Refine your query (more in Advanced-Search):
 Focus on the recent 5 years   Focus on the current year   Focus on the last 30 days   More choices ...
 Focus on articles with free fulltexts   More choices ...
 Do simple 'keyword' search (no query expansion)

[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 10 of about 15738
1. Ding C, Yu H, Yu H, Qin H: TP53 codon 72 polymorphism with hepatocellular carcinoma: a metaanalysis. J Int Med Res; 2012;40(2):446-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TP53 codon 72 polymorphism with hepatocellular carcinoma: a metaanalysis.
  • OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene - which results in a missense mutation of arginine (R) to proline (P) - and susceptibility to hepatocellular carcinoma (HCC) is controversial.
  • A metaanalysis was performed in order to define this relationship more precisely.
  • METHODS: Published studies of TP53 codon 72 polymorphism and the risk of HCC were identified.
  • Data were extracted, and summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated.
  • Pooled ORs were determined for an additive model (R/R versus P/P), a dominant model ([R/R + R/P] versus P/P) and a recessive model (R/R versus [R/P + P/P]).
  • RESULTS: The meta-analysis included seven case-control studies (total 1511 cases and 2165 controls).
  • The risk of cancer was significantly decreased in the overall dominant model and the dominant model in Asian populations.
  • A significantly decreased risk was found for all models in hospital-based but not population-based studies.
  • There was no association between polymorphism and cancer risk when data were stratified according to hepatitis B or C virus infection status.
  • CONCLUSION: The TP53 codon 72 polymorphism may be a risk factor for HCC.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Genes, p53. Hepatitis B / complications. Hepatitis C / complications. Liver Neoplasms / genetics. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Aflatoxin B1 / toxicity. Alcohol Drinking / adverse effects. Asian Continental Ancestry Group / genetics. Case-Control Studies. Female. Gene Frequency. Genetic Predisposition to Disease. Genotype. Humans. Male. Polymorphism, Single Nucleotide. Risk. Risk Factors

  • MedlinePlus Health Information. consumer health - Hepatitis B.
  • MedlinePlus Health Information. consumer health - Hepatitis C.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. AFLATOXIN B1 .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Int Med Res. 2013 Apr;41(2):519-20 [23569040.001]
  • (PMID = 22613405.001).
  • [ISSN] 1473-2300
  • [Journal-full-title] The Journal of international medical research
  • [ISO-abbreviation] J. Int. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 9N2N2Y55MH / Aflatoxin B1
  •  go-up   go-down


2. Yu H: [Qualitative research and clinical study on cancer]. Zhongguo Zhong Xi Yi Jie He Za Zhi; 2008 Feb;28(2):169-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Qualitative research and clinical study on cancer].
  • Tumor is one of the fateful diseases that human must confront.
  • Currently, quantitative research is still the principal body of the research on cancer.
  • Qualitative research can compensate the limitations of quantitative research in evaluating therapeutic effects on cancer, it can profoundly understand the attitude, experience, confidence, presumable problems and obstacles of doctors and patients to the therapy.
  • This article introduces the necessity and general situation of development in applying qualitative research methods in the researches on tumor, and the main problems and developing tendency for extending in China.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18386584.001).
  • [ISSN] 1003-5370
  • [Journal-full-title] Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine
  • [ISO-abbreviation] Zhongguo Zhong Xi Yi Jie He Za Zhi
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  •  go-up   go-down


3. Yu H: Bacteria-mediated disease therapy. Appl Microbiol Biotechnol; 2011 Dec;92(6):1107-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bacteria-mediated disease therapy.
  • Laboratory bacteria have been model systems for studying gene function or developing molecular biotechnologies; industrial bacteria have been used to produce drugs, foods, fuel etc.
  • ; while pathogenic bacteria have been the subject of infectious diseases studies with aim of controlling them.
  • Recently, with our increasing knowledge in molecular biology, bacterial genetics, and immunology, bacteria have gained increased interest in therapeutic applications.
  • This review will summarize recent advances toward applying bacteria in treatment of diseases, such as inflammatory disease, cancer, and virus infection.
  • Probiotics have long been appreciated for their immunomodulatory effect, which are discussed in the anti-inflammatory section.
  • Anaerobic bacteria have been applied for destructing tumor cells or used as a magic bullet to specifically deliver therapeutic agents to tumor tissue.
  • Examples and strategies of applying those tumor-targeting bacteria are discussed in the antitumor section.
  • Finally, the pioneer study of applying Salmonella in delivering RNase P that was specifically engineered to target essential mRNAs of virus is summarized.
  • [MeSH-major] Bacterial Physiological Phenomena. Biological Therapy. Drug Therapy. Genetic Therapy / instrumentation
  • [MeSH-minor] Animals. Bacteria / genetics. Humans. Probiotics / therapeutic use

