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Biomedical subjects

T Kishimoto

Publications and source records attributed to T Kishimoto.

At least 235 records · Page 13Linked to original sources
PubMed1999

[Cough variant asthma improving with avoidance of pet rabbit].

The concept of cough variant asthma (CVA) has been defined recently, but little is known about the relation between CVA and antigen. A case of CVA due to per rabbit was presented here. A 49-year-old man who kept a pet rabbit indoors was admitted our hospital with nocturnal dry cough. Both serum total IgE level and eosinophil count were elevated (IgE 5580 IU/L. Eosinophil 1183/L). According to Sato's criteria, this case was diagnosed to be CVA. After the patient was kept out of contact with the rabbit, his coughing disappeared and never recurred and IgE (RAST) against rabbit decreased. The out come of this case clearly shows that CVA improved due to avoidance of the antigen. These facts suggest that the cause of CVA in this case in due to mainly an immunoglobulin E-mediated allergic reaction.

Animals↗
PubMed1999

[Intrascrotal epidermoid cyst: report of two cases].

A 41-year-old man and a 47-year-old man presented with an intrascrotal mass. The routine studies and ultrasonography showed that the mass was not associated with the testis, epididymis or spermatic cord, but the magnetic resonance imaging was the most useful for making a preoperative diagnosis. Both patients received transscrotal resection of the mass, the histopathological diagnosis of which was epidermoid cyst. A total of 24 cases of epidermoid cyst have been reported in the Japanese literature.

Adult↗
PubMed1999

[Interstitial pneumonia induced by the inhalation of hard metal].

A 51-year-old man visited Okayama Rousai Hospital with the chief complaints of dyspnea and emaciation. His occupational history included 23 years as a hard-metal polisher for a shipyard. Physical examination disclosed digital clubbing and fine crackles audible in the inferior posterior lung fields. Laboratory examination revealed hypoxemia and a remarkably reduced vital capacity of the lungs. Chest x-ray films and computed tomograms disclosed interstitial pneumonia predominantly in the upper lung lobes. Lung fibrosis progressed rapidly, and the patient died of exacerbation of chronic respiratory failure 2 years after his first visit to our hospital. The histopathologic findings from tissue specimens obtained by open lung biopsy and necropsy revealed mixed patterns of atypical and usual interstitial pneumonia, but no giant cell interstitial pneumonia. X-ray analysis detected tungsten in the lung tissue and mediastinal lymph nodes, but no cobalt was found. The interstitial pneumonia observed in this patient was thought to be induced by the occupational inhalation of hard metal.

Air Pollutants, Occupational↗
PubMed1999

[Evaluation of the usefulness of a serodiagnosis kit, the determiner TBGL antibody for tuberculosis: setting reference value].

The determiner TBGL antibody developed by Kyowa-Medex co., ltd. is a new serodiagnostic kit for tuberculosis. To set cut-off point suitable for the kit, TBGL antibody titer of serum from healthy subjects were analyzed in relation to age, sex, previous and family history on tuberculosis. Based on results of healthy subjects, cut-off point was set by using several analytical methods. We propose 2U/ml as a cut-off point for screening of patients with tuberculosis considering the diagnostic efficiency by receiver operating characteristics (ROC) curve analysis and 4U/ml for diagnosis of tuberculosis, which was determined by parametric method considering its specificity.

Adolescent↗
PubMed1999

Clinical results of total cystectomy for 92 patients with bladder cancer.

The survival rate of 92 patients with primary bladder cancer who had undergone total cystectomy during a 13-year period from 1984 to 1996 was examined. The mean follow-up period was 1,886 days. The 5-year survival rate was 67.9% and the 10-year survival rate was 55.1%. When survival rates were compared pathohistologically, with 81 patients with transitional cell carcinoma divided into two groups, a high-stage group including T3 and T4 patients and a low-stage group with all other patients, the cancer-specific 5-year survival rate of the low-stage group was 88.9% while that of the high-stage group was 45.4%; this difference was significant (p = 0.0002). There were also significant differences in survival rate between those with and those without regional lymph node metastasis, those with and those without lymphatic infiltration, and those with and those without vascular infiltration. However, there was no significant difference in survival rate for the 34 patients with T3 or T4 disease when those with or without chemotherapy and/or radiation therapy were compared.

