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Biomedical subjects

K Kishi

Publications and source records attributed to K Kishi.

At least 271 records · Page 15Linked to original sources
PubMed1997

[Evaluation of hepatic encephalopathy and portal hemodynamics by Doppler ultrasonography after a transjugular intrahepatic portosystemic shunt].

TIPS (transjugular intrahepatic portosystemic shunt) is an efficacious treatment for esophagogastric varices, ascites and hypertensive gastrointestinal vasculopathy associated with portal hypertension. The main complication after the procedure is hepatic encephalopathy. We tried to elucidate the correlation between hepatic encephalopathy and changes in portal hemodynamics after TIPS, based on observation by Doppler ultrasonography. We carried out Doppler ultrasonography in 28 cases of TIPS to assess hepatopetal and hepatofugal blood flow in the right and left portal branches. Hepatic encephalopathy occurred after TIPS in 9 cases out of 28 (32%), and new onset of disease was observed in 6 of 9. Doppler ultrasonography revealed hepatofugal blood flow in both right and left portal branches in 6 cases, 5 of which showed encephalopathy. Hepatopetal blood flow of the right and left portal branches was observed in 17 of 28 cases after TIPS. Hepatic encephalopathy occurred in only 2 of 17 cases. The changes in portal vein hemodynamics after TIPS were investigated by color Doppler ultrasonography, which were considered to be very useful for prediction of hepatic encephalopathy and indication of medical treatment to prevent the occurrence of this disease.

Adult↗
PubMed1997

[Bilateral hilar and mediastinal lymphadenopathy accomporying pulmonary infiltration with eosinophilia].

A 46-year-old man had had an occasional dry cough in the early morning since about the age of 20, but had received no treatment. He had been taking an antirheumatic drug for 2 years for rheumatoid arthritis. The patient complained of fever and dry coughing that began in the middle of November 1995, and he was treated for acute bronchitis. His condition did not improve, and he was admitted to the hospital in early December. Wheezing and rhonchi were heard in both lung fields. His white blood cell count was 19,000/mm3, and the eosinophil percent age was 48%. A chest CT scan revealed macular lesions with an increased density in both lung fields, and markedly swollen mediastinal and hilar lymph nodes. Analysis of alveolar lavage fluid revealed an increased number of cells (total) and eosinophilia (37%), and examination of a transbronchial lung biopsy specimen indicated infiltration with eosinophils and lymphocytes. Our diagnosis was eosinophilic pneumonia. The patient's condition improved soon after the start of pulse therapy with steroids. Bilateral swelling of mediastinal and hilar lymph nodes is rare in patients who have pulmonary in filtration with eosinophilia (the PIE syndrome).

Humans↗
PubMed1997

The heterogeneous expression of CD80, CD86 and other adhesion molecules on leukemia and lymphoma cells and their induction by interferon.

CD80 (B7/BB-1, B7-1) and CD86 (B70, B7-2) take an important role in the interaction between T lymphocytes and antigen presenting cells (APCs) as co-stimulatory molecules. We analyzed the manifestation of adhesion molecules, including CD80 and CD86, on some leukemia and lymphoma cells. Constitutive expression of CD80 and/or CD86 was frequently observed on B cell leukemia/lymphoma cells, while it is rare on myeloid leukemia cells. Interferon-alpha (IFN-alpha) amplified the manifestation of MHC class I and interferon-gamma (IFN-gamma) did both class I and class II. We also showed CD80 could be induced by IFN-alpha on K562 cells, which were originally negative for CD80. Our data implies the immunotherapy via CD80 and CD86 for patients with hematological malignancies and the possibility to enhance it using interferons.

Antigens, CD↗
PubMed1997

[Influence of low high-density lipoprotein cholesterolemia induced by probucol on the progression of coronary atherosclerosis].

