GLORIA

GEOMAR Library Ocean Research Information Access

X
Language
Preferred search index
Number of Hits per Page
Default Sort Criterion
Default Sort Ordering
Size of Search History
Default Email Address
Default Export Format
Default Export Encoding
Facet list arrangement
Maximum number of values per filter
Auto Completion
Topics (search only within journals and journal articles that belong to one or more of the selected topics)
Show more topics
Feed Format
Maximum Number of Items per Feed
Permalink If you want to be able to use settings permanently, you must save your settings and then set a Bookmark to the permalink

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Increased mRNA expression of tumour necrosis factor-α and its converting enzyme in circulating leucocytes of patients with acute myocardial infarction
    Portland Press Ltd. ; 2003
    In:  Clinical Science Vol. 105, No. 1 ( 2003-07-01), p. 39-44
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 105, No. 1 ( 2003-07-01), p. 39-44
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20020367
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2003
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Activated tumour necrosis factor-α shedding process is associated with in-hospital complication in patients with acute myocardial infarction
    Portland Press Ltd. ; 2005
    In:  Clinical Science Vol. 108, No. 4 ( 2005-04-01), p. 339-347
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 108, No. 4 ( 2005-04-01), p. 339-347
    Abstract: TACE [TNF-α (tumour necrosis factor-α)-converting enzyme] plays an essential role in the shedding of TNF-α, which could affect the outcome of AMI (acute myocardial infarction). To investigate the clinical significance of the TACE–TNF-α system in AMI, we examined TACE-mediated TNF-α synthesis in PBMCs (peripheral blood mononuclear cells), which are a possible source of TNF-α in AMI. Forty-one pat ients with AMI and 15 healthy subjects (HS) were enrolled in the present study. PBMCs were isolated from peripheral blood on day 1 and 14 after the onset of AMI. TACE and TNF-α mRNA levels and intracellular median fluorescence intensity were measured by real-time RT (reverse transcriptase)–PCR and flow cytometry respectively. TACE-mediated TNF-α production was evaluated in cultured PBMCs with PMA, which is known to activate TACE. Spontaneous TACE and TNF-α levels were higher in AMI patients than in HS (P & lt;0.001). TACE and TNF-α levels in PMA-stimulated PMBCs were markedly increased in AMI patients compared with HS (P & lt;0.001). There was a positive correlation between TACE and TNF-α levels in AMI. Although spontaneous and stimulated levels of TACE and TNF-α decreased 14 days after the onset of AMI, levels in AMI patients were higher than in HS. In AMI patients with in-hospital complications (n=15; pump failure in ten, recurrent myocardial infarction in one, malignant ventricular arrhythmia in three and cardiac death in one), spontaneous and stimulated levels of TACE and TNF-α were higher than in patients without complications (P & lt;0.01). These levels were higher in AMI patients with in-hospital complications 14 days after onset. These results demonstrate that TACE-mediated TNF-α maturation in PBMCs may play an important role in poor outcomes from AMI, suggesting that TACE may be a potential target for the inhibition of cellular TNF-α production in AMI.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20040229
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2005
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Dysregulation of ossification-related miRNAs in circulating osteogenic progenitor cells obtained from patients with aortic stenosis
    Portland Press Ltd. ; 2016
    In:  Clinical Science Vol. 130, No. 13 ( 2016-07-01), p. 1115-1124
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 130, No. 13 ( 2016-07-01), p. 1115-1124
    Abstract: CAVD (calcific aortic valve disease) is the defining feature of AS (aortic stenosis). The present study aimed to determine whether expression of ossification-related miRNAs is related to differentiation intro COPCs (circulating osteogenic progenitor cells) in patients with CAVD. The present study included 46 patients with AS and 46 controls. Twenty-nine patients underwent surgical AVR (aortic valve replacement) and 17 underwent TAVI (transcatheter aortic valve implantation). The number of COPCs was higher in the AS group than in the controls (P & lt;0.01). Levels of miR-30c were higher in the AS group than in the controls (P & lt;0.01), whereas levels of miR-106a, miR-148a, miR-204, miR-211, miR-31 and miR-424 were lower in the AS group than in the controls (P & lt;0.01). The number of COPCs and levels of osteocalcin protein in COPCs were positively correlated with levels of miR-30a and negatively correlated with levels of the remaining miRNAs (all P & lt;0.05). The degree of aortic valve calcification was weakly positively correlated with the number of COPCs and miR-30c levels. The number of COPCs and miR-30c levels were decreased after surgery, whereas levels of the remaining miRNAs were increased (all P & lt;0.05). Changes in these levels were greater after AVR than after TAVI (all P & lt;0.05). In vitro study using cultured peripheral blood mononuclear cells transfected with each ossification-related miRNA showed that these miRNAs controlled levels of osteocalcin protein. In conclusion, dysregulation of ossification-related miRNAs may be related to the differentiation into COPCs and may play a significant role in the pathogenesis of CAVD.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20160094
