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Biomedical subjects

J Matsuda

Publications and source records attributed to J Matsuda.

At least 91 records · Page 5Linked to original sources
PubMed1997

Human leptin receptor gene in obese Japanese subjects: evidence against either obesity-causing mutations or association of sequence variants with obesity.

Leptin is an adipocyte-derived blood-borne satiety factor that acts on its cognate leptin receptor (Ob-R) in the hypothalamus, thereby regulating food intake and energy expenditure. To explore whether mutations in the Ob-R gene cause obesity in humans, we have searched for mutations in the gene for Ob-Rb, a biologically active receptor isoform, in obese Japanese subjects. We have also examined associations between such mutants and obesity in the Japanese. Genomic DNAs were used as templates in polymerase chain reaction (PCR) with primers selected to amplify exons 2 to 20 of the human Ob-Rb gene. Direct sequence analysis of the PCR products revealed 7 nucleotide sequence variants (Lys109Arg, Gln223Arg, Ser343Ser, Ser492Thr, Lys656Asn, Ala976Asp, and Pro1019Pro) in the Ob-Rb coding region from 17 obese Japanese subjects with a family history of obesity (BMI 39.3 +/- 8.4 kg/m2). No missense and nonsense mutations were found such as those in Zucker fatty (fa/fa) rats and Koletsky (fa[k]/ fa[k]) rats. Nucleotide substitutions occurred at relatively high frequencies at codons 109, 223, 976, and 1019 (79, 91, 100, and 85%, respectively). Allele frequency of each variant determined by PCR-RFLP and PCR-single strand conformation polymorphism analyses showed no significant differences between 47 obese (BMI 35.1 +/- 6.5 kg/m2) and 68 non-obese (BMI 21.6 +/- 2.2 kg/m2) subjects. The present study represents the first report of sequence variants of the Ob-Rb gene in the Japanese and provides evidence against either obesity-causing mutations or association of sequence variants with obesity in obese Japanese subjects.

Adolescent↗
PubMed1997

Neurological manifestations of knockout mice with beta-galactosidase deficiency.

We succeeded in producing the beta-galactosidase-deficient knockout mouse by gene targeting in embryonic stem cells. The mutant mice developed progressive spastic diplegia within a few months after birth, and died of emaciation at 7-10 months of age. This is an authentic murine model of human GMI-gangliosidosis, and is useful for studies of its pathogenesis and treatment.

Animals↗
PubMed1997

Increased factor VIIa levels in systemic lupus erythematosus patients with lupus anticoagulant.

Recurrent fetal loss, and/or arterio-venous thrombosis are frequent complications in patients with the antiphospholipid antibodies (aPL), anticardiolipin antibody (aCL) and/or lupus anticoagulant (LA). Furthermore, patients with LA have been found to be more susceptible to thrombosis than those with aCL, thus suggesting differences in the pathogenesis of aCL and LA. We examined the systemic lupus erythematosus (SLE) patients with aCL and/or LA for differences in the markers for hypercoagulable state, including thrombin-antithrombin complex (TAT), prothrombin fragment 1 + 2 (F1 + 2), thrombomodulin (TM) and activated factor VII (FVIIa), and lipoprotein (a) (Lp(a)), which is a well-known risk factor for thrombosis. The FVIIa concentration was significantly higher in the LA-positive patients than in the aCL-positive and aPL-negative patients. No significant differences in TAT, F1 + 2, TM, and Lp(a) values were found among the aCL-positive, LA-positive and LA-negative patients groups. These findings indicate that patients with LA were in a more prethrombotic state than those with aCL. The measurement of FVIIa may serve as a useful predictive marker for thrombosis, but further studies are needed to clarify the mechanisms of thrombosis in this clinical setting.

Adult↗
PubMed1997

In vitro susceptibility studies and detection of vancomycin resistance genes in clinical isolates of enterococci in Nagasaki, Japan.

Glycopeptide resistance in enterococci is now a cause of clinical concern in the United States and Europe. However, details of vancomycin resistance in enterococci in Japan have been unknown. We measured minimum inhibitory concentrations (MICs) of various antimicrobial agents for a total of 218 clinical strains of enterococci isolated in our hospital in 1995-6 in addition to 15 strains with known genotypic markers of resistance. We also screened vancomycin resistance genes using a single step multiplex-PCR. In clinical isolates, only two strains of Enterococcus gallinarum were of intermediate resistance to vancomycin (MIC, 8 micrograms/ml), while the others were all susceptible. Glycopeptides (vancomycin and teicoplanin) and streptogramins (RP 58500 and RPR 106972) showed potent antimicrobial effects for the isolates. In addition, ampicillin was also potent for Enterococcus faecalis, while ampicillin, minocycline and gentamicin were potent for Enterococcus avium. No vanA or vanB genes were detected, while vanC1 and vanC23 genes were detected from two and four strains, respectively. Our results suggest that incidence of VRE in Japan may be estimated as still very low at this time.