The influence of probucol-induced low high-density lipoprotein (HDL) cholesterolemia on the progression of coronary atherosclerosis was studied in 320 patients with angina pectoris or myocardial infarction, 32 patients with probucol 500 mg/day, 288 patients without probucol, who underwent follow-up angiography at intervals of at least 2 years. The 288 patients were divided into two groups depending on the serum HDL-cholesterol (HDL-C) level at the follow-up angiography: the low HDL-C group had a serum HDL-C level below 40 mg/dl (152 patients) and the control group had 40 mg/dl or above (136 patients). Coronary sclerosis index was defined as the total products of coronary scores (0-6) by segments according to the American Heart Association reporting system in the branches without angioplasty and was compared between the three groups. In the probucol group, serum HDL-C level was significantly reduced from 43.9 +/- 10.6 (at baseline) to 31.1 +/- 7.6 mg/dl (at follow-up, p < 0.01) and was lower than that in the other two groups (low HDL-C group 33.1 +/- 5.0 mg/dl, p < 0.07; control group 52.6 +/- 9.8 mg/dl, p < 0.01). Coronary sclerosis index was most increased in the low HDL-C group (8.3 +/- 5.4-->11.9 +/- 6.1, p < 0.01), whereas there was no significant change in the probucol group (7.2 +/- 5.9-->9.1 +/- 6.8, p = 0.24). Our results showed that treatment with probucol inhibits the progression of coronary atherosclerosis despite the decrease in HDL-C level. One possible reason may be remarkable improvement in the other lipid factors, especially the low-density lipoprotein cholesterol level (165.7 +/- 33.9-->123.7 +/- 29.0 mg/dl, p < 0.01).

Aged↗
PubMed1997

Simple purification method of the antiphospholipid antibody from normal human plasma.

We have reported that rabbit serum contains a phospholipid (PL)/ganglioside-binding protein which adsorbs to Sephacryl S-400 gel and agglutinates human red blood cells. A new protein similar to the PL/ganglioside-binding protein was simply purified from normal human plasma using Sephacryl S-400, Sepharose CL-4B and DEAE-Sepharose CL-6B columns. The purified protein was found to agglutinate rabbit red blood cells. The hemagglutination was specifically inhibited by two PL, phosphatidylserine and phosphatidylinositol, but not by any other PL, gangliosides, saccharides or glycoproteins tested. From analyses of the N-terminal amino acid sequence and immunological specificity, the protein was identified to be a human immunoglobulin M.

Amino Acid Sequence↗
PubMed1997

Genetic polymorphisms detectable in human urine: their application to forensic individualization.

This review describes several types of genetic polymorphism, which have recently been identified in human urine in our laboratory, and have also been found in other human body fluids such as blood, saliva and semen. These include uropepsinogen, ribonuclease, deoxyribonuclease I (DNase I), deoxyribonuclease II (DNase II), 43-kDa glycoprotein, alpha-L-fucosidase, glutamate pyruvate transaminase, alpha-2-HS-glycoprotein, transferrin and vitamin D-binding protein. Several substances can be detected more easily in urine than in plasma. The concentrations of uropepsinogen, DNase I and DNase II in blood plasma are too low for analysis, whereas those in urine are high enough for easy typing. In practice, DNase I-polymorphism is one of the most useful genetic markers for practical purposes, because of its higher content in various body fluids including urine, a well-balanced gene frequency, and its easy and accurate detectability. Furthermore, several genetic markers previously identified in blood and/or other forensic samples can be phenotyped reproducibly and easily from the corresponding urine samples. Thus, urine, in addition to the convenience and non-invasive nature of its collection, is by no means inferior to blood as a sample source for typing in the field of forensic science. Biochemical and serological typing of genetic polymorphisms present in human urine could offer useful information to practising forensic biologists for forensic individualization of urine samples.

Deoxyribonuclease I↗
PubMed1996

A transforming growth factor beta type II receptor gene mutation common in sporadic cecum cancer with microsatellite instability.

