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  1. Article ; Online: Research advances in immune cellular pathogenesis in liver fibrosis

    XIAO Chunyang

    Journal of Clinical Hepatology, Vol 31, Iss 9, Pp 1532-

    2015  Volume 1536

    Abstract: Liver fibrosis is the common pathological consequence of all chronic liver diseases with various etiologies. The mechanism of liver fibrosis is associated with the activation and proliferation of hepatic stellate cells (HSCs). The interaction between ... ...

    Abstract Liver fibrosis is the common pathological consequence of all chronic liver diseases with various etiologies. The mechanism of liver fibrosis is associated with the activation and proliferation of hepatic stellate cells (HSCs). The interaction between immune cells and HSCs can regulate the production of extracellular matrix (ECM) and lead to the excessive deposition of ECM and subsequent liver fibrosis and cirrhosis. This article reviews the current understanding of the effects and action mechanisms of immune cells in the development of liver fibrosis and summarizes the regulatory functions of the innate and adaptive immune systems in liver fibrosis. Further study of the interactions between immune cells, cytokines, and HSCs and the regulatory mechanisms of the immune system will provide novel opportunity for the treatment of liver fibrosis.
    Keywords liver cirrhosis；hepatic stellate cell; immune cell; review ; Medicine (General) ; R5-920 ; Medicine ; R
    Subject code 610
    Language Chinese
    Publishing date 2015-09-01T00:00:00Z
    Document type Article ; Online
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  2. Article ; Online: Aiming to personalized laser therapy for nevus of Ota: melanin distribution dependent parameter optimization.

    Xiao, Chunyang / Sang, Xuehao / Li, Dong / Chen, Bin / Deng, Chenggang / Wang, Jiafeng

    Lasers in medical science

    2022  Volume 38, Issue 1, Page(s) 10

    Abstract: Aiming to the personalized laser therapy of nevus of Ota (NO), a local thermal non-equilibrium model was employed to optimize laser wavelength, pulse duration, and energy density under different melanin depth and volume fraction. According to our ... ...

    Abstract Aiming to the personalized laser therapy of nevus of Ota (NO), a local thermal non-equilibrium model was employed to optimize laser wavelength, pulse duration, and energy density under different melanin depth and volume fraction. According to our simulation, the optimal pulse duration is between 15 and 150 ns to limit heat transfer inside the hyperplastic melanin, and 50 ns is recommended to decrease the energy absorption by normal melanin in epidermis. Correlations of the minimum and the maximum energy densities are proposed with respect to melanin depth and volume fraction for the 755-nm and 1064-nm lasers. For the same NO type, the therapy window of the 755-nm laser is larger than that of 1064-nm. For NO with shallow depth or low volume fraction, the 755-nm laser is recommended to make the treatment more stable owing to its lager therapy window. For deeper depth or higher volume fraction, the 1064-nm laser is recommended to avoid thermal damage of epidermis. Through comparison with clinical data, the optimized laser parameters are proved practicable since high cure rate can be achieved when energy density falls into the range of predicted therapy window. With developing of non-invasive measurement technology of melanin content and distribution, personalized treatment of NO maybe possible in the near future.
    MeSH term(s) Humans ; Nevus of Ota/radiotherapy ; Nevus of Ota/surgery ; Melanins ; Laser Therapy ; Low-Level Light Therapy ; Skin Neoplasms/radiotherapy ; Skin Neoplasms/surgery
    Chemical Substances Melanins
    Language English
    Publishing date 2022-12-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 632808-8
    ISSN 1435-604X ; 0268-8921
    ISSN (online) 1435-604X
    ISSN 0268-8921
    DOI 10.1007/s10103-022-03673-2
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    Zs.A 2148: Show issues Location:
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  3. Book ; Online: Towards Robust Aspect-based Sentiment Analysis through Non-counterfactual Augmentations

    Liu, Xinyu / Ding, Yan / An, Kaikai / Xiao, Chunyang / Madhyastha, Pranava / Xiao, Tong / Zhu, Jingbo

    2023  

    Abstract: While state-of-the-art NLP models have demonstrated excellent performance for aspect based sentiment analysis (ABSA), substantial evidence has been presented on their lack of robustness. This is especially manifested as significant degradation in ... ...

