Biomedical subjects

Y Matsuki

Publications and source records attributed to Y Matsuki.

At least 55 records · Page 3Linked to original sources

PubMed1997

Relevance of local Th2-type cytokine mRNA expression in immunocompetent infiltrates in inflamed gingival tissue to periodontal diseases.

It has been suggested that the types of inflammatory round cell infiltrates and the divergence in the cytokine production profile by macrophages and helper T cells regulate the course of infectious or inflammatory diseases, including periodontitis and gingivitis. We examined the expression of IL-1alpha, IL-1beta, IL-2, IL-4, IL-5, IL-6 and tumour necrosis factor-alpha (TNF-alpha) mRNA in the inflamed gingiva by in situ hybridization. The results of single-cell analysis were used as data sets for statistical analyses. The density of cells expressing IL-1alpha, IL-4 and IL-5 mRNA was higher in periodontitis than in gingivitis. IL-2 mRNA-expressing cells were almost absent in gingivitis specimens. Principal component analysis disclosed three factors explaining 84.8% of the variance: one accounting for 40.5% of the variance and mainly regulated by IL-1alpha, IL-1beta, IL-6 and TNF-alpha, and two others, explaining 29.9% and 14.4% of the variance, describing the relationship between the types of cytokines derived from macrophages or Th2 type. These results suggest that the cytokines produced by inflammatory cells infiltrating in the gingival tissue are influential on the progression of gingivitis, an acute and reversible inflammatory condition, to chronic and destructive periodontitis. Thus, periodontal disease progression may be regulated by the local cytokine network, and the bias in this network towards a Th2-type cytokine dominance could be an exacerbating factor.

Adult↗

PubMed1997

In situ hybridization study on tissue inhibitors of metalloproteinases (TIMPs) mRNA-expressing cells in human inflamed gingival tissue.

This study presents the exact cell types and localization of tissue inhibitors of metalloproteinases (TIMPs) production sites in periodontal diseased gingiva by means of in situ hybridization. Gingival tissue specimens were fixed, embedded and hybridized in situ with specific digoxigenin-labeled cRNA probes (386 and 496 bp). TIMP-1 and -2 mRNAs were expressed on macrophages, mononuclear cells, capillary endothelial cells and some fibroblasts throughout the gingival tissue. In periodontitis, TIMP-1 and -2 mRNA-expressing cells showed significantly different localization. TIMP-1 mRNA was broadly observed in the gingival connective tissue while TIMP-2 mRNA was predominantly expressed in the connective tissue adjacent to the pocket epithelium (p < 0.01). Fewer TIMPs mRNA were observed in minimal gingivitis than in periodontitis, especially in the middle zone of gingival tissue. Thus, TIMP-1 and TIMP-2 mRNA was detected differentially and site-specifically in periodontal diseased gingival tissue.

Aged↗

PubMed1997

Sex difference in the metabolism of pirmenol in rats.

The in vitro metabolism of pirmenol (cis-alpha-[3-(2,6-dimethyl-1-piperidinyl)propyl]-alpha-phenyl-2-pyri dinemethanol) and glucuronidation of its metabolites, a 4-hydroxylated derivative of pirmenol (M3) and 3-methylether of M3 (M5), were investigated using a hepatic 9000 x g supernatant and microsomes, respectively, of female and male rats in order to elucidate the higher urinary excretion of M3G and M5G (glucuronides of M3 and M5, respectively) in females previously observed in in vivo metabolism. Pirmenol delta1' iminium ion (M2) and M3 were formed by the oxidation of pirmenol in both sexes; however, M2 was the main metabolite in males, while M2 and M3 were formed at nearly the same level in females. On glucuronidation of M3 and M5, the Vmax values of both compounds were higher in female rats, consistent with the results in vivo. In addition, the sex difference in the urinary excretion ratio of M5G to M3G (1.1 in female, 2.5 in male) might reflect the lower availability of M3 for glucuronidation in male rats in vivo. The chromatographic separation of diastereomers of M5G was also described.

Animals↗

PubMed1997

[SMON and pharmacokinetics of chinoform with special reference to animal species difference].

