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Dr. Bing  Liu  Dmd image

Dr. Bing Liu Dmd

556 Pleasant St
Brockton MA 02301
508 831-1218
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: 20796
NPI: 1689760688
Taxonomy Codes:
1223G0001X

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Publications

[Effect of comprehensive intervention on capacity in prevention and control of chronic diseases in community medical staff in Hangzhou]. - Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi
To evaluate the effect of the Oxford Health Alliance-Community Interventions for Health on chronic diseases prevention and control capacity in community medical staff in Hangzhou.A two year comprehensive intervention on chronic disease prevention and control capacity was conducted in the medical staff in Xiacheng district and Gongshu district, Xihu district was used as control according to the study design principal of parallel comparison and non-random grouping. The intervention effect was evaluated with Cochran-Mantel-Haenszel test. A total of 985 questionnaires were completed in the baseline survey and 870 questionnaires were completed in the follow-up survey.After 2 year intervention, the detection rates of blood cholesterol, blood pressure and fasting blood glucose by community medical staff significantly increased compared with the rates before the intervention (χ(2)=7.97, P =0.05 ; χ(2)=27.21, P =0.00 ; χ(2)=21.32, P=0.00). While, in the control district, the fasting blood glucose detection rate increased from 25.37% to 31.19%, the differences showed statistical significance (χ(2)=15.29, P=0.00). The communication between community medical staff and patients about healthy diet pattern was improved after the intervention, the difference was statistical significant (χ(2)=8.64, P=0.03). However, no significant differences in communication about increasing physical activity and smoking cessation between community medical staff and patients was found before and after intervention both in intervention districts and in control district. Furthermore, multivariate logistic regression analysis indicated that the interventions on screening of common chronic diseases and management of chronic diseases patients were related with the detections of blood cholesterol, blood pressure and fasting blood glucose. Moreover, the intervention on counsel and suggestion for chronic disease prevention and control had some influence on the communication about chronic disease risk factors between community medical staff and patients.The intervention on chronic disease prevention and control capacity in community medical staff was effective to improve the detection of chronic diseases in community and the communication between the medical staff and patients.
The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression. - Oncotarget
Neuroblastoma is the most common solid tumor during early childhood. One of the key features of neuroblastoma is extensive tumor-driven angiogenesis due to hypoxia. However, the mechanism through which neuroblastoma cells drive angiogenesis is poorly understood. Here we show that the long noncoding RNA MALAT1 was upregulated in human neuroblastoma cell lines under hypoxic conditions. Conditioned media from neuroblastoma cells transfected with small interfering RNAs (siRNA) targeting MALAT1, compared with conditioned media from neuroblastoma cells transfected with control siRNAs, induced significantly less endothelial cell migration, invasion and vasculature formation. Microarray-based differential gene expression analysis showed that one of the genes most significantly down-regulated following MALAT1 suppression in human neuroblastoma cells under hypoxic conditions was fibroblast growth factor 2 (FGF2). RT-PCR and immunoblot analyses confirmed that MALAT1 suppression reduced FGF2 expression, and Enzyme-Linked Immunosorbent Assays revealed that transfection with MALAT1 siRNAs reduced FGF2 protein secretion from neuroblastoma cells. Importantly, addition of recombinant FGF2 protein to the cell culture media reversed the effects of MALAT1 siRNA on vasculature formation. Taken together, our data suggest that up-regulation of MALAT1 expression in human neuroblastoma cells under hypoxic conditions increases FGF2 expression and promotes vasculature formation, and therefore plays an important role in tumor-driven angiogenesis.
TFF3 knockout in human pituitary adenoma cell HP75 facilitates cell apoptosis via mitochondrial pathway. - International journal of clinical and experimental pathology
