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1.
Arch Pediatr ; 19(4): 396-403, 2012 Apr.
Artigo em Francês | MEDLINE | ID: mdl-22377245

RESUMO

UNLABELLED: Few data are available on the impact of a tuberculosis exposure on newborns in a maternity ward. OBJECTIVES: To describe the screening and clinical course of infants exposed during the neonatal period to a caregiver with bacillary tuberculosis. PATIENTS AND METHODS: Infants exposed during the postnatal period in a maternity unit in Paris, from March to August 2005, to a caregiver with bacillary tuberculosis were included in a standardized screening protocol. The screening performed at baseline (M0) and at 3 months (M3) included a clinical evaluation, a tuberculin skin test (TST), and a chest X-ray. A preventive treatment for tuberculosis with isoniazid and rifampicin for 3 months was systematically proposed. RESULTS: At M0, 182 of the 217 infants (84%) with significant exposure were evaluated. Data were available for 172 infants. The median age at M0 was 4.9 months (IQR=3.8-6.2). At M0, 4 of 172 infants (2.3%) had latent TB infection. Between M0 and M3, 19 infants (11%) were lost to follow-up and 1 on 153 developed a latent TB infection. No cases of tuberculosis disease were diagnosed. The treatment was administered properly in 83% of cases and side effects were observed in 11% of infants without any serious adverse event. Four infants received no treatment and 11 stopped their treatment prematurely. CONCLUSION: In the absence of neonatal massive exposure, although low (2.9%), the risk of latent TB infection requires close monitoring of the infants exposed. However, in the context of a mild exposure in the maternity unit, surveillance without systematic initiation of TB preventive treatment could be discussed.


Assuntos
Infecção Hospitalar/transmissão , Transmissão de Doença Infecciosa do Profissional para o Paciente , Tuberculose Latente/transmissão , Programas de Rastreamento , Tuberculose Pulmonar/transmissão , Antituberculosos/uso terapêutico , Estudos de Coortes , Infecção Hospitalar/diagnóstico , Infecção Hospitalar/prevenção & controle , Feminino , Seguimentos , Humanos , Lactente , Isoniazida/uso terapêutico , Tuberculose Latente/diagnóstico , Tuberculose Latente/prevenção & controle , Masculino , Radiografia Pulmonar de Massa , Unidade Hospitalar de Ginecologia e Obstetrícia , Paris , Rifampina/uso terapêutico , Fatores de Risco , Teste Tuberculínico , Tuberculose Pulmonar/diagnóstico , Tuberculose Pulmonar/prevenção & controle
2.
Arch Pediatr ; 18(7): 772-7, 2011 Jul.
Artigo em Francês | MEDLINE | ID: mdl-21571511

RESUMO

A 15-month-old boy treated with amoxicillin and clavulanic acid therapy for 8 days was admitted for persistent gastroenteritis and fever. He received ceftriaxone for pneumonia modified on day 4 for cefotaxime and josamycin due to extension of alveolar lesions. On day 7, persistent fever and worsened respiratory distress led to addition of rifampicin. The child was then admitted to an intensive care unit. A hemophagocytic syndrome was suspected based on clinical signs and laboratory findings and confirmed by cytological examination of bone marrow. Adenovirus type 7 was identified by polymerase chain reaction and culture of bronchoalveolar fluid. Prognosis was good within 3 weeks. B and T immunologic evaluations were normal 5 months after the infection. This case of severe adenovirus pneumonia was associated with hemophagocytic syndrome in a child without identified primary immunodeficiency. Adenovirus type 3 and 7 are most frequently responsible for severe or fatal respiratory infections.


