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.

Input: Consider Input: Context: The ADAMTS13-von Willebrand factor (vWF) axis has been suggested to play a critical role in the pathophysiology of ischemia-reperfusion injury (IRI) in the heart or brain. Therefore, we aimed to investigate whether this axis was involved in the pathophysiology of IRI-induced acute kidney injury.', 'We performed renal IRI in ADAMTS13 knockout (KO) or wild type (WT) mice. Functional and histological kidney damage, and inflammation were compared and the effect of anti-vWF antibodies in ADAMTS13 KO mice was assessed.', 'Following IRI, the blood and kidney ADAMTS13 levels were significantly decreased. vWF expression was significantly upregulated in both the medulla and cortex of injured kidneys as shown by immunohistochemistry and western blot analyses. There was also an increased level of vWF dimers after IRI. In ADAMTS13 KO mice, kidney vWF levels were further increased and this was associated with greater endothelial and epithelial injury compared to WT mice, suggesting an important role of vWF in renal IRI. In addition, the number of Gr-1
Answer: Our data show that the ADAMTS13-vWF axis is partially involved in the pathophysiology of kidney IR, suggesting that regulating ADAMTS13- and vWF-dependent mechanisms could have therapeutic potential to limit renal IRI. This article is protected by copyright. All rights reserved.

Output: Is the ADAMTS13-von Willebrand factor axis involved in the pathophysiology of kidney ischemia-reperfusion injury?


Input: Consider Input: Context: The aim of this article is to develop the Spanish adaptation of the internal functioning of Work Teams Scale (QFI-22).', 'The scale was adapted from the French version, and was applied to a sample of 1,055 employees working for firms operating in Spain. The article analyses the internal structure (exploratory and confirmatory factor analysis) and internal consistency, and provides convergent validity evidence of the scale.', 'The QFI-22 scale shows the same internal structure as the original. Factor analysis confirmed the existence of two factors: interpersonal support and team work management, with good internal consistency coefficients (α1 = .93, α2 = .92). Regarding validity evidence, the QFI-22 scale has significant correlations with other correlates and alternative scales used for comparison purposes. The two factors correlated positively with team vision, participation safety, task orientation and support for innovation (Team Climate Inventory, TCI scale), with progressive culture (Organisational Culture, X-Y scale), and with creating change, customer focus and organisational learning (Denison Organizational Culture Survey, DOCS scale). In contrast, the two factors correlated negatively with traditional culture (X-Y scale).
Answer: The QFI-22 scale is a useful instrument for assessing the internal functioning of work teams.

Output: Does spanish adaptation of the internal functioning of the Work team Scale ( QFI-22 )?


Input: Consider Input: Context: Overexpression of the human c-MYC (MYC) oncogene is one of the most frequently implicated events in the pathogenesis of hepatocellular carcinoma (HCC). Previously, we have shown in a conditional transgenic mouse model that MYC overexpression is restrained from inducing mitotic cellular division and tumorigenesis in the adult liver; whereas, in marked contrast, MYC induces robust proliferation associated with the very rapid onset of tumorigenesis in embryonic and neonatal mice.', 'Here, we show that non-genotoxic hepatotoxins induce changes in the liver cellular context associated with increased cellular proliferation and enhanced tumorigenesis. Both 5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride (CCl(4)) cooperate with MYC to greatly accelerate the onset of liver cancer in an adult host to less than 7 days versus a mean latency of onset of over 35 weeks for MYC alone. These hepatotoxin-enhanced liver tumors grossly and histologically resemble embryonic and neonatal liver tumors. Importantly, we found that MYC overexpression is only capable of inducing expression of the mitotic Cyclin B1 in embryonic/neonatal hosts or adult hosts that were treated with either carcinogen.
Answer: Our results suggest a model whereby oncogenes can remain latently activated, but exposure of the adult liver to hepatotoxins that promote hepatocyte proliferation can rapidly uncover their malignant potential.


Output: Do hepatotoxin-induced changes in the adult murine liver promote MYC-induced tumorigenesis?