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Biomedical subjects

M Tardieu

Publications and source records attributed to M Tardieu.

At least 19 recordsLinked to original sources
PubMed2005

[Varicella, acute postinfectious arteriopathy and cerebral arterial thrombosis in childhood: a unique clinical and etiologic framework to be fully acknowledged].

Acute arteriopathies are the etiological factor of 25% of all the cerebral arterial thrombosis cases in childhood; they give way to ischemic strokes which have specific clinical and radiological features; varicella is the etiologic factor in 60% of the cases; favorable outcome is the rule; physiopathology and treatment remain under discussion.

Acute Disease↗
PubMed2004

DSM-IV mental disorders and neurological complications in children and adolescents with human immunodeficiency virus type 1 infection (HIV-1).

AIM: - To study the types of psychiatric problem encountered in children infected with the human immunodeficiency virus (HIV) and their relationship to central nervous system disorder and the severity of infection. METHODS: - 17 HIV-infected children presenting with psychiatric problems were included. Mental disorders were evaluated according to DSM-IV criteria. Neurological disorders and progressive encephalopathy (presence or absence) diagnosis were evaluated by clinical and radiological examination. The severity of infection was assessed by the percentage of CD4 lymphocytes. RESULTS: - The most frequent diagnoses were major depression (MDD: 47%) and attention deficit hyperactivity disorder (ADHD: 29%). Major depression diagnosis was significantly associated with neuroimaging or clinical neurological abnormalities (p < 0.01). In contrast, no association was found between hyperactivity diagnosed according to DSM-IV criteria and central nervous system disorder. Percentage of CD4 lymphocytes were close to 0 for more than 80% of children presenting with psychiatric complications. CONCLUSION: - The very low % of CD4 lymphocytes of these children suggest that the appearance of a psychiatric complication should be regarded as a factor indicating severe HIV infection. Depressive disorders may be a clinical form of encephalopathy.

AIDS Dementia Complex↗
PubMed2004

Multiple sclerosis in children.

Multiple sclerosis can develop during childhood, even among children under 10 years of age, and the initial diagnosis can be difficult. A first demyelinating event in children may be an episode of monophasic acute disseminated encephalomyelitis or a first episode of a macrophage activation syndrome, angiitis affecting the central nervous system or MS. The risk of developing MS is lower if: the child is younger than 10 years old; onset is associated with severely altered consciousness; presentation is polysymptomatic; or there are large and poorly limited lesions of the white matter. MS in children probably has a slightly better outcome than MS in adults. Initial treatment mainly relies on methylprednisolone, and there is little information on the results of beta interferon treatment in children with MS.

Age Factors↗
PubMed2003

[Description and prognostic value of cerebellar MRI lesions in children with severe acute ataxia].

The aim of this work was to evaluate NMR cerebellar abnormalities in children with severe acute ataxia. Among 8 consecutively observed children, NMR performed in 6 during the acute phase was pathological in 4, demonstrating hyperintense signal in the T2-weighed sequences of dentate nuclei (2 cases, associated in 1 with hyperintense signal in the medium cerebellar peduncle) or of the cerebellar cortex associated with cerebellar swelling (2 cases). NMR performed in 7 cases after at least 1 month of evolution showed cerebellar atrophy in 4 cases. After 1 to 6 years of clinical follow-up, 4/8 children had clinical sequellae, including 3 of the 4 children with initially abnormal NMR. Conversely, the 2 patients with initially normal NMR had a good clinical recovery. NMR during the acute phase gives informations on prognosis in patients with severe acute ataxia.

Acute Disease↗
PubMed2002

Risk of early febrile seizure with perinatal exposure to nucleoside analogues.

The frequency of seizures was studied in a prospective cohort of French children born to HIV-1-infected mothers. The analysis was restricted to the 4426 uninfected children, whether or not exposed to antiretrovirals. 81 convulsions were reported up to the age of 18 months, and 30 children fulfilled the criteria for simple febrile seizures. The risk of first febrile seizure was higher for children perinatally exposed to antiretrovirals than for those not exposed (log-rank test: p=0.0198). A similar trend was noted for other non-neonatal seizures (p=0.0537) but not for neonatal seizures.

Anti-HIV Agents↗
PubMed2001

Cellular expression of functional chemokine receptor CCR5 and CXCR4 in human embryonic neurons.