Assuntos
Infecções por Adenovirus Humanos/diagnóstico , Adenovírus Humanos/classificação , Pneumonia Viral/diagnóstico , Infecções por Adenovirus Humanos/tratamento farmacológico , Infecções por Adenovirus Humanos/imunologia , Adenovírus Humanos/imunologia , Adenovírus Humanos/isolamento & purificação , Antibacterianos/uso terapêutico , Quimioterapia Combinada , Humanos , Imunocompetência/imunologia , Lactente , Linfo-Histiocitose Hemofagocítica/diagnóstico , Linfo-Histiocitose Hemofagocítica/tratamento farmacológico , Linfo-Histiocitose Hemofagocítica/imunologia , Ativação de Macrófagos/imunologia , Masculino , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/imunologia , Reação em Cadeia da Polimerase , Prognóstico
3.
Cell Death Differ ; 15(10): 1542-52, 2008 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-18551134

RESUMO

In mammals, programmed cell death (PCD) is a central event during brain development. Trophic factors have been shown to prevent PCD in postmitotic neurons. Similarly, cytokines have neurotrophic effects involving regulation of neuronal survival. Nevertheless, neuronal PCD is only partially understood and host determinants are incompletely defined. The present study provides evidence that the cytokine interleukin-9 (IL-9) and its receptor specifically control PCD of neurons in the murine newborn neocortex. IL-9 antiapoptotic action appeared to be time-restricted to early postnatal stages as both ligand and receptor transcripts were mostly expressed in neocortex between postnatal days 0 and 10. This period corresponds to the physiological peak of apoptosis for postmitotic neurons in mouse neocortex. In vivo studies showed that IL-9/IL-9 receptor pathway inhibits apoptosis in the newborn neocortex. Furthermore, in vitro studies demonstrated that IL-9 and its receptor are mainly expressed in neurons. IL-9 effects were mediated by the activation of the JAK/STAT (janus kinase/signal transducer and activator of transcription) pathway, whereas nuclear factor-kappaB (NF-kappaB) or Erk pathways were not involved in mediating IL-9-induced inhibition of cell death. Finally, IL-9 reduced the expression of the mitochondrial pro-apoptotic factor Bax whereas Bcl-2 level was not significantly affected. Together, these data suggest that IL-9/IL-9 receptor signaling pathway represents a novel endogenous antiapoptotic mechanism for cortical neurons by controlling JAK/STAT and Bax levels.


Assuntos
Apoptose/fisiologia , Córtex Cerebral/citologia , Interleucina-9/metabolismo , Neurônios/fisiologia , Receptores de Interleucina-9/metabolismo , Transdução de Sinais/fisiologia , Animais , Animais Recém-Nascidos , Caspase 3/metabolismo , Células Cultivadas , Humanos , Janus Quinases/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fatores de Transcrição STAT/metabolismo , Proteína X Associada a bcl-2/metabolismo
4.
Neuroscience ; 141(2): 875-888, 2006 Aug 25.
Artigo em Inglês | MEDLINE | ID: mdl-16725276

RESUMO

Freezing injury to the developing cortical plate results in a neocortical malformation resembling four-layered microgyria. Previous work has demonstrated that following freezing injury to the somatosensory cortex, males (but not females) have more small and fewer large cells in the medial geniculate nucleus. In the first experiment, we examined the effects of induced microgyria to the somatosensory cortex on neuronal numbers, neuronal size, and nuclear volume of three sensory nuclei: ventrobasal complex, dorsal lateral geniculate nucleus, and medial geniculate nucleus. We found that there was a decrease in neuronal number and nuclear volume in ventrobasal complex of microgyric rats when compared with shams, whereas there were no differences in these variables in the dorsal lateral geniculate nucleus or medial geniculate nucleus. We also found that there were more small and fewer large neurons in both ventrobasal complex and medial geniculate nucleus. In experiment 2, we attempted to determine the role of cell death in the thalamus on these histometric measures. We found that cell death peaked within 24 h of the freezing injury and was concentrated mostly in ventrobasal complex. In addition, there was evidence of greater cell death in males at this age. Taken together, these results support the notion that males are more severely affected by early injury to the cerebral cortex than females.