    Abstract While state-of-the-art NLP models have demonstrated excellent performance for aspect based sentiment analysis (ABSA), substantial evidence has been presented on their lack of robustness. This is especially manifested as significant degradation in performance when faced with out-of-distribution data. Recent solutions that rely on counterfactually augmented datasets show promising results, but they are inherently limited because of the lack of access to explicit causal structure. In this paper, we present an alternative approach that relies on non-counterfactual data augmentation. Our proposal instead relies on using noisy, cost-efficient data augmentations that preserve semantics associated with the target aspect. Our approach then relies on modelling invariances between different versions of the data to improve robustness. A comprehensive suite of experiments shows that our proposal significantly improves upon strong pre-trained baselines on both standard and robustness-specific datasets. Our approach further establishes a new state-of-the-art on the ABSA robustness benchmark and transfers well across domains.

    Comment: 10pages,1 figure,10 tables
    Keywords Computer Science - Computation and Language
    Subject code 006
    Publishing date 2023-06-24
    Publishing country us
    Document type Book ; Online
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  4. Article ; Online: Beneficial Effects of Moderate Hepatic Activin A Expression on Metabolic Pathways, Inflammation, and Atherosclerosis.

    Liu, Huan / Hallauer Hastings, Margaret / Kitchen, Robert / Xiao, Chunyang / Baldovino Guerra, Justin Ralph / Kuznetsov, Alexandra / Rosenzweig, Anthony

    Arteriosclerosis, thrombosis, and vascular biology

    2022  Volume 43, Issue 2, Page(s) 330–349

    Abstract: Background: Atherosclerosis is an inflammatory vascular disease marked by hyperlipidemia and hematopoietic stem cell expansion. Activin A, a member of the Activin/GDF/TGFβ/BMP (growth/differentiation factor/transforming growth factor beta/bone ... ...

    Abstract Background: Atherosclerosis is an inflammatory vascular disease marked by hyperlipidemia and hematopoietic stem cell expansion. Activin A, a member of the Activin/GDF/TGFβ/BMP (growth/differentiation factor/transforming growth factor beta/bone morphogenetic protein) family is broadly expressed and increases in human atherosclerosis, but its functional effects in vivo in this context remain unclear.
    Methods: We studied LDLR
    Results: Activin A expression decreased in both livers and aortae from LDLR
    Conclusions: Our studies reveal hepatic Activin A expression reduces inflammation, hematopoietic stem cell expansion, liver steatosis, circulating cholesterol, and fat accumulation, which likely all contribute to the observed protection against atherosclerosis. The reduced Activin A observed in LDLR
    MeSH term(s) Humans ; Animals ; Mice ; Liver/metabolism ; Inflammation/genetics ; Inflammation/prevention & control ; Inflammation/metabolism ; Atherosclerosis/genetics ; Atherosclerosis/prevention & control ; Atherosclerosis/metabolism ; Activins/genetics ; Activins/metabolism ; Fatty Liver/genetics ; Fatty Liver/prevention & control ; Cholesterol/metabolism ; Metabolic Networks and Pathways ; Receptors, LDL/genetics ; Receptors, LDL/metabolism ; Mice, Knockout ; Mice, Inbred C57BL
    Chemical Substances activin A ; Activins (104625-48-1) ; Cholesterol (97C5T2UQ7J) ; Receptors, LDL
    Language English
    Publishing date 2022-12-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.122.318138
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1705: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  5. Article ; Online: miR-222 inhibits pathological cardiac hypertrophy and heart failure.

    Liu, Xiaojun / Li, Haobo / Hastings, Margaret H / Xiao, Chunyang / Damilano, Federico / Platt, Colin / Lerchenmüller, Carolin / Zhu, Han / Wei, Xin Paul / Yeri, Ashish / Most, Patrick / Rosenzweig, Anthony

    Cardiovascular research

    2023  Volume 120, Issue 3, Page(s) 262–272

    Abstract: Aims: Physiological cardiac hypertrophy occurs in response to exercise and can protect against pathological stress. In contrast, pathological hypertrophy occurs in disease and often precedes heart failure. The cardiac pathways activated in physiological ...

