The purpose of this study is to establish the normal physiological values of glycosylated hemoglobin (HbA₁ and HbA_1C) among Japanese rural inhabitants and to evaluate its potential as a screening tool for diabetes mellitus. Six hundred and seventy-five people aged 35-64 years (210 males and 465 females) were examined. Oral glucose tolerance tests were perfomed on 135 inhabitants of them by giving a 50-gm.
Frequency distributions of HbA₁ and HbA_1C fitted approximately to the log-normal distribution.
Geometric means and standard deviations in bracket were 7.95 (1.11)% for HbA₁ in men, 8.13 (1.12)% for HbA₁ in women, 5.17 (1.10)% for HbA_1C in men and 5.16 (1.11)% for HbA_1C in women
Group average values of HbA₁ and HbA_1C tended to increase with age in both men and women except a male group aged 60 years and over. There were no significant differences between mean values of glycosylated hemoglobin in men and those in women. HbA₁ was positively correlated with age in women and negatively correlated with hemoglobin in both men and women. HbA_1C was positively correlated with age in men and women, body mass index, systolic blood pressure and serum cholesterol in women, and negatively correlated with hemoglobin in men.
In order to evaluate glycosylated hemoglobin as a screening tool for the identification of unknown persons with diabetes, we calculated the sensitivity (the extents to which the participants who were found to have a diabetic OGTT also had an abnormal glycosylated hemoglobin) and specificity (the extents to which the participants who were not diabetic had normal glycosylated hemoglobin). The sensitivities for the person aged 59 years or under using HbA₁ were 72.7-100% and the specificities 67.3-75.0 percent. Futhermore the sensitivities for the same aged person using HbA_1C were 81.8-100% and the specificities 78.8-81.3 percent. The validities for both HbA₁ and HbA_1C were higher than those for glucosuria or blood glucose. But glycosylated hemoglobin was not useful as a screening tool for the person aged 60 years and over because of the low specificity.

Objective: Sauna bathing is a popular recreational activity and has long since been used to relieve stiff necks and low back pain. Recently, low-temperature sauna has been used to treat congestive heart failure (CHF), coronary artery diseases, chronic fatigue syndrome, and chronic pain. During 1960-1970, thermal stimulation was applied to the patients with renal failure. We could not find the subsequent reports, and the long-term effects are unclear. The purpose of this experiment was to verify the safety of systemic low-temperature sauna treatment (ST) for the 5/6 remnant kidney mouse and to examine the effect of ST on urinary protein excretion. Materials and Methods: The C57BL/6 mice were divided into the following 4 groups; group 1: sham-operated and non-sauna treatment mice (sham+non-ST group: n = 5), group 2: sham-operated and ST mice (sham+ST group: n = 5), group 3: Nx and non-ST mice (Nx+non-ST group: n = 5), and group 4: Nx and ST mice (Nx+ST group: n = 5). Mice received ST at 41°Cfor 15 min and at 32°Cfor 20 min for 12 weeks using a natural convection dry sauna system. Results: After 12 weeks of ST, no differences were observed in creatinine clearance, body weight, fluid intake, urine volume, serum sodium and potassium levels between ST and non-ST groups. Our results showed a significant increase in eNOS mRNA expression in the Nx+ST group compared to that in the Nx+non-ST group. These results suggest the possibility that mild sauna treatment induces thermal vasodilation effects on glomerulus. Systolic blood pressure and urine protein levels in the Nx groups did not change throughout the intervention. Conclusion: There are no clear adverse events associated with low-temperature sauna. Therefore, this study setting is safe in the CKD model mouse. Renal eNOS mRNA expression was increased by the low-temperature sauna. The present results suggest the possibility that ST might provide a renal protective effect by suppressing glomerular hypertension via stimulation of renal NO production in the CKD model mouse.