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Biomedical subjects

T Yasuda

Publications and source records attributed to T Yasuda.

At least 433 records · Page 24Linked to original sources
PubMed1995

[Sensory ataxic neuropathy associated with Sjögren's syndrome].

One tenth of patients with Sjögren's syndrome (SS) is associated with peripheral neuropathy. Trigeminal neuropathy, mononeuropathy multiplex, sensory neuropathy, distal sensory neuropathy, ataxic sensory-autonomic neuropathy have been described as the neuropathy associated with SS. However, some of them secondary occur associated with the vasculopathy due to rheumatoid arthritis, systemic lupus erythematodes etc combined with SS. We demonstrated the clinico-patho-physiological features and spinal MRI findings of patients with primary SS in whom the sensory ataxia and autonomic dysfunctions were the predominant symptoms. The underlying pathology was lymphocytic (T cells) infiltration to the dorsal root ganglia with sensory neuronal degeneration. These findings have identified as association between SS and sensory ataxic neuropathy.

Aged↗
PubMed1995

[Effect of tepid cardiopulmonary bypass in coronary artery bypass operation].

The effect of systemic temperature during cardiopulmonary bypass (CPB) surgery was evaluated in 100 patients. The patients were divided into three groups, based on systemic temperature during CPB; 28 degrees C, 30 degrees C, or 32 degrees C (tepid). Multidose cold crystalloid cardioplegia was administered for myocardial protection. Pump flow was maintained at 75 ml/kg/min. Methoxamine hydrochloride and phenothiazine were used to maintain systemic perfusion pressures between 60 and 80 mmHg. Preoperatively, there were no differences between groups in left ventricular ejection fraction or extent of coronary artery disease. The time required for CPB and weaning from CPB were significantly shorter in the 32 degrees C group than in either the 28 degrees C or the 30 degrees C group. There were significant differences in the doses of methoxamine hydrochloride and phenothiazine required in each group. Postoperatively, there were no significant differences in the incidence of myocardial infarction, stroke, or 30-day mortality between groups. In conclusion, tepid systemic perfusion shortens the length of CPB and does not differ significantly from cold perfusion with respect to mortality and morbidity.

Aged↗
PubMed1995

Gamma-heavy chain deposition disease showing nodular glomerulosclerosis.

We describe a 35-year-old woman who had nodular glomerulosclerosis associated with deposition of fragmented gamma (gamma 1)-heavy chains. She presented with edema of lower legs, mild proteinuria, and hematuria. Laboratory examination revealed hypocomplementemia, and a small amount of monoclonal IgG-lambda (lambda) in the blood. Renal biopsy disclosed prominent nodular expansion of the mesangium. Ultrastructurally, the nodules were composed of electron dense deposits and fibrillar structures. An immunofluorescent study showed depositions of gamma-heavy chains and C3 in the central portion of nodules and capillary walls, whereas kappa (kappa)-, lambda-light chains, and Fab fragments of the heavy chain were negative. The accumulation of collagen I, IV, V, and VI was demonstrated in the mesangium. Western blot analysis of serum protein disclosed fragmented gamma-heavy chains that did not combine with light chains. Glomerular nodular lesions, thus, can occur in heavy chain deposition disease, as in light chain deposition disease. Fragmented gamma-heavy chains may also induce hypocomplementemia by the activation of the complement pathway.

Adult↗
PubMed1995

[Phenotypic heterogeneity in Japanese Charcot-Marie-Tooth disease type 1A patients with PMP-22 gene duplication].

