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T Kaneko

Publications and source records attributed to T Kaneko.

At least 343 records · Page 19Linked to original sources

Poor outcome in disseminated intravascular coagulation or thrombotic thrombocytopenic purpura patients with severe vascular endothelial cell injuries.

Various hemostatic and vascular endothelial cell markers were measured in patients with disseminated intravascular coagulation (DIC), non-DIC, or thrombotic thrombocytopenic purpura (TTP) and in healthy volunteers to examine the relationships between the hemostatic abnormalities or vascular endothelial cell injuries and the patients' outcomes. Although the plasma levels of soluble fibrin monomer, thrombin-antithrombin complex, plasmin-plasmin inhibitor complex, and D-dimer were significantly increased in the DIC patients, there were no significant differences in these markers between the DIC patients who survived and those who died, suggesting that these markers might not be directly related to the patient outcome. The plasma thrombomodulin (TM) levels in the DIC and TTP patients were significantly higher than those in the healthy volunteers, and the plasma TM levels in the patients who died were significantly higher than those in the patients who survived. These findings showed that the TM level reflected the outcome, and that the outcome of the diseases underlying DIC and TTP might depend on vascular endothelial cell injuries. The plasma protein C and antithrombin activities were markedly reduced in the DIC, non-DIC, and TTP patients who died compared to those who survived. These findings suggest that reduced plasma antithrombin and protein C activities are useful markers of systemic vascular endothelial injuries. Although the plasma tissue factor (TF) levels were significantly increased in the DIC patients, there was no significant difference in the plasma TF levels between the DIC patients who died and those who survived. In conclusion, we found that the outcome of the diseases underlying DIC and TTP is related to vascular endothelial cells, and that plasma TM, antithrombin, and protein C are useful markers for systemic vascular endothelial cell injury.

Antifibrinolytic Agents↗

Direct measurement of CD34+ blood stem cell absolute counts by flow cytometry.

For the collection of adequate numbers of peripheral blood stem cells (PBSC) for PBSC transplantation, an accurate quantification of circulating CD34+ stem cells is required for deciding the optimal time of the collection. To enumerate peripheral blood (PB) CD34+ stem cells, the percentage of CD34+ cells in the gated PB mononuclear cells should be multiplied by the percentage of the gated mononuclear cells among white blood cells (WBC) and by the total WBC count. Accordingly, a minor difference in the measured percentage of the CD34+ cells can lead to a major difference in the PB CD34+ cell concentration. In the present study, we measured the concentration of PB CD34+ stem cells with a flow cytometer designed to provide direct absolute counts of cell subsets from a single instrument. Whole blood was stained with a phycoerythrin-conjugated anti-CD34 monoclonal antibody, and, after the lysis of red blood cells, CD34+ cells were counted in a fraction of the lymphocyte and monocyte gate. The accuracy of our method was demonstrated in an experiment in which various dilutions of known numbers of CD34+ leukemic cells were mixed with normal blood; the predicted value of the CD34+ cell count was observed. The concentration of CD34+ cells in leukapheresis products was measured both by our direct assay and an indirect assay that calculates the number from the percentage of CD34+ cells in mononuclear cells, and our assay was shown to produce less variation. Further, our assay showed a significant correlation between the concentration of mobilized CD34+ cells in the PB and the number of harvested CD34+ cells in leukapheresis. These findings indicate that the monitoring of the concentration of PB CD34+ cells by the present method can be used to predict the number of stem cells collected in leukapheresis. This procedure is easy to perform and can be applied to daily monitoring to decide the appropriate timing for harvest of mobilized stem cells.

Antigens, CD34↗

Intranasal administration of HIV-DNA vaccine formulated with a polymer, carboxymethylcellulose, augments mucosal antibody production and cell-mediated immune response.

