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Biomedical subjects

M Mizuguchi

Publications and source records attributed to M Mizuguchi.

At least 91 records · Page 5Linked to original sources
PubMed1996

Gastric lesions in 76 patients with adult T-cell leukemia/lymphoma. Endoscopic evaluation.

BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is caused by human T-lymphotropic virus type I. Gastric lesions in ATLL have not been described precisely, whereas the clinical features of ATLL have been well documented. The goal of the present study was to review gastric lesions, including gastric involvement, of patients with ATLL who were admitted to our hospital. METHODS: Endoscopic examination of the upper gastrointestinal tract was performed on 76 of 110 patients who were admitted to our hospital between 1981 and 1994. Gastric involvement was diagnosed by histologic examination of biopsy specimens of gastric lesions. Types of gastric lesions, histologic features, and survival periods in patients with ATLL were summarized. RESULTS: Of the 76 patients with ATLL who underwent an endoscopic examination, 23 had gastric involvement (30.3%). Twenty-seven patients had other gastric lesions: 10 with peptic ulcers (13.2%), 8 with gastric erosions (10.5%), 3 with submucosal tumors (3.9%), 2 with hyperplastic polyps (2.6%), 1 with gastric adenoma (1.3%), and 3 with gastric carcinomas (3.9%). The most frequent endoscopic configuration of gastric involvement with ATLL was the diffuse type with ulceration, and the most common histology was large cell type. Among those with the acute type ATLL, the survival period of those patients with gastric involvement was less than that of the patients without gastric involvement. In contrast, the survival period for lymphoma type ATLL did not differ among the groups regardless of gastric involvement. CONCLUSIONS: This study demonstrated that 30.3% of patients with ATLL had gastric involvement and 13.2% had peptic ulcers. Gastric involvement of ATLL was one of the prognostic factors in acute type ATLL, whereas it had no influence on the prognosis of lymphoma type ATLL.

Female↗
PubMed1996

Structure of chromosomal DNA coding for Pseudomonas putida S-1 salicylate hydroxylase.

A gene coding for the salicylate hydroxylase has been isolated from chromosomal DNA of Pseudomonas putida S-1 and sequenced. The DNA fragment contained an open reading frame of 1266 bp encoding a polypeptide of 421 amino acid residues. The predicted amino acid sequence of the protein gave a good agreement with the sequences determined with the peptides isolated from the enzyme but methionine residue in the amino terminal was deleted in the N-terminal sequence of the enzyme protein. The nucleotide and amino acid sequences of the salicylate hydroxylase shared several common characteristics with those of the enzyme encoded on the plasmid DNA of P. putida PpG7; homology of nucleotide sequence is 58% and that of amino acid sequence is 56%. We could find two large conserved regions of the amino acid sequence at or near FAD- and NADH-binding regions. The FAD-binding site locates on the amino terminal and a lysine residue, functioning as an NADH-binding site (K. Suzuki, M. Mizuguchi, T. Gomi, and E. Itagaki, 1995, J. Biochem. 117,579-585), locates as Lys163.

Amino Acid Sequence↗
PubMed1996

Immunohistochemical expression of cell adhesion molecule L1 during development of the human brain.

We demonstrated the expression of neural cell adhesion molecule, L1, during human brain development by immunostaining with anti-L1 fibronectin domain antibody. In the human cerebellum, the inner half of the external granular and molecular layers, mostly parallel fibres, and the Purkinje cell layer were immunoreactive for L1 from the early foetal period of 13-15 gestational weeks (GW). Immunoreactivity was strongest in the molecular layer in the perinatal period. The subcortical white matter and dentate layer were immunoreactive in foetal life. In the human cerebrum, the outer half of the molecular layer, together with Cajal-Retzius cell bodies, were positively stained until 30-34 GW, when afferent fibres develop over the entire cortex. The fibres in the white matter were strongly immunopositive in the fascicles until early infancy. These results suggest that L1 is temporally and spatially expressed in the developing brain, and may play important roles in neural cell migration, neurite elongation, and axonal fasciculation.

Adolescent↗
PubMed1996

Expression of markers for both neuronal and glial cells in human amniotic epithelial cells.