We studied phenotypic heterogeneity in 18 Japanese patients with Charcot-Marie-Tooth disease type 1A (CMT1A) with PMP-22 gene duplication, together with heterogeneity of duplication size. In order to detect the duplication of PMP-22 gene region, the PMP-22 cDNA and a polymorphic marker VAW409R3 were used as probes for Southern blot analysis. As the clinical phenotypes, we assessed the degree of foot deformity, muscular weakness and atrophy, tendon reflexes, sensory impairment and electrophysiologic and sural nerve biopsy findings. Although the degree of muscular weakness and atrophy was slightly more severe in the advanced age, there was a patient with calf hypertrophy in the older age or a patient with marked muscular atrophy of the leg in the younger age. The incidence of foot deformities and sensory impairment was high and these phenotypes did not relate to aging. Diminished or absent tendon reflexes and slowing of motor conduction velocities were commonly seen, but the motor conduction velocity varied greatly among the patients. The clinical phenotypes were extensively variable among the CMT 1A patients with the same gene mutation of PMP-22 gene duplication, suggesting that there is a factor other than PMP-22 gene duplication, which influences phenotypic manifestation in CMT 1A.

Adult↗
PubMed1994

Identification of a unique antigen peptide pRL1 on BALB/c RL male 1 leukemia recognized by cytotoxic T lymphocytes and its relation to the Akt oncogene.

BALB/c radiation leukemia RL male 1 is an immunogenic tumor. We established bulk and cloned cytotoxic T lymphocyte (CTL) lines from regressor (BALB/c x C57BL/6)F1 (CB6F1) spleen cells that recognized RL male 1 specifically. We then obtained antigen peptide recognized by CTL from RL male 1 by acid extraction. Analysis of the acid extract by reversed-phase high performance liquid chromatography (HPLC) on a semipreparative C18 column revealed that fractions eluted in 23 min (peak a) and 26 min (peak b) showed sensitization activity on the P815 target for specific CTL. On further purification of these fractions by HPLC and direct sequencing by Edman degradation, we identified the CTL-recognizing RL male 1 peptide pRL1a (IPGLPLSL) in peak a and its possible precursor peptide pRL1b (SIIPGLPLSL) in peak b. Sequence homology indicated that these peptides were derived from the 5' untranslated region of c-akt oncogene.

Amino Acid Sequence↗
PubMed1994

Purification and characterization of human brain ribonuclease inhibitor.

Ribonuclease inhibitor (RI) was purified about 1300-fold from human cerebrum (including a small portion of midbrain) by a combination of ammonium sulfate precipitation, ribonuclease A-Sepharose chromatography, and high-performance anion-exchange chromatography. The purified RI appeared to be homogeneous as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Using the same method, a homogeneous RI was also obtained from human hindbrain (brainstem and cerebellum). The cerebral RI appeared to be virtually identical with the hindbrain RI on the basis of the following properties: (a) Molecular mass was estimated to be 50 kDa on SDS-PAGE under reducing conditions. (b) Composition analysis revealed that the RI was rich in leucine and cysteine residues and included no amino sugars. (c) The N-terminus was blocked and probably modified by N-acetylation. After treatment with trifluoroacetic acid, it became susceptible to Edman degradation and was sequenced as Ser-Leu-Asp-Ile-Gln-Ser-Leu-Asp-Ile-Gln-(Cys)-Glu-Glu-. (d) The RI, which showed sulfhydryl-dependent inhibitory activity on both secretory-type and nonsecretory-type ribonucleases, bound tightly to ribonuclease to form a 1:1 complex on a molar basis. (e) The RI cross-reacted strongly with anti-human placental RI antibody. These findings also indicate that human brain RI is quite similar to human placental RI. In contrast to the abundance of RI in human brain tissue (about 0.08% (w/w) of total protein), RI was undetectable in human cerebrospinal fluid, suggesting that brain RI may not be a secreted protein.

Amino Acid Sequence↗
PubMed1994

Anticardiolipin antibodies recognize beta 2-glycoprotein I structure altered by interacting with an oxygen modified solid phase surface.

