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Biomedical subjects

M Matsuda

Publications and source records attributed to M Matsuda.

At least 199 records · Page 11Linked to original sources
PubMed2000

Effect of irradiation on autogenous bone transplantation in rat parietal bone.

To determine the appropriate time for bone reconstruction after irradiation, the healing process after autogenous iliac bone transplantation in the irradiated parietal bone was examined by scanning electron microscopy and light microscopy. Bone transplantation was carried out at the second and the fourth weeks after Cobalt-sixty (60Co) irradiation with calculated dose and fractionation. Animals without irradiation were used as control. The results show the appearance of mesenchymal cells and blood vessels around the transplantation to be extremely few one week after transplantation which was carried out at the second week after irradiation. These inhibitions were still seen two weeks after transplantation. Four weeks after transplantation, there were no differences in the bone formation among the experimental groups. Bone formation in the transplantation at the fourth week after irradiation was similar to that of the control group. Microvascularization in the transplantation at the second week after irradiation was inhibited one week after transplantation. The delay in bone healing was responsible for the retardation of revascularization and caused microcirculatory failures as well as the damage of osteogenic cells. It is quite clear that damaged cells and tissues recovered by the elapse of time under the irradiation procedure employed in this study and also that bone formation was carried out in the physiological process. We think that bone transplantation after irradiation should be done after recovery from the radiation damage to the periosteal cells and the blood vessels.

Animals↗
PubMed2000

Myasthenia gravis with membranous nephropathy, successfully treated with extended total thymectomy.

A 46-year-old woman showed proteinuria and hematuria after left blepharoptosis, and revealed a histopathology of membranous nephropathy (MN) at renal biopsy. She was diagnosed as having myasthenia gravis (MG) because of a positive edrophonium test and anti-acetylcholine receptor (AchR) antibodies in serum. We found a decrease in anti-AchR antibodies after extended total thymectomy, in parallel with an improvement in both urinary findings and myasthenic symptoms. In this case, MG preceded MN and the thymectomy was effective for both diseases, suggesting that the thymus might play an important role in the pathogenesis of MN.

Female↗
PubMed2000

Bromocriptine: a novel approach to the treatment of type 2 diabetes.

OBJECTIVE: In vertebrates, body fat stores and insulin action are controlled by the temporal interaction of circadian neuroendocrine oscillations. Bromocriptine modulates neurotransmitter action in the brain and has been shown to improve glucose tolerance and insulin resistance in animal models of obesity and diabetes. We studied the effect of a quick-release bromocriptine formulation on glucose homeostasis and insulin sensitivity in obese type 2 diabetic subjects. RESEARCH DESIGN AND METHODS: There were 22 obese subjects with type 2 diabetes randomized to receive a quick-release formulation of bromocriptine (n = 15) or placebo (n = 7) in a 16-week double-blind study. Subjects were prescribed a weight-maintaining diet to exclude any effect of changes in body weight on the primary outcome measurements. Fasting plasma glucose concentration and HbA(1c) were measured at 2- to 4-week intervals during treatment. Body composition (underwater weighing), body fat distribution (magnetic resonance imaging), oral glucose tolerance (oral glucose tolerance test [OGTT]), insulin-mediated glucose disposal, and endogenous glucose production (2-step euglycemic insulin clamp, 40 and 160 mU x min(-1) x m(-2)) were measured before and after treatment. RESULTS: No changes in body weight or body composition occurred during the study in either placebo- or bromocriptine-treated subjects. Bromocriptine significantly reduced HbA(1c) (from 8.7 to 8.1%, P = 0.009) and fasting plasma glucose (from 190 to 172 mg/dl, P = 0.02) levels, whereas these variables increased during placebo treatment (from 8.5 to 9.1%, NS, and from 187 to 223 mg/dl, P = 0.02, respectively). The differences in HbA(1c) (delta = 1.2%, P = 0.01) and fasting glucose (delta = 54 mg/dl, P < 0.001) levels between the bromocriptine and placebo group at 16 weeks were highly significant. The mean plasma glucose concentration during OGTT was significantly reduced by bromocriptine (from 294 to 272 mg/dl, P = 0.005), whereas it increased in the placebo group. No change in glucose disposal occurred during the first step of the insulin clamp in either the bromocriptine- or placebo-treated group. During the second insulin clamp step, bromocriptine improved total glucose disposal from 6.8 to 8.4 mg x min(-1) kg(-1) fat-free mass (FFM) (P = 0.01) and nonoxidative glucose disposal from 3.3 to 4.3 mg min(-1) x kg(-1) FFM (P < 0.05), whereas both of these variables deteriorated significantly (P < or = 0.02) in the placebo group. CONCLUSIONS: Bromocriptine improves glycemic control and glucose tolerance in obese type 2 diabetic patients. Both reductions in fasting and postprandial plasma glucose levels appear to contribute to the improvement in glucose tolerance. The bromocriptine-induced improvement in glycemic control is associated with enhanced maximally stimulated insulin-mediated glucose disposal.