Human amniotic epithelial (HAE) cells are formed from amnioblasts, separated from the epiblast at about the 8th day after fertilization. We attempted to detect various developmental antigens specific to neural cells by immunocytochemical methods. The cultured HAE cells displayed positive immunoreactivity to RC1, vimentin, A2B5, neurofilament proteins, microtubule-associated protein 2 (MAP2) and MAP2 kinase. In addition, the cells also demonstrated immunoreactivity to glial fibrillary acidic protein, CNPase, myelin basic protein and galactocerebroside. The appearance rate of positive cells was more than 50% in cells positive to RC1, A2B5, vimentin or neuronal markers, and 20-30% to glial cell markers. Double staining showed the heterogeneous appearance of oligodendrocyte lineage cells. These data indicate that HAE cells may have the putative multipotentiality of neurons, astrocytes and oligodendrocytes.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1996

Immunochemical and immunohistochemical localization of Bcl-x protein in the rat central nervous system.

To explore the role of bcl-x in the regulation of cell death in the nervous system, we produced monoclonal antibodies against rat Bcl-xL protein, the major product of the rat bcl-x gene that inhibits apoptosis, and defined its distribution in rat neural tissues by immunochemical and immunohistochemical means. Western blotting of tissue homogenates identified the Bcl-x protein as two bands with molecular weights of about 29 and 31 kDa. The level of Bcl-x expression in the nervous system was high, being comparable to that in the hematolymphoid system, and higher in the fetal than in the adult brain. Subcellular fractionation studies localized Bcl-x to various subcellular compartments. In tissue culture, Bcl-x was produced by all the cell types examined, including neurons, astrocytes, oligodendrocytes and microglial cells. Immunohistochemistry revealed that Bcl-x immunoreactivity was more intense in the gray than in the white matter. In the fetal cerebral cortex, labeling was mostly confined to the neuronal perikarya, whereas in the more mature brain, the neuropil of the gray matter, as well as the glial cells in the white matter, was also stained.

Aging↗
PubMed1996

High expression of Bcl-x protein in the developing human cerebellar cortex.

The gene bcl-x, which is related to a bcl-2, regulates programmed cell death. bcl-x may function in the development of the nervous system. We raised a polyclonal antibody against human Bcl-x protein, and investigated its distribution in the developing human cerebellum. Western blotting revealed that Bcl-x expression in the cerebellum is higher in the fetal, than in the postnatal period. Immunohistochemical studies of fetal brains localized intense Bcl-x immunoreactivity in the granule cell processes at 13-22 gestational weeks and in the Purkinje cell bodies at 24-38 weeks. The immunoreactivity decreased after birth, but was retained in the Purkinje cells at a low level until adulthood. These results suggested that Bcl-x expression in the cerebellum is developmentally regulated and involved specifically in the development of neuronal subpopulations.

Adult↗
PubMed1996

Loss of tuberin from cerebral tissues with tuberous sclerosis and astrocytoma.

We studied the expression of tuberin, the TSC2 gene product, in cerebra with or without tuberous sclerosis. Tuberin was abundant in the gray matter of normal cerebra, but was undetectable in the subependymal astrocytomas from 3 patients with tuberous sclerosis. In 1 patient, cortical tubers and normally appearing cortical tissue also showed a marked loss of tuberin. These results indicate the critical role of tuberin in the neuropathology of tuberous sclerosis.

Adolescent↗
PubMed1996

Inhibition of HTLV-I induction and virus-induced syncytia formation by oligodeoxynucleotides.

