The Role of Internal Third-Party Interveners in Civil Resistance Campaigns: The Case of Israeli–Jewish Anti-Occupation Activists

When a non-violent resistance campaign does not have leverage to challenge powerful opponents, third-party intervention has been shown to assist. While the role of external third-party interveners – foreign activists – has been documented, less attention has been given to intervention from members of the dominant population. Drawing from the literature on civil resistance and through the study of Israeli Jews who intervene in Palestinian resistance campaigns against the Israeli military occupation, I argue that intervention from members of the dominant population is strategically desirable. Through an analysis of three Palestinian campaigns, this article identifies that the physical presence of Israeli Jews was needed to ensure the Palestinians could maintain their resistance efforts and presence on the land, despite the repression they faced. Furthermore, the skills and knowledge of the Israelis were needed to help the Palestinians achieve some of their goals, at least in the short term

Embryonic cardiomyocyte, but not autologous stem cell transplantation, restricts infarct expansion, enhances ventricular function, and improves long-term survival

Controversy exists in regard to the beneficial effects of transplanting cardiac or somatic progenitor cells upon myocardial injury. We have therefore investigated the functional short- and long-term consequences after intramyocardial transplantation of these cell types in a murine lesion model. Myocardial infarction (MI) was induced in mice (n = 75), followed by the intramyocardial injection of 1-2×10(5) luciferase- and GFP-expressing embryonic cardiomyocytes (eCMs), skeletal myoblasts (SMs), mesenchymal stem cells (MSCs) or medium into the infarct. Non-treated healthy mice (n = 6) served as controls. Bioluminescence and fluorescence imaging confirmed the engraftment and survival of the cells up to seven weeks postoperatively. After two weeks MRI was performed, which showed that infarct volume was significantly decreased by eCMs only (14.8±2.2% MI+eCM vs. 26.7±1.6% MI). Left ventricular dilation was significantly decreased by transplantation of any cell type, but most efficiently by eCMs. Moreover, eCM treatment increased the ejection fraction and cardiac output significantly to 33.4±2.2% and 22.3±1.2 ml/min. In addition, this cell type exclusively and significantly increased the end-systolic wall thickness in the infarct center and borders and raised the wall thickening in the infarct borders. Repetitive echocardiography examinations at later time points confirmed that these beneficial effects were accompanied by better survival rates. Cellular cardiomyoplasty employing contractile and electrically coupling embryonic cardiomyocytes (eCMs) into ischemic myocardium provoked significantly smaller infarcts with less adverse remodeling and improved cardiac function and long-term survival compared to transplantation of somatic cells (SMs and MSCs), thereby proving that a cardiomyocyte phenotype is important to restore myocardial functio

Embryonic cardiomyocyte, but not autologous stem cell transplantation, restricts infarct expansion, enhances ventricular function, and improves long-term survival

Contains fulltext : 118371.pdf (publisher's version ) (Open Access)AIMS: Controversy exists in regard to the beneficial effects of transplanting cardiac or somatic progenitor cells upon myocardial injury. We have therefore investigated the functional short- and long-term consequences after intramyocardial transplantation of these cell types in a murine lesion model. METHODS AND RESULTS: Myocardial infarction (MI) was induced in mice (n = 75), followed by the intramyocardial injection of 1-2x10(5) luciferase- and GFP-expressing embryonic cardiomyocytes (eCMs), skeletal myoblasts (SMs), mesenchymal stem cells (MSCs) or medium into the infarct. Non-treated healthy mice (n = 6) served as controls. Bioluminescence and fluorescence imaging confirmed the engraftment and survival of the cells up to seven weeks postoperatively. After two weeks MRI was performed, which showed that infarct volume was significantly decreased by eCMs only (14.8+/-2.2% MI+eCM vs. 26.7+/-1.6% MI). Left ventricular dilation was significantly decreased by transplantation of any cell type, but most efficiently by eCMs. Moreover, eCM treatment increased the ejection fraction and cardiac output significantly to 33.4+/-2.2% and 22.3+/-1.2 ml/min. In addition, this cell type exclusively and significantly increased the end-systolic wall thickness in the infarct center and borders and raised the wall thickening in the infarct borders. Repetitive echocardiography examinations at later time points confirmed that these beneficial effects were accompanied by better survival rates. CONCLUSION: Cellular cardiomyoplasty employing contractile and electrically coupling embryonic cardiomyocytes (eCMs) into ischemic myocardium provoked significantly smaller infarcts with less adverse remodeling and improved cardiac function and long-term survival compared to transplantation of somatic cells (SMs and MSCs), thereby proving that a cardiomyocyte phenotype is important to restore myocardial function