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 22033568.001).
  • [ISSN] 1432-0614
  • [Journal-full-title] Applied microbiology and biotechnology
  • [ISO-abbreviation] Appl. Microbiol. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  •  go-up   go-down


Advertisement
4. Yu H: China's medical savings accounts: an analysis of the price elasticity of demand for health care. Eur J Health Econ; 2017 Jul;18(6):773-785
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] China's medical savings accounts: an analysis of the price elasticity of demand for health care.
  • Although medical savings accounts (MSAs) have drawn intensive attention across the world for their potential in cost control, there is limited evidence of their impact on the demand for health care.
  • This paper is intended to fill that gap.
  • First, we built up a dynamic model of a consumer's problem of utility maximization in the presence of a nonlinear price schedule embedded in an MSA.
  • Second, the model was implemented using data from a 2-year MSA pilot program in China.
  • The estimated price elasticity under MSAs was between -0.42 and -0.58, i.e., higher than that reported in the literature.
  • The relatively high price elasticity suggests that MSAs as an insurance feature may help control costs.
  • However, the long-term effect of MSAs on health costs is subject to further analysis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Health Care Finance Econ. 2014 Mar;14(1):19-40 [24214101.001]
  • [Cites] BMC Health Serv Res. 2009 Dec 29;9:244 [20040076.001]
  • [Cites] Health Serv Res. 2011 Feb;46(1 Pt 1):155-72 [21029087.001]
  • [Cites] Health Aff (Millwood). 2008 Jul-Aug;27(4):1120-31 [18607046.001]
  • [Cites] Ann N Y Acad Sci. 1982;387:111-4 [6953855.001]
  • [Cites] J Health Econ. 2001 Jul;20(4):461-94 [11469231.001]
  • [Cites] Health Serv Res. 2004 Aug;39(4 Pt 2):1189-210 [15230920.001]
  • [Cites] Time. 2001 Oct 15;158(17 ):Y15-6 [11668851.001]
  • [Cites] J Health Soc Behav. 1995 Mar;36(1):1-10 [7738325.001]
  • [Cites] Health Aff (Millwood). 2006 Jan-Feb;25(1):57-69 [16403745.001]
  • [Cites] Health Aff (Millwood). 2006 Nov-Dec;25(6):w516-30 [17062591.001]
  • [Cites] Am J Manag Care. 2011 Jan;17(1):79-86 [21348571.001]
  • [Cites] Health Aff (Millwood). 2008 Jul-Aug;27(4):1111-9 [18607045.001]
  • [Cites] J Health Polit Policy Law. 2001 Aug;26(4):733-7 [11523960.001]
  • [Cites] Health Aff (Millwood). 2012 Jun;31(6):1339-48 [22623614.001]
  • [Cites] Health Aff (Millwood). 2002 Jan-Feb;21(1):49-64 [11900095.001]
  • [Cites] Inquiry. 2007 Spring;44(1):26-40 [17583260.001]
  • [Cites] Health Aff (Millwood). 2006 Jan-Feb;25(1):256-67 [16403762.001]
  • [Cites] J Health Econ. 1998 Jun;17(3):283-95 [10180919.001]
  • [Cites] Annu Rev Public Health. 1999;20:125-44 [10352853.001]
  • [Cites] J Health Econ. 1999 Apr;18(2):153-71 [10346351.001]
  • [Cites] Health Econ Policy Law. 2016 Jul;11(3):321-35 [26883211.001]
  • [Cites] J Health Econ. 1997 Feb;16(1):1-31 [10167341.001]
  • [Cites] J Health Econ. 1988 Dec;7(4):337-67 [10312839.001]
  • [Cites] Am J Manag Care. 2011 Mar;17 (3):222-30 [21504258.001]
  • [Cites] J Health Polit Policy Law. 2001 Aug;26(4):739-45 [11523961.001]
  • [Cites] Health Serv Res. 2008 Oct;43(5 Pt 1):1542-56 [18479407.001]
  • [Cites] J Health Econ. 2000 Sep;19(5):697-718 [11184800.001]
  • [Cites] Int J Health Care Finance Econ. 2013 Dec;13(3-4):319-31 [24085335.001]
  • [Cites] J Ment Health Policy Econ. 2010 Dec;13(4):159-65 [21368340.001]
  • [Cites] Health Serv Res. 1986 Jun;21(2 Pt 2):291-319 [3721874.001]
  • [Cites] Health Policy. 1995 Apr-Jun;32(1-3):181-91 [10156638.001]
  • [Cites] Health Serv Res. 2010 Aug;45(4):1041-60 [20528988.001]
  • [Cites] J Health Polit Policy Law. 2001 Aug;26(4):727-31 [11523959.001]
  • [Cites] J Health Econ. 1998 Jun;17(3):247-81 [10180918.001]
  • [Cites] Milbank Q. 2009 Dec;87(4):820-41 [20021587.001]
  • [Cites] Health Aff (Millwood). 1995 Spring;14(1):126-39 [7657198.001]
  • [Cites] J Health Polit Policy Law. 2001 Aug;26(4):709-26 [11523958.001]
  • [Cites] Health Serv Res. 1986 Jun;21(2 Pt 2):321-40 [3721875.001]
  • [Cites] Soc Sci Med. 2009 Jan;68(2):201-9 [19019519.001]
  • [Cites] Am J Manag Care. 2013 Dec 01;19(12):e400-7 [24512088.001]
  • [Cites] J Health Econ. 1999 Jun;18(3):365-80 [10537900.001]
  • [Cites] J Med Internet Res. 2013 Aug 29;15(8):e185 [23988296.001]
  • (PMID = 27650358.001).
  • [ISSN] 1618-7601
  • [Journal-full-title] The European journal of health economics : HEPAC : health economics in prevention and care
  • [ISO-abbreviation] Eur J Health Econ
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Keywords] NOTNLM ; China / Demand for health care / Elasticity / Health insurance / Medical savings accounts / Nonlinear price schedule
  •  go-up   go-down


