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Biomedical subjects

T Nishimura

Publications and source records attributed to T Nishimura.

At least 685 records · Page 38Linked to original sources
PubMed1993

Cellular localization of serotonin transporter mRNA in the rat brain.

Expression of serotonin (5-hydroxytryptamine, 5-HT) transporter mRNA in the rat brain was examined by in situ hybridization histochemistry with a synthetic oligonucleotide probe. 5-HT transporter mRNA was expressed in neurons in most of the raphe nuclei. The dorsal and median raphe nuclei contained intensely labeled neurons, while the caudal linear nucleus, raphe magnus nucleus, raphe pontis nucleus, raphe pallidus nucleus and the raphe obscurus nucleus contained weakly or moderately labeled neurons. The localization pattern of the 5-HT transporter mRNA-positive neurons coincides fairly well with that of 5-HT-immunoreactive neurons, indicating that 5-HT transporter is primarily located in serotonergic neurons.

Animals↗
PubMed1993

Inhibition of inflammatory liver injury by a monoclonal antibody against lymphocyte function-associated antigen-1.

When mice were given an i.v. injection of LPS 7 days after an i.v. injection of Propionibacterium acnes, liver injury and a rapid increase of serum alanine aminotransferase and asparagine acid aminotransferase occurred. The in vivo administration of mAb against LFA-1 on days 1, 2, and 3 after the i.v. injection of P. acnes resulted in a potent inhibition of all these dysfunctions. Using P. acnes and the LPS model, we found that anti-LFA-1 mAb protected the mice from P. acnes and LPS-induced lethal shock. During the course of P. acnes and LPS-induced liver injury, inflammatory cells infiltrated the liver and caused a massive hepatic cell necrosis. Flow cytometry revealed that the liver-infiltrating cells were mainly leukocytes expressing a higher level of LFA-1 antigen than that seen in the normal liver. These results suggested that the LFA-1 molecule on liver-infiltrating leukocytes may play an important role in the induction of inflammatory liver injury.

Alanine Transaminase↗
PubMed1993

Expression of sialyl Lewis(x) antigen on human T cells.

Sialyl Lewis(x) (sLe(x)) antigen, which has been introduced as tumor-associated cell surface carbohydrates, was demonstrated to be expressed on a subpopulation of human CD4+ and CD8+ T cells. It was also demonstrated that the majority of gamma delta T cells as well as natural killer cells expressed a high level of sLe(x) antigen. The sLe(x) expression on T cells were up-regulated by activation with various T cell stimulants. The sLe(x)+ CD4+ T cells were enriched in CD4+CD45RO+ memory type of T cells but not in CD4+CD45RA+ T cells. Moreover, sLe(x)+ CD4+ T cells were demonstrated to show higher proliferative responses to T cell stimulants such as CD4+CD45RO+ T cells. These results initially clarified the expression of sLe(x) carbohydrate on human T cells and indicated the important role of sLe(x)-expressing T cells in immune responses.

Antibodies, Monoclonal↗
PubMed1993

[MR cisternography using "long echo train length fast spin echo sequence" for demonstrating the inner ear].

Excellent quality of MR cisternography was acquired using "long echo train length fast spin echo sequence" (TR/TE = 2666/200, ETL = 24, 6 or 8 NEX, 3 mm thickness, 0 mm interslice gap, 19 cm FOV, 512 * 384, 2 DFT method). The inner ear anatomy such as canaliculus cochleae or lamina spiralis ossea were well visualized. The VII, VIII th nerve bundles within the internal auditory canal were detectable as 1 to 4 bundles. The vessels in the cerebellopontine angle or the internal auditory canal were also demarcated from the VII, VIII th nerve bundles because of their flow void. Signal to noise ratio seemed to be better than 3 DFT method, however limited spatial resolution in the cranio-caudal direction might require additional sagittal or coronal scan.

Adult↗
PubMed1993

Molecular defect in factor IX Tokyo: substitution of valine-182 by alanine at position P2' in the second cleavage site by factor XIa resulting in impaired activation.

