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: Hyperoxia increases oxidative stress through the generation of reactive oxygen species and may therefore enhance inflammation in the lungs. The aim of this study was to investigate whether short term supplementary oxygen (28%) increases oxidative stress and inflammation in the airways by measuring 8-isoprostane and interleukin 6 (IL-6) concentrations in exhaled breath condensate.', 'Twenty three healthy subjects (12 men, mean (SD) age 48 (7) years) and 23 patients with chronic obstructive pulmonary disease (COPD; 15 men, mean (SD) age 56 (5) years) were studied. 8-isoprostane and IL-6 concentrations were measured by immunoassay.', 'Increased concentrations of 8-isoprostane and IL-6 were found in all subjects after breathing 28% oxygen for 1 hour. In healthy subjects the concentrations of 8-isoprostane and IL-6 were 10.9 (2.9) pg/ml and 4.9 (0.8) pg/ml, respectively, compared with baseline concentrations of 6.1 (1.3) pg/ml and 2.9 (0.6) pg/ml, and in patients with COPD the concentrations were 27.9 (3.1) pg/ml and 8.3 (1.2) pg/ml), respectively, compared with baseline concentrations of 18.9 (3.6) pg/ml and 6.3 (0.6) pg/ml. By contrast, breathing air through the same face mask for 1 hour had no significant effects on 8-isoprostane or IL-6 concentrations in normal subjects or those with COPD.\Question: Does supplementary oxygen in healthy subjects and those with COPD increase oxidative stress and airway inflammation?
[A]: These findings suggest that short term supplementary oxygen may enhance oxidative stress and inflammation in the airways. Whether this happens with long term oxygen therapy needs to be determined.


[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 mean\u2009±\u2009SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey's post hoc test.", 'Creatinine clearance (μL/min) was similar between C57 (171\u2009±\u200917) and ApoE (140\u2009±\u200926) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112\u2009±\u20098, ~\u2009-\u200935%, p\u2009<\u20090.05) and ApoE (61\u2009±\u200910, ~\u2009-\u200956%, p\u2009<\u20090.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73\u2009±\u20097; OVX: 73\u2009±\u20098, p\u2009<\u20090.05) when compared to C57 animals (Sham: 49\u2009±\u20093; OVX: 60\u2009±\u20094), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1\u2009±\u20095.7; OVX: 33.7\u2009±\u20094.7) and ApoE sham animals (26.4\u2009±\u20093.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6\u2009±\u20095.8, p\u2009<\u20090.05). 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: 9.2\u2009±\u20090.4; C57 OVX: 22.9\u2009±\u20091.0; ApoE Sham: 13.9\u2009±\u20090.7; ApoE OVX: 34.0\u2009±\u20091.4 au x 103, p\u2009<\u20090.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0\u2009±\u20090; C57 OVX: 0\u2009±\u20090; ApoE Sham: 6.8\u2009±\u20091.6; ApoE OVX: 5.2\u2009±\u20090.8% x 10-2, p\u2009<\u20090.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78\u2009±\u20090.04; ApoE: 0.81\u2009±\u20090.04 au, p\u2009<\u20090.05) when compared to sham animals (C57:1.00\u2009±\u20090.04; ApoE: 1.03\u2009±\u20090.03 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.


[Q]: Context: Agonism of alpha-adrenoreceptors has a powerful anesthetic result mediated, in part, by effects on the spinal cord. Alpha-adrenoreceptor agonists (e.g., dexmedetomidine) can decrease the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetics (e.g., halothane) to zero, with an apparently additive interaction between halothane and dexmedetomidine. We tested whether the capacity of the inhaled anesthetic isoflurane to produce immobility in the face of noxious stimulation resulted from agonism of alpha-adrenoreceptors. MAC (the concentration required to eliminate movement in response to a noxious stimulus in 50% of subjects) of isoflurane was determined before and after intraperitoneal administration of the alpha-adrenoreceptor antagonists yohimbine and atipamezole. The doses of yohimbine and atipamezole equaled or exceeded those that reverse the ability of agonism of alpha-adrenoreceptors to decrease MAC. Smaller doses of yohimbine or atipamezole slightly increased (by 10%) the MAC of isoflurane, an increase we interpret as the result of blockade of a small amount of tonically active alpha-adrenoreceptor activity. Doses five-fold larger did not change MAC. Doses 10-fold larger decreased MAC. We conclude that alpha-adrenoreceptors do not or minimally mediate the capacity of inhaled anesthetics to produce immobility.\Question: Do alpha-2 adrenoreceptors probably mediate the immobility produced by inhaled anesthetics?
[A]:
Although stimulation (agonism) of alpha-2 adrenoreceptors can decrease the inhaled anesthetic concentration required to produce immobility in the face of noxious stimulation, blockade of alpha-2 adrenoreceptors minimally affects the concentration. Thus, augmentation of the effect of alpha-2 adrenoreceptors is not an appreciable part of the mechanism whereby inhaled anesthetics produce immobility.