    Abstract Aims: Physiological cardiac hypertrophy occurs in response to exercise and can protect against pathological stress. In contrast, pathological hypertrophy occurs in disease and often precedes heart failure. The cardiac pathways activated in physiological and pathological hypertrophy are largely distinct. Our prior work demonstrated that miR-222 increases in exercised hearts and is required for exercise-induced cardiac hypertrophy and cardiomyogenesis. Here, we sought to define the role of miR-222 in pathological hypertrophy.
    Methods and results: We found that miR-222 also increased in pathological hypertrophy induced by pressure overload. To assess its functional significance in this setting, we generated a miR-222 gain-of-function model through cardiac-specific constitutive transgenic miR-222 expression (TgC-miR-222) and used locked nucleic acid anti-miR specific for miR-222 to inhibit its effects. Both gain- and loss-of-function models manifested normal cardiac structure and function at baseline. However, after transverse aortic constriction (TAC), miR-222 inhibition accelerated the development of pathological hypertrophy, cardiac dysfunction, and heart failure. Conversely, miR-222-overexpressing mice had less pathological hypertrophy after TAC, as well as better cardiac function and survival. We identified p53-up-regulated modulator of apoptosis, a pro-apoptotic Bcl-2 family member, and the transcription factors, Hmbox1 and nuclear factor of activated T-cells 3, as direct miR-222 targets contributing to its roles in this context.
    Conclusion: While miR-222 is necessary for physiological cardiac growth, it inhibits cardiac growth in response to pressure overload and reduces adverse remodelling and cardiac dysfunction. These findings support the model that physiological and pathological hypertrophy are fundamentally different. Further, they suggest that miR-222 may hold promise as a therapeutic target in pathological cardiac hypertrophy and heart failure.
    MeSH term(s) Mice ; Animals ; MicroRNAs/genetics ; Cardiomegaly/metabolism ; Heart Failure/metabolism ; Heart ; Heart Diseases/pathology ; Myocytes, Cardiac/metabolism ; Disease Models, Animal ; Homeodomain Proteins/metabolism
    Chemical Substances MicroRNAs ; Hmbox1 protein, mouse ; Homeodomain Proteins ; MIRN222 microRNA, mouse
    Language English
    Publishing date 2023-12-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvad184
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    Zs.A 565: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Cardioprotective and Anti-Inflammatory Effects of FAM3D in Myocardial Ischemia-Reperfusion Injury.

    Rhee, James / Freeman, Rebecca / Roh, Kangsan / Lyons, Margaret / Xiao, Chunyang / Zlotoff, Daniel / Yeri, Ashish / Li, Haobo / Guerra, Justin / Guseh, J Sawalla / Kuznetsov, Alexandra / Houstis, Nicholas / Roh, Jason / Damilano, Federico / Liu, Xiaojun / Silverman, Michael / Kwong, Raymond / Das, Saumya / Rosenzweig, Anthony

    Circulation research

    2023  Volume 133, Issue 7, Page(s) 651–653

    MeSH term(s) Humans ; Myocardial Reperfusion Injury/prevention & control ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Cytokines
    Chemical Substances Anti-Inflammatory Agents ; FAM3D protein, human ; Cytokines
    Language English
    Publishing date 2023-08-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.123.322640
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    Ui IV Zs.70: Show issues Location:
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    Ui IV Zs.60: Show issues Location:
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  7. Article ; Online: High slope-efficiency quantum-dot lasers grown on planar exact silicon (001) with asymmetric waveguide structures.

    Wang, Jun / Liu, Zhuoliang / Liu, Hao / Bai, Yiming / Ma, Bojie / Xiao, Chunyang / Jiang, Chen / Li, Jiachen / Wang, Haijing / Jia, Yanxing / Liu, Kai / Yang, Yisu / Wang, Qi / Huang, Yongqing / Ren, Xiaomin

    Optics express

    2022  Volume 30, Issue 7, Page(s) 11563–11571

    Abstract: We report electrically pumped continuous-wave (CW) InAs/GaAs quantum dot lasers directly grown on planar exact silicon (001) with asymmetric waveguide structures. Surface hydrogen-annealing for the GaAs/ Si (001) templates and low-temperature growth for ... ...

    Abstract We report electrically pumped continuous-wave (CW) InAs/GaAs quantum dot lasers directly grown on planar exact silicon (001) with asymmetric waveguide structures. Surface hydrogen-annealing for the GaAs/ Si (001) templates and low-temperature growth for GaInP upper cladding layers were combined in the growth of the laser structure to achieve a high slope efficiency. For the broad-stripe edge-emitting lasers with 2-mm cavity length and 20-µm stripe width made from the above laser structure, a threshold current density of 203.5 A/cm
    Language English
    Publishing date 2022-04-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1491859-6
    ISSN 1094-4087 ; 1094-4087
    ISSN (online) 1094-4087
    ISSN 1094-4087
    DOI 10.1364/OE.454895
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  8. Article ; Online: lncExACT1 and DCHS2 Regulate Physiological and Pathological Cardiac Growth.

