Publications by authors named "Xiaoming Cheng"

55 Publications

Key Milestones in HCV Discovery and Therapeutics.

Innovation (N Y) 2020 Nov 6;1(3):100067. Epub 2020 Nov 6.

Liver Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.

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http://dx.doi.org/10.1016/j.xinn.2020.100067DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8454740PMC
November 2020

Fatty acid β-oxidation promotes breast cancer stemness and metastasis via the miRNA-328-3p-CPT1A pathway.

Cancer Gene Ther 2021 May 27. Epub 2021 May 27.

Thyroid and Breast Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China.

MicroRNAs (miRNA) have been shown to be associated with tumor diagnosis, prognosis, and therapeutic response. MiR-328-3p plays a significant role in breast cancer growth; however, its actual function and how it modulates specific biological functions is poorly understood. Here, miR-328-3p was significantly downregulated in breast cancer, especially in patients with metastasis. Mitochondrial carnitine palmitoyl transferase 1a (CPT1A) is a downstream target gene in the miR-328-3p-regulated pathway. Furthermore, the miR-328-3p/CPT1A/fatty acid β-oxidation/stemness axis was shown responsible for breast cancer metastasis. Collectively, this study revealed that miR-328-3p is a potential therapeutic target for the treatment of breast cancer patients with metastasis, and also a model for the miRNA-fatty acid β-oxidation-stemness axis, which may assist inunderstanding the cancer stem cell signaling functions of miRNA.
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http://dx.doi.org/10.1038/s41417-021-00348-yDOI Listing
May 2021

Clinical characteristics of COVID-19 patients with hepatitis B virus infection - a retrospective study.

Liver Int 2021 04 10;41(4):720-730. Epub 2021 Jan 10.

State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, Institute of Medical Virology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.

Background & Aims: The outbreak of coronavirus disease 2019 (COVID-19) has been declared a pandemic. Although COVID-19 is caused by infection in the respiratory tract, extrapulmonary manifestations including dysregulation of the immune system and hepatic injury have been observed. Given the high prevalence of hepatitis B virus (HBV) infection in China, we sought to study the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and HBV coinfection in patients.

Methods: Blood samples of 50 SARS-CoV-2 and HBV coinfected patients, 56 SARS-CoV-2 mono-infected patients, 57 HBeAg-negative chronic HBV patient controls and 57 healthy controls admitted to Renmin Hospital of Wuhan University were collected in this study. Complete blood count and serum biochemistry panels including markers indicative of liver functions were performed. Cytokines including IFN-γ, TNF-α, IL-2, IL-4, IL-6 and IL-10 were evaluated. T cell, B cell and NK cell counts were measured using flow cytometry.

Results: SARS-CoV-2 and HBV coinfection did not significantly affect the outcome of the COVID-19. However, at the onset of COVID-19, SARS-CoV-2 and HBV coinfected patients showed more severe monocytopenia and thrombocytopenia as well as more disturbed hepatic function in albumin production and lipid metabolism. Most of the disarrangement could be reversed after recovery from COVID-19.

Conclusions: While chronic HBV infection did not predispose COVID-19 patients to more severe outcomes, our data suggest SARS-CoV-2 and HBV coinfection poses a higher extent of dysregulation of host functions at the onset of COVID-19. Thus, caution needs to be taken with the management of SARS-CoV-2 and HBV coinfected patients.
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http://dx.doi.org/10.1111/liv.14774DOI Listing
April 2021

Physiological and Pathophysiological Roles of Ion Transporter-Mediated Metabolism in the Thyroid Gland and in Thyroid Cancer.

Onco Targets Ther 2020 3;13:12427-12441. Epub 2020 Dec 3.

Department of Thyroid and Breast Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, People's Republic of China.

Thyroid cancer is the most common type of endocrine tumor and has shown an increasing annual incidence, especially among women. Patients with thyroid cancer have a good prognosis, with a high five-year survival rate; however, the recurrence rate and disease status of thyroid cancer remain a burden for patients, which compels us to further elucidate the pathogenesis of this disease. Recently, ion transporters have gradually become a hot topic in the field of thyroid gland biology and cancer research. Additionally, alterations in the metabolic state of tumor cells and protein molecules have gradually become the focus of scientific research. This review focuses on the progress in understanding the physiological and pathophysiological roles of ion transporter-mediated metabolism in both the thyroid gland and thyroid cancer. We also hope to shed light on new targets for the treatment and prognosis of thyroid cancer.
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http://dx.doi.org/10.2147/OTT.S280797DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721308PMC
December 2020

Gancao Xiexin decoction combined with mesalazine in the treatment of ulcerative colitis: A protocol for a systematic review and meta-analysis.

Medicine (Baltimore) 2020 Nov;99(47):e23038

School of Basic Medical Science, Chengdu University of Traditional Chinese Medicine, Chengdu.

Backgroud: Ulcerative colitis (UC) is a chronic inflammatory disease that involves the rectum, colon and ileum. Gancao Xiexin decoction (GCXXD) is a classic herbal formula in Shanghanlun. More and more research evidence shows that GCXXD has a certain therapeutic effect on UC. Therefore, we designed this study protocol aim to evaluate the efficacy and safety of GCXXD combine with mesalazine for UC.

Methods: We will systematically search 6 databases, including PubMed, the Cochrane Library, EMBASE, CNKI, VIP, Wang-fang database up to July 2020 to obtain eligible studies. The primary outcomes will focus on the clinical effectiveness. Review Manager 5.3 software will be used for data analysis.

Results: This study will provide the systematic evidence of UC treated with GCXXD combine with mesalazine.

Conclusion: The findings of this meta-analysis will provide evidence to judge whether GCXXD combine with mesalazine is a more effective intervention compare to mesalazine only for patient of UC.

