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102. Influence of water temperature and feeding regime on otolith growth in Anguilla japonica glass eels and elvers: does otolith growth cease at low temperatures?

Author

FUKUDA, N., KUROKI, M., SHINODA1, A., YAMADA, Y., OKAMURA, A., AOYAMA, J., and TSUKAMOTO, K.

Subjects
*WATER temperature, *FISH feeds, *OTOLITHS, *FISH growth, *ANGUILLA japonica
Abstract

The influences of water temperature and feeding regime on otolith growth in Anguilla japonica glass eels and elvers were investigated using individuals reared at 5, 10, 15, 20, 25 and 30° C and in fed or unfed conditions at salinity 32 after their otoliths were marked with alizarin complexone (ALC). To eliminate the difficulty of observing the edges of otoliths with optical (OM) or scanning electron (SEM) microscopes, three to 10 individuals were sampled from each tank at 10, 20 and 30 days during the experiment and reared for an additional 10 days at 25° C after their otoliths were marked a second time. Otolith growth and the number of increments were measured using both OM and SEM. Most A. japonica commenced feeding after 10 days at 20–30° C or after 20 days at 15° C, but no feeding occurred at 5 and 10° C. No otolith growth occurred at 5 and 10° C except in two individuals with minimal increment deposition at 10° C. Otolith growth was proportional to water temperature within 15–25° C and not different between 25 and 30° C. At 15, 25 and 30° C, the mean otolith growth rate in fed conditions was higher than in unfed conditions. The number of increments per day was significantly different among water temperatures (0·00–0·01 day−1 at 5 and 10° C, 0·43–0·48 day−1 at 15° C and 0·94–1·07 day−1 at 20–30° C). These results indicated that otolith growth in A. japonica glass eels and elvers was affected by temperature and ceased at ≤10° C under experimental conditions. Hence, future studies analysing the otoliths of wild-caught A. japonica glass eels and elvers need to carefully consider the water temperatures potentially experienced by the juveniles in the wild. [ABSTRACT FROM AUTHOR]

Published
2009
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103. Sympatric spawning of Anguilla marmorata and Anguilla japonica in the western North Pacific Ocean.

Author

KUROKI, M., AOYAMA, J., MILLER, M. J., YOSHINAGA, T., SHINODA, A., HAGIHARA, S., and TSUKAMOTO, K.

Subjects
*ANGUILLA (Fish), *FISH larvae, *EELS, *AQUATIC habitats
Abstract

Extensive collections were made of the larvae of the temperate Japanese eel Anguilla japonica and the tropical giant mottled eel Anguilla marmorata in an overlapping area of the North Equatorial Current region of the western North Pacific Ocean. Collections of 189 A. marmorata and > 2500 A. japonica larvae during nine surveys from 1991 to 2007 showed that these two anguillid eels have similar spawning areas just west of the southern West Mariana Ridge. In July to August 2006 and August 2007, morphologically and genetically identified A. marmorata preleptocephali were mainly collected between 14·5–15° N and 142–142·5° E, where A. japonica preleptocephali were also caught in some of the same net tows. Fewer A. marmorata preleptocephali, however, were collected ( n = 31) compared to those of A. japonica ( n = c. 165), and fewer small larvae of A. marmorata were collected per tow than A. japonica ( n = 1–10 and 1–294, respectively), suggesting relatively smaller spawning aggregations of A. marmorata. The distribution of preleptocephali and small larvae was wider in longitude in A. marmorata (131– 143° E) than in A. japonica (137–143° E), while the latitudinal range was almost the same (12–17° N). Although spawning by these two species overlaps both spatially and temporally, the tropical eels of the North Pacific population of A. marmorata probably have a much longer spawning season with fewer spawners, at least in summer, and recruit to a much wider latitudinal range of growth habitats. [ABSTRACT FROM AUTHOR]

Published
2009
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106. Counterfactual-Based Prevented and Preventable Proportions

Author

Yamada Kentaro and Kuroki Manabu

Subjects
prevented fraction, preventable fraction, attributable fraction, excess fraction, vaccine efficacy, Mathematics, QA1-939, Probabilities. Mathematical statistics, QA273-280
Abstract

Prevented and preventable fractions have been widely used in medical science to evaluate the proportion of new diseases that can be averted by a protective exposure. However, most existing formulas used in practical situations cannot be interpreted as proportions without any further assumptions because they are obtained according to different target populations and may fall outside the range [0.000,1.000]$[0.000,1.000]$. To solve this problem, this paper proposes counterfactual-based prevented and preventable proportions. When both causal effects and observed probabilities are available, we show that the proposed measures are identifiable under the negative monotonicity assumption. Additionally, when the negative monotonicity assumption is violated, we formulate the bounds on the proposed measures. We also show that negative monotonicity together with exogeneity induces equivalence between the proposed measures and existing measures.

Published
2017
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107. Covariate selection for estimating the causal effect of control plans by using causal diagrams.

Author

Kuroki, M. and Miyakawa, M.

Subjects
CAUSATION (Philosophy), REGRESSION analysis, ANALYSIS of covariance
Abstract

Consider a case where cause–effect relationships between variables can be described by a causal path diagram and the corresponding linear structural equation model. The paper proposes a graphical selection criterion for covariates to estimate the causal effect of a control plan. For designing the control plan, it is essential to determine both covariates that are used for control and covariates that are used for identification. The selection of covariates used for control is only constrained by the requirement that the covariates be non–descendants of a treatment variable. However, the selection of covariates used for identification is dependent on the selection of covariates used for control and is not unique. In the paper, the difference between covariates that are used for identification is evaluated on the basis of the asymptotic variance of the estimated causal effect of an effective control plan. Furthermore, the results can be also described in terms of a graph structure. [ABSTRACT FROM AUTHOR]

Published
2003
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108. Combination therapy for chronic Pseudomonas aeruginosa respiratory infection associated with biofilm formation.

Author

Yanagihara, Katsunori, Tomono, Kazunori, Sawai, Toyomitsu, Kuroki, Misuzu, Kaneko, Yukihiro, Ohno, Hideaki, Higashiyama, Yasuhito, Miyazaki, Yoshitsugu, Hirakata, Yoichi, Maesaki, Shigefumi, Kadota, Jun-ichi, Tashiro, Takayoshi, Kohno, Shigeru, Yanagihara, K, Tomono, K, Sawai, T, Kuroki, M, Kaneko, Y, Ohno, H, and Higashiyama, Y

Abstract

There had been no reports of investigations into biofilms in chronic respiratory infection in vivo. Recently, we established a new murine model of chronic respiratory infection with Pseudomonas aeruginosa. In the present study, we examined the bacteriological effect of combined clarithromycin and levofloxacin against chronic respiratory infection with P. aeruginosa. Scanning electron micrograph of the surface of the catheter intubated in mouse bronchus for 7 days demonstrated in vivo formation of a biofilm containing blood cells, complex fibrous structures and bacteria. Treatment with either clarithromycin alone or levofloxacin alone had no statistical effect on the number of viable bacteria in lung. The combined use of both drugs resulted in a significant decrease in the number of viable bacteria. The present experiment demonstrates that the newly established murine model was useful to investigate the treatment of biofilm-associated chronic respiratory infection with P. aeruginosa, and combination therapy with clarithromycin and levofloxacin was effective in biofilm-associated chronic respiratory infection. [ABSTRACT FROM AUTHOR]

Published
2000
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109. Tumor scintigraphy by the method for subtracting the initial image with technetium-99m labeled antibody.