Assuntos
Lesões Encefálicas/patologia , Tamanho Celular , Neocórtex/patologia , Neurônios/patologia , Tálamo/patologia , Fatores Etários , Análise de Variância , Animais , Animais Recém-Nascidos , Mapeamento Encefálico , Contagem de Células/métodos , Morte Celular/fisiologia , Feminino , Fluoresceínas , Congelamento , Marcação In Situ das Extremidades Cortadas/métodos , Masculino , Neocórtex/fisiopatologia , Compostos Orgânicos , Gravidez , Distribuição Aleatória , Ratos , Fatores Sexuais , Fatores de Tempo
5.
Acta Paediatr ; 94(2): 185-90, 2005 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-15981752

RESUMO

AIM: The pathophysiology of perinatal brain lesions is probably complex and multifactorial. The development and characterization of distinct yet complementary animal models should help to unravel the cellular and molecular mechanisms underlying perinatal brain lesions. This paper reviews experimental data obtained in animal models of neonatal excitotoxic brain lesions that closely mimic some of the lesions found in human cerebral palsy. CONCLUSION: Available data point to a key role for brain macrophages and oligodendrocytes in neonatal rodent excitotoxic brain lesions and underline the impact of cytokines on these lesions.


Assuntos
Paralisia Cerebral/fisiopatologia , Animais , Animais Recém-Nascidos , Paralisia Cerebral/imunologia , Citocinas/metabolismo , Modelos Animais de Doenças , Ácido Glutâmico/metabolismo , Humanos , Recém-Nascido , Inflamação , Interleucina-9/metabolismo , Leucomalácia Periventricular/imunologia , Leucomalácia Periventricular/fisiopatologia , Camundongos , Microglia/imunologia , Modelos Neurológicos
6.
Neuroscience ; 125(1): 163-70, 2004.
Artigo em Inglês | MEDLINE | ID: mdl-15051155

RESUMO

Methylphenidate (MPH), a dopamine reuptake inhibitor, is used increasingly to treat attention deficit and hyperactivity disorders in children. Given that dopaminergic mechanisms, contribute to the structural and functional maturation of brain circuitry, consideration of the potential influence of MPH in disrupting such processes seems warranted. Following a similar logic regarding the relevance of glutamate neurotransmission in mediating aspects of brain maturation, we and others have previously utilized in vivo and in vitro studies of the developing rodent brain to establish that MK-801, an N-methyl-d-aspartate (NMDA) receptor antagonist has both neuroprotective and pro-apoptotic actions. In this study we used a neonatal murine model of excitotoxin-induced cortical injury to compare such actions between MPH and MK-801, and found that MPH shared some biological properties with MK-801. Specifically, both drugs were neuroprotective against excitotoxic challenge resulting in neonatal brain lesions and in vitro neuronal death, but both drugs also exacerbated programmed neural cell death. However, this profile of action was not shared by the dopamine reuptake blocker GBR-12783, a molecule which like MPH binds to and blocks the dopamine transporter, but which is structurally dissimilar to MPH, suggesting that inhibition of dopamine reuptake alone cannot explain the results from our MPH studies. The implications of our findings are that when studied in our developmental mouse model both drugs demonstrate similar capacities to be either neuroprotective or pro-apoptotic, depending on the specific biologic setting in which they act. Additional studies to identify some potential positive as well as negative consequences of exposure to these drugs during brain development in clinical settings are warranted.


Assuntos
Encéfalo/efeitos dos fármacos , Maleato de Dizocilpina/farmacologia , Metilfenidato/farmacologia , Neurônios/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Animais , Animais Recém-Nascidos , Apoptose/efeitos dos fármacos , Encéfalo/embriologia , Lesões Encefálicas/induzido quimicamente , Inibidores da Captação de Dopamina/farmacologia , Ácido Ibotênico/toxicidade , Marcação In Situ das Extremidades Cortadas , Camundongos , Neurônios/patologia , Piperazinas/farmacologia , Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
7.
Brain Pathol ; 12(3): 320-8, 2002 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-12146800