Inplasy Registration Number: INPLASY202080008.
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http://dx.doi.org/10.1097/MD.0000000000023038DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7676594PMC
November 2020

Application of carbon nanoparticles combined with intraoperative neuromonitoring in papillary thyroid microcarcinoma surgery.

Am J Otolaryngol 2021 Jan - Feb;42(1):102790. Epub 2020 Oct 24.

Gastroenterology Department, Affiliated Hospital of Zunyi Medical University, Zunyi, China. Electronic address:

Purposes: To improve the lymph node dissection as well as protect parathyroid gland and recurrent laryngeal nerve, the carbon nanoparticles and intraoperative neuromonitoring were applied in papillary thyroid microcarcinoma surgery.

Methods: Carbon nanoparticles and intraoperative neuromonitoring were used in the experimental group, whereas the control group were not. Routine pathological examination was performed.

Results: The lymph nodes dissected was significantly higher in the experimental group, but the metastatic lymph nodes were not. The number of mistakenly dissected parathyroid gland and postoperative hypoparathyroidism were 3 and 13 in the experimental group respectively, significantly less than 10 and 25 in the control group. The incidences of overall, transient and persistent recurrent laryngeal nerve palsy in the experimental group were 5.5%, 5.5% and 0% respectively, whereas in the control group were 8.6%, 6.9% and 1.7%.

Conclusions: Carbon nanoparticles can improve lymph node dissection in papillary thyroid microcarcinoma surgery, and the combination of carbon nanoparticles with intraoperative neuromonitoring can reduce surgical complications and improve patient quality of life.
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http://dx.doi.org/10.1016/j.amjoto.2020.102790DOI Listing
April 2021

Descriptive, Retrospective Study of the Clinical Characteristics of Asymptomatic COVID-19 Patients.

mSphere 2020 10 7;5(5). Epub 2020 Oct 7.

State Key Laboratory of Virology, School of Basic Medical Sciences, Wuhan University, Wuhan, China

Since the outbreak of coronavirus disease 2019 (COVID-19) in Wuhan, China, it has rapidly spread around the world. Persons with asymptomatic disease exhibit viral shedding, resulting in transmission, which presents disease control challenges. However, the clinical characteristics of these asymptomatic individuals remain elusive. We collected samples of 25 asymptomatic and 27 symptomatic COVID-19 patients. Viral titers of throat swabs were determined by quantitative reverse transcription-PCR (qRT-PCR). COVID-19 IgG and IgM were examined. Complete blood counts were determined, and serum biochemistry panels were performed. Cytokines, including gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), interleukin 2 (IL-2), IL-4, IL-6, and IL-10 were evaluated. T cell, B cell, and NK cell counts were measured using flow cytometry. Although similar viral loads were detected, asymptomatic patients had significantly faster virus turnover than symptomatic patients. Additionally, asymptomatic patients had higher counts of lymphocytes, T cells, B cells, and NK cells. While liver damage was observed in symptomatic patients, as indicated by elevated liver enzymes and decreased liver-synthesized proteins in the blood, asymptomatic patients showed normal liver measurements. Lactate dehydrogenase, a COVID-19 risk factor, was significantly lower in asymptomatic patients. These results suggest that asymptomatic COVID-19 patients had normal clinical indicators and faster viral clearance than symptomatic patients. Lymphocytes may play a role in their asymptomatic phenotype. Since asymptomatic patients may be a greater risk of virus transmission than symptomatic patients, public health interventions and a broader range of testing may be necessary for the control of COVID-19. Asymptomatic transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a potential problem for pandemic control through public health strategies. Our results demonstrate that asymptomatic COVID-19 patients have better outcomes than symptomatic patients. This may have been due to more active cellular immune responses and normal liver function. Since asymptomatic patients have no clinical symptoms which can easily prevent timely diagnosis and treatment, they may cause a greater risk of virus transmission than symptomatic patients, which poses a major challenge to infection control. Evidence suggests that nonpharmaceutical public health interventions, like social distancing and face mask ordinances, play important roles in the control of COVID-19. Looking forward, it may be necessary to proceed cautiously while reopening businesses in areas of epidemicity to prevent potential waves of COVID-19 in the future.
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http://dx.doi.org/10.1128/mSphere.00922-20DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568656PMC
October 2020

Mediastinal liposarcoma masquerading as penetrating aortic ulcer in the descending aorta: a case report.

Cardiovasc Diagn Ther 2020 Aug;10(4):888-891

Department of Vascular Surgery, The First Hospital of China Medical University, Shenyang, China.

A 56-year-old woman with a history of hypertension and cerebral infarction was admitted to the hospital complaining of progressive and severe chest pain for 1 day. CT scan revealed a descending penetrating ulcer. Accordingly, she underwent an uneventful endovascular repair with a thoracic endograft. One month later the patient presented to our clinic with chest and back pain again. The contrast CT indicated that the periaortic mass grew larger, which interpreted as hematoma resulting from endoleak. But no endoleak was found by angiography. CT-guided needle biopsy was carried out, the histology of the mass revealed a pleomorphic liposarcoma. Liposarcomas are malignant fat-containing tumors derived from mesenchymal cells that typically occur in the extremities and retroperitoneum, mediastinal liposarcoma account for less than 1% in mediastinal malignancies; pleomorphic liposarcoma is the least common liposarcomas. Cases of liposarcoma invading vascular system are seldom, to our knowledge, it is the first case of mediastinal pleomorphic liposarcoma invaded the descending aorta. It is worth mentioning that in the modern endovascular era, the majority of aortic diseases are being repaired by endovascular techniques. When patients with growing periaortic mass post endovascular repair and endograft-related causes have been excluded, the rare possibility of mediastinal liposarcoma should arise as a differential diagnosis. Promptly CT-guided biopsy help establish an early diagnosis.
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http://dx.doi.org/10.21037/cdt-20-287DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7487380PMC
August 2020

Pathological role of ion channels and transporters in the development and progression of triple-negative breast cancer.