In the present study we analysed expression of the chemokine receptors CCR5 and CXCR4 in human embryonic neurons. Both receptors were detected in neurons from primary cultures by immunofluorescence and confocal laser microscopy analysis. Both CCR5 and CXCR4 were mainly located inside the cell in the neuronal cell body and processes. In addition, neurons synthesised CCR5 and CXCR4 transcripts, as demonstrated by reverse transcription-polymerase chain reaction. Stimulation with the CCR5 and the CXCR4 agonists increased [Ca(2+)](i) in embryonic neurons, indicating that CXCR4 and CCR5 were functional at the neuronal surface. The inhibitory effect of pertussis toxin demonstrated that G(i)alpha protein is involved in chemokine receptor activation. The fact that chemokine receptors are expressed at embryonic stage in neurons reinforces the idea that chemokines might be cues for neuron pathfinding during brain ontogeny.

Calcium↗
PubMed2001

Role of CD23 in astrocytes inflammatory reaction during HIV-1 related encephalitis.

Soluble factors released by intra-cerebral activated cells are implicated in neuronal alterations during central nervous system inflammatory diseases. In this study, the role of the CD23 pathway in astrocyte activation and its participation in human immunodeficiency virus-1 (HIV-1)-induced neuropathology were evaluated. In human primary astrocytes, CD23 protein membrane expression was dose-dependently upregulated by gp120. It was also upregulated by gamma-interferon (gamma-IFN) and modulated by interleukin-1-beta (IL-1beta) whereas microglial cells in these stimulation conditions did not express CD23. Cell surface stimulation of CD23 expressed by astrocytes induced production of nitric oxide (NO) and IL-1beta which was inhibited by a specific inducible NO-synthase (iNOS) inhibitor (aminoguanidine), indicating the implication of this receptor in the astrocyte inflammatory reaction. On brain tissues from five out of five patients with HIV-1-related encephalitis, CD23 was expressed by astrocytes and by some microglial cells, whereas it was not detectable on brain tissue from five of five HIV-1-infected patients without central nervous system (CNS) disease or from two of two control subjects. In addition, CD23 antigen was co-localized with iNOS and nitrotyrosine on brain tissue from patients with HIV1-related encephalitis, suggesting that CD23 participates in iNOS activation of astrocytes in vivo. In conclusion, CD23 ligation is an alternative pathway in the induction of inflammatory product synthesis by astrocytes and participates in CNS inflammation.

AIDS Dementia Complex↗
PubMed2001

Beneficial use of fibroblast growth factor 2 and RGTA, a new family of heparan mimics, for endothelialization of PET prostheses.

We have studied the endothelialization of polyethylene terephtalate (PET) prostheses coated with collagen by adult human saphenous endothelial cells (EC) under various in vitro conditions. Collagenous PET was impregnated either by Fibroblast Growth Factor 2 (FGF2), heparin, a synthetic heparan sulfate mimic named RGTA 11 (for ReGeneraTing Agent), or combinations of these products. RGTA 11 belongs to a new family of drugs, which have been previously described as stabilizer and protector of heparin binding growth factors (HBGF), and to act in vivo as to stimulate wounded tissue repair. As endothelialization of prosthesis can be obtained in vivo after EC seeding and/or by transanastomotic, as well as by transprosthetic EC migrations, we have designed in vitro models to study the growth of EC seeded on PET, the EC colonization of an acellular area on PET, and the migration of EC from a collagen gel through the prosthesis. The combinations of either RGTA11 or heparin with FGF2 enhanced after a week by 5-fold the growth of seeded EC compared to RGTA or heparin alone and by 3-fold compared to FGF2 alone (p < 0.05). More than 80% of the colonization of an acellular area was achieved within 6 days when FGF2 was combined with RGTA11 or heparin. In contrast, colonization was only of 20% promoted in presence of FGF2 alone and not promoted in the presence of RGTA or heparin alone (p < 0.05). In addition, transprosthetic migration of EC and endothelialization of the luminal side were observed only when gel contained RGTA11 or heparin in combination with FGF2. The present work did strongly indicate that RGTA11 could be used in vivo as to improve endothelialization and should be the focus of continued investigation.

Adult↗
PubMed2001

Human microglial cells express a functional IL-12 receptor and produce IL-12 following IL-12 stimulation.

Microglial cells (MC) are IL-12 producers in the central nervous system. Here, we found that IL-12 receptor subunits beta1 and beta2 were both constitutively expressed, and up-regulated by IFN-gamma, in human primary MC. IL-12p70, after binding to its receptor, is internalized into vesicles that qualify as early endosomes as indicated by intracellular colocalization with transferrin. IL-12 induced tyrosine phosphorylation and nuclear translocation of STAT4. IL-12 signaling in human MC also involved members of the NFkappaB family. IL-12p70 and, more effectively, the combination of IL-12p70 and IFN-gamma, induced IL-12p40 mRNA expression and bioactive IL-12p70 production. Human MC, thus, express a functional IL-12 receptor and produce bioactive IL-12 following IL-12 stimulation.