Trefoil factor 3 (TFF3), a regulatory protein composed of 59 amino acids, has been suggested to be involved in pathogenesis, proliferation, differentiation, invasion, migration and apoptosis in multiple malignant tumors. This study thus investigated the effect of TFF3 knockout in human pituitary adenoma cell line HP75 on cell apoptosis and related pathways. RNA interference approach was used to knock down the expression of TFF3 protein. The gene silencing was validated by RNA denaturing gel electrophoresis and Western blotting. The effect of TFF3 knockout on cell apoptosis was analyzed by Western blotting and flow cytometry. TFF3 protein level in pituitary adenoma was about 3.61 ± 0.48 folds of that in normal tissues (P < 0.01). After transfecting with small interference RNA (siRNA) against TFF3, the apoptotic ration was significantly elevated (P < 0.01). Apoptosis related protein Bcl-2 and caspase-3 levels were remarkably depressed after siRNA transfection, while Bax and cleaved caspase-3 levels were elevated. TFF3 protein knockout can facilitate apoptosis of human pituitary adenoma HP75 cells via mitochondrial pathway.
Human mesenchymal and murine stromal cells support human lympho-myeloid progenitor expansion but not maintenance of multipotent haematopoietic stem and progenitors cells. - Cell cycle (Georgetown, Tex.)
A major goal in hematopoietic stem cell (HSC) research is to define conditions for the expansion of HSCs or multipotent progenitor cells (MPPs). Since human HSCs/MPPs cannot be isolated, NOD/SCID repopulating cell (SRC) assays emerged as the standard for the quantification of very primitive hematopoietic cell. However, in addition to HSCs/MPPs, lympho-myeloid primed progenitors (LMPPs) were recently found to contain SRC activities, challenging this assay as clear HSC/MPP readout. Because our revised model of human hematopoiesis predicts that HSCs/MPPs can be identified as CD133(+)CD34(+) cells containing erythroid potentials, we investigated the potential of human mesenchymal and conventional murine stromal cells to support expansion of HSCs/MPPs. Even though all stromal cells supported expansion of CD133(+)CD34(+) progenitors with long-term myeloid and long-term lymphoid potentials, erythroid potentials were exclusively found within erythro-myeloid CD133(low)CD34(+) cell fractions. Thus, our data demonstrate that against the prevailing assumption co-cultures on human mesenchymal and murine stromal cells neither promote expansion nor maintenance of HSCs and MPPs.
An Injectable Enzymatically Crosslinked Carboxymethylated Pullulan/Chondroitin Sulfate Hydrogel for Cartilage Tissue Engineering. - Scientific reports
In this study, an enzymatically cross-linked injectable and biodegradable hydrogel system comprising carboxymethyl pullulan-tyramine (CMP-TA) and chondroitin sulfate-tyramine (CS-TA) conjugates was successfully developed under physiological conditions in the presence of both horseradish peroxidase (HRP) and hydrogen peroxide (H2O2) for cartilage tissue engineering (CTTE). The HRP crosslinking method makes this injectable system feasible, minimally invasive and easily translatable for regenerative medicine applications. The physicochemical properties of the mechanically stable hydrogel system can be modulated by varying the weight ratio and concentration of polymer as well as the concentrations of crosslinking reagents. Additionally, the cellular behaviour of porcine auricular chondrocytes encapsulated into CMP-TA/CS-TA hydrogels demonstrates that the hydrogel system has a good cyto-compatibility. Specifically, compared to the CMP-TA hydrogel, these CMP-TA/CS-TA composite hydrogels have enhanced cell proliferation and increased cartilaginous ECM deposition, which significantly facilitate chondrogenesis. Furthermore, histological analysis indicates that the hydrogel system exhibits acceptable tissue compatibility by using a mouse subcutaneous implantation model. Overall, the novel injectable pullulan/chondroitin sulfate composite hydrogels presented here are expected to be useful biomaterial scaffold for regenerating cartilage tissue.
Significant enhancement of gas uptake capacity and selectivity via the judicious increase of open metal sites and Lewis basic sites within two polyhedron-based metal-organic frameworks. - Chemical communications (Cambridge, England)
Two new isomorphous polyhedron-based MOFs ( and ), with dual functionalities of OMSs and LBSs, have been synthesized by using the SBB strategy. By judiciously avoiding the DABCO axial ligand, possesses more OMSs than , and exhibits a significant enhancement of CO2 uptake capacity 210 versus 162 cm(3) g(-1) for at 273 K under 1 bar.
Nuclear AURKA acquires kinase-independent transactivating function to enhance breast cancer stem cell phenotype. - Nature communications
Centrosome-localized mitotic Aurora kinase A (AURKA) facilitates G2/M events. Here we show that AURKA translocates to the nucleus and causes distinct oncogenic properties in malignant cells by enhancing breast cancer stem cell (BCSC) phenotype. Unexpectedly, this function is independent of its kinase activity. Instead, AURKA preferentially interacts with heterogeneous nuclear ribonucleoprotein K (hnRNP K) in the nucleus and acts as a transcription factor in a complex that induces a shift in MYC promoter usage and activates the MYC promoter. Blocking AURKA nuclear localization inhibits this newly discovered transactivating function of AURKA, sensitizing resistant BCSC to kinase inhibition. These findings identify a previously unknown oncogenic property of the spatially deregulated AURKA in tumorigenesis and provide a potential therapeutic opportunity to overcome kinase inhibitor resistance.