Abdomen↗
PubMed2000

The tau and anti-tau effects in successively presented stimuli.

It was confirmed by the reproduction method with 20 adults that (a) the tau effect, i.e., the greater the temporal separation between successively presented stimuli with a constant spatial interval, the greater the apparent spatial interval, occurred, especially in the situation in which the participants were assumed to form a set easily using temporal interval as the cue for spatial interval estimation, and (b) the anti-tau effect occurred in the special situation in which the participants were assumed to form a set using speed of an imaginary movement as the cue for it. These findings supported the hypothesis of "cue-selection sets."

Adolescent↗
PubMed2000

Establishment of a myeloid cell line, YM711, characterized by retinoid resistance.

A myeloid cell line (YM711) was established by transfecting exogenous PML/RARalpha cDNA into peripheral blood stem cells. The cells were positive for CD33, CD34, CD38, CD13, CD14, and CD11b. Cytochemical examination revealed YM711 cells to be positive for peroxidase, alpha-naphtyl butyrate esterase, and acid phosphatase as well. Karyotypic analysis showed them to be nearly tetraploid (92 XXYY). Reverse-transcription polymerase chain reaction showed that, although PML/RARalpha mRNA was detected in YM711, these cells could not be differentiated by all-trans retinoic acid (ATRA). We therefore designated the YM711 cell line as being ATRA resistant. Because YM711 expressed multi drug resistance 1 (MDR-1) mRNA and p-glycoprotein cell surface protein, we assessed whether verapamil and ATRA would induce the differentiation of YM711 cells; they did not. An increased expression of cellular retinoic acid-binding protein (CRABP)-II was also detected on YM711 cells compared with that of HL-60. These results suggest that high level of expression of CRABP-II may contribute to be the mechanism of ATRA resistance. This cell line may be useful in evaluating the mechanism of resistance to retinoid.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

[A case of motor neuron disease with dementia, presenting motor aphasia as an initial symptom].

We report a case of motor neuron disease (MND) with dementia, presenting motor aphasia as an initial symptom. A 67-year-old man was admitted to our hospital because of speech disturbance slowly progressing for 2 years. On physical examination, he showed no neurological abnormalities except for non-fluent aphasia and increased deep tendon reflexes without laterality. MRI demonstrated bilateral fronto-temporal atrophy, dominating the left hemisphere. This finding was confirmed by surface anatomy scanning (SAS), showing an obvious atrophy in the left inferior frontal gyrus, compared with the right one. SPECT with 123I-IMP revealed some irregular defects in the bilateral frontotemporal region. Because he showed dementia, bulbar palsy with tongue atrophy, weakness of upper extremities and facial muscles, snout reflex, and the atrophy and fasciculation in limbs in addition to motor aphasia soon after the discharge from our hospital, he was diagnosed as having MND with dementia. At age 68, he died of a respiratory failure 3 years after the onset of the disease. MND with dementia seldom shows motor aphasia as an initial symptom. We must include, however, the MND with dementia as an differential diagnosis when we see the patients with progressive aphasia.

Aged↗
PubMed2000

Decreased IRS-2 and increased SREBP-1c lead to mixed insulin resistance and sensitivity in livers of lipodystrophic and ob/ob mice.

In mice with too little fat (lipodystrophy) or too much fat (ob/ob), leptin deficiency leads to hyperglycemia, hyperinsulinemia, and insulin resistance. In both disorders, the liver overproduces glucose as a result of resistance to the normal action of insulin in repressing mRNAs for gluconeogenic enzymes. Here we show that chronic hyperinsulinemia downregulates the mRNA for IRS-2, an essential component of the insulin-signaling pathway in liver, thereby producing insulin resistance. Despite IRS-2 deficiency, insulin continues to stimulate production of SREBP-1c, a transcription factor that activates fatty acid synthesis. The combination of insulin resistance (inappropriate gluconeogenesis) and insulin sensitivity (elevated lipogenesis) establishes a vicious cycle that aggravates hyperinsulinemia and insulin resistance in lipodystrophic and ob/ob mice.

Animals↗
PubMed2000

Structure and function of fibrinogen inferred from hereditary dysfibrinogens.