RESUMO

Shaken baby syndrome, a rotational acceleration injury, is most common between 3 and 6 months of age and causes death in about 10 to 40% of cases and permanent neurological abnormalities in survivors. We developed a mouse model of shaken baby syndrome to investigate the pathophysiological mechanisms underlying the brain damage. Eight-day-old mouse pups were shaken for 15 seconds on a rotating shaker. Animals were sacrificed at different ages after shaking and brains were processed for histology. In 31-day-old pups, mortality was 27%, and 75% of survivors had focal brain lesions consisting of hemorrhagic or cystic lesions of the periventricular white matter, corpus callosum, and brainstem and cerebellar white matter. Hemorrhagic lesions were evident from postnatal day 13, and cysts developed gradually between days 15 and 31. All shaken animals, with or without focal lesions, had thinning of the hemispheric white matter, which was significant on day 31 but not earlier. Fragmented DNA labeling revealed a significant increase in cell death in the periventricular white matter, on days 9 and 13. White matter damage was reduced by pre-treatment with the NMDA receptor antagonist MK-801. This study showed that shaking immature mice produced white matter injury mimicking several aspects of human shaken baby syndrome and provided evidence that excess release of glutamate plays a role in the pathophysiology of the lesions.


Assuntos
Encéfalo/patologia , Ácido Glutâmico/metabolismo , Leucomalácia Periventricular/patologia , Síndrome do Bebê Sacudido/patologia , Animais , Animais Recém-Nascidos , Tronco Encefálico/lesões , Tronco Encefálico/patologia , Morte Celular , Cerebelo/lesões , Cerebelo/patologia , Corpo Caloso/lesões , Corpo Caloso/patologia , Modelos Animais de Doenças , Maleato de Dizocilpina/farmacologia , Antagonistas de Aminoácidos Excitatórios/farmacologia , Feminino , Humanos , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Recém-Nascido , Leucomalácia Periventricular/etiologia , Leucomalácia Periventricular/metabolismo , Masculino , Camundongos , Fármacos Neuroprotetores/farmacologia , Receptores de N-Metil-D-Aspartato/antagonistas & inibidores , Receptores de N-Metil-D-Aspartato/metabolismo , Síndrome do Bebê Sacudido/complicações , Síndrome do Bebê Sacudido/metabolismo , Fatores de Tempo
8.
Eur J Pharmacol ; 424(3): 189-94, 2001 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-11672561

RESUMO

Antioxidant 8-alkylamino-1,4-benzoxazines, (R,S)-(3-tert-butyl-8-phenylethylamino-3,4-dihydro-2H-1,4-benzoxazin-5-yl) (phenyl) methanone (S 24429) and (R,S)-(3-cyclopentyl-8-benzylamino-3,4-dihydro-2H-1,4-benzoxazin-5-yl) (phenyl) methanone (S 24718), were prepared according to a two-step one-pot electrochemical procedure. These compounds had been selected from a previous study of structure/activity. Both compounds (1-100 microM) prevented the fall in ATP levels caused by 24 h of hypoxia in astrocytes. Both compounds (1 and 10 mg/kg i.p.) were powerful neuroprotective agents in protecting against the lesions induced by 15 microg S-bromo-willardiine injected into the cortex or white matter of 5-day old mice pups. In contrast, exifone, an antioxidant compound, was inactive at these doses. S 24429 and S 24718 appear to be novel neuroprotective agents, which are effective in a model of brain damage mimicking the lesions underlying cerebral palsy.


Assuntos
Alanina/análogos & derivados , Antioxidantes/farmacologia , Fármacos Neuroprotetores/farmacologia , Oxazinas/farmacologia , Trifosfato de Adenosina/metabolismo , Alanina/administração & dosagem , Animais , Animais Recém-Nascidos , Astrócitos/citologia , Astrócitos/efeitos dos fármacos , Astrócitos/metabolismo , Benzofenonas/farmacologia , Benzoxazinas , Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Relação Dose-Resposta a Droga , Camundongos , Oxigênio/farmacologia , Ratos
9.
Semin Neonatol ; 6(2): 185-94, 2001 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-11483023

