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Biomedical subjects

K Sakai

Publications and source records attributed to K Sakai.

At least 1,045 records · Page 58Linked to original sources

Anterior cervical fusion using the free vascularized fibular graft.

A free vascularized fibular graft with microvascular anastomoses was applied to six clinical cases of anterior cervical fusion for cervical spondylosis with myelopathy (two patients) and ossification of the posterior longitudinal ligament with myelopathy in four. The numbers of levels fused were three in five patients, and two in one. Their follow-up period ranged from 14 to 42 months (mean, 26 months). Union of the graft occurred between 2.5 and 5 months (mean, 3.4 months) postoperatively. There were no nonunions nor any serious complications. This technique is indicated for multilevel intervertebral fusion in which the nonunion or delayed union rate with conventional bone grafting may be high.

Cervical Vertebrae↗

Isolation and characterization of growth hormone from a marine fish, bonito (Katsuwonus pelamis).

Growth hormone (GH) was extracted under alkaline conditions (pH 10) from pituitary glands (6.3 g) of bonito (Katsuwonus pelamis), and subsequently purified by gel filtration, ion exchange chromatography, and reversed-phase HPLC. The GH was monitored by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and by immunoblotting with yellowtail GH antiserum at each step of purification. GH activity was determined by an in vivo bioassay. The yield of this hormone was 4.8 mg/g wet tissue. Intraperitoneal injection of bonito GH at doses of 0.1 and 1 micrograms/g body wt at 7-day intervals resulted in a significant increase in body weight and length of juvenile rainbow trout. Bonito GH antiserum exhibited both species and hormone specificity in radioimmunoassay. However, the bonito GH antiserum as well as yellowtail GH antiserum exhibited hormone specificity but not species specificity in immunoblotting. A molecular weight of 21,000 and an isoelectric point of 7.0 for bonito GH were estimated by SDS-PAGE and gel electrofocusing, respectively. The complete amino acid sequence of 185 residues was determined by sequencing fragment peptides prepared by chemical and enzymatic cleavages. Sequence comparison of bonito GH with other GHs revealed that there is a significant deletion in the middle of the molecule.

Amino Acid Sequence↗

Effects of AN-132 and quinidine, antiarrhythmic agents, on plasma digoxin concentrations in rats.

The effects of AN-132, 3-(diisopropylaminoethyl-amino)-2',6'-dimethylpropionanilide.2H 3PO4, on chloroform-induced arrhythmias and plasma digoxin concentrations have been compared with those of quinidine in rats. AN-132 (0.01-3 mg kg-1) administered orally significantly inhibited the incidence of cardiac arrhythmias in a dose-related fashion. A single dose of digoxin (1 mg kg-1) given orally for 7 consecutive days was followed, on day 8, orally by digoxin alone, or together with AN-132 (50, 100 and 200 mg kg-1) or quinidine (25 and 50 mg kg-1). The AUC0-24 and Cmax of plasma digoxin were enhanced significantly by co-administration of quinidine, but not by AN-132.

Anilides↗

Glycogenolysis in the rat isolated perfused liver as a measure of chemically induced liver toxicity.

The relationship between chemically induced glycogenolysis and decreased thiol content in the rat isolated, perfused liver has been examined. Chemicals such as 2,4-dinitrophenol (DNP), diethyl maleate, alcohols and anti-inflammatory agents (except for sodium salicylate) accelerated glycogenolysis. Protein thiol loss correlated well with a marked increased rate of glucose release. Non-protein thiol loss, without significant loss of protein thiol, caused by a slight increase in the rate of glycogenolysis compared with controls. Since it has been reported that protein thiol loss rather than non-protein thiol loss is correlated to liver cell injury, a marked glucose release from the perfused liver may be a convenient measure of hepatic toxicity for a variety of chemicals.

Animals↗

The effects of salicylate concentration on the uptake of salicylate and cefmetazole into rat isolated small intestinal epithelial cells.

The uptake of salicylate into rat isolated small intestinal epithelial cells reached an equilibrium within 15 min, but that of cefmetazole alone did not. The presence of salicylate at concentrations greater than 50 mM accelerated the uptake of cefmetazole, which reached equilibrium within 5 min. At equilibrium, the uptake clearance of salicylate (mumol (g protein)-1 M-1 initial salicylate concn) was greater than that of cefmetazole. The uptake clearance of salicylate during the first several minutes was concentration-dependent, and a 'super-uptake' clearance of salicylate, greater than equilibrium values, was observed when 100 mM salicylate was present. This indicates that some mechanism, other than a simple diffusion process, may be involved in salicylate uptake into these cells.

