Biomedical subjects
Publications and source records attributed to H Koya.
New fibrates containing piperidine, 4-hydroxypiperidine, piperidin-3-ene, and piperazine moieties in the structures were synthesized and evaluated. Among the synthesized compounds, 2-[3-[1-(4-fluorobenzoyl)-piperidin-4yl]phenoxyl-2-methylpropanoic acid (9aA: AHL-157) showed very superior activities in decreasing triglyceride, cholesterol, and blood sugar compared to bezafibrate in mice and rats.
OBJECTIVES: Our purpose was to investigate whether liver size is increased in the fetuses of pregnant women with diabetes and whether there is any relationship between fetal liver size and maternal glycemic control. STUDY DESIGN: Eighty pregnant women with diabetes had ultrasonographic measurement of fetal liver length made at 18, 28, and 36 weeks' gestation. Twenty-four obese, nondiabetic women were studied at 36 weeks as controls. RESULTS: Fetal liver length measurements were significantly greater than normal by 18 weeks' gestation (12% above normal mean values; p < 0.001) and increased further (19%, p < 0.02) by 36 weeks. In the obese controls liver length was increased 9% and was significantly lower than in the diabetic subjects (p < 0.001). CONCLUSIONS: Fetal liver size in increased in pregnant women with diabetes and cannot be explained solely by maternal obesity. The major increase in liver size occurs early in pregnancy but appears to be modifiable by glycemic control later in gestation.
Acquired inhibitor of von Willebrand factor-platelet interaction occurring in a 57 year-old female has been partially characterized. She had no personal or familial bleeding tendencies, but presented a subcutaneous hematoma of recent origin. She was diagnosed as having an acquired von Willebrand syndrome because she had low levels of FVIII complex in plasma, with platelet adhesiveness to glassbeads and RIPA decreased. This inhibitor was classified as an IgA immunoglobulin, and had no activity against any component of FVIII complex. The purified IgA by the chromatographic technology interacted with normal platelets to inhibit RIPA. Following 1-deamino-8-D-arginine vasopressin (DDAVP) infusion, she had higher immediate rise in all components of FVIII complex in plasma, with no rapid decline. Plasma von Willebrand factor (vWF) multimers analyzed by 1.5% SDS-AGE technology revealed to be identical with those of normal plasma. These studies suggest that the abnormality of ristocetin-induced vWF-platelet interaction by IgA RIPA inhibitor and the reduction of all vWF multimers (like type IA von Willebrand disease) may have a relationship with the pathogenesis of bleeding diathesis in this case.
A new case of acquired von Willebrand syndrome (AvWS) with Hashitoxicosis and pernicious anemia combined in a 73-years-old male is reported. He was admitted because of appetite loss and general malaise. Physical examination showed severe anemia and general edema. The red-cell count was 103 X 10(4)/microliters with a MCV of 122 fl; the white-cell count was 2,900/microliters with 24.5% hypersegmented neutrophils; the platelet count was 17.2 X 10(4)/microliters. the lactate dehydrogenase was 9,513 U/ml and vitamin B12 was 87 pg/dl. An aspirated specimen of bone marrow was diagnostic of megaloblastic anemia. The thyroid hormones were decreased with the thyroid stimulating hormone increased. From the immunological findings, the thyroid-test, microsome-test, and anti-intrinsic factor were positive, but M proteinemia and Bence Jones proteinuria were absent. Histology of the thyroid gland and the gastric mucosa established the diagnosis of chronic thyroiditis and chronic atrophic gastritis. Subcutaneous hemorrhages after veni-puncture were observed on admission. He had a normal bleeding time, but the coagulation studies indicated the presence of von Willebrand disease, but as his family and past history were negative, this suggested the presence of an AvWS. The analysis of von Willebrand factor (vWF) multimeric composition had showed the lack of the larger multimers in the plasma, but it was normalized after the administration of levothyroxine sodium and hydroxocobalamin with vWF: Ag/RCo ratio paralleled. As far as we know, this is the first report of AvWS with Hashitoxicosis and pernicious anemia combined.
Fujiwara trait, the first case of kininogen deficiency in Japan previously reported which did not show any clinical symptom except the prolonged activated partial thromboplastin time was further examined. The activated partial thromboplastin time of the patient was corrected by addition of normal, Factor XII deficient or Fletcher plasma, but not corrected by Fitzgerald or Williams plasma. It was also corrected by addition of highly purified bovine or human high molecular weight (HMW) kininogen, but not by low molecular weight (LMW) kininogen. When total kininogen was measured as the amount of bradykinin released by trypsin, only a trace amount was detected in Fujiwara as well as Williams plasma. No immunoreactive protein against anti-human-HMW-kininogen nor anti-human-LMW-kininogen was found in Fujiwara plasma. Acetone-kaolin-activated plasma kallikrein was not generated by Fujiwara plasma. Substitution with normal plasma in various ratios showed the generation of various plasma kallikrein activities. Calculations with these activities of mixed plasma gave the prekallikrein content of Fujiwara trait plasma about 30% of the normal level. These results suggest that Fujiwara trait is very similar to Williams trait in that both plasmas were deficient in HMW and LMW kininogens with reduced content of prekallikrein.
Explore the source record for details and available documents.
Asymptomatic, female, 56-year-old identical Japanese twins were found to have a severe abnormality in the surface-mediated intrinsic coagulation, fibrinolysis and esterolytic activity. These defects were thought to be due to the lack of Fitzgerald factor, because of the prolongations of kaolin-activated partial thromboplastin time and kaolin-activated euglobulin lysis time that were not corrected by the addition of Fitzgerald trait-plasma but were corrected to normal levels by the addition of isolated bovine high-molecular-weight kininogen, Fletcher trait-plasma or Hageman trait-plasma.
Explore the source record for details and available documents.
Asymptomatic identical twins were found to show the prolonged activated partial thromboplastin time, which was corrected by addition of normal, Hageman factor deficient or Fletcher trait plasma but not corrected by Fitzgerald or Williams plasma. The prolonged activated partial thromboplastin time was also corrected by addition of highly purified bovine high molecular weight kininogen but not by low molecular weight kininogen. When total kininogen was measured as the amount of bradykinin released by trypsin on acid treated plasma, only trace amount was detected in Fujiwara and Williams plasmas, although Fitzgerald plasma showed approximately 50% of the total kininogen of normal plasma level. Acetone-kaolin activated amidase activity of plasma kallikrein was not generated by Fujiwara plasma. Substitution with normal plasma in various ratios showed plasma kallikrein activity proportionally to the normal plasma contents. Extrapolation with the values at 120 min after activation gave the prekallikrein content of Fujiwara plasma as 30% of the normal value.
Explore the source record for details and available documents.
A blood coagulation deficiency was found at the contact phase in identical Japanese female twins. Of the four possible factors involved, Factor XI or XII can be ruled out according to cross-correction studies. The problem factor was probably not Fletcher factor, because the abnormal partial thromboplastin time was not significantly shortened by increasing the incubation period of plasma with kaolin. The deficiency is most likely due to the lack of Fitzgerald factor.
Explore the source record for details and available documents.
Explore the source record for details and available documents.