Cancer Cell Int 2020 6;20:377. Epub 2020 Aug 6.

Department of Thyroid and Breast Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, 563003 Guizhou Province China.

Breast cancer is a common malignancy in women. Among breast cancer types, triple-negative breast cancer (TNBC) tends to affect younger women, is prone to axillary lymph node, lung, and bone metastases; and has a high recurrence rate. Due to a lack of classic biomarkers, the currently available treatments are surgery and chemotherapy; no targeted standard treatment options are available. Therefore, it is urgent to find a novel and effective therapeutic target. As alteration of ion channels and transporters in normal mammary cells may affect cell growth, resulting in the development and progression of TNBC, ion channels and transporters may be promising new therapeutic targets for TNBC. This review summarizes ion channels and transporters related to TNBC and may provide new tumor biomarkers and help in the development of novel targeted therapies.
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http://dx.doi.org/10.1186/s12935-020-01464-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7409684PMC
August 2020

Profiling serum cytokines in COVID-19 patients reveals IL-6 and IL-10 are disease severity predictors.

Emerg Microbes Infect 2020 Dec;9(1):1123-1130

State Key Laboratory of Virology and Hubei Province Key Laboratory of Allergy and Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, People's Republic of China.

Since the outbreak of coronavirus disease 2019 (COVID-19) in Wuhan, China, it has rapidly spread across many other countries. While the majority of patients were considered mild, critically ill patients involving respiratory failure and multiple organ dysfunction syndrome are not uncommon, which could result death. We hypothesized that cytokine storm is associated with severe outcome. We enrolled 102 COVID-19 patients who were admitted to Renmin Hospital (Wuhan, China). All patients were classified into moderate, severe and critical groups according to their symptoms. 45 control samples of healthy volunteers were also included. Inflammatory cytokines and C-Reactive Protein (CRP) profiles of serum samples were analyzed by specific immunoassays. Results showed that COVID-19 patients have higher serum level of cytokines (TNF-α, IFN-γ, IL-2, IL-4, IL-6 and IL-10) and CRP than control individuals. Within COVID-19 patients, serum IL-6 and IL-10 levels are significantly higher in critical group ( = 17) than in moderate ( = 42) and severe ( = 43) group. The levels of IL-10 is positively correlated with CRP amount ( = 0.41,  < 0.01). Using univariate logistic regression analysis, IL-6 and IL-10 are found to be predictive of disease severity and receiver operating curve analysis could further confirm this result (AUC = 0.841, 0.822 respectively). Our result indicated higher levels of cytokine storm is associated with more severe disease development. Among them, IL-6 and IL-10 can be used as predictors for fast diagnosis of patients with higher risk of disease deterioration. Given the high levels of cytokines induced by SARS-CoV-2, treatment to reduce inflammation-related lung damage is critical.
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http://dx.doi.org/10.1080/22221751.2020.1770129DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7473317PMC
December 2020

Engineered butyrate-producing bacteria prevents high fat diet-induced obesity in mice.

Microb Cell Fact 2020 Apr 25;19(1):94. Epub 2020 Apr 25.

Department of Biochemical Engineering, School of Chemical Engineering and Technology, Key Laboratory of Systems Bioengineering, Ministry of Education, Tianjin University, Tianjin, 300072, China.

Background: Obesity is a major problem worldwide and severely affects public safety. As a metabolite of gut microbiota, endogenous butyric acid participates in energy and material metabolism. Considering the serious side effects and weight regain associated with existing weight loss interventions, novel strategies are urgently needed for prevention and treatment of obesity.

Results: In the present study, we engineered Bacillus subtilis SCK6 to exhibited enhanced butyric acid production. Compared to the original Bacillus subtilis SCK6 strain, the genetically modified BsS-RS06550 strain had higher butyric acid production. The mice were randomly divided into four groups: a normal diet (C) group, a high-fat diet (HFD) group, an HFD + Bacillus subtilis SCK6 (HS) group and an HFD + BsS-RS06550 (HE) group. The results showed BsS-RS06550 decreased the body weight, body weight gain, and food intake of HFD mice. BsS-RS06550 had beneficial effects on blood glucose, insulin resistance and hepatic biochemistry. After the 14-week of experiment, fecal samples were collected for nontargeted liquid chromatography-mass spectrometry analysis to identify and quantify significant changes in metabolites. Sixteen potentially significant metabolites were screened, and BsS-RS06550 was shown to potentially regulate disorders in glutathione, methionine, tyrosine, phenylalanine, and purine metabolism and secondary bile acid biosynthesis.

Conclusions: In this study, we successfully engineered Bacillus subtilis SCK6 to have enhanced butyric acid production. The results of this work revealed that the genetically modified live bacterium BsS-RS06550 showed potential anti-obesity effects, which may have been related to regulating the levels of metabolites associated with obesity. These results indicate that the use of BsS-RS06550 may be a promising strategy to attenuate obesity.
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http://dx.doi.org/10.1186/s12934-020-01350-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7183672PMC
April 2020

Diminished hepatic IFN response following HCV clearance triggers HBV reactivation in coinfection.

J Clin Invest 2020 06;130(6):3205-3220

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.