Author

Karube, Yoshiharu, Katsuno, Kentaro, Ito, Sanae, Matsunaga, Kazuhisa, Takata, Jiro, Kuroki, Masahide, Murakami, Masaaki, Matsuoka, Yuji, Karube, Y, Katsuno, K, Ito, S, Matsunaga, K, Takata, J, Kuroki, M, Murakami, M, and Matsuoka, Y

Abstract

The method for subtracting the initial image from the localization image was evaluated for radioimmunoscintigraphy of tumors with technetium-99m (Tc-99m) labeled antibodies. Monoclonal antibodies were parental mouse and mouse-human chimeric antibodies to carcinoembryonic antigen (CEA), designated F11-39 and ChF11-39, respectively, both of which have been found to discriminate CEA in tumor tissues from the CEA-related antigens. After reduction of the intrinsic disulfide bonds, these antibodies were labeled with Tc-99m. In vivo studies were performed on athymic nude mice bearing the human CEA-producing gastric carcinoma xenografts. Though biodistribution results showed selective and progressive accumulation of Tc-99m labeled antibodies at the tumor site, high radioactivity in blood was inappropriate for scintigraphic visualization of the tumors within a few hours. We examined the subtraction of the initial Tc-99m image from the Tc-99m localization image after a few hours. Subtracted images of the same count reflected the in vivo behavior of the Tc-99m radioactivity. The subtracted scintigrams revealed excellent tumor images with no significant extrarenal background. Visualization of the tumor site was dependent on antigen-specific binding and nonspecific exudation. These results demonstrate that a method of subtraction of the initial image may serve as a potentially useful diagnostic method for an abnormal site for agents with a low pharmacokinetic value. [ABSTRACT FROM AUTHOR]

Published
1999
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111. The KOR-SA3544 antigen predominantly expressed on the surface of Philadelphia chromosome-positive acute lymphoblastic leukemia cells is nonspecific cross-reacting antigen-50/90 (CD66c) and invariably expressed in cytoplasm of human leukemia cells.

Author

Sugita, K, Mori, T, Yokota, S, Kuroki, Ma, O-Koyama, T, Inukai, T, Iijima, K, Goi, K, Tezuka, T, Kojika, S, Shiraishi, K, Nakamura, M, Miyamoto, N, Karakida, N, Kagami, K, Nakazawa, S, Kuroki, M, and Koyama, T O

Subjects
LYMPHOBLASTIC leukemia, CELL surface antigens, FLOW cytometry, GRANULOCYTES, IMMUNOHISTOCHEMISTRY, WESTERN immunoblotting, MONOCLONAL antibodies, MEMBRANE glycoproteins, CHROMOSOME abnormalities, CELL adhesion molecules, GLYCOPROTEINS, FLUORESCENT antibody technique, TUMOR antigens, CYTOPLASM, ANTIGENS
Abstract

We previously reported a novel monoclonal antibody KOR-SA3544 which predominantly reacted with a surface antigen (sSA3544) expressed on Philadelphia chromosome (Ph1)-positive acute lymphoblastic leukemia (ALL). In the present study, we demonstrate that the antibody specifically recognized nonspecific cross-reacting antigen (NCA)-50/90 (CD66c), one of the carcinoembryonic antigen (CEA)-related glycoproteins encoded by a member of the CEA gene family. In addition, we show that the SA3544 antigen (NCA-50/90) was invariably expressed in cytoplasm of all of the human leukemic cell lines examined (sSA3544-positive B-lymphoid two, sSA3544-negative T or B-lymphoid and non-lymphoid 24) regardless of the presence or absence of surface expression of this antigen. Immunoelectromicroscopic examination revealed that the cytoplasmic antigen was mainly present in granules in sSA3544-positive leukemia cells, whereas it was diffusely present in cytosol in sSA3544-negative leukemia cells. Thus, among members of the CEA family, NCA-50/90 was first demonstrated to be expressed not only on the surface of some leukemia cells, but also in cytoplasm of various types of leukemia cells. [ABSTRACT FROM AUTHOR]

Published
1999
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114. In vivo comparative therapeutic study of optimal administration of 5-fluorouracil and cisplatin using a newly established HST-1 human squamous-carcinoma cell line.

Author

Kuroki, Mika, Nakano, Shuji, Mitsugi, Kenji, Ichinose, Ichiro, Anzai, Keizo, Nakamura, Minoru, Nagafuchi, Seiho, Niho, Yoshiyuki, Kuroki, M, Nakano, S, Mitsugi, K, Ichinose, I, Anzai, K, Nakamura, M, Nagafuchi, S, and Niho, Y

Subjects
ANIMAL experimentation, ANTINEOPLASTIC agents, CISPLATIN, COMPARATIVE studies, CLINICAL drug trials, FLUOROURACIL, RESEARCH methodology, MEDICAL cooperation, MICE, RESEARCH, SQUAMOUS cell carcinoma, TIME, EVALUATION research, CANCER cell culture
Abstract

The efficacy and toxicity of 5-fluorouracil (5-FU) and cisplatin (CDDP) given in a sequential combination were evaluated in nude mice transplanted with HST-1, a newly established human squamous-carcinoma cell line. 5-FU and CDDP were given i.p. for 5 days and 1 day, respectively, either as single agents or in a sequential manner separated by a 24-h interval. The treatment was repeated every 30 days. Although inhibition of tumor growth was seen in all of the treated groups after two cycles, the sequence of 5-FU followed by CDDP significantly reduced the tumor burdens throughout all three courses and was more effective than the reverse sequence or either drug alone. Neither treatment-related death nor significant hematologic or nephrologic toxicities were seen, even following three cycles of therapy. Significant weight loss was observed only in mice treated with CDDP followed by 5-FU. This sequence dependence of the activity and toxicity of the 5-FU and CDDP combination should thus be incorporated into the design of a clinical trial. [ABSTRACT FROM AUTHOR]

Published
1992
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122. New Traffic Conflict Measure Based on a Potential Outcome Model

Author

Yamada Kentaro and Kuroki Manabu

Subjects
traffic conflict, crash-to-conflict ratio, counterfactual conditional, potential outcome model, structural causal model, Mathematics, QA1-939, Probabilities. Mathematical statistics, QA273-280
Abstract

A key issue in the analysis of traffic accidents is to quantify the effectiveness of a given evasive action taken by a driver to avoid crashing. Since 1977, the widely accepted definition for this effectiveness measure, which is called traffic conflict, has been “the risk of a collision if the driver movement remains unchanged.” Although the definition is expressed counterfactually, the full power of counterfactual analysis was not utilized. In this paper, we propose a counterfactual measure of traffic conflict called Counterfactual Based Conflict (CBC). The CBC is interpreted as the probability that a driver avoided a crash actually by taking an evasive action in the counterfactual situation in which the crash would have occurred if he/she had not taken an evasive action and the crash would not have occurred if he/she had taken an evasive action. The CBC captures realistic aspects of the traffic situation, and lends itself to modern causal analysis. In addition, we provide some of identification conditions for the CBC. Furthermore, we formulate bounds on the CBC when the proposed identification conditions are violated. Finally, through an application of the CBC to the 100-Car Naturalistic Driving Study, we discuss the usefulness and limitations of the proposed measure.