Anticardiolipin antibodies (aCL) derived from the sera of individuals exhibiting the antiphospholipid syndrome (APS) directly bind to beta 2-glycoprotein I (beta 2-GPI), which is adsorbed to an oxidized polystyrene surface. Oxygen atoms were introduced on a polystyrene surface by irradiation with electron or gamma-ray radiation. X-ray photoelectron spectroscopy revealed the irradiated surfaces were oxidized to generate C-O and C = O moieties. aCL derived from either APS patients or (NZW x BXSB)F1 mice bound to beta 2-GPI coated on the irradiated plates, depending on the radiation dose. Antibody binding to beta 2-GPI on the irradiated plates was competitively inhibited by simultaneous addition of cardiolipin (CL)-coated latex beads mixed together with beta 2-GPI but were unaffected by addition of excess beta 2-GPI, CL micelles, or CL-coated latex beads alone. There was a high correlation between binding values of aCL in sera from 40 APS patients obtained by the anti-beta 2-GPI enzyme-linked immunosorbent assay (ELISA) using the irradiated plates and those by the beta 2-GPI-dependent aCL ELISA. Therefore, aCL have specificity for an epitope on beta 2-GPI. This epitope is expressed by a conformational change occurring when beta 2-GPI interacts with an oxygen-substituted solid phase surface.

Animals↗
PubMed1994

Protein growth factors as potential therapies for central nervous system demyelinative disorders.

Demyelinative diseases are frequently accompanied by loss of oligodendroglia; in such instances, oligodendroglial regeneration must precede remyelination. Recent studies indicate that extracellular proteins such as platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) profoundly influence the oligodendroglial lineage. PDGF stimulates the formation of oligodendroglia from partially differentiated progenitor cells, whereas bFGF induces mature oligodendroglia to proliferate and dedifferentiate. Manipulations of the central nervous system concentrations of these and other protein growth factors may prove of therapeutic value in multiple sclerosis.

Adult↗
PubMed1994

Use of antibodies against synthetic peptides for analysis of molecular multiplicity: human deoxyribonuclease I polymorphism.

Eight different antibodies were raised in rabbits and chickens by injecting them with two synthetic N- and C-peptides, which corresponded to the N- and C-terminal 15 residues of human deoxyribonuclease I (DNase I). These two peptides were used as immunogens, both free and conjugated with keyhole limpet hemocyanin (KLH). A rabbit antiserum against the C-peptide conjugated with KLH (rabbit anti-C/KLH) and two chicken antisera against the C-peptide itself (chicken anti-C) and conjugated with KLH (chicken anti-C/KLH) reacted well with purified DNase I, blotted onto a transfer membrane after isoelectric focusing in a polyacrylamide gel. A clear isoenzyme pattern identical to that detected with a rabbit antiserum against the parent enzyme (rabbit anti-DNase I) was observed. Surprisingly, the chicken anti-C antiserum was found to be a powerful and highly specific tool for the determination of urinary DNase I phenotypes (Kishi et al., Hum. Genet. 1989, 81, 295-297) and was not inferior in any respect to the rabbit anti-DNase I. These findings show that the selection of immune animal is one of the most important factors for producing an effective anti-peptide antibody. Unfortunately, the anti-peptide antisera obtained in this study neither blocked DNase I enzyme activity nor did it bind to the enzyme.

Animals↗
PubMed1994

Effects of tumour necrosis factor alpha and interleukin 1 beta on the proliferation of cultured glomerular epithelial cells.

Rat glomerular epithelial cells were cultured with human monocyte supernatant or with recombinant cytokines. A primary glomerular culture and a glomerular epithelial cell culture were made; supernatant from monocyte cultures derived from healthy humans, and recombinant tumour necrosis factor alpha (TNF alpha) or recombinant interleukin 1 beta (IL-1 beta) were added. Cell proliferation rates were assayed by the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay. In serum-free media, consistent proliferation of glomerular epithelial cells (GEC) was observed throughout the 3 week culture period. Significant growth-stimulatory effects were induced by lipopolysaccharide-treated monocyte conditioned medium and by 1-50 ng/ml of TNF alpha, growth being up to 400% more than in the control culture. The effect of TNF alpha depended mainly on its interaction with epidermal growth factor (EGF). In contrast to TNF alpha, IL-1 beta inhibited GEC proliferation; this was due to the early appearance and proliferation of mesangial cells, despite the culture being serum-free. This study showed that activated monocytes secrete growth factors for GEC in vitro, and that interaction between both TNF alpha and IL-1 beta and between TNF alpha and EGF can modulate GEC proliferation. These findings suggest that, under pathological conditions, monocytes or macrophages affect GEC proliferation, probably being involved in crescent formation.

