Given a passage, 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.

[Q]: This study investigated the isolated and combined effects of heat [temperate (22\xa0°C/30\xa0% rH) vs. hot (35\xa0°C/40\xa0% rH)] and hypoxia [sea level (FiO2 0.21) vs. moderate altitude (FiO2 0.15)] on exercise capacity and neuromuscular fatigue characteristics.', 'Eleven physically active subjects cycled to exhaustion at constant workload (66\xa0% of the power output associated with their maximal oxygen uptake in temperate conditions) in four different environmental conditions [temperate/sea level (control), hot/sea level (hot), temperate/moderate altitude (hypoxia) and hot/moderate altitude (hot\xa0+\xa0hypoxia)]. Torque and electromyography (EMG) responses following electrical stimulation of the tibial nerve (plantar-flexion; soleus) were recorded before and 5\xa0min after exercise.', 'Time to exhaustion was reduced (P\xa0<\xa00.05) in hot (-35\xa0±\xa015\xa0%) or hypoxia (-36\xa0±\xa014\xa0%) compared to control (61\xa0±\xa028\xa0min), while hot\xa0+\xa0hypoxia (-51\xa0±\xa020\xa0%) further compromised exercise capacity (P\xa0<\xa00.05). However, the effect of temperature or altitude on end-exercise core temperature (P\xa0=\xa00.089 and P\xa0=\xa00.070, respectively) and rating of perceived exertion (P\xa0>\xa00.05) did not reach significance. Maximal voluntary contraction torque, voluntary activation (twitch interpolation) and peak twitch torque decreased from pre- to post-exercise (-9\xa0±\xa01, -4\xa0±\xa01 and -6\xa0±\xa01\xa0% all trials compounded, respectively; P\xa0<\xa00.05), with no effect of the temperature or altitude. M-wave amplitude and root mean square activity were reduced (P\xa0<\xa00.05) in hot compared to temperate conditions, while normalized maximal EMG activity did not change. Altitude had no effect on any measured parameters.
[A]: Does combining heat stress and moderate hypoxia reduce cycling time to exhaustion without modifying neuromuscular fatigue characteristics?


[Q]: Previous results have shown that mice lacking in the group 1B phospholipase A(2) (Pla2g1b) are resistant to obesity and diabetes induced by feeding a diabetogenic high-fat/high-carbohydrate diet. This study examined the potential of using the Pla2g1b inhibitor methyl indoxam as therapy to suppress diet-induced obesity and diabetes.', 'Male C57BL/6 mice were fed the diabetogenic diet with or without methyl indoxam supplementation. Body weight gain, fasting plasma glucose levels, glucose tolerance and postprandial lysophospholipid absorption were compared.', 'Wild-type C57BL/6 mice fed the diabetogenic diet without Pla2g1b inhibitor showed 31 and 69% body weight gain after 4 and 10 weeks respectively. These animals also showed elevated plasma glucose levels and were glucose intolerant. In contrast, C57BL/6 mice fed the diabetogenic diet with 90 mg.kg(-1) of methyl indoxam gained only 5% body weight after 10 weeks. These animals were also euglycaemic and displayed normal glucose excursion rates in glucose tolerance test. Methyl indoxam suppression of diet-induced body weight gain and glucose intolerance was correlated with the inhibition of Pla2g1b-mediated postprandial lysophospholipid absorption.
[A]: Does the phospholipase A ( 2 ) inhibitor methyl indoxam suppress diet-induced obesity and glucose intolerance in mice?


[Q]: The chemokine CCL27 attracts skin-homing T cells. CCL27 production by keratinocytes is enhanced in skin lesions from patients with atopic dermatitis or psoriasis vulgaris. It is suggested that prostaglandin E(2) (PGE(2)) regulates skin inflammation.', 'We examined the in vitro effects of PGE(2) on CCL27 production in human keratinocytes.', 'Keratinocytes were incubated with TNF-alpha in the presence or absence of PGE(2) . CCL27 secretion and mRNA level were analyzed by means of ELISA and RT-PCR, respectively. Nuclear factor kappaB (NF-kappaB)-dependent transcriptional activity was analyzed by using luciferase assays.', 'TNF-alpha increased CCL27 secretion and mRNA levels in parallel to NF-kappaB activity in keratinocytes. NF-kappaB p50 or p65 antisense oligonucleotides suppressed TNF-alpha-induced CCL27 production, indicating the requirement of NF-kappaB for CCL27 production. PGE(2) , EP2, or EP3 agonists reduced TNF-alpha-induced CCL27 secretion and mRNA levels in parallel to NF-kappaB activity and CCL2, CCL5, CXCL8, and CXCL10 mRNA levels. Either EP3-specific or dual EP1-EP2 antagonist partially blocked the inhibitory effects of PGE(2) on CCL27 production and NF-kappaB activity, and the addition of both completely abrogated the inhibition, whereas EP1 or EP4 antagonists were ineffective. Intracellular Ca(2+) chelator BAPTA/AM or cyclic adenosine monophosphate (cAMP)-dependent protein kinase inhibitor H-89 partially blocked the inhibitory effects of PGE(2) on CCL27 production and NF-kappaB activity, and the addition of both completely abrogated the inhibition. PGE(2) or EP3 agonist increased intracellular Ca(2+) concentrations. PGE(2) or EP2 agonist increased intracellular cAMP concentrations.
[A]:
Does prostaglandin E ( 2 ) suppress CCL27 production through EP2 and EP3 receptors in human keratinocytes?