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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Question: Context: Endoplasmic reticulum (ER) stress is induced in many forms of chronic liver disease and may promote the development of hepatocellular carcinoma. The activator protein 1 (AP-1) complex is a transcription factor that promotes hepatic carcinogenesis in response to cellular stress. The aim of this study was to determine the role of ER stress in the regulation of the hepatic AP-1 complex.', 'Human hepatocellular carcinoma (HepG2) cells and C57BL/6J mice were subjected to pharmacologic ER stress and the expression of AP-1-associated genes and proteins was assessed. To determine the role of MAPK signaling in ER stress-induced AP-1 activation, ER stress was induced in JNK- and ERK-inhibited HepG2 cells.', 'Induction of ER stress promoted the activation of both Jun- and Fos-related genes and proteins of the AP-1 complex in HepG2 cells and murine liver. Inhibition of ERK phosphorylation in HepG2 cells completely prevented ER stress-induced activation of the fos-related components of AP-1 whereas activation of Jun-related components was only partially attenuated. Conversely, inhibition of JNK phosphorylation in HepG2 cells reduced ER stress-induced activation of Jun-related components but did not prevent activation of fos-related components.
Answer: ER stress activates the hepatic AP-1 complex via MAPK-dependent signaling pathways. ER stress-induced activation of Fos-related components is dependent primarily on ERK activation whereas ER stress-induced activation of Jun-related components is dependent primarily on JNK activation, although there is interplay between these regulatory pathways. These data implicate a novel signaling pathway by which sustained ER stress, as observed in many chronic liver diseases, may promote hepatic carcinogenesis.

Answer: Does endoplasmic reticulum stress activate the hepatic activator protein 1 complex via mitogen activated protein kinase-dependent signaling pathways?


Question: Context: We examined the effect of prior heating, by exercise and warm-water immersion, on core cooling rates in individuals rendered mildly hypothermic by immersion in cold water.', 'There were seven male subjects who were randomly assigned to one of three groups: 1) seated rest for 15 min (control); 2) cycling ergometry for 15 min at 70% Vo2 peak (active warming); or 3) immersion in a circulated bath at 40 degrees C to an esophageal temperature (Tes) similar to that at the end of exercise (passive warming). Subjects were then immersed in 7 degrees C water to a Tes of 34.5 degrees C.', 'Initial Tes cooling rates (initial approximately 6 min cooling) differed significantly among the treatment conditions (0.074 +/- 0.045, 0.129 +/- 0.076, and 0.348 +/- 0.117 degrees C x min(-1) for control, active, and passive warming conditions, respectively); however, secondary cooling rates (rates following initial approximately 6 min cooling to the end of immersion) were not different between treatments (average of 0.102 +/- 0.085 degrees C x min(-1)). Overall Tes cooling rates during the full immersion period differed significantly and were 0.067 +/- 0.047, 0.085 +/- 0.045, and 0.209 +/- 0.131 degrees C x min(-1) for control, active, and passive warming, respectively.
Answer: These results suggest that prior warming by both active and, to a greater extent, passive warming, may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold water. Thus, functional time and possibly survival time could be reduced when cold water immersion is preceded by whole-body passive warming, and to a lesser degree by active warming.

Answer: Does warming by immersion or exercise affect initial cooling rate during subsequent cold water immersion?


Question: Context: The susceptibility of neonates to pulmonary and systemic infection has been associated with the immaturity of both lung structure and the immune system. Surfactant protein (SP) D is a member of the collectin family of innate immune molecules that plays an important role in innate host defense of the lung.', 'We tested whether treatment with recombinant human SP-D influenced the response of the lung and systemic circulation to intratracheally administered Escherichia coli lipopolysaccharides.', 'After intratracheal lipopolysaccharide instillation, preterm newborn lambs were treated with surfactant and ventilated for 5 h.', 'Survival rate, physiologic lung function, lung and systemic inflammation, and endotoxin level in plasma were evaluated.', 'In control lambs, intratracheal lipopolysaccharides caused septic shock and death associated with increased endotoxin in plasma. In contrast, all lambs treated with recombinant human SP-D were physiologically stable and survived. Leakage of lipopolysaccharides from the lungs to the systemic circulation was prevented by intratracheal recombinant human SP-D. Recombinant human SP-D prevented systemic inflammation and decreased the expression of IL-1beta, IL-8, and IL-6 in the spleen and liver. Likewise, recombinant human SP-D decreased IL-1beta and IL-6 in the lung and IL-8 in the plasma. Recombinant human SP-D did not alter pulmonary mechanics following endotoxin exposure. Recombinant human SP-D was readily detected in the lung 5 h after intratracheal instillation.
Answer: Intratracheal recombinant human SP-D prevented shock caused by endotoxin released from the lung during ventilation in the premature newborn.

Answer:
Does intratracheal recombinant surfactant protein d prevent endotoxin shock in the newborn preterm lamb?