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.

Example Input: Context: Bacteria often form multicellular, organized communities known as biofilms, which protect cells from a variety of environmental stresses. During biofilm formation, bacteria secrete a species-specific matrix; in Bacillus subtilis biofilms, the matrix consists of protein polymers and exopolysaccharide. Many domesticated strains of B. subtilis have a reduced ability to form biofilms, and we conducted a two-month evolution experiment to test whether laboratory culturing provides selective pressure against biofilm formation in B. subtilis.', 'Bacteria grown in two-month-long batch culture rapidly diversified their biofilm-forming characteristics, exhibiting highly diverse colony morphologies on LB plates in the initial ten days of culture. Generally, this diversity decreased over time; however, multiple types of colony morphology remained in our final two-month-old populations, both under shaking and static conditions. Notably, while our final populations featured cells that produce less biofilm matrix than did the ancestor, cells overproducing biofilm matrix were present as well. We took a candidate-gene approach to identify mutations in the strains that overproduced matrix and found point mutations in the biofilm-regulatory gene sinR. Introducing these mutations into the ancestral strain phenocopied or partially phenocopied the evolved biofilm phenotypes.
Answer: Our data suggest that standard laboratory culturing conditions do not rapidly select against biofilm formation. Although biofilm matrix production is often reduced in domesticated bacterial strains, we found that matrix production may still have a fitness benefit in the laboratory. We suggest that adaptive specialization of biofilm-forming species can occur through mutations that modulate biofilm formation as in B. subtilis.
Example Output: Is sinR a mutational target for fine-tuning biofilm formation in laboratory-evolved strains of Bacillus subtilis?

Example Input: Context: Asteatotic eczema (AE) is characterized by itchy, dry, rough, and scaling skin. The treatments for AE are mainly emollients, usually containing urea, lactic acid, or a lactate salt. N-palmitoylethanolamine (PEA) and N-acetylethanolamine (AEA) are both endogenous lipids used as novel therapeutic tools in the treatment of many skin diseases. The purpose of this study was to compare a PEA/AEA emollient with a traditional emollient in the treatment of AE.', "A monocentric, randomized, double-blind, comparative trial was conducted in 60 AE patients to evaluate and compare the efficacy of the two emollients. The level of skin dryness among the subjects ranged from mild to moderate. The subjects' skin barrier function and the current perception threshold were tested for 28 days by clinical scoring and bioengineering technology.", 'The results showed that, although some aspects were improved in both groups, the group using the emollient containing PEA/AEA presented a better skin surface change in capacitance. However, the most impressive finding was the ability of the PEA/AEA emollient to increase the 5 Hz current perception threshold to a normal level after 7 days, with a significant difference between values at baseline and after 14 days. A current perception threshold of 5 Hz was positively and significantly correlated with skin surface hydration and negatively correlated with transepidermal water loss in the PEA/AEA emollient group.
Answer: Compared with traditional emollients, regular application of a topical PEA/AEA emollient could improve both passive and active skin functions simultaneously.
Example Output: Are n-palmitoylethanolamine and N-acetylethanolamine effective in asteatotic eczema : results of a randomized , double-blind , controlled study in 60 patients?

Example Input: Context: We have previously shown that the cardioprotective effect of ischemic preconditioning (IPC) is suppressed in hyperhomocysteinemic rat hearts. The present study investigated the effect of 2-chloro-N-cyclopentyladenosine (CCPA), a selective adenosine-A1 receptor agonist, in hyperhomocysteinemia-induced attenuation of the cardioprotective effect of IPC.', 'Rats were administered L-methionine (1.7 g/kg/day po) for 8 weeks to produce hyperhomocysteinemia. Isolated Langendorff perfused normal and hyperhomocysteinemic rat hearts were subjected to 30-minute global ischemia, followed by a 120-minute reperfusion. Myocardial infarct size was assessed macroscopically using triphenyltetrazolium chloride staining. Coronary effluent was analyzed for lactate dehydrogenase and CK-MB release to assess the extent of cardiac injury. The oxidative stress in the heart was assessed by measuring thiobarbituric acid reactive substance and reduced form of glutathione.', 'Ischemia and reperfusion (I/R) produced myocardial injury by increasing myocardial infarct size, elevating lactate dehydrogenase and CK-MB release in coronary effluent, decreasing coronary flow rate, and inducing oxidative stress in normal and hyperhomocysteinemic rat hearts. The hyperhomocysteinemic rat hearts showed enhanced I/R-induced myocardial injury with high oxidative stress. The IPC afforded cardioprotection against I/R-induced myocardial injury in normal rat hearts. However, IPC-mediated myocardial protection against I/R injury was abolished in hyperhomocysteinemic rat hearts. Administration of CCPA did not alter the cardioprotective effect of IPC in normal rat hearts, but its administration markedly restored the cardioprotective effect of IPC in hyperhomocysteinemic rat hearts.
Answer: It may be concluded that the activation of adenosine-A1 receptors using CCPA markedly restored the suppressed cardioprotective and infarct size-limiting effects of IPC in hyperhomocysteinemic rat hearts. Thus, the reduced availability of extracellular adenosine and impaired activation of adenosine-A1 receptors may be responsible for abolishing the cardioprotective potential of IPC against I/R-induced myocardial injury in hyperhomocysteinemic rat hearts.
Example Output:
Does adenosine-A1 receptors activation restore the suppressed cardioprotective effects of ischemic preconditioning in hyperhomocysteinemic rat hearts?