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.

Ex Input:
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?

Ex Output:
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.


Ex Input:
Context: Animals control the speed of motion to meet behavioral demands. Yet, the underlying neuronal mechanisms remain poorly understood. Here we show that a class of segmentally arrayed local interneurons (period-positive median segmental interneurons, or PMSIs) regulates the speed of peristaltic locomotion in Drosophila larvae.', 'PMSIs formed glutamatergic synapses on motor neurons and, when optogenetically activated, inhibited motor activity, indicating that they are inhibitory premotor interneurons. Calcium imaging showed that PMSIs are rhythmically active during peristalsis with a short time delay in relation to motor neurons. Optogenetic silencing of these neurons elongated the duration of motor bursting and greatly reduced the speed of larval locomotion.\Question: Does a group of segmental premotor interneurons regulate the speed of axial locomotion in Drosophila larvae?

Ex Output:
Our results suggest that PMSIs control the speed of axial locomotion by limiting, via inhibition, the duration of motor outputs in each segment. Similar mechanisms are found in the regulation of mammalian limb locomotion, suggesting that common strategies may be used to control the speed of animal movements in a diversity of species.


Ex Input:
Context: Tissue and organic venous congestion is a common pathophysiologic phenomenon. However, it is unclear whether venous congestion induces small-intestinal mucosal apoptosis. The aim of this study was to investigate whether venous congestion, or congestion followed by re-outflow, induced small-intestinal mucosal apoptosis, and whether tumor necrosis factor-alpha is involved in this apoptosis.', 'Small-intestinal venous congestion was induced in rats by occlusion of the superior mesenteric vein with a micro-bulldog clamp. At the end of the congestive period, the clamp was released to facilitate congestion followed by re-outflow. The rats were injected with a neutral anti-tumor necrosis factor-alpha antibody (0.15 mg/kg) via the jugular vein for 30 min before venous congestion or congestion followed by re-outflow. Intestinal mucosal apoptosis was evaluated and tumor necrosis factor-alpha was assayed. The amounts of caspase-8, caspase-3, and cytochrome c were determined by Western blot analysis.', 'Our results showed that venous congestion and congestion followed by re-outflow significantly increased mucosal apoptosis, the amount of mucosal tumor necrosis factor-alpha, and the levels of caspase-8 cleavage and caspase-3 activation, but did not induce cytochrome c release from mitochondria to the cytosol. Pretreatment with an anti-tumor necrosis factor-alpha antibody significantly reduced mucosal apoptosis after intestinal congestion or congestion followed by re-outflow.\Question: Does venous congestion induce mucosal apoptosis via tumor necrosis factor-alpha-mediated cell death in the rat small intestine?

Ex Output:

The present results support the view that venous congestion and congestion followed by re-outflow induce mucosal apoptosis in the rat small intestine, and show that the apoptosis occurs partly via tumor necrosis factor-alpha-mediated cell death.