Animals↗
PubMed1994

Genetically polymorphic alpha-L-fucosidase (FUCA1) isozymes detected in blood plasma.

The main isozyme patterns of desialylated blood plasma or serum alpha-L-fucosidase (FUCA) were found to be almost identical to those of semen, urine, placental extracts, and leukocyte lysates, when detected by polyacrylamide gel isoelectric focusing, and activity staining using the fluorogenic substrate 4-methylumbelliferyl-alpha-L-fucopyranoside. Three phenotypes (1, 2-1, and 2) determined from plasma samples were identical to the phenotypes from urine and leukocyte lysates from the same individuals. A population study of plasma samples collected from 485 Japanese individuals indicated that the frequencies of the FUCA1*1 and FUCA1*2 alleles were 0.7505 and 0.2495, respectively. The mean plasma enzyme activities (+/- SD) of the three phenotypes were 318.8 +/- 116.7 nmol/ml per h for type 1, 268.0 +/- 108.3 nmol/ml per h for type 2-1, and 233.2 +/- 84.4 nmol/ml per h for type 2. The mean activities of types 1 and 2 suggest that, on average, the FUCA1*1 gene product in plasma has about 1.4 times the activity of FUCA1*2.

Adult↗
PubMed1994

Overexpression of pancreatic secretory trypsin inhibitor in pancreatic cancer. Evaluation of its biological function as a growth factor.

Four clones of pancreatic secretory trypsin inhibitor (PSTI)-overexpressing cells (TF-PANC clones 1, 6, 8, and 36) were established to evaluate the physiological function of PSTI secreted by cancer cells, by means of introducing a PSTI-expression vector (pRSV-PSTI) into the human pancreatic adenocarcinoma cell line (PANC-1). No obvious changes were observed in the histological features of these transplanted tumors in nude mice, in the growth of TF-PANC and PANC-1, or that of 3T3 fibroblasts when cocultured with them. Addition of recombinant human PSTI to the cultured media resulted in no increase in proliferation of fibroblasts (3T3 and WI-38) or of four pancreatic cancer cell lines (PANC-1, CAPAN-I, MIAPaCa-2, and Hs766T). These results suggest that the estimation of tumor-bearing PSTI as a paracrine or autocrine growth factor in recent studies should be given careful consideration.

3T3 Cells↗
PubMed1994

Intraventricular conduction abnormalities in patients with clinically suspected myocarditis are associated with myocardial necrosis.

Twenty-nine patients with suspected myocarditis, either with or without intraventricular conduction abnormalities, were investigated for degree of myocardial necrosis by antimyosin scintigraphy. Among those 29 patients, 16 had intraventricular conduction abnormalities. Antimyosin scans were analyzed for heart/lung ratios and semiquantitative visual uptake scores (0 to 4+ scale). Of the 16 patients with conduction abnormalities, 15 (94%) demonstrated visual antimyosin uptake versus 7 (54%) of 13 cases without conduction abnormalities (p < 0.03). In addition, the heart/lung ratios and uptake scores were significantly higher in the group with conduction abnormalities than in the group without (1.64 +/- 0.31 vs 1.39 +/- 0.20, p < 0.03; and 2.3 +/- 0.7 vs 1.4 +/- 0.7, p < 0.005; respectively). In conclusion, intraventricular conduction abnormalities in patients with suspected myocarditis were more strongly associated with active and more severe myocardial necrosis as judged by antimyosin imaging than patients with normal electrocardiograms.

Adult↗