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Biomedical subjects

T Komai

Publications and source records attributed to T Komai.

At least 73 records · Page 4Linked to original sources

Poly(O-acyl hydroxy L-proline) (II) wetting characteristics and blood clotting on surfaces of poly O-acetyl, butyryl, hexanoyl, dodecanoyl, and benzoyl hydroxy L-proline.

Poly O-acetyl, butyryl, hexanoyl, dodecanoyl, and benzoyl hydroxy L-proline (poly[O-acyl Hyp]s) were evaluated as materials for blood contact by means of contact angle and blood clotting time measurements. Critical surface tensions obtained from Zisman plots for all materials were 22-29 dyn/cm, suggesting that these materials may exhibit good blood compatibility. Dispersion and nondispersion force contributions to the surface tension were gamma ds = 1.4, gamma ns = 49.3 dyn/cm, (11.0, 16.2), (19.8, 3.8), (21.2, 4.6) and (14.1, 10.8) for the poly(O-Acetyl, Butyryl, Hexanoyl, Dodecanoyl and Benzoyl Hyp) surfaces, respectively. The materials showed remarkable wetting differences that were dependent on the type of acyl group attached to Hyp. The values of the dispersion and nondispersion components of the surface tension for poly(O-hexanoyl Hyp) and poly(O-dodecanoyl hyp) were very close to those obtained for glutaraldehyde-treated umbilical cord vessels. The blood clotting times on the respective polymer surfaces, obtained by using the kinetic method, were normalized to those of control glass and siliconized glass surfaces. All the poly(O-acyl Hyp)s surfaces showed longer clotting times than those of the poly(L-proline) and glass surfaces. The surfaces of those polymers having longer aliphatic or aromatic acyl groups had longer clotting times than those of the polymers with relatively shorter groups.

Blood Coagulation↗

Wetting characteristics and blood clotting on surfaces of copoly(gamma-Benzyl-L-glutamate, gamma-hydroxyethyl-L-glutamine).

The film surface of poly(gamma-benzyl-L-glutamate) (PBLG) was modified with 2-aminoethanol to enhance its hydrophilicity. Controlling the reaction conditions of PBLG and 2-aminoethanol, various types of copoly(gamma-benzyl-L-glutamate, gamma-hydroxyethyl-L-glutamine) film surfaces were obtained. Surface free energy (gamma sv), the dispersive component of gamma sv (gamma dsv), the nondispersive component of gamma sv (gamma psv), and the interfacial free energy of polymer surface with water (gamma sw), which were obtained by using the contact angle measurement and calculation method proposed by Andrade et al., were changed remarkably by the aminolysis. The gamma sv value increased after 2 h of aminolysis from 48.2 (PBLG) to 65.3 dyn/cm and gradually increased to around 70 dyn/cm after 12 h reaction. (gamma dsv) and (gamma psv) changed from 31.0 and 17.2 dyn/cm (PBLG) to 26.5 and 44.3 dyn/cm, respectively. These parameters of the material surfaces, modified over 12 h reaction, were found to be similar to those of the surfaces of canine aorta, vein, and human fibrin membrane. Blood clotting times on these polymer surfaces were comparatively longer than on siliconized glass surfaces.

Blood Coagulation↗

[Traumatic hemorrhage in the basal ganglia in the child. Five cases].

Traumatic hemorrhages in the basal ganglia were seen in five children. The CT findings and the characteristics of these injuries were discussed. All of children were injured in car accidents. They ranged in age from 3 to 13 years. The patients comprised 3 boys and 2 girls. On admission, case 1 was conscious and case 2 was in a stupor. Case 1 and 2 were mild cases in which spotty hematomas were seen in the ganglionic region. They recovered fully. Case 3-5 were severe cases in which massive hematomas were seen in the ganglionic region. On admission, their consciousness ranged from stupor to coma. We performed operations on two of them but their recoveries were unsatisfactory. Their results were as follows. One had residual hemiparesis and dysarthria, one experienced tetraparesis and dysarthria and the last went from coma to a vegetative state. Concerning the directions of the impacts, 4 were hit in the frontal region or face and the last one received blows on the occipital region. Skull fractures were seen in two cases. Mandibula and clavicula fractures were seen in the other two cases. Only one child had no fractures. We conclude that pediatric traumatic hemorrhages in the basal ganglia are induced by severe impact on the frontal or occipital regions. The size of hematomas in this injury is spotty or massive. The massive type has a poor prognosis. On the other hand, the spotty type's prognosis is good. We speculate that impact to the head causes a shear strain in the ganglionic region. At that time, vessels in the area are injured.

