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  • 1
    Electronic Resource
    Electronic Resource
    CHRONIC LEVOTHYROXIN TREATMENT IS ASSOCIATED WITH ION CHANNEL ABNORMALITIES IN CARDIAC AND NEURONAL CELLS (1999)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 26 (1999), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. We investigated the ion currents responsible for repolarization of guinea-pig isolated myocytes (ICa) and rat hippocampal CA1 neurons (IA and IK) by means of the whole-cell holding technique.2. The rat hypertrophied heart, induced by levothyroxin, caused exaggerated cardiac arrhythmias after coronary ischaemia–reperfusion.3. We found an enhanced ICa in guinea-pig isolated myocytes and decreased IA and IK in rat hippocampal CA1 neurons following levothyroxin treatment. Blockade of the outward K+ current and an increment in inward Ca2+ current by chronic levothyroxin treatment contributed to the delayed repolarization and aggravated cardiac arrhythmias.4. Animals treated with chronic levothyroxin may serve as pathological models for the investigation of the pattern of ion channel disorders with regard to impaired repolarization and aggravated cardiac arrhythmias.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.1999.03135.x
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  • 2
    Electronic Resource
    Electronic Resource
    Reduction in the Sodium Currents in Isolated Ventricular Myocytes of Guinea Pigs Treated by Chronic L-Thyroxin Medication (2002)
    350 Main Street , Malden , MA 02148 , USA. , and 9600 Garsington Road , Oxford OX4 2DQ , England . : Blackwell Science Inc
    Journal of cardiac surgery 17 (2002), S. 0 
    Details
    ISSN: 1540-8191
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective: Cardiac remodeling induced by chronic medication of L-thyroxin is manifested by a much more severe cardiac arrhythmias on the occlusion/reperfusion of the coronary artery in rats. A pattern of changes in ion currents in a diseased heart (L-thyroxin induced cardiac remodeling) is possibly provided as a basis of promoting malignant cardiac arrhythmias. An enhanced delayed outward rectifier potassium currents the rapid (IKr) and slow (IKS) component was found in the remodeled heart by L-thyroxin chronic medication. It is interested to investigate the changes in the sodium currents in the L-thyroxin remodeled guinea pig ventricle. Method: The remodeling model in guinea pig was developed by L-thyroxin 4 mg po for 10 days. On d 11, the heart was removed and perfused to isolate ventricular myocytes with medium of Ca2+ free medium containing collagen. The whole cell holding technique was applied. Results: The INa density in the L-thyroxin caused hypertrophied myocytes was reduced significantly at holding potential −30 mV, −53.20 +/−10.78pA/pF against −73.78+/−14.66pA/pF in the normal. (n = 45, p 〈 0.001). No difference in the steady-state inactivation and recovery kinetics between the remodeled and the normal was found. The recovery constant 37.54+/−3.63 ms in the remodeled vs 36.57+/−2.81 ms in the normal (n = 18, p 〉 0.05). The accelerated deactivation time constant 3.67+/−0.14 of the remodeled (n = 39) against the normal 4.14+/−0.15 ms (n = 43) (p 〈 0.05). Conclusion: There is a reduced INa in the L-thyroxin remodeled ventricular myocytes and the deactivation of the current is accelerated. A changed depolarization of the affected myocardium is likely involved in the mechanism of arrhythmogenesis of the remodeled ventricle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8191.2002.101415.x
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  • 3
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    Overexpression of DNAJB6 promotes colorectal cancer cell invasion through an IQGAP1/ERK-dependent signaling pathway (2014)
    Wiley-Blackwell
    Details
    Publication Date: 2014-07-09
    Description: DNAJB6 is a member of the heat shock protein 40 (Hsp40) family. We here investigated the clinical correlation and biological role of DNAJB6 overexpression in colorectal cancer (CRC). The expression of DNAJB6 protein was examined in 200 cases of colorectal adenocarcinomas by immunohistochemistry (IHC) technology. Gene transfection and RNA interference were performed to determine the effect of DNAJB6 expression on the invasion of CRC cells and to explore the underlying molecular mechanisms in vitro and in vivo. Overexpression of DNAJB6 was found in 39% (78/200) of the CRC tissues, especially in tumors at pT4 as compared with at pT1–3 ( P  = 0.02). A Kaplan–Meier survival analysis revealed a correlation between DNAJB6 expression and overall survival (OS) times ( P  = 0.003). Multivariate analysis confirmed that DNAJB6 overexpression was an independent prognostic factor for CRC ( P  = 0.002). RNA interference-mediated silencing of the DNAJB6 gene inhibited the invasion of CRC cells in vitro were accompanied by a significant reduction in the protein levels of IQ-domain GTPase-activating protein 1 (IQGAP1) and phosphorylated ERK (pERK). An in vivo assay showed that inhibition of DNAJB6 expression decreased the lung metastases of CRC cells. IHC analysis of serial sections showed that there was a positive correlation between DNAJB6 and IQGAP1 expression in primary CRC tissues ( P  = 0.013). The data suggest that DNAJB6 plays an important oncogenic role in CRC cell invasion by up-regulating IQGAP1 and activating the ERK signaling pathway and that DNAJB6 may be used as a prognostic marker for CRC. © 2014 Wiley Periodicals, Inc.
    Print ISSN: 0899-1987
    Electronic ISSN: 1098-2744
    Topics: Medicine
    Published by Wiley-Blackwell
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