Mismatch repair genes are the responsible genes for hereditary non-polyposis colon cancer, and mutation of these genes causes replication error (RER). In several RER-positive colon cancer cell lines, mutations of repetitive sequences of transforming growth factor beta (TGF-beta) type II receptor (RII) gene have been reported. Since TGF-beta inhibits cell proliferation, loss of response to TGF-beta is an important tumor progression step. In this study, the relationship between RER status and mutation of the RII gene was analyzed in 112 cases of various types of sporadic gastrointestinal and hepatobiliary cancer (41 with gastric, 49 with colorectal, 5 with gallbladder, and 17 with hepatic cancers). RER was found in 17 cases (4 with gastric, 12 with colorectal, and 1 with gallbladder cancer), and 10 of those (3 with gastric and 7 with colorectal cancer) showed mutations of the RII gene. Of interest was that in all seven cases with colorectal cancer, tumors were located at the cecum. These data indicate that mutation of the RII gene, presumably caused by abnormality of repair gene, play an important role in carcinogenesis of sporadic gastrointestinal cancer, especially at the cecum.

Aged↗
PubMed1996

Gq-coupled receptors transmit the signal for GLUT4 translocation via an insulin-independent pathway.

Guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS) induces the translocation of glucose transporter type 4 (GLUT4) from an intracellular pool to the cell surface and increases glucose uptake in adipocytes. The GTP-binding protein(s) responsible for the translocation has remained to be identified. Using a sensitive and quantitative method to assess the translocation of c-MYC epitope-tagged GLUT4, we obtained evidence that the activation of receptor-coupled Gq (neither Gi nor Gs) triggered GLUT4 translocation in cells, independently of insulin signaling pathway(s). Platelet-activating factor (PAF) induced GLUT4 translocation in the cells expressing the Gi- and Gq-coupled PAF receptor, but the translocation was induced even after pretreatment with wortmannin, an islet-activating protein and phorbol 12, 13-dibutyrate. Norepinephrine triggered GLUT4 translocation in cells expressing the Gq-coupled alpha1-adrenergic receptor, but prostaglandin E2 did not cause GLUT4 translocation in cells expressing the Gs-coupled EP4 receptor or the Gi-coupled EP3alpha receptor. The norepinephrine-stimulated GLUT4 translocation and glucose uptake via Gq may possibly contribute to the fuel supply required for thermogenesis in brown adipocytes and for the enhanced contractility in cardiomyocytes, both of which have an abundant endogenous GLUT4.

3T3 Cells↗
PubMed1996

Characterization of manganese(II) binding site mutants of manganese peroxidase.

A series of site-directed mutants, E35Q, E39Q, and E35Q-D179N, in the gene encoding manganese peroxidase isozyme 1 (mnp1) from Phanerochaete chrysosporium, was created by overlap extension, using the polymerase chain reaction. The mutant genes were expressed in P. chrysosporium during primary metabolic growth under the control of the glyceraldehyde-3-phosphate dehydrogenase promoter. The mutant manganese peroxidases (MnPs) were purified and characterized. The molecular masses of the mutant proteins, as well as UV-vis spectral features of their oxidized states, were very similar to those of the wild-type enzyme. Resonance Raman spectral results indicated that the heme environment of the mutant MnP proteins also was similar to that of the wild-type protein. Steady-state kinetic analyses of the E35Q and E39Q mutant MnPs yielded K(m) values for the substrate MnII that were approximately 50-fold greater than the corresponding K(m) value for the wild-type enzyme. Likewise, the kcat values for MnII oxidation were approximately 300-fold lower than that for wild-type MnP. With the E35Q-D179N double mutant, the K(m) value for MnII was approximately 120-fold greater, and the kcat value was approximately 1000-fold less than that for the wild-type MnP1. Transient-state kinetic analysis of the reduction of MnP compound II by MnII allowed the determination of the equilibrium dissociation constants (KD) and first- order rate constants for the mutant proteins. The KD values were approximately 100-fold higher for the single mutants and approximately 200-fold higher for the double mutant, as compared with the wild-type enzyme. The first-order rate constants for the single and double mutants were approximately 200-fold and approximately 4000-fold less, respectively, than that of the wild-type enzyme. In contrast, the K(m) values for H2O2 and the rates of compound I formation were similar for the mutant and wild-type MnPs. The second-order rate constants for p-cresol and ferrocyanide reduction of the mutant compounds II also were similar to those of the wild-type enzyme.

