In order to reevaluate the high mortality from Hodgkin's disease (HD) in Kyushu, Japan, the chronological changes of the geographical variation of HD were analysed. The age-adjusted death rates (AADRs) for HD of the three periods 1969-71, 1974-76, and 1979-81 were calculated for each prefecture and 128 cases of HD in 1969-72 were re-examined to evaluate the difference in the diagnostic criteria of HD among these periods. AADRs for HD in Kagoshima Prefecture, which had the highest mortality from HD in Japan in the early period, has decreased drastically and the mortality from HD in Kyushu has not been high in the most recent period. The main reasons for the decreased mortality from HD in Kyushu may be as follows: (1) HD has been more strictly diagnosed by histopathological criteria in recent years; (2) adult T-cell leukemia/lymphoma (ATLL) which is prevalent in Kyushu and has similar histopathological features to those of HD may have been diagnosed as HD in the past when the concept of ATLL did not exist. Therefore, it is suggested that the mortality from HD in Kyushu has been essentially the same as for other areas in Japan even in the past.

Female↗

PubMedDate not supplied

Malignant lymphomas in Japan: epidemiological analysis on adult T-cell leukemia/lymphoma.

According to the Vital Statistics Japan Series in 1950-1981, the age-adjusted death rate for malignant lymphomas (ICDs, 200-202) in Japan has increased in recent years. A geographical clustering of malignant lymphomas in the Kyushu districts was observed both in the period 1969-1971 and more recently in 1979-1981. The excessive rate of malignant lymphomas in Kyushu was due to the high incidence of adult T-cell leukemia/lymphoma (ATLL). The distribution of healthy carriers of ATLV, a human retrovirus which is almost identical to HTLV, was closely related to that of patients with ATLL in Japan. Epidemiological features of the infectious mode of ATLV suggested two main routes of natural transmission, one from mother to child and the other from husband to wife. ATLV is considered to be a main causative agent of ATLL from virological and epidemiological evidence, but infection by this virus alone may not result in ATLL because the incidence of ATLL among ATLV carriers was apparently not very high even in endemic areas of ATLL. Thus, some risk factors other than ATLV, such as environmental and genetic factors, may contribute to the development of ATLL.

Age Factors↗

PubMedDate not supplied

Correlation of detectability of hepatitis C virus genome in saliva of elderly Japanese symptomatic HCV carriers with their hepatic function.

The hepatitis C virus (HCV) genome was sought in the saliva of 76 chronic HCV carriers (mean age nearly 60 years) in a rural Japanese town, who had high serum titers of c-100 and anti-core second generation antibodies. In 27 samples (27 cases, 36%), the HCV-RNA genome was detected by the reverse transcriptase - polymerase chain reaction with either of two sets of primers covering two regions of the HCV genome: the 5'noncoding region and the region encompassing the putative envelope (E1). Transaminase values at the time of sampling were higher in the patients with than in those without detectable HCV RNA in saliva (p = 0.04 for alanine aminotransferase, p = 0.04 for aspartate aminotransferase; Wilcoxon test). The prevalence of the positivity was higher by 5'noncoding primers (14/59 vs. 15/68). Our data show that the severity and duration of hepatic dysfunction influence the detectability of the HCV genome in the saliva. This has been a controversial point among investigators.

Adult↗

PubMedDate not supplied

Sulfur-containing metabolites of chlorobiphenyl isomers, a comparative study.

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Animals↗

PubMedDate not supplied

An immunohistochemical study of p16, pRb, p21 and p53 proteins in human esophageal cancers.

BACKGROUND: Cell cycle-associated proteins, p16, pRb, p21 and p53 are important in regulating the G1-S checkpoint in the cell cycle, and their functional alterations play key roles in carcinogenesis and cell proliferation. MATERIALS AND METHODS: We immunohistochemically examined the expression of p16, pRb, p21 and p53 proteins by using surgically resected tissues from 35 patients with primary esophageal cancers. RESULTS: In 35 esophageal cancers, the expressions of p16, pRb, p21 and p53 proteins were detectable in 4(11.4%), 25(71.4%), 11(31.4%) and 20(57.1%) respectively. Interestingly, 24 of 25 pRb positive cancers (96.0%) had negative p16, whereas three of ten pRb-negative cancers (30.0%) had high levels of p16 (p < 0.05). In 11 cases of p21 positive immunostaining, there was lymph node metastasis (pN1) in 9 (81.8%). CONCLUSIONS: These results suggest that abnormalities of p16 protein may be closely associated with the carcinogenesis or cell proliferation of esophageal cancers.

Adult↗

PubMedDate not supplied

Metabolism of 3-tert-butyl-4-hydroxyanisole by horseradish peroxidase and hydrogen peroxide.

3-Tert-butyl-4-hydroxyanisole (3-BHA) was metabolized in the presence of horseradish peroxidase and hydrogen peroxide to 2-tert-butyl-p-benzoquinone (TBQ), 2,3-epoxy-5-tert-butyl-1,4-benzoquinone (TBQ-epoxide), and two known dimers. The formation of TBQ from 3-BHA required both horseradish peroxidase and hydrogen peroxide. When 2.5 mM 3-BHA was incubated with horseradish peroxidase and hydrogen peroxide, the formation of TBQ increased with hydrogen peroxide concentration up to 5 mM and decreased gradually at higher concentrations of hydrogen peroxide. On the other hand, the formation of TBQ-epoxide from 3-BHA increased, depending on hydrogen peroxide concentration at higher concentrations than 1 mM. In incubating 2-tert-butylhydroquinone (TBHQ) with horseradish peroxidase and hydrogen peroxide, TBHQ was rapidly oxidized to TBQ, and then TBQ-epoxide was also produced at concentrations more than 2.5 mM of hydrogen peroxide. In the absence of horseradish peroxidase, the incubation of TBQ with hydrogen peroxide resulted in TBQ-epoxide production. These results suggest that 3-BHA is metabolized to TBHQ, which is rapidly oxidized to TBQ, by horseradish peroxidase and hydrogen peroxide, and then TBQ is converted to TBQ-epoxide by only hydrogen peroxide.