Hydrogen sulfide ameliorates acute lung injury induced by infrarenal aortic cross-clamping by inhibiting inflammation and angiopoietin 2 release. - Journal of vascular surgery
Infrarenal aortic cross-clamping (IAC) is a common procedure during infrarenal vascular operations. It often causes ischemia-reperfusion injury to lower limbs, resulting in systemic inflammation response and damage to remote organs (particularly lungs). Hydrogen sulfide (H2S) is a gaseous mediator that has been shown to have a protective effect against lung injury.Wistar rats underwent IAC for 2 hours, followed by 4 hours of reperfusion. GYY4137 (a slow-releasing H2S donor) and dl-propargylglycine (PAG, an inhibitor of cystathionine γ-lyase) were preadministered to rats 1 hour before IAC, and their effects on severity of lung injury and related mechanisms were investigated.IAC induced a significant increase in plasma levels of H2S, H2S-synthesizing activity, and cystathionine γ-lyase expression in lung tissues compared with sham operation. Administration of GYY4137 significantly increased the levels of H2S but had little effect on H2S-synthesizing activity, whereas PAG reduced H2S levels and H2S-synthesizing activity. Preadministration of GYY4137 significantly attenuated acute lung injury induced by IAC, evidenced by reduced histologic scores and wet lung contents; improved blood gas parameters; reduced cell counts and protein amounts in bronchoalveolar lavage fluids; and reduced myeloperoxidase activity in lung tissues and plasma levels of tumor necrosis factor α, interleukin 6, and interleukin 1β. However, PAG further aggravated the severity of lung injury and displayed opposite effects to GYY4137. In exploration of the mechanisms, we found that IAC increased the release of angiopoietin 2 (Ang2) and its expression in lung tissues. GYY4137 attenuated the increase of Ang2 release and expression and increased the phosphorylation of Akt and the activation of its downstream factors, glycogen synthase kinase 3β and ribosomal protein S6 kinase; PAG showed opposite effects.The study indicates that H2S may play a protective role in IAC-induced acute lung injury in rats by inhibiting inflammation and Ang2 release.Copyright © 2015 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
Enhanced and Differential Capture of Circulating Tumor Cells from Lung Cancer Patients by Microfluidic Assays Using Aptamer Cocktail. - Small (Weinheim an der Bergstrasse, Germany)
Collecting circulating tumor cells (CTCs) shed from solid tumor through a minimally invasive approach provides an opportunity to solve a long-standing oncology problem, the real-time monitoring of tumor state and analysis of tumor heterogeneity. However, efficient capture and detection of CTCs with diverse phenotypes is still challenging. In this work, a microfluidic assay is developed using the rationally-designed aptamer cocktails with synergistic effect. Enhanced and differential capture of CTCs for nonsmall cell lung cancer (NSCLC) patients is achieved. It is also demonstrated that the overall consideration of CTC counts obtained by multiple aptamer combinations can provide more comprehensive information in treatment monitoring.© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Genome-Wide Analysis of DNA Methylation and Cigarette Smoking in Chinese. - Environmental health perspectives
Smoking is a risk factor for many human diseases. DNA methylation has been related to smoking, but genome-wide methylation data on smoking in Chinese is limited.We aimed to investigate epigenome-wide methylation in relation to smoking in Chinese.We measured the methylation levels at >485,000 CpGs of blood leukocytes using HumanMethylation450 BeadChip and conducted a genome-wide meta-analysis of smoking in a total of 596 Chinese participants. For the smoking-related CpGs, we further evaluated their associations with internal polycyclic aromatic hydrocarbons (PAHs) biomarkers and their correlations with the expression of corresponding genes.We identified 318 CpGs whose methylation levels were associated with smoking at genome-wide significance level (false discovery rate < 0.05), among which 161 CpGs annotated to 123 genes were not associated with smoking in recent studies of Europeans and African Americans. Of these smoking-related CpGs, methylation levels at 80 CpGs showed significant correlations with the expression of corresponding genes (including RUNX3, IL6R, PTAFR, ANKRD11, CEP135 and CDH23), and methylation at 15 CpGs were significantly associated with urinary 2-hydroxynaphthalene, the most representative internal monohydroxy-PAHs biomarker for smoking.We identified DNA methylation markers associated with smoking in Chinese populations, including some that also were correlated with gene expression. Exposure to naphthalene, a by-product of tobacco smoke, may contribute to smoking-related methylation.

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