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Biomedical subjects

Y Inada

Publications and source records attributed to Y Inada.

At least 325 records · Page 18Linked to original sources
PubMed1983

Coupling between fatty acid binding and sulfhydryl oxidation in bovine serum albumin.

Albumin with and without a free sulfhydryl group (mercapt-albumin and nonmercapt-albumin) has low and high amounts of fatty acids, respectively. It was found that this difference was brought about by the following two mechanisms: (a) the binding of fatty acids increases the rate of oxidation of the sulfhydryl group, (b) the oxidation of the sulfhydryl group of the protein enhances the binding of fatty acids. The incubation of the protein with fatty acids enhanced reversibly the reaction rate of the free sulfhydryl group with 5,5'-dithiobis(2-nitrobenzoic acid). This effect of fatty acids depends on the kind of fatty acid added. Among saturated long-chain fatty acids tested, the shortest fatty acid, lauric (dodecanoic) acid, had the strongest effect. Oleic (cis-9-octadecenoic) acid, which has a long chain but also one cis-double bond, however, was as effective as lauric acid in enhancing the reactivity of the sulfhydryl group on the protein. Analyses with palmityl-Sepharose and equilibrium partitioning of palmitic acid between heptane and aqueous protein solutions have shown that nonmercapt-albumin has higher affinity to the fatty acid than mercapt-albumin. These results imply that the binding of fatty acids and the oxidation of sulfhydryl groups of the protein are intimately coupled.

Animals↗
PubMed1983

Ca2+- or Mg2+-dependent ATPase in plasma membrane of cultured endothelial cells from bovine carotid artery.

ATPase was found in plasma membrane of cultured endothelial cells from bovine carotid artery. The activity of the enzyme solubilized by octaethyleneglycol mono-n-dodecyl ether was enhanced by the addition of Ca2+ or Mg2+ and was not affected by F-actin and ouabain. Vmax was 2.8 and 10.0 mumol Pi/mg protein per h for Ca2+- and Mg2+-dependent activity, respectively, and the corresponding Km was 4.8 X 10(-4) M and 3.2 X 10(-4) M. Molecular weight of the protein was estimated to be approx. 250 000, as determined by activity-staining electrophoresis with polyacrylamide gels.

Adenosine Triphosphatases↗
PubMed1983

Modification of batroxobin with activated polyethylene glycol: reduction of binding ability towards anti-batroxobin antibody and retention of defibrinogenation activity in circulation of preimmunized dogs.

Amino groups of batroxobin (Bothrops atrox thrombic protease) were modified with 2,4-bis(O-methoxypolyethylene glycol)-6-chloro-s-triazine (activated PEG2). The modified batroxobin had the reduced binding ability towards anti-batroxobin antibody but retained its enzymic activity in vitro and in vivo. Administration of modified batroxobin in which 29% of the total amino groups in the molecule had been modified, to beagle dogs preimmunized with native batroxobin gave rise to a marked reduction of the fibrinogen level in plasma, accompanied with an increased level of fibrinogen (fibrin) degradation products, FDP. On the other hand, no reduction of fibrinogen level was observed when native batroxobin instead of modified batroxobin was injected to immunized dogs.

Animals↗
PubMed1983

Agonist-specific refractory states of bovine platelets-disappearance of synergism in aggregation.

The specificity of refractory state of bovine platelets developed by various agonists was examined. When bovine unwashed platelets were preincubated with 5-hydroxytryptamine (5HT) (or ADP), they became non responding to that agonist (refractory) but they responded quite normally to collagen, thrombin and ADP (or 5HT). When platelets became refractory to 5HT, the synergistic aggregation normally obtained with this agonist plus ADP was lost, but that with ADP plus thrombin was not changed. Platelets made refractory to ADP (or 5HT) after the aggregation and disaggregation cycle by the agonist responded normally to 5HT (or ADP). These results strongly indicate that platelets become refractory to one agonist without impairing the sensitivity to any other agonists.

Adenosine Diphosphate↗
PubMed1983

Identification of an essential histidine residue for fibrin polymerization. Essential role of histidine 16 of the B beta-chain.