5. Yu H: Typical cell signaling response to ionizing radiation: DNA damage and extranuclear damage. Chin J Cancer Res; 2012 Jun;24(2):83-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Typical cell signaling response to ionizing radiation: DNA damage and extranuclear damage.
  • To treat many types of cancer, ionizing radiation (IR) is primarily used as external-beam radiotherapy, brachytherapy, and targeted radionuclide therapy.
  • Exposure of tumor cells to IR can induce DNA damage as well as generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which can cause non-DNA lesions or extracellular damage like lipid perioxidation.
  • The initial radiation-induced cell responses to DNA damage and ROS like the proteolytic processing, as well as synthesis and releasing ligands (such as growth factors, cytokines, and hormone) can cause the delayed secondary responses in irradiated and unirradiated bystander cells through paracrine and autocrine pathways.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Science. 1993 Nov 12;262(5136):1065-9 [7694366.001]
  • [Cites] Int Rev Cytol. 1993;143:1-62 [8449662.001]
  • [Cites] Nat Immunol. 2002 Mar;3(3):221-7 [11875461.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jul 5;295(1):24-30 [12083761.001]
  • [Cites] Mol Biol Cell. 2012 Jan;23(1):7-11 [22210846.001]
  • [Cites] Radiat Res. 1994 Oct;140(1):97-104 [7938461.001]
  • [Cites] J Immunol. 1994 Jul 15;153(2):712-23 [8021507.001]
  • [Cites] J Biol Chem. 1994 Aug 5;269(31):20067-74 [8051093.001]
  • [Cites] Radiat Res. 1994 Jun;138(3):367-72 [8184011.001]
  • [Cites] Cell. 1996 Jan 26;84(2):299-308 [8565075.001]
  • [Cites] Immunity. 1996 Apr;4(4):387-96 [8612133.001]
  • [Cites] Eur J Cancer. 1997 Apr;33(4):638-44 [9274448.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10057-62 [9294162.001]
  • [Cites] Biochem J. 1998 Mar 15;330 ( Pt 3):1451-60 [9494119.001]
  • [Cites] Genes Dev. 1998 Jun 15;12(12):1769-74 [9637678.001]
  • [Cites] FASEB J. 1998 Jul;12(10):801-11 [9657520.001]
  • [Cites] Science. 1998 Sep 11;281(5383):1680-3 [9733516.001]
  • [Cites] Clin Cancer Res. 1995 Dec;1(12):1557-62 [9815956.001]
  • [Cites] Nature. 1998 Dec 10;396(6711):580-4 [9859993.001]
  • [Cites] J Urol. 1999 Feb;161(2):674-9 [9915481.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Sep 14;287(1):110-5 [11549261.001]
  • [Cites] Ernst Schering Res Found Workshop. 2002;(36):51-70 [11859564.001]
  • [Cites] Mil Med. 2002 Feb;167(2 Suppl):66-7 [11873521.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2531-4 [11980645.001]
  • [Cites] Oncogene. 2002 May 30;21(24):3898-908 [12032828.001]
  • [Cites] Science. 2002 Jul 26;297(5581):602-6 [12142538.001]
  • [Cites] Oncogene. 2002 Sep 19;21(42):6510-9 [12226754.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5436-42 [12359750.001]
  • [Cites] J Mol Biol. 2002 Oct 4;322(5):917-27 [12367518.001]
  • [Cites] J Immunol. 2002 Nov 1;169(9):5287-93 [12391248.001]
  • [Cites] Immunol Today. 1992 May;13(5):151-3 [1322675.001]
  • [Cites] Cancer Res. 1992 Nov 15;52(22):6394-6 [1423287.001]
  • [Cites] J Exp Med. 1990 Jan 1;171(1):35-47 [2104921.001]
  • [Cites] Nature. 1990 Apr 12;344(6267):678-82 [2157987.001]
  • [Cites] Mol Cell Biol. 1990 Apr;10(4):1498-506 [2181276.001]
  • [Cites] Mol Cell Biol. 1990 May;10(5):2327-34 [2183031.001]
  • [Cites] Cell. 1995 May 19;81(4):495-504 [7758105.001]
