Publications by authors named "Yuyang Chen"

25 Publications

  • Page 1 of 1

Assessing the impact of COVID-19 border restrictions on dengue transmission in Yunnan Province, China: an observational epidemiological and phylogenetic analysis.

Lancet Reg Health West Pac 2021 Sep 20;14:100259. Epub 2021 Aug 20.

State Key Laboratory of Remote Sensing Science, Center for Global Change and Public Health, College of Global Change and Earth System Science, Beijing Normal University, Beijing, China.

Background: In response to the COVID-19 pandemic, China implemented strict restrictions on cross-border travel to prevent disease importation. Yunnan, a Chinese province that borders dengue-endemic countries in Southeast Asia, experienced unprecedented reduction in dengue, from 6840 recorded cases in 2019 to 260 in 2020.

Methods: Using a combination of epidemiological and virus genomic data, collected from 2013 to 2020 in Yunnan and neighbouring countries, we conduct a series of analyses to characterise the role of virus importation in driving dengue dynamics in Yunnan and assess the association between recent international travel restrictions and the decline in dengue reported in Yunnan in 2020.

Findings: We find strong evidence that dengue incidence between 2013-2019 in Yunnan was closely linked with international importation of cases. A 0-2 month lag in incidence not explained by seasonal differences, absence of local transmission in the winter, effective reproductive numbers < 1 (as estimated independently using genetic data) and diverse cosmopolitan dengue virus phylogenies all suggest dengue is non-endemic in Yunnan. Using a multivariate statistical model we show that the substantial decline in dengue incidence observed in Yunnan in 2020 but not in neighbouring countries is closely associated with the timing of international travel restrictions, even after accounting for other environmental drivers of dengue incidence.

Interpretation: We conclude that Yunnan is a regional sink for DENV lineage movement and that border restrictions may have substantially reduced dengue burden in 2020, potentially averting thousands of cases. Targeted testing and surveillance of travelers returning from high-risk areas could help to inform public health strategies to minimise or even eliminate dengue outbreaks in non-endemic settings like southern China.

Funding: Funding for this study was provided by National Key Research and Development Program of China, Beijing Science and Technology Planning Project (Z201100005420010); Beijing Natural Science Foundation (JQ18025); Beijing Advanced Innovation Program for Land Surface Science; National Natural Science Foundation of China (82073616); Young Elite Scientist Sponsorship Program by CAST (YESS) (2018QNRC001); H.T., O.P.G. and M.U.G.K. acknowledge support from the Oxford Martin School. O.J.B was supported by a Wellcome Trust Sir Henry Wellcome Fellowship (206471/Z/17/Z). Chinese translation of the abstract (Appendix 2).
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http://dx.doi.org/10.1016/j.lanwpc.2021.100259DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8387751PMC
September 2021

Targeted cell therapy for partial-thickness cartilage defects using membrane modified mesenchymal stem cells by transglutaminase 2.

Biomaterials 2021 08 27;275:120994. Epub 2021 Jun 27.

Arthritis Clinic & Research Center, Peking University People's Hospital, Peking University, Beijing, 100044, China; Arthritis Institute, Peking University, Beijing, 100044, China. Electronic address:

Unlike full-thickness cartilage defects (FCD), partial-thickness cartilage defects (PCD) may still have residual healthy cartilage tissue, and therefore, the conventional clinical treatments such as microfracture and autologous chondrocyte implantation (ACI) are so traumatic that they may not be the suitable therapies for PCD. Although intra-articular injection of mesenchymal stem cells (MSCs) is a minimally invasive treatment, its therapeutic efficacy is markedly limited due to anoikis caused by failure of cell colonization in the injured area. By modifying a functional polypeptide on the MSC plasma membrane and exploiting the high expression of transglutaminase 2 (TGase2) in the regions of injured cartilage, we achieved targeted recognition and capture of modified MSCs by injured articular chondrocytes (ACs). In the in vitro co-culture model, MSCs improved the function of injured ACs and enhanced the chondrogenic differentiation potential of MSCs. Results of in vitro study also revealed that the activation of the AKT/mTOR signaling pathway may play an important role in the treatment of injured ACs by MSCs. Further, membrane-modified MSCs exhibited a better therapeutic effect than wide-type MSCs in a rabbit model of PCD. Thus, this unique cell membrane modification strategy provides a new cell-based therapeutic approach for the early treatment of articular cartilage defects and other joint diseases.
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http://dx.doi.org/10.1016/j.biomaterials.2021.120994DOI Listing
August 2021

Global Significant Changes in Formaldehyde (HCHO) Columns Observed From Space at the Early Stage of the COVID-19 Pandemic.

Geophys Res Lett 2021 Feb 23;48(4):2e020GL091265. Epub 2021 Feb 23.

School of Environmental Science and Engineering Southern University of Science and Technology Shenzhen China.

Satellite HCHO data are widely used as a reliable proxy of non-methane volatile organic compounds (NMVOCs) to constrain underlying emissions and chemistry. Here, we examine global significant changes in HCHO columns at the early stage of the COVID-19 pandemic (January-April 2020) compared with the same period in 2019 with observations from the TROPOspheric Monitoring Instrument (TROPOMI). HCHO columns decline (11.0%) in the Northern China Plain (NCP) because of a combination of meteorological impacts, lower HCHO yields as NO emission plunges (by 36.0%), and reduced NMVOC emissions (by 15.0%) resulting from the lockdown. HCHO columns change near Beijing (+8.4%) due mainly to elevated hydroxyl radical as NO emission decreases in a NO -saturated regime. HCHO columns change in Australia (+17.5%), Northeastern Myanmar of Southeast Asia (+14.9%), Central Africa (+7.8%), and Central America (+18.9%), consistent with fire activities. Our work also points to other changes related to temperature and meteorological variations.
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http://dx.doi.org/10.1029/2020GL091265DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7995117PMC
February 2021

Verification and comparison of three prediction models of ischemic stroke in young adults based on the back propagation neural networks.