We previously reported that intramuscular (i.m.) immunization of DNA vaccine encoding human immunodeficiency virus type 1 (HIV-1)IIIB env and rev genes alone or in combination with appropriate adjuvant induces substantial and enhanced immune response against HIV-1. In the present study, we examined whether a polymer, low-viscosity carboxymethylcellulose sodium salt (CMCS-L), has an adjuvant effect on immune response induced by DNA vaccination. BALB/c mice were immunized with HIV-DNA vaccine formulated with CMCS-L via the intranasal (i.n.) and i.m. routes. The combination with the polymer elicited higher levels of antigen-specific serum IgG and fecal IgA antibodies than DNA vaccine alone. For cell-mediated immunity, HIV-specific delayed-type hypersensitivity response and cytotoxic T lymphocyte activity were measured by the footpad-swelling test and the 51Cr-release assay, respectively. Both were enhanced by the combination with CMCS-L via i.n. and i.m. inoculation. Cytokine analysis in culture media of bulk splenocytes harvested from immunized animals showed higher levels of IL-4 production in i.n. -immunized mice compared with i.m.-immunized mice. Nevertheless, the increased IFN-gamma production resulting from the combination with CMCS-L was observed only in i.n.-immunized mice. These data indicate that i.n. immunization of HIV-DNA vaccine formulated with CMCS-L enhances HIV-specific mucosal antibody (Ab) and systemic Ab and cell-mediated immune response.

AIDS Vaccines↗

Localization of cortisol receptor in branchial chloride cells in chum salmon fry.

To clarify the involvement of cortisol in functional differentiation of branchial chloride cells, cellular gene expression and localization of cortisol receptor were examined in chum salmon (Oncorhynchus keta) fry in freshwater (FW) and those adapted to seawater (SW) by in situ hybridization and immunocytochemical staining. Sodium-potassium adenosinetriphosphatase (Na+,K(+)-ATPase) activity in the whole gill homogenate was significantly higher in SW fish than in FW fish. There were no significant differences in plasma cortisol levels nor in the expression of cortisol receptor mRNA, examined by Northern blot analysis, between SW and FW fish. The receptor gene expression, examined by in situ hybridization with biotin-labeled synthetic oligonucleotide probe, and specific immunostaining with anticortisol receptor serum were found in two types of chloride cells distributed in the gill filaments and lamellae, which were also labeled with anti-Na+,K(+)-ATPase serum, indicating that cortisol may be one of the important factors regulating chloride cell functions. Gene expression of cortisol receptor in filament chloride cells, which were highly activated in SW-adapted fry, was significantly greater in the fry adapted to SW than in FW-adapted fry, reflecting their specific role in salt secretion in SW. Cortisol receptors were also present in undifferentiated cells in the interlamellar regions adjacent to the central venous sinus, also suggesting the involvement of cortisol in the functional differentiation of chloride cells.

Animals↗

Bradykinin increases intracellular calcium levels in a human bronchial epithelial cell line via the B2 receptor subtype.

OBJECTIVE: To determine which types of kinin receptor are present in human bronchial epithelial cells we studied the capability of bradykinin to mobilize intracellular Ca2+ ([Ca2+]i) in a human bronchial epithelial cell line (16HBE cells). MATERIAL: Human bronchial epithelial cell line transformed with an original defective simian virus 40 (SV40). TREATMENT: Bradykinin (0.1 pM to 0.1 microM), des-Arg9 bradykinin (1 microM), des-Arg10) kallidin (1 microM), indomethacin (1 microM), phosphoramidon (1 microM), captopril (1 microM), des-Arg9-[Leu8]bradykinin (1 microM), HOE 140 (DArg-[Hyp3, Thi5, DTic , Oic8]-bradykinin) (1 microM), and NPC 16731 (DArg-[Hyp3, Thi5, DTic7, Tic8]-bradykinin) (1 microM). METHODS: The mobilization of [Ca2+]i was determined by the fura-2 method. Two sample Wilcoxon rank-sum (Mann-Whitney) test was used for statistical calculations. RESULTS: Bradykinin, but not the selective agonists for kinin B1 receptor des-Arg9 bradykinin and des-Arg10 kallidin, increased the mobilization of [Ca2+]i (EC50, 0.079+/-0.009nM) in 16HBE cells in a concentration-dependent manner. Pretreatment with the cyclooxygenase inhibitor indomethacin (1 microM) or the peptidase inhibitors, phosphoramidon (1 microM) or captopril (1 microM), did not affect the response to bradykinin. The kinin B1 receptor antagonist, des-Arg9-[Leu8]bradykinin (1 microM), was inactive. HOE 140 and NPC 16731, two selective antagonists of the kinin B2 receptor abolished the response to bradykinin (IC50 of HOE 140 and NPC 16731 were 0.52+/-0.037nM and 1.67 +/- 0.41 nM, respectively). CONCLUSIONS: The present data indicate the presence of kinin B2 receptors in the 16HBE cells.