  • [Cites] Radiat Res. 1994 Apr;138(1 Suppl):S47-51 [8146325.001]
  • [Cites] Biochem Mol Biol Int. 1995 Dec;37(6):1063-70 [8747536.001]
  • [Cites] Carcinogenesis. 1996 Aug;17(8):1633-9 [8761419.001]
  • [Cites] Science. 1996 Nov 1;274(5288):782-4 [8864118.001]
  • [Cites] Science. 1996 Nov 1;274(5288):784-7 [8864119.001]
  • [Cites] Cell. 1996 Nov 1;87(3):565-76 [8898208.001]
  • [Cites] Mutat Res. 1996 Nov 4;358(2):143-53 [8946019.001]
  • [Cites] Cell. 1997 Jan 24;88(2):213-22 [9008162.001]
  • [Cites] Nature. 1997 Feb 6;385(6616):540-4 [9020361.001]
  • [Cites] J Biol Chem. 1997 May 30;272(22):14183-7 [9162048.001]
  • [Cites] Nat Med. 1997 Aug;3(8):917-21 [9256286.001]
  • [Cites] Semin Cancer Biol. 1997 Apr;8(2):113-9 [9299589.001]
  • [Cites] J Exp Med. 1998 Jul 6;188(1):211-6 [9653098.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9067-9 [9689033.001]
  • [Cites] Nature. 1998 Sep 10;395(6698):124-5 [9744267.001]
  • [Cites] Radiat Res. 1998 Nov;150(5):497-504 [9806590.001]
  • [Cites] J Biol Chem. 1999 Mar 26;274(13):8531-8 [10085086.001]
  • [Cites] J Biol Chem. 2000 Nov 24;275(47):36671-5 [10970902.001]
  • [Cites] Nature. 2000 Nov 23;408(6811):433-9 [11100718.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):635-40 [11149963.001]
  • [Cites] Nat Rev Mol Cell Biol. 2000 Dec;1(3):179-86 [11252893.001]
  • [Cites] Free Radic Biol Med. 2001 Aug 15;31(4):520-9 [11498285.001]
  • [Cites] Annu Rev Genet. 2002;36:617-56 [12429704.001]
  • [Cites] Lab Invest. 2002 Dec;82(12):1661-72 [12480916.001]
  • [Cites] Hepatology. 2003 Jan;37(1):118-28 [12500196.001]
  • [Cites] Cancer Res. 2003 Jan 15;63(2):324-8 [12543783.001]
  • [Cites] Shi Yan Sheng Wu Xue Bao. 2000 Jun;33(2):129-40 [12548976.001]
  • [Cites] Genes Dev. 2003 Mar 1;17(5):615-28 [12629044.001]
  • [Cites] Science. 2003 Jun 6;300(5625):1542-8 [12791985.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Arch Dermatol Res. 2004 Aug;296(3):125-33 [15278366.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2005 Feb;32(2):229-46 [15657757.001]
  • [Cites] J Rheumatol. 2006 Jun;33(6):1061-8 [16755653.001]
  • [Cites] Curr Opin Cell Biol. 2007 Apr;19(2):124-34 [17314037.001]
  • [Cites] J Radiol Prot. 2009 Jun;29(2A):A133-42 [19454811.001]
  • [Cites] Neoplasia. 2009 Aug;11(8):720-31 [19649202.001]
  • [Cites] Mol Cell Endocrinol. 2010 Jul 8;323(1):115-23 [20385202.001]
  • [Cites] J Biol Chem. 1999 Mar 12;274(11):7264-71 [10066788.001]
  • [Cites] J Biol Chem. 1992 Jun 25;267(18):12424-7 [1618749.001]
  • [Cites] J Clin Invest. 1991 Aug;88(2):691-5 [1864978.001]
  • [Cites] Am J Respir Cell Mol Biol. 1991 Mar;4(3):278-86 [2001291.001]
  • [Cites] Cancer Res. 1991 May 15;51(10):2552-8 [2021936.001]
  • [Cites] EMBO J. 1991 Aug;10(8):2247-58 [2065663.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2336-40 [2494664.001]
  • [Cites] Cell. 1989 Jul 28;58(2):227-9 [2665943.001]
  • [Cites] Cell. 1988 Apr 22;53(2):211-7 [3129195.001]
  • [Cites] Science. 1988 Oct 28;242(4878):540-6 [3140380.001]
  • (PMID = 23357898.001).
  • [ISSN] 1000-9604
  • [Journal-full-title] Chinese journal of cancer research = Chung-kuo yen cheng yen chiu
  • [ISO-abbreviation] Chin. J. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC3555267
  • [Keywords] NOTNLM ; Bystander effect / DNA damage / Extranuclear damage / Radiation
  •  go-up   go-down