Medicine (Baltimore) 2021 Mar;100(11):e25081

The First School of Medicine.

Abstract: This work aims to explore risk factors for ischemic stroke in young adults and analyze the Traditional Vascular Risk Factors Model based on age, hypertension, diabetes, smoking history, and drinking history. Further, the Lipid Metabolism Model was analyzed based on lipoprotein a [LP (a)], high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein AI (apo AI), apolipoprotein B (apo B), and the Early Renal Injury Model based on urinary microalbuminuria/creatinine ratio (UACR). Besides, we estimated glomerular filtration rate (eGFR), cystatin C (Cys-C), homocysteine (Hcy), β2 microglobulin (β2m), and validated their predictive efficacy and clinical value for the development of ischemic stroke in young adults.We selected and retrospectively analyzed the clinical data of 565 young inpatients admitted to Zhejiang Provincial Hospital of Chinese Medicine between 2010 and 2020, 187 of whom were young stroke patients. A single-factor analysis was used to analyze the risk factors for stroke in young people and developed a traditional vascular risk factors model, a lipid metabolism model, and an early kidney injury model based on backpropagation (BP) neural networks technology to predict early stroke occurrence. Moreover, the prediction performance by the area under the receiver operating characteristics (ROC) curve (AUC) was assessed to further understand the risk factors for stroke in young people and apply their predictive role in the clinical setting.Single-factor analysis showed that ischemic stroke in young adults was associated with hypertension, diabetes, smoking history, drinking history, LP(a), HDL, LDL, apo AI, apo B, eGFR, Cys-C, and β2m (P < .05). The BP neural networks technique was used to plot the ROC curves for the Traditional Vascular Risk Factors Model, the Lipid Metabolism Model, and the Early Kidney Injury Model in enrolled patients, and calculated AUC values of 0.7915, 0.8387, and 0.9803, respectively.The early kidney injury model precisely predicted the risk of ischemic stroke in young adults and exhibited a certain clinical value as a reference for morbidity assessment. Whereas the prediction performance of the Traditional Vascular Risk Factors Model and the Lipid Metabolism Model were inferior to that of the early kidney injury model.
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http://dx.doi.org/10.1097/MD.0000000000025081DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7982175PMC
March 2021

Effect of CRRT combined with low-flow ECMO on canines with ARDS and hypercapnia.

J Artif Organs 2021 Sep 9;24(3):336-342. Epub 2021 Mar 9.

Department of ICU, the First Affiliated Hospital of Hunan University of Medicine, Huaihua, 418000, Hunan, China.

To observe the effect of continuous renal replacement therapy (CRRT) combined with low-flow extracorporeal membrane oxygenation (ECMO) of V-V mode on anti-inflammation, improving oxygenation and reducing PCO in canines with acute respiratory distress syndrome (ARDS) and hypercapnia. A total of 30 healthy adult canines were randomly divided into sham group (n = 10), ECMO (EC) group (n = 10) and CRRT + ECMO (CR + EC) group (n = 10). Sham group was only treated with invasive mechanical ventilation. EC group was also treated with ECMO. CR + EC group was treated with CRRT combined with low-flow ECMO of V-V mode besides invasive mechanical ventilation. The results showed that hazard ratio was lower in the CR + EC group. Inflammatory factors, OI values, and PaCO levels were lower in the CR + EC group. There was no significant difference in the levels of MAP, CO and T among the three groups. No significant complications or death was developed in the three groups. Compared with ECMO group at T3, T6 and T9, IL-6 [(276.13 ± 8.32, 262.04 ± 7.15, 259.33 ± 7.31)ng/L VS (352.67 ± 19.24, 360.24 ± 23.58, 362.21 ± 25.24)ng/L] and TNF-α [(50.14 ± 1.75, 50.45 ± 1.81, 48.03 ± 1.24) ng/L VS (70.25 ± 3.02, 72.45 ± 3.25, 76.69 ± 2.18)ng/L] in CR + EC group were decreased (P < 0.0001). Compared with sham group, IL-6 [(343.76 ± 21.97, 345.91 ± 19.89, 340.34 ± 22.17)ng/L]and TNF-α [(68.10 ± 2.96, 67.31 ± 3.01, 70.34 ± 3.35)ng/L] of T3, T6 and T9 in CR + EC group were lower (P < 0.0001). These findings indicated that CRRT combined with low-flow ECMO of V-V mode had a positive effect on anti-inflammation, oxygenation improvement and surplus blood CO removal in canines with ARDS and hypercapnia. These results provide a promising treatment regimen for ARDS.
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http://dx.doi.org/10.1007/s10047-021-01253-9DOI Listing
September 2021

Oxidative Stress, Endocrine Disturbance, and Immune Interference in Humans Showed Relationships to Serum Bisphenol Concentrations in a Dense Industrial Area.

Environ Sci Technol 2021 02 26;55(3):1953-1963. Epub 2021 Jan 26.

School of Environmental Science and Engineering, Southern University of Science and Technology, Shenzhen, Guangdong 518055, China.

