Institution
Shanghai Jiao Tong University
Education•Shanghai, Shanghai, China•
About: Shanghai Jiao Tong University is a education organization based out in Shanghai, Shanghai, China. It is known for research contribution in the topics: Population & Cancer. The organization has 157524 authors who have published 184620 publications receiving 3451038 citations. The organization is also known as: Shanghai Communications University & Shanghai Jiaotong University.
Topics: Population, Cancer, Microstructure, Cell growth, Metastasis
Papers published on a yearly basis
Papers
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Haidong Wang1, Zulfiqar A Bhutta2, Zulfiqar A Bhutta3, Matthew M Coates1 +610 more•Institutions (263)
TL;DR: The Global Burden of Disease 2015 Study provides an analytical framework to comprehensively assess trends for under-5 mortality, age-specific and cause-specific mortality among children under 5 years, and stillbirths by geography over time and decomposed the changes in under- 5 mortality to changes in SDI at the global level.
591 citations
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TL;DR: Results indicate that TDR is a key component of the molecular network regulating rice tapetum development and degeneration, and two genes, Os CP1 and Os c6, encoding a Cys protease and a protease inhibitor, were shown to be the likely direct targets of TDR.
Abstract: In flowering plants, tapetum degeneration is proposed to be triggered by a programmed cell death (PCD) process during late stages of pollen development; the PCD is thought to provide cellular contents supporting pollen wall formation and to allow the subsequent pollen release. However, the molecular basis regulating tapetum PCD in plants remains poorly understood. We report the isolation and characterization of a rice (Oryza sativa) male sterile mutant tapetum degeneration retardation (tdr), which exhibits degeneration retardation of the tapetum and middle layer as well as collapse of microspores. The TDR gene is preferentially expressed in the tapetum and encodes a putative basic helix-loop-helix protein, which is likely localized to the nucleus. More importantly, two genes, Os CP1 and Os c6, encoding a Cys protease and a protease inhibitor, respectively, were shown to be the likely direct targets of TDR through chromatin immunoprecipitation analyses and the electrophoretic mobility shift assay. These results indicate that TDR is a key component of the molecular network regulating rice tapetum development and degeneration.
587 citations
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TL;DR: GV-971, a sodium oligomannate that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China, suppresses gut dysbiosis and the associated phenylalanine/isoleucine accumulation, harnesses neuroinflammation and reverses the cognition impairment.
Abstract: Recently, increasing evidence has suggested the association between gut dysbiosis and Alzheimer’s disease (AD) progression, yet the role of gut microbiota in AD pathogenesis remains obscure. Herein, we provide a potential mechanistic link between gut microbiota dysbiosis and neuroinflammation in AD progression. Using AD mouse models, we discovered that, during AD progression, the alteration of gut microbiota composition leads to the peripheral accumulation of phenylalanine and isoleucine, which stimulates the differentiation and proliferation of pro-inflammatory T helper 1 (Th1) cells. The brain-infiltrated peripheral Th1 immune cells are associated with the M1 microglia activation, contributing to AD-associated neuroinflammation. Importantly, the elevation of phenylalanine and isoleucine concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of patients with mild cognitive impairment (MCI) due to AD. Furthermore, GV-971, a sodium oligomannate that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China, suppresses gut dysbiosis and the associated phenylalanine/isoleucine accumulation, harnesses neuroinflammation and reverses the cognition impairment. Together, our findings highlight the role of gut dysbiosis-promoted neuroinflammation in AD progression and suggest a novel strategy for AD therapy by remodelling the gut microbiota.
587 citations
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China Medical University (Taiwan)1, Academia Sinica2, Shanghai Jiao Tong University3, Vanderbilt University4, National University of Singapore5, University of North Carolina at Chapel Hill6, University of Tokyo7, National Taiwan University8, Seoul National University9, The Chinese University of Hong Kong10, Kyushu University11, Singapore National Eye Center12, Fudan University13, Harvard University14, Ewha Womans University15, Soongsil University16, University of San Carlos17, Agency for Science, Technology and Research18, Nagoya University19, University of Melbourne20, Aichi Gakuin University21, Kindai University22, Ajou University23, University of Oxford24, Systems Research Institute25, University of California, San Francisco26
TL;DR: The combined analysis identified eight new T2D loci reaching genome-wide significance, which mapped in or near GLIS3, PEPD, FITM2-R3HDML-HNF4A, KCNK16, MAEA, GCC1-PAX4, PSMD6 and ZFAND3, which may regulate glucose-dependent insulin secretion in the pancreas.
Abstract: We conducted a three-stage genetic study to identify susceptibility loci for type 2 diabetes (T2D) in east Asian populations. We followed our stage 1 meta-analysis of eight T2D genome-wide association studies (6,952 cases with T2D and 11,865 controls) with a stage 2 in silico replication analysis (5,843 cases and 4,574 controls) and a stage 3 de novo replication analysis (12,284 cases and 13,172 controls). The combined analysis identified eight new T2D loci reaching genome-wide significance, which mapped in or near GLIS3, PEPD, FITM2-R3HDML-HNF4A, KCNK16, MAEA, GCC1-PAX4, PSMD6 and ZFAND3. GLIS3, which is involved in pancreatic beta cell development and insulin gene expression, is known for its association with fasting glucose levels. The evidence of an association with T2D for PEPD and HNF4A has been shown in previous studies. KCNK16 may regulate glucose-dependent insulin secretion in the pancreas. These findings, derived from an east Asian population, provide new perspectives on the etiology of T2D.