6. Yu H: Universal health insurance coverage for 1.3 billion people: What accounts for China's success? Health Policy; 2015 Sep;119(9):1145-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Universal health insurance coverage for 1.3 billion people: What accounts for China's success?
  • China successfully achieved universal health insurance coverage in 2011, representing the largest expansion of insurance coverage in human history.
  • While the achievement is widely recognized, it is still largely unexplored why China was able to attain it within a short period.
  • This study aims to fill the gap.
  • Through a systematic political and socio-economic analysis, it identifies seven major drivers for China's success, including (1) the SARS outbreak as a wake-up call, (2) strong public support for government intervention in health care, (3) renewed political commitment from top leaders, (4) heavy government subsidies, (5) fiscal capacity backed by China's economic power, (6) financial and political responsibilities delegated to local governments and (7) programmatic implementation strategy.
  • Three of the factors seem to be unique to China (i.e., the SARS outbreak, the delegation, and the programmatic strategy.) while the other factors are commonly found in other countries' insurance expansion experiences.
  • This study also discusses challenges and recommendations for China's health financing, such as reducing financial risk as an immediate task, equalizing benefit across insurance programs as a long-term goal, improving quality by tying provider payment to performance, and controlling costs through coordinated reform initiatives.
  • Finally, it draws lessons for other developing countries.
  • [MeSH-major] Insurance, Health / organization & administration. Universal Coverage / organization & administration
  • [MeSH-minor] China. Cost Control / organization & administration. Disease Outbreaks. Financing, Government / organization & administration. Financing, Government / statistics & numerical data. Health Care Reform / organization & administration. Humans. Politics. Program Evaluation. Reimbursement, Incentive / organization & administration. SARS Virus. Severe Acute Respiratory Syndrome / epidemiology

