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Institution

Tokyo University of Science

EducationTokyo, Japan
About: Tokyo University of Science is a education organization based out in Tokyo, Japan. It is known for research contribution in the topics: Catalysis & Thin film. The organization has 15800 authors who have published 24147 publications receiving 438081 citations. The organization is also known as: Tōkyō Rika Daigaku & Science University of Tokyo.


Papers
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Journal ArticleDOI
TL;DR: Bi2W2O9, Bi2WO6, and Bi3TiNbO9 consisting of layered structure with perovskite slabs interleaved with Bi2O2 layers showed photocatalytic activities for H2 evolution from an aqueous methanol solution and O 2 evolution from aqueously silver nitrate solution.
Abstract: Bi2W2O9, Bi2WO6, and Bi3TiNbO9 consisting of layered structure with perovskite slabs interleaved with Bi2O2 layers showed photocatalytic activities for H2 evolution from an aqueous methanol solution and O2 evolution from an aqueous silver nitrate solution. Bi2WO6 with the Aurivillius structure and a 2.8 eV band gap was active for the O2 evolution reaction under visible light irradiation (λ > 420 nm).

442 citations

Journal ArticleDOI
TL;DR: The results indicate that cellular states are constrained by complex networks involving both positive and negative regulatory interactions among substantial numbers of transcription factors and that no single transcription factor is both necessary and sufficient to drive the differentiation process.
Abstract: Using deep sequencing (deepCAGE), the FANTOM4 study measured the genome-wide dynamics of transcription-start-site usage in the human monocytic cell line THP-1 throughout a time course of growth arrest and differentiation. Modeling the expression dynamics in terms of predicted cis-regulatory sites, we identified the key transcription regulators, their time-dependent activities and target genes. Systematic siRNA knockdown of 52 transcription factors confirmed the roles of individual factors in the regulatory network. Our results indicate that cellular states are constrained by complex networks involving both positive and negative regulatory interactions among substantial numbers of transcription factors and that no single transcription factor is both necessary and sufficient to drive the differentiation process.

441 citations

Journal ArticleDOI
TL;DR: Cilostazol seems to be non-inferior, and might be superior, to aspirin for prevention of stroke after an ischaemic stroke, and was associated with fewer haemorrhagic events.
Abstract: Summary Background The antiplatelet drug cilostazol is efficacious for prevention of stroke recurrence compared with placebo. We designed the second Cilostazol Stroke Prevention Study (CSPS 2) to establish non-inferiority of cilostazol versus aspirin for prevention of stroke, and to compare the efficacy and safety of cilostazol and aspirin in patients with non-cardioembolic ischaemic stroke. Methods Patients aged 20–79 years who had had a cerebral infarction within the previous 26 weeks were enrolled at 278 sites in Japan and allocated to receive 100 mg cilostazol twice daily or 81 mg aspirin once daily for 1–5 years. Patients were allocated according to a computer-generated randomisation sequence by means of a dynamic balancing method using patient information obtained at registration. All patients, study personnel, investigators, and the sponsor were masked to treatment allocation. The primary endpoint was the first occurrence of stroke (cerebral infarction, cerebral haemorrhage, or subarachnoid haemorrhage). The predefined margin of non-inferiority was an upper 95% CI limit for the hazard ratio of 1·33. Analyses were by full-analysis set. This trial is registered with ClinicalTrials.gov, number NCT00234065. Findings Between December, 2003, and October, 2006, 2757 patients were enrolled and randomly allocated to receive cilostazol (n=1379) or aspirin (n=1378), of whom 1337 on cilostazol and 1335 on aspirin were included in analyses; mean follow-up was 29 months (SD 16). The primary endpoint occurred at yearly rates of 2·76% (n=82) in the cilostazol group and 3·71% (n=119) in the aspirin group (hazard ratio 0·743, 95% CI 0·564–0·981; p=0·0357). Haemorrhagic events (cerebral haemorrhage, subarachnoid haemorrhage, or haemorrhage requiring hospital admission) occurred in fewer patients on cilostazol (0·77%, n=23) than on aspirin (1·78%, n=57; 0·458, 0·296–0·711; p=0·0004), but headache, diarrhoea, palpitation, dizziness, and tachycardia were more frequent in the cilostazol group than in the aspirin group. Interpretation Cilostazol seems to be non-inferior, and might be superior, to aspirin for prevention of stroke after an ischaemic stroke, and was associated with fewer haemorrhagic events. Therefore, cilostazol could be used for prevention of stroke in patients with non-cardioembolic stroke. Funding Otsuka Pharmaceutical.

