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Biomedical subjects

M Yamazaki

Publications and source records attributed to M Yamazaki.

At least 379 records · Page 21Linked to original sources
PubMed1996

[A study of soluble form of L-selectin in blood of patients with neuroimmunological disorders].

Members of the selection family mediate the first step of leukocyte-endothelial cell interaction in inflammatory lesion. We have examined the soluble form of L-selectin (sL-selectin) in patients with neuroimmunological disorders (48 multiple sclerosis, 2 Balo's sclerosis, 18 Guillain-Barré syndrome, 7 Miller-Fisher syndrome, 8 chronic inflammatory demyelinating polyneuropathy, and 25 human T-lymphotropic virus type-1 associated myelopathy). The levels of sL-selectin were measured by monoclonal antibody-based enzyme immunoassay on serum samples taken from patients with neuro immunological disorders. The level of sL-selectin were significantly decreased in the blood of patient with inactive stage of multiple sclerosis (MS), Guillain-Barré syndrome (GBS), and human T-lymphotropic virus type-1 associated myelopathy (HAM). The levels of sL-selectin in the sera of patients with active phase of MS tended to be high, but not significantly increased. The levels of sL-selectin, however, in the sort of patients with Balo's concentric sclerosis tended to be decreased. Thus, the findings that the serum concentrations of sL-selectin were decreased in stable phase of MS and acute phase of GBS and HAM suggest that sL-selectin may be differently involved in between patients with MS and patients with GBS or HAM.

Adult↗
PubMed1996

[Clinical evaluation of hepatic arterial infusion chemotherapy in patients with liver metastases from colorectal cancer].

Seventy-four cases of hepatic metastasis of colorectal cancer experienced in our hospital from January 1988 to February 1996 were examined for hepatic arterial infusion chemotherapy induced macrobiotic effect. A group (21 cases of hepatectomy and hepatic arterial infusion chemotherapy), B group (31 cases of hepatic arterial infusion chemotherapy only) and C group (22 cases of iv and po systemic chemotherapy) were comparatively examined for survival rate using Kaplan-Meier method. Single administration of adriamycin, epirubicin, cisplatin (CDDP) and 5-FU, along with CDDP-5-FU combined therapy and 5-FU 1,000 mg/5 hr intermittent continuous infusion therapy, were used. Mean survival period was 719 +/- 369, 426 +/- 417, 158 +/- 125 days for groups A, B and C, respectively. One-year survival rate by degrees of H factor was comparatively examined because of different H factor rates for these 3 groups. As a result, it proved to be 83 and 40% for groups A and B, respectively, in H1,2 cases and 32 and 11% for groups B and C, respectively, in H3 cases, with their respective significant differences (p < 0.05). Positive treatment, including hepatectomy, hepatic arterial infusion chemotherapy and the like, was suggested to contribute to patient macrobiosis.

Aged↗
PubMed1996

[The influence of intrathecal NMDA receptor antagonist on the isoflurane MAC and on the motor function].

The effect of intrathecal administration of NMDA (N-methyl-D-aspartate) receptor antagonists on the isoflurane MAC (minimum alveolar anesthetic concentration), and on the locomotor function, were studied in Wistar rats with catheters placed intrathecally. We determined the isoflurane MAC after the administration of either a competitive NMDA receptor antagonist, AP7 (0.044-132 nmole), or a non-competitive NMDA receptor antagonist, MK801 (0.3-90 nmole), as well as NMDA (0.068-204 nmole), and saline. AP7 (0.44-132 nmole) and MK801 (30-90 nmole) decreased the MAC. Intrathecal administration of NMDA reversed these decreases of MAC, but reversal effect is incomplete with AP7 132 nmole and MK801 90 nmole. In a locomotor dysfunction test, rats showed motor dysfunction with AP7 132 nmole (P < 0.05) and MK801 90 nmole (P < 0.05), but low doses did not exert these effects. Large doses of NMDA antagonist decreased the isoflurane MAC due to motor dysfunction, but low doses reduced the MAC without impairing motor function. We suspect that NMDA receptor antagonists play important roles in determining the isoflurane MAC in the spinal cord.

2-Amino-5-phosphonovalerate↗
PubMed1996

[Preparation of plasma membrane and the analysis of transport kinetics and driving forces].