  • MedlinePlus Health Information. consumer health - Health Insurance.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2015 The Author. Published by Elsevier Ireland Ltd.. All rights reserved.
  • (PMID = 26251322.001).
  • [ISSN] 1872-6054
  • [Journal-full-title] Health policy (Amsterdam, Netherlands)
  • [ISO-abbreviation] Health Policy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Keywords] NOTNLM ; China / Health care reform / Health insurance / Universal coverage
  •  go-up   go-down


7. YU H: [Epigenetics: advances of non-coding RNAs regulation in mammalian cells]. Yi Chuan; 2009 Nov;31(11):1077-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Epigenetics: advances of non-coding RNAs regulation in mammalian cells].
  • Epigenetics is the study of meiotically and mitotically heritable changes in gene expression that are not coded for in the underlying DNA sequence.
  • The term epigenetics is derived from epi- (meaning upon) and genetics.
  • Epigenetic regulation of mammalian gene expression has profound effects in controlling cell growth, differentiation and cancer development.
  • The important epigenetic mechanisms include DNA cytosine methylation, histone modifications and the more recently discovered non-coding RNAs.
  • Non-coding RNAs are functional RNA molecules that are not translated into proteins.
  • The main classes of regulatory non-coding RNAs include siRNA, miRNA, piRNA and long non-coding RNAs.
  • There is growing evidence that regulatory non-coding RNAs play essential roles in the regulation of gene expression and are impor-tant in mammalian development and disease processes.
  • Here, we review current research efforts aimed at understanding non-coding RNAs and their mechanisms of function in mammalian cells.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19933087.001).
  • [ISSN] 0253-9772
  • [Journal-full-title] Yi chuan = Hereditas
  • [ISO-abbreviation] Yi Chuan
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] China
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Small Interfering; 63231-63-0 / RNA
  • [Number-of-references] 81
  •  go-up   go-down


8. Yu H: Towards answering biological questions with experimental evidence: automatically identifying text that summarize image content in full-text articles. AMIA Annu Symp Proc; 2006;:834-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Towards answering biological questions with experimental evidence: automatically identifying text that summarize image content in full-text articles.
  • Images (i.e., figures) are important experimental evidence that are typically reported in bioscience full-text articles.
  • Biologists need to access images to validate research facts and to formulate or to test novel research hypotheses.
  • We propose to build a biological question answering system that provides experimental evidences as answers in response to biological questions.
  • As a first step, we develop natural language processing techniques to identify sentences that summarize image content.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Bioinformatics. 2001 Feb;17(2):126-36 [11238068.001]
  • [Cites] Bioinformatics. 2001;17 Suppl 1:S74-82 [11472995.001]
  • [Cites] Pac Symp Biocomput. 2003;:613-23 [12603062.001]
  • [Cites] BMC Bioinformatics. 2006;7:140 [16539745.001]
  • [Cites] Nucleic Acids Res. 1988 Nov 25;16(22):10881-90 [2849754.001]
  • [Cites] Acta Crystallogr D Biol Crystallogr. 1998 Nov 1;54(Pt 6 Pt 1):1078-84 [10089483.001]
  • [Cites] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D258-61 [14681407.001]
  • (PMID = 17238458.001).
  • [ISSN] 1942-597X
  • [Journal-full-title] AMIA ... Annual Symposium proceedings. AMIA Symposium
  • [ISO-abbreviation] AMIA Annu Symp Proc
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC1839512
  •  go-up   go-down


