Effects of Wen-Pi-Tang and its crude drug extracts on proliferation of cultured mouse mesangial cells

The efficacy of Wen-Pi-Tang and each of its crude drug extracts on the proliferation of mouse mesangial cells was determined in terms of [³H]thymidine uptake. When Wen-Pi-Tang was added to the medium of mesangial cell cultures, it suppressed the proliferation of mesangial cells markedly. Similar to the effects of Wen-Pi-Tang, Rhei Rhizoma, its main ingredient, exerted an inhibitory effect on mesangial cell proliferation at a relatively low concentration. Ginseng Radix and Aconiti Tuber were also an effective crude drug. As for Zingiberis Rhizoma, an inhibitory activity at relatively high concentration was noted. However, the proliferation of mesangial cells in the presence of Glycyrrhizae Radix showed no particular alteration. As is clear from the results of the present study, Rhei Rhizoma, Ginseng Radix, Aconiti Tuber and Zingiberis Rhizoma alone each exert an inhibitory effect. The inhibition of mesangial cell proliferation by Wen-Pi-Tang can thus be explained by the action of these crude drugs.     

The mechanism of acquired resistance to cisplatin by a human ovarian cancer cell line

The present study was designed to elucidate the mechanism of resistance to cisplatin. A cisplatin-resistant cell line (KFr) was established from KF cells derived from human serous cystadenocarcinoma of the ovary. The DNA histogram revealed an increase of S-phase cells and a decrease of G1-phase cells in cultured KFr cells, compared to that in cultured KF cells. Although the cisplatin content in the KF cells incubated with cisplatin at 10 micrograms/ml increased in a time-dependent manner, that in the KFr cells remained unchanged during the experimental period. When 0.5 mg of cisplatin was administered ip to nude mice with KF or KFr tumor, the cisplatin content in the KFr tumor was significantly lower than that in the KF tumor. The KFr cells showed a cross-resistance to L-phenylalanine mustard, while no cross-resistance to vincristine or 5-fluorouracil was observed. These findings suggest that the mechanism of cisplatin resistance in the KFr cells involves a decrease of cisplatin accumulation in the tumor cells.     

Late-arterial and portal-venous phase imaging of the liver with a multislice CT scanner in patients without circulatory disturbances: automatic bolus tracking or empirical scan delay?

The value of automatic bolus tracking in late-arterial and portal-venous phase imaging of the liver with a multislice CT scanner as compared with fixed time-delay examination in patients without circulatory disturbances is evaluated. For the evaluation of known or suspected liver disease, 98 multiphase contrast-enhanced CT examinations including double late-arterial phase imaging were randomized into either scanning with a scan delay of 30 s from the beginning of contrast material injection or scanning with automatic bolus tracking. Contrast material was injected at 0.07 ml/kg body weight/s over 30 s. Contrast enhancement in each acquisition was measured in the aorta, portal vein, liver, pancreas and hepatocellular carcinomas. The density difference between hepatocellular carcinomas and the hepatic parenchyma was calculated. The mean time to the first-pass acquisition as determined by automatic bolus tracking was 29.6 s. No statistically significant difference was observed between the two groups either in any enhancement in any acquisition or in the lesion-to-liver density difference. The use of automatic bolus tracking in late-arterial and portal-venous phase hepatic CT does not significantly improve the degree of contrast enhancement in the aorta, portal vein, liver and pancreas or lesion-to-liver conspicuity in patients without circulatory disturbances.     

Restorative effects of calmodulin antagonists on reduced cisplatin uptake by cisplatin-resistant human ovarian cancer cells

In the present study, we attempted to determine effects of calmodulin antagonists (W-7 and W-5) on cisplatin uptake by human ovarian cancer cells, using KF cells derived from serous cystadenocarcinoma of the ovary and cisplatin-resistant cells (KFr). The degree of cisplatin resistance of the KFr cells was about 3.7-fold higher than that of the parent KF cells, with regard to the concentration of cisplatin required for 50% inhibition of cell proliferation (IC50). When KF and KFr cells were incubated with 10 micrograms/ml cisplatin for 4 hr, cisplatin-content in the KF cells was significantly higher than that in the KFr cells. When KF cells were incubated in the presence of W-7 (but not W-5), cisplatin uptake significantly increased, compared to cells treated with cisplatin alone. On the other hand, when KFr cells were incubated in the presence of 5 micrograms/ml W-7 or W-5, cisplatin uptake was significantly higher than uptake by KFr cells treated with cisplatin alone, being comparable to that by KF cells treated with cisplatin alone. Such an increase in cisplatin uptake seemed to bring about adjuvant effects to cisplatin of KFr cell proliferation in vitro. The KF tumor grown in nude mice took up 24.8 ng/g dry wt of cisplatin 4 hr after intraperitoneal administration. When cisplatin was administered with calmodulin antagonists, cisplatin uptake by the KF and KFr tumors was significantly increased, compared to that after treatment with cisplatin alone. In particular, the cisplatin uptake by the KFr tumor was about 2.5-fold higher than that by the KFr tumor treated with cisplatin alone. These results suggest that coadministration of calmodulin antagonists and cisplatin may be of use in patients with refractory ovarian cancer.     

Imaging endolymphatic hydrops at 3 tesla using 3D-FLAIR with intratympanic Gd-DTPA administration.

PURPOSE: Visualization of endolymphatic hydrops by 3-dimensional fluid-attenuated inversion recovery-FLAIR using conventional turbo-spin-echo (3D-FLAIR-CONV) after intratympanic injection of Gd-DTPA has been reported in patients with Ménière's disease. Compared to 3D-FLAIR-CONV used in previous studies, the addition of a variable flip-angle technique (3D-FLAIR-VFL) enables very long echo trains and, therefore, shorter scan times. We evaluated whether 3D-FLAIR-VFL could replace 3D-FLAIR-CONV in detecting endolymphatic hydrops after intratympanic Gd-DTPA administration. METHODS: Eleven patients were included in this study. Twenty-four hours after Gd-DTPA injection, we performed 3D-FLAIR-CONV and 3D-FLAIR-VFL imaging at 3T. We compared the contrast-to-noise ratio (CNR) between cochlear fluid and the cerebellum between the 2 FLAIR sequences. We subjectively scored the size of the endolymphatic space in the cochlea and vestibule for each patient and correlated the scores with the clinical diagnoses. RESULTS: The CNR of 3D-FLAIR-CONV was significantly higher than that of 3D-FLAIR-VFL. Scores for the size of endolymphatic space in the vestibule were identical between the 2 sequences; however, those in the cochlea disagreed in 3 cases. 3D-FLAIR-CONV correlated better with the clinical diagnoses. CONCLUSIONS: Currently, we may not be able to replace 3D-FLAIR-CONV with 3D-FLAIR-VFL, at least not with the scanning parameters used in the present study.