An essential histidine residue for fibrin polymerization has been identified. It is the one located at position 16 in the B beta-chain of fibrinogen by the following experiments. Photooxidation of the activated NH2-terminal disulfide knot, which is derived from fibrin and contains the NH2-terminal binding domain, reduced the ability of this fragment to bind to fibrinogen-Sepharose conjugate. Functional and dysfunctional fragments were separated by the affinity chromatography just mentioned. Sequence analyses have revealed that the histidine residue which should be obtained in the second stage of the cleavage is missing in the dysfunctional fragment. The histidine residue which is supposed to be found at the eighth step, however, was not modified under our experimental conditions.

Amino Acid Sequence↗
PubMed1983

CV-3988 - a specific antagonist of platelet activating factor (PAF).

CV-3988, rac-3-(N-n-octadecylcarbamoyloxy)-2-methoxypropyl 2-thiazolioethyl phosphate was shown to be a specific inhibitor of platelet activating factor (PAF). This compound in concentrations of 3 x 10(-6) to 3 x 10(-5)M inhibited aggregation of rabbit platelets induced by PAF (3 x 10(-8)M), while it had no effect on the aggregation induced by arachidonic acid, ADP, collagen or A-23187. CV-3988 alone even at a concentration of 10(-3)M had no effect on platelet aggregation. The inhibitory action of CV-3988 on the PAF-induced aggregation was independent of the formation of micelles. The PAF (0.1 to 1.0 micrograms/kg, i.v.)-induced hypotension in anesthetized rats was also inhibited dose-dependently by the i.v. administration of CV-3988 (1 and 10 mg/kg), while the hypotensive actions induced by the i.v. administration of acetylcholine (1 micrograms/kg), arachidonic acid (1 mg/kg), bradykinin (10 micrograms/kg), isoproterenol (1 microgram/kg) and histamine (100 micrograms/kg) were not altered by CV-3988 (10 mg/kg, i.v.). All these findings indicate that CV-3988 specifically inhibits the action of PAF in vitro and in vivo. This is the first report of a PAF antagonist which can specifically inhibit the PAF-induced hypotension as well as the PAF-induced platelet aggregation.

Adenosine Diphosphate↗
PubMed1983

Nephelometric determination of plasminogen and plasmin inhibitors in human plasma using fibrin suspension as a substrate.

A nephelometric method is described for determination of plasminogen and two types of plasmin inhibitors in human plasma having different affinity toward plasmin. This method is based on the kinetic analysis of effects of whole plasma and plasmin inhibitor fraction obtained from plasma on the activity of exogenously added plasminogen which was determined by measuring the decrease of light scattering of fibrin suspension. With this method we have determined the activity of plasminogen and two types of inhibitors in the plasma of normal subjects and patients with high fibrinogen degradation product values. They include patients with various malignant tumors with DIC, chronic renal failure, sepsis, vascular diseases, and liver cirrhosis with hepatoma.

Female↗
PubMed1983

Studies on immune adherence (C3b) receptor activity of human erythrocytes: relationship between receptor activity and membrane osmotic fragility.

Although human erythrocytes (E) possess C3b receptors (C3b-R), their in vivo functions are unknown. We had observed that E from patients with immune complex diseases had defective or impaired C3b-R activity when circulating immune complexes (CIC) could be demonstrated. This phenomenon has been investigated in relation to membrane osmotic fragility of such E by a coil planet centrifugation (CPC) system. Osmotic fragility was defined by the hemolysis starting point (HSP), peak point (HPP) and end point (HEP) using NaCl osmotic gradient (150-30 mOsM) coiled tubes. It was observed that E with low C3b-R activity showed high osmotic fragility. Hemolysis of E with low C3b-R activity started at 104 +/- 8 mOsM (n = 133) compared to 97 +/- 3 mOsM (n = 18) of patients' E with normal C3b-R activity and 96 +/- 5 mOsM of E from normal healthy donors (n = 128). Furthermore, we observed that HSP shifted towards lower osmolarity with clinical and immunological improvement of disease activity after treatment with corticosteroids. When osmotic gradients were lower to 120-50 mOsM, 52 out of 116 E samples with low C3b-R activity separated into 2 E populations. In contrast, none of 18 E samples with normal C3b-R activity separated into 2 E populations. However, we observed broadened fragility patterns in these 18 E samples. Serial studies of C3b-R activity, osmotic fragility and the presence of CIC were performed in 7 patients. Improvement of disease activity was associated with increased C3b-R activity, decreased osmotic fragility and the disappearance of CIC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