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Biomedical subjects

S Imamura

Publications and source records attributed to S Imamura.

At least 19 recordsLinked to original sources
PubMed1997

Histidine-44 of the A subunit of Escherichia coli enterotoxin is involved in its enzymatic and biological activities.

We examined the role in toxicity of histidine-44 of the A subunit of Escherichia coli enterotoxin, which is located in the active site cavity close to glutamic acid-112. Although amino acid substitution of histidine-44 usually renders a mutant toxin unstable to trypsin, one mutant, alanine-44 (His44Ala) was found to be stable. His44Ala did not show any agmatine:ADP-ribosyltransferase activity in the presence or absence of recombinant ADP-ribosylation factor. It showed no diarrheal or rabbit skin permeability activity and was a competitor in enterotoxin-ADP-ribosyltransferase assays containing recombinant ADP-ribosylation factor. These results suggest that like glutamic acid-112, histidine-44 plays an essential role in toxicity. A tentative model, which explains NAD+ catalysis and the transfer of the ADP-ribosyl moiety to a target amino acid, is proposed for histidine-44 and glutamic acid-112.

ADP-Ribosylation Factors↗
PubMed1997

Multiple cadherins are expressed in human fibroblasts.

Although the cell-cell adhesiveness of fibroblasts is thought to be related to wound healing, the molecular basis of this adhesiveness is still unknown. We isolated five kinds of cadherin fragments from the cDNA of human fibroblasts by polymerase chain reaction (PCR). Two of the five were known cadherins: PC43, a protocadherin containing six cadherin repeats in the extracelluar domain, and human Fat, which is the human homologue of the Drosophila tumor suppressor Fat. The other three were novel cadherin fragments, and we named them cadherins FIB1, FIB2, and FIB3. The expressions of cadherins including E-, P-, and N-cadherin, PC43, human Fat, and cadherins FIB1, FIB2, and FIB3 were compared in human fibroblasts, human melanocytes, and human epidermal keratinocytes. The latter six cadherins were expressed in human fibroblasts, and cadherins FIB1 and FIB2 were fibroblast-specific. These results suggest that diverse cadherin molecules may contribute to the cell-cell adhesion in human fibroblasts.

Amino Acid Sequence↗
PubMed1997

Bromodeoxyuridine-induced expression of endothelin A in A375 human melanoma cells.

Expression of endothelin (ET) receptor subtypes was examined in an experimental model of A375 human melanoma cell differentiation using the pyrimidine analog bromodeoxyuridine (BUdR). BUdR (10 microM)-treated cells had an increased surface area and an increased dendricity, were contact-inhibited and lacked tumorigenecity in athymic nude mice. The untreated A375 cells exclusively expressed ETB and BUdR-induced phenotypical changes were accompanied by induction of ETA expression as evidenced by northern blotting, [125I]ET-1 binding assay and [Ca2+]i measurement. Thus, BUdR-induced differentiation of A375 melanoma cells may provide a model system to study the receptor subtype switch in melanocyte development.

Animals↗
PubMed1997

Increase in radiation sensitivity of human malignant melanoma cells by expression of wild-type p16 gene.

The influence of wild-type p16 expression on the radiation sensitivity of human melanoma cell lines was investigated. MeWo cells, which alone expressed intrinsic wild-type p16 among six melanoma cell lines examined, showed higher radiosensitivity in comparison with the other five melanoma cells. The introduction of human wild-type p16 cDNA into A875 cells, which homozygously lost p16 genes, and AKI cells, which retained p16 gene but did not express p16 mRNA, led to increased sensitivity of those cells to X-ray irradiation. The radiosensitizing effect by the p16 introduction to those cells was prominent after rather higher doses of X-rays (8 and 10 Gy). In both A875 and AKI, no significant difference in sensitivities to UVC and cisplatin was observed between the parental and p16-transfectant cells. These results suggest that the loss or dysfunction of p16 gives melanoma cells the radioresistant characteristics.