Utilizing polymerase chain reaction and directly sequencing the amplified exon 6 of the factor IX gene derived from a mild hemophilia Bm patient, we have identified a T to C mutation at nucleotide 20,525. This point mutation predicted a Val182 to Ala substitution in the abnormal factor IX molecule, designated as factor IX Tokyo. The patient manifested a low factor IX activity and a moderately prolonged ox-brain prothrombin time but a normal factor IX antigen level in plasma. Immunopurified factor IX derived from the patient was found to have a normal molecular weight but a reduced specific activity (23% of normal). Limited proteolysis by activated factor XI or by a snake venom-derived factor X-activating enzyme was considerably delayed, indicating the presence of structural alteration(s) most probably at or near the second enzyme-cleavage site. Once activated, however, factor IXa Tokyo was able to activate factor X normally and was inactivated by antithrombin III also in a normal fashion. The structural model of factor IXa and a docking model of factor IX and activated factor VII (factor VIIa) suggested that the Val182 to Ala substitution would not affect the local conformation of the catalytic domain. This mutation would rather loosen the fitness of the molecule into the substrate-binding pocket of factor VIIa due to a shorter side chain of the Ala substitution at the P2' position of the second cleavage site.

Adolescent↗
PubMed1993

Activation of two angiotensin-generating systems in the balloon-injured artery.

Participation of angiotensin II in the myointimal proliferation following a vascular injury was postulated. This study assessed the potential involvement of the local angiotensin II-forming enzymes in injured arteries of dogs. The potential angiotensin II-forming enzymes are angiotensin-converting enzyme (ACE) and chymostatin-sensitive angiotensin II-generating enzyme (CAGE) which is highly homologous to or could be identical to the mast cell chymase. Both ACE and CAGE catalyze the conversion of angiotensin I to angiotensin II. We found that the enzymatic activities of ACE and CAGE, and the mRNA levels of ACE and chymase were increased in the injury-induced hypertrophied vessels. The results suggest that ACE and CAGE participate in the hypertrophy through the production of angiotensin II which is a growth promoter for vascular smooth muscle cells.

Angiotensin II↗
PubMed1993

Acceleration of bovine neurofilament L assembly by deprivation of acidic tail domain.

Functions of the tail region of neurofilament L have, to date, not been clearly elucidated. Bovine neurofilament L was cleaved into tail-less neurofilament L (50 kDa) and a tail fragment (19 kDa), by thrombin. Tail-less neurofilament L was deficit of the highly acidic domain of the tail region (approximately 77% of the entire region). Assembly of tail-less neurofilament L. was observed to be accelerated by both fluorometric and centrifugal measurements, compared with intact neurofilament L. The critical concentration of tail-less neurofilament L, which constitutes the constant unassembled pool, was approximately 0.25-times lower than that of neurofilament L. Under physiological conditions, tail-less neurofilament L formed a ribbon-like structure, whereas tail-less neurofilament L could form 10-nm filaments in an extremely low ionic-strength buffer in the presence of 1 mM MgCl2. An affinity-purified antibody directed against the tail fragment also accelerated neurofilament L assembly. The tail fragment neither coassembled with neurofilament L nor affect neurofilament L assembly. The acidic domain of the tail region may regulate neurofilament assembly and may be involved in 10-nm filament formation under physiological conditions.

Amino Acid Sequence↗
PubMed1993

[Detection of myocardial damage in patients with dilated cardiomyopathy using ultrafast CT].

The myocardial characteristics of DCM patients were investigated by ultrafast CT (UFCT), left ventriculography (LVG) and T1 myocardial scintigraphy (SCINTI). Late enhancement, focal wall thinning and intramyocardial fatty components were detected as focal abnormal findings by UFCT. The regions of asynergy detected by LVG and perfusion defect detected by SCINTI were well correlated with those of focal abnormal findings detected by UFCT. There were significant differences between patients with and without focal abnormal findings, in ejection fraction and end-diastolic pressure of left ventricle and the incidence of ventricular arrhythmia. It is possible that these focal abnormal findings represented focal ischemic myocardial damage in DCM patients. DCM patients were divided into two different functional groups by UFCT findings.

Adolescent↗
PubMed1993

Dominantly inherited motor and sensory neuropathy with excessive myelin folding complex.

