// +author:h adachi +author:adachi 
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{userid:"a.agrawal", "articletype":"article","pages":"817-822","author":"Anurag Agrawal, Roberto Adachi, Michael Tuvim, Xiao-Tian Yan, Abigail H Teich, Burton F Dickey","year":"2000","title":"Gene structure and promoter function of murine Munc18-2, a nonneuronal exocytic Sec1 homolog","month":"","journal":"Biochemical and Biophysical Research Communications","publisher":"Elsevier","volume":"276","number":"3","note":"","tags":"","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"","doi":"","isi":"","pubmed":"","key":"agrawal2000gene","howpublished":"","urllink":"","refid":7}
,

{userid:"junji_yodoi", "articletype":"article","pages":"261-275","author":"T Nagai, M Adachi, N Noro, J Yodoi, H Uchino","year":"1985","title":"T and B lymphocytes with immunoglobulin E Fc receptors (Fc epsilon R) in patients with nonallergic hyperimmunoglobulinemia E: demonstration using a monoclonal antibody against Fc epsilon R-associated antigen.","month":"Jun","journal":"Clin Immunol Immunopathol","publisher":"","volume":"35","number":"3","note":"","tags":"Adult,Angiolymphoid Hyperplasia with Eosinophilia,Antibodies, Monoclonal,Antigens, Surface,B-Lymphocytes,Humans,Hypergammaglobulinemia,Immunoglobulin E,Lymphocytes,Male,Middle Aged,Receptors, Fc,Receptors, IgE,Rosette Formation,T-Lymphocytes","booktitle":"","editor":"","abstract":"T and B cells bearing Fc receptors for IgE (Fc epsilon R) were studied in 7 patients with hyperimmunoglobulinemia E (2 with hyper IgE syndrome and 5 with Kimura's disease). Fc epsilon R was detected by both rosette formation with IgE-coated red cells (Eo'-IgE) and immunofluorescence assay using H107 monoclonal antibody recognizing a determinant(s) associated with lymphocyte Fc epsilon R. A high correlation was observed between the proportions of Eo'-IgE rosette-forming cells (RFC) and H107+ cells. All patients had a large number of Fc epsilon R-positive cells (mean +\/- 1 SD; 9.7 +\/- 3.7% Eo'-IgE-RFC, 8.4 +\/- 3.4% H107+ cells) in contrast to those of 6 normal subjects (0.7 +\/- 1.2% Eo'-IgE-RFC, 0.3 +\/- 0.4% H107+ cells). In one patient with Kimura's disease, the presence of Fc epsilon R-bearing T cells was confirmed by two-dimensional flow cytometry, using fluorescein isothiocyanate (FITC)-H107 and phycoerythrin (PE)-Leu-1. H107 antigens seemed to be expressed on both helper\/inducer and suppressor T-cell populations. The direct analysis of Fc epsilon R+ T cells by 2-D flow cytometry with H107 antibody may facilitate the study of hyperimmunoglobulinemia E.","address":"","school":"","issn":"0090-1229","doi":"","isi":"","pubmed":"3157519","key":"Nagai1985","howpublished":"","urllink":"","refid":435}
,

{userid:"junji_yodoi", "articletype":"article","pages":"417-424","author":"T Nagai, K Nagai, M Adachi, H Uchino, J Yodoi, K Takatsuki","year":"1982","title":"In vitro production of IgE by human peripheral blood lymphocytes. Effect of serum from patients with Kimura's disease.","month":"","journal":"Arerugi","publisher":"","volume":"31","number":"7","note":"","tags":"Adult,Antibody Formation,Cells, Cultured,Eosinophilic Granuloma,Humans,Immune Sera,Immunoglobulin E,Lymphocytes,Male,Middle Aged,Plaque Assay","booktitle":"","editor":"","abstract":"","address":"","school":"","issn":"0021-4884","doi":"","isi":"","pubmed":"7181663","key":"Nagai1982","howpublished":"","urllink":"","refid":459}
,