9. Yu H: Sphingosine-1-Phosphate Receptor 2 Regulates Proinflammatory Cytokine Production and Osteoclastogenesis. PLoS One; 2016;11(5):e0156303
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sphingosine-1-Phosphate Receptor 2 Regulates Proinflammatory Cytokine Production and Osteoclastogenesis.
  • Sphingosine-1-phosphate receptor 2 (S1PR2) couples with the Gi, Gq, and G12/13 group of proteins, which modulate an array of cellular signaling pathways and affect immune responses to multiple stimuli.
  • In this study, we demonstrated that knockdown of S1PR2 by a specific S1PR2 shRNA lentiviral vector significantly inhibited IL-1β, IL-6, and TNF-α protein levels induced by oral pathogen Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) in murine bone marrow-derived monocytes and macrophages (BMMs) compared with controls.
  • In addition, knockdown of S1PR2 by the S1PR2 shRNA lentiviral vector suppressed p-PI3K, p-ERK, p-JNK, p-p38, and p-NF-κBp65 protein expressions induced by A. actinomycetemcomitans.
  • Furthermore, bone marrow cells treated with the S1PR2 shRNA lentiviral vector inhibited osteoclastogenesis induced by RANKL compared with controls.
  • The S1PR2 shRNA suppressed the mRNA levels of six osteoclastogenic factors including nuclear factor of activated T-cells cytoplasmic calcineurin-dependent 1 (NFATc1), cathepsin K (Ctsk), acid phosphatase 5 (Acp5), osteoclast-associated receptor (Oscar), dendritic cells specific transmembrane protein (Dcstamp), and osteoclast stimulatory transmembrane protein (Ocstamp) in bone marrow cells.
  • We conclude that S1PR2 plays an essential role in modulating proinflammatory cytokine production and osteoclastogenesis.
  • Blocking S1PR2 signaling might be a novel therapeutic strategy to treat inflammatory bone loss diseases.
  • [MeSH-major] Cytokines / metabolism. Osteoclasts / cytology. Osteogenesis. Pasteurellaceae Infections / immunology. Receptors, Lysosphingolipid / genetics
  • [MeSH-minor] Aggregatibacter actinomycetemcomitans / immunology. Animals. Cells, Cultured. Gene Knockdown Techniques. Interleukin-1beta / metabolism. Interleukin-6 / metabolism. Mice. Monocyte-Macrophage Precursor Cells / cytology. Monocyte-Macrophage Precursor Cells / immunology. Monocyte-Macrophage Precursor Cells / microbiology. Tumor Necrosis Factor-alpha / metabolism

