Human plasminogen polymorphism in Japanese: a new variant and relative activities of plasminogen among phenotypes.
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Biomedical subjects
Publications and source records attributed to K Matsui.
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In 48 normotensive women with epidemiologic high-risk factors for pregnancy-induced hypertension, the angiotensin sensitivity test was performed serially between 26 and 32 weeks of gestation. If an effective pressor dose of less than 12 ng/kg per minute was considered to be a positive test result, 20 subjects were positive at 30 weeks of gestation and destined to develop pregnancy-induced hypertension. Of ten subjects with a false-positive test result, seven patients developed proteinuria and/or clinically significant edema without apparent hypertension, and only three subjects remained normal throughout their pregnancy. Twenty-eight subjects with negative test results had uneventful pregnancies. Before 30 weeks' gestation, it was difficult to identify all patients destined for pregnancy-induced hypertension. Although high false-positive test results were detected, these results suggest that an angiotensin sensitivity test at 30 weeks' gestation represents an appropriate means of identifying women who remain normal throughout pregnancy. Careful follow-up should be undertaken in all patients with positive test results.
In nursing, if we know an elderly person's mental condition, and that which does not make him/her too tired, this method can be very useful. Using this method we predicted the MAS score from scores of Y-G scales. We obtained the MAS score results by the following formula: MAS score not equal to 0.31 X Lack of objectivity +0.41 X Inferiority feelings -0.15 X Ascendance +0.34 X Y-G Nervousness +0.30 X Y-G Depression +9.54.
Pregnant women destined to develop pregnancy-induced hypertension lose refractoriness to the pressor effects of infused angiotensin II. The effect of calcium supplementation on the vascular sensitivity to angiotensin II was investigated in pregnant women. We administered orally 600 mg of calcium L-aspartate daily to 22 pregnant women from 20 weeks of gestation to delivery. The values for the effective pressor dose of angiotensin II in the calcium-supplemented women were compared with those in 72 nonsupplemented pregnant women. The vascular sensitivity was significantly decreased after calcium supplementation. The values for the effective pressor dose of angiotensin II in the calcium-supplemented patients were 18.1 +/- 1.2 ng/kg/min at 20 weeks of gestation, 32.2 +/- 2.6 ng/kg/min at the twenty-sixth week, 41.1 +/- 3.4 ng/kg/min at the thirtieth week, and 25.9 +/- 2.9 ng/kg/min at the thirty-sixth week (mean +/- SEM), while those in the nonsupplemented patients were 17.3 +/- 1.2, 17.7 +/- 1.6, 17.6 +/- 1.2, and 15.0 +/- 1.6 ng/kg/min, respectively. Assessment of the changes in the effective pressor dose of angiotensin II in the individual patients indicated that the percentile changes from 20 weeks of gestation in the calcium-supplemented patients were also significantly greater than those in 22 nonsupplemented patients. These findings suggest that calcium supplementation tends to reduce the vascular sensitivity in pregnancy. The present dosage of calcium did not affect the blood chemical parameters and did not reduce the blood pressure. The incidence of pregnancy-induced hypertension in the calcium-supplemented patients was 4.5%, which was smaller than that (21.2%) in the nonsupplemented patients. Although there is no clear explanation of the mechanisms involved in such an effect of calcium, the present results do provide evidence to support the idea that oral calcium intake can prevent the onset of pregnancy-induced hypertension.
When guinea pig lymphocytes were cultured with 1-oleoyl-2-acetyl-glycerol (OAG), A23187, and cholera toxin, ornithine decarboxylase activity was induced synergistically, peaking at 6 h. Addition of 12-O-tetradecanoyl-phorbol 13-acetate (TPA), A23187, and dibutyryl cAMP caused the same kind of induction. Cholera toxin potentiated the ability of A23187 to induce ornithine decarboxylase, but not that of OAG. Dibutyryl cAMP augmented the induction caused by A23187 but not by TPA. These results suggest that both the activation of Ca++-sensitive, phospholipid-dependent protein kinase (protein kinase C) and the increase in intracellular levels of Ca++ and cAMP are necessary for this induction. cAMP may potentiate the induction by modulating a Ca++ messenger system other than that for protein kinase C activation.
Plasminogen activator is one of the principal enzymes involved in the fibrinolytic system. The plasminogen activator activity in placental tissue was examined using a chromogenic substrate in 9 patients with pre-eclampsia and in 9 women with uncomplicated pregnancy, who were delivered between 37 and 42 weeks of gestation. In the patients with pre-eclampsia, the plasminogen activator activity was significantly (P less than 0.05) decreased compared with that in the control group of normal pregnant women. The present findings suggest a decreased fibrinolytic activity in the placental tissue of pre-eclamptic patients, which is responsible for fibrin deposition in the placental tissue and may contribute to placental ischemia and insufficiency in pre-eclampsia.
We report a rare case of eclampsia which occurred during the 18th gestational week in the absence of hydatidiform disease or Rh isoimmunization. In spite of extensive examinations during pregnancy and postpartum, we were unable to find any underlying disease, and the patient returned to being normotensive and non-proteinuric postpartum.
A case involving transitional cell carcinoma of the renal pelvis with extension to the main renal vein and inferior vena cava as well as massive involvement of the kidney and ureter is reported. A review of the literature on renal pelvic tumors and patterns of tumor growth is presented.
