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Biomedical subjects

Y Higashi

Publications and source records attributed to Y Higashi.

At least 289 records · Page 16Linked to original sources
PubMed1988

Studies of fluorescence depolarization at high pressures of dimyristoylphosphatidylcholine liposomes containing poly(gamma-benzyl-L-glutamate).

The behaviors of four kinds of poly(gamma-benzyl-L-glutamate) (PBLG) molecules and their locations in dimyristoyl-phophatidylcholine (DMPC) liposomes were studied by fluorescence techniques at high pressures of up to 981 bar. The fluorescent substances 1,6-diphenyl-1,3,5-hexatriene (DPH), 1-aminonaphthalene-8-sulfonate (ANS) and PBLGs labeled with a dansyl group were used as probes of hydrophobic and hydrophilic spheres and the motions of polypeptides, respectively. The changes in mobilities of the PBLG molecules depended on their concentrations, degrees of polymerization and the lengths of hydrocarbon chains attached to their terminals. The molecular motions of the PBLGs were altered by increase in their contents, caused by squeezing the PBLG molecules out of the membranes. Models of the membranes and the behavior of polypeptides in the membranes at high pressures are discussed.

Dimyristoylphosphatidylcholine↗
PubMed1988

Actinomycosis of urachal remnants.

We report a case of urachal actinomycosis. The patient presented with complaints of micturition pain and a lower abdominal mass. Computerized tomography and an echogram showed the mass extending from the dome of the bladder to just beneath the rectus muscle. Exploration revealed a hard mass in the urachal cord, which was near the dome of the bladder and extended to the umbilicus. The mass and urachal cord were resected, and histopathological examination revealed actinomycosis of the urachal remnants.

Actinomycosis↗
PubMed1988

Role of phosphatidylserine in the cellular and subcellular lung distribution of quinidine in rats.

The role of phosphatidylserine in the cellular and subcellular lung distribution of quinidine was investigated in rats, since quinidine was found to bind preferentially to phosphatidylserine. The concentration of phosphatidylserine in the cellular and subcellular fractions was determined after separation by two-dimensional thin-layer chromatography. Selective accumulation of quinidine in vivo was observed in the alveolar macrophage at the cellular level and in the plasma membrane at the subcellular level. Both alveolar macrophages and plasma membranes were rich in phosphatidylserine compared to other fractions. When plasma levels were kept at steady state by i.v. infusion, the distribution of quinidine in the lung cellular and subcellular fractions was linearly correlated with the concentration of phosphatidylserine (r = 0.906). These results suggest that the concentration of phosphatidylserine is a dominant determinant of the cellular and subcellular lung distribution of quinidine.

Animals↗
PubMed1988

Aberrant splicing and missense mutations cause steroid 21-hydroxylase [P-450(C21)] deficiency in humans: possible gene conversion products.

Four steroid 21-hydroxylase B [P-450(C21)B] genes (designated P.7, P.10-1, P.10-2, and P.3) from three P-450(C21)-deficient patients were isolated to analyze their structures and functions. Several base changes were observed in the sequences of the four P-450(C21)B genes as compared to that of the functional B gene. Many of these base changes were identical to those of the P-450(C21)A pseudogene. The three DNAs (P.10-1, P.10-2, and P.3) produced no P-450(C21) activity in a functional assay for P-450(C21) by the COS cell expression system, while the P.7 DNA expressed the activity. The P.10-1 and P.10-2 DNAs were shown to have a point mutation in the second intron, causing aberrant splicing. The P.3 DNA carried three clustered missense mutations in the sixth exon, which impaired P-450(C21) activity. All these critical mutations could be seen in the corresponding site of the P-450(C21)A pseudogene. These data strongly suggest the involvement of gene conversion in this genetic disease.

Adrenal Hyperplasia, Congenital↗
PubMed1988

Evidence for frequent gene conversion in the steroid 21-hydroxylase P-450(C21) gene: implications for steroid 21-hydroxylase deficiency.

