Publications by authors named "Zhiying He"

52 Publications

Machine learning-based radiomics for histological classification of parotid tumors using morphological MRI: a comparative study.

Eur Radiol 2022 Jun 24. Epub 2022 Jun 24.

Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, 410008, People's Republic of China.

Objectives: To evaluate the effectiveness of machine learning models based on morphological magnetic resonance imaging (MRI) radiomics in the classification of parotid tumors.

Methods: In total, 298 patients with parotid tumors were randomly assigned to a training and test set at a ratio of 7:3. Radiomics features were extracted from the morphological MRI images and screened using the Select K Best and LASSO algorithm. Three-step machine learning models with XGBoost, SVM, and DT algorithms were developed to classify the parotid neoplasms into four subtypes. The ROC curve was used to measure the performance in each step. Diagnostic confusion matrices of these models were calculated for the test cohort and compared with those of the radiologists.

Results: Six, twelve, and eight optimal features were selected in each step of the three-step process, respectively. XGBoost produced the highest area under the curve (AUC) for all three steps in the training cohort (0.857, 0.882, and 0.908, respectively), and for the first step in the test cohort (0.826), but produced slightly lower AUCs than SVM in the latter two steps in the test cohort (0.817 vs. 0.833, and 0.789 vs. 0.821, respectively). The total accuracies of XGBoost and SVM in the confusion matrices (70.8% and 59.6%) outperformed those of DT and the radiologist (46.1% and 49.2%).

Conclusion: This study demonstrated that machine learning models based on morphological MRI radiomics might be an assistive tool for parotid tumor classification, especially for preliminary screening in absence of more advanced scanning sequences, such as DWI.

Key Points: • Machine learning algorithms combined with morphological MRI radiomics could be useful in the preliminary classification of parotid tumors. • XGBoost algorithm performed better than SVM and DT in subtype differentiation of parotid tumors, while DT seemed to have a poor validation performance. • Using morphological MRI only, the XGBoost and SVM algorithms outperformed radiologists in the four-type classification task for parotid tumors, thus making these models a useful assistant diagnostic tool in clinical practice.
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http://dx.doi.org/10.1007/s00330-022-08943-9DOI Listing
June 2022

Mouse Models of Liver Parenchyma Injuries and Regeneration.

Front Cell Dev Biol 2022 5;10:903740. Epub 2022 May 5.

Department of General Surgery, Ji'an Hospital, Shanghai East Hospital, School of Medicine, Tongji University, Ji'an, China.

Mice have genetic and physiological similarities with humans and a well-characterized genetic background that is easy to manipulate. Murine models have become the most favored, robust mammalian systems for experimental analyses of biological processes and disease conditions due to their low cost, rapid reproduction, a wealth of mouse strains with defined genetic conditions (both native ones as well as ones established experimentally), and high reproducibility with respect to that which can be done in experimental studies. In this review, we focus on murine models for liver, an organ with renown regenerative capacity and the organ most central to systemic, complex metabolic and physiological functions for mammalian hosts. Establishment of murine models has been achieved for all aspects of studies of normal liver, liver diseases, liver injuries, and regenerative repair mechanisms. We summarize key information on current mouse systems that partially model facets of clinical scenarios, particularly those associated with drug-induced acute or chronic liver injuries, dietary related, non-alcoholic liver disease (NAFLD), hepatitis virus infectious chronic liver diseases, and autoimmune hepatitis (AIH). In addition, we also include mouse models that are suitable for studying liver cancers (e.g., hepatocellular carcinomas), the aging process (senescence, apoptosis), and various types of liver injuries and regenerative processes associated with them.
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http://dx.doi.org/10.3389/fcell.2022.903740DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9198899PMC
May 2022

Prognostic Significance and Immunological Role of FBXO5 in Human Cancers: A Systematic Pan-Cancer Analysis.

Front Immunol 2022 3;13:901784. Epub 2022 Jun 3.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.

F-box protein 5 (FBXO5), an essential subunit of the ubiquitin protein ligase complex, is increasingly recognized to exhibit important biological effects in regulating tumor occurrence and progression. The present research was intended to systematically investigate the latent roles of FBXO5 in prognosis and immunological function across cancers. Pan-cancer analyses of FBXO5 were performed based upon publicly available online databases, mainly including the Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), UCSC Xena, cBioPortal, and ImmuCellAI, revealing the possible relationships between FBXO5 and prognosis, DNA methylation, tumor microenvironment (TME), infiltration of immune cells, immune-related genes, immune checkpoints, tumor mutation burden (TMB), and microsatellite instability (MSI). The results suggested that FBXO5 was expressed at a high level in numerous tumor cell lines with significant upregulation in most cancers as opposed to normal tissues. Of note, elevated expression of FBXO5 was significantly related to an unfavorable prognosis in many cancer types. Furthermore, DNA methylation and TME were confirmed to display evident correlation with the expression of FBXO5 in several malignancies. Moreover, FBXO5 expression was remarkably positively correlated with the levels of infiltrating Treg cells and Tcm cells in most tumors, but negatively correlated with tumor-infiltrating CD8 T cells, NK/NKT cells, and Th2 cells. Meanwhile, FBXO5 was demonstrated to be co-expressed with the genes encoding immune activating and suppressive factors, chemokines, chemokine receptors, and major histocompatibility complex (MHC). Immune checkpoints, TMB, and MSI were also overtly associated with FBXO5 dysregulation among diverse kinds of cancers. Additionally, the enrichment analyses showed close relationships between FBXO5 expression and the processes related to cell cycle and immune inflammatory response. These findings provided a detailed comprehension of the oncogenic function of FBXO5. Because of its crucial roles in cancer immunity and tumorigenesis, FBXO5 may serve as a novel prognostic indicator and immunotherapeutic target for various malignancies.
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http://dx.doi.org/10.3389/fimmu.2022.901784DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9203914PMC
June 2022

Intramyocardial injected human umbilical cord-derived mesenchymal stem cells (HucMSCs) contribute to the recovery of cardiac function and the migration of CD4 T cells into the infarcted heart via CCL5/CCR5 signaling.

Stem Cell Res Ther 2022 06 11;13(1):247. Epub 2022 Jun 11.

Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, 150 Jimo Rd, Pudong, Shanghai, 200120, People's Republic of China.

Background: Human umbilical cord-derived mesenchymal stem cells (HucMSCs) have been recognized as a promising cell for treating myocardial infarction (MI). Inflammatory response post MI is critical in determining the cardiac function and subsequent adverse left ventricular remodeling. However, the local inflammatory effect of HucMSCs after intramyocardial injection in murine remains unclear.