{userid:"junji_yodoi", "articletype":"article","pages":"65-71","author":"M Adachi, J Yodoi, N Noro, T Masuda, H Uchino","year":"1984","title":"Murine IgA binding factors produced by Fc alpha R(+) T cells: role of Fc gamma R(+) cells for the induction of Fc alpha R and formation of IgA-binding factor in Con A-activated cells.","month":"Jul","journal":"J Immunol","publisher":"","volume":"133","number":"1","note":"","tags":"Animals,Antibodies, Monoclonal,Antigens, CD,Concanavalin A,Immunoglobulin A,Leukemia L5178,Lymphocyte Activation,Lymphokines,Mice,Mice, Inbred BALB C,Mice, Inbred DBA,Prostatic Secretory Proteins,Receptors, Fc,Receptors, IgG,Stem Cells,T-Lymphocytes","booktitle":"","editor":"","abstract":"The relationship between the production of a T cell factor having affinity for IgA (IgA-binding factor(s); IgA BF) and the expression of Fc receptors specific for IgA (Fc alpha R) was studied by using murine spleen cells activated with concanavalin A (Con A blasts). Fc alpha R was detected by the cytophilic binding of anti-TNP murine IgA myeloma protein (MOPC 315 IgA) to Con A blasts as determined by an indirect rosette method with trinitrophenylated sheep red blood cells (TNP-SRBC). After 18 hr preculture with IgA, Fc alpha R was expressed on 15 to 20% of Con A blasts, which released IgA BF suppressing the in vitro IgA synthesis of the spleen cells stimulated with pokeweed mitogen (PWM). Without preculture with IgA, there was neither induction of Fc alpha R nor the production of IgA BF from Con A blasts. Fc alpha R was not induced on Con A blasts by IgA if Fc gamma R(+) cells were depleted from the blasts by rosetting with SRBC sensitized with rabbit IgG antibody (EA gamma). Even after preculture with IgA, the suppressive IgA BF was undetectable in the culture supernatant of Con A blasts depleted of the Fc gamma R(+) cell population. By using a double rosette method with EA gamma and trinitrophenylated quail red blood cells, Fc alpha R proved to be co-expressed on Fc gamma R(+) precursor T cells in the Con A blasts. The results suggested that both Fc gamma R and Fc alpha R could be co-expressed on Con A blasts, as is the case with T2D4 Fc gamma R(+), Fc alpha R(+) T hybridoma cells, which are known to produce IgG-binding factor(s) (IgG BF) and IgA BF. The relationship between Fc gamma R and Fc alpha R on a single cell was studied by using monoclonal anti-Fc gamma R antibody (2. 4G2 ). The reactivity of 2. 4G2 antibody with T cell Fc gamma R was proved by the inhibition of EA gamma rosette formation by Con A blasts or T2D4 cells. The addition of 2. 4G2 monoclonal antibody, however, did not affect the induction of Fc alpha R on Con A blasts by IgA. Furthermore, the binding of IgA to Fc alpha R already expressed on L5178Y T lymphoma cell line cells was not inhibited by the monoclonal antibody. The results confirmed that Fc alpha R are distinct from Fc gamma R co-expressed on the same Con A blasts, and that the expression of Fc alpha R on Fc gamma R(+) T cells and their production of suppressive IgA BF may be induced by the binding of IgA to Fc alpha R.","address":"","school":"","issn":"0022-1767","doi":"","isi":"","pubmed":"6233376","key":"Adachi1984","howpublished":"","urllink":"","refid":446}
,

