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  • 1
    Online Resource
    Online Resource
    Cancer survival in C hina, 2003–2005: A population‐based study
    Wiley ; 2015
    In:  International Journal of Cancer Vol. 136, No. 8 ( 2015-04-15), p. 1921-1930
    Details
    In: International Journal of Cancer, Wiley, Vol. 136, No. 8 ( 2015-04-15), p. 1921-1930
    Abstract: What's new? Because it's difficult to create good public‐health policies without good population data, China has recently made efforts to improve its systematic recording of cancer data. This paper reports the largest pooled analysis of survival data in China, the first to include data from a wide range of geographical areas. They report the various survival rates for different cancers by age, gender, and locality. The most striking finding was that those living in rural residents had far lower survival rates than urban residents. This finding may prompt efforts to improve availability of cancer prevention and treatment in rural areas of China.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v136.8
    DOI: 10.1002/ijc.29227
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 2
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    BMP4 Administration Induces Differentiation of CD133+ Hepatic Cancer Stem Cells, Blocking Their Contributions to Hepatocellular Carcinoma
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 16 ( 2012-08-15), p. 4276-4285
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 16 ( 2012-08-15), p. 4276-4285
    Abstract: CD133+ cancer stem cells (CSC) contribute to hepatocellular carcinoma (HCC) progression and resistance to therapy. Bone morphogenetic protein BMP4 plays an important role in hepatogenesis and hepatic stem cell differentiation, but little is known about its function in hepatic CSCs. In this study, we showed that high-dose exogenous BMP4 promotes CD133+ HCC CSC differentiation and inhibits the self-renewal, chemotherapeutic resistance, and tumorigenic capacity of these cells. Interestingly, we found that low-dose exogenous BMP4 upregulated CD133 protein expression in vitro, and endogenous BMP4 was preferentially expressed in CD133+ HCC CSCs, suggesting that low doses of BMP4 may facilitate CSC maintenance. A reduction in endogenous BMP4 levels decreased CD133 protein expression in vitro. In HCC tissues, expression of the BMP4 signaling target gene SMAD6 was positively correlated with CD133 expression. Activation of the Erk1/2 signaling pathway led to BMP4-mediated reduction in CD133 expression, which was reversed by treatment with MEK inhibitors. Taken together, our findings indicated that BMP4 might be a potent therapeutic agent in HCC that targets CSCs. Cancer Res; 72(16); 4276–85. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-12-1013
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
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    Abstract 198: Angiotensin II Inhibits Cardiac Angiogenesis via the Cooperation of p53 and Jagged 1
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Research Vol. 111, No. suppl_1 ( 2012-08-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 111, No. suppl_1 ( 2012-08-03)
    Abstract: It is well established that angiotension II (Ang II) is an important regulator in vascular homeostasis. Under certain conditions, Ang II could exert anti-angiogenic effects in cardiovascular system. However, the potential mechanism is unclear. P53 has been reported to suppress angiogenesis by promoting hypoxia-inducible factor-1 (Hif-1α) degradation. This study was conducted to determine the contribution of P53 and the underlying mechanism to the anti-angiogenic effect of Ang II. Angiogenesis was determined by tube formation from the cardiac microvascular endothelial cells (ECs). Microvessel density and cardiac function were analyzed in mice subjected to Ang II infusion (200 ng/kg/min ) or vehicle for 2 weeks. Ang II (1μM) greatly inhibited tube formation and stimulated phosphorylation and upregulation of P53 in cultured cardiac ECs. P53 inhibitor, pifithrin-α (PFT-α,3.0mg/kg), significantly reversed the inhibitory effect of Ang II on tube formation. Vascular endothelial growth factor (VEGF ) and Hif-1α has been reported as important pro-angiogenetic factors. The present study indicated that Ang II decreased VEGF concentration in cultured medium and downregulated Hif-1α expression in cultured ECs. Interestingly, Ang II also stimulated the upregulation of Jagged 1, a ligand of Notch, but it didn't affect the Delta-like 4 (Dll 4) , another ligand of Notch, expression in cardiac ECs. However, PFT-α partly abolished these effects of Ang II. These results were consistent with the study in vivo. Further research revealed that siRNA-Jagged 1 transfection in cultured ECs dramatically abolished the phosphorylation of P53 and the downregulation of Hif-1α induced by Ang II. Additionally, Ang II- induced inhibitory effect on capillary formation was blocked by siRNA-Jagged 1 transfection in cultured cardiac ECs. In conclusion, Ang II promoted the phosphorylation and upregulation of P53, and increased Jagged 1 expression, the upregulation of Jagged 1 in turn stimulated the phosphorylation of P53, which resulted in the downregulation of Hif-1α and VEGF, then induced the inhibitory effects of Ang II on capillary formation. The present data suggest that Ang II exerts anti-angiogenesis via the cooperation of P53 and Jagged 1 in vitro and in vivo.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.111.suppl_1.A198
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Abstract P148: Urotensin II Impairs Cardiac Functions and Proliferation of Cardiac Side Population Cells in Mice During Chronic Pressure Overload.