The experimental reproduction of SMON using several kinds of animals given a prolonged administration of chinoform has been carried out by many investigators because of the importance to solve the problem of etiology in the SMON. In these experiments, it is demonstrated that a marked species difference was observed in the relationship between the doses given to animals and the frequency of the onset of neurologic symptoms. Although dogs were accepted as the most suitable animal model for SMON, pathological changes in the peripheral nerve of the dog were not observed. The blood level or tissue distribution of chinoform after oral, intravenous or intraperitoneal administration of the drug differed in the animal species. Thus, it is considered that the species difference in the onset of neurologic symptoms is principally caused by the difference in pharmacokinetics of chinoform in each animal. Moreover, for the onset of neurologic symptoms in animals, perhaps it is necessary to maintain the level of unconjugated chinoform in the nerve tissues around several to over ten micrograms/ml for three or four weeks as well as that in SMON patients while the neurologic symptoms or pathological changes do not appear in some kinds of animals at these levels. In a study on the cellular toxicity of chinoform, many other problems remain to be solved although degeneration or uncoupling on oxidative phosphorylation in mitochondria of the axons by chinoform and lipid peroxidation of the membrane by chinoform-ferric chelate have been already shown.

Amebicides↗

PubMed1997

Rapidly progressive interstitial lung disease associated with dermatomyositis responding to intravenous cyclophosphamide pulse therapy.

Interstitial lung disease, especially the rapidly progressive type, carries a grave prognosis when associated with polymyositis (PM)/dermatomyositis (DM). We describe a case of rapidly progressive interstitial lung disease associated with DM. Pathological findings included bronchiolitis obliterans organizing pneumonia (BOOP) pattern in the right upper lung lobe and interstitial fibrosis with microscopic honeycomb lesions in the right lower lung lobe. The patient's respiratory distress was severe and persistent, and oral intubation with mechanical ventilation was transitionally introduced. The respiratory distress condition responded to intravenous cyclophosphamide pulse therapy.

Autoimmune Diseases↗

PubMed1997

SLE and Sjögren's syndrome associated with unilateral moyamoya vessels in cerebral arteries.

Moyamoya disease is a rare clinical entity, diagnosed by cerebral angiography and characterized by occlusion of the internal carotid artery system and the development of collateral arteries. A 30-year-old woman with systemic lupus erythematosus and Sjögren's syndrome recurrently presented transient right homonymous hemianopsia. Cerebral angiography showed occlusion of the left posterior cerebral artery associated with the development of collateral circulation ("moyamoya vessels"). In a young adult, as in this case, the unilaterality of the lesion and the presentation of transient ischemic attacks rather than subarachnoid hemorrhage are rare features for Moyamoya disease. Antiphospholipid syndrome was absent.

Adult↗

PubMed1997

Primary Sjögren's syndrome associated with hyaline-vascular type of Castleman's disease and autoimmune idiopathic thrombocytopenia.

We describe a case of primary Sjögren's syndrome complicated by hyaline-vascular type of Castleman's disease and autoimmune idiopathic thrombocytopenia. This type of Castleman's disease was diagnosed by biopsy of a right axillary lymph node 7 years after the onset of Sjögren's syndrome. The specimen showed small hyaline-vascular lymphoid follicles and interfollicular capillary proliferation. Serum IL-6 was slightly increased, but systemic manifestations, such as fever or weight loss, were not present. Hyaline-vascular type of Castleman's disease should be considered a lymphoproliferative disorder associated with Sjögren's syndrome.

Biopsy↗

PubMed1996

Thromboxane A2 receptor blockade suppresses intercellular adhesion molecule-1 expression by stimulated vascular endothelial cells.

Inhibition of the thromboxane A2-synthesizing enzyme (DP-1904: [+/-]-6-[1-imidazolylmethyl]-5,6,7,8-tetrahydronaphthalene-2-carbo xylic acid hydrochloride hemihydrate) reportedly suppresses intercellular adhesion molecule-1 (ICAM-1) expression on the surface of stimulated vascular endothelial cells (Ishizuka et al., 1994, Eur. J. Pharmacol 262, 113). In the present study, thromboxane A2 receptor antagonists suppressed the expression of ICAM-1 on the surface of human vascular endothelial cells that were stimulated by tumor necrosis factor alpha (TNF alpha), platelet activating factor (PAF), or U46619 (9,11-dideoxy-9 alpha, 11 alpha-epoxymethanoprostaglandin F2 alpha). Augmentation of ICAM-1 expression on human vascular endothelial cells stimulated by U46619 was suppressed by protein kinase C inhibitors. Thromboxane A2 receptor antagonist suppressed U46619 stimulation of protein kinase C activity of a cell membrane fraction. These results indicate that in human vascular endothelial cells, thromboxane A2, the production and secretion of which is stimulated by TNF alpha or PAF, binds to the thromboxane A2 receptors on cell membranes and augments ICAM-1 expression on the cell surfaces mainly through protein kinase C.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1996

Haploinsufficiency of parathyroid hormone-related peptide (PTHrP) results in abnormal postnatal bone development.