Adolescent↗

Generation of low-level chemiluminescence during the metabolism of 1-naphthol by rat liver microsomes.

The metabolism of 1-naphthol in rat liver microsomal fractions supplemented with NADPH is accompanied by low-level chemiluminescence which reflects the formation of molecular excited states. Photoemission consists of two phases which both are dependent on microsomal protein and 1-naphthol concentration. The involvement of cytochrome P-450 in the microsomal metabolism of 1-naphthol was indicated by an inhibition of chemiluminescence by aminopyrine or metyrapone. Oxygen is required for light emission. Whereas phase I is hardly influenced by superoxide dismutase, phase II is suppressed. Chemiluminescence was not associated with malondialdehyde accumulation, in contrast to NADPH-dependent lipid peroxidation in microsomal fractions in the absence of 1-naphthol. Phase I of chemiluminescence appears to directly reflect cytochrome P-450-dependent hydroxylation, and phase II is attributed to redox cycling of products arising from these reactions, e.g. the 1,4- and/or 1,2-naphthoquinones as oxidation products of the corresponding dihydroxynaphthalenes.

Aminopyrine↗

Protection against reactive oxygen species by NAD(P)H: quinone reductase induced by the dietary antioxidant butylated hydroxyanisole (BHA). Decreased hepatic low-level chemiluminescence during quinone redox cycling.

Menadione elicits low-level chemiluminescence (lambda greater than 620 nm) associated with redox cycling of the quinone in mouse hepatic postmitochondrial fractions. This photoemission is suppressed when the animals are fed a diet containing the anticarcinogenic antioxidant, 2[3]-(tert-butyl)-4-hydroxyanisole (BHA), which leads to a 13-fold increase in NAD(P)H: quinone reductase (EC 1.6.99.2). Inhibition of the enzyme by dicoumarol completely abolishes the protective effect of BHA treatment and leads to higher chemiluminescence, reaching similar photoemission for BHA-treated and control animals. These findings indicate that the two-electron reduction promoted by quinone reductase prevents redox cycling and that BHA protects against reactive oxygen species by elevating the activity of this enzyme.

Animals↗

Experimental urinary bladder reconstruction using a synthetic poly(alpha-amino acids) membrane.

Biodegradability of the poly(epsilon-benzyloxycarbonyl-L-lysine) membrane was tested for use as a biodegradable graft for the reconstruction of rabbit urinary bladder. Rabbit urinary bladder was exposed through a midline incision under general anesthesia and segmental resection with full thickness was done, with replacement by this synthetic membrane. The membrane was gradually reabsorbed, serving as a framework of support for regeneration of normal bladder tissues. Follow-up study at 1 year revealed no urinary tract complications, such as bladder stones or urinary tract infection. Also, no disturbance of renal function was demonstrated. Bladder capacity remained within normal limits and bladder functions were almost normal. These results indicate that biodegradable membrane may be well suited to this clinical use.

Animals↗

Wetting characteristics and blood clotting on surfaces of acylated chitins.

Various acylated chitins, including formyl, acetyl, propionyl, butyryl, caproyl, capryl, lauroyl, and benzoylchitin, were evaluated as materials for blood contact surfaces by means of contact angle and blood-clotting time measurements. Critical surface tensions of acylated chitins varied within the range of 20-30 dyn cm-1 and were dependent on the length of the acyl side chains. Furthermore, the dispersion and nondispersion components of the surface tension show remarkable differences which are dependent on the type of acyl group attached to chitin. The chitin derivative with 2.0 acetyl groups per N-acetylglucosamine residue gave values of the dispersive and nondispersive components of the surface tension that are very close to those obtained for glutaraldehyde-treated umbilical cord vessels. All of the acylated chitin surfaces show longer clotting times than the original chitin surface.

