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.

Restoration of posterior condylar offset during TKA is believed to be important to improving knee kinematics, maximizing ROM, and minimizing flexion instability. However, controversy exists regarding whether there are important anatomic differences between sexes and whether a unisex knee prosthesis can restore the anatomy of knees in males and females.', 'The purposes of our study were to determine if sex differences exist in (1) absolute posterior condylar offset size, (2) relative posterior condylar offset size in relation to total condylar height, and (3) posterior condylar articular cartilage thickness.', 'We identified 100 patients (50 men and 50 women) without a history of arthritis, deformity, dysplasia, osteochondral defect, fracture, or surgery about the knee who had MRI of the knee performed. All MR images were ordered by primary care medical physicians for evaluation of nonspecific knee pain. Using a previously described three-dimensional MRI protocol, we measured posterior condylar offset, total condylar height, and articular cartilage thickness at the medial and lateral femoral condyles and compared values to evaluate for potential sex differences. We performed an a priori power calculation using a 2-mm posterior condylar offset difference as the minimum clinically important difference; with 2n = 100, our power to detect such a difference was 99.8%.', 'Compared with females, males had greater medial posterior condylar offset (30 mm [95% CI, 29.3-30.7 mm; SD, 2.5 mm] vs 28 mm [95% CI, 27.0-28.5 mm; SD, 2.7 mm]), lateral posterior condylar offset (27 mm [95% CI, 26.2-27.3 mm; SD, 2.0 mm] vs 25 mm [95% CI, 24.2-25.4 mm; SD, 2.0 mm]), medial condylar height (63 mm [SD, 3.2 mm] vs 57 mm [SD, 4.4 mm]), and lateral condylar height (71 mm [SD, 5.2 mm] vs 65 mm [SD: 4.0 mm]) (all p values < 0.001). However, the mean ratio of medial posterior condylar offset to medial condylar height (0.48 [SD, 0.04] vs 0.49 [SD, 0.05]) and the mean ratio of lateral posterior condylar offset to lateral condylar height (0.38 [SD, 0.05] vs 0.38 [SD, 0.03]) were not different between sexes (p = 0.08 and p = 0.8, respectively). There also was no sex difference in mean articular cartilage thickness at either condyle (medial condyle: 2.7 mm [SD, 0.5 mm] vs 2.5 mm [SD, 0.7 mm]; lateral condyle: 2.6 mm [SD, 0.6 mm] vs 2.5 mm [SD, 0.8 mm]) (both p values ≥ 0.1).
Do no sex differences exist in posterior condylar offsets of the knee?

To evaluate whether the relationship between dietary composition and plasma lipid levels is genetically determined.', 'We have evaluated the influence of common apolipoprotein A5 (APOA5) variants (T-1131 > C, Ser19 > Trp and Val153 > Met) on plasma lipid concentrations in 117 males for whom dietary composition markedly changed and total cholesterol decreased (from 6.21 +/- 1.31 mmol/L in 1988 to 5.43 +/- 1.06 mmol/L in 1996) over an 8 year follow-up study.', 'APOA5 T-1131 > C and Val153 > Met variants did not influence the change in lipid measures over time. In Ser/Ser19 homozygotes, the plasma cholesterol was relatively stable over the years (6.1 +/- 1.2 mmol/L in 1988 and 5.6 +/- 1.0 mmol/L in 1996, -8%, P < 0.01). In contrast, in the Trp19 carriers, the decrease of the plasma cholesterol was more than 20% (6.5 +/- 1.6 mmol/L in 1988 and 5.1 +/- 1.0 mmol/L in 1996) (P < 0.001). The difference of the changes is significant (8% vs. 20%, P < 0.005). Changes in other analyzed lipid parameters have not been significantly associated with APOA5 variants.
Does aPOA5 variant Ser19Trp influence a decrease of the total cholesterol in a male 8 year cohort?

Regular physical activity is an effective non-pharmacological therapy for prevention and control of hypertension. However, the underlying mechanisms are not fully understood. Accumulating evidence shows that the elevated vascular tone in hypertension is a consequence of the 'ion channel remodelling' that occurs during sustained high BP. The present study investigated the effects of aerobic exercise on the electrical remodelling of L-type Ca(2+) (Cav 1.2) and large-conductance Ca(2+) -activated K(+) (KCa 1.1) channels in mesenteric arteries (MAs) from spontaneously hypertensive rats (SHRs).", 'SHRs and normotensive (Wistar-Kyoto) rats were subjected to aerobic training or kept sedentary, and vascular mechanical and functional properties were evaluated.', 'Exercise did not affect the heart weight, but reduced the heart rate and body weight in SHR. In mesenteric arterial myocytes, exercise normalized the increased Cav 1.2 and KCa 1.1 current density in SHRs. Exercise also ameliorated the increased open probability and mean open time of the single KCa 1.1 channel in hypertension. The isometric contraction study revealed that both nifedipine (Cav 1.2 channel blocker) and NS11021 (KCa 1.1 channel activator) induced concentration-dependent vasorelaxation in MAs precontracted with noradrenaline. Exercise normalized the increased sensitivity of tissues to nifedipine and NS11021 in SHR. Furthermore, protein expression of the Cav 1.2 α1C -subunit together with the KCa 1.1 α- and β1-subunit was significantly increased in SHRs; and exercise ameliorated these molecular alterations in hypertension.

Does chronic exercise normalize changes in Cav 1.2 and KCa 1.1 channels in mesenteric arteries from spontaneously hypertensive rats?