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AID and TET2 cooperation modulates FANCA expression by active demethylation in diffuse large B cell lymphoma. PubMed Scopus SCIE
期刊论文 | 2019 , 195 (2) , 190-201 | Clinical and experimental immunology
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Diffuse large B cell lymphoma (DLBCL) is traced to a mature B malignance carrying abnormal activation-induced cytidine deaminase (AID) expression. AID activity initially focuses on deamination of cytidine to uracil to generate somatic hypermutation and class-switch recombination of the immunoglobulin (Ig), but recently it has been implicated in DNA demethylation of genes required for B cell development and proliferation in germinal center (GC). However, it has not been characterized well whether AID activity on mutation or demethylation of genes involves oncogenesis of DLBCL. Our data demonstrate that the proto-oncogene fanconi anaemia complementation group A (FANCA) is highly expressed in DLBCL patients and cell line, respectively. AID recruits demethylation enzyme ten eleven-translocation family member TET2 to bind FANCA promoter. As a result, FANCA is demethylated and its expression increases in DLBCL. On the basis of our findings, we develop a new therapeutic strategy to significantly inhibit DLBCL cell growth by combination of proteasome inhibitor bortezomib with AID and TET2 depletion. These findings support a novel mechanism that AID has a crucial role in active demethylation for oncogene activation in DLBCL. This article is protected by copyright. All rights reserved.

Keyword :

fanconi anaemia complementation group A diffuse large B cell lymphoma activation-induced cytidine deaminase active demethylation ten-eleven translocation-2

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GB/T 7714 Jiao J , Jin Y , Zheng M et al. AID and TET2 cooperation modulates FANCA expression by active demethylation in diffuse large B cell lymphoma. [J]. | Clinical and experimental immunology , 2019 , 195 (2) : 190-201 .
MLA Jiao J et al. "AID and TET2 cooperation modulates FANCA expression by active demethylation in diffuse large B cell lymphoma." . | Clinical and experimental immunology 195 . 2 (2019) : 190-201 .
APA Jiao J , Jin Y , Zheng M , Zhang H , Yuan M , Lv Z et al. AID and TET2 cooperation modulates FANCA expression by active demethylation in diffuse large B cell lymphoma. . | Clinical and experimental immunology , 2019 , 195 (2) , 190-201 .
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p38 MAPK signaling pathway activation by phenyl benzoxime in SNU-306 cells causes induction of apoptosis. PubMed SCIE
期刊论文 | 2019 , 126 , 74-78 | Microbial pathogenesis
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The present study was aimed to investigate and understand the mechanism of inhibitory effect of phenyl benzoxime on proliferation of SNU-306 cells. Proliferation of SNU-306 cells transfected with wild-type p53-induced phosphatase 1 (Wip1)-siRNA or treated with phenyl benzoxime was examined by 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Induction of apoptosis was examined by flow cytometry using annexin V-fluorescein isothiocyanate/propidium iodide staining. In SNU-306 cells Wip1 mRNA and protein expression was found to be significantly (p < 0.05) higher compared to normal cells. However, Wip1-siRNA transfection significantly (p < 0.02) inhibited the expression of Wip1 at 60 nmol/l. The proliferation of SNU-306 cells was inhibited to 3.7% on transfection with Wip1-siRNA. Phenyl benzoxime reduced proliferation to 92.0, 75.0, 49.0, 19.0 and 4.0% at 1, 2, 4, 8 and 10 μM doses, respectively. The expression of Wip1 was significantly (p < 0.01) suppressed in SNU-306 cells on phenyl benzoxime treatment. Phenyl benzoxime induced apoptosis in 74.73% cells at 10 μM doses compared to 1.34% in control. Treatment with phenyl benzoxime markedly increased the expression of Bax, caspase-3 and p53 and decreased Bcl-2 mRNA. Moreover, addition of SB203580 to cultures of SNU-306 cells significantly (p < 0.01) prevented phenyl benzoxime mediated inhibition of cell proliferation. Phenyl benzoxime induces apoptosis and inhibits SNU-306 cell proliferation by silencing Wip1 expression through p38 MAPK signaling pathway activation. Therefore, phenyl benzoxime can act as an important chemotherapeutic agent for breast cancer treatment.