Bisphenol A (BPA) analogues, used in a range of products due to health concerns regarding BPA, have emerged as ubiquitous environmental contaminants worldwide. This study aims to evaluate the levels of nine bisphenols (BPs) and eight biomarkers (malondialdehyde, MDA; 8-hydroxy-2'-deoxyguanosine, 8-OHdG; estradiol, E2; follicle-stimulating hormone, FSH; luteinizing hormone, LH; complement compound 3, C3; immunoglobulin M, IgM and c-reaction protein, CRP) in human serum ( = 353) to explore their potential relationships. The detection rates (DRs) of eight BPs in serum samples taken from people working in a dense industrial area of Shenzhen (Guangdong Province, China) were over 72% except for bisphenol B (BPB) (DR = 27.5%). The mean concentrations of BPA, bisphenol P (BPP), BPB, bisphenol F (BPF), bisphenol FL (BPFL), 4,4'-dihydroxy-benzophenone (DHBP), bisphenol AF (BPAF), 4,4'-thiodiphenol (TDP) and bisphenol S (BPS) were 42.062, 2.083, 0.765, 0.578, 0.423, 0.402, 0.191, 0.120, and 0.071 ng/mL, respectively. BPA and BPFL were significantly correlated with the level of oxidative stress indices MDA and 8-OHdG; BPAF, BPB, and DHBP were strongly correlated with the level of endocrine disturbance indices E2, FSH, and LH; and BPF, DHBP, and BPAF were apparently related to the level of immune interference indices C3 and IgM. This study also suggests multiple impacts (oxidative stress, endocrine disturbance, and immune interference) mediated by BPs contaminants in vivo. To our knowledge, this is the first study to report the correlations among these nine serum BPs and oxidative stress and endocrine and immune system indices in human serum samples collected from dense industrial areas.
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http://dx.doi.org/10.1021/acs.est.0c07587DOI Listing
February 2021

Fine particulate matter exposure induces DNA damage by downregulating Rad51 expression in human bronchial epithelial Beas-2B cells in vitro.

Toxicology 2020 11 7;444:152581. Epub 2020 Sep 7.

The Institute for Chemical Carcinogenesis, Guangzhou Medical University, Xinzao, Panyu District, Guangzhou, 511436, PR China; State Key Laboratory of Respiratory Disease, The First Affiliated Hospital of Guangzhou Medical University, No. 151 Yanjiang Road, Yuexiu District, Guangzhou, 510120, PR China. Electronic address:

Although an accumulating body of evidence suggests that fine particulate matter (PM) can cause lung injury and lung cancer, the underlying mechanisms are not yet clear. In this study, multiple endpoints associated with the cellular response to PM exposure, including the cell proliferation rate, cell apoptosis, malondialdehyde (MDA) content and DNA damage, were evaluated in human bronchial epithelial Beas-2B cells. The mRNA expression profile in PM-treated cells was analyzed by transcriptome sequencing. The DNA repair gene Rad51 was then selected for further analysis. We found that the viability and growth of Beas-2B cells decreased while cell apoptosis increased in a dose-dependent manner after PM exposure. The comet assay showed that PM exposure induced evident DNA damage in PM-treated cells. The MDA content in the treated cells was increased, indicating that PM exposure promoted lipid peroxidation. Furthermore, Rad51 expression was downregulated in PM-treated cells, which may have contributed to the PM-induced DNA damage in Beas-2B cells. Upregulation of Rad51 expression could rescue the negative impact of PM exposure in Beas-2B cells. Taken together, our research demonstrates that PM exposure induces DNA damage and impairs the DNA repair process by downregulating Rad51 expression in Beas-2B cells. This finding is expected to provide new insight into the genotoxicity of PM exposure.
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http://dx.doi.org/10.1016/j.tox.2020.152581DOI Listing
November 2020

TGase-mediated cell membrane modification and targeted cell delivery to inflammatory endothelium.

Biomaterials 2021 02 6;269:120276. Epub 2020 Aug 6.

Department of Biomedical Engineering, School of Medicine, Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, 100084, China. Electronic address:

Targeted cell delivery to lesion sites via minimally invasive approach remains an unmet need in regenerative medicine to endow controlled cell distribution and minimized side-effects. Current cell modification approaches to improve cell delivery tend to have adverse effects on cellular phenotype and functionality. Here, we rationally developed a facile and mild cell modification and targeted delivery strategy leveraging endogenous tissue transglutaminase (TGase) expressed on the surface of MSCs (Mesenchymal Stem Cells) and inflammatory endothelial cells (ECs). Cell modification by functional peptides was accomplished simply via TGase catalyzed cross-linking with naturally-expressed MSCs membrane proteins (e.g. Annexin II), without detectable disturbance of cellular viability and functionality. The modified functional peptides could facilitate adhesion of MSCs to inflammatory ECs (with up-regulated TGase expression compared with normal ECs) in vitro, as demonstrated by a one-fold increase of the MSC-EC adhesion force measured by atomic force microscopy (AFM) and by targeted delivery of modified MSC to inflammatory ECs in a flow chamber assay. When transplanted in vivo, modified MSCs demonstrated a dramatic increase in targeted efficiency to inflammatory endothelium compared with non-modified MSCs in both mice ear inflammation and acute/chronic liver injury models. The cell membrane modification strategy and targeted cell delivery mechanism described here can be readily extended for empowering cell engineering and cell therapy with multifaceted functionalities to combat refractory diseases.
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http://dx.doi.org/10.1016/j.biomaterials.2020.120276DOI Listing
February 2021

Oxidized low-density lipoprotein inhibits the degradation of cyclophilin A via the lysosome in vascular smooth muscle cells.

Am J Transl Res 2020 15;12(7):3964-3973. Epub 2020 Jul 15.

Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University Guangzhou 510120, Guangdong, China.

Background: Cyclophilin A (CyPA) plays an important role in the progression of atherosclerosis. Additionally, it has been reported that lysosomal function is markedly impaired in atherosclerosis induced by oxidized low-density lipoprotein (ox-LDL). As the CyPA degradation pathway remains to be elucidated, we aimed to uncover the role of lysosomes and ox-LDL in the degradation of CyPA.

Methods: We exploited RNA interference (RNAi) in combination with either the lysosomal inhibitor chloroquine (CQ) or the proteasomal inhibitor MG-132 to examine CyPA turnover. We also investigated the role of ox-LDL in lysosomal function and the CyPA degradation pathway and determined whether CyPA interacts with the selective autophagy adaptor p62.

