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  • 1
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    Mineralocorticoid Receptor Affects AP-1 and Nuclear Factor-κB Activation in Angiotensin II–Induced Cardiac Injury
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Hypertension Vol. 37, No. 2 ( 2001-02), p. 787-793
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. 2 ( 2001-02), p. 787-793
    Abstract: Aldosterone is implicated in cardiac hypertrophy and fibrosis. We tested the role of the mineralocorticoid receptor in a model of angiotensin II–induced cardiac injury. We administered spironolactone (SPIRO; 20 mg · kg −1 · d −1 ), valsartan (VAL; 10 mg · kg −1 · d −1 ), or vehicle to rats double transgenic for the human renin and angiotensinogen genes (dTGR). We investigated basic fibroblast growth factor (bFGF), platelet-derived growth factor, transforming growth factor-β 1 , and the transcription factors AP-1 and nuclear factor (NF)-κB. We used immunohistochemistry, electrophoretic mobility shift assays, and TaqMan RT-PCR. Untreated dTGR developed hypertension, cardiac hypertrophy, vasculopathy, and fibrosis with a 50% mortality rates at 7 weeks. SPIRO and VAL prevented death and reversed cardiac hypertrophy, while only VAL normalized blood pressure. Both drugs prevented vasculopathy. bFGF was markedly upregulated in dTGR, whereas platelet-derived growth factor-B and transforming growth factor-β 1 were little changed. VAL and SPIRO suppressed this upregulation. Both AP-1 and NF-κB were activated in dTGR compared with controls. VAL and SPIRO reduced both transcription factors and reduced bFGF, collagen I, fibronectin, and laminin in the interstitium. These findings show that aldosterone promotes hypertrophy, cardiac remodeling, and fibrosis, independent of blood pressure. The effects involve AP-1, NF-κB, and bFGF. Mineralocorticoid receptor blockade downregulates these effectors and reduces angiotensin II–induced cardiac damage.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.37.2.787
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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  • 2
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    p38 Mitogen-Activated Protein Kinase Inhibition Ameliorates Angiotensin II–Induced Target Organ Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Hypertension Vol. 49, No. 3 ( 2007-03), p. 481-489
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 49, No. 3 ( 2007-03), p. 481-489
    Abstract: We investigated whether or not p38 mitogen-activated protein kinase inhibition ameliorates angiotensin II–induced target organ damage. We used double transgenic rats harboring both human renin and angiotensinogen genes (dTGRs). dTGR, with or without p38 inhibitor (BIRB796; 30 mg/kg per day in the diet), and nontransgenic Sprague–Dawley rats were studied in 2 protocols. In protocol 1 (week 7), systolic blood pressure of untreated dTGRs was 204±4 mm Hg, but partially reduced after BIRB796 treatment (166±7 mm Hg), whereas Sprague–Dawley rats were normotensive. The cardiac hypertrophy index was unchanged in untreated and BIRB796-treated dTGRs. The β-myosin heavy chain expression of BIRB796-treated hearts was significantly lower in BIRB796 compared with dTGRs, indicating a delayed switch to the fetal isoform. BIRB796 treatment significantly reduced cardiac fibrosis, connective tissue growth factor, tumor necrosis factor-α, interleukin-6, and macrophage infiltration. Albuminuria was not reduced in BIRB796-treated dTGRs. Tubular and glomerular damage with tumor necrosis factor-α expression was unaltered, although serum creatinine and cystatin C were normalized. Renal macrophage infiltration, fibrosis, and vessel damage were reduced. In protocol 2 (week 8), we focused on mortality and arrhythmogenic electrical remodeling. Mortality of untreated dTGRs was 100% but was reduced to 10% in the BIRB796 group. Cardiac magnetic field mapping showed prolongation of depolarization and repolarization in untreated dTGRs compared with Sprague–Dawley rats with a partial reduction by BIRB796. Programmed electrical stimulation elicited ventricular tachycardias in 81% of untreated dTGRs but only in 48% of BIRB796-treated dTGRs. In conclusion, BIRB796 improved survival, target organ damage, and arrhythmogenic potential in angiotensin II–induced target organ damage.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000256831.33459.ea