The principles of isolating plasma membrane (basolateral membrane and brush border membrane), and separating right side-out and inside-out membrane vesicles were described. We then focused on the liver plasma membrane. Liver plasma membrane vesicles have been used to investigate the mechanism for the hepatobiliary transport of ligands. We precisely describe our protocol to isolate the sinusoidal (SMV) and canalicular membrane vesicles (CMV) from rat liver using the percoll gradient. Methods to determine the purity and orientation of SMV and CMV are also mentioned. Furthermore, procedures for the transport studies with SMV and CMV are provided; we refer to the electrogenic sodium dependent transport of taurocholic acid and alanine into SMV as an example to characterize the secondary active transport system. ATP-dependent uptake of S-(2,4-dinitrophenyl)-glutathione (DNP-SG) into CMV is also cited as an example to clarify the primary active transport mechanism. Kinetic analysis for the ATP-dependent uptake of [3H] DNP-SG into CMV is also described.

Adenosine Triphosphate↗
PubMed1996

Rapid and clear detection of ABO genotypes by simultaneous PCR-RFLP method.

We reported a new approach of ABO genotyping by a polymerase chain reaction and restriction fragment length polymorphism method. Instead of amplifying the loci containing the positions of nucleotides 258 and 700 of cDNA of the A transferase separately, we successfully amplified these 2 loci together in one reaction mixture using 2 sets of primers. The amplified DNA products were digested at the same time with restriction enzymes Kpn I and Alu I. The digested DNA products were then separated by electrophoresis on polyacrylamide gel. In addition, we evaluated the influence of various amplification parameters (concentration of template DNA, primers, Taq DNA polymerase, MgCl2, and number of cycles). In particular, high Mg2+ concentration (3.5 mM) made effective amplification of this locus without producing any unspecific band. By using that optimized condition for PCR, together with a simultaneous approach, our study proved to be time saving, more economic, and convenient in interpreting the results.

ABO Blood-Group System↗
PubMed1996

[Analysis of behaviors of plasma tissue factor and tissue factor pathway inhibitor in patients with various diseases].

We measured plasma levels of tissue factor (TF), total tissue factor pathway inhibitor (TFPI) and free TFPI antigen in patients with diabetes mellitus (DM), hyperlipidemia and disseminated intravascular coagulation (DIC). The mean TF, total TFPI and free TFPI antigen concentrations were significantly higher in patients with DM than in controls and the plasma TF concentration was significantly higher in patients with retinopathy or nephropathy than in DM with no complications. The mean TF, total TFPI and free TFPI antigen concentrations were significantly higher in patients with hyperlipidemia than in controls. There was a significant positive correlation between levels of total TFPI and total cholesterol. In patients with hyperlipidemia, the level of total TFPI was significantly decreased compared to base line level by cholesterol lowering drug, however, free TFPI concentration did not change by cholesterol lowering drug. The TF and total TFPI concentrations were significantly higher in patients with DIC than in controls.

Anticoagulants↗
PubMed1996

Differentiation of binding sites of CGP12177, a beta 3-adrenoceptor partial agonist, and carteolol, a beta 1/beta 2-adrenoceptor partial agonist, to the beta-adrenoceptors in guinea-pig taenia caecum.

Differentiation of binding sites of CGP12177 and carteolol to the beta-adrenoceptors in the guinea-pig taenia caecum was investigated. Carteolol and CGP12177 competitively antagonized the relaxation responses to isoprenaline, and the pA2 values were 9.87 and 9.33, respectively. Butoxamine, a beta 2-selective antagonist, caused competitive antagonism of the relaxant responses to carteolol, and the pA2 value for butoxamine was 6.22. However, butoxamine (10(-4) M) did not significantly affect the relaxant responses to CGP12177. CGP12177 caused competitive antagonism of the relaxant responses to carteolol, and the pA2 value for CGP12177 was 9.32. However, carteolol (10(-6) M) did not significantly affect the relaxant responses to CGP12177. The competitive inhibition curve for specific binding of 50 nM [3H]befunolol by carteolol showed a biphasic shape, although the curve by CGP12177 was monophasic. Moreover, the competitive inhibition curve for specific binding of 100 nM [3H]CGP12177 by CGP12177 showed a biphasic shape, although the curve by carteolol indicated partial inhibition. These results suggest that the low affinity site of beta-adrenoceptor and beta 3-adrenoceptors are different from each other.

Adrenergic beta-Agonists↗
PubMed1996

FK960 N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate ameliorates the memory deficits in rats through a novel mechanism of action.

