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]: Enhanced activation of the mineralocorticoid receptors (MRs) in cardiovascular tissues increases oxidative stress, maladaptive immune responses, and inflammation with associated functional vascular abnormalities. We previously demonstrated that consumption of a Western diet (WD) for 16 weeks results in aortic stiffening, and that these abnormalities were prevented by systemic MR blockade in female mice. However, the cell-specific role of endothelial cell MR (ECMR) in these maladaptive vascular effects has not been explored.', 'We hypothesized that specific deletion of the ECMR would prevent WD-induced increases in endothelial sodium channel activation, reductions in bioavailable nitric oxide, increased vascular remodeling, and associated increases in vascular stiffness in females.', 'Four-week-old female ECMR knockout and wild-type mice were fed either mouse chow or WD for 16 weeks. WD feeding resulted in aortic stiffness and endothelial dysfunction as determined in vivo by pulse wave velocity and ex vivo by atomic force microscopy, and wire and pressure myography. The WD-induced aortic stiffness was associated with enhanced endothelial sodium channel activation, attenuated endothelial nitric oxide synthase activation, increased oxidative stress, a proinflammatory immune response and fibrosis. Conversely, cell-specific ECMR deficiency prevented WD-induced aortic fibrosis and stiffness in conjunction with reductions in endothelial sodium channel activation, oxidative stress and macrophage proinflammatory polarization, restoration of endothelial nitric oxide synthase activation.
[A]: Does endothelial Mineralocorticoid Receptor mediate Diet-Induced Aortic Stiffness in Females?

[Q]: Energy needs in infants are decreased after surgery because of growth inhibition (resulting from catabolic stress metabolism), decreased insensible losses, and inactivity. Using standardized formulas that account for growth, activity, and insensible losses during this stress period can lead to overfeeding in excess of 200% of the actual measured requirement. Overfeeding during this acute injury period can result in increased CO2 production from lipogenesis. This study determined the effects of a reduced rate of mixed caloric repletion on infant energy use during the early postoperative period.', 'C-reactive protein (CRP), oxygen consumption (VO2), carbon dioxide production (VCO2), measured energy expenditure (MEE), and total urinary nitrogen (TUN) were measured serially in seven infants (average age, 78 days) during the first 72 hours after abdominal or thoracic surgery. Nonprotein respiratory quotient (RQnp), and values for oxidation of carbohydrate (Ce) and fat (Fe) were calculated. Injury severity was stratified based on serum CRP concentrations of > or = 6.0 mg/dL (high stress) or < 6.0 mg/dL (low stress). Recovery from acute stress was analyzed by comparing studies in which CRP had decreased to < or = 2.0 mg/dL (resolving stress group) with those in which CRP values were greater than 2.0 mg/dL (acute stress group).', 'Average total caloric intake (64.56 +/- 18.51 kcal/kg/d; approximately 50% of predicted energy requirement) exceeded average MEE (42.90 +/- 9.98 kcal/kg/d) by approximately 50%. Average TUN was 0.18 +/- 0.07 g/kg/d (high stress 0.2 +/- 0.05 versus low stress 0.16 +/- 0.09 g/kg/d). Average RQnp was 1.05 +/- 0.13 and average Ce was 37.28 +/- 16.86 kcal/kg/d. The average calculated Fe was 0.0 +/- 12.27 kcal/kg/d, reflecting approximately equal amounts of fat oxidized compared with fat generated from excess glucose (lipogenesis). When individual studies were analyzed at a CRP cutpoint of 2.0 mg/dL, overfeeding (RQ > 1.0) was significantly less likely in the resolving (2/6 studies, 33.4%) versus acute stress (9/13 studies, 69.2%, Z test P < .001) group. Five of seven (5/7) patients (9/19 individual studies) had negative Fe values (average -9.89 +/- 10.02) reflecting net lipogenesis. The RQnp for these nine studies was 1.14 +/- 0.11 versus 0.97 +/- 0.09 for the remaining 10, and this difference was significant (P < .01). A significant correlation existed between carbohydrate intake and VCO2 (Pearson r = .6951, P < .01). In addition, there was a good correlation between carbohydrate intake and VCO2 (Pearson r = .6591, P < .01). The coefficient of variation for MEE was 8.0% (low stress) versus 30.2% (high stress).
[A]: Do early postoperative alterations in infant energy use increase the risk of overfeeding?

[Q]: A large proportion of interstitial fibroblasts actually originate from tubular epithelial cells via the epithelial-to-mesenchymal transition (EMT) in renal fibrogenesis. Transforming growth factor-beta1 (TGF-beta1) is capable of initiating and completing the entire EMT course. Bone morphogenetic protein-7 (BMP-7) is a member of the TGF-beta superfamily. Recent studies indicate that BMP-7 could reverse established renal fibrosis in mice, primarily through counteracting TGF-beta1-mediated EMT. Therefore, we tested the hypothesis that BMP-7 functions by antagonizing profibrogenic events that are induced by TGF-beta1 in cultured human renal proximal tubular epithelial (HK-2) cells.', 'Cultured HK-2 cells were treated with TGF-beta1 (3 ng/mL) or a combination of TGF-beta1 and BMP-7 (100-400 ng/mL) for 48 hours. Morphological changes were assessed by phase contrast microscopy. The expression of alpha-smooth muscle actin (alpha-SMA), E-cadherin, fibronectin, collagen I and connective tissue growth factor (CTGF) was analyzed by immunofluorescence, reverse transcriptase polymerase chain reaction and Western blotting.', 'Incubation of HK-2 cells with 3 ng/mL TGF-beta1 for 48 hours induced EMT, in association with decreased E-cadherin expression, increased alpha-SMA, fibronectin, collagen I and CTGF expression, and loss of epithelial morphology. BMP-7 inhibited all these effects in a dose-dependent manner. In addition, 200 ng/mL BMP-7 reversed TGF-beta1-induced EMT, in association with reexpression of endogenous E-cadherin.
[A]:
Does bMP-7 counteract TGF-beta1-induced epithelial-to-mesenchymal transition in human renal proximal tubular epithelial cells?