RESUMO

Foetal and neonatal brain is under the influence of environmental factors from maternal and extra-maternal origin. Based on the available data, these environmental factors can be classified into three arbitrary groups: (i) factors and maternal status with a demonstrated deleterious effect on the foetal brain (i.e. ethanol, cocaine, some drugs including anticonvulsants, some viral infections, maternal diabetes, untreated maternal phenylketonuria); (ii) factors highly suspected to interfere with foetal brain development (i.e. lead and other heavy metals, some drugs like benzodiazepines, nicotine); (iii) factors which have been shown to be safe for the developing brain in the available studies (i.e. low to moderate doses of caffeine, methadone). However, most of these studies do not address the potential risk of environmental factors on minimal to moderate cognitive and behavioural disturbances. Finally, the impact of the neonatal environment on brain development in very pre-term infants is probably underestimated.


Assuntos
Lesões Encefálicas/etiologia , Encéfalo/embriologia , Poluentes Ambientais/efeitos adversos , Doenças do Recém-Nascido/etiologia , Recém-Nascido Prematuro , Complicações na Gravidez , Transtornos Relacionados ao Uso de Substâncias/complicações , Cafeína/efeitos adversos , Cocaína/efeitos adversos , Etanol/efeitos adversos , Feminino , Humanos , Recém-Nascido , Chumbo/efeitos adversos , Compostos de Metilmercúrio/efeitos adversos , Entorpecentes/efeitos adversos , Gravidez , Fumar/efeitos adversos
10.
Pediatr Res ; 50(2): 222-30, 2001 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-11477207

RESUMO

Elevated mean IL-9 serum levels have been observed in human neonates who will later develop cerebral palsy. In earlier studies, using a newborn mouse model of excitotoxic lesions mimicking those described in human cerebral palsy, we found that IL-9 pretreatment exacerbated brain damage produced by intracerebral injections of the glutamatergic analog ibotenate. Among its different cell targets, the Th2 cytokine IL-9 is a mast cell growth and differentiation factor that can cause mast cells to release various substances including histamine. In the present study, we sought to determine whether the deleterious effects of IL-9 in our mouse model were mediated by mast cells through histamine release. All mouse pups were pretreated with intraperitoneal injections of IL-9 or saline between postnatal days (P) P1 and P5. Immunohistochemistry for murine mast cell protease-1 performed on P5 showed an increased density of labeled cells in the neopallium of IL-9-treated Swiss pups as compared with controls. Western blot analysis confirmed the increased murine mast cell protease-1 brain content of IL-9-treated Swiss mice. IL-9 pretreatment had no significant effect on ibotenate-induced excitotoxic brain lesions in mast cell-deficient P5 pups (WBB6F1/J kit(W/W-v)), whereas IL-9 exacerbated these lesions in the control littermates with normal mast cell populations. Finally, cromoglycate or antihistamine drugs significantly reduced ibotenate-induced brain lesions in IL-9-treated Swiss pups. Taken together, these data suggest that recruitment of cerebral mast cells with histamine release may contribute to the exacerbation of neonatal excitotoxic brain lesions produced by IL-9. Neuroprotective strategies targeting mast cells may be useful in some neonates at risk for cerebral palsy.


Assuntos
Encéfalo/efeitos dos fármacos , Encéfalo/patologia , Antagonistas dos Receptores Histamínicos H1/farmacologia , Interleucina-9/farmacologia , Mastócitos/efeitos dos fármacos , Mastócitos/fisiologia , Fármacos Neuroprotetores/farmacologia , Animais , Animais Recém-Nascidos , Comportamento Animal/efeitos dos fármacos , Encéfalo/crescimento & desenvolvimento , Encéfalo/fisiopatologia , Paralisia Cerebral/etiologia , Cromolina Sódica/farmacologia , Modelos Animais de Doenças , Agonistas de Aminoácidos Excitatórios/toxicidade , Feminino , Humanos , Ácido Ibotênico/toxicidade , Recém-Nascido , Inflamação/etiologia , Inflamação/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Mutantes
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