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Biomedical subjects

Azusa Futamura

Publications and source records attributed to Azusa Futamura.

3 recordsLinked to original sources

[Quantification of urinary hemoglobin by an immunological method].

The quantification method of urinary hemoglobin has not been established. We examined whether a reagent (Eiken, Tokyo) used to immunologically assay fecal hemoglobin could be utilized to quantify urinary hemoglobin. The coefficients of variation were 2.2-3.0% in the reproducibility of one-run assays using urine and 4.3-5.7% in that of multiple-run assays using the standard sample of hemoglobin. Urinary hemoglobin was unstable and decreased in a time- and temperature-dependent manner. However, addition of the hemoglobin stabilization buffer (50 mM phosphate buffer, pH 6.4) (Eiken) to urine made urinary hemoglobin stable. Urinary hemoglobin levels did not change significantly when stored at 4 degrees C for 7 days or at -80 degrees C for 30 days. The hemoglobin concentration (mean +/- SD) of urine showing 1+, 2+ and 3+ with a test strip was 385 +/- 165(n = 30), 1070 +/- 499(n = 40) and 4130 +/- 2770 ng/ml (n = 20), respectively. Urinary hemoglobin did not correlate with urinary albumin, transferrin, immunoglobulin G, N-acetyl-beta-D-glucosaminidase nor alpha 1 microglobulin. These results suggest that this immunological method using the hemoglobin stabilization buffer can be utilized for quantification of urinary hemoglobin, which may provide clinically important information.

Biomarkers↗

Relationship between genetic polymorphisms of alcohol-metabolizing enzymes and changes in risk factors for coronary heart disease associated with alcohol consumption.

BACKGROUND: There are large individual variations in the responses of risk factors for coronary heart disease to alcohol consumption. To clarify the factors responsible for these individual variations, we studied the relationship between blood pressure, serum lipids, and uric acid and the genetic polymorphisms of alcohol dehydrogenase (ADH) 2 and aldehyde dehydrogenase (ALDH) 2 in alcohol drinkers. METHODS: We examined 133 male workers who drank >300 g of alcohol per week. Information regarding lifestyle habits was obtained by questionnaire. The ADH2 genotype was determined by PCR and subsequent digestion with MaeIII. The ALDH2 genotype was determined based on amplified product length polymorphisms. RESULTS: When the workers were divided into three groups: the ADH2(1)/2(1), ADH2(1)/2(2), and ADH2(2)/2(2) groups, the mean triglycerides and gamma-glutamyl transpeptidase concentrations were significantly higher in the ADH2(2)/2(2) group than in the ADH2(1)/2(1) group. In addition, multiple logistic regression analysis showed that the frequencies of individuals whose systolic blood pressure, triglycerides, and uric acid values were in the highest one third were significantly higher in the ADH2(2)/2(2) group than in the ADH2(1)/2(1) group. In contrast, no difference was observed between the ALDH2(1)/2(1) and (ALDH2(1)/2(2) + ALDH2(2)/2(2)) groups with regard to the mean value of any variable and to the frequency of individuals with any variable value in the highest one third. CONCLUSION: Individuals with the ADH2(1)/2(1) genotype might suffer fewer negative effects of drinking.

Alcohol Dehydrogenase↗