Although apparently phenotypically normal at birth, mice heterozygous for inactivation of the gene encoding parathyroid hormone-related peptide (PTHrP) develop haplotype insufficiency by 3 months of age. In addition to histologic and morphologic abnormalities similar to those seen in homozygous mutants, heterozygous animals demonstrated alterations in trabecular bone and bone marrow. These included metaphyseal bone spicules which were diminished in volume, irregularly distributed, and less well developed than those seen in age-matched controls as well as bone marrow, which contained an inordinate number of adipocytes. A substantial reduction in PTHrP mRNA was detected in heterozygous tissue, while circulating parathyroid hormone (PTH) and calcium concentrations were normal. Thus, while a physiologic concentration of PTH was capable of maintaining calcium homeostasis, it was incapable of compensating for PTHrP haploinsufficiency in developing bone. In normal animals, both PTHrP and the PTH/PTHrP receptor were expressed predominantly in chondrocytes situated throughout the proliferative zone of the tibial growth plate. In the metaphysis, the PTH/PTHrP receptor was identified on osteoblasts and preosteoblastic cells situated in the bone marrow, while PTHrP was expressed only by osteoblasts. These observations indicate that postnatal bone development involves susceptible pathways that display exquisite sensitivity to critical levels of PTHrP and imply that the skeletal effects of PTH are influenced by locally produced PTHrP. Moreover, identification of both the ligand and its N-terminal receptor in metaphyseal osteoblasts and their progenitors suggests an autocrine/paracrine role for the protein in osteoblast differentiation and/or function. Impairment in this function as a consequence of PTHrP haploinsufficiency may critically influence the course of bone formation, resulting in altered trabecular architecture and perhaps low bone mass and increased bone fragility.

Age Factors↗

PubMed1996

Full-length sequence, localization, and chromosomal mapping of ameloblastin. A novel tooth-specific gene.

We report the full-length sequencing, cell type-specific expression, and immunolocalization of a novel gene expressed in rat incisors, which we have designated ameloblastin. Northern blot analysis of RNA from multiple rat and mouse tissues demonstrated high levels of expression of two distinct transcripts of approximately 2.0 and 1.6 kilobase pairs that were expressed only in teeth. In situ hybridization using a digoxigenin-labeled RNA probe showed that the tissue distribution of ameloblastin was limited to the ameloblast in rat incisors. Immunohistochemical staining of rat incisors using a polyclonal antibody raised against a fusion protein revealed a unique localization pattern. Ameloblastin was found to be expressed during the differentiation of inner enamel epithelium into ameloblasts, with intense localization in the Tomes' processes of secretory ameloblasts. In contrast to amelogenin, only modest amounts of ameloblastin were detected in enamel matrix. The ameloblastin gene encodes an open reading frame of 422 amino acids corresponding to a putative protein of 45 kDa. The predicted protein is acidic (pI = 5.54) and the most abundant amino acids are Pro (15.2%), Gly (9.9%), and Leu (9.9%). We have also mapped the ameloblastin gene, Ambn, to a locus on mouse chromosome 5 near other genes associated with mineralized tissues. Thus, ameloblastin represents a unique ameloblast-specific gene product that may be important in enamel matrix formation and mineralization.

Amelogenin↗

PubMed1996

Anti-DNA antibody kinetics following selective removal by adsorption using dextran sulphate cellulose columns in patients with systemic lupus erythematosus.