Keyword :

Signaling Apoptosis Proliferation Estrogen Proto-oncogene

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GB/T 7714 Chen Wei , Tan Yanni , Zhang Yu . p38 MAPK signaling pathway activation by phenyl benzoxime in SNU-306 cells causes induction of apoptosis. [J]. | Microbial pathogenesis , 2019 , 126 : 74-78 .
MLA Chen Wei et al. "p38 MAPK signaling pathway activation by phenyl benzoxime in SNU-306 cells causes induction of apoptosis." . | Microbial pathogenesis 126 (2019) : 74-78 .
APA Chen Wei , Tan Yanni , Zhang Yu . p38 MAPK signaling pathway activation by phenyl benzoxime in SNU-306 cells causes induction of apoptosis. . | Microbial pathogenesis , 2019 , 126 , 74-78 .
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Pay-it-forward strategy to enhance uptake of dual gonorrhea and chlamydia testing among men who have sex with men in China: a pragmatic, quasi-experimental study SCIE
期刊论文 | 2019 , 19 (1) , 76-82 | LANCET INFECTIOUS DISEASES
WoS CC Cited Count: 1
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Background Chinese men who have sex with men (MSM) rarely receive gonorrhoea and chlamydia testing. The purpose of this pilot study was to evaluate a pay-it-forward strategy to increase uptake of gonorrhoea and chlamydia testing among MSM. Methods We performed a quasi-experimental pragmatic study to compare a pay-it-forward model with standard of care at two HIV testing sites for MSM in Guangzhou, China: an STD clinic for MSM and a local MSM community based organisation. All men who arrived at the STD clinic or the community-based organisation were invited to participate. In the pay-it-forward programme, men were offered free gonorrhoea and chlamydia testing and given the option of donating money toward testing for future participants. In the standard-of-care group, men were offered gonorrhoea and chlamydia testing at the standard patient price of Y150 (about US$21.50). The pay-it-forward programme was implemented for 3 months, after which both sites switched to standard of care offering dual testing for 3 months. The primary outcome for this study was uptake of dual gonorrhoea and chlamydia testing, which we compared using x(2) test and logistic regression, reported as crude odds ratios (cOR) and adjusted odds ratios (aOR), by adjusting for nationality, marital status, income, and site of testing. Findings The pay-it-forward programme took place from Dec 2, 2017, to Feb 3, 2018, and the standard-of-care control took place from March 11, 2018, to May 1, 2018. 408 men were included in this study. 203 men were offered pay-it forward, and 205 were offered standard of care. Overall, 109 (54%) of 203 men in the pay-it-forward group and 12 (6%) of 205 men in the standard-of-care group received gonorrhoea and chlamydia testing (cOR 18.65, 9 78-35 54; p<0.0001; aOR 19.73, 95% CI 10. 02-38. 85; p<0.0001). Of all 121 men who tested, this was the first gonorrhoea test for 97 (80%) men and the first chlamydia test for 104 (86%) men. Five (4%) of these 121 men were diagnosed with gonorrhoea and 15 (12%) were diagnosed with chlamydia. 97 (89%) of 109 men who received testing in the pay-it forward group donated some money toward testing for future participants. Interpretation Pay-it-forward might be a sustainable model for expanding integrated HIV testing services among MSM in China. Copyright (C) 2018 Elsevier Ltd. All rights reserved.

