Specific deletion of Notch1 and RBPjκ in the mouse results in abrogation of definitive haematopoiesis concomitant with the loss of arterial identity at embryonic stage. As prior arterial determination is likely to be required for the generation of embryonic haematopoiesis, it is difficult to establish the specific haematopoietic role of Notch in these mutants. By analysing different Notch‐ligand‐null embryos, we now show that Jagged1 is not required for the establishment of the arterial fate but it is required for the correct execution of the definitive haematopoietic programme, including expression of GATA2 in the dorsal aorta. Moreover, successful haematopoietic rescue of the Jagged1‐null AGM cells was obtained by culturing them with Jagged1‐expressing stromal cells or by lentiviral‐mediated transduction of the GATA2 gene. Taken together, our results indicate that Jagged1‐mediated activation of Notch1 is responsible for regulating GATA2 expression in the AGM, which in turn is essential for definitive haematopoiesis in the mouse.
Regardless of the presence of acute rejection, delayed graft function amplifies the detrimental effect of advanced donor age on long-term graft outcome.
Chronic pulmonary thromboembolism is mainly a consequence of incomplete resolution of pulmonary thromboembolism. Increased vascular resistance due to obstruction of the vascular bed leads to pulmonary hypertension. Chronic thromboembolic pulmonary hypertension is clearly more common than previously was thought, and misdiagnosis is common because patients often present with nonspecific symptoms related to pulmonary hypertension. Computed tomography (CT) is a useful alternative to conventional angiography not only for diagnosing chronic pulmonary thromboembolism but also for determining which cases are treatable with surgery and confirming technical success postoperatively. The vascular CT signs include direct pulmonary artery signs (complete obstruction, partial obstruction, eccentric thrombus, calcified thrombus, bands, webs, poststenotic dilatation), signs related to pulmonary hypertension (enlargement of main pulmonary arteries, atherosclerotic calcification, tortuous vessels, right ventricular enlargement, hypertrophy), and signs of systemic collateral supply (enlargement of bronchial and nonbronchial systemic arteries). The parenchymal signs include scars, a mosaic perfusion pattern, focal ground-glass opacities, and bronchial anomalies. The presence of one or more of these radiologic signs arouses suspicion and allows diagnosis of this entity. Early recognition of chronic pulmonary thromboembolism may help improve the outcome, since the condition is potentially curable with pulmonary thromboendarterectomy.
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