bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhancement of Migratory and Aggregate Activities of Human Peripheral Blood Monocyte‐Derived Dendritic Cells by Stimulation with RANTES
Authors: Enomoto Makoto , Nagayama Hitomi , Takahashi Tsuneo A. 
Published: November 2013

AbstractWe examined the effects of various chemokines on the functional activation of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) plus interleukin‐4 (IL‐4)‐generated human peripheral blood monocyte‐derived immature dendritic cells (iDC). Stimulation of iDC with regulated on activation normal T cell expressed and secreted (RANTES) resulted in the promotion of their chemotactic migratory capacity in response to RANTES when compared with that of unstimulated cells. TNF‐α induced a homotypic aggregated cluster formation of iDC in a dose‐dependent manner, whereas the combination of TNF‐α and RANTES exhibited more potent induction. IDC stimulated with RANTES were more efficient than unstimulated iDC in the production of endogenous RANTES. Treatment of iDC with the combination of TNF‐α and RANTES was just little effective for the enhancement of allogeneic T‐cell stimulatory capacity as compared with that of TNF‐α treated iDC. These results suggest that endogenous secretions of RANTES from iDC stimulated with RANTES be potentially involved in RANTES‐induced changes of properties with respect to morphology and function.
A Mathematical Analysis of the Interactions between Immunogenic Tumor Cells and Cytotoxic T Lymphocytes
Authors: Takayanagi Toshiaki , Ohuchi Azuma 
Published: November 2013

AbstractRecent developments of biotechnology have enabled us to use immunotherapy against certain kinds of tumors in patients. However, it is reasonable to doubt if the immunotherapy can completely aid the rejection of tumors that have escaped from the immune system. In this paper, we propose a new mathematical model of tumor immunity by tumor‐specific cytotoxic T lymphocytes (CTLs), since tumor‐specific CTLs play an important role in tumor immunity. Using this model, we have mathematically investigated the interactions between immunogenic tumor cells (TCs) and tumor‐specific CTLs and evaluated the availability of immunotherapies for tumors. The findings herein demonstrate that three kinds of dynamics of tumor immunity exist: i.e. (1) TCs continue to proliferate with CTLs; (2) TCs are rejected by CTLs; and (3) TCs equilibrate with CTLs, but with little possibility of the equilibrium. The findings also demonstrate that a sufficient increase in CTLs by immunotherapy can aid the rejection of TCs, but an insufficient increase in CTLs by immunotherapy causes only a transient regression of TCs. Clinically the findings mean that increasing tumor‐specific CTLs, e.g., by vaccination or adoptive transfer of tumor‐specific CTLs expanded ex vivo, can theoretically aid the rejection of TCs.
Protective Effect of Wogonin on Endotoxin‐Induced Lethal Shock in D‐Galactosamine‐Sensitized Mice
Authors: Van Dien Mai , Takahashi Kazuko , Mu Mya Mya , Koide Naoki , Sugiyama Tsuyoshi , Mori Isamu , Yoshida Tomoaki , Yokochi Takashi 
Published: November 2013

AbstractThe effects of wogonin, a major flavonoid from Scutellaria baicalensis Georgi, on lipopolysaccharide (LPS)‐induced lethal shock in mice was investigated. Wogonin pretreatment prevented the lethal shock in mice injected with D‐galactosamine (D‐GalN) and LPS, but not in mice injected with a high dose of LPS. Wogonin definitely inhibited the hepatic injury in mice injected with D‐GalN, and LPS and reduced the level of circulating tumor necrosis factor (TNF)‐α. The reduction was more marked in mice injected with D‐GalN and LPS compared with that in mice injected with a high dose of LPS. Wogonin pretreatment did not inhibit the lipid peroxidation in mice receiving either D‐GalN and LPS or a high dose of LPS. Wogonin inhibited the in vitro production of TNF‐α and nitric oxide in LPS‐stimulated RAW 264.7 cells. The mechanism of the protective effect of wogonin on the lethal shock in mice injected with D‐GalN and LPS is discussed.
Effects of Mutation in Hepatitis C Virus Nonstructural Protein 5A on Interferon Resistance Mediated by Inhibition of PKR Kinase Activity in Mammalian Cells
Authors: Noguchi Tohru , Satoh Shinya , Noshi Takeshi , Hatada Eriko , Fukuda Ryuji , Kawai Akihiko , Ikeda Satoru , Hijikata Makoto , Shimotohno Kunitada 
Published: November 2013

