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Biomedical subjects

K Koike

Publications and source records attributed to K Koike.

At least 397 records · Page 22Linked to original sources

Distinguishing between acute and symptomatic chronic hepatitis B virus infection.

BACKGROUND/AIMS: Differentiating between an acute hepatitis B (AH-B) infection and an acute exacerbation of a chronic hepatitis B (CH-B) infection can present a problem for the clinician. The only current serological method of distinguishing between acute and symptomatic chronic hepatitis B virus (HBV) infection is the immunoglobulin M antibody to hepatitis B core antigen (anti-HBc) assay, which can be problematic. Therefore, in an attempt to better distinguish between acute and chronic HBV infection, sera from 26 patients with AH-B and 53 patients with CH-B were compared in a variety of experimental immunoassays. METHODS: Experimental assays have been designed to detect free antibody to hepatitis B e antigen (anti-HBe), hepatitis B e antigen (HBeAg)/anti-HBe immune complexes (ICs), and hepatitis B surface antigens (HBsAg)/antibody to hepatitis B surface antigen (anti-HBs) in the presence of excess antigen. An additional assay was developed to detect a novel anti-HBc specificity, designated antibody to woodchuck hepatitis virus (anti-HBcW), which cross-reacts with the core antigen of the woodchuck hepatitis virus. RESULTS: Sera from patients with CH-B showed significantly higher levels of free anti-HBe, HBeAg/anti-HBe ICs, and HBsAg/anti-HBs ICs compared with AH-B patient sera. Furthermore, patients with CH-B consistently produced high titer anti-HBcW, whereas patients with AH-B produced little or no anti-HBcW antibody. CONCLUSIONS: The serology of AH-B infection and symptomatic CH-B infection can be distinguished using a variety of experimental immunoassays in addition to the immunoglobulin M anti-HBc assay.

Acute Disease↗

A case of neural cell adhesion molecule-positive peripheral T-cell lymphoma associated with human T-cell lymphotrophic virus type 1 showing an unusual involvement of the gastrointestinal tract during the course of the disease.

We report a case of neural cell adhesion molecule (NCAM)-positive peripheral T-cell lymphoma (PTCL), pleomorphic, medium and large cell type according to the updated Kiel classification, which was associated with human T-cell lymphotrophic virus type 1 (HTLV-1). The patient showed an unusual involvement of the gastrointestinal tract forming a bulky mass during the course of his disease, and a relatively indolent clinical course for 53 months until death. Phenotypic analysis showed CD2+, CD3-, CD4+, CD5+, CD7+, CD8-, CD16-, CD56+, and CD57- phenotype. Human T-cell lymphotrophic virus type 1 antibody was detected by the enzyme-linked immunosorbent assay. The proviral integration of HTLV-1 and the monoclonal rearrangements of T-cell receptor beta and gamma genes also were confirmed in DNA extract from fresh material. This fact calls attention to NCAM as one of the potential factors playing a role in the localization and behavior of lymphomas even within the category of PTCL associated with HTLV-1, ie, adult T-cell leukemia/lymphoma (ATLL).

Antigens, Surface↗

Comparison of interactions of R(+)- and S(-)-isomers of beta-adrenergic partial agonists, befunolol and carteolol, with high affinity site of beta-adrenoceptors in the microsomal fractions from guinea-pig ciliary body, right atria and trachea.

1. The stereoselectivities of beta-adrenergic partial agonists for the high affinity binding site of beta-adrenoceptors in the guinea-pig ciliary body, right atria and trachea were studied. 2. The inhibition curves by the S(-)-isomers of befunolol and carteolol were not significantly different from that by the R(+)-isomers in the guinea-pig ciliary body. 3. The inhibition curves by the S(-)-isomers of befunolol and carteolol were about 10 times as potent as the R(+)-isomers in the guinea-pig atria and trachea. 4. The pKi values of the S(-)-isomers of befunolol and carteolol were significantly larger than those of R(+)-isomers in the guinea-pig atria and trachea but not larger than those of the R(+)-isomers in the guinea-pig ciliary body. 5. These results suggest that the high affinity binding site of beta-adrenoceptors in ciliary body cannot discriminate stereoselectively between the R(+)- and S(-)-isomers, while in other tissues there is stereoselectivity between the two enantiomers.