The two patients in a family having the clinical and electrodiagnostic features of hereditary motor and sensory neuropathy (HMSN) are described. The main histological features of sural nerve were segmental demyelination and remyelination with moderate to marked loss of myelinated fibers, and myelin folding complex along all of the large and small myelinated fibers. These features appeared morphologically similar to those observed in HMSN with excessive myelin outfolding, or globular neuropathy. Southern blot analysis suggests that there were neither duplication nor deletion of the peripheral myelin protein-22 gene in the patients. The presented two patients may be a rare form of dominantly inherited HMSN with myelin folding complex.

Biopsy↗
PubMed1993

Semliki Forest virus capsid protein expressed by a baculovirus recombinant.

We have constructed a recombinant baculovirus which expressed the Semliki Forest (SFV) capsid (C) gene as a fusion protein under the control of the polyhedrin gene promoter. The sequence coding for C and part of the envelope E3 region were expressed as a polyprotein precursor. Spodoptera frugiperda (Sf9) insect cells infected with the recombinant virus produced a protein reacting with polyclonal rabbit antiserum that had been raised against the 33 kDa authentic C protein purified from SFV. Primer extension analyses showed that transcription from the polyhedrin promoter started in the late/very late consensus initiation motif. Due to its autoprotease activity, the recombinant C protein was contranslationally cleaved within its C-terminus and the mature protein remained undegraded for long periods of time. Spodoptera frugiperda cells infected with recombinant virus synthesized large amounts of C protein. The recombinant protein was karyophilic as is authentic SFV C protein and it was translocated into the nucleus; there, it was associated with nucleolus-like structures.

Amino Acid Sequence↗
PubMed1993

Evaluation of agents for use in medium for selective isolation of Lyme disease and relapsing fever Borrelia species.

Barbour-Stoenner-Kelly (BSK) II medium containing fosfomycin, 5-fluorouracil, trimethoprim and sulfamethoxazole was evaluated for the selective isolation of the Borrelia species responsible for Lyme disease and relapsing fever. The maximum non-inhibitory concentrations of fosfomycin, 5-fluorouracil, trimethoprim and sulfamethoxazole for six strains of borreliae were 500 to > 1000 micrograms/ml, 250 to > 500 micrograms/ml, 125 to 500 micrograms/ml and 125 to 500 micrograms/ml, respectively. The combination of four agents (fosfomycin 400 micrograms/ml, 5-fluorouracil 100 micrograms/ml, trimethoprim 10 micrograms/ml, sulfamethoxazole 50 micrograms/ml) did not inhibit the growth of borreliae, allowing growth in cultures inoculated with a few organisms (theoretically a single organism). In contrast, the four-agent combination completely inhibited the growth of 12 of 13 other bacterial strains tested as possible contaminants. This combination also allowed the selective growth of borreliae in experimentally contaminated specimens. The four-agent combination in BSK II medium may be useful for selective isolation of Borrelia species responsible for Lyme disease and relapsing fever from clinical and environmental samples.

Bacteriological Techniques↗
PubMed1993

Effect of etodolac on type-II collagen-induced arthritis in mice.

We tested the effect of etodolac on the development of type-II collagen-induced arthritis in DBA/1J mice. It was administered orally once daily for 35 days after the primary immunization with type-II collagen. Etodolac (10 mg/kg) significantly inhibited the development of signs of arthritis on day 28 to day 35. Indomethacin (1 mg/kg) also significantly inhibited it on day 29 to day 34. Radiographic examination showed that etodolac (10 mg/kg) significantly prevented the development of osteopenia, bone erosion and new bone formation of the joints on day 35, while indomethacin (1 mg/kg) significantly prevented only the development of bone erosion. Histopathological examination showed that both etodolac (10 mg/kg) and indomethacin (1 mg/kg) significantly prevented the development of synovitis, erosion of cartilage of the joints and bone destruction of the limbs on day 35. Etodolac and indomethacin did not affect the serum level of anti-type-II collagen antibodies. These results suggest that etodolac and indomethacin suppress type-II collagen-induced arthritis without affecting humoral immune responses.

Animals↗
PubMed1993

Characterization of the T cells in aged rat bone marrow.