Methods: HucMSCs were cultured and transplanted into the mice after MI surgery. Cardiac function of mice were analyzed among MI-N.S, MI-HucMSC and MI-HucMSC-C-C Motif Chemokine receptor 5 (CCR5) antagonist groups, and angiogenesis, fibrosis and hypertrophy, and immune cells infiltration of murine hearts were evaluated between MI-N.S and MI-HucMSC groups. We detected the expression of inflammatory cytokines and their effects on CD4 T cells migration.

Results: HucMSCs treatment can significantly improve the cardiac function and some cells can survive at least 28 days after MI. Intramyocardial administration of HucMSCs also improved angiogenesis and alleviated cardiac fibrosis and hypertrophy. Moreover, we found the much higher numbers of CD4 T cells and CD4FoxP3 regulatory T cells (Tregs) in the heart with HucMSCs than that with N.S treatment on day 7 post MI. In addition, the protein level of C-C Motif Chemokine Ligand 5 (CCL5) greatly increased in HucMSCs treated heart compared to MI-N.S group. In vitro, HucMSCs inhibited CD4 T cells migration and addition of CCL5 antibody or CCR5 antagonist significantly reversed this effect. In vivo results further showed that addition of CCR5 antagonist can reduce the cardioprotective effect of HucMSCs administration on day 7 post MI injury.

Conclusion: These findings indicated that HucMSCs contributed to cardiac functional recovery and attenuated cardiac remodeling post MI. Intramyocardial injection of HucMSCs upregulated the CD4FoxP3 Tregs and contributed to the migration of CD4 T cells into the injured heart via CCL5/CCR5 pathway.
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http://dx.doi.org/10.1186/s13287-022-02914-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9188247PMC
June 2022

Effect of aerobic exercise as a treatment on type 2 diabetes mellitus with depression-like behavior zebrafish.

Life Sci 2022 Jul 27;300:120578. Epub 2022 Apr 27.

Department of Endocrinology and Metabolism, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China. Electronic address:

Background: Depression is the most known complication of type 2 diabetes mellitus (T2DM). Aerobic exercise improves glycemic control in T2DM, although the underlying mechanisms of comorbid depression-like behaviors in T2DM have not yet been fully elucidated.

Methods: 120 zebrafish were randomly assigned to four groups: Control, T2DM, T2DM + metformin, and T2DM + aerobic exercise. Then, all animals except the control group were fed with high glucose fairy shrimp (~40 g/kg/day) and exposed reserpine (40 μg/ml for 20 min) for 10 days. Here, behavioral tests were used for model verification. Following the verification, all groups were treated as before. Additionally, the T2DM + metformin group received metformin (~10.6 mg/kg/day) at the same time, while the T2DM + aerobic exercise group received aerobic exercise 30 min/day. Finally, blood glucose and behavioral tests, as well as protein and molecular levels were determined at Day 11 and 12.

Results: Aerobic exercise alleviated depressive-like behavior and enhanced the levels of antidepressant biomarkers (NE, 5-HIAA) in zebrafish after 10 consecutive days of exercise. Additionally, 10 consecutive days of aerobic exercise decreased the levels of inflammatory biomarkers (IFN-γ, IL-1, IL-4) and depressive biomarkers (cortisol). Meanwhile, it also aided in the reduction of CD11b, IL-6, IL-6R, and caspase-3 expression to combat the neuroinflammation induced by T2DM, mediated the BDNF-TrkB pathway, and increased Bcl-2/Bax levels.

Conclusion: Given the remarkable similarity in neurochemistry between humans and zebrafish, this study supports the effectiveness of aerobic exercise as clinical guidance in preventing and treating T2DM complicated with depression.
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http://dx.doi.org/10.1016/j.lfs.2022.120578DOI Listing
July 2022

Editorial: Stem Cells in Tissue Homeostasis and Disease.

Front Cell Dev Biol 2022 9;10:876060. Epub 2022 Mar 9.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.

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http://dx.doi.org/10.3389/fcell.2022.876060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8959411PMC
March 2022

Stathmin 1 is a biomarker for diagnosis of microvascular invasion to predict prognosis of early hepatocellular carcinoma.

Cell Death Dis 2022 02 24;13(2):176. Epub 2022 Feb 24.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University School of Medicine, Shanghai, 200123, P. R. China.

Microvascular invasion (MVI) is presently evaluated as a high-risk factor to be directly relative to postoperative prognosis of hepatocellular carcinoma (HCC). Up to now, diagnosis of MVI mainly depends on the postoperative pathological analyses with H&E staining assay, based on numbers and distribution characteristics of MVI to classify the risk levels of MVI. However, such pathological analyses lack the specificity to discriminate MVI in HCC specimens, especially in complicated pathological tissues. In addition, the efficiency to precisely define stages of MVI is not satisfied. Thus, any biomarker for both conforming diagnosis of MVI and staging its levels will efficiently and effectively promote the prediction of early postoperative recurrence and metastasis for HCC. Through bioinformatics analysis and clinical sample verification, we discovered that Stathmin 1 (STMN1) gene was significantly up-regulated at the locations of MVI. Combining STMN1 immunostaining with classic H&E staining assays, we established a new protocol for MVI pathological diagnosis. Next, we found that the degrees of MVI risk could be graded according to expression levels of STMN1 for prognosis prediction on recurrence rates and overall survival in early HCC patients. STMN1 affected epithelial-mesenchymal transformation (EMT) of HCC cells by regulating the dynamic balance of microtubules through signaling of "STMN1-Microtubule-EMT" axis. Inhibition of STMN1 expression in HCC cells reduced their lung metastatic ability in recipients of mouse model, suggesting that STMN1 also could be a potential therapeutic target for inhibiting HCC metastasis. Therefore, we conclude that STMN1 has potentials for clinical applications as a biomarker for both pathological diagnosis and prognostic prediction, as well as a therapeutic target for HCC.
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http://dx.doi.org/10.1038/s41419-022-04625-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8873260PMC
February 2022

Flexural behaviour and evaluation of ultra-high-performance fibre reinforced concrete beams cured at room temperature.

Sci Rep 2021 Sep 24;11(1):19069. Epub 2021 Sep 24.

School of Civil Engineering, The University of Sydney, Sydney, NSW, 2006, Australia.