Novel cloning vectors for glutamic acid-producing bacteria have been constructed. Two cryptic plasmids, pAM330 from Brevibacterium lactofermentum and pHM1519 from Corynebacterium glutamicum, were used as precursors, and recombined with pBR325 or pUB110. Resultant composite plasmids were able to propagate and to express the CmR or KmR phenotype in B. lactofermentum and C. glutamicum. A smaller, high-copy-number plasmid, pAJ43, was also isolated following deletion of a part of the pAM330-pBR325 composite plasmid. Furthermore, a cosmid vector, which can be packaged and transduced through phage infection, has been developed using a cohesive-end fragment of the f1A phage and plasmid pAJ43. These plasmids are suitable for use as cloning vectors in the glutamic acid-producing bacteria.
Human urine urokinase [EC 3.4.21.31] was found to be inactivated by dithiothreitol (DTT) much more severely than by 2-mercaptoethanol at the same concentration on the basis of -SH groups. Removal of DTT by dialysis restored the activities of esterase toward acetyl-glycyl-L-lysine methyl ester, plasminogen activation, and amidase toward 7-(glutaryl-glycyl-L-arginine-amido)-4-methyl coumarin. But the restoration of amidase activity was much less than that of esterase activity. The addition of DTT mediated the conversion of high molecular weight urokinase to low molecular weight urokinase, releasing several peptides. This suggests that the urokinase consists of several polypeptides linked by disulfide bonds. The molecular weight of urokinase produced with DTT was smaller than that of low molecular weight urokinase obtained by autodigestion of high molecular weight urokinase. The autodigestion was also accompanied by liberation of some peptides. But, those peptides released on autodigestion of high molecular weight urokinase were different from those appearing in the presence of DTT.
3-Ketovalidoxylamine A C-N lyase was purified about 900-fold from the cell-free extract of Flavobacterium saccharophilum by ammonium sulfate fractionation, column chromatography on CM cellulose and gel filtration on Sephacryl S-200. The purified enzyme was homogeneous as judged by sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis. The molecular weight of the enzyme was estimated to be 36,000 by gel filtration on Sephacryl S-200 and by SDS polyacrylamide gel electrophoresis, indicating that the enzyme is a monomer. The optimum pH was found at 9.0. The enzyme activity was inhibited by EDTA or ethyleneglycol bis(beta-aminoethylether)-N,N'-tetraacetic acid and the inhibition was reversed by Ca2+ ion. The enzyme was able to eliminate p-nitroaniline or p-nitrophenol from p-nitrophenyl-3-ketovalidamine (IV) or p-nitrophenyl-alpha-D-3-ketoglucoside (VI), but not from p-nitrophenyl-1-epi-3-ketovalidamine or p-nitrophenyl-beta-D-3-ketoglucoside. Apparent Km values for IV and VI were 0.24 mM and 0.5 mM, respectively.
Chronic renal lesion with membranous changes and massive proteinuria similar to human membranous nephropathy was induced in rats through repeated intravenous injections of gamma-globulin fraction of rabbit anti-rat F X 1A antisera (GRAFA) 0.37-1.5 mg/100 g body weight. The injections were administered every 2 or 3 days over a 68-day period for a total of 26 times. It is suggested that a sufficient amount of GRAFA was given to the rats to induce renal lesion, judging from the result that no remarkable differences were observed between the severity of the histopathological and clinical changes in each rat given the various doses of GRAFA. Furthermore, this renal lesion is considered to correspond to human membranous nephropathy morphologically and clinically, judging from the fact that the protein excretion was kept at a plateau, and the capillary lumen was kept almost intact with advanced membranous changes.
Chronic chemical denervation of the sympathetic nervous system with 6-OH dopamine resulted in an augmentation of the coronary blood flow (CBF) increase inherent in the canine heart-lung preparation, but not in an augmented accumulation of 6-keto PGF1 alpha in the circulating blood. In denervated HLP, 6-keto PGF1 alpha was lower and the vasodilator response to PGI2 larger at the start of the experiments. It was concluded that exaggerated increase in CBF was due to a potentiation of the vasodilator response to PGI2.
Using the microelectrode technique, the effects of l-carnitine (LC) and acetyl-l-carnitine (ALC) on the changes in the transmembrane action potential of the canine ventricular muscle induced by palmityl-l-carnitine (PLC) were studied in comparison with those of disopyramide (D). LC (5 X 10(-3) M) itself had no effect on the electrophysiological parameters of the ventricular muscle. ALC (5 X 10(-3) M) increased the maximum rate of rise (dV/dt max) slightly and decreased the action potential duration (APD), although these changes were not statistically significant. D (1.5 X 10(-3) M) decreased dV/dt max and prolonged APD and the absolute refractory period (ARP). PLC (3 X 10(-4) M) decreased the resting membrane potential, action potential amplitude and dV/dt max, and it shortened APD and ARP. LC and ALC (5 X 10(-3) M) improved the electrophysiological derangement produced by PLC to the same degree. On the other hand, application of D (1.5 X 10(-5) M) resulted in no improvement of the electrophysiological derangement produced by PLC.
The effects of thiamine tetrahydrofurfuryl disulfide (TTFD) on the gradual increase in the coronary blood flow (CBF) inherent in the canine heart-lung preparation were studied. TTFD is a disulfide-type derivative of thiamine reported to have an antiinflammatory effect in experimental animals. Since it was found that the substance could reverse the gradual increase in CBF, the possibility that the reversal was brought about through an inhibition of activation of the arachidonic acid cascade-line was tested, examining the effects of this substance on the CBF increase produced by arachidonic acid (AA) and prostacyclin (PGI2). The vasodilator response to AA, which was barely detectable at the start of the experiment at which CBF was at a physiological low level, became potentiated as the gradual increase in CBF occurred, returning to the initial magnitude after TTFD, while the vasodilator response to PGI2 remained essentially unchanged during the entire course of the experiment. It was concluded that TTFD reversed the gradual increase in CBF in the HLP through the inhibition of the arachidonic acid cascade-line activation.
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