Published
2019
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124. Affinity purification of Helicobacter pylori urease. Relevance to gastric mucin adherence by urease protein.

Author

Icatlo, F C, Kuroki, M, Kobayashi, C, Yokoyama, H, Ikemori, Y, Hashi, T, and Kodama, Y

Abstract

A simple, reproducible and high yield method of Helicobacter pylori urease enzyme purification was developed using a heparinoid (Cellufine sulfate) affinity gel. The purification method involved two sequential steps using the same gel that takes advantage of the differential affinity of urease to the heparinoid at two levels of hydrogen ion concentration. SDS-polyacrylamide gel electrophoresis analysis of affinity-purified urease revealed two major protein bands with about 62- and 30-kDa molecular mass. When whole cell lysates of clinical and laboratory strains of H. pylori were probed by Western blot, anti-urease hyperimmune serum produced by affinity-purified urease in rabbit recognized only the two bands corresponding to the urease A and B subunits. To probe the molecular relevance of affinity gel adherence to mucin adherence, the purified urease was derivatized with N-hydroxysuccinimidobiotin and used in adherence assays. Competitive inhibition tests revealed commonality of urease receptors among gastric mucin, heparin, and heparinoid. Composite data on adherence kinetics modulated by pH, salt, incubation time, and concentration of urease or mucin were indicative of conformation-dependent ligand-receptor interaction.

Published
1998

125. Evidence for carboxyl-terminal processing and glycolipid-anchoring of human carcinoembryonic antigen.

Author

Takami, N, Misumi, Y, Kuroki, M, Matsuoka, Y, and Ikehara, Y

Abstract

We have investigated the post-translational modification of carcinoembryonic antigen (CEA) for membrane-anchoring in QGP-1 cells derived from a human pancreatic carcinoma. Pulse-chase experiments with [3H]leucine demonstrated that CEA was initially synthesized as a precursor form with Mr 150,000 having N-linked high-mannose-type oligosaccharides, which was then converted to a mature form with Mr 200,000 containing the complex type sugar chains. The mature protein thus labeled was found to be released from the cell surface by treatment with phosphatidylinositol-specific phospholipase C, suggesting that CEA is a phosphatidylinositol-linked membrane protein. This was confirmed by metabolic incorporation into CEA of 3H-labeled compounds such as ethanolamine, myo-inositol, palmitic acid, and stearic acid. The 3H-labeled fatty acids incorporated were specifically removed from the protein by nitrous acid deamination as well as by phosphatidylinositol-specific phospholipase C treatment. Since the available cDNA sequence predicts that CEA contains a single methionine residue only in its carboxyl-terminal hydrophobic domain, processing of the carboxyl terminus was examined by pulse-chase experiments with [35S]methionine. It was found that CEA with Mr 150,000 was initially labeled with [35S]methionine but its radioactivity was immediately lost with chase. Taken together, these results suggest that CEA is anchored to the membrane by simultaneously occurring proteolysis of the carboxyl terminus and replacement by the glycophospholipid immediately after the synthesis.

Published
1988
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126. A euthymic hairless mouse model of Helicobacter pylori colonization and adherence to gastric epithelial cells in vivo.

Author

Kimura, N, Ariga, M, Icatlo, F C, Kuroki, M, Ohsugi, M, Ikemori, Y, Umeda, K, and Kodama, Y

Abstract

The hairless mouse strain NS:Hr/ICR was examined as a potential small animal model of Helicobacter pylori colonization, adherence to gastric epithelial cells in vivo, and gastritis. Among several small animals tested, NS:Hr/ICR mice proved to be the most highly susceptible to H. pylori infection. Challenge with clinical isolates of H. pylori consisting of either phenotype I or II (VacA and CagA positive and negative, respectively) resulted in colonization by mucus-resident and epithelial cell-adherent bacterial populations. Cell-adherent bacteria resisted 80 cycles of top-speed Vortex washing and were recovered only by homogenization of serially washed glandular stomach tissue, indicating intimate association with the mucosal surface. Immunoperoxidase staining of paraffin sections of gastric tissue from infected mice revealed H. pylori antigens localized in the glandular region of the mucosa, with some colonized areas seen in the vicinity of submucosal mononuclear cell infiltration. The latter inflammatory reaction was observed as a function of the H. pylori phenotype (only type I induced inflammation) and the challenge dose (only those mice challenged with 10(8) CFU or higher showed the reaction). The NS:Hr/ICR strain of mice is a suitable miniature model of H. pylori infection and may prove useful in the quest for an efficacious mode of treatment for this common infection in humans.

Published
1998

127. Cyclic ADP-ribose and inositol 1,4,5-trisphosphate as alternate second messengers for intracellular Ca2+ mobilization in normal and diabetic beta-cells.

Author

Takasawa, S, Akiyama, T, Nata, K, Kuroki, M, Tohgo, A, Noguchi, N, Kobayashi, S, Kato, I, Katada, T, and Okamoto, H

Abstract

Intracellular Ca2+ mobilization occurs in a variety of cellular processes and is mediated by two major systems, the inositol 1,4, 5-trisphosphate (IP3) and cyclic ADP-ribose (cADPR) systems. cADPR has been proposed to be a second messenger for insulin secretion induced by glucose in pancreatic beta-cells (Takasawa, S., Nata, K., Yonekura, H., and Okamoto, H. (1993) Science 259, 370-373). Here we show that the cADPR signal system for insulin secretion is replaced by the IP3 system in diabetic beta-cells such as ob/ob mouse islets and RINm5F cells. We measured the cADPR content in these beta-cells by radioimmunoassay and found that the increase of the cADPR content by glucose did not occur in ob/ob mouse islets and RINm5F cells, whereas the increased cADPR level by glucose was observed in normal rat and mouse islets. Microsomes of these diabetic beta-cells released Ca2+ in response to IP3 but not to cADPR. In the diabetic beta-cells, CD38 (ADP-ribosyl cyclase/cADPR hydrolase) and type 2 ryanodine receptor mRNAs were scarcely detected and, in contrast, an increased expression of IP3 receptor mRNAs was observed. The diabetic beta-cells secreted insulin rather by carbamylcholine than by glucose.

Published
1998

128. Carbohydrate structures of nonspecific cross-reacting antigen-2, a glycoprotein purified from meconium as an antigen cross-reacting with anticarcinoembryonic antigen antibody

Author

Yamashita, K, Totani, K, Iwaki, Y, Kuroki, M, Matsuoka, Y, Endo, T, and Kobata, A