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GB/T 7714 Li, Katherine T. , Tang, Weiming , Wu, Dan et al. Pay-it-forward strategy to enhance uptake of dual gonorrhea and chlamydia testing among men who have sex with men in China: a pragmatic, quasi-experimental study [J]. | LANCET INFECTIOUS DISEASES , 2019 , 19 (1) : 76-82 .
MLA Li, Katherine T. et al. "Pay-it-forward strategy to enhance uptake of dual gonorrhea and chlamydia testing among men who have sex with men in China: a pragmatic, quasi-experimental study" . | LANCET INFECTIOUS DISEASES 19 . 1 (2019) : 76-82 .
APA Li, Katherine T. , Tang, Weiming , Wu, Dan , Huang, Wenting , Wu, Feng , Lee, Amy et al. Pay-it-forward strategy to enhance uptake of dual gonorrhea and chlamydia testing among men who have sex with men in China: a pragmatic, quasi-experimental study . | LANCET INFECTIOUS DISEASES , 2019 , 19 (1) , 76-82 .
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TGF-beta Upregulated Mitochondria Mass through the SMAD2/3 -> C/EBP beta -> PRMT1 Signal Pathway in Primary Human Lung Fibroblasts SCIE PubMed
期刊论文 | 2019 , 202 (1) , 37-47 | JOURNAL OF IMMUNOLOGY
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Tissue remodeling of subepithelial mesenchymal cells is a major pathologic condition of chronic obstructive pulmonary disease and asthma. Fibroblasts contribute to fibrotic events and inflammation in both airway diseases. Recent mechanistic studies established a link between mitochondrial dysfunction or aberrant biogenesis leading to tissue remodeling of the airway wall in asthma. Protein arginine methyltransferase-1 (PRMT1) participated in airway wall remodeling in pulmonary inflammation. This study investigated the mechanism by which PRMT1 regulates mitochondrial mass in primary human airway wall fibroblasts. Fibroblasts from control or asthma patients were stimulated with TGF-beta for up to 48 h, and the signaling pathways controlling PRMT1 expression and mitochondrial mass were analyzed. PRMT1 activity was suppressed by the pan-PRMT inhibitor AMI-1. The SMAD2/3 pathway was blocked by SB203580 and C/EBP beta by small interference RNA treatment. The data obtained from unstimulated cells showed a significantly higher basal expression of PRMT1 and mitochondrial markers in asthmatic compared with control fibroblasts. In all cells, TGF-beta significantly increased the expression of PRMT1 through SMAD2/3 and C/EBP beta. Subsequently, PRMT1 upregulated the expression of the mitochondria regulators PGC-1 alpha and heat shock protein 60. Both the inhibition of the SAMD2/3 pathway or PRMT1 attenuated TGF-beta-induced mitochondrial mass and C/EBP beta and alpha-SMA expression. These findings suggest that the signaling sequence controlling mitochondria in primary human lung fibroblasts is as follows: TGF-beta -> SMAD2/3 -> C/EBP beta -> PRMT1 -> PGC-1 alpha . Therefore, PRMT1 and C/EBP beta present a novel therapeutic and diagnostic target for airway wall remodeling in chronic lung diseases.

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GB/T 7714 Sun, Qingzhu , Fang, Lei , Tang, Xuemei et al. TGF-beta Upregulated Mitochondria Mass through the SMAD2/3 -> C/EBP beta -> PRMT1 Signal Pathway in Primary Human Lung Fibroblasts [J]. | JOURNAL OF IMMUNOLOGY , 2019 , 202 (1) : 37-47 .
MLA Sun, Qingzhu et al. "TGF-beta Upregulated Mitochondria Mass through the SMAD2/3 -> C/EBP beta -> PRMT1 Signal Pathway in Primary Human Lung Fibroblasts" . | JOURNAL OF IMMUNOLOGY 202 . 1 (2019) : 37-47 .
APA Sun, Qingzhu , Fang, Lei , Tang, Xuemei , Lu, Shemin , Tamm, Michael , Stolz, Daiana et al. TGF-beta Upregulated Mitochondria Mass through the SMAD2/3 -> C/EBP beta -> PRMT1 Signal Pathway in Primary Human Lung Fibroblasts . | JOURNAL OF IMMUNOLOGY , 2019 , 202 (1) , 37-47 .
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Epidemic pattern of hand-foot-and-mouth disease in Xi'an, China from 2008 through 2015 SCIE PubMed
期刊论文 | 2019 , 19 | BMC INFECTIOUS DISEASES
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BackgroundHand, foot and mouth disease (HFMD) is an infectious disease caused by enteroviruses that has a severely impair for those high incidence countries such as China.The current study aimed to investigate the epidemic pattern of HFMD by time and region in Northwestern China.MethodsAll reported HFMD cases from 2008 to 2015 were collected from local Disease Control and Prevention.The HFMD was diagnosed in accordance with the guidebook provided by the National Health and Family Planning Commission of the People's Republic of China.ResultsA total of 154,869 cases of probable HFMD were reported. The overall incidence of HFMD has been increased from 91.68 per 100/000 in 2008 to 335.64 per 100/000 in 2015.The case mortality is decreased from 0.014 per100/000 to 0.011 per 100/000 during the time period. Most HFMD (93.82%) occurred in children younger than 5years. The seasonal peak of HFMD infections occurred in April-July and September-November and Central regions of Xi'an city were the major locations of the clusters (incidence rate 245.75/100,000; relative risk 1.19, P<0.01). EVA71 was the predominant enterovirus serotype, accounting for 50.0% of all reported HFMD cases since 2011.The most susceptible group infected by HFMD was children younger than 5years, especially boys.ConclusionsIncidence of HFMD has been increasing in the past few years, however, the case fatality is decreasing. Season and region shall be considered as influence factors in the prevention of HFMD.