AbstractThe IFN‐induced double‐stranded RNA (dsRNA)‐activated protein kinase PKR is one of the key molecules in the antiviral effects of IFN. To clarify the effects of hepatitis C virus nonstructural protein 5A (NS5A) on antiviral activity of IFN, in particular on PKR kinase activity, in mammalian cells, we established inducible NS5A‐expressing cell lines derived from human osteosarcoma (Saos‐2). The cells expressing NS5A derived from an IFN‐resistant clone (NS5A‐1b) that interacted with endogenous PKR in vitro, showed a suppressive effect on IFN function as determined by interference with vesicular stomatitis virus (VSV) infection, whereas NS5A (NS5A‐2a) from an IFN‐sensitive clone did not block the antiviral effect of IFN. A mutant with deletion of the IFN sensitivity determining region (ISDR) in NS5A‐1b (NS5A‐ΔISDR) also interacted with PKR and suppressed its activity in vitro. However, neither NS5A‐2a nor the C‐terminal truncated mutant of NS5A‐1b (NS5A‐ΔC) blocked PKR activity. These observations confirmed the previous report that the inhibitory effect of NS5A on IFN activity is mediated at least in part by the repression of PKR. In addition, we showed that IFN sensitivity was determined not only by the ISDR but that the involvement of the C‐terminal region of NS5A‐1b is important for the suppression of PKR activity.
Characterization of Mumps Virus Isolated in Saitama Prefecture, Japan, by Sequence Analysis of the SH Gene
Authors: Uchida Kazue , Shinohara Michiyo , Shimada Shin‐ichi , Segawa Yukari , Hoshino Yoji 
Published: November 2013

AbstractMumps virus (MuV) strains isolated from cerebrospinal fluid and throat swabs from patients in Saitama Prefecture and Tokyo, Japan, from 1997 to 2000 were examined by analyzing the SH gene nucleotide sequence (316‐nt). Eighteen of the 20 strains studied were divided into three genotypes, recognized as B, G, and H in previous reports. Two genotypes (G and H) are believed to be new in Japan. Two of the 20 strains belonged to none of the previously reported genotypes (A–I), but were closely related to two known strains, MP94‐H and Lougl/UK97. We propose that the two strains identified in this study together with the previously reported strains, MP94‐H and Lougl/UK97, form a new genotype, designated J, based on the divergence of the SH gene nucleotide sequences between these four strains and other strains reported (genotypes A–I). Our results also suggest that more than two genotypes circulated in Saitama Prefecture from 1997 to 1999, but only one, genotype G, was in evidence in 2000. Genotype B was earlier reported as the predominant strain in Japan, but it became undetectable by the year 2000. These results provide important epidemiological data on mumps in Japan.
Location of the Epitope for 7D5, a Monoclonal Antibody Raised against Human Flavocytochrome b558, to the Extracellular Peptide Portion of Primate gp91phox
Authors: Yamauchi Akira , Yu Lixin , Pötgens Andy J.G. , Kuribayashi Futoshi , Nunoi Hiroyuki , Kanegasaki Shiro , Roos Dirk , Malech Harry L. , Dinauer Mary C. , Nakamura Michio 
Published: November 2013

AbstractFlavocytochrome b558 is the membrane component of the phagocyte NADPH oxidase, and is a heterodimer composed of gp91phox and p22phox subunits. Human flavocytochrome b558 is recognized by monoclonal antibody 7D5 at an unidentified extracellular domain, although our previous study suggested it might recognize p22phox. 7D5 has proven useful in rapid screening of individuals for X‐linked chronic granulomatous disease by flow‐cytometry. Therefore, we re‐evaluated the location of the 7D5 epitope using gene‐engineered cell lines expressing hybrid flavocytochromes composed of human and murine subunit homologues. The current study demonstrates that the 7D5 recognizes epitope only of primate gp91phox. Flow‐cytometric analyses showed that 7D5 consistently bound to cells expressing human gp91phox. In addition, 7D5 immunoprecipitated the ~58 kDa unglycosylated gp91phox protein from solubilized membrane fractions of tunicamycin‐treated PLB‐985 granulocytes, indicating that glycans were not required for 7D5 binding. Transgenic COS7 cells expressing human gp91phox but not p22phox were recognized by 7D5. These results localized the epitope of 7D5 to an extracellular peptide portion of primate gp91phox and indicate that the antibody will be useful for monitoring the efficiency of gene therapy in patients with flavocytochrome b558‐deficient chronic granulomatous disease and for elucidating structural characteristics of flavocytochrome b558.
Characterization of an Extended‐Spectrum Class C β‐Lactamase of Citrobacter freundii
Authors: Haruta Shin , Nukaga Michiyoshi , Sawai Tetsuo 
Published: November 2013