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2016
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    MicroRNA-34a regulates the longevity-associated protein SIRT1 in coronary artery disease: effect of statins on SIRT1 and microRNA-34a expression
    Portland Press Ltd. ; 2012
    In:  Clinical Science Vol. 123, No. 3 ( 2012-08-01), p. 161-171
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 123, No. 3 ( 2012-08-01), p. 161-171
    Abstract: Endothelial senescence is thought to play a role in CAD (coronary artery disease). miR-34a (microRNA-34a) and other SIRT1 (silent information regulator 1)-related miRs have recently been found to target SIRT1 leading to endothelial senescence. In the present study, we investigated whether SIRT1-related miRs, including miR-9, miR-34a, miR-132, miR-181a, miR-195, miR-199a, miR-199b and miR-204, and SIRT1 were expressed in EPCs (endothelial progenitor cells) obtained from patients with CAD, and whether statins (atorvastatin or rosuvastatin) affected these levels. To determine the effects of miR-34a on SIRT1, cultured EPCs transfected with miR-34a were analysed for total SIRT1 protein levels. EPCs were obtained from 70 patients with CAD and 48 subjects without CAD. Patients with CAD were randomized to 8 months of treatment with atorvastatin or rosuvastatin. EPCs were obtained from peripheral blood at baseline and after 8 months of statin therapy. Levels of miRs and SIRT1 in EPCs were measured by real-time RT–PCR (reverse transcription–PCR) and FACS. Functional approaches to miR-34a have shown that transfection of miR-34a into EPCs resulted in regulation of SIRT1 expression. Levels of miR-34a were higher in the CAD group than in the non-CAD group, whereas levels of SIRT1 protein were lower in the CAD group than in the non-CAD group. There were no significant differences in other miRs (miR-9, miR-132, miR-181a, miR-195, miR-199a, miR-199b and miR-204) between the two groups. Levels of miR-34a were mildly negatively correlated with SIRT1 protein levels. A randomized clinical study has shown that the atorvastatin group had markedly decreased miR-34a levels and increased SIRT1 levels, whereas the rosuvastatin group showed no change in these levels. Levels of other miRs remained unchanged in the atorvastatin and rosuvastatin groups. In conclusion the results of the present study suggest that miR-34a may regulate SIRT1 expression in EPCs and that atorvastatin up-regulates SIRT1 expression via inhibition of miR-34a, possibly contributing to the beneficial effects of atorvastatin on endothelial function in CAD.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20110563
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2012
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Effect of intensive lipid-lowering therapy on telomere erosion in endothelial progenitor cells obtained from patients with coronary artery disease
    Portland Press Ltd. ; 2009
    In:  Clinical Science Vol. 116, No. 11 ( 2009-06-01), p. 827-835
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 116, No. 11 ( 2009-06-01), p. 827-835
    Abstract: Telomere erosion of EPCs (endothelial progenitor cells) may be a key factor in endothelial cell senescence and is highly dependent on cellular oxidative damage. The aim of the present study was to investigate whether LLT (lipid-lowering therapy) with statins could attenuate EPC telomere erosion in patients with CAD (coronary artery disease). The study included 100 patients with stable CAD and 25 subjects without CAD as controls. CAD patients were randomized to 12 months of intensive LLT with atorvastatin or moderate LLT with pravastatin. EPCs were obtained from peripheral blood at baseline and after 12 months of statin therapy. Telomere length in EPCs was measured by FISH (fluorescence in situ hybridization) and oxidative DNA damage by flow cytometry of oxidized DNA bases. EPC telomere length was shorter in the CAD group than in the controls, and oxidative DNA damage to EPCs was higher in the CAD group compared with controls. After 12 months of therapy, changes in lipid profiles were greater in the intensive LLT group than in the moderate LLT group. Intensive LLT markedly increased EPC number and decreased oxidative DNA damage in EPCs (both P & lt;0.05), with no change in telomere length. In contrast, moderate LLT did not change EPC counts or oxidative DNA damage, but showed telomere shortening (P & lt;0.05). There was a weak negative correlation between changes in EPC number and LDL (low-density lipoprotein)-cholesterol levels after intensive LLT, whereas there was no correlation between them after moderate LLT. With in vitro culturing of EPCs subjected to oxidative stress, atorvastatin led to the prevention of EPC telomere shortening compared with pravastatin. In conclusion, the present study has demonstrated that intensive LLT may prevent EPC telomere erosion in patients with CAD, possibly contributing to the beneficial effects of intensive LLT in this disorder.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20080404
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2009
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Aldosterone synthase (CYP11B2) expression and myocardial fibrosis in the failing human heart
    Portland Press Ltd. ; 2002
    In:  Clinical Science Vol. 102, No. 4 ( 2002-4-1), p. 381-
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 102, No. 4 ( 2002-4-1), p. 381-
    Type of Medium: Online Resource
    ISSN: 0143-5221
    URL: Article
    DOI: 10.1042/CS20010219
    Language: Unknown
    Publisher: Portland Press Ltd.