Angiotensin-Converting Enzyme Inhibitors↗

Effective TAE therapy using Lipiodol with epirubicin for liver metastases of nonfunctioning islet cell carcinoma of the pancreas.

We report the response of two patients with advanced nonfunctioning islet cell carcinoma of the pancreas with liver metastases treated with a combination of surgi-cal resection and transarterial embolization (TAE), using Lipiodol with epirubicin. After pretreatment evaluation, the two patients were diagnosed with nonfunctioning islet cell carcinoma of the pancreas with liver metastases. Preoperatively, in both patients, TAE was performed through the hepatic arteries, using Lipiodol and sponzel plus epirubicin. Surgical resection of the primary tumor (radical distal pancreatectomy and pancreaticoduodenectomy) was performed. After surgical resection and evaluation of the malignant histopathological features of the neoplasms, chemotherapy, which included oral 5-fluorouracil (FU), and transarterial infusion therapy, using Lipiodol with epirubicin, was administered to the patients. Follow-up evaluation of the two patients by computerized tomography (CT) scan showed a reduction in the size of the metastatic hepatic masses after several chemoembolizations through the hepatic arteries. This combined treatment modality may be an effective therapeutic strategy for improved management of patients with advanced nonfunctioning islet cell carcinoma of the pancreas with liver metastases.

Adult↗

Intraportal endovascular ultrasonography for assessment of vascular invasion by biliary tract cancer.

BACKGROUND: This study was performed to investigate the diagnostic accuracy of intraportal endovascular ultrasonography (IPEUS) in assessing vascular invasion by biliary tract cancer. METHODS: A prospective study of 31 consecutive patients with biliary tract cancer was performed. All patients underwent surgery. The sonographic criterion for right hepatic artery invasion was interruption of the hyperechoic layer or encasement by tumor. The sonographic criterion for portal vein invasion was obliteration of the echogenic band of the portal vein. IPEUS findings were confirmed by surgical exploration and pathologic examination of resected specimens. RESULTS: Right hepatic artery invasion was confirmed in resected specimens in seven patients and by operative findings in four patients. Portal vein invasion was confirmed in resected specimens in six patients and by operative findings in five patients. For diagnosis of right hepatic artery invasion, the sensitivity, specificity, and overall accuracy of IPEUS were all 100%; respective values were 63.6%, 84.2%, and 76.7% for angiography. For diagnosis of portal vein invasion, the sensitivity, specificity, and overall accuracy of IPEUS were 100%, 95%, and 96.8%, respectively. The corresponding values were 63.6%, 89.5%, and 80% for portography and 54.5%, 85%, and 74.2%, respectively, for CT. CONCLUSION: IPEUS will improve the assessment of vascular invasion at the hepatic hilum by biliary tract cancer.

Aged↗

Direct projections from the entorhinal cortical layers to the dentate gyrus, hippocampus, and subicular complex in the cat.