Results: CQ markedly reversed the CyPA downregulation induced by RNAi and increased intracellular levels of LC3 and p62. MG-132 significantly suppressed polyubiquitinated protein degradation but did not inhibit RNAi-induced CyPA downregulation. Additionally, neither CQ nor MG-132 influenced the gene-silencing efficiency of CyPA siRNA. Moreover, ox-LDL induced cytosolic accumulation of p62 was inconsistent with increased expression of LC3-II. Meanwhile, ox-LDL inhibited RNAi-induced downregulation of CyPA. Immunofluorescence indicated colocalization of endogenous CyPA with ubiquitin and with p62 in response to CQ treatment, and co-immunoprecipitation analysis confirmed interaction between CyPA and p62.

Conclusion: CyPA is degraded by a lysosome-dependent pathway that may involve p62-mediated selective autophagy. Furthermore, ox-LDL modulates the degradation of CyPA via its inhibitory role in lysosomes, contributing to increased expression of CyPA in atherosclerotic plaques.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407676PMC
July 2020

Review of surgical robotic systems for keyhole and endoscopic procedures: state of the art and perspectives.

Front Med 2020 Aug 29;14(4):382-403. Epub 2020 Jul 29.

State Key Laboratory of Mechanical System and Vibration, School of Mechanical Engineering, Shanghai Jiao Tong University, Shanghai, 200240, China.

Minimally invasive surgery, including laparoscopic and thoracoscopic procedures, benefits patients in terms of improved postoperative outcomes and short recovery time. The challenges in hand-eye coordination and manipulation dexterity during the aforementioned procedures have inspired an enormous wave of developments on surgical robotic systems to assist keyhole and endoscopic procedures in the past decades. This paper presents a systematic review of the state-of-the-art systems, picturing a detailed landscape of the system configurations, actuation schemes, and control approaches of the existing surgical robotic systems for keyhole and endoscopic procedures. The development challenges and future perspectives are discussed in depth to point out the need for new enabling technologies and inspire future researches.
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http://dx.doi.org/10.1007/s11684-020-0781-xDOI Listing
August 2020

A High-Performance Li-Mn-O Li-rich Cathode Material with Rhombohedral Symmetry via Intralayer Li/Mn Disordering.

Adv Mater 2020 Apr 4;32(16):e2000190. Epub 2020 Mar 4.

Beijing Key Laboratory of Theory and Technology for Advanced Batteries Materials, College of Engineering, Peking University, Beijing, 100871, P. R. China.

The search for new high-performance and low-cost cathode materials for Li-ion batteries is a challenging issue in materials research. Commonly used cobalt- or nickel-based cathodes suffer from limited resources and safety problems that greatly restrict their large-scale application, especially for electric vehicles and large-scale energy storage. Here, a novel Li-Mn-O Li-rich cathode material with symmetry is developed via intralayer Li/Mn disordering in the Mn-layer. Due to the special atomic arrangement and higher symmetry with respect to the C2/m symmetry, the oxygen redox activity is modulated and the Li in the Li-layer is preferentially thermodynamically extracted from the crystal structure instead of Li in the Mn-layer. The as-obtained material delivers a reversible capacity of over 300 mAh g at 25 mA g and rate capability of up to 260 mAh g at 250 mA g within 2.0-4.8 V. The excellent performance is attributed to its highly structural reversibility, mitigation of Jahn-Teller distortion, lower bandgap, and faster Li-ion 2D channels during the lithium-ion de/intercalation process. This material is not only a promising cathode material candidate but also raises new possibilities for the design of low-cost and high-performance cathode materials.
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http://dx.doi.org/10.1002/adma.202000190DOI Listing
April 2020

Nuclear Factor-κB Increases Intracellular Calcium by Upregulation of Na+-Ca2+ Exchanger 1 in Cerulein-Induced Acute Pancreatitis.

Pancreas 2020 01;49(1):111-119

From the Department of Gastroenterology, Xinqiao Hospital, Army Medical University.

Objectives: The mechanisms underlying pathogenesis of acute pancreatitis (AP) are still not completely understood. An early, critical feature of AP is aberrant calcium (Ca) signaling, termed Ca overload, within pancreatic acinar cells. This study aimed to develop a model system in rats for AP induction to study the contribution of the Na-Ca exchanger 1 (NCX1) ion channel in AP pathogenesis.

Methods: To establish a rat model of AP induction, cerulein or L-arginine were intraperitoneally injected and tissue was histologically analyzed by hematoxylin and eosin staining. A cell culture-based model for AP induction was similarly created through cerulein treatment of AR42J cells. Induction of AP was also examined following exposure to the NXC1-targeted inhibitor KB-R7943. The expression of each gene was detected by Western blotting, immunofluorescence, immunohistochemistry, or quantitative reverse transcription polymerase chain reaction. Transcriptional regulation by nuclear factor (NF)-κB was detected using an NCX1 promoter-fusion dual luciferase reporter system. Cytosolic Ca was measured using a fluorescent calcium indicator.

Results: We found that cerulein induced NCX1 expression via activation of nuclear factor NF-κB, which potentially binds to the NCX1 promoter to induce its transcription.

Conclusions: Our findings reveal a regulatory pathway through NF-κB/NCX1 governing Ca overload in AP development, thus providing potential targets for AP treatment.
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http://dx.doi.org/10.1097/MPA.0000000000001465DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946105PMC
January 2020

A Pattern-Based Method for Medical Entity Recognition From Chinese Diagnostic Imaging Text.

Front Artif Intell 2019 14;2. Epub 2019 May 14.

School of Computer Science, South China Normal University, Guangzhou, China.