Chromosomes, Human, Pair 9↗
PubMed1997

OX40 expressed on fresh leukemic cells from adult T-cell leukemia patients mediates cell adhesion to vascular endothelial cells: implication for the possible involvement of OX40 in leukemic cell infiltration.

We demonstrated previously that OX40 and its ligand, gp34, directly mediate adhesion of activated normal CD4+ T cells, as well as human T-cell leukemia virus type I (HTLV-I)-transformed T cells to vascular endothelial cells. In the present study, we examined expression of OX40 on fresh leukemic cells from patients with adult T-cell leukemia (ATL) and its possible involvement in cell adhesion. Flow cytometric analysis showed that peripheral blood mononuclear cells (PBMC) or lymph node tumor cells from 15 of 17 cases expressed significant levels of OX40 without stimulation. On the other hand, gp34 was not expressed on these cells, although its expression is also known to be associated with HTLV-I-infection. In Western blot analysis, a 50-kD protein band was detected by anti-OX40 monoclonal antibody (MoAb) in two ATL cases examined, as well as phytohemagglutinin (PHA) blasts and Hut102, an HTLV-I-infected T-cell line, but not in resting PBMC or Jurkat. Expression of OX40 mRNA was shown by reverse transcriptase-polymerase chain reaction in all ATL cases tested, PHA-blasts, and Hut102, but not in resting PBMC or Jurkat. We could not detect expression of HTLV-I viral mRNA in any of the cases tested. Cell adhesion assay was performed and in at least three cases, fresh ATL cells exhibited adhesion to human umbilical vein endothelial cells that could be considerably inhibited by either anti-OX40 MoAb or anti-gp34 MoAb. Immunohistochemical staining of skin biopsy specimens indicated that infiltrating mononuclear cells express OX40 in vivo. Taken together, these data indicate that leukemic cells from most, but not all, ATL patients constitutively express OX40, which may play a role in leukemic cell infiltration in addition to cell adhesion in vivo.

Adult↗
PubMed1997

A unique DNA sequence of human enterotoxigenic Escherichia coli enterotoxin encoded by chromosomal DNA.

We detected Ent plasmids in 300 strains of human enterotoxigenic Escherichia coli, but one strain, E. coli 240-3, had neither a small nor a large plasmid and encoded the heat-labile enterotoxin (LTh(240-3)) gene on its chromosome. DNA sequences showed that LTh(240-3) differed by 12 and 14 base pairs from LT (LTh) and LT (LTp) from human H10407 and porcine EWD299 strains, respectively. In deduced precursor toxins, LTh(240-3), LTh and LTp differed from LTh, LTp and LTh(240-3) at nine, eight and eleven positions, respectively. These data suggest that although LTh(240-3) encoded in the chromosome is antigenically similar to LTh, it cannot be grouped with LTh due to differences in its DNA and amino acids sequences.

Amino Acid Sequence↗
PubMed1997

Mitogen-inducible SIPA1 is mapped to the conserved syntenic groups of chromosome 19 in mouse and chromosome 11q13.3 centromeric to BCL1 in human.

Sipa1, previously called Spa1, is transcriptionally induced in the murine lymphoid cells following mitogenic stimulation and encodes a protein with a domain related to Rap1 GTPase activating protein (Rap1GAP) at the N-terminus and to PEST sequences followed by a leucine zipper motif at the C-terminus. Herein mouse genomic Sipa1, which consisted of 16 exons, was cloned. Gene linkage analysis using (BXD) recombinant inbred strains indicated that Sipa1 was mapped to the most centromeric region of chromosome 19 syntenic with the long arm of human chromosome 11. Human SIPA1 cDNA exhibited a striking homology to that of mouse throughout the entire region, with the overall identity being 90% at the amino acid level. Human genomic clones, which hybridized with both mouse and human SIPA1 cDNA but not with RAP1GAP cDNA, were then isolated. Fluorescence in situ hybridization (FISH) analysis using the human genomic clones indicated that SIPA1 was indeed mapped to chromosome 11q13, most likely to the 11q13.3 subregion. It was further indicated by double-color FISH that SIPA1 was located in the centromeric neighborhood of CCND1/ PRAD1, a presumed BCL1 oncogene.