Heat treatment is often required for ultra-high-performance concrete (UHPC) to achieve high strength. To broad its use in construction, the effect of different curing conditions on the properties of UHPC has been developed for many years. The experimental investigation of large scale ultra-high-performance fibre reinforced concrete (UHPFRC) beams is limited. In the present study, UHPFRC specimens and concrete cured at 20 °C were prepared to investigate the properties and flexural behaviour. The standard cubic compressive strength of UHPFRC specimens cannot be achieved at curing temperature of 20 °C. The bearing capacity under flexure was enhanced with the increase of reinforcement ratio. The failure modes of beams changed from ductile to brittle as the reinforcement ratio increased from 1.26 to 9.50%. The flexural behaviour of UHPFRC beams cured at room temperature was in accordance with the UHPFRC beams cured at high temperature in previous studies. In addition, the calculation model of CECS38-2004 underestimated the bending moment capacity of the under-reinforced UHPFRC beams (with reinforcement ratio from 0 to 7.85%) and overestimated the bending moment capacity of the UHPFRC beams with high reinforcement ration of 9.50%.
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http://dx.doi.org/10.1038/s41598-021-98502-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8463697PMC
September 2021

A Three-Dimensional Imaging Method for the Quantification and Localization of Dynamic Cell Tracking Posttransplantation.

Front Cell Dev Biol 2021 7;9:698795. Epub 2021 Sep 7.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.

Cell transplantation has been proposed as a promising therapeutic strategy for curing the diseases requiring tissue repairing and functional restoration. A preclinical method to systematically evaluate the fates of donor cells in recipients, spatially and temporally, is demanded for judging therapeutic potentials for the particularly designed cell transplantation. Yet, the dynamic cell tracking methodology for tracing transplanted cells is still at its early phase. Here, we created a practical protocol for dynamically tracking cell a three-dimensional (3D) technique which enabled us to localize, quantify, and overall evaluate the transplanted hepatocytes within a liver failure mouse model. First, the capacity of 3D bioluminescence imaging for quantifying transplanted hepatocytes was defined. Images obtained from the 3D bioluminescence imaging module were then combined with the CT scanner to reconstruct structure images of host mice. With those reconstructed images, precise locations of transplanted hepatocytes in the liver of the recipient were dynamically monitored. Immunohistochemistry staining of transplanted cells, and the serology assay of liver panel of the host mice were applied to verify the successful engraftment of donor cells in the host livers. Our protocol was practical for evaluating the engraftment efficiency of donor cells at their preclinical phases, which is also applicable as a referable standard for studying the fates of other transplanted cells, such as stem cell-derived cell types, during preclinical studies with cell transplantation therapy.
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http://dx.doi.org/10.3389/fcell.2021.698795DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8452970PMC
September 2021

Patch grafting, strategies for transplantation of organoids into solid organs such as liver.

Biomaterials 2021 10 25;277:121067. Epub 2021 Aug 25.

Departments of Cell Biology and Physiology, Program in Molecular Biology and Biotechnology, UNC School of Medicine, Chapel Hill, NC, 27599, USA. Electronic address:

Epithelial cell therapies have been at an impasse because of inefficient methods of transplantation to solid organs. Patch grafting strategies were established enabling transplantation of ≥10 organoids/patch of porcine GFP+ biliary tree stem/progenitors into livers of wild type hosts. Grafts consisted of organoids embedded in soft (~100 Pa) hyaluronan hydrogels, both prepared in serum-free Kubota's Medium; placed against target sites; covered with a silk backing impregnated with more rigid hyaluronan hydrogels (~700 Pa); and use of the backing to tether grafts with sutures or glue to target sites. Hyaluronan coatings (~200-300 Pa) onto the serosal surface of the graft served to minimize adhesions with neighboring organs. The organ's clearance of hyaluronans enabled restoration of tissue-specific paracrine and systemic signaling, resulting in return of normal hepatic histology, with donor parenchymal cells uniformly integrated amidst host cells and that had differentiated to mature hepatocytes and cholangiocytes. Grafts containing donor mature hepatocytes, partnered with endothelia, and in the same graft biomaterials as for stem/progenitor organoids, did not engraft. Engraftment occurred if porcine liver-derived mesenchymal stem cells (MSCs) were co-transplanted with donor mature cells. RNA-seq analyses revealed that engraftment correlated with expression of matrix-metalloproteinases (MMPs), especially secreted isoforms that were found expressed strongly by organoids, less so by MSCs, and minimally, if at all, by adult cells. Engraftment with patch grafting strategies occurred without evidence of emboli or ectopic cell distribution. It was successful with stem/progenitor organoids or with cells with a source(s) of secreted MMP isoforms and offers significant potential for enabling cell therapies for solid organs.
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http://dx.doi.org/10.1016/j.biomaterials.2021.121067DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8826591PMC
October 2021

Translational Attenuation Mechanism of Induction by Erythromycin Is Dependent on Two Leader Peptides.

Front Microbiol 2021 28;12:690744. Epub 2021 Jun 28.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.

Ribosome stalling on at the tenth codon (Asp) is believed to be a major mechanism of induction by erythromycin (Ery). In this study, we demonstrated that the mechanism of induction by Ery depends not only on expression but also on previously unreported expression. Introducing premature termination codons in , we proved that translation of the N-terminal region of is the key component for induced by Ery, whereas translation of the C-terminal region of did not affect Ery-induced . Mutation of the tenth codon (Asp10) of with other amino acids showed that the degree of induction was not completely consistent with the data from toe printing assay. Alanine-scanning mutagenesis of demonstrated that both N-terminal residues (R7-K11) and the latter part of (K20-K27) are critical for Ery induction of ermB. The frameshifting reporter plasmid showed that a new leader peptide, , exists in the regulatory region. Further, introducing premature termination mutation and alanine-scanning mutagenesis of demonstrated that the N-terminus of is essential for induction by Ery. Therefore, the detailed function of requires further study.
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http://dx.doi.org/10.3389/fmicb.2021.690744DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8274638PMC
June 2021

A MicroRNA-Based Network Provides Potential Predictive Signatures and Reveals the Crucial Role of PI3K/AKT Signaling for Hepatic Lineage Maturation.

Front Cell Dev Biol 2021 1;9:670059. Epub 2021 Jun 1.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University School of Medicine, Shanghai, China.

Background: Functions of miRNAs involved in tumorigenesis are well reported, yet, their roles in normal cell lineage commitment remain ambiguous. Here, we investigated a specific "transcription factor (TF)-miRNA-Target" regulatory network during the lineage maturation of biliary tree stem cells (BTSCs) into adult hepatocytes (hAHeps).

