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BACKGROUND: Evidence suggests a rise in childhood disability rates across the United States with males and those with lower socioeconomic status bearing greater burden. We investigated childhood disability rates in the Mississippi Delta (MDR) and Appalachian regions (AR) in comparison to other parts of the country. METHODS: Using data from the US Census Bureau, we calculated childhood disability rates by type and sex at national, regional, and subregional levels. We used risk ratios (RR) to compare childhood disability rates by sex, type, and region. We generated choropleth maps to represent the geographic distribution of disability. RESULTS: Childhood disability was more prevalent, at the national level, among boys (6.64%) than girls (4.08%). Children in the MDR (boys = 8.60%; girls = 5.08%) and AR (boys = 7.81%; girls = 4.83%) had greater risk of disability than those elsewhere in the country (boys = 6.47%; girls = 3.98%), with rates generally higher in rural compared to urban areas in said regions. CONCLUSIONS: Childhood disability affects rural areas of the country more extensively, with the MDR and AR affected to an even greater extent. School‐based health centers, in particular, which are disproportionately located in urban areas, could benefit disabled children living in the MDR and AR. [ABSTRACT FROM AUTHOR]

Normal human prostate (NHP) epithelial cells undergo senescence in vitro and in vivo but the potential role of senescent NHP cells in prostate tumorigenesis remain unclear. Here we show that senescent NHP cells enhance the in vivo tumorigenicity of low-tumorigenic LNCaP prostate cancer and low/non-tumorigenic subset of cells (called L cells) isolated from multiple bulk-cultured prostate (and other) cancer cell lines. Subsequent studies suggest cell-cell fusion as a potential mechanism for senescent NHP cell-enhanced tumor development. Using fluorescently tagged tumor cells and/or NHP cells, we find that NHP cells, like fibroblasts, can undergo fusion with unfractionated tumor cells or the L cells. Using 293T-L cells as the model cell system, we verify NHP and 293T-L cell fusion by using differential RT-PCR, karyotyping, and gene expression analyses. Further experiments demonstrate that senescent NHP cells that have lost progenitor markers, accumulated p16INK4a (p16) protein expression, and acquired the AR mRNA expression, appear to be the preferential fusion targets. Strikingly, the tumorigenicity of the NHP/293T-L hybrid cells was inhibited by exogenous p16 as well as hTERT. Chromosomal analyses revealed that hTERT probably inhibited the in vivo tumorigenicity by maintaining genomic stability. These results suggest that senescent NHP cells, like senescent fibroblasts, may promote tumor development and that one of the mechanisms underlying the senescent NHP cell-enhanced tumorigenicity could be through cell fusion. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Recent experimental research suggests an association between negative affect and potentiation of the human startle reflex, as well as enhancement of this effect among fearful compared to low fear subjects. In the present study, 32 undergraduates were selected for high or low total Fear Survey Schedule scores. Acoustic startle probes were presented while subjects received warned presentations of aversive and neutral photographic slides. High fear but not low fear subjects showed potentiated short-latency cardiac acceleration and blink magnitude, and reduced blink latency, during aversive compared to neutral slides. These results support the hypothesis that affective modulation of startle is enhanced among high fear compared to low fear subjects. Considered in the context of prior findings, the results suggest that this individual difference effect generalizes across psychophysiological components of the startle reflex and diverse procedures for manipulating affect. [ABSTRACT FROM AUTHOR]