Abstract

Nonspecific cross-reacting antigen-2 (NCA-2) is a glycoprotein purified from meconium as a closely correlated entity with carcinoembryonic antigen (CEA). As in the case of CEA, only asparagine-linked sugar chains are included in NCA-2. In order to elucidate the structural characteristics of the sugar chains of NCA-2, they were quantitatively released from the polypeptide backbone by hydrazinolysis and reduced with NaB3H4after N-acetylation. The radioactive oligosaccharides were fractionated by paper electrophoresis, serial chromatography on immobilized lectin columns, and Bio-Gel P-4 (under 400 mesh) column chromatography. Structures of the oligosaccharides were estimated from the data of the binding specificities of immobilized lectin columns and the effective size of each oligosaccharide determined by passing through a Bio-Gel P-4 column and were then confirmed by endo-β-galactosidase digestion, sequential digestion with exoglycosidases with different aglycon specificities, and methylation analysis. NCA-2 contains a similar number (27 mol) of sugar chains in one molecule compared with CEA (24-26 mol). However, all sugar chains of NCA-2 were complex-type in contrast to CEA, approximately 8% of the sugar chains of which were high mannose-type (Yamashita, K., Totani, K., Kuroki, M., Matsuoka, Y., Ueda, I., and Kobata, A. (1987) Cancer Res. 47, 3451-3459). About 80% of the oligosaccharides from NCA-2 contain bisecting N-acetylglucosamine residues, and the percent molar ratio of mono-, bi, tri, and tetraantennary oligosaccharides was 2:14:57:27. (± Fucα1→2)Galβ1→4(± Fucα1→3)GlcNAc, (± Fucα1→2)Galβ1→3(± Fucα1→4)GlcNAc, (± Fucα1→2)Galβ1→4(± Fucα1→3)GlcNAcβ1→ 3Galβ1→4GlcNAc, (± Fucα1→2)Galβ1→3(± Fucα1→4)GlcNAcβ1→ 3Galβ1→4GlcNAc, and GalNAcβ1→3Galβ1→3GlcNAcβ1→3Galβ1→4GlcNAc were found as their outer chain moieties. Approximately 60% of the oligosaccharides from NCA-2 contain the Galβ1→4 or 3GlcNAcβ1→3Galβ1→4GlcNAcβ1→group in their outer chains.

Published
1989
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129. The mouse gene for vascular endothelial growth factor. Genomic structure, definition of the transcriptional unit, and characterization of transcriptional and post-transcriptional regulatory sequences.

Author

Shima, D T, Kuroki, M, Deutsch, U, Ng, Y S, Adamis, A P, and D'Amore, P A

Abstract

We describe the genomic organization and functional characterization of the mouse gene encoding vascular endothelial growth factor (VEGF), a polypeptide implicated in embryonic vascular development and postnatal angiogenesis. The coding region for mouse VEGF is interrupted by seven introns and encompasses approximately 14 kilobases. Organization of exons suggests that, similar to the human VEGF gene, alternative splicing generates the 120-, 164-, and 188-amino acid isoforms, but does not predict a fourth VEGF isoform corresponding to human VEGF206. Approximately 1. 2 kilobases of 5'-flanking region have been sequenced, and primer extension analysis identified a single major transcription initiation site, notably lacking TATA or CCAT consensus sequences. The 5'-flanking region is sufficient to promote a 7-fold induction of basal transcription. The genomic region encoding the 3'-untranslated region was determined by Northern and nuclease mapping analysis. Investigation of mRNA sequences responsible for the rapid turnover of VEGF mRNA (mRNA half-life, <1 h) (Shima, D. T. , Deutsch, U., and D'Amore, P. A. (1995) FEBS Lett. 370, 203-208) revealed that the 3'-untranslated region was sufficient to trigger the rapid turnover of a normally long-lived reporter mRNA in vitro. These data and reagents will allow the molecular and genetic analysis of mechanisms that control the developmental and pathological expression of VEGF.

Published
1996

130. 5-Oxo-eicosanoids and hematopoietic cytokines cooperate in stimulating neutrophil function and the mitogen-activated protein kinase pathway.

Author

O'Flaherty, J T, Kuroki, M, Nixon, A B, Wijkander, J, Yee, E, Lee, S L, Smitherman, P K, Wykle, R L, and Daniel, L W

Abstract

The newly defined eicosatetraenoates (ETEs), 5-oxoETE and 5-oxo-15(OH)-ETE, share structural motifs, synthetic origins, and bioactions with leukotriene B4 (LTB4). All three eicosanoids stimulate Ca2+ transients and chemotaxis in human neutrophils (PMN). However, unlike LTB4, 5-oxoETE and 5-oxo-15(OH)-ETE alone cause little degranulation and no superoxide anion production. However, we show herein that, in PMN pretreated with granulocyte-macrophage or granulocyte colony-stimulating factor (GM-CSF or G-CSF), the oxoETEs become potent activators of the last responses. The oxoETEs also induce translocation of secretory vesicles from the cytosol to the plasmalemma, an effect not requiring cytokine priming. To study the mechanism of PMN activation in response to the eicosanoids, we examined the activation of mitogen-activated protein kinase (MAPK) and cytosolic phospholipase A2 (cPLA2). PMN expressed three proteins (40, 42, and 44 kDa) that reacted with anti-MAPK antibodies. The oxoETEs, LTB4, GM-CSF, and G-CSF all stimulated PMN to activate the MAPKs and cPLA2, as defined by shifts in these proteins' electrophoretic mobility and tyrosine phosphorylation of the MAPKs. However, the speed and duration of the MAPK response varied markedly depending on the stimulus. 5-OxoETE caused a very rapid and transient activation of MAPK. In contrast, the response to the cytokines was rather slow and persistent. PMN pretreated with GM-CSF demonstrated a dramatic increase in the extent of MAPK tyrosine phosphorylation and electrophoretic mobility shift in response to 5-oxoETE. Similarly, 5-oxoETE induced PMN to release some preincorporated [14C]arachidonic acid, while GM-CSF greatly enhanced the extent of this release. Thus, the synergism exhibited by these agents is prominent at the level of MAPK stimulation and phospholipid deacylation. Pertussis toxin, but not Ca2+ depletion, inhibited MAPK responses to 5-oxoETE and LTB4, indicating that responses to both agents are coupled through G proteins but not dependent upon Ca2+ transients. 15-OxoETE and 15(OH)-ETE were inactive while 5-oxo-15(OH)-ETE and 5(OH)-ETE had 3- and 10-fold less potency than 5-oxoETE, indicating a rather strict structural specificity for the 5-keto group. LY 255283, a LTB4 antagonist, blocked the responses to LTB4 but not to 5-oxoETE. Therefore, the oxoETEs do not appear to operate through the LTB4 receptor. In summary, the oxoETEs are potent activators of PMN that share some but not all activities with LTB4. The response to the oxoETEs is greatly enhanced by pretreatment with cytokines, indicating that combinations of these mediators may be very important in the pathogenesis of inflammation.

Published
1996

133. Regulatory functions of hapten-reactive helper and suppressor T lymphocytes. II. Selective inactivation of hapten-reactive suppressor T cells by hapten-nonimmunogenic copolymers of D-amino acids, and its application to the study of suppressor T-cell effect on helper T-cell development