Method: Bioinformatic analysis was conducted based on our RNA-seq and microRNA-seq datasets with four human hepatic-lineage cell lines, including hBTSCs, hepatic stem cells (hHpSCs), hepatoblasts (hHBs), and hAHeps. Short time-series expression miner (STEM) analysis was performed to reveal the time-dependent dynamically changed miRNAs and mRNAs. GO and KEGG analyses were applied to reveal the potential function of key miRNAs and mRNAs. Then, the miRDB, miRTarBase, TargetScan, miRWalk, and DIANA-microT-CDS databases were adopted to predict the potential targets of miRNAs while the TransmiR v2.0 database was used to obtain the experimentally supported TFs that regulate miRNAs. The TCGA, Kaplan-Meier Plotter, and human protein atlas (HPA) databases and more than 10 sequencing data, including bulk RNA-seq, microRNA-seq, and scRNA-seq data related to hepatic development or lineage reprogramming, were obtained from both our or other published studies for validation.

Results: STEM analysis showed that during the maturation from hBTSCs to hAHeps, 52 miRNAs were downwardly expressed and 928 mRNA were upwardly expressed. Enrichment analyses revealed that those 52 miRNAs acted as pluripotency regulators for stem cells and participated in various novel signaling pathways, including PI3K/AKT, MAPK, and etc., while 928 mRNAs played important roles in liver-functional metabolism. With an extensive sorting of those key miRNAs and mRNAs based on the target prediction results, 23 genes were obtained which not only functioned as the targets of 17 miRNAs but were considered critical for the hepatic lineage commitment. A "TF-miRNA-Target" regulatory network for hepatic lineage commitment was therefore established and had been well validated by various datasets. The network revealed that the PI3K/AKT pathway was gradually suppressed during the hepatic commitment.

Conclusion: A total of 17 miRNAs act as suppressors during hepatic maturation mainly by regulating 23 targets and modulating the PI3K/AKT signaling pathway. The regulatory network uncovers possible signatures and guidelines enabling us to identify or obtain the functional hepatocytes for future study.
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http://dx.doi.org/10.3389/fcell.2021.670059DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8204022PMC
June 2021

Endoscopy-Assisted Transoral Approach to Resect Parapharyngeal Space Tumors: A Systematic Review and Meta-Analysis.

Laryngoscope 2021 10 22;131(10):2246-2253. Epub 2021 Feb 22.

Department of Otolaryngology Head and Neck Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, People's Republic of China.

Objectives: By comparing the endoscopy-assisted transoral approach (EATA) with external approaches (EAs) for the resection of parapharyngeal space tumors (PPSTs), we determined whether the EATA has advantages in terms of operation time, intraoperative bleeding volume, postoperative hospitalization, drainage volume, and complications. At the same time, we summarized the surgical indications for the EATA.

Methods: Systematic literature retrieval was performed in the PubMed, Web of Science, Embase, CNKI, Wanfang, and CQVIP databases up to February 2020. We calculated the mean difference (MD) with a 95% confidence interval (CI) for continuous outcomes and pooled odds ratio (OR) with 95% CI for dichotomous outcomes. The measured outcomes were operative time, bleeding volume, postoperative hospitalization, drainage volume, and complications.

Results: Seven studies involving 318 patients were eligible. Of these patients, 145 patients underwent EATA and 173 patients underwent EA surgery. All the former tumors were benign and located medial or anteromedial to the carotid sheath except for the unrecorded tumors. Compared with EAs, the EATA significantly shortened the operation time (MD = -5.56 min, 95% CI: -9.58 to -1.55), shrank the bleeding volume (MD = -89.02 ml, 95% CI: -126.16 to -51.88), shortened the postoperative hospitalization (MD = -2.44 days, 95% CI: -3.37 to -1.51), reduced the drainage volume (MD = -32.97 ml, 95% CI: -36.24 to -29.70), and lowered the incidence of complications (OR = 0.30, 95% CI: 0.16 to 0.59).

Conclusion: As for PPSTs, with an appropriate and precise patient selection, the EATA is a safe, effective, minimally invasive, and aesthetic surgical modality. Laryngoscope, 131:2246-2253, 2021.
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http://dx.doi.org/10.1002/lary.29458DOI Listing
October 2021

Hepatocellular Senescence: Immunosurveillance and Future Senescence-Induced Therapy in Hepatocellular Carcinoma.

Front Oncol 2020 27;10:589908. Epub 2020 Nov 27.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, China.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. The lack of effective targeted drugs has become a challenge on treating HCC patients. Cellular senescence is closely linked to the occurrence, development, and therapy of tumor. Induction of cellular senescence and further activation of immune surveillance provides a new strategy to develop HCC targeted drugs, that is, senescence-induced therapy for HCC. Precancerous hepatocytes or HCC cells can be induced into senescent cells, subsequently producing senescence-associated secretory phenotype (SASP) factors. SASP factors recruit and activate various types of immune cells, including T cells, NK cells, macrophages, and their subtypes, which carry out the role of immune surveillance and elimination of senescent cells, ultimately preventing the occurrence of HCC or inhibiting the progression of HCC. Specific interventions in several checkpoints of senescence-mediated therapy will make positive contributions to suppress tumorigenesis and progression of HCC, for instance, by applying small molecular compounds to induce cellular senescence or selecting cytokines/chemokines to activate immunosurveillance, supplementing adoptive immunocytes to remove senescent cells, and screening chemical drugs to induce apoptosis of senescent cells or accelerate clearance of senescent cells. These interventional checkpoints become potential chemotherapeutic targets in senescence-induced therapy for HCC. In this review, we focus on the frontiers of senescence-induced therapy and discuss senescent characteristics of hepatocytes during hepatocarcinogenesis as well as the roles and mechanisms of senescent cell induction and clearance, and cellular senescence-related immunosurveillance during the formation and progression of HCC.
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http://dx.doi.org/10.3389/fonc.2020.589908DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7732623PMC
November 2020

The mRNA of TCTP functions as a sponge to maintain homeostasis of TCTP protein levels in hepatocellular carcinoma.

Cell Death Dis 2020 11 12;11(11):974. Epub 2020 Nov 12.

Department of Hepatobiliary Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi Province, 710032, China.