Cell Nucleus↗
PubMed2001

[Specifics in pediatric arterial cerebral infarctions].

Despite the number of potential causes, most children with ischemic cerebrovascular disease are classified into a few major categories: 1) cardioembolic stroke; 2) moyamoya syndrome; 3) complication(s) connected with systemic disease, with a known risk of a cerebrovascular event; 4) cervicocephalic arterial dissection; and 5) transient cerebral arteriopathy of undefined origin (probable arteritis). The etiological diagnosis is rapidly established by complementary investigations based on the initial clinical and imaging findings: cardiac exploration, magnetic resonance imaging and angiography or echo-doppler of the cervical arteries if cervical dissection is suspected; intra-arterial catheter cerebral angiography and analysis of the cerebrospinal fluid to investigate an intracranial arteriopathy. The outcome and treatment depend on the type of stroke, on its accurate identification, and on prediction regarding the risk of recurrence. Although there is a constitutional predisposition to cerebrovascular accidents, environmental triggers such as trauma, infectious disease and cardiac surgery also play a major role.

Age Factors↗
PubMed2001

Parental origin of de novo MECP2 mutations in Rett syndrome.

Rett syndrome (RTT) is a neurodevelopmental disorder occurring almost exclusively in females as sporadic cases. Recently, DNA mutations in the MECP2 gene have been detected in approximately 70% of patients with RTT. To explain the sex-limited expression of RTT, it has been suggested that de novo X-linked mutations occur exclusively in male germ cells resulting therefore only in affected daughters. To test this hypothesis, we have analysed 19 families with RTT syndrome due to MECP2 molecular defects. In seven informative families we have found by DHPLC a nucleotide variant which could be used to differentiate between the maternal and the paternal allele. In each subject investigated from these families, we have amplified specifically each allele and sequenced allele-specific PCR products to identify the allele bearing the mutation as well as the parental origin of each X chromosome. This approach allowed us to determine the parental origin of de novo mutations in all informative families. In five cases, the de novo MECP2 mutations have a paternal origin and in the two other cases a maternal origin. In all transitions at CpG, the de novo mutation observed was of paternal origin. The high frequency of male germ-line transmission of the mutation (71% of RTT informative cases) is consistent with a predominant occurrence of the disease in females.

Base Sequence↗
PubMed2001

Mitochondrial respiratory chain deficiency revealed by hypothermia.

We observed a 17-month-old girl with profound and initially isolated episodes of hypothermia. Thereafter, she developed growth delay, repetitive corneal and bone lesions. Persistent hyperlactataemia in plasma and in CSF prompted us to investigate respiratory chain enzymes. A deficit in respiratory chain complexes III and IV was demonstrated in isolated skeletal muscle mitochondria, circulating lymphocytes and fibroblasts by spectrophotometric and polarographic studies. Moreover, UCP3 mRNA expression in muscle was decreased.

Biopsy↗
PubMed2001

Segregation of a totally skewed pattern of X chromosome inactivation in four familial cases of Rett syndrome without MECP2 mutation: implications for the disease.

BACKGROUND: Rett syndrome is a neurodevelopmental disorder affecting only girls; 99.5% of Rett syndrome cases are sporadic, although several familial cases have been reported. Mutations in the MECP2 gene were identified in approximately 70-80% of sporadic Rett syndrome cases. METHODS: We have screened the MECP2 gene coding region for mutations in five familial cases of Rett syndrome and studied the patterns of X chromosome inactivation (XCI) in each girl. RESULTS: We found a mutation in MECP2 in only one family. In the four families without mutation in MECP2, we found that (1) all mothers exhibit a totally skewed pattern of XCI; (2) six out of eight affected girls also have a totally skewed pattern of XCI; and (3) it is the paternally inherited X chromosome which is active in the patients with a skewed pattern of XCI. Given that the skewing of XCI is inherited in our families, we genotyped the whole X chromosome using 32 polymorphic markers and we show that a locus potentially responsible for the skewed XCI in these families could be located on the short arm of the X chromosome. CONCLUSION: These data led us to propose a model for familial Rett syndrome transmission in which two traits are inherited, an X linked locus abnormally escaping X chromosome inactivation and the presence of a skewed XCI in carrier women.

Alleles↗