    Publication Date: 2002
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Expression of Toll-like receptor 4 is associated with enteroviral replication in human myocarditis
    Portland Press Ltd. ; 2003
    In:  Clinical Science Vol. 104, No. 6 ( 2003-06-01), p. 577-584
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 104, No. 6 ( 2003-06-01), p. 577-584
    Abstract: Previous studies have demonstrated that inflammatory cytokine expression associated with enteroviral (EV) infection may play an important role in human myocarditis. However, the mechanism of the host immune response against viral pathogens has not been fully understood. The aim of the present study was to determine whether Toll-like receptor 4 (TLR4) and EV RNA are present in human myocarditis. Endomyocardial biopsy samples were obtained from 44 patients with myocarditis and five controls. Levels of plus- and minus-strand EV RNAs and TLR4 mRNA were measured by real-time reverse transcriptase–PCR. Immunohistochemical analysis was performed to identify the cellular source of TLR4 and the EV capsid protein VP1. EV RNA was present in 21 patients with myocarditis and these patients were defined as having either active viral replication (n=15) or latent viral persistence (n=6). Neither strand of EV RNA was detected in controls. TLR4 mRNA expression levels were higher in myocarditis patients than in controls (TLR4/glyceraldehyde-3-phosphate dehydrogenase ratio 1.48±0.17 compared with 0.08±0.06, P & lt;0.001). A positive correlation was found between EV RNA and TLR4 levels (plus-strand vs TLR4: r=0.66, P & lt;0.001; minus-strand vs TLR4: r=0.48, P & lt;0.001). TLR4 immunostaining was observed in infiltrating cells and myocytes in patients with myocarditis. The EV capsid protein VP1 was also found in myocytes. The myocarditis group with EV replication and high levels of TLR4 showed significantly lower systolic function. The present study has shown that increased expression of TLR4 is associated with EV replication and that these RNA levels are related to cardiac dysfunction in human myocarditis.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20020263
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2003
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Aldosterone synthase (CYP11B2) expression and myocardial fibrosis in the failing human heart
    Portland Press Ltd. ; 2002
    In:  Clinical Science Vol. 102, No. 4 ( 2002-04-01), p. 381-386
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 102, No. 4 ( 2002-04-01), p. 381-386
    Abstract: The pathway of tissue aldosterone production may exist in the heart, and may be an important contributory factor to myocardial fibrosis and cardiac remodelling in the failing heart. CYP11B2 (aldosterone synthase) catalyses the final step of aldosterone production. The aim of the present study was to determine whether CYP11B2 and CYP11B1 (11β-hydroxylase) are expressed in myocardial tissues, and whether these enzymes contribute to collagen accumulation and myocardial dysfunction in the failing human heart. Endomyocardial tissues were obtained from 23 patients with chronic heart failure (CHF) and 10 controls. CYP11B2 and CYP11B1 mRNA levels were measured by real-time quantitative reverse transcriptase-PCR. The myocardial collagen volume fraction (CVF) was determined by digital planimetry. CYP11B2 mRNA expression was greater in the CHF group than in the controls (P 〈 0.05), while CYP11B1 mRNA was barely expressed in either group. There was a positive correlation between CYP11B2 mRNA levels and CVF (r = 0.64, P =0.001). CYP11B2 mRNA was particularly highly expressed in subgroups of CHF patients with a large left ventricular end-systolic diameter ( 〉 55mm) or a low left ventricular ejection fraction ( 〈 30%). CYP11B2 mRNA expression and CVF were lower in a CHF subgroup treated with a combination of spironolactone and angiotensin-converting enzyme inhibitors (ACEIs) than in a subgroup not treated with these drugs. In conclusion, this study has shown that increased myocardial expression of CYP11B2 mRNA is associated with increased myocardial fibrosis and with the severity of left ventricular dysfunction in human CHF. In addition, CYP11B2 expression and cardiac fibrosis are found to be decreased in CHF patients on drug therapy comprising spironolactone combined with ACEIs.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/cs1020381
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2002
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Expression of miR-23a induces telomere shortening and is associated with poor clinical outcomes in patients with coronary artery disease