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
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  • 3
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    Angiotensin II induced inflammation in the kidney and in the heart of double transgenic rats
    Springer Science and Business Media LLC ; 2002
    In:  BMC Cardiovascular Disorders Vol. 2, No. 1 ( 2002-12)
    Details
    In: BMC Cardiovascular Disorders, Springer Science and Business Media LLC, Vol. 2, No. 1 ( 2002-12)
    Type of Medium: Online Resource
    ISSN: 1471-2261
    URL: Article
    DOI: 10.1186/1471-2261-2-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2002
    detail.hit.zdb_id: 2059859-2
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  • 4
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    Spironolactone Ameliorates Angiotensin Ii-Induced Renal Damage Via the Inhibition of Ap-1 and Nf-κB
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 723-723
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 723-723
    Abstract: P168 Recently, clinical trials have demonstrated the efficacy of spironolactone (SPIRO) in men. Nevertheless the molecular mechanism of action not completely understood. Locally generated angiotensin II (ANG II) stimulates aldosterone. Therefore, we have tested the hypothesis that SPIRO ameliorates ANG II-induced renal damage. Furthermore, we investigated the effect of SPIRO on the transcription factors AP-1 and NF-κB. We treated transgenic rats overexpressing the human renin and angiotensinogen genes (dTGR) from week 5 to 7 with SPIRO (20 mg/kg/d). Plasma aldosterone was significantly increased in dTGR vs. SPIRO treated and non-transgenic (SD) rats (p 〈 0.05). Untreated dTGR showed high systolic blood pressure (182±8 mm Hg), severe renal damage with 150-fold increased albuminuria, vasculopathy and perivascular and interstitial fibrosis. Chronic SPIRO treatment reduced mortality and vasculopathy completely, despite blood pressure levels of 161±11. 24-hour albuminuria was reduced from 59±15 in dTGR to 3.5±2 mg/d; p 〈 0.01). Electrophoretic mobility gel shift analysis demonstrated a reduction of renal AP-1 and NF-κB DNA binding activity after SPIRO treatment. Immunohistological analysis showed that SPIRO also prevented the expression of AP-1 and/or NF-kB regulated matrix molecules fibronectin and laminin. The reno-protective effect of SPIRO was accompanied with a reduction of monocyte/macrophage infiltration. These findings show that blockade of aldosterone signaling ameliorates ANG II-induced renal damage. SPIRO action was at least partially mediated via AP-1 and NF-κB.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.723-d
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 5
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    Aspirin Inhibits Renal I-κB Kinase Activity, Nf-κB and Protects Against Renal and Cardiac Damage in Rats with Human Renin and Angiotensinogen Genes (dTGR)
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 693-693
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 693-693
    Abstract: P4 In a recent report, aspirin (ASA) inhibited I-κB kinase beta in vitro; however, in vivo relevance has not been shown. We previously showed that NF-κB activation and inflammation are crucial role in the pathogenesis of Ang II-induced vasculopathy. We now tested the hypothesis that ASA inhibits NF-κB and ameliorates renal and cardiac end-organ damage. dTGR feature hypertension, renal and cardiac damage and die at 7 weeks. We treated rats chronically with ASA (600 and 25 mg/kg/d ip). Only ASA 600 prevented mortality, while untreated dTGR and ASA 25 showed mortality 〉 50% at 7 weeks. ASA 600 reduced cardiac hypertrophy (4.0±0.2 vs. 5.7±0.2 mg/g, p 〈 0.001) compared to dTGR. Blood pressure levels in ASA 600 were slightly, but not significantly lower (158±8 vs. 182±8 mm Hg, p=0.2). In contrast, ASA 600 reduced albuminuria by 85 % (p 〈 0.01) and perivascular fibrosis, while ASA 25 had no effect on cardiac and renal damage. ASA 600 inhibited renal I-κB kinase activity and NF-κB DNA binding activity, which were increased in dTGR. Immunostaing of the activated p65 NF-κB subunit was increased in the endothelium, smooth muscles cells, infiltrated cells, glomeruli, and tubules of dTGR and markedly reduced by ASA 600. ASA 600 also reduced immunostaining of NF-κB-regulated genes laminin, ICAM-1, and IL-6. Monocyte infiltration was increased in dTGR hearts and kidneys and reduced by ASA 600, and not by ASA 25. These results demonstrate that high-dose ASA inhibits NF-κB, suppresses inflammation, and protects against ANG II-induced end-organ damage. The data underscore the role of inflammation and identify a novel drug target in this model.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.693-c