Aspartic Acid↗
PubMed1996

Forensic applications of genetic polymorphisms detected in human body fluids (urine, semen and blood).

The development of a new genetic marker with forensic usefulness is difficult and costly work, but it is necessary. We discovered several new markers detected in urine, semen and blood. In particular, deoxyribonuclease I-polymorphism is one of the most useful markers for practical purposes, since it has a well-balanced gene frequency, high concentration in body fluids, stability against severe conditions, and easy and accurate detectability.

Blood Chemical Analysis↗
PubMed1996

Glutathione depletion impairs transcriptional activation of heat shock genes in primary cultures of guinea pig gastric mucosal cells.

When primary cultures of guinea pig gastric mucosal cells were exposed to heat (43 degree C), ethanol, hydrogen peroxide (H2O2), or diamide, heat shock proteins (HSP90, HSP70, HSP60, and HSC73) were rapidly synthesized. The extent of each HSP induction varied with the type of stress. Ethanol, H2O2, and diamide increased the syntheses of several other undefined proteins besides the HSPs. However, none of these proteins were induced by exposure to heat or the reagents, when intracellular glutathione was depleted to <10% of the control level by pretreatment with DL-buthionine-[S,R]-sulfoximine. Gel mobility shift assay using a synthetic oligonucleotide coding HSP70 heat shock element showed that glutathione depletion inhibited the heat- and the reagent-initiated activation of the heat shock factor 1 (HSF1) and did not promote the expression of HSP70 mRNA. Immunoblot analysis with antiserum against HSF1 demonstrated that the steady-state level of HSF1 was not changed in glutathione-depleted cells, but glutathione depletion inhibited the nuclear translocation of HSF1 after exposure to heat stress. These results suggest that intracellular glutathione may support early and important biochemical events in the acquisition by gastric mucosal cells of an adaptive response to irritants.

Animals↗
PubMed1996

Roles of insulin, guanosine 5'-[gamma-thio]triphosphate and phorbol 12-myristate 13-acetate in signalling pathways of GLUT4 translocation.

Insulin, guanosine 5'-[gamma-thio]triphosphate (GTP[S] and phorbol 12-myristate 13-acetate (PMA) trigger the translocation of Gl UT4 (type 4 glucose transporter; insulin-sensitive glucose transporter) from an intracellular pool to the cell surface. We have developed a highly sensitive and quantitative method to detect GLUT4 immunologically on the surface of intact 3T3-L1 adipocytes and Chinese hamster ovary (CHO) cells, using c-myc epitope-tagged GLUT4 (GLUT4myc). We examined the roles of insulin, GTP[S] and PMA in the signalling pathways of GLUT4 translocation in the CHO cell system. Among small molecular GTP-binding proteins, ras, rab3D, rad and rho seem to be candidates as signal transmitters of insulin-stimulated GLUT4 translocation. Overexpression of wild-type H-ras and the dominant negative mutant H-rass17N in our cell system respectively enhanced and blocked insulin-stimulated activation of mitogen-activated protein kinase, but did not affect insulin-stimulated GLUT4 translocation. Overexpression of rab3D or rad in the cells did not affect GLUT4 translocation triggered by insulin, GTP[S] or PMA. Treatment with Botulinum C3 exoenzyme, a specific inhibitor of rho, had no effect on GLUT4 translocation induced by insulin, GTP[S] or PMA. Therefore these small molecular GTP-binding proteins are not likely to be involved in GLUT4 translocation. In addition, insulin, GTP[S] and PMA apparently stimulate GLUT4 translocation through independent pathways.

3T3 Cells↗
PubMed1996

Induction of heat shock proteins and their possible roles in macrophages during activation by macrophage colony-stimulating factor.