With passive avoidance (PA), Morris water maze (WM) and eight-arm radial maze tasks, we evaluated the memory-enhancing action of FK960 [N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate], a compound which we have found through rational drug screening based on our hypothesis that penile erection is a valid predictor of central cholinergic activation. Memory performance in the tasks was impaired in aged (24- to 26-months-old) rats as well as in rats with nucleus basalis magnocellularis lesions. Scopolamine (1 mg/kg i.p.) treatment induced memory impairment in PA and WM; treatment with cysteamine (200 mg/kg s.c.) induced memory impairment in PA but not in WM, whereas fimbria fornix lesioning affected the rats in the opposite manner. FK960 (0.1-10 mg/kg i.p.) ameliorated all the memory impairments except those induced by cysteamine or fimbria fornix lesion, and the dose-response curves were bell shaped with maximal response at 1 to 3.2 mg/kg. The effects of FK960 on the scopolamine-induced memory impairment in the PA and/or WM were abolished by cysteamine (200 mg/kg s.c.), dl-p-chlorophenylalanine methyl ester hydrochloride (150 mg/kg i.p. for 3 days) or raphe lesioning, but not by neonatal 6-hydroxydopamine (35 micrograms/head) treatment. Neurochemical analysis revealed that cysteamine and raphe lesions reduced brain somatostatin and serotonin contents, respectively. The treatment with FK960 (0.32-320 mg/kg p.o.) dose-dependently increased both serotonin and 5-hydroxyindoleacetic acid levels in the brain areas examined and significantly increased hippocampal somatostatin contents at the smaller doses. From these results, we conclude that FK960 ameliorates cognitive dysfunction through an activation of the somatostatinergic-serotonergic link.

Aging↗
PubMed1995

Role of tissue factor in disseminated intravascular coagulation.

We examined plasma antigen levels of tissue factor (TF) in 95 cases of disseminated intravascular coagulation (DIC), to investigate the role of TF in DIC. A significant elevation of plasma antigen levels of TF was observed in cases of DIC associated with cancer. However, no such significant elevation was observed in cases of DIC associated with acute promyelocytic leukemia (APL), acute leukemia except APL, blastic crisis of chronic myelogenous leukemia, non-Hodgkin lymphoma (NHL), sepsis or fulminant hepatitis. No significant elevation of TF was observed in patients without DIC, except 4 cases of cancer who developed DIC thereafter. Plasma antigen levels of TF were higher in both cases of DIC with renal failure and chronic renal failure without DIC than its levels in those without renal failure. Therefore, plasma antigen levels of TF in DIC patients with renal failure were considered to be carefully estimated. The levels of TF were decreased with the clinical improvement in some cases of DIC but were further increased or remained at high levels in patients who showed no improvement of DIC. Thus, plasma antigen levels of TF is an important marker to predict the development and/or prognosis of DIC, especially in patients with cancer.

Adult↗
PubMed1995

Nucleotide sequence surrounding the locus marker D21S246 on human chromosome 21.

Most of the human Not I linking clones identified to date are considered to be derived from CpG islands because of the recognition sequence of this enzyme, and CpG islands have been reported to be located around the 5' regions of genes. As a pilot study, we determined the complete nucleotide sequence (41,924 bp) of a human cosmid clone (LL21NC02Q7A10) containing the marker D21S246 originating from a Not I linking clone. As a result of sequence analysis, we successfully mapped and revealed the genomic gene structure for KIAA0002 previously reported as a cDNA clone. This gene consists of 15 exons and was shown to exist at the D21S246 locus on human chromosome 21q21.3-q22.1. These results demonstrated that genomic marker-anchored DNA sequencing is a useful approach for the human genome project.

Base Sequence↗
PubMed1995

Inhibition of TNF-triggering activity of lipopolysaccharide by a proteinaceous factor from normal mouse liver extract.

Recent studies have revealed that animals have evolved a wide range of protective systems against the deleterious effects of LPS, but the molecular mechanisms in the barrier functions of liver against enterobacterial LPS, particularly in mammals, are poorly understood. In this study, we extracted a soluble fraction from the liver of normal mice (normal liver extract, NLE) and examined its effect on biologic activities of LPS. Preincubation of NLE and LPS suppressed serum-dependent TNF induction (TNF-triggering activity) of LPS; the effect was dose-dependent and overcome by increasing LPS concentration, but treatment of macrophages with NLE showed no effect. Separation by ultrafiltration and protease sensitivity demonstrated that the factor(s) in NLE was a protein(s). We tentatively called this liver LPS-inactivating factor (LLIF). LPS inactivation by LLIF was temperature-dependent and required the coexistence of divalent cations. LLIF also suppressed a synthetic lipid A analogue, ONO-4007. Pretreatment of LPS with serum rendered LPS refractory to the action of LLIF. However, LLIF was unable to inhibit limulus amebocyte lysate activation by LPS. Direct interaction of LLIF and lipid A was evident by the method of [1-14C]ONO-4007 binding to solid-phase LLIF, but treatment of [1-14C]ONO-4007 with LLIF generated no degradative products. These results suggest that LLIF probably interacts with the lipid A portion of LPS and interferes with the association of LPS and LBP (LPS-binding protein) in serum, and that LLIF may be one of the protective molecules in liver against the gastrointestine-derived LPS.

