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Biomedical subjects

Y Hidaka

Publications and source records attributed to Y Hidaka.

At least 199 records · Page 11Linked to original sources
PubMed1988

Identification of a single nucleotide change in a mutant gene for hypoxanthine-guanine phosphoribosyltransferase (HPRT Ann Arbor).

HPRT Ann Arbor is a variant of hypoxanthine (guanine) phosphoribosyl-transferase (HPRT: EC 2.4.2.8), which was identified in wo brothers with hyperuricemia and nephrolithiasis. In previous studies, this mutant enzyme was characterized by an increased Km for both substrates, a normal Vmax, a decreased intracellular concentration of enzyme protein, a normal subunit molecular weight and an acidic isoelectric point under native isoelectric focusing conditions. We have cloned a full-length cDNA for HPRT Ann Arbor and determined its complete nucleotide sequence. A single nucleotide change (T----G) at nucleotide position 396 has been identified. This transversion predicts an amino acid substitution from isoleucine (ATT) to methionine (ATG) in codon 132, which is located within the putative 5'-phosphoribosyl-1-pyrophosphate (PRPP)-binding site of HPRT.

Base Sequence↗
PubMed1988

Chronic recurrent anterior luxation of the mandible. A review of 12 patients treated by the LeClerc procedure.

A follow-up study was performed on 12 patients surgically treated because of chronic recurrent anterior dislocation of the temporomandibular joint by the LeClerc procedure which was refined by Gosserez & Dautrey. In all of the 12 patients, there had been no recurrence of the dislocation since the operation (follow-up period: up to 5 years and 3 months). This procedure did not disturb normal functional movement of the joint, yet prevented excessive forward excursion of the condyle. The surgical technique is presented and the results of this operation are evaluated.

Adolescent↗
PubMed1988

Human adenine phosphoribosyltransferase deficiency. Demonstration of a single mutant allele common to the Japanese.

Complete adenine phosphoribosyltransferase (APRT) deficiency causes 2,8-dihydroxyadenine urolithiasis. In previous reports, analysis of the kinetic properties of APRT from APRT-deficient Japanese subjects revealed strikingly similar abnormalities suggesting a distinct "Japanese-type" mutation. In this paper, we report studies of 11 APRT-deficient lymphoblast cell lines. Nucleotide sequence analysis of APRT genomic DNA from WR2, a Japanese-type homozygote, identified a T to C substitution in exon 5, giving rise to the substitution of threonine for methionine at position 136. RNase mapping analysis confirmed this mutation in WR2 and revealed that six other Japanese-type homozygotes carry the same mutation on at least one allele. The remaining Japanese subject, who does not express the Japanese-type phenotype, did not demonstrate this mutation. Southern blot analysis showed that all seven Japanese-type subjects were confined to one TaqI restriction fragment length polymorphism (RFLP) haplotype. These studies provide direct evidence for the nature of the mutation in the Japanese-type APRT deficiency.

Adenine Phosphoribosyltransferase↗
PubMed1987

Mode of disulfide bond formation of a heat-stable enterotoxin (STh) produced by a human strain of enterotoxigenic Escherichia coli.

To determine the modes of three disulfide linkages in the heat-stable enterotoxin (STh) produced by a human strain of enterotoxigenic Escherichia coli, we synthesized STh(6-18), which consists of 13 amino acid residues and has the same intramolecular disulfide linkages as native STh [(1985) FEBS Lett. 181, 138-142], by stepwise and selective formation of disulfide bonds using different types of removable protecting groups for the Cys residues. Synthesis of the peptide with different modes of disulfide bond formation provided three peptides consistent with standard STh(6-18) in their physicochemical and biological properties, thereby indicating that the disulfide bonds in STh(6-18) are Cys-Cys-Glu-Leu-Cys-Cys-Asn-Pro-Ala-Cys-Thr-Gly-Cys.

Animals↗
PubMed1987

Human adenine phosphoribosyltransferase. Identification of allelic mutations at the nucleotide level as a cause of complete deficiency of the enzyme.

This study reports the first demonstration of specific mutations leading to human adenine phosphoribosyltransferase (APRT) deficiency. The molecular basis of the deficiency was investigated by determining the sequence of both alleles of a patient with a complete deficiency in APRT activity. A trinucleotide deletion, corresponding to phenylalanine on the deduced amino acid sequence, was confirmed on one allele. A single nucleotide insertion, immediately adjacent to the splice site at the 5' end of the fourth intervening sequence, was confirmed on the other allele. This insertion lead to aberrant splicing, as was demonstrated by the absence of exon 4 in the complementary DNA sequence and by altered RNase mapping analysis of the abnormal messenger RNA.

Adenine Phosphoribosyltransferase↗
PubMed1987

[Almost complete disappearance of metastatic pulmonary tumor and reduction of the main hepatic mass in a case of hepatocellular carcinoma treated with UFT].

A 61-year-old female patient with a low density area indicated by abdominal CT was admitted to hospital. Several circular shadows 5-20-mm in diameter were visible on the chest photos. Primary hepatocellular carcinoma complicated by compensatory cirrhosis accompanying pulmonary metastasis was diagnosed from blood biochemistry tests, a high AFP value (390,000 ng/ml) and angiogram findings. After two months of daily administration of 400 mg of UFT as ftorafur, both reduced AFP (46,000 ng/ml) and a reduction of the primary nidus were observed; after four months, the circular shadows were almost completely eliminated on chest photos. Although UFT administration was discontinued (total FT dose 33.6g) due to jaundice, in the eight months after discontinuation no enlargement of the primary nidus, recurrent shadows on chest photos, or recurrent rise of AFP were observed. This case is considered to suggest the effectiveness of UFT against primary hepatocellular carcinoma with accompanying pulmonary metastasis.

Administration, Oral↗
PubMed1987

[Videodensitometric assessment of right and left ventricular functions by digital subtraction angiography].

Right and left ventricular volumes and systolic indices were determined by intravenous digital subtraction ventriculography in 50 patients with various heart diseases. Using a constant injection speed of 35 ml Renografin-76 contrast medium, serial right and left ventriculograms were obtained in the 30 degree right anterior oblique projection. Right ventriculograms were also obtained in the 60 degree left anterior oblique projection. The videotape recordings of subtracted images were continuously digitized into 128 X 128 eight bit (256 gray scales) pixel matrices using an image-processing computer. The endocardial outlines of the right and left ventricles were drawn manually using a joystick, frame by frame, for each cardiac cycle. By integrating overall the pixel densitometric counts within this outline for each frame, the computer generated a time-density curve with maxima and minima represented in the end-diastolic and end-systolic frames, respectively. Systolic indices including ejection fraction (EF), one-third ejection fraction (1/3 EF) and the peak ejection rate (PER) were derived from the time-density curve. Right ventricular volume was determined by the single-plane or biplane mathematical formulae of Ferlinz et al., and left ventricular volume was calculated by the area-length method in the 30 degree right anterior oblique projection. Results by the two geometric methods correlated well for right ventricular volume (r = 0.84) and for EF (r = 0.80). Right ventricular densitometric counts correlated closely with single-plane volume (r = 0.91). Right ventricular ejection fraction (RVEF) determined by videodensitometry also correlated satisfactorily with that by single-plane angiography (r = 0.74).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