Adrenergic beta-Agonists↗

Canthin-6-one alkaloids from Brucea mollis var. tonkinensis.

Three new alkaloids were isolated from the root-wood of Brucea mollis var. tonkinensis collected in China. Their structures were determined to be 11-O-beta-D-glucopyranosyl-(1-->6)-beta- D-glucopyranosylcanthin-6-one, 5-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosylcanthin-6-o ne and 11-hydroxycanthin-6-one-N-oxide, by chemical and spectral methods. In addition, two known alkaloids, canthin-6-one and canthin-6-one-N-oxide, were isolated.

Alkaloids↗

Triterpenoid saponins from Ardisia crenata.

Two novel triterpenoid saponins, ardisicrenoside A [3 beta-O-(alpha-L-rhamnopyranosyl-(1-->2)-[beta-D-glucopyranosyl- (1-->4)-[beta-D-glucopyranosyl-(1-->2)]-alpha-L-arabinopyranosyl)- 13 beta,28-epoxy-16 alpha,30-oleananediol] and ardisicrenoside B [3 beta-O-(beta-D-xylopyranosyl-(1-->2)-[beta-D- glucopyranosyl-(1-->4)-[beta-D-glucopyranosyl-(1-->2)]- alpha-L-arabinopyranosyl)-13 beta,28-epoxy-16 alpha,30-oleananediol] were isolated from the roots of Ardisia crenata. Two known triterpenoid saponins, ardisiacrispins A and B were also isolated from this source. Their structures were determined mainly by 2D NMR (COSY, HOHAHA, HETCOR, HMBC and ROESY) experiments. The aglycones are the new 13 beta,28-epoxy-3 beta,16 alpha,30-oleananetriol for ardisicrenosides A and B.

Carbohydrate Sequence↗

Triterpenoid saponins from Dianthus chinensis.

Two novel triterpenoid saponins, dianchinenoside C [23-O-beta-D-glucopyranosyl 3 beta, 16 alpha-dihydroxyolean-12-ene 23 alpha, 28 beta-dioic acid 28-O-beta-D-glucopyranoside] and dianchinenoside D [3 beta, 16 alpha-dihydroxyolean-12-ene 23 alpha, 28 beta-dioic acid 28-O-beta-D-glucopyranosyl [1-->6)-beta-D-glucopyranoside] were isolated from the aerial parts of Dianthus chinensis. Their structures were determined by spectroscopic methods and chemical evidence. We also report the revision of a previous misassignment of hainanenside, isolated from Ilex hainanensis Merr. In addition, known compounds, 3-O-alpha-L-arabinopyranosyl hederagenin 28-O-beta-D-glucopyranosyl (1-->6)-beta-D-glucopyranoside, sitosterol 3 beta-O-beta-D-glucopyranoside, isoorientin-2"-O-glucoside, isovitexin-2"-O-glucoside, and chrysoeriol-7-O-glucoside, were also identified.

Carbohydrate Sequence↗

Gut ischemia/reperfusion produces lung injury independent of endotoxin.

OBJECTIVE: Bacterial translocation from the gut has been invoked as a common inciting event for postinjury multiple organ failure. We previously showed that gut ischemia/reperfusion induces remote organ injury. The purpose of this study was to ascertain if endotoxin has a pivotal mechanistic role in this process. DESIGN: Prospective, randomized study. SETTING: Animal laboratory. SUBJECTS: Sprague-Dawley rats weighing 300 to 350 g. INTERVENTIONS: Anesthetized animals underwent 45 mins of superior mesenteric artery occlusion and 2 hrs of reperfusion; sham laparotomy served as controls. Endotoxin was eliminated with the murine immunoglobulin (Ig) M antibody E5, 3 mg/kg i.v. before the study. MEASUREMENTS AND MAIN RESULTS: Plasma endotoxin was measured by the limulus amebocyte lysate assay. At 2 hrs of reperfusion, circulating neutrophil priming was determined by the difference in superoxide generation with and without the activating stimulus, N-formyl-Met-Leu-Phe. Neutrophil sequestration in the lung was quantitated by myeloperoxidase activity, and by lung endothelial permeability by 125I albumin lung/blood ratio. Endotoxin concentrations were not significantly (significance determined as p < .05) different between the gut ischemia/reperfusion and laparotomy groups (n = > or = 5) during ischemia or reperfusion. Circulating neutrophil priming, neutrophil accumulation in the lung, and lung injury were provoked by gut ischemia/reperfusion, but not altered by endotoxin elimination. CONCLUSION: Gut ischemia/reperfusion primes circulating neutrophils and produces lung injury by a mechanism independent of endotoxin.