Acylation↗

Arylsulfatases of human-lung tumors transplanted into athymic mice. Cancer-associated modification of arylsulfatase B variant.

The activities and properties of arylsulfatase A and B from human lung carcinoma transplanted into athymic mice were demonstrated. The activities of arylsulfatase A and B from transplanted carcinomas with four histological types were more than twofold higher as compared to those from surgical tumors, except for arylsulfatase A activity in blastoma. Arylsulfatase B in transplanted tumors was almost completely replaced, except for blastoma, by an anionic B variant (B1) which was a minor component of arylsulfatase B in surgical lung tumor and absent in normal human lung. The properties of arylsulfatases A and B from transplanted tumors were essentially identical, respectively, with those from normal lung or surgical tumors in respect of molecular weight, heat stability, pH optimum, isoelectric point (pI), Km, time course profile and substrate specificity. Arylsulfatase B1 showed the properties similar to B enzyme except for net charge. The cause of the negative charge of tumor B1 enzyme was investigated. By the action of phosphatase, which was added exogenously or had been persistently included in the partially purified enzyme preparation, B1 enzyme (pI 7.5) shifted to about pI 8.2. Treatment of B1 enzyme with neuraminidase, concomitant with the endogenous phosphatase, resulted in marked increase (pI 9.5) of the isoelectric point, identical to that of arylsulfatase B. Thus, it is most probable that tumor B1 enzyme is modified by additional sialic acid and phosphate bound to arylsulfate B.

Animals↗

Relationship between inhibition of pressor response to angiotensin I and blood concentration of captopril following a single oral administration to dogs.

The time courses for the inhibition of the pressor response to AI and for the blood concentration of captopril and its metabolites were determined following a single oral administration of captopril at a dose of 0.8 or 2.5 mg/kg to normal dogs. Captopril was rapidly absorbed from the gastro-intestinal tract attaining a maximum blood concentration 1-1.5h after its administration. The inhibition of the pressor response to AI was closely related with the blood concentration of unchanged captopril but not of total captopril. The blood concentrations of captopril which produced 50 and 100% inhibition were estimated to be 0.1 and 0.4 millimicron/ml respectively. At 2.5 mh/kg the maximum blood concentration attained was 4 times higher than the concentration required to completely inhibit the pressor response to AI, suggesting that a fraction of the absorbed captopril was in excess of the therapeutic requirement.

Administration, Oral↗

In vitro studies on the metabolic pathway of SQ 14225 (Captopril) and mechanism of mixed disulfide formation.

The metabolic pathway of SQ 14225 (Captopril) and the mechanism of the mixed disulfide formation with endogenous sulfhydryl compounds were studied in in vitro cell free systems. In the rat liver 9000 x g supernatants, SQ 14225-14C was metabolized to one major metabolite, glutathione-SQ 14225 mixed disulfide (GSSQ), and two minor metabolites including SQ 14551, a symmetrical disulfide of SQ 14225. The formation of GSSQ was markedly accelerated by the addition of oxidized glutathione (GSSG), but not affected by the addition of reduced glutathione (GSH), indicating that GSSQ was formed by the thiol-disulfide interchange between SQ 14225 and GSSG. Although the thiol-disulfide interchange was also observed between SQ 14225 and L-cystine, L-homocystine and SQ 14551 as well as GSSG, only the formation of GSSQ was a rapid reaction and markedly decreased by heat treatment of the liver 9000 x g supernatants. These findings demonstrate that the formation of GSSQ is catalyzed by a GSSG specific enzyme which is supposed to be thioltransferase (Glutathione: Disulfide Oxidoreductase). Although GSSQ was stable in the rat liver 9000 x g supernatants, it was rapidly hydrolyzed to cysteine-SQ 14225 mixed disulfide (CySSQ) in the rat kidney 9000 x g supernatants. A specific inhibitor of gamma-glutamyltranspeptidase, anthglutin, inhibited the hydrolysis. GSSQ-14C administered to a beagle dog was excreted into the urine in the form of CySSQ. Thus, it was speculated that CySSQ excreted into the urine as a major metabolite of SQ 14225 was derived from GSSQ formed in the liver followed by hydrolysis in the kidney.

Animals↗