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation Research Vol. 109, No. suppl_1 ( 2011-12-09)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 109, No. suppl_1 ( 2011-12-09)
    Abstract: Urotensin II (UII), a potent vasoactive “somatostatin-like” peptide, has been known to play a role in cardiovascular diseases including cardiac hypertrophy and heart failure. But its effect on cardiac side population cells (CSPs), one of somatic stem cells in the heart potentially participating in cardiac protection after injury, is unclear. The present study was therefore conducted to examine influences of UII on the differentiation, proliferation and function of CSPs. CSPs were isolated from neonatal rat hearts by fluorescence-activated cell sorting (FACS) and cultured in the absence or at the presence of UII. The expressions of alpha-cardiac myosin heavy chain, alpha-smooth muscle actin and Von Willebrand factor at mRNAs and protein levels were analyzed by reverse transcriptional PCR (RT-PCR) and immunofluoresence to evaluate the differentiation of CSPs into cardiomyocytes, smooth muscle cells and endothelial cells, respectively. The proliferation of CSPs was assessed by Luminescent Cell Viability Assay. The influence of UII on the proliferation of CSPs in vivo was also evaluated by FACS. Our results revealed that UII did inhibit the proliferation of CSPs through up-regulation of phosphorylated c-Jun N-terminal protein kinase (JNK), although it didn’t affect the differentiation of cultured CSPs into cardiaomyocytes, smooth muscle cells and endothelial cells. In vivo experiments also showed that injection of UII reduced the number of CSPs and impaired cardiac functions compared with vehicle injection in mice subjected to a chronic pressure overload, and an UII antagonist urantide induced a preserved cardiac function with an increased number of CSPs. These data indicate that UII reduces the number of CSPs by inhibiting the proliferation of CSPs possibly through increase of JNK phosphorylation, and blockage of UII may be a useful strategy for cardiac protection in the hypertensive.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.109.suppl_1.AP148
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 1467838-X
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  • 5
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    Online Resource
    CD133 positive hepatocellular carcinoma cells possess high capacity for tumorigenicity
    Wiley ; 2007
    In:  International Journal of Cancer Vol. 120, No. 7 ( 2007-04-01), p. 1444-1450
    Details
    In: International Journal of Cancer, Wiley, Vol. 120, No. 7 ( 2007-04-01), p. 1444-1450
    Type of Medium: Online Resource
    ISSN: 0020-7136
    URL: Article
    DOI: 10.1002/ijc.22476
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 6
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    Multiple introductions and onward transmission of HIV-1 subtype B strains in Shanghai, China
    Elsevier BV ; 2017
    In:  Journal of Infection Vol. 75, No. 2 ( 2017-08), p. 160-168
    Details
    In: Journal of Infection, Elsevier BV, Vol. 75, No. 2 ( 2017-08), p. 160-168
    Type of Medium: Online Resource
    ISSN: 0163-4453
    URL: Article
    DOI: 10.1016/j.jinf.2017.05.009
    RVK:
    XA 54270
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
    detail.hit.zdb_id: 2012883-6
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  • 7
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    Berberine Modulates Macrophage Activation by Inducing Glycolysis
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 208, No. 10 ( 2022-05-15), p. 2309-2318
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 208, No. 10 ( 2022-05-15), p. 2309-2318