Translationally controlled tumor protein (TCTP) is a highly conserved protein that accumulated in the tumorigenesis of various malignancies. Despite the important role of TCTP protein in tumor progression, the precise function and underlying mechanistic regulation of TCTP mRNA in hepatocellular carcinoma (HCC) remain unclear. In this study, we found that TCTP protein was overexpressed in HCC patients but TCTP mRNA expression levels were reversed. TCTP knockout HCC cells exhibited attenuated abilities of proliferation, migration, and invasion. The knockdown of TCTP by siRNA effectively reduced TCTP mRNA levels but not protein levels in HCC cells. Moreover, although the constitutive knockdown of TCTP inhibited almost 80% of TCTP protein expression levels in tumors of wildtype transgenic mice (TCTP KD/WT), partial restoration of TCTP protein expression was observed in the tumors of heterozygous TCTP mice (TCTP KD/TCTP±). The blockage of mRNA synthesis with ActD stimulated TCTP protein expression in HCC cells. In contrast, combined treatment with ActD and CHX or MG132 treatment alone did not lead to the TCTP protein accumulation in cells. Furthermore, following the introduction of exogenous TCTP in cells and orthotopic HCC tumor models, the endogenous TCTP protein did not change with the recombinational TCTP expression and kept a rather stable level. Dual-luciferase assays revealed that the coding sequence of TCTP mRNA functions as a sponge to regulate the TCTP protein expression. Collectively, our results indicated that the TCTP mRNA and protein formed a closed regulatory circuit and works as a buffering system to keep the homeostasis of TCTP protein levels in HCC.
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http://dx.doi.org/10.1038/s41419-020-03149-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7665032PMC
November 2020

Extensively expanded murine-induced hepatic stem cells maintain high-efficient hepatic differentiation potential for repopulation of injured livers.

Liver Int 2020 09 8;40(9):2293-2304. Epub 2020 Jun 8.

Department of Cell Biology, Center for Stem Cell and Medicine, Navy Medical University (Second Military Medical University), Shanghai, P. R. China.

Background & Aim: Shortage of donor hepatocytes limits hepatocyte transplantation for clinical application. Induced hepatic stem cells (iHepSCs) have capacities of self-renewal and bipotential differentiations. Here, we investigated whether iHepSCs could be extensively expanded, and whether they could differentiate into sufficient functional hepatocytes as donors for transplantation therapy after their extensive expansions.

Methods: Murine extensively expanded iHepSCs (50-55 passages) were induced to differentiate into iHepSC-Heps under a chemically defined condition. iHepSC-Heps were proved for carrying morphological hepatocyte characters and hepatocytic functions including low-density lipoprotein uptake, glycogen storage, CLF secretion, ICG uptake and release, Alb secretion, urea synthesis and metabolism-relative gene expressions respectively. Next, both iHepSCs and iHepSC-Heps were transplanted into Fah-/- mice respectively. Both liver repopulation and alleviation of liver function were compared between two transplantation groups.

Results: Murine iHepSCs still maintained the capacities of self-renewal and bipotential differentiations after extensive expansion. The efficiency for the functional hepatocyte differentiation from extensively expanded iHepSCs reached to 72.64%. Transplantations of both extensively expanded iHepSCs and iHepSC-Heps resulted in liver engraftment in Fah-/- mice. Survival rate of Fah-/- mice recipients and level of liver repopulation were 50% and 20.32 ± 4.58% respectively in iHepSC-Heps group, while 33% and 10.4 ± 4.3% in iHepSCs group.

Conclusions: Extensively expanded iHepSCs can efficiently differentiate into hepatocytes in chemical defined medium. Transplantation of iHepSC-Heps was more effective and more efficient than transplantation of iHepSCs in Fah-/- mice. Our results suggested an innovative system to obtain sufficient hepatocytes through hepatic differentiation of iHepSCs generated by lineage reprogramming.
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http://dx.doi.org/10.1111/liv.14509DOI Listing
September 2020

A New Polyphase Down-Sampling Based Multiple Description Image Coding.

IEEE Trans Image Process 2020 Apr 7. Epub 2020 Apr 7.

Multiple description coding (MDC) is an efficient source coding technique for error-prone transmission over multiple channels. In this paper, we focus on the design of a new polyphase down-sampling based MDC (NPDS-MDC) for image signals. The encoding of our proposed NPDS-MDC consists of three steps. First, we perform down-sampling on each N×N image block according to the quincunx down-sampling pattern. Second, we propose a new transform and apply it to the down-sampled pixels to produce the side descriptions. Third, we develop an error compensation algorithm to reduce the compression distortion occurring on the down-sampled pixels. In our scheme, the side decoding is performed posterior to image interpolation with reference to the down-sampled compressed pixels. Moreover, the central decoding is achieved by interlacing the side descriptions. We also propose a compression-constrained central deblocking algorithm to further improve the efficiency of the central decoding. The experimental results indicate that our proposed MDC scheme offers clearly superior performance, especially at high bit rates, as compared to the state-of-the-art methods for various types of images.
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http://dx.doi.org/10.1109/TIP.2020.2984876DOI Listing
April 2020

TRAF6 suppresses the apoptosis of hemocytes by activating pellino in Crassostrea hongkongensis.

Dev Comp Immunol 2020 02 18;103:103501. Epub 2019 Oct 18.

Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Science, Guangzhou, 510301, China; Innovation Academy of South China Sea Ecology and Environmental Engineering (ISEE), Chinese Academy of Sciences, China. Electronic address:

Tumor necrosis factor receptor-associated factor 6 (TRAF6), an E3 ubiquitin ligase, participates in both innate and adaptive immunity and regulates the apoptotic process. In this study, we observed that an ortholog of TRAF6 could inhibit the activity of p53 and suppress the apoptotic process in the Hong Kong oyster, Crassostrea hongkongensis. To investigate the possible molecular mechanism of the ChTRAF6-induced antiapoptotic effect, a GST pull-down screening assay was conducted, and ChPellino was found to physically interact with ChTRAF6. In addition, the interaction between them was confirmed by Co-immunoprecipitation. Furthermore, western blotting revealed that the phosphorylation level of ChPellino was decreased after the RNAi of ChTRAF6, demonstrating that ChTRAF6 may be an upstream regulator of Pellino activation. Furthermore, the apoptosis level of hemocytes increased after ChPellino knockdown, and ChPellino overexpression suppressed ChTRAF6-dependent p53 activation. Taken together, these results indicate that ChPellino plays a critical role in suppressing ChTRAF6-dependent anti-apoptosis in the hemocytes of Crassostrea hongkongensis.
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http://dx.doi.org/10.1016/j.dci.2019.103501DOI Listing
February 2020

microRNA-17 functions as an oncogene by downregulating Smad3 expression in hepatocellular carcinoma.

Cell Death Dis 2019 09 26;10(10):723. Epub 2019 Sep 26.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Life Sciences and Technology, Tongji University, Shanghai, 200123, P. R. China.