(1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Gel electrophoresis of pulse-labelled proteins with L-[35S]methionine showed that a number of proteins were induced during activation by M-CSF. Immunoblot analysis with antibody against heat shock protein (HSP) 90, HSP70, or HSP60 demonstrated that M-CSF induced these stress-inducible HSPs; the timing of induction and level of each HSP correlated with the increase in O2- production. The activated macrophages acquired resistance to H2O2-induced damage. M-CSF also stimulated the synthesis of a heat shock cognate protein (HSC70); however, the induction occurred at 1 h, when O2- production was not yet augmented, but at which time L-[35S]methionine incorporation into cell proteins was already enhanced. (2) Gel mobility shift assay with oligonucleotide coding for the heat shock element showed that M-CSF activated the heat shock factor within 15 min, and the activation continued for at least 8 h. Northern-blot analysis with a cDNA probe for human HSP70 or HSC70 showed that accumulations of HSP70 and HSC70 mRNAs coincided with the inductions of the respective proteins. (3) These results suggest that M-CSF may induce the transcriptional activation of heat shock genes, and that the stress-inducible HSPs as well as HSC70 may play an important role in the activation of macrophages by functioning as molecular chaperones and by protecting the macrophage against the auto-oxidative damage associated with the respiratory burst.

Animals↗
PubMed1996

Dual termination modes of corticothalamic fibers originating from pyramids of layers 5 and 6 in cat visual cortical area 17.

Terminal morphology of corticothalamic fibers originating from cat area 17 was examined. Injections of an anterograde axonal tracer, phaseolus vulgaris leucoagglutinin (PHA-L), in area 17 resulted in labeling of small boutons in the dorsal lateral geniculate, perigeniculate, and thalamic reticular nuclei and in labeling of large boutons in the lateral nucleus of lateral posterior-pulvinar, ventral lateral geniculate, and pulvinar nuclei. Since it is well known that the dorsal geniculate nucleus is a major corticothalamic target for layer 6 pyramids and the lateral posterior-pulvinar complex is that for layer 5 pyramids, the findings indicate that layer 5 pyramids in cat area 17 project axons ending with large boutons, while layer 6 pyramids project those ending with small boutons.

Animals↗
PubMed1996

Fine Needle Aspiration Cytology of Argyrophilic Mucinous Carcinoma of the Male Breast.

The results of fine needle aspiration (FNA) cytology of case of argyrophilic mucinous carcinoma of the male breast is presented. The smear obtained from the tumor showed many loose clusters of atypical cells with abundant granular cytoplasm in the mucous background. Most tumor cells showed a plasmacytoid appearance with eccentric nuclei. Numerous fine granules and a few large droplets were found in the cytoplasm. The characteristic light microscopic feature of this lesion was organoid nest formation of tumor cells in mucous lakes. The Grimelius method revealed numerous argyrophilic granules in the cytoplasm and immunohistochemistry showed a positive reaction for chromogranin A. Thus, this tumor revealed the cytomorphologic characteristics of mucinous as well as argyrophilic carcinoma, simultaneously.

Journal Article↗
PubMed1996

Relation of TGF-beta 2 to inhibition of limb bud chondrogenesis by retinoid in rats.

A newly synthesized retinoid, Am-80 (4-[5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl] carbamoxyl) benzoic acid, induced limb reduction defects in rats in vivo. The present study was designed to investigate the mechanisms of its teratogenic action and also to examine whether transforming growth factor-beta (TGF-beta) is involved in limb reduction defects by using a rat limb bud cell culture system. Am-80 inhibited DNA synthesis and chondrogenesis of limb bud cells from day 12 embryos at concentrations of 1-4 ng/ml in a concentration-dependent manner. Quantities of TGF-beta 1 and 2 in culture medium from limb bud cells treated with Am-80 were evaluated using sandwich ELISAs. Although TGF-beta 1 was not detected in conditioned medium with or without Am-80, TGF-beta 2 increased in a concentration-dependent manner at drug concentrations that inhibited DNA synthesis and chondrogenesis. In addition, when TGF-beta 2 was exogenously added to limb bud cell culture medium, the synthesis of glycosaminoglycan (GAGs) was reduced even without Am-80 treatment. Neutralization of TGF-beta 2 with antibody prevented the inhibition of GAGs synthesis induced by Am-80. These results suggest that TGF-betas, especially beta 2, are involved in the inhibition of chondrogenesis caused by Am-80 in limb bud cells.

Animals↗