Animals↗

Protective effect of salicylate against 2,4-dinitrophenol-induced protein thiol loss in the small intestine of rats.

The effect of the content of protein thiols and non-protein thiols in the tissue of the rat small intestinal loop on the absorption of cefmetazole has been investigated. 2,4-Dinitrophenol (DNP), at a concentration of 500 microM, caused rapid protein thiol loss, followed by non-protein thiol loss, along with a decrease of cefmetazole absorption by the intestine. The coadministration of 75 mM salicylate with DNP inhibited the effect of DNP on protein thiols and cefmetazole absorption but not on non-protein thiol loss by DNP.

2,4-Dinitrophenol↗

Enhancement of adenosine-induced relaxant responses of the guinea-pig isolated taenia coli and aortae by a novel nootropic agent BY-1949: comparison with dipyridamole.

In muscle strips of guinea-pig taenia coli and aortae, the effects of 3-methoxy-11-methyldibenz[b,f][1,4]oxazepine-8-carboxylate (BY-1949) on the relaxant response to adenosine have been compared with those of dipyridamole. BY-1949 (3 x 10(-5)-10(-4) M) as well as dipyridamole (3 x 10(-7)-10(-5) M) resulted in a significant potentiation of relaxant responses to a cumulative administration of adenosine (10(-6)-10(-3) M), but the drugs did not affect the response to noradrenaline and acetylcholine. The results indicate that BY-1949 exerts a selective potentiating effect on reactivity to exogenous adenosine.

Adenosine↗

Differences in cytopathogenicity and host cell range among infectious molecular clones of human immunodeficiency virus type 1 simultaneously isolated from an individual.

A cytopathic human immunodeficiency virus type 1 (HIV-1) isolate containing multiple virus genotypes was molecularly cloned, and the biological activity of six randomly selected clones was assessed by transfection into human lymphoid or glial cell lines. Five infectious clones of HIV-1, termed N1T-A through -E, were isolated in this manner. Clones N1T-A, -B, -C, and -E could be distinguished by restriction endonuclease mapping whereas clones N1T-B and -D had identical maps with the enzymes used. Each clone exhibited a distinct host cell range as well as markedly different infection kinetics and cytopathogenic properties when tested in human cell lines of T-lymphocytic, monocytic, and astrocytic origin. In particular, infection with HIV-1 clone N1T-E was characterized by slow kinetics and lack of significant cytopathic effects in acutely and chronically infected cells. Clone N1T-A, similar to the parental isolate N1T, exhibited a wide host cell range, fast kinetics of infection, and high cytopathogenicity. These data indicate that HIV-infected individuals may carry multiple HIV-1 genotypes with distinct cytopathogenic potential and cell tropism. Analysis of virus isolates must take into account the contribution, or masking, of individual virus clones.

Acquired Immunodeficiency Syndrome↗

Investigations into the mechanism of the antihypertensive effect of SGB-1534, a novel alpha 1-adrenoceptor antagonist, in rats.

Experiments in vitro and in vivo were undertaken to examine possible involvement of a central effect in the hypotensive mechanism of SGB-1534. SGB-1534 selectively antagonized the contraction of isolated rat aortae to phenylephrine with a pA2 value of 10.57, 3.9 times higher than prazosin, and markedly displaced the alpha 1-adrenoceptor ligand 3H-prazosin (pKi: 8.81) in rat brain. In anesthetized spontaneously hypertensive rats (SHRs), SGB-1534 (0.3-3 micrograms/kg) and prazosin (3-30 micrograms/kg) given intravenously (i.v.) and intracerebroventricularly (i.c.v.) produced a dose-dependent and long-lasting depressor response associated with no change in heart rate (HR). The two drugs (i.c.v.), however, significantly attenuated the pressor response to i.v. noradrenaline. Single i.v. injections of SGB-1534, prazosin and yohimbine dose-dependently inhibited the St 587 (a highly specific and centrally acting alpha 1-adrenoceptor agonist) enhanced flexor reflex and the pressor response to i.v. phenylephrine in pithed rats. However, the activities of SGB-1534 and prazosin in inhibiting the St 587-enhanced flexor reflex were 16,000 and 660 times, respectively, less than those in attenuating the pressor response to i.v. phenylephrine. It seems that the hypotensive action of SGB-1534 is due to the peripheral alpha 1-adrenoceptor antagonistic mechanism rather than the central one.

Adrenergic alpha-Antagonists↗