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 6
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    Aliskiren, a Human Renin Inhibitor, Ameliorates Cardiac and Renal Damage in Double-Transgenic Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Hypertension Vol. 46, No. 3 ( 2005-09), p. 569-576
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. 3 ( 2005-09), p. 569-576
    Abstract: We tested the hypothesis that the renin inhibitor aliskiren ameliorates organ damage in rats transgenic for human renin and angiotensinogen genes (double transgenic rat [dTGR]). Six-week-old dTGR were matched by albuminuria (2 mg per day) and divided into 5 groups. Untreated dTGR were compared with aliskiren (3 and 0.3 mg/kg per day)-treated and valsartan (Val; 10 and 1 mg/kg per day)-treated rats. Treatment was from week 6 through week 9. At week 6, all groups had elevated systolic blood pressure (BP). Untreated dTGR showed increased BP (202±4 mm Hg), serum creatinine, and albuminuria (34±5.7 mg per day) at week 7. At week 9, both doses of aliskiren lowered BP (115±6 and 139±5 mm Hg) and albuminuria (0.4±0.1 and 1.6±0.6 mg per day) and normalized serum creatinine. Although high-dose Val lowered BP (148±4 mm Hg) and albuminuria (2.1±0.7 mg per day), low-dose Val reduced BP (182±3 mm Hg) and albuminuria (24±3.8 mg per day) to a lesser extent. Mortality was 100% in untreated dTGR and 26% in Val (1 mg/kg per day) treated rats, whereas in all other groups, survival was 100%. dTGR treated with low-dose Val had cardiac hypertrophy (4.4±0.1 mg/g), increased left ventricular (LV) wall thickness, and diastolic dysfunction. LV atrial natriuretic peptide and β-myosin heavy chain mRNA, albuminuria, fibrosis, and cell infiltration were also increased. In contrast, both aliskiren doses and the high-dose Val lowered BP to a similar extent and more effectively than low-dose Val. We conclude that in dTGR, equieffective antihypertensive doses of Val or aliskiren attenuated end-organ damage. Thus, renin inhibition compares favorably to angiotensin receptor blockade in reversing organ damage in dTGR.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.0000179573.91016.3f
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
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  • 7
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    Prorenin and Renin-Induced Extracellular Signal-Regulated Kinase 1/2 Activation in Monocytes Is Not Blocked by Aliskiren or the Handle-Region Peptide
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Hypertension Vol. 51, No. 3 ( 2008-03), p. 682-688
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 51, No. 3 ( 2008-03), p. 682-688
    Abstract: The recently cloned (pro)renin receptor [(P)RR] mediates renin-stimulated cellular effects by activating mitogen-activated protein kinases and promotes nonproteolytic prorenin activation. In vivo, (P)RR is said to be blocked with a peptide consisting of 10 amino acids from the prorenin prosegment called the “handle-region” peptide (HRP). We tested whether human prorenin and renin induce extracellular signal-regulated kinase (ERK) 1/2 activation and whether the direct renin inhibitor aliskiren or the HRP inhibits the receptor. We detected the (P)RR mRNA and protein in isolated human monocytes and in U937 monocytes. In U937 cells, we found that both human renin and prorenin induced a long-lasting ERK 1/2 phosphorylation despite angiotensin II type 1 and 2 receptor blockade. In contrast to angiotensin II-ERK signaling, renin and prorenin signaling did not involve the epidermal growth factor receptor. A mitogen-activated protein kinase kinase 1/2 inhibitor inhibited both renin and prorenin-induced ERK 1/2 phosphorylation. Neither aliskiren nor HRP inhibited binding of 125 I-renin or 125 I-prorenin to (P)RR. Aliskiren did not inhibit renin and prorenin-induced ERK 1/2 phosphorylation and kinase activity. Fluorescence-activated cell sorter analysis showed that, although fluorescein isothiocyanate-labeled HRP bound to U937 cells, HRP did not inhibit renin or prorenin-induced ERK 1/2 activation. In conclusion, prorenin and renin-induced ERK 1/2 activation are independent of angiotensin II. The signal transduction is different from that evoked by angiotensin II. Aliskiren has no (P)RR blocking effect and did not inhibit ERK 1/2 phosphorylation or kinase activity. Finally, we found no evidence that HRP affects renin or prorenin binding and signaling.