Animals↗
PubMed1997

Age-related changes in the compound action potentials of the eighth nerve in guinea pigs.

The eighth nerve compound action potential (CAP) in 95 guinea pigs was measured using click stimuli to investigate age-related changes in their neural auditory thresholds. The animals were separated into three groups: group A (n = 43, 86 ears; 2-4 months old); group B (n = 29; 58 ears, 13-15 months old); and group C (n = 23; 46 ears, 23-25 months old). With increasing age, a gradual elevation of CAP thresholds was clearly seen among the three groups. The negative peak (N1) latencies of the CAP were prolonged, and the N1 amplitudes of the CAP decreased. There were significant differences in N1 latencies among the three groups and in N1 amplitudes between groups A and B, and between groups A and C. However, the rate of decline of the thresholds as well as the input-output function curves of the CAP varied in some of the oldest animals, suggesting that there were some individual differences in degenerative aging processes of the auditory system.

Acoustic Stimulation↗
PubMed1997

Human melanoma cells generate leukotrienes B4 and C4 from leukotriene A4.

We examined the synthesis of leukotrienes (LTs) in human melanoma cells in order to assess the function of LTs in human melanocytes. LTA4 hydrolase, which catalyzes the conversion of LTA4 to LTB4, was detected in the supernatant of cultured human melanoma (MeWo) cells and melanoma cells obtained from patients. Immunoblotting analysis using an antihuman LTA4 hydrolase antibody showed LTA4 hydrolase to be a 70-kDa protein in both MeWo and melanoma cells. Considerable activity of LTC4 synthase, which catalyzes the conversion of LTA4 to LTC4, was detected in the microsomal fraction of both MeWo and melanoma cells. The HPLC profile of the LTC4 synthase reaction products revealed that LTC4 was the main product. LTD4 was not detected under these conditions, indicating that the microsomal fraction of human melanoma cells lacks the membrane-bound gamma-glutamyl transferase that converts LTC4 to LTD4. LTC4 synthase activity was inhibited by the addition of MK-886, and was not altered by treatment with N-ethylmaleimide or 1-chloro-2,4-dinitrobenzene. These results indicate that the enzyme responsible for the conversion of LTA4 to LTC4 in human melanoma cells is LTC4 synthase rather than a nonspecific or microsomal glutathione-S-transferase. These results also suggest that human melanoma cells can generate LTB4 and LTC4 from LTA4, and that this process is catalyzed by two enzymes: LTA4 hydrolase and LTC4 synthase.

Dinitrochlorobenzene↗
PubMed1997

Flow cytometry analysis of the Fas ligand expression of activated lymph node T-cells.

There is increasing evidence for the role of the Fas/Fas ligand interaction in the immunoregulation of T-cells. We studied the expression of the Fas ligand (FasL) in activated peripheral T-cell in vitro, and its relation to autonomous cell death by flow cytometry. Following the stimulation of lymph node T-cells with anti-CD3 and rIL2, the mRNA level of FasL increased more than four times during the first 2 days over the level before stimulation. The surface expression of FasL was observed on 27% of the population at day 2 after stimulation and increased to approximately 50% at day 3. Kinetic analysis by flow cytometry, however, indicated that all T-blasts transformed during activation did not express FasL. FasL expression became evident simultaneously with the termination of cell expansion. Since cells remained viable (> 90%) at day 3 as judged by trypan blue-exclusion, cell membranes expressing FasL were supposed to be still intact. Concomitantly with FasL-expression, spontaneous DNA fragmentation was observed. These observations support the idea that autonomous Fas/FasL interaction mediates apoptosis in activated peripheral T-cells as demonstrated in T-cell hybridoma or established T-cells.

