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T Kawano

Publications and source records attributed to T Kawano.

At least 73 records · Page 4Linked to original sources
PubMed2001

Thrombin promotes fibroblast proliferation during the early stages of experimental radiation pneumonitis.

Huang, L., Ogushi, F., Tani, K., Ogawa, H., Kawano, T., Endo, T., Izumi, K., Ueno, J., Nishitani, H. and Sone, S. Thrombin Promotes Fibroblast Proliferation during the Early Stages of Experimental Radiation Pneumonitis. Radiat. Res. 156, 45-52 (2001). To clarify the role of thrombin in the pathogenesis of radiation-induced pneumonitis, we measured the thrombin activity and fibroblast growth-inducing activity in bronchoalveolar lavage fluid obtained from the irradiated lungs of rats at 1, 2, 4, 8 and 18 weeks after irradiation. Thrombin activity was not detected in the bronchoalveolar lavage fluid from unirradiated rats, but the bronchoalveolar lavage fluid from irradiated rats showed significantly increased thrombin activity which reached a maximum at 4 weeks after treatment. Higher fibroblast growth-inducing activity was detected in the bronchoalveolar lavage fluid from irradiated rats at 4 and 18 weeks than in fluid from unirradiated rats. Bronchoalveolar lavage fluid from irradiated rats that were pretreated with the thrombin inhibitors antithrombin III and argatroban showed significantly inhibited fibroblast growth-inducing activity and thrombin activity at 4 weeks. However, these thrombin inhibitors did not inhibit fibroblast growth-inducing activity in bronchoalveolar lavage fluid from irradiated rats at 18 weeks. Purified rat thrombin similarly induced proliferation of fibroblasts derived from irradiated and unirradiated rats. These findings suggest that thrombin may play an important role as a fibroblast growth-inducing factor during the early stages of radiation pneumonitis.

Animals↗
PubMed2001

Intracranial meningeal malignant fibrous histiocytoma mimicking parasagittal meningioma--case report.

A 69-year-old female presented with a rare intracranial meningeal malignant fibrous histiocytoma (MFH). The neuroimaging appearance of this tumor was very similar to parasagittal meningioma. The tumor was grossly totally removed, and local irradiation of 50 Gy was performed. The histological diagnosis was MFH. The patient recovered from the preoperative deficits, and no recurrence was observed by 27 months after surgery.

Aged↗
PubMed2001

[Utilization of emergency ambulances in Yokohoma City, Japan].

OBJECTIVE: In recent years, the annual number of emergency ambulance (EA) calls has increased in Yokohama city, Japan. A questionnaire study was carried out to describe behavioral features of the users in Yokohama city, and to investigate their relationship with the increase in EA utilization. METHODS: We randomly recruited 2,910 citizens, aged 15 years or older, for the questionnaire study and a total of 2,294 (78.8%) replied. The questionnaire included questions about their demographic characteristics, history of EA use, existence of family doctors, and knowledge of emergency medical services and emergency medical information centers. Additionally, respondents who had used EA previously were asked about their reasons for this. RESULTS: A total of 513 (22.4%) respondents answered that they had used EA previously. A slightly higher rate of EA use was shown among elderly people, 65 years old or over (a rate of 26.2%). The major reason for requesting EA use was the urgency of the disease or the injury (61.8%). 182 respondents answered that they requested EA as a means of transportation. However, most of them also mentioned that the urgency of the disease or the injury was one of the reasons for their request. This survey showed no evidence that the citizens of Yokohama have used EA improperly. Elderly people, among whom the annual number of EA uses has increased rapidly over the years, tended to employ EA in a way more in line with regulations than other generations. CONCLUSION: This study suggested that the basic reason for the increase of EA utilization in Yokohama city was not due to inappropriate demand but to the aging of the population.

Adolescent↗
PubMed2001

[Drug-induced interstitial pneumonia associated with inhalation of fibrinolysin-deoxyribonuclease (ElaseR)].