The sekelsky mothers against dpp3 (Smad3) functions as a transcriptional modulator activated by transforming growth factor-β (TGF-β). Accumulated evidences indicated that Smad3 played the important roles in carcinogenesis and progression of hepatocellular carcinoma (HCC). Up to now, the regulatory mechanism of Smad3 in HCC still remains unclear. It has been known that some particular microRNAs (miRNAs) involve in carcinogenesis through the regulation of gene expressions with targeting mRNAs. In our study, the unknown candidates of miRNAs that target Smad3 mRNA were searched by using a newly established in vivo approach, the miRNA in vivo precipitation (miRIP). Using a loss-of-function assay, we demonstrated that miR-17 directly targeted Smad3 in HCC cells and inhibition on miR-17 increased Smad3 expression. Furthermore, we found that downregulation on Smad3 expression was consistent with high level of miR-17 in HCC tissues of patients when compared with around normal liver tissues. The manipulated miR-17 silence in HCC cells suppressed their growth of both in vitro and in vivo. Such suppression on cell growth could be recovered through downregulating Smad3. In addition, miR-17 affected cell proliferation through arresting cell cycle in G1 phase. The negative correlation between levels of miR-17 and protein levels of Smad3 was supported by the results of analysis with HCC tissue chip. In summary, for the first time, we confirmed that miR-17 directly targeted Smad3 mRNA and downregulated Smad3 protein expression in HCC. Our results indicated that the increased expression of miR-17 promoted carcinogenesis of HCC through down-regulations of Smad3, suggesting miR-17 might serve as the potential diagnostic and therapeutic targets for clinical HCC.
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http://dx.doi.org/10.1038/s41419-019-1960-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6763424PMC
September 2019

Molecular characteristics of AMPK and its role in regulating the phagocytosis of oyster hemocytes.

Fish Shellfish Immunol 2019 Oct 30;93:416-427. Epub 2019 Jul 30.

Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, Institution of South China Sea Ecology and Environmental Engineering, South China Sea Institute of Oceanology, Chinese Academy of Science, Guangzhou, 510301, China. Electronic address:

Phagocytosis is one of the fundamental cellular immune defense parameter that helps in the elimination of the invading pathogens in both vertebrates and invertebrates, which require plenty of energy for functioning. In the present study, we identified the critical energy regulator AMP-activated protein kinase (AMPK) in Crassostrea hongkongensis which is composed of three subunits, named ChAMPK-α, ChAMPK-β, and ChAMPK-γ, and then analyzed the function of AMPK in regulating hemocyte phagocytosis. All the three ChAMPK subunits mRNA were detected to be expressed at various embryological stages, and also constitutively expressed in multiple tissues with high expression in gill and mantle. The phylogenetic tree showed that the three subunits of AMPK were correspondingly clustered with its orthologue branches. Furthermore Western Blot analysis revealed that the AMPK pharmacological inhibitors Compound C could effectively down-regulate the Thr phosphorylation level of AMPK-α, and the hemocyte phagocytosis was inhibited by Compound C (CC), which indicate its existence in the oyster. Our results showed that treatment of AMPK inhibitors significantly attenuated the capacity of hemocytes phagocytosis. Moreover, Compound C could also change the organization of actin cytoskeleton in the oyster hemocytes, demonstrating the crucial role of AMPK signaling in control of phagocytosis.
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http://dx.doi.org/10.1016/j.fsi.2019.07.075DOI Listing
October 2019

Conversion of hepatoma cells to hepatocyte-like cells by defined hepatocyte nuclear factors.

Cell Res 2019 02 18;29(2):124-135. Epub 2018 Dec 18.

International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital/Institute, the Second Military Medical University, Shanghai, China.

Normal cells become cancer cells after a malignant transformation, but whether cancer cells can be reversed to normal status remains elusive. Here, we report that the combination of hepatocyte nuclear factor 1A (HNF1A), HNF4A and forkhead box protein A3 (FOXA3) synergistically reprograms hepatocellular carcinoma (HCC) cells to hepatocyte-like cells (reprogrammed hepatocytes, rHeps). Our results show that rHeps lose the malignant phenotypes of cancer cells and retrieve hepatocyte-specific characteristics including hepatocyte-like morphology; global expression pattern of genes and specific biomarkers of hepatocytes; and the unique hepatic functions of albumin (ALB) secretion, glycogen synthesis, low-density lipoprotein (LDL) uptake, urea production, cytochrome P450 enzymes induction and drug metabolism. Intratumoral injection of these three factors efficiently shrank patient-derived tumor xenografts and reprogrammed HCC cells in vivo. Most importantly, transplantation of rHeps in the liver of fumarylacetoacetate hydrolase-deficient (Fah) mice led to the reconstruction of hepatic lobules and the restoration of hepatic function. Mechanistically, exogenous expression of HNF1A, HNF4A and FOXA3 in HCC cells initiated the endogenous expression of numerous hepatocyte nuclear factors, which promoted the conversion of HCC cells to hepatocyte-like cells. Collectively, our results indicate the successful conversion of hepatoma cells to hepatocyte-like cells, not only extending our current knowledge of cell reprogramming but also providing a route towards a novel therapeutic strategy for cancer.
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http://dx.doi.org/10.1038/s41422-018-0111-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6355772PMC
February 2019

Systematic review: diagnostic accuracy of non-invasive tests for staging liver fibrosis in autoimmune hepatitis.

Hepatol Int 2019 Jan 15;13(1):91-101. Epub 2018 Nov 15.

National Clinical Research Center of Digestive Diseases, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.

Background And Aims: Non-invasive fibrosis assessment has been highly recommended in many liver diseases. However, comparative diagnostic accuracy of laboratory markers, ultrasound and magnetic resonance elastography (MRE) for fibrosis in autoimmune hepatitis (AIH) patients has not been established.

Methods: Medline, Embase and Cochrane Library were searched. Primary outcome was significant fibrosis (SF), advanced fibrosis (AF) and cirrhosis, defined as Metavir stage F ≥ 2, F ≥ 3 and F = 4 according to liver biopsy. Hierarchical summary receiver operating characteristic curve (ROC) model was used to evaluate diagnostic accuracy of non-invasive methods. Summary area under ROC (AUROC) and diagnostic odds ratio (DOR) with 95% confidence interval (CI) were calculated. The Grading of Recommendations Assessment, Development and Evaluation system was used to assess quality of evidence.