In patients with HBV and HCV coinfection, HBV reactivation leading to severe hepatitis has been reported with the use of direct-acting antivirals (DAAs) to treat HCV infection. Here we studied the molecular mechanisms behind this viral interaction. In coinfected cell culture and humanized mice, HBV replication was suppressed by HCV coinfection. In vitro, HBV suppression was attenuated when interferon (IFN) signaling was blocked. In vivo, HBV viremia, after initial suppression by HCV superinfection, rebounded following HCV clearance by DAA treatment that was accompanied by a reduced hepatic IFN response. Using blood samples of coinfected patients, IFN-stimulated gene products including C-X-C motif chemokine 10 (CXCL10), C-C motif chemokine ligand 5 (CCL5), and alanine aminotransferase (ALT) were identified to have predictive value for HBV reactivation after HCV clearance. Taken together, our data suggest that HBV reactivation is a result of diminished hepatic IFN response following HCV clearance and identify serologic markers that can predict HBV reactivation in DAA-treated HBV-HCV-coinfected persons.
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http://dx.doi.org/10.1172/JCI135616DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7259999PMC
June 2020

JAZF1 Suppresses Papillary Thyroid Carcinoma Cell Proliferation and Facilitates Apoptosis via Regulating TAK1/NF-κB Pathways.

Onco Targets Ther 2019 2;12:10501-10514. Epub 2019 Dec 2.

Medical Center of Breast and Thyroid Disease, Affiliated Hospital of ZunYi Medical University, ZunYi, Guizhou 563003, People's Republic of China.

Purpose: Juxtaposed with another zinc finger gene 1 (JAZF1) is involved in gluconeogenesis, insulin sensitivity, cell differentiation, lipid metabolism and inflammation, but its role in carcinoma remains inexplicit.

Patients And Methods: We explored the JAZF1 expression in human papillary thyroid cancer (PTC) tissues, adjacent normal thyroid tissues and nodular goitre tissues, as well as Ki67 expression in PTC tissues, using immunohistochemistry staining. Western blotting and RT-qPCR were performed to explore the JAZF1 expression levels in Nthy-ori 3-1, BCPAP and TPC-1 cells. BCPAP cells overexpressing JAZF1 were constructed using an Adv-JAZF1-GFP recombinant adenovirus vector. Next, the cell proliferation assay, colony formation assay, cell cycle analysis, apoptosis and immunofluorescence were performed. The mRNA expression level of nuclear factor-κB p65 (NF-κB p65) was examined using RT-qPCR. The expression of Bcl-2, Bax, transforming growth factor beta-activated kinase 1 (TAK1), NF-κB p65 and NF-κB p-p65 were examined using Western blotting.

Results: The expression of JAZF1 in human PTC tissues was downregulated compared with adjacent thyroid tissues or nodular goitre. Additionally, JAZF1 expression was associated with the location and lymph node metastasis of PTC. The expression level of JAZF1 had a negative correlation with Ki67 labelling index (LI). Compared to Nthy-ori 3-1 cells and TPC-1 cells, BCPAP cells expressed the lowest JAZF1. JAZF1 overexpressed significantly inhibited proliferation, caused G0/G1 cell cycle arrest and promoted apoptosis in BCPAP cells. Furthermore, JAZF1 overexpressed in BCPAP cells clearly upregulated the expression level of Bax protein, whereas decreased the expression of Bcl-2, TAK1, NF-κB but did not affect the mRNA or protein expression level of NF-κB p65.

Conclusion: JAZF1 inhibits proliferation and induces apoptosis in BCPAP cells by suppressing the activation of TAK1/NF-κB signalling pathways, suggesting that JAZF1 may serve as a reliable molecular marker in PTC.
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http://dx.doi.org/10.2147/OTT.S230597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6897071PMC
December 2019

Chest wall lymph node metastasis from follicular thyroid carcinoma: a rare case report.

Diagn Pathol 2019 Nov 20;14(1):130. Epub 2019 Nov 20.

Gastroenterology Department, The First Affiliated Hospital of Zunyi Medical University, Zunyi, China.

Background: Distant metastases from follicular thyroid carcinoma are mainly hematogenous and are commonly observed in the lungs and bones. Other rare sites are the parotid gland, skin, brain, ovary, adrenal gland, kidney, pancreas and breast, with chest wall lymph node metastasis being even more rare.

Case Presentation: Over the past 10 years, three surgeries were performed on a 69-year-old women with a history of follicular thyroid cancer and its metastatic lesions. The patient presented with a 3-month history of masses in the left chest. She underwent detailed examination of the chest wall tumors, and surgery was then performed to resect all of the tumors. Based on the histopathology, these lymph nodes were confirmed to harbor metastatic follicular thyroid carcinoma.

Conclusion: This study reports the first case of follicular thyroid carcinoma metastasis to the chest wall lymph node.
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http://dx.doi.org/10.1186/s13000-019-0907-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6864998PMC
November 2019

Function of ion transporters in maintaining acid-base homeostasis of the mammary gland and the pathophysiological role in breast cancer.

Am J Physiol Regul Integr Comp Physiol 2020 01 25;318(1):R98-R111. Epub 2019 Sep 25.

Department of Thyroid and Breast Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, China.

The incidence of breast cancer is increasing year by year, and the pathogenesis is still unclear. Studies have shown that the high metabolism of solid tumors leads to an increase in hypoxia, glycolysis, production of lactic acid and carbonic acid, and extracellular acidification; a harsh microenvironment; and ultimately to tumor cell death. Approximately 50% of locally advanced breast cancers exhibit hypoxia and/or local hypoxia, and acid-base regulatory proteins play an important role in regulating milk secretion and maintaining mammary gland physiological function. Therefore, ion transporters have gradually become a hot topic in mammary gland and breast cancer research. This review focuses on the research progress of ion transporters in mammary glands and breast cancer. We hope to provide new targets for the treatment and prognosis of breast cancer.
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http://dx.doi.org/10.1152/ajpregu.00202.2019DOI Listing
January 2020

An ascent guidance algorithm for the energy management of solid rockets.

ISA Trans 2020 Mar 20;98:309-319. Epub 2019 Aug 20.

