Bulbar signs in normal population.

BACKGROUND AND OBJECTIVES: There is lack of published data on bulbar signs among the healthy population. This study aims to determine the range of normality of bulbar signs particularly among the elderly. METHODS: Systemic examination of bulbar signs was carried out according to a predetermined protocol on a cohort of young and elderly healthy subjects. RESULTS: A total of 206 subjects were recruited in the study, 104 young adults with mean age of 20 years, and 102 elderly with mean age of 73 years. Uvula deviation was seen in 28 (26.9%) young subjects and 22 (21.6%) elderly. Irregular tongue border was seen in 17 subjects, unilateral in 4 subjects. Fourteen (6.8%) subjects had deviation on tongue protrusion. Occasional tremor of tongue on protrusion is common in both young and old. Persistent (severe) tongue tremor on protrusion was seen in 18.6% of the elderly, and 4.8% of the young. None of the subjects had tremor of tongue at rest. In gag reflex, absence of gagging response was common in elderly, seen in two thirds of the subjects on stimulation of the posterior pharyngeal wall. However, all the subjects had uvular movement. Habituation or suppression of gagging response was seen in close to 90% of young males. CONCLUSION: There is wide range of normality in bulbar signs in normal population, particularly among the elderly.

Inhibition of aflatoxin B1-induced cell injury by selenium: an in vitro study.

Dietary selenium is an essential trace element in human nutrition. Selenium has been shown in animal studies to inhibit aflatoxin hepatocarcinogenesis. However, the cellular mechanism responsible for the inhibition has not been thoroughly studied. This study examines the effect of two selenium compounds, namely, sodium selenite and selenium-enriched yeast extract (SeY), on the cytotoxicity, DNA-binding and mutagenicity of aflatoxin B1 (AFB1) in cultured Chinese hamster ovary (CHO) cells. CHO cells, after treatment with 2 micrograms ml-1 selenite or 80 micrograms ml-1 SeY, exhibited increased resistance to AFB1-induced cell killing. At a concentration of 50 micrograms ml-1 AFB1, cell survival, measured by the clonogenicity assay, was increased by 21- and 10-fold in selenite- and SeY-treated cells, respectively. However, selenium treatment did not appear to affect AFB1-DNA binding. Similarly, no effect was observed on AFB1 mutagenicity, as determined by the hypoxanthine-guanine phosphoribosyl transferase (HPRT) gene mutation assay. The results showed that selenium could effectively protect cells from AFB1 cytotoxicity in cultured cells but had no effect on AFB1-DNA adduct formation or mutagenesis. It is suggested that there are multiple pathways of AFB1 toxicity and that selenium can modulate AFB1-induced cell killing independent of its genotoxicity.