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  • 1
    Electronic Resource
    Electronic Resource
    Structure of the blue copper(II) complex {[7R(S),14R(S)]-5,5,7,12,12,14-hexamethyl-1,4,8,11-tetraazacyclotetradecane}nitratocopper(II) perchlorate, [Cu(NO3)(C16H36N4)](ClO4) (1984)
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 40 (1984), S. 641-644 
    Details
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108270184005175
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Structure of tripotassium hexahydrogenhexamolybdoaluminate(III) heptahydrate (1991)
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 47 (1991), S. 1959-1961 
    Details
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1107/S0108270191002159
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    Paper (German National Licenses)
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  • 3
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    Hypoxia enhances the expression of prostate-specific antigen by modifying the quantity and catalytic activity of Jumonji C domain-containing histone demethylases (2013)
    Oxford University Press
    Details
    Publication Date: 2013-12-01
    Description: Oxygen concentration in prostate cancer tissue is significantly low, i.e. ~0.3% O 2 . This study showed that pathological hypoxia (〈0.5% O 2 ) increased the expression of androgen receptor (AR) target genes such as prostate-specific antigen (PSA) and kallikrein-related peptidase 2 in LNCaP human prostate cancer cells by modifying the quantity and activity of related Jumonji C domain-containing histone demethylases (JMJDs). Under pathological hypoxia, the catalytic activities of JMJD2A, JMJD2C and Jumonji/ARID domain-containing protein 1B (JARID1B) were blocked due to the lack of their substrate, i.e. oxygen. Chromatin immunoprecipitation analyses showed that hypoxia increased the appearance of H3K9me3 and H3K4me3, substrates of JMJD2s and JARID1B, respectively, in the PSA enhancer. In contrast, JMJD1A, which demethylates both H3K9me2 and H3K9me1, maintained its catalytic activity even under severe hypoxia. Furthermore, hypoxia increased the expression of JMJD1A. Hypoxia and androgen additively increased the recruitment of JMJD1A and p300 on the enhancer region of PSA through interaction with the hypoxia-inducible factor-1α and AR, both of which bind the PSA enhancer. Thus, hypoxia enhanced the demethylation of H3K9me2 and H3K9me1, leading to provide unmethylated H3K9 residues that are substrates for histone acetyltransferase, p300. Consequently, hypoxia increased the acetylation of histones of the PSA enhancer, which facilitates its transcription.
    Print ISSN: 0143-3334
    Electronic ISSN: 1460-2180
    Topics: Medicine
    Published by Oxford University Press
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  • 4
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    Combating Resistance to Anti-IGFR Antibody by Targeting the Integrin {beta}3-Src Pathway (2013)
    Oxford University Press
    Details
    Publication Date: 2013-10-16
    Description: Background Several phase II/III trials of anti–insulin-like growth factor 1 receptor (IGF-1R) monoclonal antibodies (mAbs) have shown limited efficacy. The mechanisms of resistance to IGF-1R mAb-based therapies and clinically applicable strategies for overcoming drug resistance are still undefined. Methods IGF-1R mAb cixutumumab efficacy, alone or in combination with Src inhibitors, was evaluated in 10 human head and neck squamous cell carcinoma (HNSCC) and six non–small cell lung cancer (NSCLC) cell lines in vitro in two- or three-dimensional culture systems and in vivo in cell line– or patient-derived xenograft tumors in athymic nude mice (n = 6–9 per group). Cixutumumab-induced changes in cell signaling and IGF-1 binding to integrin β3 were determined by Western or ligand blotting, immunoprecipitation, immunofluorescence, and cell adhesion analyses and enzyme-linked immunosorbent assay. Data were analyzed by the two-sided Student t test or one-way analysis of variance. Results Integrin β3–Src signaling cascade was activated by IGF-1 in HNSCC and NSCLC cells, when IGF-1 binding to IGF-1R was hampered by cixutumumab, resulting in Akt activation and cixutumumab resistance. Targeting integrin β3 or Src enhanced antitumor activity of cixutumumab in multiple cixutumumab-resistant cell lines and patient-derived tumors in vitro and in vivo. Mean tumor volume of mice cotreated with cixutumumab and integrin β3 siRNA was 133.7mm 3 (95% confidence interval [CI] = 57.6 to 209.8mm 3 ) compared with those treated with cixutumumab (1472.5mm 3 ; 95% CI = 1150.7 to 1794.3mm 3 ; P 〈 .001) or integrin β3 siRNA (903.2mm 3 ; 95% CI = 636.1 to 1170.3mm 3 ; P 〈 .001) alone. Conclusions Increased Src activation through integrin αβ3 confers considerable resistance against anti–IGF-1R mAb-based therapies in HNSCC and NSCLC cells. Dual targeting of the IGF-1R pathway and collateral integrin β3–Src signaling module may override this resistance.