Animals↗
PubMed1997

The relationship between orthostatic dizziness and hypotension in male medical students.

We carried out a questionnaire survey regarding symptoms of orthostatic dysregulation (OD) and administered the Schellong test (orthostatic test) to 123 normal male medical students aged 21-29 years to investigate the relationship between orthostatic dizziness and hypotension. OD was identified in 15 (12.2%) of the subjects based on the questionnaire results. Orthostatic dizziness was noted in 40.7% of the subjects (50/123). The occurrence of orthostatic dizziness was most significantly related to systolic pressure decrease during the procedure for the Schellong test. These results suggest that the testing procedure introduced by Schellong can be useful, and clinically applicable to the assessment of orthostatic dizziness, since it presents the advantage of being simple enough to carry out in clinical practice.

Adult↗
PubMed1997

The relationship between psychosomatic factors and orthostatic dysregulation in young men.

We carried out a questionnaire survey regarding symptoms of orthostatic dysregulation and administered the Japanese Edition of the Cornell Medical Index-Health Questionnaire (JCMI) and the Yatabe-Guilford Personality Test (Y-G test) to 151 male medical students (mean age, 24.6 yr). Orthostatic dysregulation was identified in 19 (12.5%) of the subjects based on the questionnaire results. The percentage classed as types III (possible neurotic) and IV (probable neurotic) according to the health questionnaire was 47.3% in the 19 with orthostatic dysregulation and 8.9% in the controls (n = 78). The percentage classed as types B and E, suggestive of emotional or psychological disturbance according to the personality test, was 42.1% in those with orthostatic dysregulation and 8.9% in the controls. These differences were significant (P < 0.01). These results suggest that psychosomatic factors influence the occurrence of orthostatic dysregulation in young men.

Abdominal Pain↗
PubMed1997

Identification of novel cadherins expressed in human melanoma cells.

Cadherin molecules are essential for tissue morphogenesis and are also related to cancer invasion and metastasis. Although normal melanocytes express E- and P-cadherin, the activity and expression of E- and P-cadherin in melanoma cells are still unknown. We measured the homophilic adhesion activity of human normal epidermal melanocytes and the melanoma cell lines MeWo and A375. The melanoma cells showed stronger homophilic adhesion activity than did the melanocytes, despite the lower expression of E- and P-cadherin in the melanoma cells. This result suggested that melanoma cells expressed other types of homophilic adhesion molecules. Using degenerate primers to amplify multiple cadherin subtypes, we performed a polymerase chain reaction (PCR) with the first strand of cDNAs generated by reverse transcription of the mRNAs of the melanoma cells, and we isolated two known cadherin fragments, N-cadherin and PC42, and six novel cadherin fragments, cadherins ME1-ME6. The reverse transcriptase-PCR using specific primers of cadherins including E-, P-, and N-cadherins, PC42, and cadherins ME1-ME6 revealed that the melanoma cells expressed more kinds of cadherin molecules than did the melanocytes. Such cadherins may play an important role in melanoma cell-cell adhesion.

Amino Acid Sequence↗
PubMed1997

Foot ulcer due to arteriovenous malformation: report of a case.

A 41-year-old woman had erosive eruptions surrounded by irregularly shaped pigmentation on the lateral aspect of her right foot, where she had noted gradually increasing warmth and pain for 10 years. The eruptions waxed and waned without complete healing, and an ulcer which had formed one year previously did not respond to topical treatments. Arteriography performed on the right lower extremity disclosed multiple diffuse arteriovenous malformations in the right lower leg and foot. The ulcer was treated by bed rest, surgical debridement, and topical application of bucladesine sodium ointment. After three months, the ulcer healed, leaving a shallow scar and pigmentation.

Administration, Cutaneous↗
PubMed1997

Involvement of tumor necrosis factor-alpha, interleukin-1 beta, interleukin-8, and interleukin-1 receptor antagonist in acute lung injury caused by local Shwartzman reaction.