HTLV-I is an exogenous human retrovirus that is a causative agent of adult T cell leukemia (ATL). In addition to the structural genes (gag, pol and env), a gene termed pX is postulated to be associated with leukemogenesis in ATL. Since no effective chemotherapy is currently available, it is important to find suitable therapeutic means against ATL. Here, we tested the inhibitory effect of antisense oligodeoxynucleotides (ODNs) on HTLV-I infection in different systems. ODNs were synthesized with the phosphorothioate backbone targeted to either structural genes or transactivator genes. The phosphorothioate ODNs were found to have two distinct target sites to exert their effect on HTLV-I infection: 1) Several ODNs, including sense ODNs and random oligomers, blocked syncytium formation induced by HTLV-I at a concentration of 0.1 microM. Their inhibitory effect on syncytium formation seemed to be exerted in a nonantisense manner, most probably due to their interaction with the cell membrane. 2) Efficient suppression by ODNs of gag gene expression after chemical induction was observed in HTLV-I-transformed T cells in an antisense manner. In this suppression, tax-antisense ODN showed virtually complete inhibition of gag protein expression, but not RNA expression, at the concentration of 0.1 microM, whereas tax-sense ODN displayed a weak inhibitory effect. Our results suggest that the influence of the phosphorothioate compound should be considered from the aspect of two separated mechanisms of antiviral activity, the effects on early (viral adsorption) and late (translation) phase infection.

Animals↗
PubMed1996

Neuronal and vascular pathology produced by verocytotoxin 2 in the rabbit central nervous system.

To study the pathogenesis of the central nervous system (CNS) involvement associated with verocytotoxin-producing Escherichia coli infection, we developed an animal model by administering verocytotoxin 2 to rabbits either intravenously or intrathecally. After an interval of 2-9 days, the rabbits became paralyzed in a dose-dependent manner and in the absence of renal impairment. The minimal intravenous and intrathecal doses that produced these neurological signs were 250 and 0.4 ng/kg, respectively. After intravenous administration, most of the toxin was cleared from the serum within 24 h, with concomitant transition of a small amount into the cerebrospinal fluid. Pathological examination revealed that neurons in various CNS regions showed atrophy, cytoplasmic hyperchromasia and nuclear pyknosis as early as 6 h after administration. The distribution of affected neurons was constant and irrespective of the route of administration. Abnormalities of the blood vessels, such as the thickening of arterioles walls, were noted from 2 days after administration. The vascular lesions became more prominent after the intrathecal injection, which caused thrombosis and multiple infarction. Selective deposition of the toxin on the vessel walls was demonstrated immunohistochemically. Thus, the pathological manifestations of verocytotoxin 2 neurotoxicity consisted essentially of two types of lesions, early neuronal and late vascular, both of which might have developed under the influence of the toxin that had entered the CNS by crossing or circumventing the blood-brain barrier.

Animals↗
PubMed1996

Transient expression of apolipoprotein-E in neonates with pontosubicular neuron necrosis.

An apolipoprotein-E (Apo-E) immunohistochemical study was performed on neonates with pontosubicular neuron necrosis (PSN), aged 38-42 weeks of gestation, and compared to findings for age-matched neonates without PSN. Apo-E was expressed in neurons in both the pontine nuclei and pyramidal layer of the hippocampus, as well as astrocytes of only the PSN cases. The immunoreactive neurons did not exhibit karyorrhexis and were found in neonates by the age of 6 days. Apo-E may be produced by astrocytes and taken up by neurons on membrane remodeling during early responses to cerebral hypoxic or ischemic insult in PSN neonates.

Apolipoproteins E↗
PubMed1996

Immunohistochemical expression of tumor necrosis factor alpha in neonatal leukomalacia.

The expression of tumor necrosis factor alpha (TNF alpha) was examined in infants with leukomalacia by means of immunohistochemical methods with an antihuman TNF alpha monoclonal antibody. We studied 23 patients with neonatal leukomalacia, classified as having "focal," "widespread," or "diffuse" disease according to the distribution of the lesions, and 18 age-matched controls. TNF alpha immunoreactivity was positive in 19 of the 23 (83%) patients with leukomalacia, and in 7 of the 18 (39%) controls. TNF alpha was expressed mainly in glial cells in the deep white matter in both groups, and was most abundant around the necrotic foci in the focal group. TNF alpha immunoreactivity appeared earlier in patients with leukomalacia than in controls, being first detected at 25 and 29 weeks gestation, respectively. Immunofluorescence double-labeling revealed the TNF alpha -immunoreactive cells were Ricinus communis agglutinin-1 (RCA-1)-positive microglial cells. Thus, our study revealed increasing expression of TNF alpha in the normally developing brain during the late fetal period, and overproduction of TNF alpha by microglial cells associated with the pathogenesis of neonatal leukomalacia.