Keyword :

Distribution Serotype Epidemic Hand-foot-and-mouth disease

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GB/T 7714 Liu, JiFeng , Xiang, XiaoMei , Pu, ZhongShu et al. Epidemic pattern of hand-foot-and-mouth disease in Xi'an, China from 2008 through 2015 [J]. | BMC INFECTIOUS DISEASES , 2019 , 19 .
MLA Liu, JiFeng et al. "Epidemic pattern of hand-foot-and-mouth disease in Xi'an, China from 2008 through 2015" . | BMC INFECTIOUS DISEASES 19 (2019) .
APA Liu, JiFeng , Xiang, XiaoMei , Pu, ZhongShu , Long, Yong , Xiao, Dan , Zhang, WeiLu et al. Epidemic pattern of hand-foot-and-mouth disease in Xi'an, China from 2008 through 2015 . | BMC INFECTIOUS DISEASES , 2019 , 19 .
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Epidemiology and risk factors for nosocomial infection in the respiratory intensive care unit of a teaching hospital in China: A prospective surveillance during 2013 and 2015. PubMed SCIE
期刊论文 | 2019 , 19 , 145 | BMC infectious diseases
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To determine the epidemiology and risk factors for nosocomial infection (NI) in the Respiratory Intensive Care Unit (RICU) of a teaching hospital in Northwest China.An observational, prospective surveillance was conducted in the RICU from 2013 to 2015. The overall infection rate, distribution of infection sites, device-associated infections and pathogen in the RICU were investigated. Then, the logistic regression analysis was used to test the risk factors for RICU infection.In this study, 102 out of 1347 patients experienced NI. Among them, 87 were device-associated infection. The overall prevalence of NI was 7.57% with varied rates from 7.19 to 7.73% over the 3 years. The lower respiratory tract (43.1%), urinary tract (26.5%) and bloodstream (20.6%) infections accounted for the majority of infections. The device-associated infection rates of urinary catheter, central catheter and ventilator were 9.8, 7.4 and 7.4 per 1000 days, respectively.The most frequently isolated pathogens were Staphylococcus aureus (20.9%), Klebsiella pneumoniae (16.4%) and Pseudomonas aeruginosa (10.7%). Multivariate analysis showed that the categories D or E of Average Severity of Illness Score (ASIS), length of stay (10-30, 30-60, ≥60 days), immunosuppressive therapy and ventilator use are the independent risk factors for RICU infection with an adjusted odds ratio (OR) of 1.65 (95% CI: 1.15~2.37), 5.22 (95% CI: 2.63~10.38)), 2.32 (95% CI: 1.19~4.65), 8.93 (95% CI: 3.17~21.23), 31.25 (95% CI: 11.80~63.65)) and 2.70 (95% CI: 1.33~5.35), respectively.A relatively low and stable rate of NI was observed in our RICU through year 2013-2015. The ASIS-D、E, stay ≥10 days, immunosuppressive therapy and ventilator use are the independent risk factors for RICU infection.

Keyword :