Animals↗

Induction of cell cycle progression by hepatitis B virus HBx gene expression in quiescent mouse fibroblasts.

The HBx gene of hepatitis B virus has been shown to induce hepatic tumors in transgenic mice and is implicated in hepatocarcinogenesis in human hepatitis B virus infection. To further characterize the role of HBx gene in carcinogenesis, we established mouse fibroblast cell lines in which the expression of HBx gene could be controlled by glucocorticoid hormone and examined the effect of HBx gene expression on cell growth in vitro. Along with the expression of HBx gene, most cells in the G0/G1 phase moved into the S phase in 24 h, and the cell cycle progressed further toward 48 h. Induction of DNA synthesis was also demonstrated by bromo-deoxyuridine labeling analysis. These results indicate that HBx gene has a function to trigger the synthesis of cellular DNA and suggest that HBx gene may play a role in hepatocarcinogenesis in human infection by driving deregulated cell cycle progression.

3T3 Cells↗

Studies on the constituents of Ailanthus integrifolia.

A new phenolic glycoside, 3,4,5-trimethoxyphenol-1-(6-xylopyranosyl)glucopyranoside, was isolated together with twenty known compounds identified as koaburaside, 3,4,5-trimethoxyphenol, 5,7-dihydroxychromone-7-neohesperidoside, naringin, neoeriocitrin, p-coumaric acid, vanillin, vanillic acid, coniferyl aldehyde, ferulic acid, trans-triacontyl-4-hydroxy-3-methoxycinnamate, p-methoxycinnamic acid, 2,6-dimethoxybenzoquinone, 2-(1-hydroxyethyl)naphtho[2,3-b]furan-4,9-dione, 2-acetylnaphtho[2,3-b]furan-4,9-dione, 2-(1-hydroxyethyl)-6-methoxynaphtho[2,3-b]furan-4,9-dione, 2-acetyl-6-methoxynaphtho[2,3-b]furan-4,9-dione, specioside, jioglutin C and rehmaglutin D from the bark of Ailanthus integrifolia Lamk (Simaroubaceae).

Glycosides↗

Triterpenoid saponins from Ardisia crenata and their inhibitory activity on cAMP phosphodiesterase.

Two novel triterpenoid saponins, ardisicrenoside C (1) [3 beta-O-(alpha-L-rhamnopyranosyl-(1-->2)-beta-D-glucopyranosyl-(1-->4)- [beta-D-glucopyranosyl-(1-->2)]-alpha-L-arabinopyranosyl)-16 alpha, 28-dihydroxy-olean-12-en-30-oic acid 30-O-beta-D-glucopyranosyl ester] and ardisicrenoside D (2) [3 beta-O-(beta-D-xylopyranosyl-(1-->2)- beta-D-glucopyranosyl-(1-->4)-[beta-D-glucopyranosyl-(1-->2)]-alpha-L- arabinopyranosyl)-16 alpha, 28-dihydroxy-olean-12-en-30-oic acid 30-O-beta-D-glucopyranosyl ester] were isolated from the roots of Ardisia crenata. Structure assignments are based on spectroscopic data including 2D-NMR (correlation spectroscopy (COSY), homonuclear Hartmann-Hahn spectroscopy (HOHAHA), heteronuclear correlated spectroscopy (HETCOR), heteronuclear multiple bond correlation (HMBC) and rotating frame NOE spectroscopy (ROESY)) experiments and some chemical reactions. In addition, the isolated saponins along with their prosapogenins and sapogenins have been evaluated for their inhibitory activity on cAMP phosphodiesterase as a primary screening test for new medicinal compounds.

3',5'-Cyclic-AMP Phosphodiesterases↗

Steroidal constituents from the underground parts of Reineckea carnea and their inhibitory activity on cAMP phosphodiesterase.