    Li, Haobo / Trager, Lena E / Liu, Xiaojun / Hastings, Margaret H / Xiao, Chunyang / Guerra, Justin / To, Samantha / Li, Guoping / Yeri, Ashish / Rodosthenous, Rodosthenis / Silverman, Michael G / Das, Saumya / Ambardekar, Amrut V / Bristow, Michael R / González-Rosa, Juan Manuel / Rosenzweig, Anthony

    Circulation

    2022  Volume 145, Issue 16, Page(s) 1218–1233

    Abstract: Background: The heart grows in response to pathological and physiological stimuli. The former often precedes cardiomyocyte loss and heart failure; the latter paradoxically protects the heart and enhances cardiomyogenesis. The mechanisms underlying these ...

    Abstract Background: The heart grows in response to pathological and physiological stimuli. The former often precedes cardiomyocyte loss and heart failure; the latter paradoxically protects the heart and enhances cardiomyogenesis. The mechanisms underlying these differences remain incompletely understood. Although long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis.
    Methods: RNA sequencing was applied to hearts from mice after 8 weeks of voluntary exercise-induced physiological hypertrophy and cardiomyogenesis or transverse aortic constriction for 2 or 8 weeks to induce pathological hypertrophy or heart failure. The top lncRNA candidate was overexpressed in hearts with adeno-associated virus vectors and inhibited with antisense locked nucleic acid-GapmeRs to examine its function. Downstream effectors were identified through promoter analyses and binding assays. The functional roles of a novel downstream effector, dachsous cadherin-related 2 (DCHS2), were examined through transgenic overexpression in zebrafish and cardiac-specific deletion in Cas9-knockin mice.
    Results: We identified exercise-regulated cardiac lncRNAs, called lncExACTs. lncExACT1 was evolutionarily conserved and decreased in exercised hearts but increased in human and experimental heart failure. Cardiac lncExACT1 overexpression caused pathological hypertrophy and heart failure; lncExACT1 inhibition induced physiological hypertrophy and cardiomyogenesis, protecting against cardiac fibrosis and dysfunction. lncExACT1 functioned by regulating microRNA-222, calcineurin signaling, and Hippo/Yap1 signaling through DCHS2. Cardiomyocyte DCHS2 overexpression in zebrafish induced pathological hypertrophy and impaired cardiac regeneration, promoting scarring after injury. In contrast, murine DCHS2 deletion induced physiological hypertrophy and promoted cardiomyogenesis.
    Conclusions: These studies identify lncExACT1-DCHS2 as a novel pathway regulating cardiac hypertrophy and cardiomyogenesis. lncExACT1-DCHS2 acts as a master switch toggling the heart between physiological and pathological growth to determine functional outcomes, providing a potentially tractable therapeutic target for harnessing the beneficial effects of exercise.
    MeSH term(s) Animals ; Cadherin Related Proteins/metabolism ; Cardiomegaly/metabolism ; Disease Models, Animal ; Heart Failure ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Myocytes, Cardiac/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Zebrafish/genetics
    Chemical Substances Cadherin Related Proteins ; MIRN222 microRNA, human ; MicroRNAs ; RNA, Long Noncoding
    Language English
    Publishing date 2022-02-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.121.056850
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    Ui IV Zs.60: Show issues Location:
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  9. Article ; Online: A 6 gene signature identifies the risk of developing cirrhosis in patients with chronic hepatitis B.

    Xu, Ming-Yi / Qu, Ying / Li, Zhenghong / Li, Fei / Xiao, Chun-Yang / Lu, Lun-Gen

    Frontiers in bioscience (Landmark edition)

    2016  Volume 21, Issue 3, Page(s) 479–486

    Abstract: Clinical factors and liver biopsy cannot accurately predict the risk of developing cirrhosis in chronic hepatitis B (CHB).This study was to develop a predictive gene signature for cirrhosis in CHB patients. A total of 183 untreated CHB patients were ... ...

