Behavior of various indices of lead poisoning in rabbits.
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Biomedical subjects
H Yagyu
Publications and source records attributed to H Yagyu.
Clinical evaluation of CYFRA 21-1 in malignant pleural fluids.
The diagnostic value of the novel tumor marker CYFRA 21-1 in malignant pleural fluid was assessed in comparison to carcinoembryonic antigen (CEA). CYFRA 21-1 and CEA were measured in pleural fluid obtained from patients with 108 malignant and benign diseases. The levels of pleural fluid CYFRA 21-1 in malignant diseases (median: 84.5 ng/ml) were statistically higher than those in benign diseases (median: 13.9 ng/ml; p < 0.01). The CYFRA 21-1 test was able to discriminate significantly between squamous cell lung cancer and pneumonia (p < 0.01), while pleural fluid CEA levels could not. Receiver operating characteristic (ROC) curve analysis showed that the CYFRA 21-1 test has an advantage over CEA because of its higher specificity. These results indicate that measurement of CYFRA 21-1 in pleural fluid is a new tool, in addition to cytologic examination, to discriminate between malignant and benign diseases.
Adult↗
Subthreshold hyperoxia potentiates TNF-alpha-induced ICAM-1 expression on cultured pulmonary microvascular endothelial cells.
The effects of combined exposure to subthreshold hyperoxia and the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) on the expression of intercellular adhesion molecule-1 (ICAM-1) were examined in bovine lung microvascular endothelial cells (BLuEC). The expression of total ICAM-1 was not affected by 50% hyperoxia conditions alone, indicating that this level is subthreshold for BLuEC. In the presence of 5 ng/mL TNF-alpha, which has minimal influence on BLuEC alone, the amount of total ICAM-1 expression under 50% hyperoxia was higher than that in normoxic conditions (approximately 30%) throughout the culture period. The amount of soluble ICAM-1 that has been released into the culture medium increased after joint exposure to hyperoxia and TNF-alpha. These results suggest that exposure to subthreshold hyperoxia, which does not by itself cause damage to the endothelial cells or induce ICAM-1 expression, potentiates the effects of low-level TNF-alpha exposure.
Animals↗