In this study, we determined the characteristics of CD3-positive (CD3+) T cells existing in rat bone marrow (BM). In contrast to splenic T cells, BM CD3+ T cells are composed of a higher proportion of CD8+ T cells, and the number of both cell types increased with age. Such CD3+ T cells in aged rats showed a similar usage of TCR V beta as splenic T cells, suggesting that BM CD3+ T cells are thymus-dependent and composed of an ordinary population in view of the expression of the TCR beta-chain. Purified T cells obtained from aged rat BM showed a markedly proliferative response by stimulation with immobilized anti-CD3 mAb, as did splenic T cells. However, the addition of BM non-T cells completely inhibited the response of both BM and splenic T cells in vitro. These results suggest that T cells in rat BM are negatively regulated by BM non-T cells in their response to the TCR-mediated signal not to disrupt the microenvironment of the BM.

Aging↗
PubMed1993

Thymic nurse cell clone supports the differentiation of CD4-8- thymocytes into CD4+8+ thymocytes in vitro.

A previously reported thymic nurse cell clone, TNC-R3.1 could form a unique complex with isolated adult mouse CD4-8- (DN) thymocytes and greatly sustained the cell viability of DN thymocytes in suspension culture. In addition, the TNC-R3.1 clone supported the differentiation of DN thymocytes into CD4+8+ (DP) thymocytes in a short-term culture. Addition of IL-7 into the coculture markedly enhanced DN thymocyte-TNC interaction and induced the proliferation and differentiation of DN thymocytes, though IL-7 alone did not induce the differentiation of DN thymocytes. Separation of DN thymocytes from TNC-R3.1 monolayer using a Millicell caused a great inhibition of the DN thymocyte differentiation, suggesting that direct contact between TNC-R3.1 cells and immature thymocytes was required for the differentiation of DN thymocytes. The kinetics study demonstrated that DN thymocytes started to differentiate into DP thymocytes through CD3-CD4+J11d+ intermediate cells 8-12 h after the initiation of the culture with TNC-R3.1 plus IL-7. The generation of DP thymocytes became maximal 20 h after coculture and gradually decreased thereafter. Furthermore, we demonstrated that TNC-R3.1 could support the differentiation of CD3+CD4+CD8- or CD3+CD4-CD8+ thymocytes from CD3-CD4-CD8- thymocytes in the presence of IL-7 and IL-2. These data indicate that our established in vitro culture system mimics the early stage of the intrathymic T cell developing pathway.

Animals↗
PubMed1993

Ontogeny of dopamine transporter mRNA expression in the rat brain.

The ontogeny of dopamine transporter (DAT) gene expression was studied in the rat brain. DAT mRNA was first detected in neurons of the ventrocaudal mesencephalon on embryonic day 14 (E14). By E18, intensely expressing neurons in the ventral tegmental area and substantia nigra resembled the pattern found in adult midbrain. DAT mRNA is not abundant in the hypothalamus and the olfactory bulb at any stage of development. These results parallel those noted for tyrosine hydroxylase gene expression in mesencephalon.

Animals↗
PubMed1993

Differential vulnerability in the hindbrain neurons and local cerebral blood flow during bilateral vertebral occlusion in gerbils.

Differential vulnerability in the hindbrain neurons was examined immunohistochemically during hindbrain ischemia in the gerbil. Hindbrain ischemia was produced by extracranial occlusion of the bilateral vertebral arteries just before their entry into the transverse foramen of the cervical vertebra. Local cerebral blood flow was measured by quantitative autoradiographic technique after 5 min of ischemia and was reduced to less than 5 ml/100 g per min in the cerebellum, the pons, and the medulla, indicating that severe and reproducible hindbrain ischemia was induced immediately after occlusion. For immunohistochemical investigation, four gerbils each were used for each ischemic period of 5, 10, 15, and 30 min. Immunohistochemical lesions, detected by the reaction for microtubule-associated protein 2, were visible in the lateral vestibular nucleus and the cerebellar interpositus nucleus even after 5 min of ischemia. These results suggested that these areas were more vulnerable than others, although blood flow was markedly reduced in various regions of the hindbrain. In contrast, areas related to respiratory or cardiovascular control were rather resistant to ischemia. The present study suggests that selective vulnerability during hindbrain ischemia depends mainly on different metabolic characteristics inherent to various neurons in the hindbrain.

Animals↗