{userid:"junji_yodoi", "articletype":"article","pages":"1246-1251","author":"M Adachi, J Yodoi, T Masuda, K Takatsuki, H Uchino","year":"1983","title":"Altered expression of lymphocyte Fc alpha receptor in selective IgA deficiency and IgA nephropathy.","month":"Sep","journal":"J Immunol","publisher":"","volume":"131","number":"3","note":"","tags":"Animals,Antigens, CD,Dysgammaglobulinemia,Glomerulonephritis,Humans,IgA Deficiency,Immunoglobulin A,Lymphocyte Culture Test, Mixed,Lymphocytes,Mice,Mice, Inbred BALB C,Mice, Inbred C3H,Plasmacytoma,Receptors, Fc,Rosette Formation","booktitle":"","editor":"","abstract":"To study the expression of FcR specific for IgA (Fc alpha R) on human peripheral lymphocytes (PBL), PBL from normal donors were incubated with 300 to 500 micrograms\/ml MOPC 315 IgA having anti-trinitrophenyl (TNP) antibody activity at 4 degrees C or 37 degrees C for 60 min. Under this condition, less than 2% of total cells could form rosettes with TNP-coated ox red blood cells (TNP-ORBC). When cultured with MOPC 315 IgA at 37 degrees C for 18 hr, however, there was a dose-dependent increase of the rosette-forming cells (RFC) binding TNP-ORBC. Because 15 to 20% of the total cells bound TNP-ORBC but not unsensitized ORBC, the rosette formation appeared to be due to the cytophilic binding of IgA to the cells. The binding of MOPC 315 IgA was competed by TEPC 15 IgA and human myeloma IgA, but not by murine myeloma proteins of other classes, indicating that the receptor is specific for IgA. Fc alpha R was induced on 15 to 20% of fractionated T and B cells, as well as on 15 to 18% of concanavalin A-(Con A) activated lymphocytes when cultured with IgA. The induction of the receptor was dependent on protein and RNA synthesis, but not on DNA synthesis as suggested by the sensitivity to metabolic inhibitors, such as mitomycin C, actinomycin D, puromycin, and cycloheximide. In five patients with selective IgA deficiency (serum IgA, 0 to 4 mg\/dl), only 5.1% +\/- 1.7 of PBL formed rosettes with TNP-ORBC after culture with MOPC 315 IgA, whereas 12.5% +\/- 2.5 of PBL from normal donors (serum IgA, 90 to 330 mg\/dl) formed rosettes. Fc alpha R was induced on more than 15% of the cells from these patients, however, when cultured with IgA in the presence of a conditioned medium obtained from mixed lymphocyte culture from two normal donors. The results suggested that the abnormality in the patients' PBL might be in the induction mechanism rather than in the number of precursor cells that could express Fc alpha R in the presence of IgA. On the other hand, Fc alpha R was induced on 10.4% +\/- 1.5 of PBL from the patients with IgA nephropathy (serum IgA, 382 +\/- 11 mg\/dl) when they were incubated with IgA for 1 hr at 37 degrees C. Because Fc alpha R on normal PBL was not induced by 1 hr of incubation with IgA, it appeared that the receptor was already expressed in vivo on the cells of these patients.","address":"","school":"","issn":"0022-1767","doi":"","isi":"","pubmed":"6224855","key":"Adachi1983","howpublished":"","urllink":"","refid":450}
,

{userid:"chikara.ohtsuki", "refid":170,"repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Synthesis and insulin-mimetic activities of metal complexes with 3-hydroxypyridine-2-carboxylic acid","year":"2005","author":"M Nakai, F Sekiguchi, M Obata, C Ohtsuki, Y Adachi, H Sakurai, C Orvig, D Rehder and S Yano","journal":"Journal of Inorgic Biochemistry","volume":"99","number":"6","pages":"1275-1282","month":"April","doi":"10.1016\/j.jinorgbio.2005.02.026 ","pubmed":"15917081","pdflink":"","urllink":"","abstract":"","note":"","tags":""}
,

{userid:"junji_yodoi", "articletype":"article","pages":"551-559","author":"J Yodoi, M Adachi, K Teshigawara, T Masuda, W H Fridman","year":"1983","title":"T-cell hybridoma co-expressing Fc receptors for different isotypes. I. Reciprocal regulation of Fc alpha R and Fc gamma R expression by IgA and interferon.","month":"Mar","journal":"Immunology","publisher":"","volume":"48","number":"3","note":"","tags":"Animals,Antibody Specificity,Antigens, CD,Hybridomas,Immunoglobulin A,Interferon Type I,Mice,Mice, Inbred Strains,Neoplasms, Experimental,Receptors, Fc,Receptors, IgG,Rosette Formation,T-Lymphocytes","booktitle":"","editor":"","abstract":"To clarify the co-expression phenomenon of T-cell Fc receptors (FcR) specific for different isotypes on the clonal level, a murine hybridoma clone T2D4 was studied. T2D4 cells originally reported to bear FcR for IgG (Fc gamma R) and to release a Fc gamma R-related T-cell factor binding to IgG (immunoglobulin binding factor; IBF) proved to have also the receptor for IgA. The binding of IgA was detected by rosette formation with trinitrophenylated ox red blood cells (TNP-ORBC) after preincubation of T2D4 cells with MOPC 315 IgA having anti-TNP activity, or directly with TNP-ORBC sensitized with MOPC 315 IgA. While the binding of MOPC 315 IgA was competed for by IgA but not by IgG2A nor IgG2B, IgA failed to inhibit the rosette formation of the cells with ORBC sensitized with rabbit IgG antibody (EA ox gamma), proving that T2D4 cells express FcR specific for IgA (Fc alpha R) in addition to Fc gamma R. Co-expression of both receptors on the same cell surface was demonstrated by a double rosette technique using TNP-quail red blood cells (TNP-QRBC) and EAox gamma. Fc alpha R activity of the cells was completely abrogated by 15 min. incubation with 0.1 mg\/ml trypsin, whereas Fc gamma R was resistant even to 1 mg\/ml trypsin. The expression of Fc alpha R was augmented (up-regulation) by IgA at the concentration above 300 micrograms\/ml and inhibited (down-regulation) by 1000 u.\/ml of murine beta-interferon (beta-IFN). Conversely, the expression of Fc gamma R was down-regulated by IgA and up-regulated by alpha-IFN. Thus, Fc gamma R and Fc alpha R are co-expressed and reciprocally regulated on these cell lines. The possible co-production of IBF and the Fc alpha R-related binding factor specific for IgA is discussed.","address":"","school":"","issn":"0019-2805","doi":"","isi":"","pubmed":"6219065","key":"Yodoi1983","howpublished":"","urllink":"","refid":454}
,