Butylated Hydroxyanisole↗

PubMedDate not supplied

[Research on nursing of bedridden elderly persons (1). Concerning the terminology of "the bedridden old persons"].

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Aged↗

PubMedDate not supplied

Multidrug resistance in Yoshida rat ascites hepatoma cell lines.

Rat ascites hepatoma (AH) cell lines that were induced by dimethylaminoazobenzene and established as transplantable tumors had different sensitivities to vinblastine (VBL). The most VBL-resistant cells, AH66, showed more cross-resistance to vincristine and anthracyclines than AH66F cells. The resistance of AH66 cells was significantly decreased by verapamil. VBL-resistance of AH66 cells was inhibited by other drugs reported as overcoming acquired multidrug resistance, while the sensitivity of AH66F cells was hardly influenced by these drugs. The lowered uptake and enhanced extrusion of the antitumor drug in AH66 cells were suppressed by verapamil. M(r) 160,000 protein in the plasma membrane from AH66 was labeled with a photoactive VBL analog and was immunopositive to a monoclonal antibody against P-glycoprotein, C219. The sensitive cells had barely detectable levels of the surface membrane components. Specific photo-labeling with a VBL analog of P-glycoprotein of AH66 cell membrane was inhibited by reserpine and verapamil which restored the VBL resistance. These results indicate that AH66 cells are a naturally acquired multidrug-resistant cell line overexpressing a P-glycoprotein, and AH cell lines are useful to study multidrug resistance of hepatic carcinomas and development of counteracting drugs.

Affinity Labels↗

PubMedDate not supplied

Identification and structure characterization of S-containing metabolites of 3-tert-butyl-4-hydroxyanisole in rat urine and liver microsomes.

After ip administration of 3-tert-butyl-4-hydroxyanisole (3-BHA) to rats, two previously undocumented metabolites 2-tert-butyl-5-methylthiohydroquinone (TBHQ-5-SMe) and 2-tert-butyl-6-methylthiohydroquinone (TBHQ-6-SMe) were identified in the urine by comparison with the authentic samples by GC/MS. In addition to these metabolites, 3-tert-butyl-4,5-dihydroxyanisole was also detected in the urine hydrolyzed by beta-glucuronidase/sulfatase. Administration of tert-butylhydroquinone (TBHQ), an O-demethylated metabolite of 3-BHA, also resulted in the formation of the S-containing metabolites, TBHQ-5-SMe and TBHQ-6-SMe. After incubation of TBHQ with rat liver microsomes in the presence of glutathione (GSH), two metabolites were isolated and purified by HPLC. The metabolites were identified as 2-tert-butyl-5-(glutathion-S-yl)hydroquinone and 2-tert-butyl-6-(glutathion-S-yl)hydroquinone by 1H- and 13C-NMR spectrometry and by fast atom bombardment-mass spectrometry. The formation of TBHQ-GSH conjugates required NADPH, molecular oxygen, and GSH. Cytochrome P-450 inhibitors such as SKF 525-A and metyrapone markedly inhibited the formation of TBHQ-GSH conjugates in vitro. These results suggest that TBHQ is converted by cytochrome P-450-mediated monooxygenases to a reactive metabolite, 2-tert-butyl-p-benzoquinone (TBQ), which then conjugates with GSH to form TBHQ-GSH conjugates. GSH S-transferase activities do not seem to play a role in GSH conjugation reaction to TBQ because cytosol fraction from rat liver homogenates did not enhance the microsome-mediated production of TBHQ-GSH conjugates.

Animals↗

PubMedDate not supplied

A clonal human chondrosarcoma cell line produces an anti-angiogenic antitumor factor.

Previously we reported that rabbit costal chondrocytes in primary culture produced an anti-angiogenic anti-tumor factor. We also established a clonal human chondrosarcoma cell line, HCS-2/8, which had typical cartilage phenotypes. In the present study, we investigated whether HCS-2/8 cells produce an anti-angiogenic anti-tumor factor. Serum-free medium conditioned by exposure to HCS-2/8 cells in culture inhibited the proliferation of bovine pulmonary artery endothelial cells in culture. The inhibition was not due to general cytotoxicity because the endothelial cells started to proliferate after the conditioned medium was removed from the cultures. The factor in conditioned medium also inhibited DNA synthesis in bovine pulmonary artery endothelial cells, but not in B16 melanoma cells, normal rat kidney cells or chick embryo fibroblasts. Production of the factor by HCS-2/8 cells did not change during serial passages. It also inhibited angiogenesis in the chorioallantoic membrane of chick embryos induced by B16 melanoma and growth of the tumor transplanted onto the membrane. Treatment with protease destroyed the inhibitory activities of conditioned medium on angiogenesis and tumor growth. These findings suggest that HCS-2/8 cells produce a peptide factor with anti-angiogenic, antitumor activity and that the cell line should be a useful source of the factor.

Animals↗