Projections from each layer of the entorhinal cortex (EC) of the cat were traced to the dentate gyrus (DG), Ammon's horn (CA), prosubiculum (ProSb), subiculum (Sb), presubiculum (PreSb) and parasubiculum (ParaSb); the anterograde or retrograde labeling method was used after stereotaxic injection of wheat germ agglutinin-horseradish peroxidase, cholera toxin B subunit, or Phaseolus vulgaris leucoagglutinin. On the side ipsilateral to the tracer-injection, layer II of the EC projected most abundantly to the outer half of the molecular layer (ML) of the DG, less abundantly to the almost entire thickness of the stratum lacunosum-moleculare (SLM) of CA2-3, moderately to the almost entire thickness of the SLM of CA1, and less to the outer part of the ML of the ProSb and Sb. Layer III projected abundantly to the almost entire thickness of the SLM of CA1 and outer part of the ML of the ProSb and Sb, and sparsely to the SLM of CA2-3. Layer IV projected sparsely to the pyramidal cell layer of the ProSb and Sb; Layer IV of the medial part (toward the ParaSb) of the EC projected further to the ML of the DG. Layer VI projected sparsely to the outer part of the ML of the DG, almost entire thickness of the SLM of CA1-3, and outer part of the ML of the ProSb and Sb. More temporal parts of the hippocampal region received the projections from progressively more medial and more rostral parts of layers II and III, and from progressively more rostral parts of layers IV and VI. The ML of the PreSb and ParaSb received projections from all layers of the medial part of the ipsilateral EC. The SLM of CA1 and ML of the ProSb, Sb and ParaSb received projections from layer II and/or III of the contralateral medial entorhinal area.

Animals↗

Baseline factors affecting the efficacy of troglitazone on plasma glucose in Japanese patients with non-insulin-dependent diabetes mellitus.

In order to assess the relationship between clinical efficacy of troglitazone on glycemic control and baseline characteristics of patients with NIDDM, we analyzed the data of ten clinical studies on troglitazone carried out in Japan. The study consisted of 604 subjects with NIDDM whose glycemic control had been unsatisfactory (fasting plasma glucose (FPG) > or = 8.3 mM) with diet or sulfonylureas (SU) and who had been assigned to one of ten clinical studies at a dose of 400 mg/day troglitazone for 12-16 weeks. In patients who had been treated with SU, troglitazone was given in combination with the SU drugs. The percentage decrease in FPG was adopted as the index of clinical efficacy. The relationship between this index and various baseline parameters of patients was analyzed. It was found that FPG and triglycerides decreased significantly with troglitazone (pre- and post-treatment: FPG 10.3 +/- 2.0 and 8.7 +/- 2.2 mM; triglyceride 1.82 +/- 1.27 and 1.51 +/- 0.99 mM, respectively). The percentage decrease in FPG after treatment did not differ between groups treated with troglitazone alone and those treated with troglitazone in combination with SU drugs (14.7 vs. 15.5%). Patients were classified into two groups according to the percentage decrease in FPG, greater and less than 15%. The group with greater decrease in FPG included more females and had the older mean age, greater body mass index (BMI), higher pre-treatment FPG, and higher pre-treatment C-peptide values. In the multiple regression analysis, female gender, age, BMI and pre-treatment FPG level were selected as the variables for the best regression model. The results indicate that troglitazone at 400 mg/day decreased FPG significantly in patients with NIDDM and the percentage decrease in FPG was positively correlated with female gender, higher pre-treatment FPG, older age, greater BMI and higher C-peptide level. The results suggest that this drug is more effective in patients with greater insulin resistance, in keeping with its proposed mode of effect.

Aged↗

Dietary carbohydrate intake plays an important role in preventing alcoholic fatty liver in the rat.