    Electronic ISSN: 1460-2105
    Topics: Medicine
    Published by Oxford University Press
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  • 5
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    Cellular Mechanism by Which Estradiol Protects Female Ovariectomized Mice From High-Fat Diet-Induced Hepatic and Muscle Insulin Resistance (2013)
    Oxford University Press
    Details
    Publication Date: 2013-02-22
    Description: Estrogen replacement therapy reduces the incidence of type 2 diabetes in postmenopausal women; however, the mechanism is unknown. Therefore, the aim of this study was to evaluate the metabolic effects of estrogen replacement therapy in an experimental model of menopause. At 8 weeks of age, female mice were ovariectomized (OVX) or sham (SHAM) operated, and OVX mice were treated with vehicle (OVX) or estradiol (E2) (OVX+E2). After 4 weeks of high-fat diet feeding, OVX mice had increased body weight and fat mass compared with SHAM and OVX+E2 mice. OVX mice displayed reduced whole-body energy expenditure, as well as impaired glucose tolerance and whole-body insulin resistance. Differences in whole-body insulin sensitivity in OVX compared with SHAM mice were accounted for by impaired muscle insulin sensitivity, whereas both hepatic and muscle insulin sensitivity were impaired in OVX compared with OVX+E2 mice. Muscle diacylglycerol (DAG), content in OVX mice was increased relative to SHAM and OVX+E2 mice. In contrast, E2 treatment prevented the increase in hepatic DAG content observed in both SHAM and OVX mice. Increases in tissue DAG content were associated with increased protein kinase C activation in liver of SHAM and OVX mice compared with OVX+E2 and protein kinase C activation in skeletal muscle of OVX mice compared with SHAM and OVX+E2. Taken together, these data demonstrate that E2 plays a pivotal role in the regulation of whole-body energy homeostasis, increasing O 2 consumption and energy expenditure in OVX mice, and in turn preventing diet-induced ectopic lipid (DAG) deposition and hepatic and muscle insulin resistance.
    Print ISSN: 0013-7227
    Topics: Medicine
    Published by Oxford University Press on behalf of The Endocrine Society.