{userid:"junji_yodoi", "articletype":"article","pages":"303-310","author":"J Yodoi, M Adachi, K Teshigawara, M Miyamainaba, T Masuda, W H Fridman","year":"1983","title":"T cell hybridomas coexpressing Fc receptors (FcR) for different isotypes. II. IgA-induced formation of suppressive IgA binding factor(s) by a murine T hybridoma bearing Fc gamma R and Fc alpha R.","month":"Jul","journal":"J Immunol","publisher":"","volume":"131","number":"1","note":"","tags":"Animals,Antibody-Producing Cells,Hemolytic Plaque Technique,Hybridomas,Immune Tolerance,Immunoglobulin A,Immunoglobulin Allotypes,Immunoglobulin M,Mice,Mice, Inbred BALB C,Receptors, Fc,Receptors, IgG,Rosette Formation,T-Lymphocytes","booktitle":"","editor":"","abstract":"T2D4 murine T hybridoma cells have previously been shown to express Fc receptors (FcR) for IgG (Fc gamma R) and for IgA (Fc alpha R) and to produce an IgG binding factor (IgGBF) that suppresses IgG and IgM responses. In the present work we report on the behavior of IgA bound to T2D4 cells and on the production of IgA binding factor (IgABF) and its ability to suppress IgA antibody production. A dose-dependent binding of MOPC315 IgA with anti-TNP activity by T2D4 cells was demonstrated by rosette formation with trinitrophenylated ox red blood cells (TNP-ORBC) and fixation of iodinated DNP-BSA. IgA bound to the cells disappeared after a short-term culture of 3 hr at 37 degrees C, but not at 4 degrees C. Because this phenomenon was inhibited by 0.1% sodium azide and 100 microM dansylcadaverine, a transglutaminase inhibitor, Fc alpha R-IgA complexes seemed to be released by an active process involving receptor movement. In the culture supernatant of IgA-treated T2D4 cells, we detected a factor(s) that binds to IgA-Sepharose and competitively inhibits the binding of IgA to T2D4 cells. The factor (IgABF) failed to inhibit the rosette formation of Fc gamma R(+) cells with IgG-sensitized ORBC (EAox gamma), indicating that it binds specifically to IgA. IgABF was undetectable in the culture supernatants of untreated T2D4 cells of Fc alpha R(-) BW5147 T lymphoma cells used as parent cells for the establishment of the hybridoma. To study the effect of IgABF on antibody formation, culture filtrates of IgA-treated or untreated T2D4 cells were fractionated on IgA-Sepharose beads and were added to BALB\/c spleen cells cultured with pokeweed mitogen. By use of a reverse plaque assay, it was shown that the IgA plaque-forming cell (PFC) response was suppressed by the acid eluate but not by the effluent of IgA-Sepharose beads incubated with the filtrates of IgA-treated T2D4 cell cultures. The suppression was IgA specific, because neither IgG nor IgM responses were suppressed by the eluate. As expected, there was no significant IgA suppressive activity in the acid eluates of the beads incubated with the culture filtrate of untreated T2D4 cells or IgA-treated BW5147 cells. IgA-specific suppressive activity proved to be due to IgA binding factor(s), because suppressive activity in the eluate was completely adsorbed by IgA-Sepharose but not by IgG- nor BSA-Sepharose.","address":"","school":"","issn":"0022-1767","doi":"","isi":"","pubmed":"6223074","key":"Yodoi1983","howpublished":"","urllink":"","refid":452}
,