School of Astronautics, Beihang University, Beijing 100191, China. Electronic address:

Efficient energy management for the solid rocket is very important to exhaust excess energy and to meet the various terminal constraints. Based on the online planning of the velocity capability curve, a Double-arcs Energy Management (DAEM) guidance algorithm is proposed in this paper. In the DAEM, the velocity capability curve is designed with two tangential arcs. By using the elegant geometric characteristic of the arcs, the closed-loop guidance problem is transformed as a problem of solving a system of nonlinear equations about the parameters (radius and center position) of the two arcs, and the nonlinear equations can be solved in real time. The main advantages of this algorithm are that the height increment constraint, which is difficult to be satisfied in traditional energy management methods, can be satisfied theoretically, and the convergence of the solution of the DAEM is quadratic. The effectiveness and advantages of the proposed DAEM algorithm are demonstrated by simulations and comparisons with other energy management algorithms.
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http://dx.doi.org/10.1016/j.isatra.2019.08.031DOI Listing
March 2020

Osteogenic Potential of Electrospun Poly(3-hydroxybutyrate-co-4-hydroxybutyrate)/ Poly(ethylene glycol) Nanofiber Membranes.

J Biomed Nanotechnol 2019 Jun;15(6):1280-1289

Nanofibers as niche-biomimetic scaffolds exhibit potential in bone tissue engineering (BTE). Here, poly(3-hydroxybutyrate-co-4-hydroxybutyrate) co-polymer (P34HB)/poly(ethylene glycol) (PEG) nanofiber membranes with a high hydrophilicity and mechanical properties were fabricated by introducing PEG to P34HB via electrospinning. The P34HB/PEG nanofibrous scaffolds were investigated for their potential in the osteogenic differentiation and mineralization of bone marrow mesenchymal stem cells (BMSCs). By adjusting the ratio of PEG to P34HB, three scaffolds, including P34HB, P34HB/10 wt%PEG, and P34HB/30 wt%PEG, were successfully fabricated. The composite P34HB/PEG nanofiber membranes showed an enhanced hydrophilicity, a decreased fiber size, and an increased mechanical strength compared with those of P34HB. studies showed that the P34HB/PEG membranes better supported cell adhesion, spreading, and proliferation than those of P34HB. The incorporation of PEG into the P34HB scaffold also promoted the osteoinduction capacity, as evidenced by activation of the alkaline phosphatase activity (ALP) activity, increased gene expression of bone specific markers (such as ), and mineral nodules formation. Comparatively, P34HB/10 wt%PEG showed a higher hydrophilicity and mechanical properties, as well as a better biological performance than the other membranes. Thus, the electrospun P34HB/PEG nanofiber membranes may be potentially developed as regenerative materials for BTE applications.
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http://dx.doi.org/10.1166/jbn.2019.2757DOI Listing
June 2019

Hepatitis B Surface Antigen Activates Unfolded Protein Response in Forming Ground Glass Hepatocytes of Chronic Hepatitis B.

Viruses 2019 04 25;11(4). Epub 2019 Apr 25.

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Ground glass hepatocytes (GGHs), a histological hallmark of chronic hepatitis B virus (HBV) infection, contain excessive hepatitis surface antigen (HBsAg) in the endoplasmic reticulum (ER), which is linked to unfolded protein response (UPR). The mechanism by which HBV activates UPR has not been fully defined. To investigate this, HepG2-NTCP cells and primary human hepatocytes (PHHs) were either infected with HBV or transduced with adenoviral vectors expressing replication-competent HBV genome or individual HBV genes. UPR markers were evaluated by qPCR, Western blotting, and immunofluorescence. Apoptosis and cell viability were measured by Caspase-3/7 and ATPlite assay respectively. We found that UPR markers were induced by the overexpression of HBsAg in HepG2-NTCP cells and PHHs. Elevation of UPR-induced genes showed a dose-dependent correlation with HBsAg levels. In HBV-infected livers, GGHs also demonstrated excessive accumulation of HBsAg associated with increased BIP/GRP78 staining, a marker of UPR. Prolonged activation of UPR by HBsAg overexpression induced signs of apoptosis. Overexpression of HBsAg can induce ER stress through protein kinase RNA-like endoplasmic reticulum kinase (PERK) pathway in vitro, and may be linked to the appearance of GGHs. The activation of UPR by HBsAg may sensitize hepatocytes to cell death and result in possible subsequent cellular changes leading to a premalignant phenotype.
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http://dx.doi.org/10.3390/v11040386DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6520809PMC
April 2019

PASylated interferon α efficiently suppresses hepatitis B virus and induces anti-HBs seroconversion in HBV-transgenic mice.

Antiviral Res 2019 01 12;161:134-143. Epub 2018 Nov 12.

Institute of Virology, Technische Universität München/Helmholtz Zentrum München, 81675, Munich, Germany; German Center for Infection Research (DZIF), Munich Partner Site, 81675, Munich, Germany. Electronic address:

Interferon α (IFNα) so far is the only therapeutic option for chronic hepatitis B virus (HBV) infection that can lead to virus clearance. Unfortunately, its application is limited by side effects and response rates are low. The aim of this study was to generate a novel long-acting IFNα with the help of PASylation technology that adds a polypeptide comprising Proline, Alanine and Serine (PAS) to increase plasma half-life. Following evaluation of four selected recombinant murine IFNα (mIFNα) subtypes in cell culture, the most active subtype, mIFNα11, was fused with a 600 amino acid PAS chain. The activity of PAS-mIFNα was assessed by interferon bioassay and further evaluated for induction of interferon-stimulated genes (ISG) and antiviral efficacy in cell culture as well as in HBV-transgenic mice. PAS-mIFNα induced expression of ISG comparable to unmodified mIFNα and, likewise, evoked dose-dependent reduction of HBV replication in vitro. In vivo, PAS-mIFNα led to pronounced suppression of HBV replication without detectable liver damage whereas conventional mIFNα treatment only had a modest antiviral effect. Importantly, all PAS-mIFNα treated mice showed an anti-HBs antibody response, lost HBsAg and achieved seroconversion after three weeks. PASylated IFNα showed a profoundly increased antiviral effect in vivo compared to the non-modified version without toxicity, providing proof-of-concept that an improved IFNα can achieve higher rates of HBV antiviral and immune control.
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http://dx.doi.org/10.1016/j.antiviral.2018.11.003DOI Listing
January 2019

Overexpression of LASS2 inhibits proliferation and causes G0/G1 cell cycle arrest in papillary thyroid cancer.