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  • 6
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    Serum alkaline phosphatase is a predictor of mortality, myocardial infarction, or stent thrombosis after implantation of coronary drug-eluting stent (2013)
    Oxford University Press
    Details
    Publication Date: 2013-03-22
    Description: Aims The association between alkaline phosphatase (ALP) and mortality was reported in several subgroups of patients. But, the role of ALP in overall coronary artery disease (CAD) patients after percutaneous coronary intervention (PCI) remains unknown. The aim of this study was to examine the prognostic value of the ALP level in patients with CAD who underwent PCI with drug-eluting stent (DES). Methods and results We prospectively included CAD patients who underwent PCI with DES. After exclusion of patients with liver disease and cancer, 1636 patients were selected for the analysis of clinical outcomes (median duration of follow-up; 762 days, inter-quartile range; 494–1068 days), and were classified into tertiles by baseline measurements of ALP (〈63, 63–78, and 〉78 IU/L). After adjustment of potential confounders including angiographic data, the independent and dose-dependent association was observed between tertile of ALP and the adjusted hazard ratio (HR) of all-cause mortality ( P for trend 〈 0.0001). Specifically, compared with the lowest ALP tertile, the adjusted HR of all-cause mortality in the highest tertile was 4.21 (95% confidence interval 2.03–8.71). In subgroup of patients with stable or unstable angina, a similar association was noted ( P for trend 〈 0.0001). In terms of cardiovascular mortality, myocardial infarction, and stent thrombosis, the adjusted HRs in the highest ALP tertile were 3.92 (1.37–11.20), 1.98 (0.91–4.29), and 2.73 (1.33–5.61), respectively, compared with the lowest tertile. Furthermore, evaluation of both ALP and C-reactive protein provided better predictive value than either alone. Interesting result suggesting the mechanism was that ALP was significantly associated with the presence of angiographic coronary calcification ( P for trend = 0.046). Conclusion Our study demonstrated that the higher serum ALP level is an independent predictor of mortality, myocardial infarction, and stent thrombosis in CAD patients after PCI with DES.
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press
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  • 7
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    Effects of Celecoxib On Restenosis after Coronary Intervention and Evolution of Atherosclerosis (Mini-COREA) Trial: celecoxib, a double-edged sword for patients with angina (2012)
    Oxford University Press
    Details
    Publication Date: 2012-11-02
    Description: Aims In the previous COREA-TAXUS trial, a 6-month adjunctive use of celecoxib reduced target-lesion revascularization (TLR) without increased thrombotic risk. We aimed to confirm the effects of 3-month celecoxib in patients receiving drug-eluting stent (DES) implantation in the larger prospective, randomized trial. Methods and results Patients ( n = 909) treated for native coronary lesions were randomized into four groups: the control or the celecoxib group with stratification by stents: paclitaxel-eluting stent (PES) or zotarolimus-eluting stent (ZES). In the celecoxib group, 200 mg of celecoxib was given twice daily for 3 months after the procedure. The primary endpoint was in-stent late loss (LL) at 6 months. In-stent LL was significantly lower in the celecoxib group than the control group (0.64 ± 0.54 vs. 0.55 ± 0.47 mm, P = 0.02). The trend of LL reduction in the celecoxib group was maintained in the ZES and PES subgroups, although it did not reach statistical significance. There was a trend towards the reduced clinically driven TLR in the celecoxib group (5.7 vs. 3.2%, log-rank P = 0.09), but adverse cardiac events rate did not differ between the two groups (composite of cardiac death, non-fatal myocardial infarction, and TLR; 8.6 vs. 7.7%, log-rank P = 0.84). Non-fatal myocardial infarction and cardiac death occurred in 1.6% of the patients in the celecoxib group when compared with 0.2% in the control group (log-rank P = 0.03). Conclusion Three-month adjunctive celecoxib would be useful to reduce LL of DES. However, this study may raise the concern about increased thrombotic risk with celecoxib even in patients receiving dual anti-platelet therapy.