Acute-Phase Proteins↗
PubMed1995

Purification and characterization of the cytotoxic factor in rat peritoneal exudate cells: its identification as the calcium binding protein complex, calprotectin.

We previously reported the existence of a growth inhibitory factor for mitogen-stimulated lymphocytes and murine tumor cell lines, MM46 and L-929, in inflammatory polymorphonuclear leukocytes. In this study, by using mouse MM46 mammary carcinoma as target, we purified the inhibitor from lysate of rat inflammatory peritoneal exudate cells by ammonium sulfate precipitation, gel filtration, isoelectrofocusing, and anion exchange chromatography. Although the in vitro inhibitory activity for MM46 growth was partitioned into three peaks in the final step, it was found that these inhibitory samples all consist of 8- and 13-kDa peptides. Analysis of amino acid sequences revealed that the partial sequences of the 8- and 13-kDa peptides completely agree with the smaller and larger components of rat calprotectin, which are predicted from cDNA, respectively, suggesting the cell growth inhibitory factor is calprotectin. In addition to MM46, the partially purified calprotectin inhibited the growth of a rat, three mice, and a human tumor cell line in similar dose-response relationships in vitro. Moreover, it exerted a cytolytic effect against all examined tumor cells. It was confirmed that the purified calprotectin induces growth inhibition and the lysis of MM46 cells and that the minimum effective concentration is between 50 and 100 micrograms/ml. The factor also inhibited the growth of bone marrow cells and macrophages. These results suggest that calprotectin is a negative regulatory factor for the growth and/or survival states of normal and tumor cells.

Amino Acid Sequence↗
PubMed1995

Induction of apoptotic cell death in mouse lymphoma and human leukemia cell lines by a calcium-binding protein complex, calprotectin, derived from inflammatory peritoneal exudate cells.

We have previously shown that the calcium-binding protein complex, calprotectin, purified from rat inflammatory peritoneal cells exerts marked cytotoxic activity against rat, mouse, and human tumor cells. We studied here whether the cytotoxicity is caused by induction of apoptosis, using mouse EL-4 lymphoma and human MOLT-4 leukemia lines as targets. The rat calprotectin sample inhibited [3H]thymidine incorporation into these cells by partially 24 h and almost completely in 48 h of culture at concentrations of 100-200 micrograms/ml. Morphological changes, that is, loss of cell volume and nuclear condensation and/or fragmentation, appeared in both cell types cultured with calprotectin from 20 h, and such apoptotic cells subsequently increased in number to compose the great majority of the cells at 40 h. Cell death, measured by stainability with trypan blue, lagged behind the emergence of the apoptotic morphology by about 2 and 10 h in EL-4 and MOLT-4 cells, respectively. DNA fragmentation was observed in EL-4 cells cultured with calprotectin, whereas it was not observed in MOLT-4 cells, consistent with results of flow cytometry showing that loss of cell DNA content caused by the factor was greater in EL-4 cells. The data indicate that calprotectin induces the apoptosis of certain tumor cells but that the occurrence of DNA fragmentation is dependent on cell type. Finally, the apoptosis-inducing activity of the calprotectin sample was abrogated by the presence of 10 microM zinc, whereas it was not affected by 5 mM calcium or magnesium.

Animals↗
PubMed1995

Quantitation of heteroplasmy of mitochondrial tRNA(Leu(UUR)) gene using PCR-SSCP.

We have devised a novel method for quantitative analysis of the MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) tRNA(Leu(UUR)) mutation of mitochondrial DNA using a PCR-SSCP (polymerase chain reaction-single-strand conformation polymorphism) method, and compared the results obtained using the PCR-SSCP method with those obtained using other methods including Southern blotting, last one cycle hot PCR, and conventional PCR-RFLP (restriction fragment length polymorphism). The standard curve obtained using the PCR-SSCP method is linear, with a correlation coefficient of 0.999; it was determined that this method is more accurate than other methods for quantitative analysis. The PCR-SSCP method does not require restriction digestions, thereby avoiding potential problems of partial digestions or heteroduplex formation during PCR. The method is quite simple and should have a broad range of application for quantitation of mutant mtDNAs in various mitochondrial encephalomyopathies. We applied the method for quantitation of mutant mitochondrial DNA carrying a single base substitution in the tRNA(Leu(UUR)) gene in two autopsied cases of MELAS. In both cases, the mutant mtDNA is abundantly present (82-95%) withd little variation among tissues.

Base Sequence↗