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  • 1
    Call number: QZ266.6:23
    Keywords: Thermotherapy ; Hyperthermia, Induced ; Tumor / Therapie
    Pages: ix, 84 p. : ill.
    ISBN: 3540545603
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  PTCOG 48; Meeting of the Particle Therapy Co-Operative Group; 20090928-20091003; Heidelberg; DOC09ptcog139 /20090924/
    Publication Date: 2009-09-25
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 3
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  PTCOG 48; Meeting of the Particle Therapy Co-Operative Group; 20090928-20091003; Heidelberg; DOC09ptcog140 /20090924/
    Publication Date: 2009-09-25
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 4
    Keywords: CANCER ; SURVIVAL ; LUNG ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; screening ; COHORT ; cohort study ; DEATH ; MORTALITY ; RISK ; BREAST ; BREAST-CANCER ; prevention ; NUMBER ; AGE ; WOMEN ; CIGARETTE-SMOKING ; RANDOMIZED CONTROLLED TRIAL ; smoking ; DIETARY ; ALCOHOL-CONSUMPTION ; relapse ; PROGRAM ; RE ; NONSMOKING WOMEN ; ENVIRONMENTAL TOBACCO-SMOKE ; duration ; BODY-MASS INDEX ; survival analysis ; smoking cessation ; FACTOR INTERVENTION TRIAL ; UNITED-STATES POPULATIONS
    Abstract: PURPOSE: To determine the impact of smoking cessation on lung cancer mortality among women. METHODS: Survival analysis is used to assess the effect of smoking cessation on lung cancer death in the dietary cohort of 49,165 women aged 40 to 59 years enrolled in the Canadian National Breast Screening Study. RESULTS: During an average of 10.3 years of follow-up, 106 women died of lung cancer. The risk of lung cancer mortality among women who quit before age 50 (HR = 0.26; 95% CI, 0.13-0.55 among women who quit at ages 40-49) or quit in the previous 10 years (HR = 0.39; 95% CI, 0.22-0.69) is substantially lower than the risk among current smokers. Women who quit after age 40 or have quit for less than 20 years are at substantially higher risk of lung cancer mortality compared with never smokers. Both duration of smoking cessation and age at quitting have independent effects on lung cancer mortality, after controlling for number of cigarettes smoked per day and number of years smoked, as well as other potential confounding variables. CONCLUSION: These findings suggest that programs and policies to promote early cessation of smoking and prevention of relapse should be a public health priority. (c) 2005 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15780778
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  • 5
    Keywords: RECEPTOR ; CELLS ; proliferation ; CELL ; IN-VIVO ; KINASE ; VIVO ; TOOL ; PROTEIN ; DIFFERENTIATION ; MOLECULES ; TRANSDUCTION ; ACTIVATION ; LIGAND ; DOMAIN ; BINDING ; DOWN-REGULATION ; GROWTH-FACTOR RECEPTOR ; PHOSPHORYLATION ; signal transduction ; SIGNAL ; MOLECULE ; FORM ; MUTANT ; hormone ; resistance ; DECREASE ; SIGNAL-TRANSDUCTION ; SURFACE ; DIMERIZATION ; ENDOPLASMIC-RETICULUM ; ERYTHROPOIETIN RECEPTOR ; TYROSINE PHOSPHORYLATION ; ER ; POTENT ; COMPARTMENTS ; MOTIF ; CELL-SURFACE EXPRESSION ; Janus kinase 2 ; PROTEIN-TYROSINE-PHOSPHATASE ; PTP1B ; PTP1B (protein tyrosine phosphatase 1B) 'substrate-trapping' mutant ; TYROSINE-PHOSPHORYLATION
    Abstract: Erythropoietin (EPO) is the principal hormone regulating the proliferation of erythroid precursors and their differentiation into erythrocytes. Binding of ligand to the cell-surface EPO-R (EPO receptor) induces dimerization and JAK2 (Janus kinase 2)-mediated tyrosine phosphorylation of the receptor. Less than 1% of the EPO-Rs are displayed on the cell Surface; most of the receptor molecules are retained in intracellular compartments, including the ER (endoplasmic reticulum). Using pervanadate (PV) as a potent tool to inhibit cellular PTPs (protein tyrosine phosphatases), we demonstrated previously the accumulation of mature (endoglycosidase H-resistant) tyrosine-phosphorylated EPO-R [Cohen, Altaratz, Zick, Klingmuller and Neumann (1997) Biochem. J. 327, 391-397]. In the present study, we investigated the participation of the ER-associated PTP1B in the dephosphorylation of intracellular EPO-R. We demonstrate tyrosine phosphorylation of EPO-R in BOSC-23T cells co-expressing EPO-R and the 'substrate- trapping' mutant form of PTP1B, PTP1B D181A (referred to as PTP1BD). In vivo interaction between EPO-R and PTP1B suggested that PTP1B dephosphorylates the EPO-R intracellularly. Endoglycosidase H resistance of tyrosine-phosphorylated EPO-R in cells expressing PTP1BD suggested that mature EPO-R is dephosphorylated by PTP1B. Stimulation with EPO of cells co-expressing EPO-R and either PTP1BD or PTP1B resulted in an increase or decrease respectively in phosphotyrosine EPO-R. We thus suggest that PTP1B dephosphorylates EPO-stimulated EPO-R and participates in the downregulation cascade of EPO-mediated signal transduction
    Type of Publication: Journal article published
    PubMed ID: 14527337
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  • 6
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2018-11-02
    Keywords: Immunology, Medicine, Diseases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2018-06-15
    Keywords: Epidemiology, Medicine, Diseases, Science and Policy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2018-06-22
    Keywords: Biotechnology, Development, Evolution
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    American Society of Hematology (ASH)
    In: Blood
    Publication Date: 2018-06-29
    Description: T-cell chronic active Epstein-Barr virus (CAEBV) is a rare disease in which EBV is present predominantly in T cells that infiltrate the tissues; patients have high levels of EBV in the blood. If untreated, patients often develop liver failure, hemophagocytic lymphohistiocytosis, coronary artery aneurysms, EBV infiltrating T cells impairing organ function, or T-cell lymphomas refractory to treatment. At present, hematopoietic stem-cell transplantation is the only curative therapy, and it is critical to make a proper diagnosis and initiate transplantation before the disease progresses to an irreversible stage. Specific medications such as high-dose systemic corticosteroids or ganciclovir combined with either histone deacetylase inhibitors or bortezomib may temporarily reduce systemic toxicity associated with T-cell CAEBV and allow the patient time to receive a transplant. Relapses of the disease after transplantation have also occurred, and the use of donor-derived virus-specific T cells may help to treat these relapses.
    Keywords: How I Treat, Free Research Articles, Lymphoid Neoplasia
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 10
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    American Association for the Advancement of Science (AAAS)
    In: Science
    Publication Date: 2018-06-15
    Keywords: Epidemiology, Medicine, Diseases, Science and Policy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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