Phytochemical analysis of the underground parts of Reineckea carnea resulted in the finding of twelve steroidal constituents, five of which appeared to be new compounds and one to be the first isolation from a natural source. The identification and structural determination of the steroidal compounds were established by spectroscopic analysis and hydrolysis. The isolated saponins were evaluated for inhibitory activity on cAMP phosphodiesterase as a primary screening test to find new medicinal materials.

3',5'-Cyclic-AMP Phosphodiesterases↗

Involvement of beta 3-adrenoceptor in the relaxation response in guinea pig taenia caecum.

beta-Adrenoceptors in the guinea pig taenia caecum were investigated by measuring relaxation responses to agonists and by a radioligand binding assay using [3H]CGP 12177. The rightward shift of the isoprenaline concentration-response curve was observed by butoxamine, a beta 2-selective antagonist, and the pA2 value for butoxamine was 6.46. In control preparations, catecholamines caused relaxation with the following rank order of potency: isoprenaline > adrenaline > noradrenaline. However, in the presence of 10(-6) M phentolamine, 3 x 10(-4) M atenolol and 10(-4) M butoxamine, the rank order of potency of the agonists was: isoprenaline > noradrenaline > adrenaline. CGP 12177 caused graded relaxation of the guinea pig taenia caecum, and this response was not influenced by 10(-6) M phentolamine, 3 x 10(-4) M atenolol, 10(-4) M butoxamine or 10(-6) M propranolol. The Scatchard plot of the specific [3H]CGP 12177 binding to microsomal fractions from the guinea pig taenia caecum showed two affinity sites of the receptor: high affinity (KD = 0.64 nM) and low affinity (KD = 142.21 nM) sites. The pKD value of the high affinity site of [3H]CGP 12177 was in agreement with its pA2 value, and that of the low affinity site was in agreement with its pD2 value. These results suggest that isoprenaline-, noradrenaline- and adrenaline-induced relaxations of the guinea pig taenia caecum predominantly involve beta 2- and beta 3-adrenoceptors, whereas CGP 12177-induced relaxation is mediated solely through beta 3-adrenoceptors.

Adrenergic beta-Antagonists↗

Hematopoietic progenitors and synergism of interferon-gamma and stem cell factor.

Interferon-gamma (IFN-gamma), an immunoregulatory cytokine produced by activated T cells and natural killer cells in response to viral infection or other stimuli, is generally recognized as a suppressor of hematopoiesis. IFN-gamma inhibited in vitro colony formation by granulocyte-macrophage (GM), erythroid and multipotential progenitors. This cytokine exerted direct suppression on the proliferation process, but not on the commitment, of GM progenitors. The antiproliferative effects of IFN-gamma may, in part, result from the prolongation of the doubling time of GM progenitors. Clinically, IFN-gamma may play an important role in the pathogenesis of pancytopenia in aplastic anemia and in the hemophagocytic syndrome. However, as well as showing inhibitory effects, IFN-gamma increased the number of pure and mixed megakaryocyte colonies formed by post-5-fluorouracil treated bone marrow cells and, moreover, the addition of IFN-gamma to culture containing stem cell factor resulted in a synergistic effect on the development of both primitive hematopoietic progenitors and mature populations. These findings suggest that IFN-gamma has bifunctional activity in hematopoiesis.

Animals↗

[Granulocyte colony-stimulating factor combination therapy of acute myeloid leukemia complicated with severe infection].

We report the usefulness of granulocyte-colony stimulating factor (G-CSF) for the treatment of severe infection with neutropenia after chemotherapy for acute myeloid leukemia (AML, M3). A 5-year-old boy was admitted because of the first relapse of AML. After 2 courses of chemotherapy, he suffered from right mandibular phlegmon due to Pseudomonas aeruginosa. Since various types of antimicrobial therapy were not effective and neutropenia was still present, we started to give him G-CSF (400 micrograms/m2/day, sc). After 5 days, there was increase in the neutrophil count and remarkable clinical improvements. There was no evidence of AML relapse after the G-CSF the rapy. He was given another course of chemotherapy and then underwent allogeneic bone marrow transplantation from his HLA non-identical, MLC non-reactive sister. This successful case indicates that we should use G-CSF for the management of neutropenic AML patients complicated with severe infection.