The identification of medical entities and relations from electronic medical records is a fundamental research issue for medical informatics. However, the task of extracting valuable knowledge from these records is challenging due to its high complexity. The accurate identification of entity and relation is still an open research problem in medical information extraction. A pattern-based method for extracting certain tumor-related entities and attributes from Chinese unstructured diagnostic imaging text is proposed. This method is a composition of three steps. Firstly, an algorithm based on keyword matching is designed to obtain the primary sites of tumors. Then a set of regular expressions is applied to identify primary tumor size information. Finally, a set of rules is defined to acquire metastatic sites of tumors. Our method achieves a recall of 0.697, a precision of 0.825 and an F1 score of 0.755 using an overall weighted metric. For each of the extraction tasks, the F1 scores are 0.784, 0.822 and 0.740. The method proves to be stable and robust with different amounts of testing data. It achieves a comparatively high performance in the CHIP 2018 open challenge, demonstrating its effectiveness in extracting tumor-related entities from Chinese diagnostic imaging text.
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http://dx.doi.org/10.3389/frai.2019.00001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7861250PMC
May 2019

Aberrant Brain Function in Active-Stage Ulcerative Colitis Patients: A Resting-State Functional MRI Study.

Front Hum Neurosci 2019 3;13:107. Epub 2019 Apr 3.

Department of Radiology, XinQiao Hosptial, Third Military Medical University, ChongQing, China.

: Patients with ulcerative colitis (UC) usually display cognitive impairments, such as memory loss, attention deficits, and declining executive functions, particularly during the active stage of the disease. However, the potential neurological mechanisms of these symptoms remain unclear. : Forty-one patients with mildly to moderately active UC, as well as 42 matched healthy controls, were recruited for an examination using psychological scales, cognitive function tests and resting-state functional magnetic resonance imaging (rs-fMRI). Seed points were identified analysis of amplitude of low-frequency fluctuation (ALFF), and functional connectivity (FC) was calculated between these seed regions and other voxels in the whole brain. Correlation analyses were performed among clinical indexes, neuropsychological assessments and neuroimaging data. : Compared with the healthy controls, patients with UC exhibited lower ALFF values in the bilateral hippocampal/parahippocampal (HIPP/ParaHIPP) region and higher ALFF values in the left posterior cingulate cortex (PCC.L) and left middle frontal gyrus (MFG.L). With HIPP/ParaHIPP as the seed point, the strengths of the FC in the bilateral middle frontal gyri (MFG), anterior cingulate cortex (ACC), and left caudate nucleus (CAU.L) increased; using the PCC.L as the seed point, the strengths of the FC in the middle cingulate cortex (MCC) and the left angular gyrus (AUG.L) increased. These abnormal brain regions were mainly located in the limbic system. By analyzing the correlations between these brain regions and behavioral data, we observed a close correlation between decreased HIPP/ParaHIPP activity and memory loss; increased PCC activity and strength of FC with the AUG.L were related to dysfunction of executive function and attention network in patients with UC. : Based on these results, the limbic lobe might be the core of the brain-gut axis (BGA) and play an important role in cognitive impairments, suggesting potential mechanisms for cognitive impairment in patients with UC in the active stage of the disease.
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http://dx.doi.org/10.3389/fnhum.2019.00107DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6457314PMC
April 2019

Three-dimensional atomic-scale observation of structural evolution of cathode material in a working all-solid-state battery.

Nat Commun 2018 08 21;9(1):3341. Epub 2018 Aug 21.

Beijing National Laboratory for Condensed Matter Physics, Institute of Physics, Chinese Academy of Sciences, 100190, Beijing, China.

Most technologically important electrode materials for lithium-ion batteries are essentially lithium ions plus a transition-metal oxide framework. However, their atomic and electronic structure evolution during electrochemical cycling remains poorly understood. Here we report the in situ observation of the three-dimensional structural evolution of the transition-metal oxide framework in an all-solid-state battery. The in situ studies LiNiMnO from various zone axes reveal the evolution of both atomic and electronic structures during delithiation, which is found due to the migration of oxygen and transition-metal ions. Ordered to disordered structural transition proceeds along the <100>, <110>, <111> directions and inhomogeneous structural evolution along the <112> direction. Uneven extraction of lithium ions leads to localized migration of transition-metal ions and formation of antiphase boundaries. Dislocations facilitate transition-metal ions migration as well. Theoretical calculations suggest that doping of lower valence-state cations effectively stabilize the structure during delithiation and inhibit the formation of boundaries.
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http://dx.doi.org/10.1038/s41467-018-05833-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6104093PMC
August 2018

Current Visceral Leishmaniasis Research: A Research Review to Inspire Future Study.

Biomed Res Int 2018 10;2018:9872095. Epub 2018 Jul 10.

Department of Industrial and Manufacturing Systems Engineering, Kansas State University, 2061 Rathbone Hall., Manhattan, KS 66506, USA.

Visceral leishmaniasis (VL), one of the deadliest parasitic diseases in the world, causes more than 50,000 human deaths each year and afflicts millions of people throughout South America, East Africa, South Asia, and Mediterranean Region. In 2015 the World Health Organization classified VL as a neglected tropical disease (NTD), prompting concentrated study of the VL epidemic using mathematical and simulation models. This paper reviews literature related to prevalence and prevention control strategies. More than thirty current research works were reviewed and classified based on VL epidemic study methods, including modeling approaches, control strategies, and simulation techniques since 2013. A summarization of these technical methods, major findings, and contributions from existing works revealed that VL epidemic research efforts must improve in the areas of validating and verifying VL mathematical models with real-world epidemic data. In addition, more dynamic disease control strategies must be explored and advanced simulation techniques must be used to predict VL pandemics.
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http://dx.doi.org/10.1155/2018/9872095DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6076917PMC
January 2019

Effect of Endoplasmic Reticulum Stress and Autophagy in the Regulation of Post-infarct Cardiac Repair.