AbstractCitrobacter freundii GC3 is a clinical isolate which showed moderate resistance to oxyimino β‐lactams such as ceftazidime and aztreonam. This drug resistance was due to an extended‐spectrum class C β‐lactamase encoded by chromosomal gene(s). The GC3 β‐lactamase showed high amino acid sequence homology to a known C. freundii β‐lactamase, i.e., 346 of 361 amino acids were identical with those of C. freundii GN346 β‐lactamase (Tsukamoto, K. et al, Eur. J. Biochem. 188, 15–22, 1990). Asp198 was the only dissimilar amino acid found in the omega loop region, known as the hot spot for extended‐spectrum resistance in class C β‐lactamases (Haruta, S. et al, Microbiol. Immunol. 42, 165–169, 1998). However, Asp198 was eliminated as a cause of the extended‐spectrum resistance by the substitution of Asn for Asp198. Subsequent investigation suggested that the moderate resistance to oxyimino β‐lactams is attributable to the replacement of amino acids on the enzyme's surface area, far from the active‐site. Some or all of the replacements are assumed to delicately modify the active‐site configuration. The GC3 β‐lactamase is the first example of an extended‐spectrum class C β‐lactamase in which mutations are independent of the omega loop.
Nucleotide Sequence and Molecular Characterization of a Dextranase Gene from Streptococcus downei
Authors: Igarashi Takeshi , Yamamoto Ayako , Goto Nobuichi 
Published: November 2013

AbstractDNA fragments encoding the Streptococcus downei dextranase were amplified by PCR and inverse PCR based on a comparison of the dextranase gene (dex) sequences from S. sobrinus, S. mutans, and S. salivarius, and the complete nucleotide sequence of the S. downei dex was determined. An open reading frame (ORF) of dex was 3,891 bp long. It encoded a dextranase protein (Dex) consisting of 1,297 amino acids with a molecular mass of 139,743 Da and an isoelectric point of 4.49. The deduced amino acid sequence of S. downei Dex had homology to those of S. sobrinus, S. mutans and S. salivarius Dex in the conserved region (made of about 540 amino acid residues). DNA hybridization analysis showed that a dex DNA probe of S. downei hybridized to the chromosomal DNA of S. sobrinus as well as that of S. downei, but did not to other species of mutans streptococci. The C terminus of the S. downei Dex had a membrane‐anchor region which has been reported as a common structure of C termini of both the S. mutans and S. sobrinus Dex. The recombinant plasmid which harbored the dex ORF of S. downei produced a recombinant Dex enzyme in Escherichia coli cells. The analysis of the recombinant enzyme on SDS‐PAGE containing blue dextran showed multiple active forms as well as dextranases of S. mutans, S. sobrinus and S. salivarius.
Analysis of Seawaters for the Recovery of Culturable Vibrio parahaemolyticus and Some Other Vibrios
Authors: Alam Muhammad Jahangir , Tomochika Ken‐ichi , Miyoshi Shin‐ichi , Shinoda Sumio 
Published: November 2013

AbstractWe investigated the recovery of dormant and injured cells along with the normally culturable cells of Vibrio species with special emphasis on V. parahaemolyticus using both selective and non‐selective media at moderate (20 C) and standard (37 C) culture temperatures from a bay water environment. Culture temperatures (20 or 37 C) did not affect the recovery of V. parahaemolyticus but did for other vibrios. We observed similar seasonality of V. parahaemolyticus as in most other environmental studies. V. parahaemolyticus and other Vibrio species were recovered in higher numbers by a replica plating method compared to most probable number (MPN) and direct TCBS (thiosulfate citrate bile‐salt sucrose) agar counts. Even with the replica plating method, however, vibrios number goes down to a minimum level and V. parahaemolyticus was undetectable during the cool temperature period of the year, although total bacterial cells and CFU on nutrient agar (with 2% NaCl) did not vary so much during the study period.
Protective Effect of OK‐432 on Mice against Endotoxemia and Infection with Pseudomonas aeruginosa and Salmonella enteritidis
Authors: Hashimoto Masahito , Kirikae Fumiko , Toyooka Kiminori , Kaneko Aki , Yamasu Hiromi , Iwai Hiroki , Nakano Masayasu , Kirikae Teruo 
Published: November 2013

