Ontogeny of arousal.

Ontogeny of arousal data constitute a vital supplement to the sparse literature on spontaneous neuronal activity. These data demonstrate that measurable infant spontaneous arousals (SAs) with an inherent oscillatory entrainment occur six times more in active sleep than in quiet sleep of the same duration and are identifiable as a human neurobiologic function. These SAs are not significantly associated with race or ethnicity, gender, total hours spent sleeping, percent time spent in active or quiet sleep, preterm status, history of a life-threatening event, having had a sibling who died of sudden infant death syndrome (SIDS), or having had a mother who smoked during this pregnancy. As measurable neurophysiologic events, SAs establish parameters for research at molecular and molar levels focusing on several critical areas: (1) the neuronal control of SA related to neurotransmitters, (2) as a significant antecedent factor in clinical cardiorespiratory events occurring in infants at high epidemiologic risk for SIDS; (3) as a regulatory biologic factor underlying temperament and executive cognitive functioning, and (4) morbidity and mortality effects possibly related to therapeutic interventions that alter SA levels.     

表皮生长因子对TPN大鼠肠粘膜机械屏障的影响

本文旨在探讨表皮生长因子（ＥＧＦ）对ＴＰＮ大鼠小肠粘膜机械屏障的保护作用。将４８只ＳＤ大鼠随机分为正常对照组、ＴＰＮ组以及ＴＰＮ－ＥＧＦ组。结果显示ＴＰＮ组大鼠小肠绒毛面积、高度、隐窝深度、隐窝细胞数及有丝分裂指数均较对照组明显降低（Ｐ〈０．０１）；ＴＰＮ－ＥＧＦ组与对照组比较无显著差异（Ｐ〉０．０５）。提示外源性补充ＥＧＦ能促进ＴＰＮ大鼠隐窝细胞增殖，恢复隐窝细胞生成率，从而达到保护肠粘膜机械屏     

A genetic selection for Caenorhabditis elegans synaptic transmission mutants.

We have isolated 165 Caenorhabditis elegans mutants, representing 21 genes, that are resistant to inhibitors of cholinesterase (Ric mutants). Since mutations in 20 of the genes appear not to affect acetylcholine reception, we suggest that reduced acetylcholine release contributes to the Ric phenotype of most Ric mutants. Mutations in 15 of the genes lead to defects in a gamma-aminobutyric acid-dependent behavior; these genes are likely to encode proteins with general, rather than cholinergic-specific, roles in synaptic transmission. Ten of the genes have been cloned. Seven encode homologs of proteins that function in the synaptic vesicle cycle: two encode cholinergic-specific proteins, while five encode general presynaptic proteins. Two other Ric genes encode homologs of G-protein signaling molecules. Our assessment of synaptic function in Ric mutants, combined with the homologies of some Ric mutants to presynaptic proteins, suggests that the analysis of Ric genes will continue to yield insights into the regulation and functioning of synapses.     

A comparison of histological and immunohistochemical methods for quantifying the pathological lesions of Pick's disease

Counts of Pick bodies (PB), Pick cells (PC), senile plaques (SP) and neurofibrillary tangles (NFT) were made in the frontal and temporal cortex from patients with Pick's disease (PD). Lesions were stained histologically with hematoxylin and eosin (HE) and the Bielschowsky silver impregnation method and labeled immunohistochemically with antibodies raised to ubiquitin and tau. The greatest numbers of PB were revealed by immunohistochemistry. Counts of PB revealed by ubiquitin and tau were highly positively correlated which suggested that the two antibodies recognized virtually identical populations of PB. The greatest numbers of PC were revealed by HE followed by the anti-ubiquitin antibody. However, the correlation between counts was poor, suggesting that HE and ubiquitin revealed different populations of PC. The greatest numbers of SP and NFT were revealed by the Bielschowsky method indicating the presence of Alzheimer-type lesions not revealed by the immunohistochemistry. In addition, more NFT were revealed by the anti-ubiquitin compared with the anti-tau antibody. The data suggested that in PD: (i) the anti-ubiquitin and anti-tau antibodies were equally effective at labeling PB; (ii) both HE and anti-ubiquitin should be used to quantitate PC; and (iii) the Bielschowsky method should be used to quantitate SP and NFT.     

Retained intracranial metallic foreign bodies. Report of two cases.

The authors discuss two examples of extensive migration of retained metallic foreign bodies. The potential for further neurological injury from migration, formation of neurotoxic breakdown products, and the danger of infection are factors to be assessed when considering the removal of retained intracranial metallic foreign bodies.