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111.
Mario Iannaccone Mohamed Abdirashid Umberto Annone Gaëlle Saint‐Hilary Pascal Meier Alaide Chieffo Sl Chen Carlo di Mario Federico Conrotto Pierluigi Omed Antonio Montefusco Michele De Benedictis Sara Rettegno Baldassare Doronzo Mauro Gasparini Mauro Rinaldi Maurizio D'Amico Fabrizio D'Ascenzo 《Catheterization and cardiovascular interventions》2020,95(7):1259-1266
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Peyrol M Sbragia P Orabona M Casalta AC Laine M Decourt A Quatre A Jacquier A Siddo ND Paganelli F 《Journal of electrocardiology》2012,45(4):394-397
Ventricular allorhythmia is an electrocardiogram feature leading to a pattern of "regularly irregular" arrhythmia mainly reported during non-life-threatening organized atrial tachycardia. We report the infrequent case of a patient presenting with ventricular allorhythmia during infarct-related ventricular tachycardia. The potential mechanisms of this tachycardia are discussed. 相似文献
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J Uhlendorf A Miermont T Delaveau G Charvin F Fages S Bottani G Batt P Hersen 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(35):14271-14276
Gene expression plays a central role in the orchestration of cellular processes. The use of inducible promoters to change the expression level of a gene from its physiological level has significantly contributed to the understanding of the functioning of regulatory networks. However, from a quantitative point of view, their use is limited to short-term, population-scale studies to average out cell-to-cell variability and gene expression noise and limit the nonpredictable effects of internal feedback loops that may antagonize the inducer action. Here, we show that, by implementing an external feedback loop, one can tightly control the expression of a gene over many cell generations with quantitative accuracy. To reach this goal, we developed a platform for real-time, closed-loop control of gene expression in yeast that integrates microscopy for monitoring gene expression at the cell level, microfluidics to manipulate the cells' environment, and original software for automated imaging, quantification, and model predictive control. By using an endogenous osmostress responsive promoter and playing with the osmolarity of the cells environment, we show that long-term control can, indeed, be achieved for both time-constant and time-varying target profiles at the population and even the single-cell levels. Importantly, we provide evidence that real-time control can dynamically limit the effects of gene expression stochasticity. We anticipate that our method will be useful to quantitatively probe the dynamic properties of cellular processes and drive complex, synthetically engineered networks. 相似文献
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Anon E Serra-Picamal X Hersen P Gauthier NC Sheetz MP Trepat X Ladoux B 《Proceedings of the National Academy of Sciences of the United States of America》2012,109(27):10891-10896
Fundamental biological processes such as morphogenesis and wound healing involve the closure of epithelial gaps. Epithelial gap closure is commonly attributed either to the purse-string contraction of an intercellular actomyosin cable or to active cell migration, but the relative contribution of these two mechanisms remains unknown. Here we present a model experiment to systematically study epithelial closure in the absence of cell injury. We developed a pillar stencil approach to create well-defined gaps in terms of size and shape within an epithelial cell monolayer. Upon pillar removal, cells actively respond to the newly accessible free space by extending lamellipodia and migrating into the gap. The decrease of gap area over time is strikingly linear and shows two different regimes depending on the size of the gap. In large gaps, closure is dominated by lamellipodium-mediated cell migration. By contrast, closure of gaps smaller than 20 μm was affected by cell density and progressed independently of Rac, myosin light chain kinase, and Rho kinase, suggesting a passive physical mechanism. By changing the shape of the gap, we observed that low-curvature areas favored the appearance of lamellipodia, promoting faster closure. Altogether, our results reveal that the closure of epithelial gaps in the absence of cell injury is governed by the collective migration of cells through the activation of lamellipodium protrusion. 相似文献
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Virginie Pascal Brice Laffleur Arnaud Debin Armelle Cuvillier Marjolein van Egmond Daniel Drocourt Laurent Imbertie C��line Pangault Karin Tarte G��rard Tiraby Michel Cogn�� 《Haematologica》2012,97(11):1686-1694