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.

Context: Ischemic postconditioning protects the reperfused heart from infarction, and this protection is dependent on the occupancy of adenosine receptors. We further explored the role of adenosine receptors in this salvage.', 'In situ rabbit hearts underwent 30 min of regional ischemia and 3 h of reperfusion, and postconditioning was effected with four cycles of 30-s reperfusion/30-s coronary artery occlusion at the end of ischemia.', "Postconditioning reduced infarct size from 40.2+/-3.4% of the risk zone in untreated hearts to 15.5+/-2.5%. Protection by postconditioning was blocked by either the non-selective adenosine receptor blocker 8-p-(sulfophenyl)theophylline or the A2b-selective antagonist MRS 1754, injected intravenously 5 min before reperfusion. The protein kinase C (PKC) antagonist chelerythrine also aborted postconditioning's salvage, indicating a PKC-dependent mechanism. Neither the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine nor the A2a-selective antagonist 8-(13-chlorostyryl)caffeine had an effect on protection. The non-selective but A2b-potent adenosine agonist 5'-(N-ethylcarboxamido)adenosine (NECA) infused from 5 min before to 1h after reperfusion mimicked postconditioning's effect on infarct size (17.2+/-2.7% infarction) and MRS 1754 blocked the NECA-induced cardioprotection, confirming that A2b activation was protective. The PKC activator phorbol 12-myristate 13-acetate delivered just before reperfusion also duplicated the protective effect of postconditioning (16.3+/-4.1% infarction), and co-administration of the PKC antagonist chelerythrine aborted PMA's protection, confirming that the protection was the result of PKC activation. NECA's protective effect was not affected by chelerythrine, but rather MRS 1754 blocked PMA's salutary effect (42.8+/-1.0% infarction), suggesting that the A2b receptor's effect is under control of PKC. Finally, wortmannin, a blocker of phosphatidylinositol 3-kinase, also abrogated protection by PMA.\Question: Does postconditioning protect rabbit hearts through a protein kinase C-adenosine A2b receptor cascade?
Salvage of ischemic myocardium by postconditioning is dependent on activation of A2b receptors, which in turn depends on activation of PKC. It is still unclear why PKC activation is required to make the heart's adenosine become protective.

Context: To investigate the clinical logistics of laboratory routines at primary health care centres (PHCs).', 'Prospective registration was carried out for each PHC using questionnaires during 2-week intervals between the end of November 2001 and mid-January 2002. The study included 9 PHCs in the county of Ostergötland and 4 in the county of Jönköping, Sweden, with different numbers of blood tests analysed using point-of-care testing (POCT). Data for B-glucose, HbA1c, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), thyroid-stimulating hormone (TSH), T4, cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides were collected. Main outcome measures were median time from sampling to available test result (TATa) and median time from sampling to clinical decision (TATd), and the proportion of patients informed of the outcome of the blood test in question during the sampling occasion.', 'A total of 3542 samples were collected. The median TATa showed that B-glucose, ESR and CRP were immediately analysed at all 13 PHCs. For the other tests, TATa varied from immediately to about two days. The median TATd varied from immediately to about a week. When POCT was used, 30% of the patients were informed about the outcome of the test during the sampling occasion.\Question: Does point-of-care testing have a limited effect on time to clinical decision in primary health care?
POCT has a limited effect on the clinical logistics in PHCs.

Context: This research note discusses a common misconception in speech science and speech-language pathology textbooks that rib torque (i.e., rotational stress) assists resting tidal expiration and conversational speech production.', 'The nature of this misconception is considered.\Question: Does rib torque assist resting tidal expiration or most conversational speech expiration?

An alternate conceptualization is offered that is consistent with knowledge from respiratory biomechanics.