440 citations

Journal ArticleDOI
TL;DR: In this system, photogenerated electrons in the TiO2 with an n-type semiconductor character transferred to the metal sulfide through a reduced graphene oxide to achieve water splitting, and this system was active for solar water splitting.
Abstract: Z-schematic water splitting was successfully demonstrated using metal sulfide photocatalysts that were usually unsuitable for water splitting as single particulate photocatalysts due to photocorrosion. When metal sulfide photocatalysts with a p-type semiconductor character as a H2-evolving photocatalyst were combined with reduced graphene oxide-TiO2 composite as an O2-evolving photocatalyst, water splitting into H2 and O2 in a stoichiometric amount proceeded. In this system, photogenerated electrons in the TiO2 with an n-type semiconductor character transferred to the metal sulfide through a reduced graphene oxide to achieve water splitting. Moreover, this system was active for solar water splitting.

436 citations

Journal ArticleDOI
08 Sep 2011-Nature
TL;DR: It is demonstrated that T SLP promotes systemic basophilia, that disruption of TSLP–TSLPR interactions results in defective basophil responses, and that TSLPR-sufficient basophils can restore TH2-cell-dependent immunity in vivo.
Abstract: CD4(+) T-helper type 2 (T(H)2) cells, characterized by their expression of interleukin (IL)-4, IL-5, IL-9 and IL-13, are required for immunity to helminth parasites and promote the pathological inflammation associated with asthma and allergic diseases. Polymorphisms in the gene encoding the cytokine thymic stromal lymphopoietin (TSLP) are associated with the development of multiple allergic disorders in humans, indicating that TSLP is a critical regulator of T(H)2 cytokine-associated inflammatory diseases. In support of genetic analyses, exaggerated TSLP production is associated with asthma, atopic dermatitis and food allergies in patients, and studies in murine systems demonstrated that TSLP promotes T(H)2 cytokine-mediated immunity and inflammation. However, the mechanisms through which TSLP induces T(H)2 cytokine responses remain poorly defined. Here we demonstrate that TSLP promotes systemic basophilia, that disruption of TSLP-TSLPR interactions results in defective basophil responses, and that TSLPR-sufficient basophils can restore T(H)2-cell-dependent immunity in vivo. TSLP acted directly on bone-marrow-resident progenitors to promote basophil responses selectively. Critically, TSLP could elicit basophil responses in both IL-3-IL-3R-sufficient and -deficient environments, and genome-wide transcriptional profiling and functional analyses identified heterogeneity between TSLP-elicited versus IL-3-elicited basophils. Furthermore, activated human basophils expressed TSLPR, and basophils isolated from eosinophilic oesophagitis patients were distinct from classical basophils. Collectively, these studies identify previously unrecognized heterogeneity within the basophil cell lineage and indicate that expression of TSLP may influence susceptibility to multiple allergic diseases by regulating basophil haematopoiesis and eliciting a population of functionally distinct basophils that promote T(H)2 cytokine-mediated inflammation.

436 citations


Authors

Showing all 15878 results

NameH-indexPapersCitations
Kazunori Kataoka13890870412
Yoichiro Iwakura12970564041
Kouji Matsushima12459056995
Masaki Ishitsuka10362439383
Shinsuke Tanabe9872237445
Tatsumi Koi9741150222
Hirofumi Akagi9461843179
Clifford A. Lowell9125823538
Teruo Okano9160528346
László Á. Gergely8942660674
T. Sumiyoshi8885562277
Toshinori Nakayama8640525275
Akihiko Kudo8632839475
Hans-Joachim Gabius8569928085
Motohide Tamura85100732725
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202356
2022137
20211,357
20201,481
20191,510
20181,429