Author

Hamaoka, T, Yoshizawa, M, Yamamoto, H, Kuroki, M, and Kitagawa, M

Abstract

An experimental condition was established in vivo for selectively eliminating hapten-reactive suppressor T-cell activity generated in mice primed with a para-azobenzoate (PAB)-mouse gamma globulin (MGG)-conjugate and treated with PAB-nonimmunogenic copolymer of D-amino acids (D- glutamic acid and D-lysine; D-GL). The elimination of suppressor T-cell activity with PAB-D-GL treatment from the mixed populations of hapten- reactive suppressor and helper T cells substantially increased apparent helper T-cell activity. Moreover, the inhibition of PAB-reactive suppressor T-cell generation by the pretreatment with PAB-D-GL before the PAB-MGG-priming increased the development of PAB-reactive helper T-cell activity. The analysis of hapten-specificity of helper T cells revealed that the reactivity of helper cells developed in the absence of suppressor T cells was more specific for primed PAB-determinants and their cross-reactivities to structurally related determinants such as meta-azobenzoate (MAB) significantly decreased, as compared with the helper T-cell population developed in the presence of suppressor T lymphocytes. In addition, those helper T cells generated in the absence of suppressor T cells were highly susceptible to tolerogenesis by PAB-D- GL. Similarly, the elimination of suppressor T lymphocytes also enhanced helper T-cell activity in a polyclonal fashion in the T-T cell interactions between benzylpenicilloyl (BPO)-reactive T cells and PAB- reactive T cells after immunization of mice with BPO-MGG-PAB. Thus inhibition of BPO-reactive suppressor T-cell development by the BPO-v-GL- pretreatment resulted in augmented generation of PAB-reactive helper T cells with higher susceptibility of tolerogenesis to PAB-D-GL. Thus, these results support the notion that suppressor T cells eventually suppress helper T-cell activity and indicate that the function of suppressor T cells related to helper T-cell development is to inhibit the increase in the specificity and apparent affinity of helper T cells in the primary immune response. The hapten-reactive suppressor and helper T lymphocytes are considered as a model system of T cells that regulate the immune response, and the potential applicability of this system to manipulating various T cell-mediated immune responses is discussed in this context.

Published
1977
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134. Regulatory functions of hapten-reactive helper and suppressor T lymphocytes. I. Detection and characterization of hapten-reactive suppressor T-cell activity in mice immunized with hapten-isologous protein conjugate

Author

Yamamoto, H, Hamaoka, T, Yoshizawa, M, Kuroki, M, and Kitagawa, M

Abstract

Helper and suppressor T-cell activities were detected simultaneously in the spleen cells of mice immunized with para-azobenzoate (PAB)-mouse gammaglobulin (MGG). Dinitrophenyl (DNP)-specific B cells were raised by immunization with DNP-keyhole limpet hemocyanin (KLH) and used as the indicator B-cell population. The helper and suppressor T-cell activities were determined after adoptively transferring spleen cells from PAB-MGG- primed donors and DNP-KLH-primed donors into X-irradiated recipients. Stimulation of these recipients with DNP-MGG-PAB detected helper T-cell activity, which was measured in terms of increased anti-DNP antibody responses of DNP-KLH-primed cells over these responses in the presence of unprimed cells. On the other hand, when DNP-KLH-primed cells were stimulated with DNP-KLH-PAB in the presence of PAB-MGG-primed cells, anti-DNP antibody responses were substantially lower than in unprimed normal cells. This suppressor cell population was (a) hapten-reactive, (b) present in B-cell-depleted spleen cells, (c) Thy-1 positive, (d) detectable earlier than the helper T-cell activities after priming (e) more radiosensitive than helper cells, and (f) found in the spleen but not the lymph nodes in contrast to helper T cells. These data indicate that these suppressor T cells are distinct from the helper T cells. PAB-reactive T cells clearly suppressed the antibody response by inhibiting KLH-reactive helper T-cell functions. The hapten-reactive T-lymphocyte system described here should be useful for analyzing and manipulating the immune response and for studying regulatory interactions of helper and suppressor T cells in the induction of antibody responses.

Published
1977
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138. Tips & timesavers.

Author

Morgan NJ, Marshall B, Hedlund B, Reisdorfer J, Zabresky J, Lebel M, Blais H, Lewis M, Mendenhall C, Kuroki M, Widman J, Boydstun SM, Dirks JL, and Handerhan B

Published
1984

139. Transient rise in serum interleukin-8 concentration during acute myocardial infarction.

Author

Abe, Y, Kawakami, M, Kuroki, M, Yamamoto, T, Fujii, M, Kobayashi, H, Yaginuma, T, Kashii, A, Saito, M, and Matsushima, K

Abstract

OBJECTIVE--To determine whether interleukin-8 (IL-8, a potent activator of neutrophils) is involved in tissue injury during ischaemia and reperfusion in patients with acute myocardial infarction. SETTING--Teaching hospital. SUBJECTS--Five consecutive patients with acute Q-wave myocardial infarction, two patients with stable angina who underwent elective percutaneous transluminal coronary angioplasty, and 10 normal controls. MAIN OUTCOME MEASURE--Serum IL-8 concentration measured by enzyme linked immunosorbent assay (ELISA) over time (every four, eight or 12 hours for 36-72 hours). RESULTS--All five patients with acute myocardial infarction had a transient but significant rise in serum IL-8 concentration (13-1100 ng/l) within 22 hours after the onset of symptoms, whereas IL-8 was not detected in any of the samples from patients with angina pectoris or normal controls. One patient who died of pump failure and two patients who had mild congestive heart failure showed the highest values (1100, 920, and 190 ng/l respectively). CONCLUSIONS--Serum IL-8 concentration showed a transient rise during the very early phase of acute myocardial infarction. In combination with several recent lines of evidence indicating the importance of injurious activities of neutrophils as a cause of tissue damage in acute myocardial infarction and the potent stimulation of neutrophils by IL-8, these results strongly suggest that IL-8 is important in the development of myocardial injury in acute myocardial infarction. [ABSTRACT FROM PUBLISHER]

Published
1993
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140. Up-regulation of vascular endothelial growth factor production by iron chelators

Author

Laurens Victor Beerepoot, Dt, Shima, Kuroki M, Kt, Yeo, and Ee, Voest

Subjects
Vascular Endothelial Growth Factor A, Lymphokines, Mice, Vascular Endothelial Growth Factors, Animals, Humans, Endothelial Growth Factors, RNA, Messenger, Deferoxamine, Iron Chelating Agents, Cell Line, Rats, Up-Regulation
Abstract

Agents that modulate cellular iron availability have been studied for their antitumor activity. Based on encouraging in vitro studies, the iron chelator deferoxamine (DFO) has been used in clinical studies to treat cancer patients. The observation that DFO induced macular edema in several cancer patients led to the present investigation of vascular endothelial growth factor (VEGF) as a possible mediator of the encountered side effects. Both normal and malignant cell lines were incubated with DFO and a variety of other iron chelators. DFO, at concentrations achievable in humans, induced a 3-5-fold increase in VEGF mRNA expression in all cell lines studied. This increased VEGF mRNA expression was dose and time dependent. A panel of structurally different iron chelators induced an even more potent increase in VEGF mRNA expression. The DFO-induced increase in VEGF mRNA expression translated into 6- and 4-fold increases in VEGF protein secretion in conditioned media of retinal pigment epithelial and C6 glioblastoma cells, respectively. These findings suggest that VEGF may act as a mediator of the side effects induced by iron chelation therapy. In addition, because VEGF is an important regulator of angiogenesis, iron chelators should be given with caution to cancer patients.

