ABSTRACT
We describe a 38-year-old, severely emaciated female with slowly progressive type 1 diabetes mellitus (SPIDDM), who had hypoglycemia due to fasting and an extremely low energy intake. After being diagnosed with diabetes mellitus (DM), she took in only 300-500 kcal per day and her weight had decreased to 30 kg, with a body mass index (BMI) of 11.4 kg/m<sup>2</sup>. She was admitted with hypoglycemia, and SPIDDM was confirmed by nearly-completely ceased insulin secretion and seropositivity towards anti-GAD antibody. After appropriate dietary therapy and insulin administration, she recovered from a state of emaciation and her glucose metabolism was restored. With this patient it proved very effective for the general physician to coordinate treatment for both diabetes and an eating disorder.
ABSTRACT
Objective: We analyzed the number of deaths due to poisoning by pesticides over 38 years through vital statistics published annually by the Ministry of Health, Labour and Welfare of the Japanese government, from 1968 through 2005. Materials and Methods: Data not published as vital statistics were obtained from the Ministry of Health, Labour and Welfare Statistics and Information Department. The vital statistics provide the numbers of deaths with individual causes of death classified by sex and 5-year age group. We also calculated age-adjusted death rates by this classification, using a direct method based on the 1985 Japanese model population. Results: Deaths from pesticide poisoning increased rapidly beginning in 1982, reached a peak in 1986 (death rate per 100,000 population: 2.6 in males and 1.7 in females) and declined gradually thereafter. In the most recent several years, these figures have declined to levels previously unseen (death rate per 100,000 population: 0.4 in males and 0.3 in females). A difference in death rates between the sexes was observed at every age level, with death rates of males approximately 1.1-1.5-fold those of females. In the 1985-1987 data, these figures were highest in the three prefectures of northern Kanto (Tochigi, Gunma, and Ibaraki Prefectures; crude death rates per 100,000 population: 6.8, 6.8, 6.2, respectively), followed by that in Kagoshima Prefecture (5.0). In the 2003-2005 data, the figure was highest in southern Kyushu (Miyazaki Prefecture; crude death rate per 100,000 population: 1.9), followed by Tochigi (1.6), Ibaraki (1.4), and Kagoshima (1.4). Conclusions: Deaths from pesticide poisoning were extremely well correlated to the history of paraquat. Through the 1985 Advisory Resolution on Paraquat Regulations by the Japanese Association of Rural Medicine and other public health-oriented efforts, the concentration of highly fatal paraquat formulations was reduced, leading to discontinuation of its production, customer identification was strictly enforced when purchasing pesticides, and people's safety consciousness regarding pesticides improved. We regard and these developments as having had the greatest contribution to the reduction in deaths from pesticide poisoning.
Subject(s)
Pesticides , Mortality , Vital StatisticsABSTRACT
Angiotensin II AT(2) receptor gene-disrupted mice have increased blood pressure and response to angiotensin II, behavioral alterations, greater response to stress, and increased adrenal AT(1) receptors. We studied hypothalamic AT(1) receptor binding and mRNA by receptor autoradiography and in situ hybridization, adrenal catecholamines by HPLC, adrenal tyrosine hydroxylase mRNA by in situ hybridization and pituitary and adrenal hormones by RIA in AT(2) receptor-gene disrupted mice and wild-type controls. To confirm the role of adrenal AT(1) receptors, we treated wild-type C57 BL/6J mice with the AT(1) antagonist candesartan for 2 weeks, and measured adrenal hormones, catecholamines and tyrosine hydroxylase mRNA. In the absence of AT(2) receptor transcription, we found increased AT(1) receptor binding in brain areas involved in the regulation of the hypothalamic-pituitary-adrenal axis, the hypothalamic paraventricular nucleus and the median eminence, and increased adrenal catecholamine synthesis as shown by higher adrenomedullary tyrosine hydroxylase mRNA and higher adrenal dopamine, norepinephrine and epinephrine levels when compared to wild-type mice. In addition, in AT(2) receptor gene-disrupted mice there were higher plasma adrenocorticotropin (ACTH) and corticosterone levels and lower adrenal aldosterone content when compared to wild-type controls. Conversely, AT(1) receptor inhibition in CB57 BL/6J mice reduced adrenal tyrosine hydroxylase mRNA and catecholamine content and increased adrenal aldosterone content. These results can help to explain the enhanced response of AT(2) receptor gene-disrupted mice to exogenous angiotensin II, support the hypothesis of cross-talk between AT(1) and AT(2) receptors, indicate that the activity of the hypothalamic-pituitary-adrenal axis parallels the AT(1) receptor expression, and suggest that expression of AT(1) receptors can be dependent on AT(2) receptor expression. Our results provide an explanation for the increased sensitivity to stress in this model.