Risk factors Respiratory intensive care unit Nosocomial infection

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GB/T 7714 Wang Linchuan , Zhou Kai-Ha , Chen Wei et al. Epidemiology and risk factors for nosocomial infection in the respiratory intensive care unit of a teaching hospital in China: A prospective surveillance during 2013 and 2015. [J]. | BMC infectious diseases , 2019 , 19 : 145 .
MLA Wang Linchuan et al. "Epidemiology and risk factors for nosocomial infection in the respiratory intensive care unit of a teaching hospital in China: A prospective surveillance during 2013 and 2015." . | BMC infectious diseases 19 (2019) : 145 .
APA Wang Linchuan , Zhou Kai-Ha , Chen Wei , Yu Yan , Feng Si-Fang . Epidemiology and risk factors for nosocomial infection in the respiratory intensive care unit of a teaching hospital in China: A prospective surveillance during 2013 and 2015. . | BMC infectious diseases , 2019 , 19 , 145 .
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Probenecid Relieves Cerebral Dysfunction of Sepsis by Inhibiting Pannexin 1-Dependent ATP Release. PubMed
期刊论文 | 2019 | Inflammation
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Acute brain dysfunction and the following neurological manifestation are common complications in septic patients, which are associated with increased morbidity and mortality. However, the therapeutic strategy of this disorder remains a major challenge. Given the emerging role of a clinically approved drug, probenecid (PRB) has been recently identified as an inhibitor of pannexin 1 (PANX1) channel, which restrains extracellular ATP release-induced purinergic pathway activation and inflammatory response contributing to diverse pathological processes. In this study, we explored whether PRB administration attenuated neuroinflammatory response and cognitive impairment during sepsis. In mice suffered from cecal ligation and puncture (CLP)-induced sepsis, treatment with PRB improved memory retention and lessened behavioral deficits. This neuroprotective effect was coupled with restricted overproduction of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and interleukin (IL)-1β in the hippocampus. Since this damped neuroinflammation was replicated by inhibition of ATP release, it suggested that PANX1 channel modulates a purinergic-related pathway contributing to the neurohistological damage. Therefore, we identified PRB could be a promising therapeutic approach for the therapy of cerebral dysfunction of sepsis.

Keyword :

pannexin 1 neuroinflammation cecal ligation and puncture cognitive impairment probenecid

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GB/T 7714 Zhang Zhanqin , Lei Yi , Yan Chaoying et al. Probenecid Relieves Cerebral Dysfunction of Sepsis by Inhibiting Pannexin 1-Dependent ATP Release. [J]. | Inflammation , 2019 .
MLA Zhang Zhanqin et al. "Probenecid Relieves Cerebral Dysfunction of Sepsis by Inhibiting Pannexin 1-Dependent ATP Release." . | Inflammation (2019) .
APA Zhang Zhanqin , Lei Yi , Yan Chaoying , Mei Xiaopeng , Jiang Tao , Ma Zhi et al. Probenecid Relieves Cerebral Dysfunction of Sepsis by Inhibiting Pannexin 1-Dependent ATP Release. . | Inflammation , 2019 .
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IL-17A contributes to myocardial ischemic injury by activating NLRP3 inflammasome in macrophages through AMPKα/p38MAPK/ERK1/2 signal pathway in mice. PubMed SCIE
期刊论文 | 2019 , 105 , 240-250 | Molecular immunology
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Acute myocardial infarction (AMI) is followed by an acute inflammation involving inflammasome activation, thereby inducing cardiac dysfunction. Interleukin-17A (IL-17A) involves in many inflammatory diseases, but its roles in inflammation following AMI are still obscure. The aim of this study is to investigate the roles of IL-17A in the inflammatory response following AMI and its underlying mechanisms.NLRP3 inflammasome and AMPKα/p38MAPK/ERK1/2 signaling pathway were significantly activated under the induction of IL-17A in mouse peritoneal macrophages, which could be inhibited by AMPK inhibitor compound C (CC). Both p38MAPK and ERK1/2 inhibitors could partially inhibit the activation of NLRP3 inflammasome in macrophages treated by IL-17A. In vivo, IL-17A knockout not only decreased the infiltration of macrophages and the activation of NLRP3 inflammasome and AMPKα/p38MAPK/ERK1/2 signaling pathway in ischemic myocardium, but also improved cardiac function and reduced infarction size after the ligation of descending segment from left coronary artery for 3 days in mice, while IL-17A administration further aggravated the myocardial ischemic injury, which were prevented by CC administration.IL-17A aggravates inflammatory response during AMI by inducing macrophages infiltration and activating NLRP3 inflammasome through AMPKα/p38MAPK/ERK1/2 pathway.