Arch Med Res 2018 11 13;49(8):576-582. Epub 2018 Jul 13.

Department of Cardiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China. Electronic address:

Background: Acute myocardial infarction (AMI) is reported to be accompanied by endoplasmic reticulum (ER) stress and autophagy induction. Nevertheless, the roles of ER stress and autophagy in post-infarct reparative fibrosis remain to be elucidated.

Aim: To investigate the effects of ER stress and autophagy on the regulation of post-infarct reparative fibrosis.

Methods: The expression of GRP78 and LC3 in cardiac fibroblasts in human heart tissues obtained from patients with or without AMI was assessed by immunofluorescence. In vitro, human cardiac fibroblasts (HCFs) were stimulated by various agents, the expression of GRP78, LC3 and fibronectin in these was evaluated by immunoblot and/or immunofluorescence.

Results: After AMI, HCFs expressed significantly higher levels of GRP78 and LC3. ER stress inducer, tunicamycin (200 ng/mL) significantly increased the level of autophagy and reduced expression of fibronectin in HCFs, both of which were reversed by 4 Phenylbutyric acid. Under the condition of ER stress, the expression of fibronectin in HCFs was regulated by different levels of autophagy. LC3 co-localized with fibronectin when stimulated HCFs with tunicamycin.

Conclusion: AMI induces ER stress in cardiac fibroblasts, down-regulating fibronectin via enhanced autophagy. These findings suggest that ER stress and autophagy may be a therapeutic target to improve prognosis of patients with AMI.
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http://dx.doi.org/10.1016/j.arcmed.2018.07.001DOI Listing
November 2018

High throughput scaffold-based 3D micro-tumor array for efficient drug screening and chemosensitivity testing.

Biomaterials 2019 04 16;198:167-179. Epub 2018 May 16.

Department of Biomedical Engineering, School of Medicine, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Tsinghua University, Beijing, 100084, PR China. Electronic address:

Oncology drug development is greatly hampered by inefficient drug screening using 2D culture. Herein, we present ready-to-use micro-scaffolds in 384-well format to generate uniform 3D micro-tumor array (3D-MTA, CV < 0.15) that predicts in vivo drug responses more accurately than 2D monolayer. 3D-MTA generated from both cell lines and primary cells achieved high screen quality (Z' > 0.5), and were compatible with standard high throughput and high content instruments. Doxorubicin identified by 3D-MTA and 2D successfully inhibited tumor growth in mice bearing lung cancer cell line (H226) xenografts, but not gemcitabine and vinorelbine, which were selected solely by 2D. Resistance towards targeted therapy was modeled on 3D-MTA, which elicited SK-BR-3 to express higher proliferation-related genes in response to gefitinb, as compared to 2D. Screening of 56 MAPK inhibitors identified pisamertib to synergistically improve cytotoxicity effect in combination with gefitinib. Primary tumor cells derived from patient-derived xenografts further attested concordance of drug response in 3D-MTA with in vivo response. 3D-MTA was further extended to realize chemosensitivity testing using patient-derived cells. Overall, 3D-MTA demonstrated strong potential to accelerate drug discovery and improve cancer treatment by providing efficient drug screening.
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http://dx.doi.org/10.1016/j.biomaterials.2018.05.020DOI Listing
April 2019

Understanding Surface Structural Stabilization of the High-Temperature and High-Voltage Cycling Performance of Al-Modified LiMnO Cathode Material.

ACS Appl Mater Interfaces 2018 Jan 2;10(1):550-559. Epub 2018 Jan 2.

Beijing National Laboratory for Condensed Matter Physics, Institute of Physics, Chinese Academy of Sciences , Beijing 100190, China.

Stabilization of the atomic-level surface structure of LiMnO with Al ions is shown to be significant in the improvement of cycling performance, particularly at a high temperature (55 °C) and high voltage (5.1 V). Detailed analysis by X-ray photoelectron spectroscopy, secondary ion mass spectrometry, scanning transmission electron microscopy-energy-dispersive X-ray spectroscopy, etc. reveals that Al ions diffuse into the spinel to form a layered Li(Al,Mn)O structure in the outmost surface where Al concentration is the highest. Other Al ions diffuse into the 8a sites of spinel to form a (MnAl)O structure and the 16d sites of spinel to form Li(MnAl)O. These complicated surface structures, in particular the layered Li(Al,Mn)O, are present at the surface throughout cycling and effectively stabilize the surface structure by preventing dissolution of Mn ions and mitigating cathode-electrolyte reactions. With the Al ions surface modification, a stable cycle performance (∼78% capacity retention after 150 cycles) and high Coulombic efficiency (∼99%) are achieved at 55 °C. More surprisingly, the surface-stabilized LiMnO can be cycled up to 5.1 V without significant degradation, in contrast to the fast capacity degradation found in the unmodified case. Our findings demonstrate the critical role of ions coated on the surface in modifying the structural evolution of the surface of spinel electrode particles and thus will stimulate future efforts to optimize the surface properties of battery electrodes.
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http://dx.doi.org/10.1021/acsami.7b14535DOI Listing
January 2018

Unusual Spinel-to-Layered Transformation in LiMnO Cathode Explained by Electrochemical and Thermal Stability Investigation.

ACS Appl Mater Interfaces 2017 Oct 2;9(40):35463-35475. Epub 2017 Oct 2.

Beijing National Laboratory for Condensed Matter Physics, Institute of Physics, Chinese Academy of Sciences , Beijing, 100190, China.