Adult↗
PubMed1998

Accelerated apoptosis of lymphocytes by augmented induction of Bax in SSI-1 (STAT-induced STAT inhibitor-1) deficient mice.

Growth, differentiation, and programmed cell death (apoptosis) are mainly controlled by cytokines. The Janus kinase-signal transducers and activators of transcription (JAK-STAT) signal pathway is an important component of cytokine signaling. We have previously shown that STAT3 induces a molecule designated as SSI-1, which inhibits STAT3 functions. To clarify the physiological roles of SSI-1 in vivo, we generated, here, mice lacking SSI-1. These SSI-1-/- mice displayed growth retardation and died within 3 weeks after birth. Lymphocytes in the thymus and spleen of the SSI-1-/- mice exhibited accelerated apoptosis with aging, and their number was 20-25% of that in SSI-1+/+ mice at 10 days of age. However, the differentiation of lymphocytes lacking SSI-1 appeared to be normal. Among various pro- and anti-apoptotic molecules examined, an up-regulation of Bax was found in lymphocytes of the spleen and thymus of SSI-1-/- mice. These findings suggest that SSI-1 prevents apoptosis by inhibiting the expression of Bax.

Animals↗
PubMed1998

IL-6 receptor (CD126'IL-6R') expression is increased on monocytes and B lymphocytes in HIV infection.

Interleukin-6 (IL-6) is a multifunctional cytokine, with a wide range of effects on various cell types, including several types of cells involved in immune responses. IL-6 is believed to be involved in the pathogenesis of several diseases and may contribute to AIDS pathogenesis in various ways. Elevated levels of IL-6 occur in HIV infection. The objective of this study was to define the distribution of the expression of the 80-kDa alpha subunit of the IL-6 receptor (CD126'IL-6R') on immune cell subpopulations in HIV-infected subjects. CD126 is responsible for IL-6 binding, and its expression determines which cells respond to this cytokine. An elevated number of monocytes, B cells, and CD4 T cells expressing CD126 were seen in the peripheral circulation of HIV-infected subjects when compared to HIV-seronegative control subjects. Also, an increase in the density of CD126 expression was noted on monocytes. Generally, the observed increases in CD126 did not correlate with CD4 levels in HIV-infected subjects or with disease status, with the exception of CD126 expression on CD8 T cells, which was lower in those HIV-infected subjects that had AIDS. In some cases, increased CD126 expressing cells showed higher levels of STAT3 phosphorylation on exposure to recombinant IL-6. These results indicate that greatly elevated levels of CD126-expressing cells, particularly B cells and monocytes, are seen in HIV infection and suggest that the altered expression of CD126 may contribute directly or indirectly to immune dysfunction and to AIDS pathogenesis in HIV infection.

Adult↗
PubMed1998

Angiotensin II interferes with leukemia inhibitory factor-induced STAT3 activation in cardiac myocytes.

Recently, we reported that leukemia inhibitory factor (LIF), a member of the interleukin (IL)-6 cytokine family, transduced hypertrophic and cytoprotective signals via Januas Kinase-signal transducer and activator of transcription (JAK-STAT) pathway in cardiac myocytes. Angiotensin II (AII) is also known to activate STATs and reported to induced apoptosis in adult rat ventricular myocytes. In the present study, we investigated potential interactions between gp130 dependent and AII signaling pathways, by examining AII regulation of LIF-induced anti-apoptotic effect and STAT3 activation in cardiac myocytes. Although LIF attenuated the DNA fragmentation induced by serum depletion, AII augmented the DNA fragmentation in cultured neonatal rat cardiac myocytes. Furthermore, LIF-mediated cytoprotective effect was inhibited by AII pretreatment. LIF rapidly and transiently tyrosine phosphorylated STAT3 in cardiac myocytes which was not observed by AII. AII pretreatment inhibited LIF-induced phosphorylation of STAT3 in a dose dependent manner. This inhibitory effect of AII on STAT3 activation was blocked by the AII type I (AT1) receptor antagonist CV11974. These results demonstrate that negative crosstalk between gp130 and AT1 receptor dependent signaling exists in cardiac myocytes. This crosstalk may contribute to the modulation of pathophysiological process in myocardial disease.