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell Mol Life Sci. 2013 Sep;70(18):3341-53 [23296124.001]
  • [Cites] Nat Rev Drug Discov. 2013 Sep;12(9):688-702 [23954895.001]
  • [Cites] J Lipid Res. 2013 Jan;54(1):189-201 [23139430.001]
  • [Cites] Int Immunopharmacol. 2014 Jun;20(2):298-306 [24735815.001]
  • [Cites] Science. 2002 Apr 12;296(5566):346-9 [11923495.001]
  • [Cites] Proc Natl Acad Sci U S A. 2013 Apr 23;110(17):7009-13 [23569273.001]
  • [Cites] Biochim Biophys Acta. 2002 May 23;1582(1-3):72-80 [12069812.001]
  • [Cites] J Inflamm (Lond). 2012 Jan 12;9(1):1 [22239975.001]
  • [Cites] J Immunol. 2011 Jan 1;186(1):13-8 [21172874.001]
  • [Cites] Eur J Immunol. 2005 Feb;35(2):533-45 [15657952.001]
  • [Cites] Genome Res. 2009 Jun;19(6):1057-67 [19261841.001]
  • [Cites] Nat Rev Immunol. 2011 Jun;11(6):403-15 [21546914.001]
  • [Cites] Scientifica (Cairo). 2013;2013:125705 [24278766.001]
  • [Cites] Arch Biochem Biophys. 2008 May 15;473(2):132-8 [18424258.001]
  • [Cites] Cytokine Growth Factor Rev. 2011 Feb;22(1):45-53 [21051273.001]
  • [Cites] Nihon Rinsho. 2005 Sep;63(9):1541-6 [16164209.001]
  • [Cites] Biochem Biophys Res Commun. 2015 May 29;461(2):334-41 [25887803.001]
  • [Cites] FASEB J. 2015 Aug;29(8):3357-69 [25911610.001]
  • [Cites] Lipids Health Dis. 2015 Jul 04;14:66 [26138336.001]
  • [Cites] Biochim Biophys Acta. 2002 May 23;1582(1-3):94-9 [12069815.001]
  • [Cites] Int J Biochem Cell Biol. 2010 May;42(5):576-9 [20035895.001]
  • [Cites] Adv Drug Deliv Rev. 2005 May 25;57(7):959-71 [15876398.001]
  • [Cites] Pathol Res Pract. 2012 Feb 15;208(2):82-8 [22244964.001]
  • [Cites] Blood. 2013 Jul 18;122(3):443-55 [23723450.001]
  • [Cites] Keio J Med. 2011;60(4):101-5 [22200633.001]
  • [Cites] J Exp Med. 2010 Dec 20;207(13):2793-8 [21135136.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2011 Jan;31(1):81-5 [20947824.001]
  • [Cites] Front Immunol. 2014 Oct 20;5:511 [25368616.001]
  • [Cites] J Periodontol. 2008 Aug;79(8 Suppl):1585-91 [18673014.001]
  • [Cites] Biochem J. 1999 Jan 1;337 ( Pt 1):67-75 [9854026.001]
  • [Cites] Osteoarthritis Cartilage. 2002 Dec;10(12):961-7 [12464556.001]
  • [Cites] Steroids. 2014 Aug;86:62-8 [24819989.001]
  • [Cites] J Periodontal Res. 2016 Feb;51(1):38-49 [25900155.001]
  • [Cites] Nature. 2009 Mar 26;458(7237):524-8 [19204730.001]
  • [Cites] FASEB J. 2004 Mar;18(3):551-3 [14715694.001]
  • [Cites] J Biol Chem. 2002 Jun 14;277(24):21453-7 [11967257.001]
  • [Cites] J Clin Invest. 2010 May;120(5):1429-40 [20407207.001]
  • (PMID = 27224249.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / P30 GM103331; United States / NIDCR NIH HHS / DE / R03 DE025026
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / IL1B protein, mouse; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Receptors, Lysosphingolipid; 0 / Tumor Necrosis Factor-alpha; 0 / sphingosine-1-phosphate receptor-2, mouse
  • [Other-IDs] NLM/ PMC4880337
  •  go-up   go-down


10. Yu H: Management of pleural effusion, empyema, and lung abscess. Semin Intervent Radiol; 2011 Mar;28(1):75-86
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of pleural effusion, empyema, and lung abscess.
  • Pleural effusion is an accumulation of fluid in the pleural space that is classified as transudate or exudate according to its composition and underlying pathophysiology.
  • Empyema is defined by purulent fluid collection in the pleural space, which is most commonly caused by pneumonia.
  • A lung abscess, on the other hand, is a parenchymal necrosis with confined cavitation that results from a pulmonary infection.
  • Pleural effusion, empyema, and lung abscess are commonly encountered clinical problems that increase mortality.
  • These conditions have traditionally been managed by antibiotics or surgical placement of a large drainage tube.
  • However, as the efficacy of minimally invasive interventional procedures has been well established, image-guided small percutaneous drainage tubes have been considered as the mainstay of treatment for patients with pleural fluid collections or a lung abscess.
  • In this article, the technical aspects of image-guided interventions, indications, expected benefits, and complications are discussed and the published literature is reviewed.

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 22379278.001).
  • [ISSN] 1098-8963
  • [Journal-full-title] Seminars in interventional radiology
  • [ISO-abbreviation] Semin Intervent Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC3140254
  • [Keywords] NOTNLM ; Pleural effusion / empyema / interventional radiology / lung abscess / malignant pleural effusion
  •  go-up   go-down






Advertisement