Given a passage with a context and an answer, 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.

[EX Q]: Context: We analyzed the involvement of thromboxane (TX) A2/prostaglandin (PG) H2 (TP) receptor in ischemia-induced neovascularization in mice.', 'Unilateral hindlimb ischemia was induced by right femoral artery ligature in male C57BL/6J mice (n=7 per group). Animals were then treated with or without TP receptor antagonist (S18886, 5 or 10 mg/kg per day; ramatroban, 10 mg/kg per day) or aspirin (30 mg/kg per day) in drinking water for 21 days. Hindlimb ischemia raised plasma level of TXB2, the stable metabolite of TXA2, by 4.7-fold. This increase was blocked by aspirin treatment whereas S18886 (5 or 10 mg/kg per day) had no effect. However, neither S 18886 nor aspirin affected postischemic neovascularization. We next assessed the putative involvement of TXA2 signaling in angiotensin II (Ang II) proangiogenic pathway. Ang II (0.3 mg/kg per day) enhanced TXB2 plasma levels by 2.6-fold over that of control (P<0.01). Ang II-induced TXB2 upregulation was reduced by cotreatment with Ang II type I receptor antagonist (candesartan, 20 mg/kg per day). Angiographic score, capillary number, and foot perfusion were improved by 1.7-, 1.7-, and 1.4-fold, respectively, in Ang II-treated mice compared with controls (P<0.05). Ang II proangiogenic effect was associated with a 1.6-fold increase in VEGF-A protein content (P<0.05) and a 1.4-fold increase in the number of Mac-3-positive cells (ie, macrophages) in ischemic areas (P<0.05). Interestingly, treatments with TP receptor antagonists or aspirin hampered the proangiogenic effects of Ang II.
Answer: Endogenous activation of TXA2 receptor by eicosanoids did not modulate spontaneous neovascularization in the setting of ischemia. Conversely, TXA2 signaling is involved in Ang II-induced AT1-dependent vessel growth.
[EX A]: Does thromboxane A2/prostaglandin H2 receptor activation mediate angiotensin II-induced postischemic neovascularization?

[EX Q]: Context: Smoking cessation rapidly reduces cardiovascular risk. The pathophysiological mechanisms involved are still being debated. We measured structural and functional arterial wall properties of the femoral and carotid arteries after smoking cessation to investigate their possible role in cardiovascular risk reduction.', 'Out of 127 smokers, 33 proved to stop smoking for two years. They were compared with 50 nonsmokers and 55 persistent smokers in a prospective study. Cross-sectional compliance and distensibility coefficients as well as intima-media thickness of both carotid arteries and of the right common femoral artery were measured ultrasonographically at baseline and 3, 6, 12 and 24 months after smoking cessation. The nonsmoking and persistent smokers group were measured twice at an interval of 24 months.', 'Persistent smoking and two years of smoking cessation did not affect cross-sectional compliance and distensibility coefficients. Although at baseline intimal-medial layers were thicker in smokers, the change over time in intima-media thickness did not differ significantly between all three groups.
Answer: Two years of smoking cessation was not accompanied by a slower progression or a regression in intima-media thickness nor by an improved cross-sectional compliance or distensiblity coefficient. Nevertheless, smoking cessation should be recommended as it reduces cardiovascular risk rapidly after smoking cessation.
[EX A]: Does two years of smoking cessation reduce arterial wall thickness and stiffness?

[EX Q]: Context: This study investigated whether anxiety, fear of pain, or pain catastrophizing were predictive of pain-related outcomes after induced delayed onset muscle soreness (DOMS) at the shoulder.', 'Healthy participants (19 males and 23 females) were eligible for participation if they had (a) no history of neck or shoulder pain, (b) no sensory or motor impairments of the upper-extremity, (c) not regularly participating in upper-extremity weight training, (d) not currently or regularly taking pain medication, and (e) no history of upper-extremity surgery. Participants completed self-report measures for fear of pain, pain catastrophizing, and anxiety. Then, participants underwent a standard fatigue protocol to induce DOMS in the shoulder external rotator muscles. Participants were reassessed 24 hours after DOMS induction on clinical and evoked pressure pain reports, muscle force production, self-report of upper-extremity disability, and kinesiophobia. Stepwise regression models considered sex, anxiety, pain intensity, fear of pain, and pain catastrophizing as outcome predictors.', 'Fear of pain alone explained 16% (P=0.008) of the variance in clinical pain and 10% (P=0.047) evoked pressure pain intensity. Clinical pain intensity alone explained 11% (P<0.031) of the variance in muscle force production. Clinical pain intensity and fear of pain explained 50% (P<0.001) of the variance in upper-extremity disability, whereas fear of pain and sex accounted for 26% (P=0.005) of the variance in kinesiophobia.
Answer: With the exception of muscle force production, fear of pain had a consistent influence on shoulder DOMS outcomes, even after controlling for pain intensity. This study suggests fear of pain may be a relevant psychologic factor to consider in clinical studies investigating the development and treatment of chronic shoulder pain.
[EX A]:
Does fear of pain influence outcomes after exercise-induced delayed onset muscle soreness at the shoulder?