Anti-Bacterial Agents↗
PubMed1997

Chromosomes of mouse primary spermatocytes undergo meiotic divisions after incorporation into homologous immature oocytes.

The primary spermatocytes used were male germ cells at prophase I. The present study was undertaken to see whether bivalent chromosomes of mouse primary spermatocytes can undergo meiotic divisions within maturing oocytes and participate in subsequent embryonic development. Primary spermatocytes (pachytene to diplotene) freshly collected from the testes of mature males were electrofused with immature oocytes shortly before or after germinal vesicle breakdown. After culture in MEM-alpha medium for 15 h, most (> 90%) of the oocytes containing spermatocyte chromosomes underwent maturation and arrested at metaphase II (MII). Among 23 MII oocytes examined, 17 (74%) had one group of chromosomes and one polar body, indicating that male chromosomes had intermingled with those of the females and completed the first meiotic division. Chromosome analyses of these MII oocytes demonstrated their diploidy. The metaphase chromosomes were transferred to enucleated MII oocytes freshly recovered from superovulated mice. After artificial activation, the reconstructed MII oocytes resumed meiosis and developed to the morula/blastocyst stage. However, no pups were born following embryo transfer into recipient females. These findings indicate that the chromosomes of primary spermatocytes undergo meiotic divisions in maturing oocytes and participate in the formation of diploid embryos.

Animals↗
PubMed1997

Biochemical and molecular analysis of an X-linked case of Leigh syndrome associated with thiamin-responsive pyruvate dehydrogenase deficiency.

We report molecular analysis of thiamin-responsive pyruvate dehydrogenase complex (PDHC) deficiency in a patient with an X-linked form of Leigh syndrome. PDHC activity in cultured lymphoblastoid cells of this patient and his asymptomatic mother were normal in the presence of a high thiamin pyrophosphate (TPP) concentration (0.4 mmol/L). However, in the presence of a low concentration (1 x 10(-4) mmol/L) of TPP, the activity was significantly decreased, indicating that PDHC deficiency in this patient was due to decreased affinity of PDHC for TPP. The patient's older brother also was diagnosed as PDHC deficiency with Leigh syndrome, suggesting that PDHC deficiency in these two brothers was not a de novo mutation. Sequencing of the X-linked PDHC E1 alpha subunit revealed a C-->G point mutation at nucleotide 787, resulting in a substitution of glycine for arginine 263. Restriction enzyme analysis of the E1 alpha gene revealed that the mother was a heterozygote, indicating that thiamin-responsive PDHC deficiency associated with Leigh syndrome due to this mutation is transmitted by X-linked inheritance.

DNA↗
PubMed1997

Beta-galactosidase-deficient mouse as an animal model for GM1-gangliosidosis.

GM1-gangliosidosis is a progressive neurological disease in humans caused by deficiency of lysosomal acid beta-galactosidase, which hydrolyses the terminal beta-galactosidic residue from ganglioside GM1 and other glycoconjugates. In this study, we generated a mouse model for GM1-gangliosidosis by gene targeting in embryonic stem cells. The mouse homozygous for the disrupted beta-galactosidase gene showed beta-galactosidase deficiency, presented with progressive spastic diplegia, and died of emaciation at 7-10 months of age. Pathologically, PAS-positive intracytoplasmic storage was observed in neuronal cells of various areas in the brain. Biochemical analysis revealed a marked accumulation of ganglioside GM1 and asialo GM1 in brain tissue. This animal model will be useful for pathogenetic analysis and therapeutic trial of human GM1-gangliosidosis.

Animals↗
PubMed1997

Anti-endothelial cell antibodies to the endothelial hybridoma cell line (EAhy926) in systemic lupus erythematosus patients with antiphospholipid antibodies.

The endothelial hybridoma (EAhy926) cell line was employed to clarify whether antiphospholipid antibodies (aPA) [lupus anticoagulant (LA), antiprothrombin antibody (aPT) and/or anticardiolipin antibody (aCL)] and anti-endothelial cell antibodies (AECA) are identical, and establish whether beta2-glycoprotein I (beta2-GPI) is needed for reactivity of aPA to endothelial cells. Ig-G AECA was positive in 9/30 SLE patients with aPA (30.0%) and 10/22 SLE patients negative for aPA (45.5%). Ig-M AECA was positive in one SLE patient with aPA and one SLE patient without aPA. AECA-positivity was not significantly different among unfixed, TNF-stimulated and fixed EAhy926. The influence of beta2-GPI on the reactivity of serum to EAhy926 was minimal, and absorption experiments of serum with cardiolipin-liposome/beta2-GPI or phosphatidylserine-liposome/prothrombin gave little evidence of cross-reactivity of aPA and AECA. The results of our study suggest that aPA and AECA may have partially cross-reacted, but were different antibodies. However, further study is needed to clarify the clinico-pathological significance of AECA.

