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The possible association between the risk of gastric cancer and the levels of calcium, magnesium, and nitrate in drinking water from municipal supplies was investigated in a matched case-control study in Taiwan. Records of gastric cancer deaths among eligible residents in Taiwan from 1987 through 1991 were obtained from the Bureau of Vital Statistics of the Taiwan Provincial Department of Health. Controls were deaths from other causes and were pair-matched to the cases by sex, year-of-birth, and year-of-death. Each matched control was selected randomly from the set of possible controls for each case. Data on calcium, magnesium, and nitrate levels in drinking water throughout Taiwan were obtained from the Taiwan Water Supply Corporation. The municipality of residence of the cases and controls was assumed to be the source of the subject's calcium, magnesium, and nitrate exposure via drinking water. The subjects were divided into tertiles according to the levels of calcium, magnesium, and nitrate in their drinking water. The results of the present study show that there is a significant positive association between drinking water nitrate exposure and gastric cancer mortality. The present study also suggests that there was a significant protective effect of calcium intake from drinking water on the risk of gastric cancer. Magnesium also exerts a protective effect against gastric cancer, but only for the group with the highest levels.

Many investigators have examined urbanization gradients in cancer rates. The purpose of this report was to identify urban-rural trends in cancer mortality rates (1982-1991) for municipalities in Taiwan. For this purpose, Taiwan's municipalities were classified as rural, suburban, urban, or metropolitan, using population density as an ordinal indicator of the degree of urbanization. Average annual age-adjusted, site-specific cancer mortality rates were calculated for both sexes within each population density group. Significant increasing trends with more urbanization were observed in mortality rates for cancers of the lung, pancreas, and kidney among both males and females, as well as male prostate cancer, and female breast and ovary cancer. In addition, this study revealed a significant rural excess for nonmelanoma skin cancer among both males and females, as well as male non-Hodgkin's lymphoma, and cancers of the female bone, and female connective tissue. Analytic studies for sites with consistent urban-rural trends may be fruitful in identifying the aspect of population density, or other unmeasured factors, that contribute to these trends.Almost all studies which have reported variation in cancer incidence and mortality rates across urbanization gradients have found higher rates in urban populations than in rural areas. Findings are presented from a study conducted to identify urban-rural trends in cancer mortality rates during 1982-91 for municipalities in Taiwan. The countries municipalities were classified as rural, suburban, urban, or metropolitan, using population density as an ordinal indicator of the degree of urbanization. Average annual age-adjusted, site-specific cancer mortality rates were calculated for both sexes within each population density group. Significant increasing trends with more urbanization were observed in mortality rates for cancers of the lung, pancreas, and kidney among both men and women, as well as male prostate cancer and female breast and ovary cancer. The study also found a significant rural excess for non-melanoma skin cancer among men and women, as well as male non-Hodgkin's lymphoma and cancers of the female bone and connective tissue.

The role of N-methyl-d-aspartate (NMDA) receptor in mediating the effect of testosterone exposure prenatally on neuronal apoptosis in the sexual dimorphic nucleus of the preoptic area (SDN-POA) of rats was studied. The endogenous testosterone was diminished by prenatal stress (PNS) or simulated by testosterone exposure (TE) to understand the effect of testosterone on NR1(a functional subunit protein of NMDA receptor) expression and neuronal apoptosis. To further study whether the testosterone, after being converted into estradiol, modulates NR1expression, 4-androstein-4-ol-3,17-dione (ATD; an aromatase inhibitor) was used to block the conversion of estradiol from testosterone. The expressions of the NR1mRNA and NR1subunit protein were quantified by RT-PCR and western blotting analysis, respectively. In addition, a noncompetitive antagonist of NMDA receptor, MK-801, was used to find out whether blockage of NMDA receptor affects the naturally occurring apoptosis in SDN-POA. The results showed the following. 1) Expression of perinatal NR1subunit protein in the central part of the medial preoptic area of male rats was significantly higher than that of females, especially on postnatal days 1 and 3. 2) The testosterone level of male fetuses on embryonic day 18 was significantly higher than that of females, while the testosterone level of TE females or PNS males was similar to that of intact males or intact females, respectively. 3) The apoptotic incidence of intact male rats was significantly less than that of females, and the apoptosis was stimulated by PNS in male or inhibited by TE in female. 4) The expression of NR1subunit protein could be inhibited by PNS or ATD-treatment in male, while stimulated by TE in female. 5) NR1mRNA showed no significant difference among intact male, PNS male, ATD-treated male, TE female and intact female rats. 6) The low apoptotic incidence of male rats was significantly increased when NMDA receptor was blocked by MK-801. These results suggest that testosterone, after being converted to estradiol, may prevent the SDN-POA neurons of male rats from apoptosis through enhancing the expression of NR1at the posttranscriptional level.