    Portland Press Ltd. ; 2017
    In:  Clinical Science Vol. 131, No. 15 ( 2017-08-01), p. 2007-2017
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 131, No. 15 ( 2017-08-01), p. 2007-2017
    Abstract: Telomeric repeat binding factor (TRF) 2 (TRF2) plays an important role in telomere maintenance. miR-23a may directly inhibit TRF2 expression, thereby, inducing telomere shortening and cellular senescence. The present study aimed to determine whether miR-23a and TRF2 are expressed in patients with coronary artery disease (CAD), and whether pitavastatin might affect these levels. The present study included 104 patients with CAD and 50 controls. Patients with CAD were randomly divided into two subgroups (a moderate lipid lowering therapy (LLT) group and an aggressive LLT group). Peripheral blood mononuclear cells (PBMCs) were taken from patients with CAD and from controls at baseline and after 12 months. Levels of miR-23a were higher in the CAD group than in the controls. Levels of TRF2 protein were lower in the CAD group than in the controls. Our randomized clinical study showed that aggressive LLT decreased miR-23a and increased TRF2 levels, whereas moderate LLT generated no change in these levels. Our transfected cell model showed that miR-23a controlled TRF2 expression. After a mean follow-up of 339 days, cardiovascular events were associated with high miR-23a, low TRF2 or low relative telomere length. Multivariate analysis showed that levels of miR-23a (RR: 4.9, 95% CI: 1.9–14.3) were a strong predictor of cardiovascular events after adjustment for baseline characteristics. In conclusion, elevated levels of miR-23a play an important role in coronary atherosclerosis via down-regulated TRF2, and may provide important prognostic information in patients with CAD. Additionally, aggressive LLT may prevent telomere erosion via down-regulated miR-23a.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20170242
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2017
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Expression of miR-146a/b is associated with the Toll-like receptor 4 signal in coronary artery disease: effect of renin–angiotensin system blockade and statins on miRNA-146a / b and Toll-like receptor 4 levels
    Portland Press Ltd. ; 2010
    In:  Clinical Science Vol. 119, No. 9 ( 2010-10-01), p. 395-405
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 119, No. 9 ( 2010-10-01), p. 395-405
    Abstract: The TLR4 (Toll-like receptor 4) signal plays an important role in immunity in CAD (coronary artery disease). miR-146a/b (where miR is microRNA) regulates the TLR4 downstream molecules IRAK1 (interleukin-1-receptor-associated kinase 1) and TRAF6 (tumour-necrosis-factor-receptor-associated factor 6). It has also been reported that statins and RAS (renin–angiotensin system) inhibition and have anti-atherosclerotic properties. In the present study, we have investigated whether miR-146a/b was expressed with the TLR4 signal in CAD patients, and whether combined treatment with a statin and RAS inhibition might affect these levels. A total of 66 patients with CAD and 33 subjects without CAD (non-CAD) were enrolled. Patients with CAD were randomized to 12 months of combined treatment with atorvastatin and telmisartan [an ARB (angiotensin II receptor blocker)] or atorvastatin and enalapril [an ACEI (angiotensin-converting enzyme inhibitor)] . PBMCs (peripheral blood mononuclear cells) were obtained from peripheral blood at baseline and after 12 months. Levels of miR-146a/b, IRAK1 mRNA, TRAF6 mRNA and TLR4 mRNA/TLR4 protein were significantly higher in the CAD group than in the non-CAD group (all P & lt;0.01). Levels of miR-146a/b were positively correlated with IRAK1 mRNA and TRAF6 mRNA levels. After 12 months of treatment, these levels were markedly decreased in the ARB and ACEI groups, with the decrease in the ARB group being greater than that in the ACEI group (all P & lt;0.05). In our 12-month follow-up study, high levels of miR-146a and TLR4 mRNA/TLR4 protein at baseline were independent predictors of cardiac events. The present study demonstrates that combined treatment with an ARB and a statin decreases miR-146a/b and the TLR4 signal in CAD patients, possibly contributing to the anti-atherogenic effects of ARBs and statins in this disorder.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20100003
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2010
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...