The roles of the hepatitis B virus (HBV), cigarette smoking and alcohol consumption in the etiology of hepatocellular carcinoma (HCC) were examined in a case-control study involving 204 patients with HCC and 410 control subjects in Fukuoka prefecture, where HCC risk is among the highest in Japan. Information on smoking and drinking habits was obtained by a detailed interview survey, and the results were analyzed in conjunction with serum hepatitis B surface antigen (HBsAg) status after adjustment for sex, age and other possible confounding factors. Individuals positive for serum HBsAg showed a relative risk (RR) for HCC of 13.8 (95% confidence interval, Cl 5.9 to 32.5), whereas heavy drinkers experienced about a 2-fold risk increase compared with non-drinkers. Light or moderate drinkers, however, demonstrated RRs near the unity. Some risk excess was observed among ex-smokers (RR = 1.5, 95% CI 0.8 to 2.8) and current smokers (RR = 1.5, 0.8 to 2.7) compared with non-smokers, but without evidence for a dose-response relationship in terms of pack-years. Analysis among HBsAg-negative subjects revealed similar non-significant association with smoking, and there was no clear interaction between alcohol and cigarette consumption on HCC risk. Other significant risk factors included positive histories of blood transfusion (RR = 3.7, 2.2 to 6.3) and familiar liver disease (RR = 2.6, 1.6 to 4.2). Attributable risk calculations suggest that chronic HBV infection and heavy drinking may account for 17% and 13% of HCC occurrence, respectively, in this high risk area. The association of cigarette smoking with HCC was not evident in our study.

Three hundred and sixty‐eight case‐control sets (male 287 pairs; female 81 sets) were collected for a hospital‐based case‐control study of primary hepatocellular carcinoma (HCC) conducted in Northern Kyushu, Japan. All incident cases of HCC were collected weekly from the inpatients (aged 40–69) of the Second Department of Internal Medicine, Kurume University Hospital between April, 1986 and May, 1992. One control for a male case and 4 controls for a female case were sampled, being matched to a case on age (same 5‐year age class), sex, residence (prefecture) and time of hospitalization (within 2 months after a case interview) from the inpatients of two general hospitals in Kurume. Information was collected by interview in person by a well‐trained interviewer and from a review of hospital records by the authors. Multivariatc analyses based on a conditional logistic regression model without an interaction term revealed that hepatitis B surface antigen (HBsAg) positive status (odds ratio (OR) = 8.67; 95% confidence Interval (95%CI) = 2.54–29.57), history of blood transfusion over 10 years previously (2.40; 1.26–4.56), parental history of hepatic diseases (2.31; 1.11–4.80) and heavy alcohol drinking (60≦ drink‐years) by age 40 (3.23; 1.61–6.51) were statistically significant risk factors of male HCC. Univariate analysis for females also showed an elevated OR of HBsAg (7.58; 1.96–29.35). Although the sample size was limited, univariate analysis indicated that anti‐hepatitis C virus antibody by c100‐3 antigen positive status had a statistically significant OR for HCC in both sexes.

The relationship between the occurrence of breast cancer and dietary intake, in particular a high-fat diet, has attracted much attention in recent years. In addition, the prognosis of breast cancer patients on the basis of dietary intake is also an interesting subject. The present study utilized breast cancer patients whose dietary intake was carefully assessed about one decade previously in a case-control study to determine whether dietary intake was indeed related to the patients' prognosis. The study included 212 patients who underwent a surgical operation between 1975 and 1978. They were followed-up until 1987, and a total of 47 breast cancer deaths were certified. The 5- and 10-year relative survival rates were 78.5% and 75.3%, respectively. The older patients tended to ingest smaller amounts of all nutrients, except animal fat from fish. Height was significantly correlated with total animal protein intake, whereas there was no significant correlation between body mass index and intake of any nutrient. Although the age-adjusted mean values of the nutrient intakes, other than vegetable fat, decreased with advancing stage, the differences were statistically insignificant. The results of multivariate analyses, in which some confounding factors (e.g., clinical stage) were adjusted using a proportional hazards model, showed that all hazards ratios in each nutrient were close to unity, and no dose-response relationship was seen. The present investigation did not provide any support for the hypothesis that a high-fat diet is a survival determinant for breast cancer patients.(ABSTRACT TRUNCATED AT 250 WORDS)

1. The response of renal beta-glucuronidase with time to the injection of gonadotrophin was investigated in each submicrosomal fraction of rough and smooth microsomal fractions of mouse kidney homogenate. 2. The increase in beta-glucuronidase activity appeared initially in membranes of the rough microsomal fraction, 24h after injection. 3. Afterwards the newly synthesized enzyme appeared in the contents of the rough microsomal fraction and was subsequently found in the smooth microsomal fraction, reaching a maximum concentration in this fraction at 72h. 4. At this juncture, a decrease in the enzyme activity was observed in rough microsomal contents whereas the lysosomal fraction had reached its maximum value. 5. The time-course of the appearance of beta-glucuronidase in the submicrosomal fractions after the gonadotrophin stimulation suggests that the newly synthesized enzyme at the site of membrane-bound ribosomes is transferred across the membrane into cisternae of the rough endoplasmic reticulum, and then is transported into lysosomes via the smooth endoplasmic reticulum. 6. The properties of microsomal and lysosomal beta-glucuronidases were compared.

1. Sodium (N-acetyl-N-phenylhydroxylamine beta-d-glucosid)uronate was isolated from the urine of rabbits receiving N-acetyl-N-phenylhydroxylamine. 2. Its chemical structure was confirmed by the correspondence of the infrared spectrum of its tri-O-acetyl methyl ester derivative with the tri-O-acetyl methyl ester derivative of an authentic specimen prepared by the Koenigs-Knorr synthesis.