Cancer Cell Int 2018 1;18:151. Epub 2018 Oct 1.

2College of Laboratory Medicine, Affiliated Hospital of ZunYi Medical College, Zunyi, 563003 Guizhou People's Republic of China.

Background: The aim of this study was to investigate the role of LAG1 longevity-assurance homologue 2 (LASS2) in papillary thyroid cancer (PTC).

Methods: Immunohistochemistry staining was conducted to explore the expression levels of LASS2 in PTC tissues and adjacent normal thyroid tissues and nodular goiter tissues. Western blotting and RT-qPCR were performed to explore the expression levels of LASS2 in three PTC cell lines (TPC-1, K1, BCPAP). An Adv-LASS2-GFP recombinant adenovirus vector was constructed and transduced into BCPAP cells. Then CCK-8 assay, colony formation assay, cell cycle distribution, and apoptosis were performed. Western blotting was used to examine the expression of p21, cyclin D1, cyclin-dependent kinase 4, p53 and p-p53.

Results: LASS2 was downregulated in PTC tissues compared with adjacent thyroid tissues or nodular goiter tissues. In addition, the expression of LASS2 was found to be associated with TNM stage and lymph node metastasis. BCPAP cells expressed the lowest LASS2 compared to TPC-1 cells or K1 cells. Overexpression of LASS2 significantly inhibited proliferation, promoted apoptosis and caused G0/G1 cell cycle arrest in BCPAP cells. Furthermore, overexpression of LASS2 significantly increased the expression of p21, inhibited the expression of cyclin D1 and cyclin-dependent kinase 4, and increased the expression of p-p53, but did not effect the expression of p53 in BCPAP cells.

Conclusion: Our findings indicate that overexpression of LASS2 inhibits PTC cell proliferation, promotes apoptosis and causes G0/G1 cell cycle arrest via a p53-dependent pathway. Thus, LASS2 may serve as a novel biomarker in PTC.
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http://dx.doi.org/10.1186/s12935-018-0649-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6167791PMC
October 2018

Hepatitis B Virus Deregulates the Cell Cycle To Promote Viral Replication and a Premalignant Phenotype.

J Virol 2018 10 12;92(19). Epub 2018 Sep 12.

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA

Hepatitis B virus (HBV) infection is a major health problem worldwide, and chronically infected individuals are at high risk of developing cirrhosis and hepatocellular carcinoma (HCC). The molecular mechanisms whereby HBV causes HCC are largely unknown. Using a biologically relevant system of HBV infection of primary human hepatocytes (PHHs), we studied how HBV perturbs gene expression and signaling pathways of infected hepatocytes and whether these effects are relevant to productive HBV infection and HBV-associated HCC. Using a human growth factor antibody array, we first showed that HBV infection induced a distinct profile of growth factor production by PHHs, marked particularly by significantly lower levels of the transforming growth factor β (TGF-β) family of proteins in the supernatant. Transcriptome profiling next revealed multiple changes in cell proliferation and cell cycle control pathways in response to HBV infection. A human cell cycle PCR array validated deregulation of more than 20 genes associated with the cell cycle in HBV-infected PHHs. Cell cycle analysis demonstrated that HBV-infected PHHs are enriched in the G/M phase compared to the predominantly G/G phase of cultured PHHs. HBV proviral host factors, such as PPARA, RXRA, and CEBPB, were upregulated upon HBV infection and particularly enriched in cells in the G/M phase. Together, these results support the notion that HBV deregulates cell cycle control to render a cellular environment that is favorable for productive HBV infection. By perturbing cell cycle regulation of infected cells, HBV may coincidently induce a premalignant phenotype that predisposes infected hepatocytes to subsequent malignant transformation. Hepatitis B virus (HBV) infection is a major health problem with high risk of developing hepatocellular carcinoma (HCC). By using a biologically relevant system of HBV infection of primary human hepatocytes (PHHs), we studied how HBV perturbs gene expression and whether these effects are relevant to HBV-associated HCC. HBV induced a distinct profile of growth factor production, marked particularly by significantly lower levels of the transforming growth factor β (TGF-β) family of proteins. Transcriptome profiling revealed multiple changes in cell proliferation and cell cycle control pathways. Cell cycle analysis demonstrated that HBV-infected PHHs are enriched in the G/M phase. HBV proviral host factors were upregulated upon infection and particularly enriched in cells in the G/M phase. Together, these results support the notion that HBV deregulates cell cycle control to render a cellular environment that is favorable for productive infection. This may coincidently induce a premalignant phenotype that predisposes infected hepatocytes to subsequent malignant transformation.
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http://dx.doi.org/10.1128/JVI.00722-18DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6146796PMC
October 2018

Lung Defense through IL-8 Carries a Cost of Chronic Lung Remodeling and Impaired Function.

Am J Respir Cell Mol Biol 2018 11;59(5):557-571

1 Lung Immunology Group, Infectious Disease and Immunity, Department of Medicine, Imperial College London, London, United Kingdom.

