In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: Hypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction.', "Apolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as meanSEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey's post hoc test.", 'Creatinine clearance (L/min) was similar between C57 (17117) and ApoE (14026) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (1128, ~-35%, p<0.05) and ApoE (6110, ~-56%, p<0.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 737; OVX: 738, p<0.05) when compared to C57 animals (Sham: 493; OVX: 604), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.15.7; OVX: 33.74.7) and ApoE sham animals (26.43.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.65.8, p<0.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.20.4; C57 OVX: 22.91.0; ApoE Sham: 13.90.7; ApoE OVX: 34.01.4 au x 103, p<0.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 00; C57 OVX: 00; ApoE Sham: 6.81.6; ApoE OVX: 5.20.8% x 10-2, p<0.05). Ovariectomy resulted in a similar reduction in ER- protein expression in the renal cortex (C57: 0.780.04; ApoE: 0.810.04 au, p<0.05) when compared to sham animals (C57:1.000.04; ApoE: 1.030.03 au).\Question: Do endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice?

A: Taken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women.
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Q: Context: Trauma centers are currently benchmarked on mortality outcomes alone. However, pay-for-performance measures may financially penalize centers based on complications. Our objective was to determine whether the results would be similar to the current standard method of mortality-based benchmarking if trauma centers were profiled on complications.', 'We analyzed data from the National Trauma Data Bank from 2007 to 2010. Patients 16 years or older with blunt or penetrating injuries and an Injury Severity Score (ISS) of 9 or higher were included. Risk-adjusted observed-to-expected (O/E) mortality ratios for each center were generated and used to rank each facility as high, average, or low performing. We similarly ranked facilities on O/E morbidity ratios defined as occurrence of any major complication. Concordance between hospital performance rankings was evaluated using a weighted statistic. Correlation between morbidity- and mortality-based O/E ratios was assessed using Pearson coefficients. Sensitivity analyses were performed to mitigate the competing risk of death for the morbidity analyses.', 'A total of 449,743 patients from 248 facilities were analyzed. The unadjusted morbidity and mortality rates were 10.0% and 6.9%, respectively. No correlation was found between morbidity- and mortality-based O/E ratios (r = -0.01). Only 40% of the centers had similar performance rankings for both mortality and morbidity. Of the 31 high performers for mortality, only 11 centers were also high performers for morbidity. A total of 78 centers were ranked as average, and 11 ranked as low performers on both outcomes. Comparison of hospital performance status using mortality and morbidity outcomes demonstrated poor concordance (weighted = 0.03, p = 0.22).\Question: Does benchmarking trauma centers on mortality alone reflect quality of care : implications for pay-for-performance?

A: Mortality-based external benchmarking does not identify centers with high complication rates. This creates a dichotomy between current trauma center profiling standards and measures used for pay-for-performance. A benchmarking mechanism that reflects all measures of quality is needed.
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Q: Context: To investigate the effect of premenopausal obesity on circulating levels of estradiol, estrone, free testosterone, androstenedione, DHEAS, and immuno- and bioactive FSH and LH.', 'University clinic.', 'Premenopausal hirsute women, four obese and four nonobese, received leuprolide acetate depot [LD in monthly injections (7.5 mg, i.m.)] until estradiol levels decreased to menopausal values; single monthly injections of 15 and then 22.5 mg LD were given if estradiol remained higher than menopausal after 3 months.', 'Estradiol levels of nonobese women reached menopausal values with the 7.5-mg dose, and those of obese women were not significantly reduced with any LD dose. Estrone declined to menopausal levels with 7.5 mg LD, while free testosterone and androstenedione were diminished with 7.5 mg, but not further with 15 or 22.5 mg. Bioactive LH and the bioactive/immunoactive LH ratio were maximally suppressed with 7.5 mg LD; however, LD did not change bioactive FSH levels or the bioactive/immunoactive FSH ratio. These findings were not related to adiposity.\Question: Does obesity affect circulating estradiol levels of premenopausal hirsute women receiving leuprolide acetate depot?

A:
Premenopausal obesity affects circulating estradiol levels of hirsute women receiving LD. The effect does not reflect weight-related differences in circulating levels of androgens or bioactive gonadotropins. Premenopausal adiposity in hirsute women may influence the estrogenic milieu associated with desensitization to GnRH.
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