The aim of this study is to determine by mathematical analysis which of two models, the one- or the two-compartment model, more closely approximates the kinetics of anti-dsDNA following immunoadsorption procedures in patients with systemic lupus erythematosus. Titers of anti-dsDNA were measured at specified intervals after apheresis to each model by nonlinear least-squares methods, and Akaike's Information Criterion (AIC) was calculated to determine which model most approximately described the kinetics. The AIC of the two-compartment model was larger than that of the one-compartment model in all 14 SLE patients (P < .001). Therefore, the one-compartment model is thought to be suitable. The generation rate and catabolic rate of anti-dsDNA were obtainable using this model. The anti-dsDNA replenishment curve after an immunoadsorption session was defined by only two parameters: the generation and catabolic rates of anti-dsDNA.

Adolescent↗

PubMed1996

High-avidity anti-DNA antibody removal from the serum of systemic lupus erythematosus patients by adsorption using dextran sulfate cellulose columns.

The purpose of this study is to determine whether immunoadsorption treatment using a dextran sulfate (DS) column can remove high-avidity anti-double-stranded DNA (anti-dsDNA) antibody from the blood of patients with systemic lupus erythematosus (SLE). Before and after each immunoadsorption therapy routine, titers of the high-avidity anti-dsDNA antibody of 11 SLE patients were measured by using a newly developed assay kit to exclusively detect high avidity anti-DNA antibody. Patients with active SLE showed significantly higher titers of high-avidity antibody than did those with inactive SLE, and their titers were significantly reduced by immunoadsorption procedures. Removal of high-avidity antibodies in vitro was also confirmed by mixing patients' sera and DS gel. Immunoadsorption therapy using DS columns is effective in the removal of high-avidity anti-dsDNA antibodies that are closely associated with pathogenicity in SLE.

Adult↗

PubMed1996

Anti-dsDNA antibody kinetics during in vivo apheresis in systemic lupus erythematosus patients and in an in vitro apheresis model.

Levels of anti-dsDNA measured just after an immunoadsorption procedure in systemic lupus erythematosus (SLE) patients are sometimes paradoxically larger than those measured just before the procedure. A 1:100 in vitro single-compartment immunoadsorption system model was devised to determine which of two models, one- or two-compartment, more closely approximates the kinetics of anti-dsDNA during apheresis procedures. Ten SLE patients were employed in this study. A total of 4,100 ml of plasma was passed through the dextran sulfate cellulose columns during one clinical apheresis session. In eight of ten patients, the log of RIA-measured anti-dsDNA titers decreased linearly as treated plasma volume increased, in both the clinical procedure and the experimental model. The mean adsorption efficacy in the clinical apheresis procedure and in the in vitro model was 0.37 and 0.27, respectively. However, in one patient the RIA-measured level of anti-dsDNA increased during the apheresis procedure; this phenomenon was mirrored in the model (definitely a single pool model). In contrast, the level of anti-dsDNA, as measured by ELISA, decreased in accordance with the increase of treated plasma volume in both the clinical and the in vitro apheresis procedures. Therefore, an increased titer of anti-dsDNA as measured by RIA immediately following clinical apheresis cannot be accounted for exclusively by an inflow of antibodies from a secondary (extravascular) pool into the circulating plasma. In short, a one-compartment model is applicable and an explanation must be sought elsewhere.

Adult↗

PubMed1996

Synthesis of N-acetylcysteine conjugates of catechol estrogens.

The synthesis of N-acetylcysteine conjugates of 2-hydroxyestrone (2-OHE1) and 4-hydroxyestrone (4-OHE1) is described. The reaction of estrone 2,3-quinone with N-acetylcysteine provided 2-OHE1 and its C-4 and C-1 thioether conjugates in a ratio of 1:1, while estrone 3,4-quinone with N-acetylcysteine gave 4-OHE1 and its C-2 thioether conjugate as a sole product. Their structures were characterized by inspection of NMR spectra, chemical derivatization (methylation and acetylation), and comparison with the reactivity of 4-bromoestrone 2,3-quinone or 2-bromoestrone 3,4-quinone toward N-acetylcysteine.

Acetylcysteine↗

PubMed1996

Preparation of specific antiserum to 17 alpha-estradiol 17-N-acetylglucosaminide.