The structure-function relationships of human fibrinogen and their clinical implications are discussed on the basis of data provided by biochemical and electron microscopic analyses of normal and abnormal fibrinogen and by recent crystallographic studies on certain functional domains and segments of normal fibrinogen. Particularly, ultrastructure studies of individual fibrinogen molecules and fibrin networks of structurally elucidated dysfibrinogens enable us to understand the structure-function relationships of these dysfibrinogens more clearly than ever. Electron micrographs of some representative dysfibrinogen molecules are provided.

Binding Sites↗
PubMed2000

[Japanese encephalitis presenting with left hemiplegia and thalamic neglect--a case report].

This report concerns a 51-year-old right-handed man with Japanese encephalitis, showing left hemiplegia and left hemispatial neglect. On admission, he had a slight fever, mild consciousness disturbance, left hemiplegia, and left hemispatial neglect but no neck stiffness, headache nor nausea. He was treated on the basis of cerebral infarction, but his fever and consciousness disturbance worsened. We found pleocytosis (145/mm3) in the cerebrospinal fluid (CSF) and right thalamic edema on a brain CT scan obtained 4 days later. He was finally diagnosed as having Japanese encephalitis on the basis of an increase in anti-viral antibodies observed in paired CSF and serum samples. In the exacerbation phase, 123I-IMP single photon emission CT (SPECT) demonstrated a marked decrease in cerebral perfusion in the right hemisphere, while a brain MRI revealed irregular lesions localized the right thalamus (mainly posterior and medial parts), showing low intensity on T1-weighted and high intensity on T2-weighted images. In the recovery phase, asymmetrical perfusion was no longer observed on SPECT and the symptoms including the left hemispatial neglect had improved. These findings suggest that the left hemispatial neglect in this patient might been caused by the right thalamic lesion resulting in damage to the activating system of the right hemisphere. This case thus shows that acute onset of hemispatial neglect could be caused by cerebral encephalitis.

Cerebral Infarction↗
PubMed1999

Simultaneous core 2 beta1-->6N-acetylglucosaminyltransferase up-regulation and sialyl-Le(X) expression during activation of human tonsillar B lymphocytes.

We have investigated the regulation mechanism of the surface sialyl-Le(X) (sLe(X)) expression level in tonsillar B cells during activation. sLe(X) antigen became strongly positive after activation, while resting B cells were weakly positive. sLe(X) structures were mainly located on O-linked oligosaccharide chains of glycoprotein. Transcripts of FucT-VII and core 2 GlcNAc transferase (C2GnT) were up-regulated after activation, while those of ST3GalIV and beta1-->4GalT-I were expressed constitutively. However, the up-regulation of C2GnT was more dramatic than that of FucT-VII. These results suggest that sLe(X) expression level is regulated by C2GnT during tonsillar B cell activation.

B-Lymphocytes↗
PubMed1999

Fibrinogen Niigata with impaired fibrin assembly: an inherited dysfibrinogen with a Bbeta Asn-160 to Ser substitution associated with extra glycosylation at Bbeta Asn-158.

A novel BbetaAsn-160 (TAA) to Ser (TGA) substitution has been identified in fibrinogen Niigata derived from a 64-year-old asymptomatic woman, who is heterozygotic for this abnormality. The mutation creates an Asn-X-Ser-type glycosylation sequence, and a partially sialylated biantennary oligosaccharide was linked to the BbetaAsn-158 residue. The functional abnormality was attributed to delayed lateral association of normally formed double-stranded protofibrils based on normal cross-linking of fibrin gamma-chains and tissue-type plasminogen activator-catalyzed plasmin generation by polymerizing fibrin monomers. Enzymatic removal of all the N-linked oligosaccharides from fibrinogen Niigata accelerated fibrin monomer polymerization that reached the level of untreated normal fibrin monomers, but the thrombin time was prolonged from 18.2 seconds to 113 seconds (normal: 11.2 seconds to 8.9 seconds). By scanning electron micrographic analysis, Niigata fibrin fibers were found to be more curvilinear than normal fibrin fibers. After deglycosylation, Niigata fibers became straight being similar to untreated normal fibrin fibers, whereas normal deglycosylated fibrin appeared to be less-branched than untreated normal or deglycosylated Niigata fibrin. Although normal and Niigata fibrins were similar to each other in permeation and compaction studies, deglycosylated normal and Niigata fibrins had much higher permeability and compaction values, indicating that deglycosylation had brought about the formation of more porous networks. The enzymatic deglycosylation necessitates an Asn to Asp change at position Bbeta-158 that is responsible for reducing the fiber thickness because of either local repulsive forces or steric hindrance in the coiled-coil region.

Amino Acid Substitution↗
PubMed1999

Free-living nematodes Caenorhabditis elegans possess in their mitochondria an additional rhodoquinone, an essential component of the eukaryotic fumarate reductase system.

