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.

To describe the variability in rheumatology visits and referrals to other medical specialties of patients with spondyloarthritis (SpA) and to explore factors that may influence such variability.', 'Nation-wide cross-sectional study performed in 2009-2010. Randomly selected records of patients with a diagnosis of SpA and at least one visit to a rheumatology unit within the previous 2\xa0years were audited. The rates of rheumatology visits and of referrals to other medical specialties were estimated-total and between centres-in the study period. Multilevel regression was used to analyse factors associated with variability and to adjust for clinical and patient characteristics.', "1168 patients' records (45 centres) were reviewed, mainly ankylosing spondylitis (55.2\xa0%) and psoriatic arthritis (22.2\xa0%). The patients had incurred in 5908 visits to rheumatology clinics (rate 254 per 100 patient-years), 4307 visits to other medical specialties (19.6\xa0% were referrals from rheumatology), and 775 visits to specialised nurse clinics. An adjusted variability in frequenting rheumatology clinics of 15.7\xa0% between centres was observed. This was partially explained by the number of faculties and trainees. The adjusted intercentre variability for referrals to other specialties was 12.3\xa0%, and it was associated with urban settings, number of procedures, and existence of SpA dedicated clinics; the probability of a patient with SpA of being referred to other specialist may increase up to 25\xa0% depending on the treating centre.
Do centre characteristics determine ambulatory care and referrals in patients with spondyloarthritis?

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?

To investigate whether cyclooxygenase-2 (COX-2) and heme oxygenase-1 (HO-1) are involved in the bradykinin-induced delayed protection.', 'Cardiac contractility, lactate dehydrogenase (LDH) and infarct area were analyzed in isolated rat hearts undergoing ischemia-reperfusion injury induced by Langendorff method.', 'Conscious rats received bradykinin (40 microg/kg), and the isolated hearts were subjected to 30 min of regional ischemia and 120 min of reperfusion 24 h later. Bradykinin pretreatment would improve post-ischemic performance, and reduced the release of LDH and infarct size. COX-2 inhibitor celecoxib (3 mg/kg) abolished bradykinin-induced protection, leading to poorer myocardial performance, release of more LDH and larger infarct sizes. Administration of HO-1 inhibitor ZnPP IX(20 microg/kg) before bradykinin partially abrogated the delayed protection. Pretreatment with the mitochondrial ATP sensitive potassium channel(mitoK(ATP) antagonist 5-HD before or 24 h after bradykinin administration also abolished the effect of protection.

Are [ COX-2 and HO-1 involved in the delayed preconditioning elicited by bradykinin in rat hearts ]?