IL-8-dependent inflammation is a hallmark of host lung innate immunity to bacterial pathogens, yet in many human lung diseases, including chronic obstructive pulmonary disease, bronchiectasis, and pulmonary fibrosis, there are progressive, irreversible, pathological changes associated with elevated levels of IL-8 in the lung. To better understand the duality of IL-8-dependent host immunity to bacterial infection and lung pathology, we expressed human IL-8 transgenically in murine bronchial epithelium, and investigated the impact of overexpression on lung bacterial clearance, host immunity, and lung pathology and function. Persistent IL-8 expression in bronchial epithelium resulted in neutrophilia, neutrophil maturation and activation, and chemotaxis. There was enhanced protection against challenge with Pseudomonas aeruginosa, and significant changes in baseline expression of innate and adaptive immunity transcripts for Ccl5, Tlr6, IL-2, and Tlr1. There was increased expression of Tbet and Foxp3 in response to the Pseudomonas antigen OprF, indicating a regulatory T-cell phenotype. However, this enhanced bacterial immunity came at a high price of progressive lung remodeling, with increased inflammation, mucus hypersecretion, and fibrosis. There was increased expression of Ccl3 and reduced expression of Claudin 18 and F11r, with damage to epithelial organization leading to leaky tight junctions, all of which resulted in impaired lung function with reduced compliance, increased resistance, and bronchial hyperreactivity as measured by whole-body plethysmography. These results show that IL-8 overexpression in the bronchial epithelium benefits lung immunity to bacterial infection, but specifically drives lung damage through persistent inflammation, lung remodeling, and damaged tight junctions, leading to impaired lung function.
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http://dx.doi.org/10.1165/rcmb.2018-0007OCDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236688PMC
November 2018

Genetic Analysis of Fusarium Head Blight Resistance in CIMMYT Bread Wheat Line C615 Using Traditional and Conditional QTL Mapping.

Front Plant Sci 2018 1;9:573. Epub 2018 May 1.

Key Laboratory of Wheat Biology and Genetic Improvement for Low & Middle Yangtze Valley Ministry of Agriculture, Lixiahe Agricultural Institute of Jiangsu Province, Yangzhou, China.

Fusarium head blight (FHB) is a destructive wheat disease present throughout the world, and host resistance is an effective and economical strategy used to control FHB. Lack of adequate resistance resource is still a main bottleneck for FHB genetics and wheat breeding research. The synthetic-derived bread wheat line C615, which does not carry the gene, is a promising source of FHB resistance for breeding. A population of 198 recombinant inbred lines (RILs) produced by crossing C615 with the susceptible cultivar Yangmai 13 was evaluated for FHB response using point and spray inoculations. As the disease phenotype is frequently complicated by other agronomic traits, we used both traditional and multivariate conditional QTL mapping approaches to investigate the genetic relationships (at the individual QTL level) between FHB resistance and plant height (PH), spike compactness (SC), and days to flowering (FD). A linkage map was constructed from 3,901 polymorphic SNP markers, which covered 2,549.2 cM. Traditional and conditional QTL mapping analyses found 13 and 22 QTL for FHB, respectively; 10 were identified by both methods. Among these 10, three QTL from C615 were detected in multiple years; these QTL were located on chromosomes 2AL, 2DS, and 2DL. Conditional QTL mapping analysis indicated that, at the QTL level, SC strongly influenced FHB in point inoculation; whereas PH and SC contributed more to FHB than did FD in spray inoculation. The three stable QTL (, and ) for FHB were partly affected by or were independent of the three agronomic traits. The QTL detected in this study improve our understanding of the genetic relationships between FHB response and related traits at the QTL level and provide useful information for marker-assisted selection for the improvement of FHB resistance in breeding.
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http://dx.doi.org/10.3389/fpls.2018.00573DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5946024PMC
May 2018

A Combined Association Mapping and Linkage Analysis of Kernel Number Per Spike in Common Wheat ( L.).

Front Plant Sci 2017 18;8:1412. Epub 2017 Aug 18.

College of Agronomy, Shanxi Agricultural UniversityJinzhong, China.

Kernel number per spike (KNPS) in wheat is a key factor that limits yield improvement. In this study, we genotyped a set of 264 cultivars, and a RIL population derived from the cross Yangmai 13/C615 using the 90 K wheat iSelect SNP array. We detected 62 significantly associated signals for KNPS at 47 single nucleotide polymorphism (SNP) loci through genome-wide association analysis of data obtained from multiple environments. These loci were on 19 chromosomes, and the phenotypic variation attributable to each one ranged from 1.53 to 39.52%. Twelve (25.53%) of the loci were also significantly associated with KNPS in the RIL population grown in multiple environments. For example, , , , and were significantly associated with KNPS in all environments. Our findings demonstrate the effective integration of association mapping and linkage analysis for KNPS, and underpin KNPS as a target trait for marker-assisted selection and genetic fine mapping.
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http://dx.doi.org/10.3389/fpls.2017.01412DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5563363PMC
August 2017

Hepatitis B virus evades innate immunity of hepatocytes but activates cytokine production by macrophages.

Hepatology 2017 12;66(6):1779-1793

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.

Hepatitis B virus (HBV) infects hepatocytes specifically and causes immune-mediated liver damage. How HBV interacts with the innate immunity at the early phase of infection, either with hepatocytes or other cells in the liver, remains controversial. To address this question, we utilized various human cell-culture models and humanized Alb-uPA/SCID mice. All these models were unable to mount an interferon (IFN) response despite robust HBV replication. To elucidate the mechanisms involved in the lack of IFN response, we examined whether HBV actively inhibits innate immune functions of hepatocytes. By treating HBV-infected cells with known inducers of the IFN signaling pathway, we observed no alteration of either sensing or downstream IFN response by HBV. We showed that the DNA innate sensing pathways are poorly active in hepatocytes, consistent with muted innate immune recognition of HBV. Upon exposure to high-level HBV, human macrophages could be activated with increased inflammatory cytokine expressions.