Keyword :

AMI IL-17A AMPKα Inflammasome Macrophage

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GB/T 7714 Zhang Lisha , Liu Peining , Wen Wen et al. IL-17A contributes to myocardial ischemic injury by activating NLRP3 inflammasome in macrophages through AMPKα/p38MAPK/ERK1/2 signal pathway in mice. [J]. | Molecular immunology , 2019 , 105 : 240-250 .
MLA Zhang Lisha et al. "IL-17A contributes to myocardial ischemic injury by activating NLRP3 inflammasome in macrophages through AMPKα/p38MAPK/ERK1/2 signal pathway in mice." . | Molecular immunology 105 (2019) : 240-250 .
APA Zhang Lisha , Liu Peining , Wen Wen , Bai Xiaofang , Zhang Yan , Liu Mengping et al. IL-17A contributes to myocardial ischemic injury by activating NLRP3 inflammasome in macrophages through AMPKα/p38MAPK/ERK1/2 signal pathway in mice. . | Molecular immunology , 2019 , 105 , 240-250 .
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Dentin matrix protein 1 correlates with the severity of hemorrhagic fever with renal syndrome and promotes hyper-permeability of endothelial cells infected by Hantaan virus. PubMed
期刊论文 | 2019 | Microbes and infection
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Hantaviruses is the major causative agents of hemorrhagic fever with renal syndrome (HFRS) in humans, which is characterized by increased capillary permeability. Dentin matrix protein 1 (DMP1) has been shown to degrade components of the basal membrane and interendothelial junctions via matrix metalloproteinase-9. To study the changes of serum DMP1 in HFRS, we determined the concentration of DMP1 using sandwich enzyme-linked immunosorbent assay. We found that serum DMP1 concentrations increased significantly, and reached peak value during the oliguric phase and in the critical group in HFRS patients. Moreover, serum DMP1 concentrations were closely related to blood urea nitrogen, creatinine, cystatin C, and vascular endothelial growth factor (VEGF). We further explored the role of DMP1 in HTNV-infected human umbilical vein endothelial cells (HUVECs) model. Data from immunocytochemistry showed that VEGF and tumor necrosis factor-α (TNF-α) promote expression of DMP1 on HTNV-infected HUVECs. Results from transwell assays demonstrated that the permeability of HUVECs increases significantly after HTNV infection with the addition of DMP1, VEGF, and TNF-α. This study suggests that elevated DMP1 concentrations may be associated with disease stage, severity, and the degree of acute kidney injury. DMP1 is involved in the regulation of capillary permeability in HFRS caused by hantavirus infection.

Keyword :

hyper-permeability vascular endothelial growth factor hantavirus dentin matrix protein 1 tumor necrosis factor-α hemorrhagic fever with renal syndrome

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GB/T 7714 Shi Dongsha , Dong Yanying , Dai Pengfei et al. Dentin matrix protein 1 correlates with the severity of hemorrhagic fever with renal syndrome and promotes hyper-permeability of endothelial cells infected by Hantaan virus. [J]. | Microbes and infection , 2019 .
MLA Shi Dongsha et al. "Dentin matrix protein 1 correlates with the severity of hemorrhagic fever with renal syndrome and promotes hyper-permeability of endothelial cells infected by Hantaan virus." . | Microbes and infection (2019) .
APA Shi Dongsha , Dong Yanying , Dai Pengfei , Gao Juan , Yin Jingjing , Xie Ming . Dentin matrix protein 1 correlates with the severity of hemorrhagic fever with renal syndrome and promotes hyper-permeability of endothelial cells infected by Hantaan virus. . | Microbes and infection , 2019 .
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PM2.5 Exposure Induced Autophagy Activation via the ROS/AMPK/mTOR/ULK1 Signaling Axis in Macrophages CPCI-S SCIE
会议论文 | 2019 , 143 (2) , AB230-AB230 | Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology (AAAAI)
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GB/T 7714 Liu, Lu , Liu, Qun , Wen, Dongqing et al. PM2.5 Exposure Induced Autophagy Activation via the ROS/AMPK/mTOR/ULK1 Signaling Axis in Macrophages [C] . 2019 : AB230-AB230 .
MLA Liu, Lu et al. "PM2.5 Exposure Induced Autophagy Activation via the ROS/AMPK/mTOR/ULK1 Signaling Axis in Macrophages" . (2019) : AB230-AB230 .
APA Liu, Lu , Liu, Qun , Wen, Dongqing , Rule, Ana , Koehler, Kirsten , Li, Manxiang et al. PM2.5 Exposure Induced Autophagy Activation via the ROS/AMPK/mTOR/ULK1 Signaling Axis in Macrophages . (2019) : AB230-AB230 .
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