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.
question:
Context: Neonatal respiratory distress syndrome is a restrictive lung disease characterized by surfactant deficiency. Decreased vascular endothelial growth factor (VEGF), which demonstrates important roles in angiogenesis and vasculogenesis, has been implicated in the pathogenesis of restrictive lung diseases. Current animal models investigating VEGF in the etiology and outcomes of RDS require premature delivery, hypoxia, anatomically or temporally limited inhibition, or other supplemental interventions. Consequently, little is known about the isolated effects of chronic VEGF inhibition, started at birth, on subsequent developing lung structure and function.', 'To determine whether inducible, mesenchyme-specific VEGF inhibition in the neonatal mouse lung results in long-term modulation of AECII and whole lung function.', 'Triple transgenic mice expressing the soluble VEGF receptor sFlt-1 specifically in the mesenchyme (Dermo-1/rtTA/sFlt-1) were generated and compared to littermate controls at 3 months to determine the impact of neonatal downregulation of mesenchymal VEGF expression on lung structure, cell composition and function. Reduced tissue VEGF bioavailability has previously been demonstrated with this model.', 'Triple transgenic mice demonstrated restrictive lung pathology. No differences in gross vascular development or protein levels of vascular endothelial markers was noted, but there was a significant decrease in perivascular smooth muscle and type I collagen. Mutants had decreased expression levels of surfactant protein C and hypoxia inducible factor 1-alpha without a difference in number of type II pneumocytes.
Answer: These data show that mesenchyme-specific inhibition of VEGF in neonatal mice results in late restrictive disease, making this transgenic mouse a novel model for future investigations on the consequences of neonatal RDS and potential interventions.
answer:
Does sequestration of Vascular Endothelial Growth Factor ( VEGF ) induce Late Restrictive Lung Disease?


question:
Context: Left ventricular hypertrophy (LVH) is common in patients with autosomal dominant polycystic kidney disease (ADPKD). Although insulin resistance contributes to cardiac hypertrophy, the relationship between insulin resistance and LVH in patients with ADPKD has not been previously studied.', 'We performed M-mode and color Doppler echocardiography on 176 family members (106 patients and 70 healthy relatives) from 16 families with polycystic kidney disease type 1 (PKD1). Left ventricular mass index (LVMI) was calculated using the Penn equation and corrected for body surface area. Fasting insulin and glucose concentrations were measured and insulin resistance was evaluated by means of the homeostasis model assessment.', 'In multivariate regression analysis, insulin resistance was significantly associated with LVMI in healthy relatives (P < 0.01) and patients with PKD1 (P < 0.05) independent of age, weight, systolic blood pressure, and albuminuria.
Answer: Insulin resistance is associated with LVMI in patients with PKD1 independently of other factors known to increase LVMI.
answer:
Is insulin resistance related to left ventricular hypertrophy in patients with polycystic kidney disease type 1?


question:
Context: 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.
Answer: Moderate hypoxia in combination with heat stress reduces cycling time to exhaustion without modifying neuromuscular fatigue characteristics. Impaired oxygen delivery or increased cardiovascular strain, increasing relative exercise intensity, may have also contributed to earlier exercise cessation.
answer:

Does combining heat stress and moderate hypoxia reduce cycling time to exhaustion without modifying neuromuscular fatigue characteristics?