AbstractOK‐432 has been used clinically as a biological response modifier for cancer therapy. We investigated here the protective effects of OK‐432 against endotoxic shock and infectious death caused by Pseudomonas aeruginosa and Salmonella enteritidis in mice and proposed a possible mechanism. Pre‐treatment of OK‐432 reduced the lethality of lipopolysaccharide (LPS)‐induced endotoxic shock in d‐(+)‐galactosamine‐sensitized C3H/HeN mice. OK‐432 did not affect the TNFα production in blood, but it did decrease the susceptibility to TNFα. Furthermore, an acceleration of LPS clearance from blood was detected. The pretreatment of OK‐432 also decreased the lethality of mice in bacterial infection caused by P. aeruginosa and S. enteritidis. The rapid decrease of the viable bacteria from the circulating blood and in spleen and liver in mice was observed in a manner similar to LPS clearance. These findings indicate that the protective effect of OK‐432 against the endotoxemia and bacteremia may depend on an up‐regulation of clearance of LPS and bacteria and the augmented resistance to TNFα.
Suppressive Mechanisms of EPA on Human T Cell Proliferation
Authors: Terada Sachiyo , Takizawa Mari , Yamamoto Shigeru , Ezaki Osamu , Itakura Hiroshige , Akagawa Kiyoko S. 
Published: November 2013

AbstractIn vivo and in vitro experiments show that polyunsaturated fatty acids (PUFAs) including eicosapentaenoic acid (EPA) inhibit mitogen‐ or antigen‐stimulated proliferation of T cells in rodents and humans. However, the exact manner and mechanisms by which PUFA inhibits T cell proliferation is not clear. In the present study, we investigated the suppressive effects of EPA, an n‐3 PUFA, on PHA stimulated human peripheral blood T cells. Our results showed that EPA suppresses mitogen‐ or antigen‐stimulated human T cell proliferation by at least 2 steps; step 1) EPA suppresses T cell proliferation by inhibiting IL‐2Rα expression and IL‐2 production; step 2) EPA induces cell death of blast T cells without reducing the expression of IL‐2Rα. We also showed that EPA selectively stimulates the cell death of blast T cells but not resting T cells. The suppressive effect of EPA was mediated via the production of reactive oxygen products, because EPA‐stimulated H2O2 production and the suppressive effect of EPA was restored by addition of catalase or NAC. These results taken together suggest that such immunosuppressive effects of EPA may explain the apparent benefits of EPA‐enriched diets for patients with inflammatory disorders.
Role of V3 Independent Domains on a Dualtropic Human Immunodeficiency Virus Type 1 (HIV‐1) Envelope gp120 in CCR5 Coreceptor Utilization and Viral Infectivity
Authors: Foda Mohamed , Harada Shinji , Maeda Yosuke 
Published: November 2013

AbstractThe molecular mechanism of human immunodeficiency virus type 1 (HIV‐1) entry into cells involves specific interactions between the viral envelope glycoprotein gp120 and two target cell proteins, CD4 and either CCR5 or CXCR4 chemokine receptors. In order to delineate the functional role of HIV‐1 gp120 subdomains of dualtropic strains in CCR5 coreceptor usage, we used a panel of chimeric viruses in which the V1/V2 and V3 domains of gp120 from the dualtropic HIV‐1KMT isolate were introduced either alone or in combination into the T‐tropic HIV‐1NL4–3 background. These chimeric constructs were employed in cell‐cell fusion and cell‐free virus infectivity assays using cell lines expressing CD4 and the CCR5 chemokine receptor. In both assays, the V3 domain of HIV‐1KMT but not the V1/V2 domain proved to be the principal determinant of CCR5 coreceptor usage. However, in the cell‐free viral infectivity assay although a chimeric virus with a combined V1/V2 and V3 domains of HIV‐1KMT efficiently fused with coreceptor expressing cells, yet its infectivity was markedly diminished in CCR5 as well as CXCR4 expressing cells. Restoring a comparable level of infection of such chimeric virus required the C3‐V5 domain from HIV‐1KMT to be introduced. Our present findings confirmed that the V3 domain is the major determinant of fusion activity and cellular tropism, and demonstrated a dispensable role for the V1/V2 domain. In addition the C3‐V5 domain appeared to play an important role in viral infectivity when the corresponding V1/V2 and V3 domains are present.
Molecular Ecology of Toxigenic Vibrio cholerae
Authors: Faruque Shah M. , Nair G. Balakrish 
Published: November 2013