Brain↗
PubMed1996

Hypertrophy of the cerebral white matter in hemimegalencephaly.

We morphometrically measured the cut surface of the cerebral hemisphere and localized epidermal growth factor (EGF)-like immunoreactivity in 4 patients with hemimegalencephaly. On the affected side, the area of cerebral white matter was more than twice as large as that on the unaffected side, while the area of the cerebral cortex on the affected side was relatively small. EGF-like immunoreactivity was demonstrated in cortical neurons (4 of 4 patients) and glial cells (3 of 4 patients), notably in astrocytes. Significant enlargement of the cerebral white matter compared to the cerebral cortex and the expression of EGF-like molecules in astrocytes suggest excessive proliferation in the white matter with hemimegalencephaly and the possible relevance of EGF to these events.

Brain↗
PubMed1996

A tyrosine kinase-like molecule is localized in the nuclear membrane of neurons: hippocampal behavior under stress.

Protein tyrosine kinases play important roles in the development of the mammalian nervous system during embryogenesis and in the maintenance of function of the adult brain. Using a semi-nested PCR technique based on a short amino acid motif of protein tyrosine kinases, we isolated a human genomic DNA encoding a peptide whose sequence was related to known mammalian protein tyrosine kinases. The expression was examined by Northern blot analysis, and transcripts were detected almost exclusively in the brain. The corresponding cDNA was sequenced, and it was revealed that the gene designated as byk coded for a receptor-like molecule with a motif of protein tyrosine kinase. Immunohistochemical analysis demonstrated that the Byk protein was expressed in neurons and was located in the nuclear envelope. To understand the physiological significance of the Byk protein, we investigated the behavior of this molecule in the hippocampus after ischemia. Byk-like immunoreactivity disappeared from the neurons in the fields CA1 through CA3 and the dentate gyrus of the hippocampus following 20 min of ischemia. After recirculation of blood flow, neurons in the CA3 field and the dentate gyrus re-expressed Byk-like antigen but CA1 neurons did not. Interestingly, Byk-like immunoreactivity was detected in microglial cells and astrocytes in the CA1 field that were activated after ischemia. Byk could be a new tool to study the neuron-glia and glia-glia interactions.

Amino Acid Sequence↗
PubMed1996

Excessive glutamate receptor 1 immunoreactivity in adult Down syndrome brains.

We studied the immunohistochemical localization of the glutamate receptor subunits GluR1, GluR2/3, and GluR4 in brains of Down syndrome patients and of normal controls. In cerebral cortex of both the control and Down syndrome patients, weak GluR1 immunoreactivity was observed in the cytoplasm of neurons, especially pyramidal neurons, after 34 weeks of gestation. In Down syndrome patients, the staining of the neurons became more distinct after 21 years of age. After 32 years of age in Down syndrome patients, GluR1 immunoreactivity was also observed in the senile plaques, including the diffuse, primitive, and classic plaques. The immunoreactivity was observed in a cluster of several small swollen neurites in the senile plaques. GluR2/3 and GluR4 immunoreactivity was also observed in the cytoplasm of neurons, especially pyramidal neurons, after 34 weeks of gestation in controls and Down syndrome patients, but not in senile plaques. GluR4 immunoreactivity was also observed in the cell processes of astrocytes in both the normal and the Down syndrome brains. Excessive immunoreactivity of GluR1 may be involved in degeneration of neurons and the early formation of senile plaques in Down syndrome.

Adolescent↗
PubMed1996

Involvement of NK2 receptors rather than NK1 receptors in bronchial hyperresponsiveness induced by allergic reaction in guinea-pigs.