Angiotensin II↗
PubMed1998

Okadaic acid-stimulated degradation of p35, an activator of CDK5, by proteasome in cultured neurons.

Degradation of p35, a neuron-specific activator of CDK5, was studied in rat cortical neurons in primary culture. Treatment of cultured neurons with cyclohexamide induced the rapid disappearance of p35 accompanied by parallel inactivation of the kinase activity of CDK5. The disappearance of p35 was blocked with proteasome inhibitors benzyloxycarbonyl-leucyl-leucyl-leucinal and lactacystin, indicating the involvement of proteasome. The degradation of p35 was induced with okadaic acid in the presence of ATP in neuron extracts. The degradation of p35 by proteasome in cultured neurons was stimulated by okadaic acid in the absence of cyclohexamide. These results indicate that p35 is degraded by proteasome in a phosphorylation-dependent manner in neurons.

Adenosine Triphosphate↗
PubMed1998

Postnatally induced inactivation of gp130 in mice results in neurological, cardiac, hematopoietic, immunological, hepatic, and pulmonary defects.

The pleiotrophic but overlapping functions of the cytokine family that includes interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin M, ciliary neurotrophic factor, and cardiotrophin 1 are mediated by the cytokine receptor subunit gp130 as the common signal transducer. Although mice lacking individual members of this family display only mild phenotypes, animals lacking gp130 are not viable. To assess the collective role of this cytokine family, we inducibly inactivated gp130 via Cre-loxP-mediated recombination in vivo. Such conditional mutant mice exhibited neurological, cardiac, hematopoietic, immunological, hepatic, and pulmonary defects, demonstrating the widespread importance of gp130-dependent cytokines.

Animals↗
PubMed1998

Stat3 activation is responsible for IL-6-dependent T cell proliferation through preventing apoptosis: generation and characterization of T cell-specific Stat3-deficient mice.

Stat3, a member of STAT, is activated by a variety of cytokines such as IL-6 family of cytokines, granulocyte CSF, epidermal growth factor, and leptin. A recent study with mice genetically deficient in the Stat3 gene has revealed its important role in the early embryogenesis. To assess the function of Stat3 in adult tissues, we disrupted the Stat3 gene specifically in T cells by conditional gene targeting using Cre-loxP system. In Stat3-deficient T cells, IL-6-induced proliferation was severely impaired. IL-6 did not enhance cell cycle progression, but prevented apoptosis of normal T cells. In contrast, IL-6 did not prevent apoptosis of Stat3-deficient T cells. Antiapoptotic protein, Bcl-2, was normally up-regulated in response to IL-6 even in Stat3-deficient T cells. These results demonstrate that Stat3 activation is involved in IL-6-dependent T cell proliferation through prevention of apoptosis independently of Bcl-2.

Amino Acid Sequence↗
PubMed1998

NF-kappaB activation in CD27 signaling: involvement of TNF receptor-associated factors in its signaling and identification of functional region of CD27.

CD27 belongs to TNF receptor family, and it is unique in this family for its disulfide-linked homodimerization of 55-kDa monomers. In the present study we demonstrate that overexpression of CD27 in 293 cells induces a low level of NF-kappaB activation, and the ligation of the receptor by its corresponding ligand (CD70) augments this signal dramatically. Either TNF receptor-associated factor-2 (TRAF2) or TRAF3 binds to the CD27 molecule from the coimmunoprecipitation experiment. This NF-kappaB activation signal is inhibited by dominant negative TRAF2 or intact TRAF3, indicating that TRAF2 and TRAF3 works as a mediator and an inhibitor, respectively. The activated NF-kappaB complex contains at least two components, p50 and p65, but not p52. All these phenomena have also been observed in the TNF receptor type II, CD30 and CD40 signaling system, indicating that this receptor family uses the common or similar molecules for this signal. Finally, we identified the 13-amino acid alignment in the cytoplasmic region of the CD27 molecule (residues 238-250 amino acids), which is critical for the NF-kappaB activation signal and also for its association with TRAFs. This amino acid alignment contains the EEEG sequence, which is essential for interaction of CD30 or CD40 with TRAFs (TRAF1 and TRAF2, but not TRAF3), and also contains the PIQED sequence, which is similar to PXQXT that is known to be necessary for interaction of TNF receptor II and CD30 with TRAFs (TRAF1, 2, and 3).