Results: Overall, 16 studies with 861 patients were included, comparing aspartate aminotransferase to platelet ratio index (APRI), fibrosis-4 index (FIB-4), aspartate aminotransferase/alanine aminotransferase ratio, transient elastography (TE), acoustic radiation force impulse, shear wave elastography and MRE versus liver biopsy. Among all non-invasive markers, TE had good performance for fibrosis staging. Summary AUROCs and DORs of TE were 0.90 (95% CI 0.87, 0.92) and 23.7, 0.91 (95% CI 0.89, 0.93) and 31.6, 0.89 (95% CI 0.86, 0.92) and 80.5 for staging SF, AF and cirrhosis, whereas APRI and FIB-4 showed poor performance for detecting AF (DOR, 4.6 and 4.7) and cirrhosis (DOR, 5.5 and 12.9).

Conclusions: TE performs well to stage liver fibrosis in patients with AIH, compared with other laboratory non-invasive indexes. Nevertheless, diagnostic accuracy of APRI and FIB-4 is poor.
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http://dx.doi.org/10.1007/s12072-018-9907-5DOI Listing
January 2019

Structural and functional analysis of interferon regulatory factors (IRFs) reveals a novel regulatory model in an invertebrate, Crassostrea gigas.

Dev Comp Immunol 2018 12 2;89:14-22. Epub 2018 Aug 2.

Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Science, Guangzhou, 510301, China. Electronic address:

Interferon regulatory factors (IRF), a family of transcription factors, are involved in the regulation of interferon to response the pathogen infection. Here, three IRF-like genes including CgIRF1a, CgIRF1b and CgIRF8 were identified in the genome of the oyster C. gigas. Among these genes, CgIRF1a and CgIRF1b, which are tandemly located in adjacent loci of scaffold 4, share the same domains. Phylogenetic analysis indicated that CgIRF1a and CgIRF1b were two paralogs that may originate from duplication of the same ancestral IRF gene. Subcellular localization analysis confirmed the nuclear distribution of CgIRF1a and CgIRF1b. Dual-luciferase reporter assay showed that CgIRF1a significantly activated the ISRE reporter gene, whereas CgIRF1b did not. Additionally, overexpression of CgIRF1b could significantly suppress the activation effect of CgIRF1a, which strongly suggests that CgIRF1b may serve as a regulator of the IRF signaling pathway. Furthermore, the result of native page revealed that CgIRF1a would form homologous dimers, and CgIRF1b would interact with CgIRF1a to inhibit the activity of the latter. Taken together, one novel regulatory model of IRF signaling pathways has been raised one paralog of IRF has evolved and appears to be a regulator of IRF.
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http://dx.doi.org/10.1016/j.dci.2018.07.027DOI Listing
December 2018

Engineering Two-Dimensional Mass-Transport Channels of the MoS Nanocatalyst toward Improved Hydrogen Evolution Performance.

ACS Appl Mater Interfaces 2018 Aug 18;10(30):25409-25414. Epub 2018 Jul 18.

Institute for Regenerative Medicine, Shanghai East Hospital, School of Materials Science and Engineering , Tongji University , Shanghai 200123 , China.

In addition to the intrinsic catalytic activity, the mass transport should be taken into adequate account in order to realize the superior performance of electrocatalysts. Here, we engineer the interstitial space between MoS nanosheets via the introduction of "spacers" to construct two-dimensional (2D) channels for favorable mass transport. The nano-sized spacers effectively separate MoS nanosheets, generating open and connective channels to fulfill timely reactant supply and rapid gas release. Besides, the spacer served as the physical support can prevent the collapse of 2D channels. Because of the engineering of nanostructured channels, a reduction in overpotential by approximately 100 and 360 mV at -10 and -100 mA cm, respectively, a decrease in the Tafel slope from 66.7 to 39.4 mV dec, and a more stable operation can be achieved. After being integrated by carbon paper, a further improved performance of 198 mV at -200 mA cm and 36 mV dec can be obtained. This work emphasizes the importance of mass-transport channels and paves a way to enhance the hydrogen evolution reaction performance.
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http://dx.doi.org/10.1021/acsami.8b07163DOI Listing
August 2018

The Molecular Mechanism Underlying Pro-apoptotic Role of Hemocytes Specific Transcriptional Factor Lhx9 in .

Front Physiol 2018 28;9:612. Epub 2018 May 28.

CAS Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, China.

Hemocytes are the central organ of immune defense against pathogens by means of inflammation, phagocytosis, and encapsulation in mollusks. The well-functioning of the host immune system relies on the hemocytes' task exertion and frequent renewal, but the underlying renewal mechanism remains elusive at the gene level. Here, we identified one transcription factor, LIM homeobox 9, in (Lhx9) that could be involved in hemocyte apoptosis or renewal. Lhx9 contains a homeodomain and two LIM domains. The expression profile of Lhx9 showed that it was specific and had high expression in hemocytes, and it significantly increased under the bacterial challenge. RNA interference of Lhx9 dramatically decreased the apoptosis rate of hemocytes when compared with a control group, which strongly implies its pro-apoptotic role in hemocytes. Furthermore, the genomic responses to the knockdown of Lhx9 were examined through RNA-seq, which showed that multiple pathways associated with cell apoptosis, including the apoptosis pathway, hippo signal pathway and p53 signaling pathway, were significantly down-regulated. Meanwhile, seven of the key apoptotic genes were confirmed to be upregulated by Lhx9, among which ASPP1 (apoptosis stimulating protein of p53) was confirmed to induce hemocyte apoptosis strongly, which demonstrates that ASPP1 was a downstream target mediated by Lhx9 that caused apoptosis. In conclusion, tissue-specific transcription factor Lhx9 induces hemocyte apoptosis through activating apoptotic genes or pathways, which could contribute to hemocyte renewal and immune defense in oysters.
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http://dx.doi.org/10.3389/fphys.2018.00612DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5985316PMC
May 2018

Compression-Dependent Transform-Domain Downward Conversion for Block-Based Image Coding.

IEEE Trans Image Process 2018 Jun;27(6):2635-2649

Transform-domain downward conversion (TDDC) for image coding is usually implemented by discarding some high-frequency components from each transformed block. As a result, a block of fewer coefficients is formed, and a lower compression cost is achieved due to the coding of only a few low-frequency coefficients. In this paper, we focus on the design of a new TDDC-based coding method by using our proposed interpolation-compression directed filtering (ICDF) and error-compensated scalar quantization (ECSQ), leading to the compression-dependent TDDC (CDTDDC)-based coding. More specifically, ICDF is first used to convert each macro-block into an coefficient block. Then, this coefficient block is compressed with ECSQ, resulting in a smaller compression distortion for those pixels that locate at some specific positions of a macro-block. We select these positions according to the 4:1 uniform sub-sampling lattice and use the pixels locating at them to reconstruct the whole macro-block through an interpolation. The proposed CDTDDC-based coding can be applied to compress both grayscale and color images. More importantly, when it is used in the color image compression, it offers not only a new solution to reduce the data-size of chrominance components but also a higher compression efficiency. Experimental results demonstrate that applying our proposed CDTDDC-based coding to compress still images can achieve a significant quality gain over the existing compression methods.
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http://dx.doi.org/10.1109/TIP.2018.2806281DOI Listing
June 2018

Senescence and cell death in chronic liver injury: roles and mechanisms underlying hepatocarcinogenesis.

