In order to improve the efficiency and cost-effectiveness of the PCB analysis, the DMSO partition and SPE extraction were applied to clean up the PCB-contaminated transformer oils and PCB level was determined by means of the quadrupole GC/MS. The analysis data obtained from this method were compared statistically to that from the standard method.

Chemistry Techniques, Analytical↗

PubMedDate not supplied

Mutagenicity of the L-rhamnose-ammonia-hydrogen sulfide Browning reaction mixture.

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Ammonia↗

PubMedDate not supplied

The bilateral effect of stellate ganglion block on the facial skin blood flow.

BACKGROUND AND OBJECTIVES: It is our hypothesis that stellate ganglion block increases regional blood flow on the blocked side, but does not change cardiac output, suggesting that the corresponding regional blood flow on the contralateral side may decrease, which would be disadvantageous for patients with bilateral sympathetically-maintained pain. The aim of this study is to examine the effect of stellate ganglion block on facial skin blood flow. METHODS: Skin blood flow on the right and left forehead was measured by a laser blood flowmeter before stellate ganglion block and 15 minutes after the block. The block was performed for 8 outpatients with acute or chronic pain in the head or neck using a 24-gauge needle, 5 mL of 1% mepivacaine, and a paratracheal approach at the C6 transverse process. Time control without the block was obtained with 9 healthy volunteers. RESULTS: All the patients developed the Horner's syndrome on the blocked side, but not on the contralateral side. The facial skin blood flow increased from 7.5 +/- 1.1 mL/min/100 g to 14.5 +/- 1.4 mL/min/100 g on the blocked side (P < .01) and from 8.8 +/- 1.2 mL/min/100 g to 12.8 +/- 1.7 mL/min/100 g on the contralateral side (P < .05). The healthy volunteers without the block showed no significant change (from 10.1 +/- 0.8 mL/min/100 g to 10.3 +/- 0.7 mL/min/100 g). CONCLUSIONS: Our study suggests that stellate ganglion block may increase the contralateral regional skin blood flow.

Adult↗

PubMedDate not supplied

Comparison of effects of doxorubicin and radiation on p53-dependent apoptosis in vivo.

The effects of doxorubicin and radiation on apoptosis, p53 expression, and tumor growth in human tumor xenografts were investigated. Human ependymoblastoma (NNE), primitive neuroectodermal tumor (YKP), glioblastoma (KYG) and small cell lung carcinoma (GLS) that are all transplantable to nude mice were treated with doxorubicin (8 mg/kg) or radiation (1 Gy). The histological study was performed by using TUNEL and p53 staining. Cytotoxic effects of doxorubicin and radiation were compared with no-treatment group by the growth curves and apoptotic index of tumor to each treatment. In NNE with wild-type p53, doxorubicin induced growth delay of tumors (tumor volume doubling time; 13.7+/-3.3 days in control group vs 30.4+/-1.5 days in doxorubicin group), but no growth delay of tumors in KYG and GLS with mutant type p53. While radiation-induced apoptosis appeared most frequently at 6 h after irradiation, doxorubicin-induced apoptosis had a tendency to appear later. Furthermore, although the frequency of doxorubicin-induced apoptosis was lower than that of apoptosis by 1 Gy irradiation, apoptotic cells appeared for many hours after the treatment. Doxorubicin-induced apoptosis may be correlated with p53 phenotype because apoptosis was induced only in tumor with wild-type p53, but it appeared less frequently and later than radiation-induced apoptosis.

Animals↗

PubMedDate not supplied

Effect of paclitaxel pretreatment on radiation-induced p53-dependent apoptosis.

The aim of this study was to investigate the effect of paclitaxel on radiation-induced p53-dependent apoptosis. A human ependymoblastoma transplanted to nude mice was used. They were treated with paclitaxel (40 mg/kg), irradiation (2 Gy), or a combination of both. Apoptosis was markedly increased in the irradiation group. p53 protein expression was well correlated with the frequency of radiation-induced apoptosis. There was only a slight increase in apoptosis in the paclitaxel group, with little p53 protein expression. In the combination group, the frequency of apoptosis varied with the time intervals, and the group irradiated 12 h after paclitaxel administration showed much less apoptosis than the irradiation group. The Ki-67 labeling index in the paclitaxel group was always higher than before administration. The present study indicates that p53-dependent apoptosis was frequently induced in the human tumor in vivo by irradiation, but not by paclitaxel alone. When combined with irradiation, the timing affected the frequency of apoptosis and the degree of p53 protein expression.

Animals↗

PubMedDate not supplied

Experimental induction of apoptosis by a combination of etoposide and radiation treatment.

The present study was undertaken to investigate cell death (particularly apoptosis) induced by etoposide, radiation, and both, and to examine p53 protein expression in relation to cell death. Nude mice transplanted with a human tumor (ependymoblastoma) were treated with etoposide (5-40 mg/kg) or 1-2 Gy X-ray irradiation or both. The tumor was excised at different points after treatment, and tumor tissue specimens were used to check for apoptosis and p53 protein expression by TUNEL, p53 protein staining, etc. Induction of p53-dependent apoptosis was observed in the etoposide treatment group, the X-ray irradiation group, and the combined (etoposide + X-ray irradiation) group. Etoposide 10 mg/kg was found to be approximately equivalent to 1 Gy X-ray irradiation in ability to induce apoptosis. When etoposide treatment was combined with X-ray irradiation at intervals of 3-6 hours, an approximately additive effect was observed.

Animals↗