A local Shwartzman reaction (LSR) was prepared in rabbit lung as a model of acute lung injury. To induce LSR, intratracheal injection of lipopolysaccharide (LPS) 10 micrograms into the lower lobe of the right lung, followed 24 h later by i.v. injection of LPS (10 micrograms/kg). In the lung with the LSR, myeloperoxidase activity, representing neutrophil accumulation, peaked at 1-2 h and was sustained for 48 h after challenge with i.v. LPS. The lung water content peaked at 12 h, and decreased gradually. Histological findings showed diffuse interstitial widening, intra-alveolar leukocyte infiltration with hemorrhage, and alveolar exudate formation. The production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), interleukin-8 (IL-8), and IL-1 receptor antagonist (IL-1 Ra) in the lung was analyzed. TNF-alpha first elevated and peaked at 0.5 h (66.5 +/- 16.7 ng/g.lung), subsequently, IL-1 beta and IL-8 increased and peaked at 2 h (17.8 +/- 3.4 ng/g.lung and 336.9 +/- 49.6 ng/g.lung, respectively). IL-1Ra was present even before the challenge, and the production increased to show a dual peak (0.5 h, 1.5 +/- 0.2 micrograms/g.lung; and 2 h, 1.6 +/- 0.1 micrograms/g.lung), and a large concentration of IL-1Ra was sustained for 48 h. Immunohistochemistry showed that the cellular source of these cytokines was alveolar macrophages and infiltrating neutrophils. Thus, disclosing the kinetics of the generation of cytokines led to a better understanding of their roles, namely TNF-alpha as an initiator, IL-1 and IL-8 as amplifier and effector, and IL-1Ra as regulator of the intensity of acute inflammation.

Animals↗
PubMed1997

Clinicopathologic study of leptomeningeal carcinomatosis involving the temporal bone.

The temporal bone pathology of a 71-year-old man with bilateral sensorineural hearing loss and facial paralysis caused by diffuse metastatic leptomeningeal carcinomatosis is described. The origin of this malignant disease was an extremely rare entity, a transitional cell carcinoma of the renal pelvis. Histopathologic study of the temporal bone demonstrated that tumor cells filled the internal auditory meatus, infiltrated into the Rosenthal's canals, and reached the scala tympani of the basal turn of the bilateral cochleas. The vestibulocochlear nerve and facial nerve trunks in the internal auditory meatus had been destroyed by the bilateral tumor invasion. Case reports of temporal bone metastases of leptomeningeal carcinomatosis published since 1965 were reviewed. In leptomeningeal carcinomatosis, it is suggested that tumor cells infiltrate the internal auditory meatus of both ears simultaneously from the cerebrospinal fluid, involving the seventh and eighth nerve trunks, and then cause bilateral sensorineural hearing loss and facial paralysis.

Aged↗
PubMed1997

Electrophysiologic effects of nitrous oxide, a volatile anesthetic, in dogs following myocardial infarction in comparison with other anesthetics.

The present study was undertaken to examine the electrophysiologic effects of nitrous oxide in the dog heart after inducing myocardial infarction, and to compare these with those of other anesthetics. Myocardial infarction was produced by two-stage ligation of the left anterior descending coronary artery in dogs. Seven days after ligation, bipolar electrodes were sutured on the ventricular surface of the infarcted and normal regions for applying electrical stimulation or recording ventricular activation. Ventricular activation time and QT interval on the bipolar electrocardiogram and PQ interval from the standard limb lead II were measured during atrial pacing. Nitrous oxide 80% did not significantly prolong ventricular activation time, PQ interval or QT interval. However, halothane 1 minimum alveolar concentration (MAC), thiopental 5 and 10 mg/kg and fentanyl 30 microg/kg did prolong ventricular activation time; thiopental and fentanyl prolonged the QT interval. Nitrous oxide did not potentiate the effects of fentanyl. Therefore, electrophysiologic effects of nitrous oxide are much weaker compared with those of thiopental, fentanyl or halothane.

Anesthetics, Inhalation↗