Genetic polymorphism of human plasminogen in the Japanese population was studied using agarose gel isoelectric focusing followed by immunofixation. A new basic variant, PLG B, was found as a heterozygous state PLG 1-B, which was genetically determined. The allele frequencies calculated from 258 individuals were PLG^1=0.958, PLG^2=0.020 and PLG^B=0.022.
BACKGROUD:
Helicobacter pylori
infection and serum pepsinogen values are strongly related with stomach cancer. The aim of this study was to know what were these factors among general population.
METHODS: Subjects were randomly selected 633 control subjects in a nested case-control study for risk of stomach cancer. Most of them were from rural areas of Japan. Using frozen sera, pepsinogen I (PG I) and II (PG II) values and
H. pylori
antibody were measured. Those with PG I less than 50 ng/mL and the ratio of PG I to PG II (PG I/II) was less than 2.0 were defined as severe, those with PG I less than 70 ng/ml and PG I/II less than 3.0 were defined as mild and the other subjects were defined as no serological atrophy.
RESULTS: About 70% of the subjects were
H. pylori
seropositive and the seroprevalence did no depend on age or sex. Percentages of those with severe serological atrophy increased with age from 10% in those aged 40-49 years to 38% in 70 and more, and percentages of those with mild serological atrophy were about 30% independent of age.
CONCLUSIONS: The subjects, who were expected to represent populations of rural area of Japan, had high prevalence of both
H. pylori
infection and serological atrophy of gastric mucosa. These facts should be considered in discussing results of the nested case-control study.
The hereditary and environmental influences shared by parents and offspring are likely to play a strong aetiological role in colorectal or liver cancer versus a weaker but still significant role in stomach cancer. In contrast, the aetiological role of familial predisposition to lung cancer was indeterminate, which suggests a predominant role of non-familial factors in the development of lung cancer.
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