141. Progress report on damage investigation after Kocaeli earthquake by Architectural Institute of Japan

Author

Kabeyasawa, T., Shiohara, H., Kudo, K., Fujita, K., Kusu, K., Suzuki, N., Kitayama, K., Takahashi, I., Kanata, K., Kimura, H., Kanno, T., Okada, H., Masuda, Y., Tanaka, H., Kono, S., Kobayashi, K., Kikuchi, K., Kobayashi, J., Arai, H., Kuroki, M., Yoshimura, K., Nagao, T., Watanabe, H., Altay, G., Kilic, S., Erdik, M., Yuzugullu, O., Özel, O., Karadogan, F., Boduroglu, H., and Polat Gulkan

142. Intratumoral distribution of radiolabeled antibody and radioimmunotherapy in experimental liver metastases model of nude mouse

Author

Noriko Sato, Saga T, Sakahara H, Yao Z, Nakamoto Y, Zhang M, Kuroki M, Matsuoka Y, Iida Y, and Konishi J

Subjects
Iodine Radioisotopes, Mice, Mice, Inbred BALB C, Liver Neoplasms, Animals, Antibodies, Monoclonal, Humans, Mice, Nude, Female, Tissue Distribution, Radioimmunotherapy, Colorectal Neoplasms, Carcinoembryonic Antigen
Abstract

The biodistribution and intratumoral distribution of radiolabeled anticarcinoembryonic antigen (CEA) monoclonal antibody in experimental liver metastases and the therapeutic effect of 131I-labeled anti-CEA antibody on the metastases were studied.Three weeks after an intrasplenic injection of human colon cancer cells, mice received an intravenous injection of 125I- or 111In-labeled anti-CEA antibody F33-104. The biodistribution and tumor penetration of radiolabeled antibody were examined by using quantitative autoradiography. To evaluate the therapeutic effect, 5.55, 9.25 or 11.1 MBq (150, 250 or 300 microCi) 131I-labeled F33-104 were injected into groups of mice that had micrometastases smaller than 1 mm. Control groups were injected with phosphate-buffered saline or 131I-labeled control antibody. Mice were killed 3 wk later to determine the size of liver metastases.1251-labeled F33-104 showed a high accumulation in the liver metastases (percentage of injected dose per gram of metastases [%ID/g]24%, metastasis-to-liver ratio9.8, metastasis-to-blood ratio2.1); however, its accumulation was heterogeneous or peripheral in the nodules more than 1 mm in diameter. When the antibody dose was increased, antibody penetration was improved, but tumor uptake of radioactivity and specificity ratios decreased. In mice with large metastases, radioactivity in the normal tissue was lower than that in mice with small metastases, resulting in higher metastasis-to-background ratios. 111In-labeled antibody showed even higher tumor uptake than 125I-labeled antibody (51 %ID/g). Metastases formation was suppressed in a dose-dependent manner by 131I-labeled F33-104 injection (5 of 8 mice had no macroscopic tumor after an injection of 5.55 MBq (150 microCi), and all mice had no visible metastasis after an injection of 9.25 or 11.1 MBq [250 or 300 microCi]), whereas tumor progression was seen in the control groups.Liver metastases had easy accessibility to the antibody. Micrometastases of less than 0.5 mm in diameter showed homogeneous intratumoral distribution of injected antibody and were successfully treated with 131I-labeled antibody. Very high uptake and satisfactory metastasis-to-liver ratios with 111In-labeled antibody suggest that the use of a radiometal with high beta-energy, such as 90Y or 188Re, is preferable for the successful radioimmunotherapy of metastases larger than 1 mm.

143. 5-Oxo-eicosatetraenoate is a broadly active, eosinophil-selective stimulus for human granulocytes

Author

Flaherty Jt, O., Kuroki M, Ab, Nixon, jonny wijkander, Yee E, Sl, Lee, Pk, Smitherman, Rl, Wykle, and Lw, Daniel

Subjects
Enzyme Activation, Eosinophils, Mitogen-Activated Protein Kinase 3, Neutrophils, Chemotactic Factors, Eosinophil, Calcium-Calmodulin-Dependent Protein Kinases, Hydroxyeicosatetraenoic Acids, Humans, Arachidonic Acids, Mitogen-Activated Protein Kinases, Cell Degranulation
Abstract

5-Oxo-eicosatetraenoate (5-oxoETE) is gaining recognition as a chemotactic factor for eosinophilic (Eo) as well as neutrophilic (Neu) polymorphonuclear leukocytes. We found that the eicosanoid was far stronger than C5a, platelet-activating factor (PAF), leukotriene B4 (LTB4), or FMLP in stimulating Eo chemotaxis. Moreover, it had weak intrinsic degranulating effects on otherwise unstimulated Eo, produced prominent degranulation responses in Eo primed by granulocyte-macrophage CSF, and enhanced the Eo-degranulating potencies of PAF, C5a, LTB4, and FMLP by up to 10,000-fold. Low picomolar levels of 5-oxoETE also induced Eo to activate mitogen-activated protein kinases (MAPKs), as defined by shifts in the electrophoretic mobility and tyrosine phosphorylation of two immunodetectable proteins, p44 and p42. 5-OxoETE wasor = 100-fold weaker or unable to stimulate any of these responses in Neu. Finally, 5-oxo-15-hydroxy-ETE and 5-hydroxy-ETE activated both cell types, but were weaker than 5-oxoETE and had Eo/Neu potency ratios approaching unity. 5-OxoETE, thus, is uniquely potent and selective in promoting Eo not only to migrate, but also to release granule enzymes and activate MAPKs. By triggering MAPK activation, the eicosanoid may also influence the production of anaphylactoid lipids (e.g., PAF), arachidonic acid metabolites, and cytokines. 5-OxoETE therefore possesses a biologic profile well suited for mediating Eo-dominated allergic reactions in vivo.

148. Reply

Author

Kuroki, M., primary, Tanaka, R., additional, and Hondo, H., additional

Published
1989
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149. General lectures (II)

