Institution
Osaka University
Education•Osaka, Japan•
About: Osaka University is a education organization based out in Osaka, Japan. It is known for research contribution in the topics: Laser & Population. The organization has 83778 authors who have published 185669 publications receiving 5158122 citations. The organization is also known as: Ōsaka daigaku.
Topics: Laser, Population, Catalysis, Thin film, Gene
Papers published on a yearly basis
Papers
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University of Cologne1, University of Freiburg2, Fred Hutchinson Cancer Research Center3, University of Regensburg4, University of Liverpool5, Lund University6, University of Basel7, Discovery Institute8, Imperial College London9, Northwestern University10, National Institutes of Health11, Stanford University12, University of Manchester13, French Institute of Health and Medical Research14, Washington University in St. Louis15, Yokohama City University16, Karolinska Institutet17, Vanderbilt University18, Harvard University19, Max Planck Society20, Osaka University21, University of Copenhagen22, Thomas Jefferson University23, University of Helsinki24, University of Erlangen-Nuremberg25, Rutgers University26
TL;DR: A new identification system for a trimer using three Arabic numerals, based on the alpha, beta and gamma chain numbers is introduced, which is introduced for laminin trimers.
836 citations
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TL;DR: A stromal cell line, PA6, was found to produce a soluble mediator, which was distinct from interleukin 7 (IL-7) and stem cell factor and supported the proliferation of a stromAL cell-dependent pre-B-cell clone, DW34.
Abstract: Generation and proliferation of early B-cell progenitors have been known to require stromal cell-derived molecules. A stromal cell line, PA6, was found to produce a soluble mediator, which was distinct from interleukin 7 (IL-7) and stem cell factor and supported the proliferation of a stromal cell-dependent pre-B-cell clone, DW34. A cDNA clone encoding this DW34 growth-stimulating factor was isolated by expression cloning. The nucleotide sequence contained a single substantial open reading frame of 267 nucleotides encoding an 89-amino acid polypeptide. The amino acid sequence of this cytokine, designated pre-B-cell growth-stimulating factor (PBSF), revealed that it is a member of intercrine alpha subfamily. Recombinant PBSF stimulated the proliferation of DW34 cells for itself and, furthermore, synergistically augmented the growth of DW34 as well as bone marrow B-cell progenitors in the presence of IL-7.
833 citations
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TL;DR: Results indicate that TRAF2 plays crucial roles not only in the signaling of the c-Jun N-terminal kinase pathway but also in activation of caspase-12 to transduce signals from IRE1s, providing a missing link in the ER stress-induced apoptosis-signaling pathway.
831 citations
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TL;DR: Results suggest that conversion of Asp-816 to Val in human c-kitR may be an activating mutation and responsible for the constitutive activation of c-KitR in HMC-1 cells.
Abstract: The c-kit proto-oncogene encodes a receptor tyrosine kinase. Binding of c-kit ligand, stem cell factor (SCF) to c-kit receptor (c-kitR) is known to activate c-kitR tyrosine kinase, thereby leading to autophosphorylation of c-kitR on tyrosine and to association of c-kitR with substrates such as phosphatidylinositol 3-kinase (PI3K). In a human mast cell leukemia cell line HMC-1, c-kitR was found to be constitutively phosphorylated on tyrosine, activated, and associated with PI3K without the addition of SCF. The expression of SCF mRNA transcript in HMC-1 cells was not detectable by means of PCR after reverse transcription (RT-PCR) analysis, suggesting that the constitutive activation of c-kitR was ligand independent. Sequencing of whole coding region of c-kit cDNA revealed that c-kit genes of HMC-1 cells were composed of a normal, wild-type allele and a mutant allele with two point mutations resulting in intracellular amino acid substitutions of Gly-560 for Val and Val-816 for Asp. Amino acid sequences in the regions of the two mutations are completely conserved in all of mouse, rat, and human c-kit. In order to determine the causal role of these mutations in the constitutive activation, murine c-kit mutants encoding Gly-559 and/or Val-814, corresponding to human Gly-560 and/or Val-816, were constructed by site-directed mutagenesis and expressed in a human embryonic kidney cell line, 293T cells. In the transfected cells, both c-kitR (Gly-559, Val-814) and c-kitR (Val-814) were abundantly phosphorylated on tyrosine and activated in immune complex kinase reaction in the absence of SCF, whereas tyrosine phosphorylation and activation of c-kitR (Gly-559) or wild-type c-kitR was modest or little, respectively. These results suggest that conversion of Asp-816 to Val in human c-kitR may be an activating mutation and responsible for the constitutive activation of c-kitR in HMC-1 cells.
826 citations
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King's College1, Carlos III Health Institute2, King's College London3, Georgia Regents University4, Baylor College of Medicine5, Osaka University6, Southern General Hospital7, University of Naples Federico II8, Tel Aviv University9, Icahn School of Medicine at Mount Sinai10, St Thomas' Hospital11, Royal College of Nursing12, Emory University13, Fukuoka University14, North Tyneside General Hospital15, University of Kent16, Royal Free Hospital17
TL;DR: NMSS can be used to assess the frequency and severity of NMS in PD patients across all stages in conjunction with the recently validated non‐motor questionnaire.
Abstract: Non-motor symptoms (NMS) in Parkinson's disease (PD) are common, significantly reduce quality of life and at present there is no validated clinical tool to assess the progress or potential response to treatment of NMS. A new 30-item scale for the assessment of NMS in PD (NMSS) was developed. NMSS contains nine dimensions: cardiovascular, sleep/fatigue, mood/cognition, perceptual problems, attention/memory, gastrointestinal, urinary, sexual function, and miscellany. The metric attributes of this instrument were analyzed. Data from 242 patients mean age 67.2 +/- 11 years, duration of disease 6.4 +/- 6 years, and 57.3% male across all stages of PD were collected from the centers in Europe, USA, and Japan. The mean NMSS score was 56.5 +/- 40.7, (range: 0-243) and only one declared no NMS. The scale provided 99.2% complete data for the analysis with the total score being free of floor and ceiling effect. Satisfactory scaling assumptions (multitrait scaling success rate >95% for all domains except miscellany) and internal consistency were reported for most of the domains (mean alpha, 0.61). Factor analysis supported the a prori nine domain structure (63% of the variance) while a small test-retest study showed satisfactory reproducibility (ICC > 0.80) for all domains except cardiovascular (ICC = 0.45). In terms of validity, the scale showed modest association with indicators of motor symptom severity and disease progression but a high correlation with other measures of NMS (NMSQuest) and health-related quality of life measure (PDQ-8) (both, rS = 0.70). In conclusion, NMSS can be used to assess the frequency and severity of NMS in PD patients across all stages in conjunction with the recently validated non-motor questionnaire.
826 citations
Authors
Showing all 84130 results
Name | H-index | Papers | Citations |
---|---|---|---|
Shizuo Akira | 261 | 1308 | 320561 |
Thomas C. Südhof | 191 | 653 | 118007 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Yusuke Nakamura | 179 | 2076 | 160313 |
H. S. Chen | 179 | 2401 | 178529 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Kenji Kangawa | 153 | 1117 | 110059 |
Jongmin Lee | 150 | 2257 | 134772 |
Yoshio Bando | 147 | 1234 | 80883 |
Takeo Kanade | 147 | 799 | 103237 |
Olaf Reimer | 144 | 716 | 74359 |
Yuji Matsuzawa | 143 | 836 | 116711 |
Kim Nasmyth | 142 | 294 | 59231 |
Tasuku Honjo | 141 | 712 | 88428 |