Distorted surface regions (5-6 nm) with an unusual layered-like structure on LiMnO cathode material were directly observed after it was cycled (3-4.9 V), indicating a possible spinel-to-layered structural transformation. Formation of these distorted regions severely degrades LiMnO cathode capacity. As we attempt to get a better understanding of the exact crystal structure of the distorted regions, the structural transformation pathways and the origins of the distortion are made difficult by the regions' nanoscopic size. Inspired by the reduction of Mn to Mn in surface electronic structures that might be associated with oxygen loss during cycling, we further investigated the atomic-level surface structure of LiMnO by heat-treatments between 600 and 900 °C in various atmospheres, finding similar surface spinel-to-layered structural transformation only for LiMnO heat-treated in argon atmosphere for a few minutes (or more). Controllable and measurable oxygen loss during heat-treatments result in Mn for charge compensation. The ions then undergo a disproportionation reaction, driving the spinel-to-layered transformation by way of an intermediate LiMnO-like structure. The distortion of the surface regions can be extended to the whole bulk by heat-treatment for 300-600 min, ultimately enabling us to identify the bulk-level structure as layered LiMnO (C2/m). This work demonstrates the critical role of Mn in controlling the kinetics of the structural transformation in spinel LiMnO and suggests heat-treatment in argon as a convenient method to control the surface oxygen loss and consequently reconstruct the atomic-level surface structure.
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http://dx.doi.org/10.1021/acsami.7b11303DOI Listing
October 2017

Oxidized Low-Density Lipoprotein-Induced Cyclophilin A Secretion Requires ROCK-Dependent Diphosphorylation of Myosin Light Chain.

J Vasc Res 2016 9;53(3-4):206-215. Epub 2016 Nov 9.

Department of Cardiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, and Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China.

Objective: Accumulation of cyclophilin A (CyPA) within atherosclerotic lesions is thought to be implicated in the progression of atherosclerosis. However, the source of CyPA within atherosclerotic lesions is still unknown. The aim of this study is to determine the role of oxidized low-density lipoproteins (ox-LDL) in vascular smooth muscle cell (VSMC)-derived CyPA secretion and the underlying mechanism.

Methods And Results: Abundant CyPA and α-smooth muscle actin (α-SMA) expressed in atherosclerotic lesions was observed in apolipoprotein E-deficient mice. ox-LDL induced CyPA secretion from a primary culture of rat aortic smooth muscle cells in a dose- and time-dependent manner. Sulfosuccinimidyloleate, a CD36 inhibitor, prevented the ox-LDL-induced CyPA secretion. Pre-exposure to either the actin-depolymerizing agent cytochalasin D or the actin-polymerizing agent jasplakinolide inhibited CyPA secretion induced by ox-LDL. Gene silencing of vesicle-associated membrane protein 2 suppressed ox-LDL-induced CyPA secretion. ox-LDL caused the phosphorylation of myosin light chain (MLC). Inhibition of MLC by blebbistatin reversed the secretion of CyPA and the phosphorylation of MLC induced by ox-LDL. MLC kinase inhibitor ML-7 reduced the monophosphorylation of MLC but did not reduce CyPA secretion. Pretreatment with the rho-associated coiled-coil kinase (ROCK) inhibitor Y27632 blocked diphosphorylation of MLC and secretion of CyPA induced by ox-LDL.

Conclusions: ox-LDL-induced CyPA secretion requires vesicle transportation, actin remodeling and ROCK-dependent diphosphorylation of MLC. VSMC-derived CyPA induced by ox-LDL may be associated with increased CyPA expression in atherosclerotic lesions.
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http://dx.doi.org/10.1159/000449387DOI Listing
May 2017

Knockdown of EMMPRIN improves adverse remodeling mediated by IL-18 in the post-infarcted heart.

Am J Transl Res 2015 15;7(10):1908-16. Epub 2015 Oct 15.

Department of Cardiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University Guangzhou, China ; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology Guangzhou, China.

Interleukin-18 (IL-18) exacerbates cardiac dysfunction following myocardial infarction (MI). Extracellular matrix metalloproteinase inducer (EMMPRIN) has been shown to exacerbate ventricular remodeling via induction of extracellular matrix metalloproteinase (MMP) synthesis. While up-regulation of EMMPRIN expression by IL-18 has been demonstrated in vitro, little is known regarding its in vivo effects. Here, we investigated the role of EMMPRIN in progressive post-infarct ventricular remodeling induced by IL-18. Cardiac function was impaired on echocardiography and organ weight was increased in mice receiving daily intraperitoneal injection of IL-18 following MI. Accompanying these adverse functional effect were increased EMMPRIN levels. Gene silencing of cardiac EMMPRIN by intramyocardial RNA interference rescued IL-18 mediated adverse effects on post-infarct cardiac function. Finally, EMMPRIN silencing reduced MMP-9 expression in the post-infarcted left ventricular myocardium. In conclusion, progressive post-infarct left ventricular remodeling induced by IL-18 can be reversed by gene silencing of EMMPRIN. Knock down of EMMPRIN may be a potential therapeutic strategy to abrogate the adverse effects of IL-18 on post-infarct left ventricular remodeling likely via MMP-9 inhibition.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4656767PMC
December 2015

microRNA-378 promotes mesenchymal stem cell survival and vascularization under hypoxic-ischemic conditions in vitro.

Stem Cell Res Ther 2014 Nov 23;5(6):130. Epub 2014 Nov 23.

Introduction: Mesenchymal stem cells (MSCs) transplantation has been demonstrated to be an effective strategy for the treatment of cardiovascular disease. However, the low survival rate of MSCs at local diseased tissue reduces the therapeutic efficacy. We therefore investigated the influence of MicroRNA-378 (miR-378) transfection on MSCs survival and vascularization under hypoxic-ischemic condition in vitro.