Author

Segawa, K., primary, Nakazawa, S., additional, Koide, N., additional, Imai, K., additional, Matsuo, N., additional, Yamamoto, Y., additional, Shiobara, M., additional, Shimada, H., additional, Kawai, K., additional, Machida, K., additional, Okabe, N., additional, Hoshi, Y., additional, Koizumi, Y., additional, Watanuki, T., additional, Hiroshima, Y., additional, Matsusaka, Y., additional, Katase, K., additional, Sakuma, Y., additional, Matoba, N., additional, Murata, N., additional, Toyama, Y., additional, Murai, S., additional, Nukaga, A., additional, Ishimatsu, N., additional, Watanabe, Y., additional, Abe, M., additional, Ono, Y., additional, Hirai, K., additional, Iwabuchi, S., additional, Suzuki, K., additional, Aoki, T., additional, Masamura, K., additional, Yoshida, K., additional, Ikeuchi, J., additional, Nagao, F., additional, Kobayashi, A., additional, Toriie, S., additional, Nakajima, M., additional, Kohli, M., additional, Ida, K., additional, Masuda, M., additional, Hattori, T., additional, Fujita, S., additional, Tamada, T., additional, Inoue, K., additional, Usui, T., additional, Yamaya, S., additional, Ohtsuka, K., additional, Shiraki, Y., additional, Fujishima, S., additional, Tochikubo, O., additional, Miyamoto, S., additional, Ueda, A., additional, Asano, K., additional, Kunisada, M., additional, Miyake, H., additional, Fujii, Y., additional, Yoshimoto, S., additional, Hiramatsu, K., additional, Nakano, S., additional, Takeda, T., additional, Kitamura, K., additional, Horiguchi, Y., additional, Okada, K., additional, Okada, M., additional, Kuwabara, T., additional, Tanaka, M., additional, Konno, K., additional, Isobe, K., additional, Iwasaki, A., additional, Unoura, T., additional, Matsumoto, M., additional, Yoshida, T., additional, Takahashi, I., additional, Maeda, H., additional, Hayashi, T., additional, Koizumi, H., additional, Iwasaki, M., additional, Takahashi, K., additional, Honda, T., additional, Ariga, K., additional, Mohri, S., additional, Suga, Y., additional, Ono, T., additional, Kobayashi, K., additional, Mizuno, T., additional, Sameshima, Y., additional, Shiozaki, Y., additional, Sasakawa, M., additional, Hiramatsu, A., additional, Ikehara, K., additional, Nagata, T., additional, Tatsumi, K., additional, Aoki, M., additional, Iwasaki, S., additional, Aizawa, T., additional, Kajiwara, K., additional, Sata, K., additional, Omata, S., additional, Imamura, K., additional, Kondo, K., additional, Sajima, H., additional, Sato, Y., additional, Kiryu, H., additional, Mimoto, S., additional, Masuoka, T., additional, Kira, K., additional, Mizumoto, R., additional, Kuratsuka, H., additional, Honjo, I., additional, Hojo, Y., additional, Nakajima, H., additional, Tosaka, T., additional, Arai, O., additional, Kobayashi, N., additional, Obata, N., additional, Ito, S., additional, Takaoka, T., additional, Uragami, Y., additional, Kitamura, Y., additional, Kishi, S., additional, Fujii, S., additional, Okuda, H., additional, Hirano, K., additional, Kano, H., additional, Ogino, M., additional, Ueda, Y., additional, Nishiwaki, K., additional, Iwamura, N., additional, Kamada, T., additional, Suematsu, T., additional, Fusamoto, H., additional, Abe, H., additional, Katayama, S., additional, Yamaguchi, K., additional, Fukuda, M., additional, Ishii, T., additional, Kaito, I., additional, Sato, S., additional, Sasaki, H., additional, Onodera, H., additional, Yamanaka, M., additional, Akagi, K., additional, Miyazaki, S., additional, Okumura, M., additional, Omae, T., additional, Nakamura, Y., additional, Wada, M., additional, Nakai, Y., additional, Inoue, S., additional, Arima, T., additional, Yamasaki, S., additional, Takano, T., additional, Katsuta, Y., additional, Yano, T., additional, Isoda, K., additional, Aramaki, T., additional, Fukuda, N., additional, Ichikawa, T., additional, Okumura, H., additional, Adachi, Y., additional, Inoue, R., additional, Iwasaki, Y., additional, Tanaka, S., additional, Yamamoto, T., additional, Wakisaka, G., additional, Nakaya, H., additional, Takase, S., additional, Ikegami, F., additional, Takada, A., additional, Takeuchi, J., additional, Kato, Y., additional, Funayama, A., additional, Kakumu, S., additional, Okuyama, S., additional, Taoka, Y., additional, Endo, T., additional, Chizuka, R., additional, Yanagida, T., additional, Chizuka, S., additional, Usui, H., additional, Ando, T., additional, Takai, T., additional, Wakahara, T., additional, Kojima, M., additional, Fukazawa, T., additional, Takahashi, Y., additional, Miyamura, S., additional, Urakawa, T., additional, Shima, T., additional, Miyaji, K., additional, Okazaki, T., additional, Kashimura, S., additional, Koyama, K., additional, Yamauchi, H., additional, Matsuo, Y., additional, Takagi, Y., additional, Muto, I., additional, Owada, Y., additional, Otowa, T., additional, Sato, T., additional, Naito, C., additional, Sugawara, K., additional, Nokiba, T., additional, Kido, H., additional, Sasaki, M., additional, Sugai, Y., additional, Nishimura, G., additional, Nanbu, H., additional, Kamiyama, Y., additional, Yamada, T., additional, Yamaoka, Y., additional, Takeda, H., additional, Ohsawa, T., additional, Kamano, T., additional, Mizukami, T., additional, Kitamura, O., additional, Ozawa, K., additional, Takasan, H., additional, Miyasaki, R., additional, Katayama, T., additional, Amakawa, T., additional, Hirose, K., additional, Furukawa, Y., additional, Noguchi, M., additional, Okamoto, M., additional, Maezawa, H., additional, Tanaka, N., additional, Yamada, S., additional, Hisata, T., additional, Hata, C., additional, Sawa, J., additional, Mituda, Y., additional, Oohira, S., additional, Hayasaka, A., additional, Okuyama, T., additional, Fukui, S., additional, Furuichi, T., additional, Yamamitsu, S., additional, Yamauchi, K., additional, Konishi, Y., additional, Maeda, S., additional, Setoyama, S., additional, Otsuji, S., additional, Ibata, T., additional, Niu, H., additional, Ogawa, A., additional, Tujioka, E., additional, Maeda, T., additional, Takewa, M., additional, Matumoto, T., additional, Tamada, K., additional, Maeda, A., additional, Sumita, H., additional, Iseki, Y., additional, Yukawa, S., additional, Nitta, Y., additional, Isida, K., additional, Nomoto, H., additional, Sato, R., additional, Sato, G., additional, Toyokawa, S., additional, Yamamoto, G., additional, Ohtomi, S., additional, Haga, M., additional, Ueno, Y., additional, Endo, R., additional, Yokota, T., additional, Ohsawa, J., additional, Kohno, A., additional, Ohtoshi, E., additional, Yasugi, H., additional, Ichikawa, H., additional, Ando, K., additional, Suzuki, H., additional, Nishiwaki, T., additional, Kishimoto, T., additional, Miki, T., additional, Takeshige, K., additional, Sawada, M., additional, Hidemura, R., additional, Yamamoto, S., additional, Itoh, S., additional, Kashiwagi, T., additional, Kishida, M., additional, Imamura, O., additional, Suematus, T., additional, Sakoda, K., additional, Kawada, T., additional, Arima, Y., additional, Kamimura, T., additional, Takesue, M., additional, Katsuki, T., additional, Akita, H., additional, Yakeishi, Y., additional, Takehisa, I., additional, Miyasato, K., additional, Yoshida, H., additional, Kubota, K., additional, Aoki, S., additional, Suzuki, S., additional, Miyahara, T., additional, Fujiwara, K., additional, Sakai, T., additional, Oda, T., additional, Igarashi, S., additional, Fukuhara, M., additional, Tsujii, T., additional, Tamura, T., additional, Matsuoka, Y., additional, Takahashi, H., additional, Sakamoto, T., additional, Fukuda, S., additional, Oku, M., additional, Matsui, T., additional, Morita, T., additional, Oyazato, Y., additional, Kimura, K., additional, Moriya, W., additional, Morimoto, S., additional, Tsuiki, S., additional, Shoji, K., additional, Hata, M., additional, Kubo, J., additional, Yoshizawa, K., additional, Nagayama, K., additional, Ozawa, Y., additional, Yoshida, M., additional, Horiguchi, M., additional, Machii, A., additional, Aiso, Y., additional, Kitahara, N., additional, Kitazawa, E., additional, Fukuda, K., additional, Saiti, N., additional, Murakami, Y., additional, Nao, Y., additional, Okazaki, I., additional, Funatsu, K., additional, Maruyama, K., additional, Takagi, B., additional, Yasuraoka, S., additional, Ishii, K., additional, Matsuzaki, S., additional, Ishii, H., additional, Kamegaya, K., additional, Sambe, K., additional, Ishikawa, H., additional, Tajima, Y., additional, Kuroda, A., additional, Ishihara, Y., additional, Sato, N., additional, Ishikawa, I., additional, Noro, T., additional, Kakumoto, Y., additional, Mekjian, H. S., additional, Thomford, N. R., additional, Yokomura, T., additional, Adachi, S., additional, Yamamoto, A., additional, Saito, I., additional, Kawamura, A., additional, Miyata, M., additional, Kasai, S., additional, Kawanishi, N., additional, Tamaki, A., additional, Mito, M., additional, Kasai, Y., additional, Hasumi, A., additional, Uchiyama, T., additional, Tachikawa, Y., additional, Takanashi, T., additional, Kanke, T., additional, Matsuda, K., additional, Hamana, G., additional, Sakuma, M., additional, Sugita, T., additional, Tomita, K., additional, Tsuzuki, T., additional, Uekusa, M., additional, Matsuzaki, M., additional, Tsuchiya, M., additional, Uchimura, M., additional, Murohisa, T., additional, Muto, Y., additional, Ishigaki, J., additional, Waki, S., additional, Tsuchiya, R., additional, Sho, M., additional, Furukawa, M., additional, Suzuki, N., additional, Nagashima, H., additional, Matsushiro, T., additional, Saitoh, T., additional, Nakamura, N., additional, Hatanaka, T., additional, Tooi, K., additional, Tanaka, Y., additional, Kadokura, N., additional, Okada, Y., additional, Yanakgi, I., additional, Sekiya, V. M., additional, Adachi, K., additional, Miyashita, M., additional, Moriyama, Y., additional, Onda, M., additional, Yoshioka, M., additional, Teraoka, T., additional, Shimizu, Y., additional, Fujishima, G., additional, Ookawa, K., additional, Miki, M., additional, Shirota, A., additional, Aihara, K., additional, Shiga, T., additional, Sano, H., additional, Hayashi, S., additional, Hori, M., additional, Sato, H., additional, Chuman, Y., additional, Tsukase, S., additional, Nakahara, N., additional, Ehira, S., additional, Nishimata, H., additional, Irisa, T., additional, Tokutome, K., additional, Nakashima, Y., additional, Koga, H., additional, Yokoyama, H., additional, Otsuji, T., additional, Chujo, Y., additional, Gotoda, S., additional, Uchiyama, S., additional, Kosaki, G., additional, Ohkura, H., additional, Mukojima, T., additional, Hattori, N., additional, Sasaki, O., additional, Soejima, K., additional, Inokuchi, K., additional, Utsunomiya, J., additional, Maki, T., additional, Iwama, T., additional, Matsunaga, Y., additional, Shimomura, T., additional, Nakajima, T., additional, Ichikawa, S., additional, Miyanaga, T., additional, Sengoku, K., additional, Hamaguchi, E., additional, Aoki, N., additional, Nomura, T., additional, Matsuoka, A., additional, Nagahama, A., additional, Kazumi, T., additional, Miyawaki, H., additional, Miyasaki, K., additional, Kato, K., additional, Miyazaki, Y., additional, Harada, N., additional, Yamada, K., additional, Tashiro, S., additional, Sakai, K., additional, Ho, N., additional, Murayama, H., additional, Yada, M., additional, Sakabe, T., additional, Shimizu, H., additional, Kuroki, M., additional, Nishida, S., additional, Ishiyama, S., additional, Yukawa, K., additional, Hayashi, M., additional, Soh, K., additional, Doi, K., additional, Nakagawa, A., additional, Yukawa, E., additional, Uematsu, Y., additional, Nara, K., additional, Hattori, H., additional, Watanabe, M., additional, Sato, K., additional, Okuse, S., additional, Murotani, T., additional, Takasu, S., additional, Konta, M., additional, Uchiya, T., additional, Fujimaki, N., additional, Yoshikawa, K., additional, Uchida, M., additional, Kawana, S., additional, Tamura, K., additional, Hashimoto, T., additional, Hara, T., additional, Nosaka, J., additional, Fukui, O., additional, Inaba, E., additional, Otsukasa, S., additional, Sanada, K., additional, Hiraide, H., additional, Senyo, G., additional, Ootani, A., additional, Nakayama, T., additional, Takei, S., additional, Miki, H., additional, Minota, S., additional, Nakayama, K., additional, Nakagawa, K., additional, Shiraishi, T., additional, Kawauchi, H., additional, Nagaya, H., additional, Mizushima, K., additional, Tachimi, Y., additional, Namiki, M., additional, Masuda, K., additional, Mitsutani, N., additional, Mukuta, T., additional, Koizumi, T., additional, Takeuchi, T., additional, Nemoto, T., additional, Takabayashi, H., additional, Takagi, M., additional, Hongo, Y., additional, Kojima, H., additional, Nishimura, M., additional, Hino, S., additional, Hirayama, J., additional, Nakamura, M., additional, Koga, S., additional, Hirayama, C., additional, Kikuch, S., additional, Ito, M., additional, Hidano, S., additional, Ooya, T., additional, Banno, H., additional, Tomura, A., additional, Koyama, T., additional, Takei, T., additional, Tomimura, T., additional, Yamauchi, M., additional, Nakaya, Y., additional, Matsuda, Y., additional, Udo, K., additional, Hukuda, N., additional, Kametani, M., additional, Miyagawa, T., additional, Imaeda, T., additional, Senda, K., additional, Okubo, H., additional, Kanoda, K., additional, Miyashita, B., additional, Ishizuka, H., additional, Goto, T., additional, Oto, K., additional, Kaneda, H., additional, Hase, M., additional, Matsuda, J., additional, Kawai, T., additional, Ikehara, H., additional, Baba, S., additional, Ishii, M., additional, Tozawa, T., additional, Inoue, E., additional, Mizuno, N., additional, Saeki, S., additional, Nakaji, T., additional, Narabayashi, T., additional, Okuno, T., additional, Yamada, H., additional, Tanno, M., additional, Chiba, K., additional, Iio, M., additional, Shibata, K., additional, Furuhashi, F., additional, Mizuochi, K., additional, Ohashi, S., additional, Nakano, M., additional, Otsuka, S., additional, Irie, M., additional, Akima, M., additional, Maruyama, Y., additional, Oyamada, F., additional, Nagata, E., additional, Kubo, Y., additional, Arishima, T., additional, Otsuyama, Y., additional, Kaneto, A., additional, Shimogawa, Y., additional, Tanigawa, K., additional, Nakajima, K., additional, Onishi, S., additional, Kasahara, A., additional, Shimizu, T., additional, Ikehara, Y., additional, Tajima, H., additional, Okamoto, A., additional, Komibuchi, T., additional, Negoro, T., additional, Nihonsugi, A., additional, Ogawa, Y., additional, Otani, H., additional, Ishida, M., additional, Yashima, H., additional, Ryo, M., additional, Tanaka, T., additional, Taketa, K., additional, Watanabe, A., additional, Yumoto, Y., additional, Tanaka, A., additional, Takesue, A., additional, Aoe, H., additional, Ueda, M., additional, Shimamura, J., additional, Kosaka, K., additional, Kashiwara, E., additional, Orita, K., additional, Konaga, E., additional, Kaneda, S., additional, Ogawa, K., additional, Tamura, H., additional, Okanishi, S., additional, Ueda, T., additional, Horie, H., additional, Kamachi, M., additional, Asihara, T., additional, Daido, R., additional, Izumi, T., additional, Kurihara, M., additional, Sumida, M., additional, Haraikawa, M., additional, Hayakawa, H., additional, Shirakabe, H., additional, and Yasui, A., additional

Published
1974
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