Amino Acid Sequence↗
PubMed1998

Cloning of a novel rat gene, DB83, that encodes a putative membrane protein.

Using a partial cDNA sequence and a 5'-RACE technique, we isolated a novel cDNA from rat liver referred to as DB83. DB83 had four hydrophobic trans-membrane domains and one N-myristoylation site as well as multiple possible phosphorylation sites. The db83 gene was highly expressed in the liver and significantly in brain, lungs and kidneys. We suggest that DB83 is a tissue-specific putative membrane protein. p6

Amino Acid Sequence↗
PubMed1998

Three distinct domains of SSI-1/SOCS-1/JAB protein are required for its suppression of interleukin 6 signaling.

Cytokine-inducible protein SSI-1 [signal transducers and activators of transcription (STAT)-induced STAT inhibitor 1, also referred to as SOCS-1 (suppressor of cytokine signaling 1) or JAB (Janus kinase-binding protein)] negatively regulates cytokine receptor signaling by inhibition of JAK kinases. The SSI family of proteins includes eight members that are structurally characterized by an SH2 domain and a C-terminal conserved region that we have called the SC-motif. In this study, we investigated the roles of these domains in the function of SSI-1. Results of reporter assays demonstrated that the pre-SH2 domain (24 aa in front of the SH2 domain) and the SH2 domain of SSI-1 were required for the suppression by SSI-1 of interleukin 6 signaling. Coexpression studies of COS7 cells revealed that these domains also were required for inhibition of three JAKs (JAK1, JAK2, and TYK2). Furthermore, deletion of the SH2 domain, but not the pre-SH2 domain, resulted in loss of association of SSI-1 with TYK2. Thus, SSI-1 associates with JAK family kinase via its SH2 domain, and the pre-SH2 domain is required for the function of SSI-1. Deletion of the SC-motif markedly reduced expression of SSI-1 protein in M1 cells, and this reduction was reversed by treatment with proteasome inhibitors, suggesting that this motif is required to protect the SSI-1 molecule from proteolytic degradation. Based on these findings, we concluded that three distinct domains of SSI-1 (the pre-SH2 domain, the SH2 domain, and the SC-motif) cooperate in the suppression of interleukin 6 signaling.

Amino Acid Sequence↗
PubMed1998

Impaired B-lymphopoiesis, myelopoiesis, and derailed cerebellar neuron migration in CXCR4- and SDF-1-deficient mice.

The chemokine stromal cell-derived factor 1, SDF-1, is an important regulator of leukocyte and hematopoietic precursor migration and pre-B cell proliferation. The receptor for SDF-1, CXCR4, also functions as a coreceptor for T-tropic HIV-1 entry. We find that mice deficient for CXCR4 die perinatally and display profound defects in the hematopoietic and nervous systems. CXCR4-deficient mice have severely reduced B-lymphopoiesis, reduced myelopoiesis in fetal liver, and a virtual absence of myelopoiesis in bone marrow. However, T-lymphopoiesis is unaffected. Furthermore, the cerebellum develops abnormally with an irregular external granule cell layer, ectopically located Purkinje cells, and numerous chromophilic cell clumps of abnormally migrated granule cells within the cerebellar anlage. Identical defects are observed in mice lacking SDF-1, suggesting a monogamous relationship between CXCR4 and SDF-1. This receptor-ligand selectivity is unusual among chemokines and their receptors, as is the function in migration of nonhematopoietic cells.

Animals↗