Antibodies↗
PubMed1997

Serum leptin concentration in cord blood: relationship to birth weight and gender.

To investigate the effect of leptin on fetal growth, serum leptin concentrations in venous cord blood were measured in 82 newborns (male = 43, female = 39, gestational age 36-42 weeks, birth weight 2,306-4,128 g). Serum leptin concentrations in cord blood ranged from 2.0 to 84.5 ng/mL (mean 19.9 +/- 17.4 ng/mL). Serum leptin concentrations in males (mean 15.3 +/- 15.6 ng/mL, range 2.0 to 79.3 ng/mL) were significantly (P = 0.011) lower than those in females (mean 25.0 +/- 18.0 ng/mL, range 2.1 to 84.5 ng/mL). Serum leptin concentrations in cord blood were positively correlated with birth weight (r = 0.555, P <0.0001), birth weight SD (r = 0.540, P <0.0001), Kaup index (r = 0.505, P <0.0001) and body weight/body height (r = 0.560, P <0.0001). The serum concentrations of estradiol and testosterone did not differ between males and females and did not correlate with the leptin concentration. It is unlikely that the gender difference in fetal leptin levels is due either to body fat content or distribution or to reproductive hormone status, but may be attributed to genetic differences between males and females.

Birth Weight↗
PubMed1997

[A study of the association between HLA phenotype and serum concentration of soluble HLA class I].

We investigated the association between the phenotypes of human leucocyte antigens (HLA) class I on the surface of lymphocytes and serum concentrations of soluble HLA (sHLA) in normal and Human immunodeficiency virus (HIV) infected subjects. Serum concentrations of sHLA inn normal subjects with HLA-A 24 were significantly higher than those in such subject without HLA-A 24. The similar relation was found in HIV infected subjects whose levels of sHLA significantly increased compared with that of normal subjects. These results might suggest that the mechanism which causes the increase in secretion of sHLA in HIV infected subjects does not change the association between HLA phenotype and serum concentration of sHLA.

Adult↗
PubMed1997

[Clinical results of extracorporeal shock wave lithotripsy for upper urinary tract stone using Siemens Lithostar2].

Between May 1994 and March 1996, a total of 427 cases of upper urinary tract stones were treated by extracorporeal shock wave lithotripsy (ESWL) using a Siemens Lithostar2. Of 427 patients, 167 had renal stones and 260 had ureteral calculi. A double J stent was inserted preoperatively for patients with stones > or = 20 mm in diameter. The success rate after 3 months, defined as complete disappearance of stone or partial disintegration with residual stones < or = 4 mm in diameter, was 82.4% and 88.1% for the renal and ureteral calculi, respectively. Additional treatments were required in 9 cases (transurethral ureterolithotripsy in 5, percutaneous nephrostomy in 2, nephrolithotripsy and ureterolithotomy in 1 each). There were no serious side effects requiring surgical treatment or blood transfusion, although perirenal hematoma developed in 5 patients, who were treated conservatively. It is concluded that ESWL using Simens Lithostar 2 is safe and useful for treating upper urinary tract stones.

Adult↗
PubMed1997

[A case of bilateral upper urinary tract tumors after radical cystectomy].

We report a case of bilateral upper urinary tract tumors after total cystectomy. A 67-year-old male with multiple bladder tumors underwent total cystectomy and ileal conduit urinary diversion. Pathological diagnosis was transitional cell carcinoma, grade 3 (G3), pT1b. Followup urinary cytology continued to be negative. Percutaneous antegrade pyelography revealed multiple bilateral upper urinary tract tumors 21 months post-operatively. Bilateral nephroureterectomy and resection of ileal conduit were performed. Pathological examination revealed transitional cell carcinoma, G3 in bilateral pelvis and ureter. Routine careful examination is necessary after total cystectomy.

Aged↗
PubMed1997

Recurrent syncope induced by left ventricular outflow tract obstruction: demonstration in a patient with hypertrophic obstructive cardiomyopathy.

A 70-year-old man presented with repeated syncope induced by left ventricular outflow tract obstruction. He was referred to us because of repeated syncope with convulsion at rest. During syncope, electrocardiography showed marked ST segment depression with negative T waves in leads I, II, aVL, aVF and V2-V5 but no arrhythmias. Echocardiography revealed asymmetric septal hypertrophy and complete obstruction of the left ventricular outflow tract due to systolic anterior movement of anterior mitral leaflet and concomitant severe mitral regurgitation. During the catheterization study, syncope with convulsion developed repeatedly without antecedent cause, and was associated with a decrease in systemic blood pressure. Simultaneous pressure monitoring of the left ventricle and femoral artery showed a significant pressure gradient (maximum 110 mmHg). During each episode, systemic blood pressure rose spontaneously with the recovery of consciousness over several minutes. He received temporary atrioventricular sequential pacing and underwent successful mitral valve replacement. Four years later, he was doing well.

Aged↗