A 73-year-old man was referred to our department because of sputum production and fever. He had under-gone a total laryngectomy for laryngeal cancer. His chest radiograph showed patchy ground-glass shadows in both lung fields. He was treated with antibiotics for pneumonia, but his symptoms continued, and the size of the patchy shadows in the chest radiograph increased. Inhalation therapy with ElaseR had been started from one day before fever arose. Withdrawal of ElaseR treatment resolved his symptoms. We therefore suspected drug-induced interstitial pneumonia. Transbronchial lung biopsy specimens showed infiltration of lymphocytes in the alveolar septa and thickening of those septa. A bronchoalveolar lavage revealed an increased number of lymphocytes, and the CD4/CD8 ratio was 0.3. A drug lymphocyte stimulation test (DLST) with peripheral blood lymphocytes was strongly positive (S.I. 2127%) for ElaseR. The anti-nuclear antigen (ANA) was detected (x640), and the anti-single strand DNA antibody titer was also high (123.4 IU/ml). About 10 weeks after the withdrawal of ElaseR, the infiltrative shadows and the abnormal laboratory findings improved spontaneously. On the basis of these findings, we arrived at a diagnosis of drug-induced interstitial pneumonia associated with inhalation of ElaseR.

Administration, Inhalation↗
PubMed2001

[Lowe syndrome].

Explore the source record for details and available documents.

DNA, Complementary↗
PubMed2001

Autoantibodies to IL-1 alpha in sera from rapidly progressive idiopathic pulmonary fibrosis.

To clarify the clinical significance of autoantibodies to interleukin-1 alpha (IL-1 alpha autoantibodies) in rapidly progressive idiopathic pulmonary fibrosis (IPF), we measured the level of IL-1 alpha autoantibodies in serum of 11 patients on the first hospital day, when patients were admitted due to severe symptoms, and on the 21st hospital day. IL-1 alpha autoantibodies in serum were measured using radioimmunoassay, and the limitation of this assay for IL-1 alpha autoantibodies was 5 ng/ml. These antibodies were detected in 5 of 11 patients on the first hospital day. On the 21st hospital day, these antibodies were detected in all patients, and its level was increased compared with that on the first hospital day. IL-1 alpha autoantibodies that appeared in patients corresponded to that of IgG. The half life of exogenous autoantibodies was investigated following administration of autoantibody rich plasma obtained from healthy blood donors to 6 control patients (CP) and 6 progressive IPF patients. These autoantibody levels in their serum were less than 5 ng/ml before administration. Serum was obtained at the indicated time after administration of IL-1 alpha autoantibodies and the level of these autoantibodies in serum was measured, then the half life was calculated. Half life of exogenous IL-1 alpha autoantibodies in progressive IPF patients was significantly shorter than that in CP (71.3 +/- 31.8 hr vs 352.0 +/- 98.3 hr, p < 0.01). These findings suggested that IL-1 alpha autoantibodies were generated in response to the inflammatory process of rapidly progressive IPF and may act as a regulatory factor for IL-1 alpha.

Aged↗
PubMed2001

A new concept for precise patella resection in total knee arthroplasty.

We developed a new patella-cutting guide that simplifies proper alignment and enables resection of the correct thickness of bone. This guide consists of a central shaft, two support frames, and a ring. The ring consists of upper and lower disks, with a slot between the disks. The central shaft and the lower disk have holes for fixation pins. The distance from the distal end of the central shaft to the lowest level of the slot is 8 mm. Bone of the same thickness as that of the patellar component can be automatically resected using this guide. A feeler gauge is inserted through the slot, and the periarticular region is felt. This procedure enables the guide to be set at the correct angulation. A laboratory study using fresh-frozen cadaver patella specimens and a clinical study showed that proper alignment and proper resection were achieved using this guide.

Arthroplasty, Replacement, Knee↗
PubMed2000

Monocyte chemotactic protein-1 receptor CCR2B is a glycoprotein that has tyrosine sulfation in a conserved extracellular N-terminal region.

Monocyte chemotactic protein-1 (MCP-1) binding to its receptor, CCR2B, plays an important role in a variety of diseases involving infection, inflammation, and/or injury. In our effort to understand the molecular basis of this interaction and its biological consequences, we recognized a conserved hexad of amino acids at the N-terminal extracellular domain of several chemokine receptors, including CCR2B. Human embryonic kidney 293 cells expressing Flag-tagged CCR2B containing site-directed mutations in this region, 21-26, including a consensus tyrosine sulfation site were used to determine MCP-1 binding and its biological consequences. The results showed that several of these amino acids are important for MCP-1 binding and consequent lamellipodium formation, chemotaxis, and signal transduction involving adenylate cyclase inhibition and Ca(2+) influx into cytoplasm. Mutations that prevented adenylate cyclase inhibition and Ca(2+) influx did not significantly inhibit lamellipodium formation and chemotaxis, suggesting that these signaling events are not involved in chemotaxis. CCR2B was found to be sulfated at Tyr(26); this sulfation was abolished by the substitution of Tyr with Ala and severely reduced by substitution of Asp(25), a part of the consensus sulfation site. The expressed CCR2B was found to be N:-glycosylated, as N:-glycosidase F treatment of the receptor or growth of the cells in tunicamycin reduced the receptor size to the same level, from 50 to 45 kDa. Thus, CCR2B is the first member of the CC chemokine receptor family shown to be a glycoprotein that is sulfated at the N-terminal Tyr. These post-translational modifications probably have significant biological functions.