AbstractToxigenic Vibrio cholerae is the etiological agent of cholera, an acute dehydrating diarrhea that occurs in epidemic form in many developing countries. Although V. cholerae is a human pathogen, aquatic ecosystems are major habitats of Vibrio species, which includes both pathogenic and nonpathogenic strains that vary in their virulence gene content. V. cholerae belonging to the O1 and O139 serogroups is commonly known to carry a set of virulence genes necessary for pathogenesis in humans. Recent studies have indicated that virulence genes or their homologues are also dispersed among environmental strains of V. cholerae belonging to diverse serogroups, which appear to constitute an environmental reservoir of virulence genes. Although the definitive roles of the virulence‐associated factors in the environment, and the environmental selection pressures for V. cholerae‐carrying virulence genes or their homologues is not clear, the potential for origination of new epidemic strains from environmental progenitors seems real. It is likely that the aquatic environment harbors different virulence‐associated genes scattered among environmental vibrios, which possess a lower virulence potential than the epidemic strains. The ecosystem comprising the aquatic environment, V. cholerae, genetic elements mediating gene transfer, and the mammalian host appears to support the clustering of critical virulence genes in a proper combination leading to the origination of new V. cholerae strains with epidemic potential.
Association of a Regulatory Gene, slyA with a Mouse Virulence of Salmonella Serovar Choleraesuis
Authors: Kaneko Aki , Mita Masaharu , Sekiya Kachiko , Matsui Hidenori , Kawahara Kazuyoshi , Danbara Hirofumi 
Published: November 2013

AbstractThe influence of slyA gene, originally found in Salmonella serovar Typhimurium as a regulatory gene for the expression of virulence genes, on a mouse virulence of S. serovar Choleraesuis was investigated by using an slyA‐defective mutant. The defective mutant was constructed by the insertion of a kanamycin‐resistance gene (aph) into the cloned slyA gene, and the homologous recombination with the intact slyA gene on the chromosome. The mutant strain showed the LD50 value for BALB/c mouse approximately 105 higher than that of the parent strain. The increase of the LD50 value was the same order as that shown by the mutation of the slyA gene of S. serovar Typhimurium, although LD50 of the wild‐type strain of S. serovar Choleraesuis was 40‐fold higher than that of S. serovar Typhimurium. The time course of infection observed in the mice organs also proved the clear difference of the virulence between the parent and the mutant strains. These results suggested that the slyA gene product functions as a virulence‐associated regulator also in S. serovar Choleraesuis.
Chemokine Production by Rat Macrophages Stimulated with Streptolysin O from Streptococcus pyogenes
Authors: Mitsui Ken‐ichiro , Takano Katsuhiko , Nakatani Sumie , Nambu Hidemi , Shibata Futoshi , Nakagawa Hideo 
Published: November 2013

AbstractThe contribution of streptolysin O (SLO) from Streptococcus pyogenes to neutrophil infiltration in inflammatory lesions was determined by production of cytokine‐induced neutrophil chemoattractant (CINC)−1, −2 and −3, and macrophage inflammatory protein (MIP)‐1α by rat macrophages stimulated with SLO in culture. Active SLO induced the production of CINCs and MIP‐1α in dose‐ and time‐dependent manners. These inductions were ascertained by chemokine mRNA expression in macrophages. Streptolysin S was without effect. The SLO‐cholesterol complex induced the chemokine production in proportion to the residual hemolytic activity of the complex. In addition, the effects of SLO on the chemokine production were confirmed by the injection of active SLO into the preformed air pouch on the back of rats. The infiltration of neutrophils into the pouch fluid (exudate) increased steadily with a lag phase of about 2 hr. The major chemokine found in exudates was MIP‐1α but not CINCs. In this study, it became clear that active SLO, but not the inactive one, contributed to the production of MIP‐1α and CINCs in the conditioned medium and in exudates.
Characterization of the Outermembrane Proteins of Vibrio cholerae Expressed in In Vivo Culture
Authors: Nakasone Noboru , Iwanaga Masaaki 
Published: November 2013

AbstractTwo outer membrane proteins (Omps) of Vibrio cholerae O1, expressed in the intestine (in vivo) but not in culture media (in vitro), were investigated. The molecular masses of those proteins were 116 kDa and 15 kDa, and they were not associated with iron‐regulated proteins. Convalescent cholera patients' sera reacted with the 15 kDa protein but not with the 116 kDa protein. The N‐terminal amino acid sequence of the 15 kDa protein was homologous to V. cholerae OmpT. Anti‐serum to the 15 kDa protein caused agglutination of the organisms grown in the intestine, but not the organisms in in vitro culture. The antiserum was bactericidal, but it did not inhibit the adhesion of the organisms to the intestine and HEp‐2 cells. These findings suggest the possibility that the 15 kDa protein could be involved in post‐infection immunity.