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: The apolipoprotein B (apoB)/apoA-I ratio represents the balance of proatherogenic and antiatherogenic lipoproteins. The purpose of this study was to determine whether the apoB/apoA-I ratio was superior to any of the cholesterol ratios - total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C), low-density lipoprotein cholesterol (LDL-C)/HDL-C and non-HDL-C/HDL-C - in predicting the risk of coronary disease. Moreover, we examined whether any lipids, lipoproteins or cholesterol ratios add significant predictive information beyond that provided by the apoB/apoA-I ratio.', 'Plasma lipids, lipoproteins, apoB, and apoA-I were measured in 69,030 men and 57,168 women above 40 years of age. After a mean follow-up of 98 months, 1183 men and 560 women had died from a myocardial infarction in this prospective apolipoprotein-related mortality risk (AMORIS) study.', 'High apoB and a high apoB/apoA-I ratio were strongly related to increased coronary risk, while high apoA-I was inversely related to risk. The apoB/apoA-I ratio was superior to any of the cholesterol ratios in predicting risk. This advantage was most pronounced in subjects with LDL-C levels <3.6 mmol/l. Addition of lipids, lipoproteins or any cholesterol ratio to apoB/apoA-I in risk models did not further improve the strong predictive value of apoB/apoA-I.

A: Is the apoB/apoA-I ratio better than the cholesterol ratios to estimate the balance between plasma proatherogenic and antiatherogenic lipoproteins and to predict coronary risk?
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Q: Both diet quality (DQ) and physical activity (PA) have been shown to play a role in the prevention of functional capacity (FC) decline. Because older adults (OA) with T2D are at a higher risk of FC decline compared to their non-diabetic counterparts, our aim was to determine if DQ alone, or combined with PA is associated with FC decline in OA with T2D over a 3-year follow-up in a secondary analysis of the NuAge cohort.', "In 159 OA with T2D (mean age=75 years), FC change was calculated as the difference in FC scores at T1 and T4 measured by the SMAF (Système de Mesure de l'Autonomie Fonctionnelle). Baseline DQ was calculated from three non-consecutive 24-h dietary recalls collected at T1 using the validated Canadian Healthy Eating Index (C-HEI). PA change was calculated from Physical Activity Scale for the Elderly (PASE) as T4-T1. Associations were evaluated between FC decline and four combinations of variables: C-HEI score < or ≥70 with PASE change < or > median and analyzed by GLM while controlling for covariates.", 'Neither DQ alone nor DQ combined with PA change were associated with FC decline over follow-up.

A: Is decline in functional capacity unaffected by diet quality alone or in combination with physical activity among generally healthy older adults with T2D from the NuAge cohort?
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Q: In the past years the interaction of GH and 11beta hydroxysteroid dehydrogenase (11betaHSD) in the pathogenesis of central obesity has been suggested.', 'We studied the effects of 9 months of GH treatment on 11betaHSD activity and its relationship with body composition and insulin sensitivity in 30 men with abdominal obesity, aged 48-66 years, in a randomised, double-blind, placebo-controlled trial.', 'Urinary steroid profile was used to estimate 11betaHSD type 1 and 2 (11betaHSD1 and 11betaHSD2) activities. Abdominal s.c. and visceral adipose tissues were measured using computed tomography. Glucose disposal rate (GDR) obtained during a euglycaemic-hyperinsulinaemic glucose clamp was used to assess insulin sensitivity.', 'In the GH-treated group the 11betaHSD1 activity decreased transiently after 6 weeks (P < 0.01) whereas 11betaHSD2 increased after 9 months of treatment (P < 0.05). Between 6 weeks and 9 months, GDR increased and visceral fat mass decreased. Changes in 11betaHSD1 correlated with changes in visceral fat mass between baseline and 6 weeks. There were no significant correlations between 11betaHSD1 and 11betaHSD 2 and changes in GDR.

A:
Is gH effect on enzyme activity of 11betaHSD in abdominal obesity dependent on treatment duration?
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