Quantification of cardiac function by MRI.

<p>Representative in vivo end-diastolic MR-images two weeks after myocardial infarction in A) short-axis (mid-LV) and B) long-axis orientation for each experimental group. Global cardiac morphology and function were obtained from in vivo cine MR-images: C) EDV, D) ESV, E) EF and F) CO. No MI: n = 6, MI+eCM: n = 5, MI+SM: n = 7, MI+MSC: n = 7 and MI: n = 8. *  =  p<0.05 vs. MI, †  =  p<0.05 vs. MI+eCM.</p

Quantification of infarct size by MRI.

<p>A) Representative in vivo T₁-weighted mid-LV short-axis LGE MR-images two weeks after myocardial infarction for each experimental group. Infarct size was quantified from LGE images as B) relative transmural infarct volume and C) relative epicardial infarct surface area. No MI: n = 6, MI+eCM: n = 5, MI+SM: n = 5, MI+MSC: n = 7 and MI: n = 8. *  =  p<0.05 vs. MI, †  =  p<0.05 vs. MI+eCM. The infarct volume and area measured in wild type mice (no MI) was indicative for the accuracy of the analysis.</p

Long-term cell survival and treatment outcome.

<p>A) Survival curves of mice with myocardial infarction transplanted with eCMs (n = 17), SMs (n = 14) and MSCs (n = 16), followed 7 weeks postoperatively. B) In vivo longitudinal BLI of representative mice at 5, 13 and 49 days after transplantation of eCMs (top) SMs (middle) and MSCs (bottom) to monitor long-term cell survival in infarcted myocardium. C) Longitudinal evaluation of heart function with echocardiography at day 5 and 49 after transplantation of eCMs, SMs and MSCs.</p

Assessment of regional contractile function by MRI.

<p>Regional contractile function two weeks after myocardial infarction, described by group-averaged A) end-systolic wall thickness and B) wall thickening after segmentation of the LV according to the 16 segment AHA model for mice with no MI (n = 6), MI+eCM (n = 5), MI+SM (n = 7), MI+MSC (n = 7) and MI (n = 8). *  =  p<0.05 vs. MI, †  =  p<0.1 vs. MI. The segment numbering is clarified in A).</p

Fluorescence microscopy and histology of myocardial tissues of treatment and control groups.

<p>A) Ex vivo fluorescence microscopy of GFP expressing eCMs, SMs and MSCs two weeks after transplantation in infarcted myocardium to evaluate cell engraftment and survival. GFP is depicted in green and autofluorescence is shown in red. Scale bar = 20 µm. B) Ex vivo picrosirius red staining to determine general infarct composition two weeks postoperatively. Engrafted eCMs and SMs can be identified within the lesion (arrows). Scale bar = 1 mm. C) Ex vivo fluorescence microscopy to evaluate cell differentiation at 7 weeks (no MI, MI+eCM, MI+SM, MI) or 2 weeks (MI+MSC) after surgery and transplantation. For all groups, GFP fluorescence is depicted in green and cell nuclei in blue. For eCM (top) and SM (middle) the cardiomyocyte marker Connexin43 is shown in red and α-actinin in white, whereas for MSC (bottom) the mesenchymal stem cell marker CD73 is shown in red. Scale bars = 20 µm.</p