Institution
Binzhou Medical College
Education•Yantai, China•
About: Binzhou Medical College is a education organization based out in Yantai, China. It is known for research contribution in the topics: Apoptosis & Cancer. The organization has 959 authors who have published 619 publications receiving 7642 citations.
Topics: Apoptosis, Cancer, Cell growth, Metastasis, Genotype
Papers published on a yearly basis
Papers
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Joan B. Soriano1, Parkes J Kendrick2, Katherine R. Paulson2, Vinay Gupta2 +311 more•Institutions (178)
TL;DR: It is shown that chronic respiratory diseases remain a leading cause of death and disability worldwide, with growth in absolute numbers but sharp declines in several age-standardised estimators since 1990.
829 citations
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TL;DR: To assess current trajectories towards the GPW13 UHC billion target—1 billion more people benefiting from UHC by 2023—the authors estimated additional population equivalents with UHC effective coverage from 2018 to 2023, and quantified frontiers of U HC effective coverage performance on the basis of pooled health spending per capita.
304 citations
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TL;DR: It is shown that claudin‐14 promoter activity and transcript are exclusively localized in the TAL, establishing a key regulatory role for claudIn‐14 in renal Ca++ homeostasis.
Abstract: The paracellular claudin channel of the thick ascending limb (TAL) of Henle is critical for Ca++ reabsorption in the kidney. Genome-wide association studies (GWASs) have identified claudin-14 associated with hypercalciuric nephrolithiasis. Here, we show that claudin-14 promoter activity and transcript are exclusively localized in the TAL. Under normal dietary condition, claudin-14 proteins are suppressed by two microRNA molecules (miR-9 and miR-374). Both microRNAs directly target the 3′-UTR of claudin-14 mRNA; induce its mRNA decay and translational repression in a synergistic manner. Through physical interaction, claudin-14 blocks the paracellular cation channel made of claudin-16 and -19, critical for Ca++ reabsorption in the TAL. The transcript and protein levels of claudin-14 are upregulated by high Ca++ diet, while downregulated by low Ca++ diet. Claudin-14 knockout animals develop hypermagnesaemia, hypomagnesiuria, and hypocalciuria under high Ca++ dietary condition. MiR-9 and miR-374 transcript levels are regulated by extracellular Ca++ in a reciprocal manner as claudin-14. The Ca++ sensing receptor (CaSR) acts upstream of the microRNA-claudin-14 axis. Together, these data have established a key regulatory role for claudin-14 in renal Ca++ homeostasis.
227 citations
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University of Texas Southwestern Medical Center1, University of Texas Health Science Center at Houston2, Shanghai Jiao Tong University3, Binzhou Medical College4, Wenzhou Medical College5, Xiamen University6, Central South University7, Fudan University8, Osaka University9, University of Texas MD Anderson Cancer Center10
TL;DR: It is shown that LILRB4, an immunoreceptor tyrosine-based inhibition motif-containing receptor and a marker of monocytic leukaemia, supports tumour cell infiltration into tissues and suppresses T cell activity via a signalling pathway that involves APOE, LIL RB4, SHP-2, uPAR and ARG1 in acute myeloid leukaemis (AML) cells.
Abstract: Immune checkpoint blockade therapy has been successful in treating some types of cancer but has not shown clinical benefits for treating leukaemia1. This result suggests that leukaemia uses unique mechanisms to evade this therapy. Certain immune inhibitory receptors that are expressed by normal immune cells are also present on leukaemia cells. Whether these receptors can initiate immune-related primary signalling in tumour cells remains unknown. Here we use mouse models and human cells to show that LILRB4, an immunoreceptor tyrosine-based inhibition motif-containing receptor and a marker of monocytic leukaemia, supports tumour cell infiltration into tissues and suppresses T cell activity via a signalling pathway that involves APOE, LILRB4, SHP-2, uPAR and ARG1 in acute myeloid leukaemia (AML) cells. Deletion of LILRB4 or the use of antibodies to block LILRB4 signalling impeded AML development. Thus, LILRB4 orchestrates tumour invasion pathways in monocytic leukaemia cells by creating an immunosuppressive microenvironment. LILRB4 represents a compelling target for the treatment of monocytic AML.
140 citations
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TL;DR: The results indicated that the up/down-regulation of BDNF and TrkB were affected by aging and the stimulus paradigm, which might reflect important mechanisms by which the hippocampus copes with stressful stimuli.
Abstract: Purpose
The purpose of this study is to explore the dynamic change of brain-derived neurotrophic factor (BDNF) mRNA, protein, and tyrosine kinase-coupled receptor (TrkB) mRNA of the rat hippocampus under different stress conditions and to explore the influence of senescence on the productions expression.
124 citations
Authors
Showing all 959 results
Name | H-index | Papers | Citations |
---|---|---|---|
Yuming Guo | 73 | 492 | 37180 |
Mingwen Zhao | 55 | 361 | 10884 |
Philip H.-S. Jen | 30 | 137 | 3644 |
Qiusheng Zheng | 28 | 117 | 2352 |
Qiang Fu | 19 | 62 | 1094 |
Haixia Zhang | 17 | 38 | 1155 |
Ling-Qun Kong | 15 | 20 | 931 |
Xuemei Hu | 14 | 30 | 395 |
Jichun Han | 14 | 28 | 447 |
Bao-guang Hu | 11 | 20 | 732 |
Xianbing Liu | 11 | 21 | 301 |
Xiaoyan Xu | 10 | 15 | 260 |
Yongfeng Gong | 10 | 10 | 521 |
Jingjing Xie | 10 | 13 | 457 |
Xiling Sun | 10 | 18 | 404 |