A specific enzyme immunoassay (EIA) method has been developed for 17 alpha-estradiol 17-N-acetylglucosaminide as a model compound instead of 15 alpha-hydroxyestrogen 15-N-acetylglucosaminides. Two new haptens, 3-(omega-carboxyalkyl) ether derivatives of 17-alpha-estradiol 17-N-acetylglucosaminide, were synthesized and conjugated with bovine serum albumin (BSA). The EIA was newly established using specific antiserum elicited against 3-(1-carboxypropyl) ether of 17 alpha-estradiol 17-N-acetylglucosaminide (17NAG CPE)-BSA conjugate and beta-galactosidase-labeled 17NAG CPE as a labeled antigen. An appropriate dose-response curve of EIA for 17 alpha-estradiol 17-N-acetylglucosaminide was obtained in the range of 20-1000 pg/tube. The specificity of EIA proved to be satisfactory in terms of cross-reactivities to related compounds including 15 alpha-N-acetylglucosaminides. The proposed method will be applicable to the preparation of antisera for use in EIA of 15 alpha-hydroxyestrogen 15-N-acetylglucosaminides.

Acetylglucosamine↗

PubMed1996

[Swyer-James syndrome with pneumomediastinum and subcutaneous emphysema due to bronchial asthma].

A 24-year-old woman was admitted to our hospital due to moderate asthmatic attacks. Dyspnea and hypoxemia progressed gradually despite medication. A chest roentgenogram revealed left unilateraly hyperlucency with pneumomediastiumn and subcutaneous emphysema. Swyer-James syndrome was diagnosed. Several cases of Swyer-James syndrome with bronchial asthma airway hyperresponsiveness have been reported, but we know of no reports of Swyer-James syndrome with pneumomediastinum and subcutaneous emphysema due to prolonged asthmatic attacks. Pneumomediastinum and subcutaneous emphysema may be caused by abnormally high pressures in the bronchial lumen and alveolar space during asthmatic attacks, because the emphysematous lesion may be structurally weak.

Adult↗

PubMed1996

Ameloblastin expression in rat incisors and human tooth germs.

We recently identified ameloblastin as an ameloblast-specific gene product from a rat incisor cDNA library (Krebsbach et al., J. Biol. Chem. 271: 4431-4435, 1996). Here we report the developmental pattern of expression of ameloblastin in rat incisors and human tooth germs as visualized by in situ hybridization and immunochemistry. Compared to the expression of amelogenin, the major ameloblast product, ameloblastin mRNA was more widely expressed in ameloblasts from the presecretory to the late maturation stage of development. Ameloblastin mRNA was first observed in the juxtanuclear cytoplasm or presecretory stage ameloblasts, gradually increased in the distal cytoplasm of secretory stage ameloblasts and was found throughout the cytoplasm of early to late maturation stage ameloblasts. The immunostaining of ameloblastin, using a monospecific antibody raised against a recombinant protein, showed intense reactivity in Tomes' processes of secretory stage ameloblasts and surrounding enamel. The immunoreaction was concentrated in the juxtanuclear cytoplasm of late maturation stage ameloblasts. High-resolution colloidal gold immunocytochemistry established the presence of ameloblastin antigenicity in the Golgi apparatus, secretory granules in Tomes' process and enamel. Human tooth germs in early to late bell stage also expressed ameloblastin mRNA and ameloblastin antigenicity in the ameloblasts. Western blot analysis of protein extracts from rat incisor tissues indicated that ameloblastin can be found in the enamel epithelial tissue and in mineralized enamel, as well as in the EDTA decalcification solution. These data indicate that ameloblastin is an ameloblast secretory product which is sequentially expressed from the presecretory to the late maturation stage in rat and human teeth. This unique developmental pattern suggests that ameloblastin may have a broader role in amelogenesis than amelogenin and tuftelin.

Ameloblasts↗

PubMed1995

Gene expression of epimorphin in rat incisor ameloblasts.

Epimorphin has been recently identified as an important factor in the morphogenesis of epithelial cells. A cDNA encoding epimorphin from skin of newborn mice was cloned by the polymerase chain-reaction technique before the preparation of digoxigenin-labelled cRNA probes. In situ hybridization of longitudinal sections of rat incisors revealed a distinct pattern of expression of epimorphin mRNA in the ameloblast layer. Epimorphin mRNA was detected from the presecretory stage up to the beginning of the maturation stage of amelogenesis. With the identification of this expression by epithelial-derived cells, i.e. ameloblasts, it is thought likely that epimorphin is one of the factors that modulate the differentiation cascade of ameloblasts in the course of amelogenesis.

Ameloblasts↗