Oligonucleotide probes specific for the deleterious mutations harbored in the P-450(C21)A pseudogene and oligonucleotide probes specific for the corresponding sequences in the B gene were prepared to examine the molecular lesions in the P-450(C21) gene of P-450(C21)-deficient patients. Using these gene-specific probes, we performed Southern blot analyses of genomic DNAs from 11 patients and eight normal individuals. At least one allele of the B gene (the 3.7-kb TaqI fragment) in a patient was inactivated by mutations caused by recombination with the A gene. The A genes in normal individuals and patients seemed to be replaced frequently (i.e., 10/19 individuals) in their 3' portions by B gene sequences. All of these alterations occurred without changing the characteristic length (3.2 kb) of the TaqI fragment of the A gene, a result strongly suggesting that frequent gene conversions and/or intragenic recombinations have happened in the P-450(C21) genes. Densitometric analysis of the autoradiograms from hybridization experiments revealed extensive variation (from one to five copies) in the copy number of the A gene (the 3.2-kb TaqI fragment) whereas that of the B gene (the 3.7-kb TaqI fragment) was relatively constant at two or three copies.

Adrenal Hyperplasia, Congenital↗
PubMed1988

Fumaraldehydic acid-induced inactivation of aspartase.

Fumaraldehydic acid (FAA) induced a time-dependent inactivation of aspartase (L-aspartate ammonia-lyase, EC 4.3.1.1) from Escherichia coli at 30 degrees C and pH 7.4 following pseudo-first order kinetics. The rate of inactivation increased in proportion to the FAA concentration. In addition, the rate of inactivation increased, as the pH was increased. Determination of sulfhydryl groups showed that approximately one among 11 sulfhydryl groups was modified by FAA concomitant with the inactivation. L-Aspartate and fumarate protected the enzyme against FAA-inactivation, when Mg2+ ions were present. Unlike E. coli aspartase, P. fluorescens aspartase was not inactivated by FAA.

Ammonia-Lyases↗
PubMed1988

[Clinical study of extracorporeal shock-wave lithotripsy (ESWL) for renal and ureteral stones. The first report: end-results of 1,000 cases].

Between April, 1985 and May, 1987, we experienced 1,000 cases of extracorporeal shock-wave lithotripsy (ESWL) using a Dornier HM3. In the treatment of smaller stones, no auxiliary treatment was required. On the other hand, endourological treatments such as percutaneous nephrostomy, percutaneous nephroureterolithotomy, transurethral ureterolithotripsy or double J catheterization were combined in the treatment of larger stones. Sixteen percent of the cases were stone-free at the time of discharge from hospital but after more than 3 months 58.4% were stone-free, and including cases with insignificant residual fragments, the outcome was good in 84.2%. As major complications, cerebral bleeding due to autonomic nerve hyperreflexia was observed in one spinal cord injury patient, but generally speaking, the frequency of complications after ESWL was lower than after open surgery and the post ESWL period was rather comfortable for the patient. Surgical therapy for renal and ureteral stones will be performed mainly by ESWL. Manipulations of post-ESWL stone street or residual fragments are important, and detection of late complications is also important.

Adolescent↗
PubMed1988

Specific inhibition of aspartase by S-2,3-dicarboxyaziridine.

Aspartase of Escherichia coli was inhibited in a competitive manner by S-2,3-dicarboxyazirdine (DCAZ), an antibacterial substance against Aeromonas salmonesida. The inhibition constant (Ki) was 55 microM, which was as low as less than one tenth that of the Km value for the substrate, L-aspartate. In view of the fact that both aspartase and fumarase (J. Greenhut et al. (1985) J. Biol. Chem. 260, 6684-6686) were inhibited by DCAZ in competitive manners, common features of the reaction mechanism of the two enzymes were discussed.

Ammonia-Lyases↗