. Three hundred thirty-eight probands with autism-spectrum disorder (ASD) including 208 probands with autism were studied along with 147 parents, 149 siblings, and typically developing controls. ASDs were diagnosed, and head circumference and clinical variables measured in a standardized manner across all sites.

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Background: Valproic acid (VPA) exposure in utero has been associated with an increased risk of both neural tube defects and autism spectrum disorders (ASDs). The terata induced by VPA suggest interference with pattern formation. Retinoic acid produces similar terata and is known to act in part by increasing the expression of Hoxa1.

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We performed a genome-wide linkage scan using highly polymorphic microsatellite markers. To minimize genetic heterogeneity, we focused on sibpairs meeting the strict diagnosis of autism. In our primary analyses, we observed a strong linkage signal (P=0.

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Autism is a neurodevelopmental disorder manifesting early in childhood. Some symptoms of autism are alleviated by treatment with selective serotonin reuptake inhibitors, which are known to interact with the serotonin transporter. Moreover, variation in the gene that encodes the transporter (SLC6A4), especially the HTTLPR locus, is known to modulate its expression.

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Autism spectrum disorders affect behaviors that emerge at ages when typically developing children become increasingly social and communicative, but many lines of evidence suggest that the underlying alterations in the brain occur long before the period when symptoms become obvious. Studies of the behavior of children in the first year of life demonstrate that symptoms are often detectable in the first 6 months. The environmental factors known to increase the risk of autism have critical periods of action during embryogenesis.

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The central nervous system is the most vulnerable of all body systems to developmental injury. This review focuses on developmental processes by which the nervous system is formed and how those processes are known or suspected to be injured by toxic agents. The processes discussed are establishment of neuron numbers; migration of neurons; establishment of connections, neurotransmitter activity, and receptor numbers; deposition of myelin; and 2 processes that are prominent in postnatal development, trimming back of connections and postnatal neurogenesis.

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A recent study by Persico et al. [2001: Mol Psychiatry 6:150-159] suggests alleles of a CGG polymorphism, just 5' of the reelin gene (RELN) initiator codon, confer liability for autism, especially alleles bearing 11 or more CGG repeats (long alleles). The association is consistent across both a case-control and family-based sample.

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Background: The HOXA1 gene plays a major role in brainstem and cranial morphogenesis. The G allele of the HOXA1 A218G polymorphism has been previously found associated with autism.

Methods: We performed case-control and family-based association analyses, contrasting 127 autistic patients with 174 ethnically matched controls, and assessing for allelic transmission disequilibrium in 189 complete trios.

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The hypothesis that brain stem injury plays a role in the autism spectrum disorders was suggested by evidence that exposure to thalidomide during the earliest stages of brain development increases the risk of autism spectrum disorders. The implications for the embryological origin of autism first led to studies of neuroanatomy in a human case and an animal model and then to examinations of minor craniofacial features in autism. But the general hypothesis had much broader implications.

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Background: Family studies have demonstrated that the autism spectrum disorders (ASDs) have a major genetic etiologic component, but expression and penetrance of the phenotype are variable. Mice with null mutations of Hoxa1 or Hoxb1, two genes critical to hindbrain development, have phenotypic features frequently observed in autism, but no naturally occurring variants of either gene have been identified in mammals.

Methods: By sequencing regions of genomic DNA of patients with autism spectrum disorders, we detected a substitution variant at HOXA1 and an insertion variant at HOXB1, both in coding regions of the genes.

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Abnormalities in anatomy and function of the cranial nerve motor nuclei have been demonstrated in some people with autism and can be modeled in rats by exposure to valproic acid during neural tube closure. Reductions in Purkinje cell number and cerebellar volume, particularly of the posterior lobe, have also been reported in people with autism. Thus, a stereological examination of cerebellar morphology was undertaken in valproate-exposed rats.

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In the context of an epidemiological study of autism in Nova Scotia, subjects were evaluated for minor physical anomalies and physical measurements. Normal control children, children with autism and their siblings, and children with developmental disabilities and their siblings were compared. Posterior rotation of the external ears was found to be a characteristic related to autism specifically, rather than to developmental disabilities in general.

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