{userid:"l.mbuagbaw", "articletype":"article","pages":"","author":"Guowei Li, Lawrence Mbuagbaw, Zainab Samaan, Yanling Jin, Ikunna Nwosu, Mitchell A H Levine, Jonathan D Adachi, Lehana Thabane","year":"2017","title":"State of reporting of primary biomedical research: a scoping review protocol.","month":"Mar","journal":"BMJ open","publisher":"","volume":"7","number":"3","note":"","tags":"Biomedical Research,Data Collection,Guideline Adherence,Humans,Practice Guidelines as Topic,Quality Assurance, Health Care,Research Report,Selection Bias,Review Literature as Topic","booktitle":"","editor":"","abstract":"Incomplete or inconsistent reporting remains a major concern in the biomedical literature. Incomplete or inconsistent reporting may yield the published findings unreliable, irreproducible or sometimes misleading. In this study based on evidence from systematic reviews and surveys that have evaluated the reporting issues in primary biomedical studies, we aim to conduct a scoping review with focuses on (1) the state-of-the-art extent of adherence to the emerging reporting guidelines in primary biomedical research, (2) the inconsistency between protocols or registrations and full reports and (3) the disagreement between abstracts and full-text articles.","address":"","school":"","issn":"2044-6055","doi":"10.1016\/j.jclinepi.2011.10.016","isi":"","pubmed":"28360252","key":"Li2017","howpublished":"","urllink":"","refid":126,"weight":126}
,

{userid:"jerilynn.prior", "refid":"109","repocollections":"","attachment":"","_thumb":"","articletype":"article","sectionheading":"","title":"Vertebral fracture status and the World Health Organization risk factors for predicting osteoporotic fracture risk.","year":"2009","author":"Peiqi Chen, John H Krege, Jonathan D Adachi, Jerilynn C Prior, Alan Tenenhouse, Jacques P Brown, Emmanuel Papadimitropoulos, Nancy Kreiger, Wojciech P Olszynski, Robert G Josse, David Goltzman,  ","journal":"Journal of Bone and Mineral Research ","volume":"24","number":"3","pages":"495-502","month":"Mar","doi":"10.1359\/jbmr.081103","pubmed":"19016585","pdflink":"","urllink":"","abstract":"Vertebral fractures are the most common osteoporotic fracture, and patients with prevalent vertebral fractures have a greater risk of future fractures. However, radiographically determined vertebral fractures are not identified as a distinct risk factor in the World Health Organization (WHO) fracture risk assessment tool. The objective of this study was to evaluate and compare potential risk factors including morphometric spine fracture status and the WHO risk factors for predicting 5-yr fracture risk. We hypothesized that spine fracture status provides prognostic information in addition to consideration of the WHO risk factors alone. A randomly selected, population-based community cohort of 2761 noninstitutionalized men and women > or =50 yr of age living within 50 km of one of nine regional centers was enrolled in the Canadian Multicentre Osteoporosis Study (CaMOS), a prospective and longitudinal cohort study following subjects for 5 yr. Prevalent and incident spine fractures were identified from lateral spine radiographs. Incident nonvertebral fragility fractures were determined by an annual, mailed fracture questionnaire with validation, and nonvertebral fragility fracture was defined by investigators as a fracture with minimal trauma. A model considering the WHO risk factors plus spine fracture status provided greater prognostic information regarding future fracture risk than a model considering the WHO risk factors alone. In univariate analyses, age, BMD, and spine fracture status had the highest gradient of risk. A model considering these three risk factors captured almost all of the predictive information provided by a model considering spine fracture status plus the WHO risk factors and provided greater predictive information than a model considering the WHO risk factors alone. The use of spine fracture status along with age and BMD predicted future fracture risk with greater simplicity and higher prognostic accuracy than consideration of the risk factors included in the WHO tool.","note":"","tags":"Adult,Aging,Area Under Curve,Canada,Demography,Female,Femur Neck,Health Status,Humans,Incidence,Male,Middle Aged,Multivariate Analysis,Osteoporosis,Risk Factors,Spinal Fractures,Time Factors,World Health Organization","weight":"112.50000","publisher":"","booktitle":"","editor":"","address":"","school":"","issn":"1523-4681","isi":"","key":"Chen2009","howpublished":""}
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