Conclusion: HBV behaves like a "stealth" virus and is not sensed by, nor actively interferes with, the intrinsic innate immunity of infected hepatocytes. Macrophages are capable of sensing HBV, but require exposure to high HBV titers, potentially explaining the long "window period" during acute infection and HBV's propensity to chronic infection. (Hepatology 2017;66:1779-1793).
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http://dx.doi.org/10.1002/hep.29348DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706781PMC
December 2017

HMOX-1 inhibits TGF-β-induced epithelial-mesenchymal transition in the MCF-7 breast cancer cell line.

Int J Mol Med 2017 Aug 14;40(2):411-417. Epub 2017 Jun 14.

Department of Breast and Thyroid Surgery, The Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.

Epithelial‑mesenchymal transition (EMT) is a key mechanism underlying metastatic breast cancer. Reactive oxygen species (ROS) play an important role in EMT. Heme oxygenase‑1 (HMOX‑1) can reduce oxidative stress. However, the effect of HMOX‑1 on the EMT process in breast cancer cells is unknown. We treated the MCF‑7 breast cancer cell line with the HMOX‑1 inducer hemin and observed that hemin induced HMOX‑1 expression and inhibited migration, invasion and ROS generation in transforming growth factor‑β (TGF‑β)‑treated MCF‑7 cells using quantitative RT‑qPCR, western blotting, wound‑healing and cell invasion assays as well as fluorescent probe DCFDA. Hemin inhibited TGF‑β‑induced EMT in the MCF‑7 cells, whereas HMOX‑1 siRNA attenuated the suppressive effect of hemin as determined by the expression and cellular distribution of selected EMT markers. In summary, our results revealed that hemin treatment increased HMOX‑1 expression and inhibited TGF‑β‑induced EMT in MCF‑7 cells.
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http://dx.doi.org/10.3892/ijmm.2017.3027DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5505025PMC
August 2017

Secreted Interferon-Inducible Factors Restrict Hepatitis B and C Virus Entry In Vitro.

J Immunol Res 2017 6;2017:4828936. Epub 2017 Mar 6.

Institute of Virology, Technische Universität München/Helmholtz Zentrum München, 81675 Munich, Germany; German Center for Infection Research (DZIF), Partner Site Munich, Munich, Germany.

Interferon- (IFN-) has been used for more than 20 years as the first-line therapy for hepatitis B virus (HBV) and hepatitis C virus (HCV) infection, because it has a number of antiviral effects. In this study, we describe a novel mode of its antiviral action. We demonstrate that the supernatant from IFN--treated cultured cells restricted HBV and HCV infection by inhibiting viral entry into hepatoma cells. The factors contained in the supernatant competed with the virus for binding to heparan glycosaminoglycans-the nonspecific attachment step shared by HBV and HCV. Secreted factors of high molecular mass that bind to heparin columns elicited the antiviral effect. In conclusion, IFN- is able to induce soluble factors that can bind to heparan glycosaminoglycans thus leading to the inhibition of viral binding.
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http://dx.doi.org/10.1155/2017/4828936DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5358466PMC
May 2017

Human stem cell-derived hepatocytes as a model for hepatitis B virus infection, spreading and virus-host interactions.

J Hepatol 2017 03 14;66(3):494-503. Epub 2016 Oct 14.

Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States. Electronic address:

Background & Aims: One major obstacle of hepatitis B virus (HBV) research is the lack of efficient cell culture system permissive for viral infection and replication. The aim of our study was to establish a robust HBV infection model by using hepatocyte-like cells (HLCs) derived from human pluripotent stem cells.

Methods: HLCs were differentiated from human embryonic stem cells and induced pluripotent stem cells. Maturation of hepatocyte functions was determined. After HBV infection, total viral DNA, cccDNA, total viral RNA, pgRNA, HBeAg and HBsAg were measured.

Results: More than 90% of the HLCs expressed strong signals of human hepatocyte markers, like albumin, as well as known host factors required for HBV infection, suggesting that these cells possessed key features of mature hepatocytes. Notably, HLCs expressed the viral receptor sodium-taurocholate cotransporting polypeptide more stably than primary human hepatocytes (PHHs). HLCs supported robust infection and some spreading of HBV. Finally, by using this model, we identified two host-targeting agents, genistin and PA452, as novel antivirals.

Conclusions: Stem cell-derived HLCs fully support HBV infection. This novel HLC HBV infection model offers a unique opportunity to advance our understanding of the molecular details of the HBV life cycle; to further characterize virus-host interactions and to define new targets for HBV curative treatment.

Lay Summary: Our study used human pluripotent stem cells to develop hepatocyte-like cells (HLCs) capable of expressing hepatocyte markers and host factors important for HBV infection. These cells fully support HBV infection and virus-host interactions, allowing for the identification of two novel antiviral agents. Thus, stem cell-derived HLCs provide a highly physiologically relevant system to advance our understanding of viral life cycle and provide a new tool for antiviral drug screening and development.
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http://dx.doi.org/10.1016/j.jhep.2016.10.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5316493PMC
March 2017

[Advances in molecular targeted therapy of thyroid carcinoma].

Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2015 Dec;29(24):2188-90

Thyroid carcinoma is the most common endocrine maligancy, and the worldwide incidence has been rising in recent years. Differentiated thyroid carcinoma is the most common thyroid malignancy, which include thyroid papillary carcinoma and follicular thyroid carcinoma, accounting for about 90 percent of thyroid carcinoma incidence. Currently, surgical treatment, iodine radiotherapy and TSH suppressive therapy are the commonly accepted effective treatments for differentiated thyroid carcinoma, and most patients can be cured. But there are still some patients not sensitive to the general treatments, who have lost the treatment of opportunity. Molecular targeted therapy is an agonistic or suppressive treatment for molecular biology targets of malignant tumor, and currently is a frontier research in the field of malignancy treatment. By retrieving and analyzing the related literature of molecular targeted therapy of thyroid carcinoma through PUBMED in the past 5 years, the article introduced the current status of molecular targeted therapy of thyroid carcinoma.
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December 2015
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