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press
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  • 8
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    Five-year results of intracoronary infusion of the mobilized peripheral blood stem cells by granulocyte colony-stimulating factor in patients with myocardial infarction (2012)
    Oxford University Press
    Details
    Publication Date: 2012-12-15
    Description: Aim To evaluate the long-term effects of peripheral blood stem cell therapy in myocardial infarction (MI) patients. Methods and results A total of 163 patients with MI who were successfully revascularized with drug-eluting stents were enrolled and randomly assigned to four groups: acute MI (AMI) cell infusion, AMI control, old MI (OMI) cell infusion, and OMI control. We compared 5 years' clinical outcomes between the cell infusion group (57 and 22 patients with AMI and OMI, respectively) and the control (60 and 24 patients with AMI and OMI, respectively). In the time-sequence comparison from baseline to 6 and 24 months follow-up after AMI, left ventricular ejection fraction (LVEF) by cardiac magnetic resonance imaging was significantly improved in the cell infusion group ( n = 57), but not in the control group ( n = 60). In the between-group comparison, the difference in improvement of LVEF for 2 years after AMI did not reach statistical significance between cell infusion and control groups. Intriguingly, the major adverse cardiac events for 5 years were significantly reduced in the cell infusion group ( n = 79) compared with the control ( n = 84; composite of cardiac death, non-fatal MI, hospitalization for heart failure and angina, and target vessel revascularization; 22.8 vs. 39.3%, P = 0.015). Conclusions Peripheral blood stem cell therapy has potential to improve long-term cardiovascular outcomes in MI patients.
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press
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  • 9
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    Master regulatory GATA transcription factors: mechanistic principles and emerging links to hematologic malignancies (2012)
    Oxford University Press
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    Publication Date: 2012-07-22
    Description: Numerous examples exist of how disrupting the actions of physiological regulators of blood cell development yields hematologic malignancies. The master regulator of hematopoietic stem/progenitor cells GATA-2 was cloned almost 20 years ago, and elegant genetic analyses demonstrated its essential function to promote hematopoiesis. While certain GATA-2 target genes are implicated in leukemogenesis, only recently have definitive insights emerged linking GATA-2 to human hematologic pathophysiologies. These pathophysiologies include myelodysplastic syndrome, acute myeloid leukemia and an immunodeficiency syndrome with complex phenotypes including leukemia. As GATA-2 has a pivotal role in the etiology of human cancer, it is instructive to consider mechanisms underlying normal GATA factor function/regulation and how dissecting such mechanisms may reveal unique opportunities for thwarting GATA-2-dependent processes in a therapeutic context. This article highlights GATA factor mechanistic principles, with a heavy emphasis on GATA-1 and GATA-2 functions in the hematopoietic system, and new links between GATA-2 dysregulation and human pathophysiologies.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 10
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    FOXO1 impairs whereas statin protects endothelial function in diabetes through reciprocal regulation of Kruppel-like factor 2 (2012)
    Oxford University Press
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    Publication Date: 2012-12-22
    Description: Aims Krüppel-like factor 2 (KLF2) is implicated as a key molecule maintaining endothelial function. This study was designed to evaluate the reciprocal regulation of KLF2 by the forkhead transcription factor FOXO1, and the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor atorvastatin, in hyperglycaemic conditions. Methods and results Exposure of human umbilical vein endothelial cells to 30 mM glucose activated FOXO1 and suppressed KLF2. These effects were reversed by FOXO1 small interfering RNA. Adenoviral transfection of constitutively active FOXO1 suppressed KLF2 expression. Interestingly, atorvastatin inhibited FOXO1 by increasing phosphorylation and also by inhibiting nuclear localization and replenished KLF2 in high-glucose conditions. This effect of atorvastatin was attenuated by mevalonate. Chromatin immunoprecipitation analysis demonstrated that glucose increased whereas atorvastatin decreased FOXO1 binding to the promoter region of the KLF2 gene. In the vessels of Otsuka Long-Evans Tokushima Fatty rats, animal models of type 2 diabetes, FOXO1 was activated and KLF2 was suppressed, and this was reversed by atorvastatin treatment. The arteries from Otsuka Long-Evans Tokushima Fatty rats showed impairment of endothelium-dependent vasodilatation, and both atorvastatin and KLF2 gene therapies restored it. Conclusions Suppression of KLF2 by FOXO1 may be a plausible mechanism of diabetic endothelial dysfunction. High-glucose-induced, FOXO1-mediated KLF2 suppression was reversed by atorvastatin, suggesting that intensive statin treatment could be a therapeutic option in diabetic vascular dysfunction.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
    Published by Oxford University Press
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