    Abstract Clinical factors and liver biopsy cannot accurately predict the risk of developing cirrhosis in chronic hepatitis B (CHB).This study was to develop a predictive gene signature for cirrhosis in CHB patients. A total of 183 untreated CHB patients were enrolled. GeneChip, significant analysis of microarray (SAM) and prediction analysis of microarray (PAM) were used to select predictor genes (PGs) in liver tissues. The Cirrhosis Risk Score (CRS) was calculated based on 6 PG variables and the predictive value of CRS was evaluated. Firstly differentially expressed genes were filtered from a genome scan and SAM, and 87 significant genes were selected for the signature building. Secondly a signature consisting of 6 PGs (CD24, CXCL6, EHF, ITGBL1, LUM and SOX9) most predictive for cirrhosis risk in CHB patients was developed in the selection set (n=40) by use of PAM and PCR approach. Finally the CRS was calculated to estimate the risk of developing cirrhosis and then tested in validation cohort (n=143). The area under the ROC curves (AUROC) of the CRS was 0.944 and exceeded to 6 PGs and clinical factors. A low CRS cutoff of 6.43 to identify low-risk patients would misclassify only 8.16% of high-risk patients, while a high cutoff of 8.32 to identify high-risk patients would misclassify 0% of low-risk patients. So CRS is a better predictor than clinical factors in differentiating high-risk versus low-risk for cirrhosis and application of CRS in clinical practice could help to reduce the rate of liver biopsy in patients with CHB.
    MeSH term(s) Algorithms ; Gene Expression Profiling ; Genetic Predisposition to Disease ; Hepatitis B, Chronic/genetics ; Humans ; Liver Cirrhosis/genetics ; Risk Factors
    Language English
    Publishing date 2016-01-01
    Publishing country Singapore
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Validation Study
    ZDB-ID 2704569-9
    ISSN 2768-6698 ; 1093-9946
    ISSN (online) 2768-6698
    ISSN 1093-9946
    DOI 10.2741/4403
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  10. Article ; Online: Gelatin Methacryloyl Bioadhesive Improves Survival and Reduces Scar Burden in a Mouse Model of Myocardial Infarction.

    Ptaszek, Leon M / Portillo Lara, Roberto / Shirzaei Sani, Ehsan / Xiao, Chunyang / Roh, Jason / Yu, Xuejing / Ledesma, Pablo A / Hsiang Yu, Chu / Annabi, Nasim / Ruskin, Jeremy N

    Journal of the American Heart Association

    2020  Volume 9, Issue 11, Page(s) e014199

    Abstract: Background Delivery of hydrogels to the heart is a promising strategy for mitigating the detrimental impact of myocardial infarction (MI). Challenges associated with the in vivo delivery of currently available hydrogels have limited clinical translation ... ...

    Abstract Background Delivery of hydrogels to the heart is a promising strategy for mitigating the detrimental impact of myocardial infarction (MI). Challenges associated with the in vivo delivery of currently available hydrogels have limited clinical translation of this technology. Gelatin methacryloyl (GelMA) bioadhesive hydrogel could address many of the limitations of available hydrogels. The goal of this proof-of-concept study was to evaluate the cardioprotective potential of GelMA in a mouse model of MI. Methods and Results The physical properties of GelMA bioadhesive hydrogel were optimized in vitro. Impact of GelMA bioadhesive hydrogel on post-MI recovery was then assessed in vivo. In 20 mice, GelMA bioadhesive hydrogel was applied to the epicardial surface of the heart at the time of experimental MI. An additional 20 mice underwent MI but received no GelMA bioadhesive hydrogel. Survival rates were compared for GelMA-treated and untreated mice. Left ventricular function was assessed 3 weeks after experimental MI with transthoracic echocardiography. Left ventricular scar burden was measured with postmortem morphometric analysis. Survival rates at 3 weeks post-MI were 89% for GelMA-treated mice and 50% for untreated mice (
    MeSH term(s) Animals ; Disease Models, Animal ; Drug Compounding ; Fibrosis ; Gelatin/administration & dosage ; Gelatin/chemistry ; Hydrogels ; Methacrylates/administration & dosage ; Methacrylates/chemistry ; Mice, Inbred C57BL ; Myocardial Infarction/drug therapy ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardium/pathology ; Proof of Concept Study ; Tissue Adhesives/administration & dosage ; Tissue Adhesives/chemistry ; Ventricular Function, Left
    Chemical Substances Hydrogels ; Methacrylates ; Tissue Adhesives ; gelatin methacryloyl ; Gelatin (9000-70-8)
    Language English
    Publishing date 2020-05-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.119.014199
    Database MEDical Literature Analysis and Retrieval System OnLINE

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