Biomedical subjects
Publications and source records attributed to Stephen M Maricich.
Advances in understanding basic developmental and physiological processes often have direct relevance to human disease. They provide insights into pathogenic mechanisms and reveal new pathways that can be exploited in diagnosis and the development of therapeutics.
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OBJECTIVES: Our objectives were to (1) describe the clinical characteristics of and viruses isolated from patients who presented with neurologic symptoms associated with influenza A infection and were hospitalized at Texas Children's Hospital during October and November 2003 and (2) to raise awareness of the neurologic complications of influenza among US children. METHODS: We reviewed the medical and laboratory records of all children who were hospitalized with neurologic symptoms and who also had evidence of influenza virus infection by rapid antigen testing or viral isolation. RESULTS: Eight children aged 5 months to 9 years with neurologic complications associated with influenza A were identified. None of the children had received the influenza vaccine. Four presented with seizures, 3 with mental status changes, and 1 with mutism. All but 1 of the patients had influenza A viral antigen detected in nasal wash samples. Influenza A virus was isolated in culture from nasal wash specimens obtained from 6 of the patients; influenza A virus was also isolated from the cerebrospinal fluid of 1 of these patients. None of the patients had serum metabolic abnormalities or other cerebrospinal fluid abnormalities. Three of the patients had brain imaging abnormalities. Five of the patients were treated with antivirals. All 8 of the patients survived, 6 with complete recovery and 2 with sequelae (1 mild and 1 severe). CONCLUSIONS: Neurologic symptoms and sequelae were associated with influenza A virus infection in children during the 2003-2004 influenza season in Houston, Texas. Influenza should be considered in the differential diagnosis in patients with seizures and mental status changes, especially if they present with respiratory symptoms or during an influenza outbreak.
The mouse homeodomain protein, Engrailed-1, is generally viewed as an essential player in the early establishment and maintenance of the midbrain/hindbrain region that gives rise to the cerebellum and midbrain. In keeping with this, engineered null mutations at this locus have been reported to lead to perinatal lethality accompanied by near-total absence of cerebellar and caudal midbrain structures. We report here that these cerebellar phenotypes are nearly completely suppressed on a C57BL/6J genetic background. All cell types are present and arranged properly in both the cortex and the deep nuclei, and cell counts reveal no significant absence of cerebellar Purkinje cells. Folial patterns are nearly normal, although an apparent fusion of lobules IV and V is consistently noted. Significantly, no change in the Engrailed-2 mutant phenotype occurs after a similar background switch, and whole-mount in situ hybridization reveals identical En2 expression patterns in wild-type C57BL/6J and 129/Sv mice. One likely mechanism for the En1-/- phenotype suppression is a temporal and/or spatial change in the pattern of Engrailed-2 expression apparent only in the absence of Engrailed-1. In support of this, C57BL/6-En1-/- embryos that are also En2+/- lack a cerebellum and caudal midbrain: a phenotype identical to 129/Sv-En1-/- mice.