Oncotarget 2018 Feb 22;9(9):8772-8784. Epub 2017 Dec 22.

Department of Cell Biology, Center for Stem Cell and Medicine, Second Military Medical University, Shanghai, China.

Chronic liver injury (CLI) is a complex pathological process typically characterized by progressive destruction and regeneration of liver parenchymal cells due to diverse risk factors such as alcohol abuse, drug toxicity, viral infection, and genetic metabolic disorders. When the damage to hepatocytes is mild, the liver can regenerate itself and restore to the normal state; when the damage is irreparable, hepatocytes would undergo senescence or various forms of death including apoptosis, necrosis and necroptosis. These pathological changes not only promote the progression of the existing hepatopathies via various underlying mechanisms but are closely associated with hepatocarcinogenesis. In this review, we discuss the pathological changes that hepatocytes undergo during CLI, and their roles and mechanisms in the progression of hepatopathies and hepatocarcinogenesis. We also give a brief introduction about some animal models currently used for the research of CLI and progress in the research of CLI.
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http://dx.doi.org/10.18632/oncotarget.23622DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5823588PMC
February 2018

Dual roles of cystatin A in the immune defense of the pacific oyster, Crassostrea gigas.

Fish Shellfish Immunol 2018 Apr 31;75:190-197. Epub 2018 Jan 31.

Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Science, Guangzhou 510301, China. Electronic address:

Cystatins are a large family of the proteins that function as reversible and tight-binding inhibitors of cysteine proteases, which consequently regulate multiple physiological activities including apoptosis and innate immunity. In the present study, we cloned a gene from Crassostrea gigas encoding cystatin, which is related to cystatin A superfamily. CgCytA was comprised of a cystatin-like domain with two conserved glycine residues (GG) near the N-terminal and a highly conserved glutamine-valine-glycine (Q-X-V-X-G) motif in the form of QVVAG loop. Transcription analysis of CgCytA indicated its constitutive expression in all tissues including mantle, gill, digestive tract, hemocytes, heart, adductor muscle, and gonads. Immune challenge with Vibrio alginolyticus, resulted in significant down-regulation of CgCytA expression at the initial stages of infection (till 12 h post infection) and the expression of cystatin increased 48 h post infection. Protease assay demonstrated the concentration of cystatin needed to inhibit half of the maximum biological response of cysteine protease is 14.4 μg/L (IC). Furthermore, RNAi of CgCytA resulted in increase of apoptotic cell population in hemocytes of C. gigas, suggesting protection role of CgCytA from hemocytes apoptosis. Unexpectedly, knockdown of CgCytA leaded to enhancement of bacterial clearance in vivo, implying that CgCytA may negatively regulate immune defense by suppressing endogenous cysteine protease. Therefore, CgCytA plays dual roles in protection of host hemocytes from apoptosis and control of bacterial clearance, which may server as one of key endogenous balancer between apoptosis and innate immunity in oyster.
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http://dx.doi.org/10.1016/j.fsi.2018.01.041DOI Listing
April 2018

Genomic and Proteomic Resolution of Heterochromatin and Its Restriction of Alternate Fate Genes.

Mol Cell 2017 12;68(6):1023-1037.e15

Institute for Regenerative Medicine , Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Epigenetics Program , Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA; Department of Cell and Developmental Biology , Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA. Electronic address:

Heterochromatin is integral to cell identity maintenance by impeding the activation of genes for alternate cell fates. Heterochromatic regions are associated with histone 3 lysine 9 trimethylation (H3K9me3) or H3K27me3, but these modifications are also found in euchromatic regions that permit transcription. We discovered that resistance to sonication is a reliable indicator of the heterochromatin state, and we developed a biophysical method (gradient-seq) to discriminate subtypes of H3K9me3 and H3K27me3 domains in sonication-resistant heterochromatin (srHC) versus euchromatin. These classifications are more accurate than the histone marks alone in predicting transcriptional silence and resistance of alternate fate genes to activation during direct cell conversion. Our proteomics of H3K9me3-marked srHC and functional screens revealed diverse proteins, including RBMX and RBMXL1, that impede gene induction during cellular reprogramming. Isolation of srHC with gradient-seq provides a genome-wide map of chromatin structure, elucidating subtypes of repressed domains that are uniquely predictive of diverse other chromatin properties.
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http://dx.doi.org/10.1016/j.molcel.2017.11.030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5858919PMC
December 2017

Systematic review on the reporting quality of randomized controlled trials in patients with hepatitis B or C in China.

Int J Infect Dis 2018 Feb 11;67:58-64. Epub 2017 Nov 11.

Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing Key Laboratory of Translational Medicine on Liver Cirrhosis, National Clinical Research Center for Digestive Disease, Beijing, China. Electronic address:

Background: The numbers of articles reporting randomized controlled trials (RCTs) on viral hepatitis in China have been increasing, but there have been few systematic studies evaluating the reporting quality of RCTs in this field. This study was performed to assess the reporting quality of RCTs on the treatment of hepatitis B and C in China from 1991 to 2015.

Methods: Articles published between January 1991 and December 2015 were identified via the PubMed, MEDLINE, and Embase databases using the key words "randomized clinical trials", "treatment", "therapy", "hepatitis B", "HBV", "hepatitis C", "HCV", "China", and "Chinese". The reporting quality was assessed against the Consolidated Standards of Reporting Trials (CONSORT) checklist.

Results: In total, 211 RCTs on the treatment of hepatitis B or C were included. The number of articles focusing on these RCTs increased rapidly over time, while the reporting quality improved steadily over time. Overall, compliance with the key components of the CONSORT checklist was low, with only 8.5%, 3.8%, and 11.4% of the articles fulfilling the reporting requirements of randomization, allocation concealment, and blinding, respectively.

Conclusions: Both the number and the quality of RCT articles were found to have increased steadily over the last two decades. However, compliance with the key components of the CONSORT checklist still needs improvement. It is hoped that the results of this study will lead to improvements in the reporting quality of clinical trials on hepatitis B and C in China.
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http://dx.doi.org/10.1016/j.ijid.2017.11.011DOI Listing
February 2018
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