BACKGROUND/AIMS: Dietary carbohydrate intake during ethanol ingestion augments the induction of hepatic cytochrome P450 2E1 (CYP2E1) by ethanol. This study addresses the role of carbohydrate intake in the development of alcoholic fatty liver in the rat. METHODS: Male Sprague-Dawley rats were pair-fed on liquid diets containing ethanol (3.5 g/day, 36% of total calories) with different amounts of carbohydrate and fat for 4 weeks, and the development of fatty liver was observed biochemically and morphologically. RESULTS: An ethanol-containing low-carbohydrate diet (protein 17%; fat 36%; carbohydrate 11%; ethanol 36%) had more markedly adverse effects on the liver of rats than did an isocaloric ethanol-containing high-carbohydrate diet (protein 17%; fat 5%; carbohydrate 42%; ethanol 36%). The hepatic triglyceride level in the rats that consumed the low-carbohydrate diet was higher than that in the rats kept on the high-carbohydrate diet, a finding that was confirmed histologically. The ethanol-containing low-carbohydrate diet caused a marked increase in the activity of hepatic CYP2E1. The CYP2E1 protein level, as measured by Western blot analysis, matched the activity of CYP2E1, as measured by the rates of dimethylnitrosamine, p-nitrophenol and ethanol metabolism. The severity of the fatty liver was well correlated with the increased CYP2E1 activity. CONCLUSIONS: Dietary carbohydrate intake plays an important role in the development of alcoholic fatty liver by affecting CYP2E1 activity in the liver. A liquid diet containing ethanol in which the ethanol is included at the expense of fat is more acceptable to rats than a diet in which the ethanol replaces carbohydrate.

Animals↗

Characterization of neocortical non-pyramidal neurons expressing preprotachykinins A and B: a double immunofluorescence study in the rat.

Neurons expressing preprotachykinin A and preprotachykinin B, which are the precursor prepropeptides of substance P and neurokinin B (neuromedin K), respectively, were characterized immunocytochemically in the rat neocortex. Antibodies raised against C-terminal portions of preprotachykinins were used for labeling cell bodies of preprotachykinin-producing neurons. Neurons immunoreactive for preprotachykinin B were encountered four times more frequently in the neocortex than those immunoreactive for preprotachykinin A. Preprotachykinin A-immunoreactive neurons were scattered more frequently in the deep cortical layers (layers IV-VI) than in the superficial layers (layers I-III), whereas preprotachykinin B-immunoreactive neurons were distributed more frequently in the superficial layers than in the deep layers. Almost all preprotachykinin-expressing neurons were immunoreactive for GABA, suggesting that they were non-pyramidal cells. However, co-expression of the two preprotachykinin immunoreactivities in single neurons was not found. Preprotachykinin-expressing neocortical neurons were further examined with markers for subpopulations of GABAergic cortical neurons. Immunoreactivities for parvalbumin, calbindin and somatostatin were found in 69%, 27% and 11%, respectively, of preprotachykinin A-immunoreactive neurons. Conversely, preprotachykinin A-immunoreactive neurons constituted only 6% of parvalbumin-immunoreactive neurons, 4% of calbindin-immunoreactive neurons and 1% of somatostatin-immunoreactive neurons. Immunoreactivities for calretinin, choline acetyltransferase, vasoactive intestinal polypeptide, corticotropin-releasing factor and cholecystokinin were detected in 13-39% of preprotachykinin B-immunoreactive neurons. Preprotachykinin B immunoreactivity was seen in 33% of calretinin-positive neurons, 45% of cholinergic neurons, 47% of vasoactive intestinal polypeptide-positive neurons, 59% of corticotropin-releasing factor-positive neurons and 83% of cholecystokinin-positive neurons. These results indicate that preprotachykinin A- and preprotachykinin B-expressing neurons constitute separate populations of GABAergic non-pyramidal neurons in the neocortex. Since receptors for substance P and neurokinin B are expressed in GABAergic neurons [Kaneko T. et al. (1994) Neuroscience 60, 199-211] and pyramidal neurons [Ding Y. Q. et al. (1996) J. comp. Neurol. 364, 290-310], respectively, cortical neurons may use two separate lines of tachykinin signals; substance P serves as a signal between GABAergic non-pyramidal neurons, whereas neurokinin B acts as a signal of GABAergic neurons to pyramidal neurons.

