Using the 2003 National Survey of Children’s Health (NSCH) sponsored by the federal Maternal and Child Health Bureau, we calculated prevalence estimates of eczema nationally and for each state among a nationally representative sample of 102,353 children 17 years of age and under. Our objective was to determine the national prevalence of eczema/atopic dermatitis in the United States pediatric population and to further examine geographic and demographic associations previously reported in other countries. Overall, 10.7% of children were reported to have a diagnosis of eczema in the last 12 months. Prevalence ranged from 8.7% to 18.1% between states and districts, with the highest prevalence reported in many of the East Coast states, as well as Nevada, Utah, and Idaho. After adjusting for confounders, metropolitan living was found to be a significant factor in predicting a higher disease prevalence with an OR of 1.67 (95% confidence interval of 1.19-2.35, p=0.008). Black race (OR 1.70, p=0.005) and education level in the household greater than high school (OR 1.61, p=0.004) were also significantly associated with a higher prevalence of eczema. The wide range of prevalence suggests social or environmental factors may influence disease expression.

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Summary: Neuronal injury may be dependent upon the gen eration of the free radical nitric oxide (NO) and the subsequent induction of programed cell death (PCD). Although the nature of this injury may be both preventable and reversible, the un derlying mechanisms that mediate PCD are not well under stood. Using the agent nicotinamide as an investigative tool in primary rat hippocampal neurons, the authors examined the ability to modulate two independent components of PCD, namely the degradation of genomic DNA and the early expo sure of membrane phosphatidylserine (PS) residues. Neuronal injury was determined through trypan blue dye exclusion, DNA fragmentation, extemalization of membrane PS residues, cys teine protease activation, and the measurement of intracellular pH (pHJ Exposure to the NO donors SIN-I and NOC-9 (300 f,LmoIlL) alone rapidly increased genomic DNA fragmentation from 20 ± 4% to 71 ± 5% and membrane PS exposure from 14 ± 3% to 76 ± 9% over a 24-hour period. Administration of a Neuronal injury can be initiated by several differ ent stimuli that ultimately lead to either apoptosis or necrosis. Neuronal apoptosis or programed cell death (PCD) is an active, controlled, and deliberate process of cell destruction that is present during cell development and injury (Kerr et aI., 1972). In contrast, neurons that undergo necrosis suffer diffuse organelle damage with

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Corticotropin releasing hormone (CRH) and its family of related peptides are involved in regulating physiologic responses to multiple stressors, including stroke. Although CRH has been implicated in the exacerbation of injury after stroke, the mechanism remains unclear. After ischemia, both excitotoxic damage and inflammation contribute to the pathology of stroke. CRH is known to potentiate excitotoxic damage in the brain and has been shown to modulate inflammatory responses in the periphery. Here the present authors examine the relative contribution of the two known CRH receptors, CRH-R1 and CRH-R2, to ischemic injury using CRH receptor knockout mice. These results implicate CRH-R1 as the primary mediator of ischemic injury in this mouse model of stroke. In addition, the authors examine a potential role for CRH in inflammatory injury after stroke by identifying functional CRH receptors on astrocytes and microglia, which are cells that are known to be involved in brain inflammation. By single cell PCR, the authors show that microglia and astrocytes express mRNA for both CRH-R1 and CRH-R2. However, CRH-R1 is the primary mediator of cAMP accumulation in response to CRH peptides in these cells. The authors suggest that astrocytes and microglia are cellular targets of CRH, which could serve as a link between CRH and inflammatory responses in ischemic injury via CRH-R1.