1. In this study, the role of neuropeptides in antigen-induced bronchoconstriction and bronchial responsiveness in guinea-pigs was evaluated by use of phosphoramidon, the inhibitor of neutral endopeptidases (NEP), the NK1 receptor antagonist, FK888, and the dual NK1/NK2 receptor antagonist, FK224. The role of endogenous tachykinins in bronchial hyperresponsiveness induced by inhaled capsaicin was also observed with FK888 and FK224. 2. Allergic bronchoconstriction and bronchial responsiveness was evoked by inhalation of ovalbumin (OA), and increasing doses of methacholine were inhaled at 5-min intervals for 30 min after OA challenge in passively sensitized and artificially ventilated guinea-pigs. Animals were treated with a 30 s inhalation of phosphoramidon (10(-3)M) or saline 10 min before the OA challenge. FK888 (1.0 or 10 mg kg-1) or FK224 (1.0 or 10 mg kg-1) was administered intravenously 5 min before the OA challenge. 3. Treatment with phosphoramidon did not alter the increase in the lateral pressure at the tracheal tube (Pao) caused by OA inhalation or the increase in bronchial response to methacholine following the allergic reaction. Pretreatment with FK224 did not inhibit the increase in Pao after antigen provocation but did significantly inhibit antigen-induced bronchial hyperresponsiveness in a dose-dependent manner, while FK888 did not affect either allergic bronchoconstriction or post-allergic bronchial hyperresponsiveness. 4. Histamine, 25, 50, 100 or 200 micrograms ml-1 was inhaled for 20 s at 5-min intervals in non-sensitized guinea-pigs which were pretreated with inhalation of subthreshold dose of capsaicin (10(-7) M). FK888 or FK224, each at a dose of 0.1 or 1.0 mg kg-1, or vehicle was given to guinea-pigs intravenously 3 min before inhalation of capsaicin. The capsaicin inhalation significantly potentiated bronchial responsiveness to histamine, compared with control. The capsaicin-induced bronchial hyperresponsiveness was completely blocked by FK224 in a dose-dependent manner but not by FK888. 5. These results suggest that NK2 receptors rather than NK1 receptors may play an important role in bronchial hyperresponsiveness induced by antigen challenge as well as capsaicin while tachykinins do not play a primary role in the acute bronchospasm elicited by antigen challenge in passively sensitized guinea-pigs.

Animals↗
PubMed1996

[Classification and pathogenesis of cerebral cortical malformations].

Cerebral cortical malformation is now diagnosed by neuroimagings, and important as a cause of developmental disorder or epilepsy. The classification of cortical malformations was tried from developmental aspect, and agyria in Miller-Dieker syndrome and polymicrogyria in Fukuyama-type congenital muscular dystrophy were compared on their pathogeneses. Unilateral hemimegalencephaly and focal cortical dysplasia were reviewed on literatures.

Brain Diseases↗
PubMed1996

Sensory neuropeptides are not directly involved in bronchial hyperresponsiveness induced by interleukin-8 in guinea-pigs in vivo.

BACKGROUND: Interleukin-8 (IL-8) has been shown to be a chemotactic factor for neutrophils, T-lymphocytes and eosinophils. Repeated intranasal administration of IL-8 enhances bronchial responsiveness to inhaled histamine in guinea-pigs. Neuropeptides which are released from C-fibre nerve-endings have been postulated to induce bronchial hyperresponsiveness through neurogenic inflammation. OBJECTIVE: This study was conducted to examine whether sensory neuropeptides are involved in the IL-8-induced bronchial hyperresponsiveness. METHODS: IL-8 at a dose of 5 micrograms/kg was administered intranasally to guinea-pigs twice a week for 3 weeks. One day after the last administration, animals were anesthetized and artificially ventilated through tracheal cannula, and lateral pressure at the tracheal cannula (Pao) was measured as an overall index of airway responses to increasing concentrations of inhaled histamine (25, 50, 100, and 200 micrograms/mL). A NK1 and NK2 dual antagonist FK224 (10 mg/kg), a selective NK1 antagonist FK888 (10 mg/kg) or vehicle was intravenously administered 10 min before measurement of bronchial responsiveness. RESULTS: The IL-8 treatment significantly enhanced bronchial responsiveness to histamine (ANOVA P < 0.01). FK224 or FK888 did not alter the IL-8-induced bronchial hyperresponsiveness. CONCLUSION: We conclude that repeated intranasal administration of IL-8 causes bronchial hyperresponsiveness (BHR) and that neuropeptides such as neurokinin A and substance P do not directly contribute to the development of BHR induced by IL-8.

Animals↗