Amino Acid Sequence↗

Neutrophils, lipid peroxidation, and nitric oxide in gastric reperfusion injury in rats.

Nitric oxide (NO) modulation of ischemia-reperfusion injury was investigated by measuring lipid peroxide and neutrophil accumulation in rat stomachs treated with NG-nitro-L-arginine (L-NNA), a specific NO synthase inhibitor. Ischemia-reperfusion injury was induced in the rat stomach. Treatment with L-NNA for 3 days at a dose of 3 mg/kg/day significantly enhanced this injury. This enhancement was reversed by the simultaneous administration of L-arginine at a dose of 30 mg/kg/day. Both thiobarbituric acid (TBA)-reactive substances, an index of lipid peroxidation, and myeloperoxidase (MPO) activity, an index of tissue-associated neutrophil accumulation, were increased in the gastric mucosa after ischemia-reperfusion. L-NNA treatment enhanced these increases in TBA-reactive substances and MPO activity. The increase in the area of gastric erosions correlated closely with accumulation of TBA-reactive substances as well as the increase in MPO activity. Enhancement of ischemia-reperfusion injury by L-NNA treatment was inhibited by injection with anti-neutrophil antibody, anti-platelet activating factor (PAF) antagonist, and anti-leukotriene B4 (LTB4) receptor antagonist. In addition, the increase in TBA-reactive substances and MPO activity was decreased by these antibodies or antagonists. Enhancement of reperfusion-induced gastric mucosal injury associated with inhibition of NO synthesis may involve neutrophil infiltration and lipid peroxide accumulation in the gastric mucosa, mediated by PAF and LTB4.

Animals↗

Amino acid formation in gas mixtures by high energy particle irradiation.

Amino acids were formed from carbon monoxide, nitrogen and water, which are possible constituents of the primitive earth's atmosphere, by irradiation with high energy particles (components of cosmic rays). Glycine yield was proportional to the total energy deposited to the gas mixture, and its G-value was as high as 0.02 when the carbon monoxide/nitrogen ratio was 1. Based on an estimate of the effective energies of various types of energy sources available in the primitive earth's atmosphere for amino acid synthesis, it is suggested that cosmic rays were one of the most important energy sources for the synthesis of amino acids on the primitive earth.

Amino Acids↗

Isolation of genes identified in mouse renal proximal tubule by comparing different gene expression profiles.

An expression profile is a list based on a large scale sequencing of 1000 cDNA clones, showing the expressed genes and the abundance of their transcripts in a given cell or tissue (Okubo K et al: Nature Genet 2:173, 1992). We constructed an expression profile of mouse renal proximal tubules (PT) carefully isolated by microdissection in order to characterize its gene expression. Altogether 1000 clones were analyzed; there were 646 types of transcripts in PT, among which 196 were identical or homologous to the previously reported genes. The most abundant transcript was kidney-androgen regulated protein. By comparing the expression profile of PT with those obtained from other sources, several genes were identified only in PT. They included known transcripts and transcripts that were not homologous to the known genes. Three (GS4001, 3991, and 4059) of the non-homologous genes were analyzed by Northern blotting and in situ hybridization, and GS4001 and 4059 were predominantly expressed in the kidney, whereas GS3991 was detected in the liver as well as in the kidney. The sequence analysis of the full-size cDNAs demonstrated that GS4001 was a new member of aspartic proteinases and GS4059 was a novel gene. It also revealed that GS3991 was a mouse homologue of SA gene known to be expressed in PT. The expression profile of mouse PT and its comparison with those of other tissues and cells provide an alternate way of isolating genes predominantly expressed in PT, and also provides probes to study the molecular mechanisms of gene expression in the kidney.

3T3 Cells↗