587 citations
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TL;DR: In this article, the authors investigated whether the addition of a limited course (two cycles) of chemotherapy to this combination would further enhance the clinical benefit of first-line nivolumab plus ipilimumab for advanced non-small-cell lung cancer (NSCLC).
Abstract: Summary Background First-line nivolumab plus ipilimumab has shown improved overall survival in patients with advanced non-small-cell lung cancer (NSCLC). We aimed to investigate whether the addition of a limited course (two cycles) of chemotherapy to this combination would further enhance the clinical benefit. Methods This randomised, open-label, phase 3 trial was done at 103 hospitals in 19 countries. Eligible patients were aged 18 years or older with treatment-naive, histologically confirmed stage IV or recurrent NSCLC, and an Eastern Cooperative Oncology Group performance status of 0–1. Patients were randomly assigned (1:1) by an interactive web response system via permuted blocks (block size of four) to nivolumab (360 mg intravenously every 3 weeks) plus ipilimumab (1 mg/kg intravenously every 6 weeks) combined with histology-based, platinum doublet chemotherapy (intravenously every 3 weeks for two cycles; experimental group), or chemotherapy alone (every 3 weeks for four cycles; control group). Randomisation was stratified by tumour histology, sex, and PD-L1 expression. The primary endpoint was overall survival in all randomly assigned patients. Safety was analysed in all treated patients. Results reported here are from a pre-planned interim analysis (when the study met its primary endpoint) and an exploratory longer-term follow-up analysis. This study is active but no longer recruiting patients, and is registered with ClinicalTrials.gov , number NCT03215706 . Findings Between Aug 24, 2017, and Jan 30, 2019, 1150 patients were enrolled and 719 (62·5%) randomly assigned to nivolumab plus ipilimumab with two cycles of chemotherapy (n=361 [50%]) or four cycles of chemotherapy alone (n=358 [50%]). At the pre-planned interim analysis (median follow-up 9·7 months [IQR 6·4–12·8]), overall survival in all randomly assigned patients was significantly longer in the experimental group than in the control group (median 14·1 months [95% CI 13·2–16·2] vs 10·7 months [9·5–12·4]; hazard ratio [HR] 0·69 [96·71% CI 0·55–0·87]; p=0·00065). With 3·5 months longer median follow-up (median 13·2 months [IQR 6·4–17·0]), median overall survival was 15·6 months (95% CI 13·9–20·0) in the experimental group versus 10·9 months (9·5–12·6) in the control group (HR 0·66 [95% CI 0·55–0·80]). The most common grade 3–4 treatment-related adverse events were neutropenia (in 24 [7%] patients in the experimental group vs 32 [9%] in the control group), anaemia (21 [6%] vs 50 [14%]), diarrhoea (14 [4%] vs two [1%]), increased lipase (22 [6%] vs three [1%]), and febrile neutropenia (14 [4%] vs ten [3%]). Serious treatment-related adverse events of any grade occurred in 106 (30%) patients in the experimental group and 62 (18%) in the control group. Seven (2%) deaths in the experimental group (acute kidney failure, diarrhoea, hepatotoxicity, hepatitis, pneumonitis, sepsis with acute renal insufficiency, and thrombocytopenia; one patient each) and six (2%) deaths in the control group (anaemia, febrile neutropenia, pancytopenia, pulmonary sepsis, respiratory failure, and sepsis; one patient each) were treatment related. Interpretation Nivolumab plus ipilimumab with two cycles of chemotherapy provided a significant improvement in overall survival versus chemotherapy alone and had a favourable risk–benefit profile. These data support this regimen as a new first-line treatment option for patients with advanced NSCLC. Funding Bristol Myers Squibb. Translations For the Polish and Russian translations of the Article see Supplementary Materials section.
586 citations
Authors
Showing all 158621 results
Name | H-index | Papers | Citations |
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Meir J. Stampfer | 277 | 1414 | 283776 |
Richard A. Flavell | 231 | 1328 | 205119 |
Jie Zhang | 178 | 4857 | 221720 |
Yang Yang | 171 | 2644 | 153049 |
Lei Jiang | 170 | 2244 | 135205 |
Gang Chen | 167 | 3372 | 149819 |
Thomas S. Huang | 146 | 1299 | 101564 |
Barbara J. Sahakian | 145 | 612 | 69190 |
Jean-Laurent Casanova | 144 | 842 | 76173 |
Kuo-Chen Chou | 143 | 487 | 57711 |
Weihong Tan | 140 | 892 | 67151 |
Xin Wu | 139 | 1865 | 109083 |
David Y. Graham | 138 | 1047 | 80886 |
Bin Liu | 138 | 2181 | 87085 |
Jun Chen | 136 | 1856 | 77368 |