Methods: MSCs were isolated from bone marrow of Sprague-Dawley rats and cultured in vitro. The third passage of MSCs were divided into the miR-378 group and control group. For the miR-378 group, cells were transfected with miR-378 mimic. Both groups experienced exposure to hypoxia (1% O2) and serum deprivation for 24 hours, using normoxia (20% O2) as a negative control during the process. After 24 hours of reoxygenation (20% O2), cell proliferation and apoptosis were evaluated. Expressions of apoptosis and angiogenesis related genes were detected. Both groups were further co-cultured with human umbilical vein endothelial cells to promote vascular differentiation for another 6 hours. Vascular density was assessed thereafter.

Results: Compared with the control group, MSCs transfected with miR-378 showed more rapid growth. Their proliferation rates were much higher at 72 h and 96 h under hypoxic condition (257.33% versus 246.67%, P <0.01; 406.84% versus 365.39%, P <0.05). Cell apoptosis percentage in the miR-378 group was significantly declined under normoxic and hypoxic condition (0.30 ± 0.10% versus 0.50 ± 0.10%, P <0.05; 0.60 ± 0.40% versus 1.70 ± 0.20%, P <0.01). The miR-378 group formed a larger number of vascular branches on matrigel. BCL2 level was decreased accompanied with an upregulated expression of BAX in the two experimental groups under the hypoxic environment. BAX expression was reduced in the miR-378 group under the hypoxic environment. In the miR-378 group, there was a decreased expression of tumor necrosis factor-α on protein level and a reduction of TUSC-2 under normoxic environment. Their expressions were both downregulated under hypoxic environment. For the angiogenesis related genes, enhanced expressions of vascular endothelial growth factorα, platelet derived growth factor-β and transforming growth factor-β1 could be detected both in normoxic and hypoxic-ischemic conditions.

Conclusion: MiR-378 transfection could effectively promote MSCs survival and vascularization under hypoxic-ischemic condition in vitro.
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http://dx.doi.org/10.1186/scrt520DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4446090PMC
November 2014

Impact of preoperative anemia on relapse and survival in breast cancer patients.

BMC Cancer 2014 Nov 18;14:844. Epub 2014 Nov 18.

Anesthesiology Department, State Key Laboratory in South China, Sun Yat-Sen University Cancer Center, 651 Dongfeng East Road, Guangzhou, PR China.

Background: Previous studies have shown that preoperative anemia is correlated with the prognoses of various solid tumors. This study was performed to determine the effect of preoperative anemia on relapse and survival in patients with breast cancer.

Methods: A total of 2960 patients with breast cancer who underwent surgery between 2002 and 2008 at the Sun Yat-sen University Cancer Center (Guangzhou, PR China) were evaluated in a retrospective analysis. A total of 2123 qualified patients were divided into an anemic group [hemoglobin (Hb) < 12.0 g/dL, N = 535)] and a nonanemic group (Hb ≥ 12.0 g/dL, N = 1588). The effects of anemia on local relapse-free survival (LRFS), lymph node metastasis-free survival (LNMFS), distant metastasis-free survival (DMFS), relapse-free survival (RFS), and overall survival (OS) were assessed using Kaplan-Meier analysis. Independent prognostic factors were identified in the final multivariate Cox proportional hazards regression model.

Results: Among the 2123 women who qualified for the analysis, 535 (25.2%) had a Hb level < 12.0 g/dL. The Kaplan-Meier curves showed that anemic patients had worse LRFS, LNMFS, DMFS, RFS, and OS than nonanemic patients, even in the same clinical stage of breast cancer. Cox proportional hazards regression model indicated that preoperative anemia was an independent prognostic factor of LRFS, LNMFS, DMFS, RFS, and OS for patients with breast cancer.

Conclusions: Preoperative anemia was independently associated with poor prognosis of patients with breast cancer.
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http://dx.doi.org/10.1186/1471-2407-14-844DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242544PMC
November 2014

Inflammatory stress exacerbates hepatic cholesterol accumulation via disrupting cellular cholesterol export.

J Gastroenterol Hepatol 2012 May;27(5):974-84

Chongqing Key Laboratory of Lipid and Glucose Metabolism, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.

Background And Aim: Both inflammation and cholesterol accumulation play important roles in the development of non-alcoholic fatty liver disease. This study was undertaken to investigate whether inflammation aggravated cholesterol accumulation via disrupting hepatic cholesterol export and we explored the underlying mechanisms.

Methods: We used casein injection in C57BL/6J mice, and tumor necrosis factor alpha (TNF-α) stimulation in human hepatoblastoma cell line (HepG2) cells to induce inflammation. Intracellular cholesterol level was examined by Oil Red O staining and quantitative analysis. Bile acid level was quantified by colorimetric analysis. (3)[H] cholesterol assay by scintillation counting was performed to evaluate the cholesterol efflux. The mRNA and protein expression was examined by real-time polymerase chain reaction and Western blot.

Results: Inflammation increased cholesterol accumulation in livers of C57BL/6J mice and in HepG2 cells. High-fat diet in mice and low-density lipoprotein (LDL) loading in HepG2 cells increased bile acid synthesis and cholesterol efflux, enhanced the mRNA and protein expression of liver X receptor α (LXRα), peroxisome proliferator-activated receptors (PPARα, γ), cholesterol 7α-hydroxylase (CYP7A1) and ATP-binding cassette transporter A1 (ABCA1). However, inflammation reduced bile acid synthesis and cholesterol efflux even in high-fat-diet-fed mice and HepG2 cells in the presence of LDL loading. The enhanced effects of these genes and proteins expression due to high-fat diet and LDL loading were inhibited by inflammation both in vivo and in vitro.

Conclusions: Inflammation disrupted PPAR-LXR-CYP7A1/ABCA1-mediated bile acid synthesis and cholesterol efflux resulting in exacerbated cholesterol accumulation in livers of C57BL/6J mice and HepG2 cells.
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http://dx.doi.org/10.1111/j.1440-1746.2011.06986.xDOI Listing
May 2012
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