    Abstract: Classical activation of macrophage and monocyte differentiation induced by β-glucan is accompanied with metabolic change in glucose. However, the role of the metabolic rewiring in monocyte/macrophage activation remains elusive. In this study, we show that berberine induces aerobic glycolysis by blocking the tricarboxylic acid cycle and modulates cytokine responses in bone marrow–derived macrophages (BMDMs) from mice and human PBMC. 13-Methyberberine had activities on glucose metabolism and BMDM activation similar to those of berberine, whereas other tested derivatives lost both activities. Glucose transporter (GLUT)1 expression and total cellular hexokinase activity increased gradually in BMDMs in the presence of berberine. In the contrast, LPS upregulated GLUT1 and 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3) levels in 6 h. Extracellular glucose levels and replacing glucose with galactose in culture medium affected the cytokine secretion of BMDMs. Berberine alleviated enteritis of Salmonella typhimurium infection and protected mice against endotoxic shock. In mice i.p. injected with LPS, the increase of serum TNF-α and the drop of blood glucose were attenuated by berberine treatment. These data together demonstrated that macrophage activation was closely related with glucose metabolism.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2100716
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 8
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    Abstract 140: Knockdown of Nucleosome Assembly Protein 1-like 1 Promotes Cardiomyocytes Differentiation by Mesoderm induction through Notch Signaling in Mouse Induced Pluripotent Stem Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation Research Vol. 113, No. suppl_1 ( 2013-08)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 113, No. suppl_1 ( 2013-08)
    Abstract: Recently, we used a functional proteomic analysis to screen out nucleosome assembly protein 1-like 1 (Nap1l1) which was downregulated during the differentiation of P19CL6 cells into cardiomyocytes. Here, we attempted to study the role of Nap1l1 in the cardiogenesis of mouse iPSCs. We observed Nap1l1 was downregulated during the differentiation of iPSCs. Knockdown of Nap1l1 dramatically enhanced the differentiation of iPSCs to cardiomyocytes characterized by the increased number of beating embryonic bodies (EBs), the larger alpha-myosin heavy chain (α-MHC)-stained area and the upregulation of cardiac transcription factors (Nkx2.5, GATA4, Mef2c, Tbx5). The effects were sharply inhibited by Nap1l1 overexpression in iPSCs. Cardiomyocytes derived from Nap1l1-knockdown-iPSCs exhibited proper cell biological characteristics. Further study revealed that Nap1l1 knockdown in iPSCs promoted mesoderm (Flk-1, Brachyury and Mesp1) development, but Nap1l1 overexpression inhibited the effect. To explore whether Nap1l1 knockdown in iPSCs enhances cardiomyocytes differentiation by mesoderm induction. Mesoderm cells (Flk-1 positive cells) from iPSCs development were sorted by fluorescent-assisted cell sorting (FACS) and recultured to induce cardiomyocytes differentiation. The result revealed that the same number of Flk-1(mesodermal marker) positive cells from Nap1l1 knockdown, Nap1l1 overexpression or their control iPSCs didn’t show obvious difference in cardiomyocyte differentiation. Loss of Notch signaling in ES cells has been reported to favor commitment to a mesoderm and to induce cardiogenesis. The present study revealed that NICD and downstream genes (Hes1, Hes5, Hey1 and Hey 2) were positively regulated by Nap1l1 expression during differentiation of iPSCs. Notch signaling inhibitor greatly rescued the inhibitory effects of Nap1l1 overexpression on mesoderm induction and cardiogenesis. These findings demonstrate that downregulation of Nap1l1 significantly enhances mesodermal induction and subsequently promotes cardiogenesis from mouse iPSCs via regulating Notch signaling, which will facilitate application of iPSCs for heart diseases.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.113.suppl_1.A140
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1467838-X
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  • 9
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    Diagnostic Performance and Clinical Impact of Metagenomic Next-Generation Sequencing for Pediatric Infectious Diseases
    American Society for Microbiology ; 2023
    In:  Journal of Clinical Microbiology Vol. 61, No. 6 ( 2023-06-20)
    Details
    In: Journal of Clinical Microbiology, American Society for Microbiology, Vol. 61, No. 6 ( 2023-06-20)