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.107.101444
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 8
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    Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Hypertension Vol. 51, No. 5 ( 2008-05), p. 1372-1378
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 51, No. 5 ( 2008-05), p. 1372-1378
    Abstract: Mineralocorticoid receptor blockade protects from angiotensin II–induced target-organ damage. 11β-Hydroxysteroid dehydrogenase type 2 protects the mineralocorticoid receptor from activation by glucocorticoids; however, high glucocorticoid concentrations and absent 11β-hydroxysteroid dehydrogenase type 2 in some tissues make glucocorticoids highly relevant mineralocorticoid receptor ligands. We investigated the effects of corticosterone (10 −6 to 10 −12 mol/L) on early vascular mineralocorticoid receptor signaling by Western blotting, confocal microscopy, and myography. Corticosterone initiated extracellular signal–regulated kinase 1/2 phosphorylation in rat vascular smooth muscle cells at ≥10 −11 mol/L doses. Protein synthesis inhibitors had no effect, indicating a nongenomic action. Corticosterone also stimulated c-Jun N-terminal kinase, p38, Src, and Akt phosphorylation at 15 minutes and enhanced angiotensin II–induced signaling at 5 minutes. A specific epidermal growth factor receptor blocker, AG1478, as well as the Src inhibitor PP2, markedly reduced corticosterone-induced extracellular signal–regulated kinase 1/2 phosphorylation, as did preincubation of cells with the mineralocorticoid receptor antagonist spironolactone. Silencing mineralocorticoid receptor with small interfering RNA abolished corticosterone-induced effects. Corticosterone (10 −9 mol/L) enhanced phenylephrine-induced contraction of intact aortic rings. These effects were dependent on the intact endothelium, mineralocorticoid receptor, and mitogen-activated protein kinase kinase 1/extracellular signal-regulated kinase signaling. We conclude that corticosterone induces rapid mineralocorticoid receptor signaling in vascular smooth muscle cells that involves mitogen-activated protein kinase kinase/extracellular signal–regulated kinase–dependent pathways. These new mineralocorticoid receptor–dependent signaling pathways suggest that glucocorticoids may contribute to vascular disease via mineralocorticoid receptor signaling, independent of circulating aldosterone.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.107.105718
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 9
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    Cyclosporin A Protects Against Angiotensin II–Induced End-Organ Damage in Double Transgenic Rats Harboring Human Renin and Angiotensinogen Genes
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 35, No. 1 ( 2000-01), p. 360-366
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 1 ( 2000-01), p. 360-366
    Abstract: Abstract —Leukocyte infiltration and adhesion molecule activation play a central role in the pathogenesis of angiotensin II (Ang II)–induced end-organ damage in double transgenic rats (dTGR) harboring human renin and angiotensinogen genes. We tested the hypothesis that the immunosuppressive agent cyclosporine (CsA) protects against the Ang II–induced myocardial and renal damage in dTGR. Furthermore, we investigated the influence of CsA on interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) expression and the DNA binding activity of transcription factor necrosis factor-κB (NF-κB). The 4-week-old rats were divided into 4 groups: (1) control dTGR (n=20), (2) dTGR plus CsA (5 mg/kg SC for 3 weeks, n=15), (3) normotensive Sprague-Dawley (SD) rats (n=10), and (4) SD rats plus CsA (n=8). In dTGR, CsA completely prevented cardiovascular death (0 of 15 versus 9 of 20), decreased 24-hour albuminuria by 90% and systolic blood pressure by 35 mm Hg, and protected against the development of cardiac hypertrophy. Whole blood CsA concentrations 24 hours after the last drug treatment were 850±15 ng/mL. Semiquantitative ED-1 and Ki-67 (a nuclear cell proliferation–associated antigen) scoring showed that CsA prevented perivascular monocyte/macrophage infiltration and prevented cell proliferation in the kidneys and hearts of dTGR, respectively. The beneficial effects of CsA were, at least in part, mediated by the suppression of IL-6 and iNOS expression. Electrophoretic mobility shift assay revealed that CsA regulated inflammatory response in part through the NF-κB transcriptional pathway. In contrast to dTGR, CsA increased blood pressure in normotensive SD rats by 10 mm Hg and had no effect on cardiac mass or 24-hour urinary albumin excretion. Perivascular monocyte/macrophage infiltration, IL-6, and iNOS expression or cell proliferation were not affected by CsA in SD rats. Our findings indicate that CsA protects against Ang II–induced end-organ damage and underscore the central role of vascular inflammatory response in the pathogenesis of myocardial and renal damage in dTGR. The beneficial effects of CsA in the kidney and heart are mediated, at least in part, by suppression of IL-6 and iNOS expression via NF-κB transcriptional pathway.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.35.1.360
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 10
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    Formation of translational risk score based on correlation coefficients as an alternative to Cox regression models for predicting outcome in patients with NSCLC
    Springer Science and Business Media LLC ; 2011
    In:  Theoretical Biology and Medical Modelling Vol. 8, No. 1 ( 2011-12)
    Details
    In: Theoretical Biology and Medical Modelling, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2011-12)
    Abstract: Personalised cancer therapy, such as that used for bronchial carcinoma (BC), requires treatment to be adjusted to the patient's status. Individual risk for progression is estimated from clinical and molecular-biological data using translational score systems. Additional molecular information can improve outcome prediction depending on the marker used and the applied algorithm. Two models, one based on regressions and the other on correlations, were used to investigate the effect of combining various items of prognostic information to produce a comprehensive score. This was carried out using correlation coefficients, with options concerning a more plausible selection of variables for modelling, and this is considered better than classical regression analysis. Methods Clinical data concerning 63 BC patients were used to investigate the expression pattern of five tumour-associated proteins. Significant impact on survival was determined using log-rank tests. Significant variables were integrated into a Cox regression model and a new variable called integrative score of individual risk (ISIR), based on Spearman's correlations, was obtained. Results High tumour stage (TNM) was predictive for poor survival, while CD68 and Gas6 protein expression correlated with a favourable outcome. Cox regression model analysis predicted outcome more accurately than using each variable in isolation, and correctly classified 84% of patients as having a clear risk status. Calculation of the integrated score for an individual risk (ISIR), considering tumour size (T), lymph node status (N), metastasis (M), Gas6 and CD68 identified 82% of patients as having a clear risk status. Conclusion Combining protein expression analysis of CD68 and GAS6 with T, N and M, using Cox regression or ISIR, improves prediction. Considering the increasing number of molecular markers, subsequent studies will be required to validate translational algorithms for the prognostic potential to select variables with a high prognostic power; the use of correlations offers improved prediction.
    Type of Medium: Online Resource
    ISSN: 1742-4682
    URL: Article
    DOI: 10.1186/1742-4682-8-28
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 2156462-0
    SSG: 12
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