Antineoplastic Combined Chemotherapy Protocols↗

[A randomized controlled trail of intensive and usual community-based education for blood pressure control].

A 1.5 year community-based hypertension education program was conducted and evaluated for the feasibility and effectiveness as a program for primary prevention of cardiovascular disease. The subjects were determined to be hypertensive from cardiovascular examinations and composed of 104 untreated men and women aged 35-69 whose blood pressure levels were between 140 and 179 mmHg for systolic and/or between 90 and 109 mmHg for diastolic and who had no evidence of hypertensive end organ effects in the 1990 examination. They were randomly assigned to either an intensive education (IE) group (n = 53) or a usual education (UE) group (n = 51) and invited to education classes six months later. The IE consisted of four education classes in the first six months and another 4 classes in the next 12 months. For the UE, one class in the first 6 months and another class in the next 12 months were held. Health education was focused on reduction of sodium intake, a 30 minutes of walking, and if necessary, reduction of alcohol and sugar intake. Mean (SD) values of systolic blood pressure at the start of the education program were 144.8 (11.7) mmHg in IE and 144.5 (12.2) mmHg in UE. The respective diastolic means (SD) were 80.6 (7.8) mmHg and 80.3 (8.6) mmHg. The proportion of persons who started to receive antihypertensive medication was 8-9% in both groups at six months, and 13% in IE and 29% in UE at 1.5 years. IE showed a 6 mmHg greater reduction in mean systolic blood pressure than UE at both six months and 1.5 years. No significant difference was found in diastolic blood pressure levels over time between the two groups. Dietary improvements related to reduction of salt intake were more evident in IE than in UE. There was no significant changes in means and distributions of relative weight index and alcohol intake in either group. Subgroup analysis according to antihypertensive medication use indicated that reduction of systolic blood pressure levels was significantly larger in IE than in UE for both no medication and medication subgroups at 6 months and 1.5 years. While it was difficult to evaluate an effect of the program at 1.5 years because of the difference in the proportion of medication use between IE and UE, the results at 6 months suggest that this community-based program was effective in reducing systolic blood pressure levels.

Adult↗

[Effect of amurinone on human pulmonary artery in vitro].

We studied the effect of amurinone, a phosphodiesterase inhibitor, on human pulmonary arterial smooth muscle in vitro. Amurinone caused dose-dependent relaxation of pulmonary arterial strips precontracted with 60 mM KCl. Preincubation with either meclofenamate (31 microM), a cyclooxygenase inhibitor, or L-NG-nitroarginine (100 microM), an endothelium-derived relaxing factor (EDRF) production inhibitor, failed to inhibit amurinone-induced pulmonary vasodilation. The cyclic AMP (cAMP) levels in the supernatant of the lung vessel homogenates significantly increased after incubation with amurinone. These results indicate that amurinone causes relaxation of human pulmonary artery in vitro, and suggest a role for cAMP in the mechanisms of amurinone-induced pulmonary vasodilation.

Adult↗

Transcription from the P2 promoter of human protooncogene myc is suppressed by retinoic acid through an interaction between the E2F element and its binding proteins.

When human promyelocytic leukemia cell line HL60 was treated with retinoic acid (RA), considerable suppression of protooncogene myc expression was achieved before granulocytic differentiation became evident. From transient transfection experiments using the reporter plasmid containing exon 1 and its 2.3 kilobases upstream of the c-myc gene fused to the chloramphenicol acetyltransferase gene, it was indicated that this suppression was mainly attributable to the level of transcription initiation. Deletion down to 95 base pairs upstream of the P2 promoter did not change the suppressive effect of RA on c-myc gene expression. Mobility shift assays with respect to the P2 promoter region revealed that the 15-base pair fragment located between P1 and P2 promoters was responsive to the RA treatment. This fragment included the E2F binding site in the c-myc P2 promoter region, and a difference of shifted bands between RA-treated and untreated HL60 cells was due to complex formation of E2F and retinoblastoma protein. The present results suggest that E2F plays an important role in the process of cell differentiation by RA and that a change of the E2F binding pattern induced by RA contributes to the suppression of c-myc gene expression preceding granulocytic differentiation.

Base Sequence↗