Adenylyl Cyclase Inhibitors↗
PubMed2000

Molecular cloning and characterization of a new insulin/IGF-like peptide of the nematode Caenorhabditis elegans.

Diapause, aging, and fat accumulation in Caenorhabditis elegans are regulated by DAF-2, a homolog of mammalian insulin/insulin-like growth factor-I (IGF-I) receptors. We have cloned and characterized a C. elegans gene encoding a new insulin/IGF-like peptide. The gene containing three exons encodes a precursor protein 95 residue long. Although the putative precursor contains a signal peptide, B chain, C peptide, and A chain like the preproinsulin, the mature peptide consists of one polypeptide-like IGF. The predicted tertiary structure seems similar to crystal structure of insulin. Therefore, the peptide may be a hybrid molecule of insulin and IGF. The peptide expression was detected at the embryonic and several larval stages. Disruption of the peptide production led to an extended life span like the daf-2 mutation, suggesting that the peptide should be one of the ligands of the DAF-2. This is the first description of the peptide that mediates animal longevity.

Amino Acid Sequence↗
PubMed2000

A conformationally reliable spacer for molecular tweezers

[figure: see text] A reliable and rigid spacer, trans,trans,trans-perhydronaphthacene, for molecular tweezers was designed. A synthesis and molecular recognition study of its 1,14-disubstituted derivatives was carried out.

Journal Article↗
PubMed2000

G(i)-dependent activation of c-Jun N-terminal kinase in human embryonal kidney 293 cells.

Heterotrimeric G proteins stimulate the activities of two stress-activated protein kinases, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase in mammalian cells. In this study, we examined whether alpha subunits of G(i) family activate JNK using transient expression system in human embryonal kidney 293 cells. Constitutively activated mutants of Galpha(i1), Galpha(i2), and Galpha(i3) increased JNK activity. In contrast, constitutively activated Galpha(o) and Galpha(z) mutants did not stimulate JNK activity. To examine the mechanism of JNK activation by Galpha(i), kinase-deficient mutants of mitogen-activated protein kinase kinase 4 (MKK4) and 7 (MKK7), which are known to be JNK activators, were transfected into the cells. However, Galpha(i)-induced JNK activation was not blocked effectively by kinase-deficient MKK4 and MKK7. In addition, activated Galpha(i) mutant failed to stimulate MKK4 and MKK7 activities. Furthermore, JNK activation by Galpha(i) was inhibited by dominant-negative Rho and Cdc42 and tyrosine kinase inhibitors, but not dominant-negative Rac and phosphatidylinositol 3-kinase inhibitors. These results indicate that Galpha(i) regulates JNK activity dependent on small GTPases Rho and Cdc42 and on tyrosine kinase but not on MKK4 and MKK7.

Cells, Cultured↗
PubMed2000

Differential tumor surveillance by natural killer (NK) and NKT cells.

Natural tumor surveillance capabilities of the host were investigated in six different mouse tumor models where endogenous interleukin (IL)-12 does or does not dictate the efficiency of the innate immune response. Gene-targeted and lymphocyte subset-depleted mice were used to establish the relative importance of natural killer (NK) and NK1.1(+) T (NKT) cells in protection from tumor initiation and metastasis. In the models examined, CD3(-) NK cells were responsible for tumor rejection and protection from metastasis in models where control of major histocompatibility complex class I-deficient tumors was independent of IL-12. A protective role for NKT cells was only observed when tumor rejection required endogenous IL-12 activity. In particular, T cell receptor Jalpha281 gene-targeted mice confirmed a critical function for NKT cells in protection from spontaneous tumors initiated by the chemical carcinogen, methylcholanthrene. This is the first description of an antitumor function for NKT cells in the absence of exogenously administered potent stimulators such as IL-12 or alpha-galactosylceramide.

Animals↗
PubMed2000

Involvement of decidual Valpha14 NKT cells in abortion.

