instruction:
Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
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Context: Human induced pluripotent stem cells (iPSCs) play an important role in disease modeling and drug testing. However, the current methods are time-consuming and lack an isogenic control.', 'This study sought to establish an efficient technology to generate human PSC-based disease models with isogenic control.', 'The ion channel genes KCNQ1 and KCNH2 with dominant negative mutations causing long QT syndrome types 1 and 2, respectively, were stably integrated into a safe harbor AAVS1 locus using zinc finger nuclease technology.', 'Patch-clamp recording revealed that the edited iPSC-derived cardiomyocytes (iPSC-CMs) displayed characteristic long QT syndrome phenotype and significant prolongation of the action potential duration compared with the unedited control cells. Finally, addition of nifedipine (L-type calcium channel blocker) or pinacidil (KATP-channel opener) shortened the action potential duration of iPSC-CMs, confirming the validity of isogenic iPSC lines for drug testing in the future.
Answer: Our study demonstrates that iPSC-CM-based disease models can be rapidly generated by overexpression of dominant negative gene mutants.
answer:
Does genome editing of isogenic human induced pluripotent stem cells recapitulate long QT phenotype for drug testing?

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Context: In mice, a subpopulation of gut dendritic cells (DCs) expressing CD103 drives the development of regulatory T (T(reg)) cells. Further, it was recently described that the cross-talk between human intestinal epithelial cells (IECs) and DCs helps in maintaining gut immune homeostasis via the induction of non-inflammatory DCs. In this study, an analysis was carried out to determine whether IECs could promote the differentiation of CD103+ tolerogenic DCs, and the function of primary CD103+ DCs isolated from human mesenteric lymph nodes (MLNs) was evaluated.', "Monocyte-derived DCs (MoDCs) and circulating CD1c+ DCs were conditioned or not with supernatants from Caco-2 cells or IECs isolated from healthy donors or donors with Crohn's disease and analysed for their ability to induce T(reg) cell differentiation. In some cases, transforming growth factor beta (TGFbeta), retinoic acid (RA) or thymic stromal lymphopoietin (TSLP) were neutralised before conditioning. CD103+ and CD103- DCs were sorted by fluorescence-activated cell sorting (FACS) from MLNs and used in T(reg) cell differentiation experiments.", "It was found that human IECs promoted the differentiation of tolerogenic DCs able to drive the development of adaptive Foxp3+ T(reg) cells. This control was lost in patients with Crohn's disease and paralleled a reduced expression of tolerogenic factors by primary IECs. MoDCs differentiated with RA or IEC supernatant upregulated the expression of CD103. Consistently, human primary CD103+ DCs isolated from MLNs were endowed with the ability to drive T(reg) cell differentiation. This subset of DCs expressed CCR7 and probably represents a lamina propria-derived migratory population.
Answer: A population of tolerogenic CD103+ DCs was identified in the human gut that probably differentiate in response to IEC-derived factors and drive T(reg) cell development.
answer:
Do human intestinal epithelial cells promote the differentiation of tolerogenic dendritic cells?

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Context: Determination of endothelial function has emerged as a crucial factor in the assessment of individual cardiovascular risk. Sonographic measurement of flow-mediated dilation (FMD) is the most widespread technique to assess endothelial function, but analysis is very time-consuming and requires an experienced examiner. Recently, it was speculated that a reduction of small artery compliance (C2) measured by pulse wave analysis might be an indicator of endothelial dysfunction. In the present study, we investigated the correlation of pulse wave analysis parameters and endothelial function with special regard to patients who are at increased risk for endothelial dysfunction.', 'One hundred and thirty-six subjects (65 male, 71 female) were included in the study. One hundred and twenty-three probands were hypertensive. Endothelium-dependent vasodilation was assessed sonographically (flow-mediated dilation) using standard protocols and as a change of reflection index (deltaRI) after application of salbutamol by photoplethysmography. Small artery compliance, large artery compliance (C1), and systemic vascular resistance (SVR) were measured by computerized pulse wave analysis of the radial artery (CR-2000; Hypertension Diagnostics, Eagan, Minnesota, USA) and were tested for correlation with FMD.', 'Mean FMD was 6.29 +/- 2.86%. Means of pulse wave analysis-derived vascular parameters were 4.91 +/- 2.86 ml/mmHg x 100 (C2), 13.35 +/- 5.41 ml/mmHg x 10 (C1) and 1611.6 +/- 348.5 dynes x s x cm(-5) (SVR). Regression analysis excluded a significant correlation between FMD, C2, C1 and SVR (r2 < 0.05 each) both in hypertensives and normotensives. There was no significant correlation between C2 and deltaRI (r2 = 0.023).
Answer: Our findings show that static measurement of vascular parameters by an automated pulse-wave analysis procedure cannot be used to assess endothelial function. Further studies are needed to examine whether a dynamic measurement of arterial compliance before and after stimulation of the endothelium (e.g. by ischemia) might quantify endothelial dilatory capacity in a better way.
answer:
Is small artery elasticity assessed by pulse wave analysis no measure of endothelial dysfunction?