The respiratory chain of Caenorhabditis elegans was characterized in mitochondria isolated from aerobically grown nematodes. Nematode mitochondria contain ubiquinone-9 as a major component and rhodoquinone-9 as a minor component. The ratio of ubiquinone-9/rhodoquinone-9 is higher in C. elegans mitochondria than in mitochondria from second-stage larvae of Ascaris suum, the free-living stage of porcine gut-dwelling nematode. The individual oxidoreductase activities comprising succinate oxidase and the amount of substrate-reducible cytochromes are comparable to those of mitochondria from second-stage larvae of A. suum. The specific activity of fumarate reductase is lower in C. elegans mitochondria than in mitochondria from second-stage larvae of A. suum, but still higher than in mammalian mitochondria. These results indicate that the free-living nematode C. elegans is capable of synthesizing rhodoquinone, as distinguished from aerobic mammalian species, although its mitochondria appear more aerobic than A. suum larval mitochondria.

Aerobiosis↗
PubMed1999

Non-adherent cell-specific expression of DOCK2, a member of the human CDM-family proteins.

Human DOCK180, which was originally identified as a major protein bound to the Crk oncogene product, is an archetype of the CDM family of proteins, including Ced-5 of Caenorhabditis elegans and Mbc of Drosophila melanogaster. After DOCK180, at least three putative human proteins that manifest high amino acid sequence similarity to DOCK180 have been registered in the GenBank/EMBL database. We have designated one of them, KIAA0209, as DOCK2 and characterize here. DOCK2 mRNA was expressed mostly in peripheral blood cells, followed by slight expression in the spleen and thymus, whereas DOCK180 was expressed in all tissues tested except in peripheral blood cells. Immunostaining of human cadaver tissues revealed that the expression of DOCK2 was limited to the lymphocytes and macrophages of various organs. DOCK2 bound to and activated Rac1, as did DOCK180; however, DOCK2 did not bind to CrkII, which transduces signals at focal adhesions. Thus, DOCK180 and DOCK2 are regulators of Rac and function in adherent and non-adherent cells, respectively.

Amino Acid Sequence↗
PubMed1999

An infectious DNA clone of HIV type 1 subtype C.

Among the 10 subtypes of the M group of human immunodeficiency virus type 1, subtype C is the most prevalent in India and may dominate worldwide in the near future; however, there has been no report on the infectious DNA clone of this subtype. We have isolated an infectious DNA clone of the 93IN101 strain of HIV-1 subtype C, which was isolated in India in 1993. MAGIC5 cells, which are derived from HeLa-CD4-LTR-beta-gal (MAGI) cells and express CCR5, were inoculated with the 93IN101 strain of HIV-1 subtype C. The genomic DNA of the infected cells was used as a template for amplification of the HIV-1 genome. The genome DNA obtained was subcloned into pBR322, and the resulting plasmid was designated as pIndie-C1. The insert of pIndie-C1 was 9680 bp in length and had an intact genomic organization with open reading frames of all structural, regulatory, and accessory proteins. Phylogenetic analysis confirmed that the nucleotide sequence of pIndie-C1 is closely related to those of HIV-1 subtype C isolated in India. Transfection of pIndie-C1 into 293T cells yielded as much virus as did pNL432, one of the most widely used HIV DNA clones. The recovered Indie-C1 virus infected MAGIC5 but not the parent MAGI cells, indicating that Indie-C1 is CCR5 tropic. Expressed Env protein was reacted efficiently with the sera of HIV-1-infected patients of India, but not of Japan. Expression of Nef and Vpr was also confirmed by immunoblotting.

Gene Products, env↗
PubMed1999

Sphingosylphosphorylcholine induces cytosolic Ca(2+) elevation in endothelial cells in situ and causes endothelium-dependent relaxation through nitric oxide production in bovine coronary artery.

Sphingosylphosphorylcholine (SPC) increased intracellular Ca(2+) concentration ([Ca(2+)]i) and nitric oxide (NO) production in endothelial cells in situ on bovine aortic valves, and induced endothelium-dependent relaxation of bovine coronary arteries precontracted with U-46619. The SPC-induced vasorelaxation was inhibited by N(omega)-monomethyl-L-arginine, an inhibitor of both constitutive and inducible NO synthase (NOS), but not by 1-(2-trifluoromethylphenyl) imidazole, an inhibitor of inducible NOS (iNOS). Immunoblotting revealed that endothelial constitutive NOS, but not iNOS, was present in endothelial cells in situ on the bovine aortic valves. We propose that SPC activates [Ca(2+)]i levels and NO production of endothelial cells in situ, thereby causing an endothelium-dependent vasorelaxation.

Animals↗