The immunological mechanisms that regulate abortion are largely unknown. Here, we found that a distinct subset of lymphocytes, Valpha14 NKT cells expressing an invariant antigen receptor encoded by Valpha14/Jalpha281 and Vbeta7 segments, accumulated in the decidua during pregnancy and provoked abortion upon stimulation with alpha-galactosylceramide (alpha-GalCer), a specific ligand for Valpha14 NKT cells. The alpha-GalCer-mediated abortion was not observed in Valpha14 NKT-, IFN-gamma-, tumor necrosis factor alpha-, or perforin-knock-out mice and appeared to be due to the degeneration of embryonic trophoblasts mediated by the activated Valpha14 NKT cells whose perforin-dependent killing and production of IFN-gamma and tumor necrosis factor alpha were essential. The possible role of the decidual Valpha14 NKT cells in the pathogenesis of abortion is discussed.

Abortion, Induced↗
PubMed2000

alpha-galactosylceramide induces early B-cell activation through IL-4 production by NKT cells.

alpha-Galactosylceramide (alpha-GalCer), a glycolipid antigen, specifically activates natural killer T (NKT) cells by a CD1d-restricted mechanism. In this work, we found that in vivo administration of alpha-GalCer resulted in the activation of B cells in addition to NKT cells, namely, alpha-GalCer administration caused upregulation of the early activation marker, CD69, on both NKT and B cells. In addition, expression of B7.2 and I-A(b) on B cells was greatly upregulated by alpha-GalCer. However, serum levels of IgE, IgG1, and IgG2a were not significantly changed within 48 h. In the present experiments, it was also demonstrated that the upregulation of CD69 expression by alpha-GalCer was strongly blocked by anti-IL-4 monoclonal antibody. Moreover, B-cell activation by alpha-GalCer was not observed in NKT-deficient mice. These results suggested that antigen-stimulated NKT cells might play a critical role not only in early defense mechanisms but also in early B-cell activation through IL-4 production.

Animals↗
PubMed2000

Augmentation of Valpha14 NKT cell-mediated cytotoxicity by interleukin 4 in an autocrine mechanism resulting in the development of concanavalin A-induced hepatitis.

The administration of concanavalin A (Con A) induces a rapid severe injury of hepatocytes in mice. Although the Con A-induced hepatitis is considered to be an experimental model of human autoimmune hepatitis, the precise cellular and molecular mechanisms that induce hepatocyte injury remain unclear. Here, we demonstrate that Valpha14 NKT cells are required and sufficient for induction of this hepatitis. Moreover, interleukin (IL)-4 produced by Con A-activated Valpha14 NKT cells is found to play a crucial role in disease development by augmenting the cytotoxic activity of Valpha14 NKT cells in an autocrine fashion. Indeed, short-term treatment with IL-4 induces an increase in the expression of granzyme B and Fas ligand (L) in Valpha14 NKT cells. Moreover, Valpha14 NKT cells from either perforin knock-out mice or FasL-mutant gld/gld mice fail to induce hepatitis, and hence perforin-granzyme B and FasL appear to be effector molecules in Con A-induced Valpha14 NKT cell-mediated hepatocyte injury.

Adoptive Transfer↗
PubMed2000

Chymase is a potent chemoattractant for human monocytes and neutrophils.

Chymase is a major chymotrypsin-like serine protease expressed in the secretory granules of mast cells in many mammalian species. In this study, we revealed the chemotactic activity of chymase for human mononuclear cells and neutrophils with a 48-well microchemotaxis chamber technique. Human chymase showed the potent chemotactic activity for monocytes and neutrophils dose-dependently in a concentration range from 0.1 to 10 microg/mL, corresponding to about 4-400 microM. The activity was as potent as that of N-formyl-methionyl-leucyl-phenylalanine. Chymase also stimulated cell migration of lymphocytes and purified T cells, but checkerboard analysis revealed that the effect was chemokinetic rather than chemotactic. Inhibition of chymase activities with chymase inhibitors, such as antileukoprotease and Bowman-Birk soybean trypsin inhibitor, significantly inhibited the chemotactic activity of chymase, suggesting that the proteolytic activity of chymase participates in the chemotactic activity. Our results suggest that mast cell chymase acts as a chemoattractant, and may play a role in the accumulation of inflammatory cells in development of the chronic inflammatory responses of allergic and nonallergic diseases.

Chemotactic Factors↗