    Abstract: Metagenomic next-generation sequencing (mNGS) has shown promise in the diagnosis of infectious diseases in adults, while its efficacy in pediatric infections remains uncertain. We performed a retrospective analysis of 1,493 mNGS samples from pediatric patients with blood, central nervous system, and lower respiratory tract infections. The positive percent agreement (PPA) and the negative percent agreement (NPA) of mNGS were compared to conventional microbiological tests (CMT) based on clinical diagnosis. The agreement of mNGS compared to CMT, as well as the clinical impact of mNGS, were valuated. Using the clinical diagnosis as a reference, mNGS demonstrated a significantly higher overall PPA compared to CMT (53.1% [95% CI = 49.7 to 56.6%] versus 25.8% [95% CI = 22.8 to 28.9%] ), while maintaining a comparable overall NPA (93.2% [95% CI = 91.3 to 95.1%] versus 97.2% [95% CI = 95.9 to 98.4%] ). In septic patients under 6 years of age or with immunosuppressive status, mNGS showed a higher PPA and a comparable NPA compared to CMT. The overall PPA and NPA of mNGS compared to CMT were 75.3 and 75.0%, respectively. The majority of cases of Streptococcus pneumoniae , Streptococcus agalactiae , Mycobacterium tuberculosis complex, and Pneumocystis jirovecii infections were identified by mNGS. A positive clinical impact of 14.0% (206/1,473), a negative impact of 0.8% (11/1,473), a nonimpact of 84.7% (1,248/1,473), and an unknown impact of 0.5% (8/1,473) were observed in the mNGS results. Notably, the positive impact was greater among immunosuppressed patients than among nonimmunosuppressed individuals (67/247, 27.1% versus 139/1,226, 11.3%; P  〈   0.001). mNGS is valuable for pathogen detection, diagnosis, and clinical management of infections among pediatric patients. mNGS was thus effective for the diagnosis of pediatric infections, which may guide clinical management. Patients with immunosuppressive conditions benefited more from mNGS testing.
    Type of Medium: Online Resource
    ISSN: 0095-1137 , 1098-660X
    URL: Article
    DOI: 10.1128/jcm.00115-23
    RVK:
    XA 10000
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2023
    detail.hit.zdb_id: 1498353-9
    SSG: 12
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  • 10
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    The nationwide distribution and trends of hepatitis C virus genotypes in mainland China
    Wiley ; 2019
    In:  Journal of Medical Virology Vol. 91, No. 3 ( 2019-03), p. 401-410
    Details
    In: Journal of Medical Virology, Wiley, Vol. 91, No. 3 ( 2019-03), p. 401-410
    Abstract: Comprehensive data on hepatitis C virus (HCV) genotypes distribution is critical for treatment regimen selection, vaccine design, and drug development. This study aimed to understand the dynamic distribution of HCV genotypes in Mainland China. Three hundred sixty‐two studies published from January 1993 to December 2017 involving 64 891 samples (5133 injecting drug users, 2748 volunteer blood donors, 1509 former paid plasma donors, 160 sexually encounters, and 1992 human immunodeficiency virus (HIV)/HCV coinfection patients) were eligible for the quantitative synthesis estimation. Pooled proportion of HCV genotypes (and 95% confidence intervals [CIs]) was estimated through the Freeman‐Tukey double arcsine transformation by period, region, and risk group. A sharp decline of the subtype 1b was observed in all regions except in northwestern and central regions. The genotypes 3 and 6 showed an obvious increase in southern and southwestern regions and have already spread nationwide. After 2010, subtype 1b was the most dominant variant in all regions and risk groups, accounting for 54.0% (95% CI, 51.9‐56.1) of all national infections. Subtype 2a was the second most prevalent strain in all regions except in the south and southwest, with 15.4% (95% CI, 13.1‐17.8) national infections. The subtype 6a in southern region and 3b and 3a in southwestern region had a higher proportion of infections than that in other regions. In addition, the genotypes 3 and 6 are already prevalent in almost all risk groups. The distribution of HCV genotypes were sharply shifting in China in the past three decades. The HCV subtype 1b posed a sharp decline, whereas genotypes 3 and 6 played an increasing role in the regional and populational HCV pandemic.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
    URL: Article
    DOI: 10.1002/jmv.v91.3
    DOI: 10.1002/jmv.25311
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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