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.

Example Input: Context: Chronic inflammation in periodontal disease is associated with increased plasminogen activation and elevated levels of chemokines. It is unknown whether chemokines can regulate the activation of plasminogen via modulation of plasminogen activators (PA) and the corresponding plasminogen activator inhibitors (PAI) in periodontal tissue.', 'To establish a link between chemokines and activation of plasminogen, human periodontal ligament fibroblasts (PDL) and gingival fibroblasts (GF) were incubated with IL-8, monocyte chemoattractant protein-1, macrophage inflammatory protein-1alpha, and platelet factor-4, either alone or in the presence of the inflammatory mediators TGF-beta and IL-1. The potential of the cell lysates to activate plasminogen was based on kinetic studies with the substrate casein. Casein zymography was performed to determine the molecular sizes of the PA. Total PAI-1 in the cell-conditioned medium was quantified by immunoassay.', 'We report that the chemokines did not affect activation of plasminogen by PDL and GF. Even in the presence of TGF-beta which suppressed, and IL-1 which stimulated plasminogen activation, the chemokines had no direct effect. Inhibition of PA and plasmin, but not of matrix metalloproteinases and cysteine proteinases prevented caseinolysis. The plasminogen activation capacity of the cell lysates was represented by a single band with features of uPA. The immunoassay showed that the release of PAI-1 in PDL and GF remained unaffected by the chemokines, also when stimulated with TGF-beta.\Question: Is plasminogen activation by fibroblasts from periodontal ligament and gingiva directly affected by chemokines in vitro?
Example Output: These results suggest that plasminogen activation by PDL and GF is not directly affected by the chemokines even in the presence of the inflammatory mediators TGF-beta and IL-1.

Example Input: Context: Intrathecal adenosine is antinociceptive under conditions of central sensitization, but not in response to acute stimuli in normals. The reasons for this selective circumstance of action remain unclear, but some evidence links adenosine's antinociceptive effects to release of norepinephrine by terminals in the spinal cord. The purpose of this study was to test whether spinal adenosine induces norepinephrine release selectively in settings of hypersensitivity.", 'Rats randomly assigned to spinal nerve ligation, sham operation, or no operation were anesthetized. A microdialysis fiber was implanted in the spinal cord dorsal horn at the L5-L6 level and perfused with artificial cerebrospinal fluid. After washout and a baseline sample period, adenosine at various concentrations was infused through the fiber for 150 min, and samples were collected every 15 min.', "In ligated, but not in sham or normal animals, adenosine perfusion increased norepinephrine in spinal cord microdialysates in a concentration-dependent manner. The effects of adenosine plateaued after 75 min and remained stable until the end of the experiment. Intravenous injection of selective adenosine A1 and A2 receptor antagonists revealed that adenosine's effect on spinal norepinephrine release was A1 receptor mediated.\Question: Does intraspinal adenosine induce spinal cord norepinephrine release in spinal nerve-ligated rats but not in normal or sham controls?
Example Output: This is the first study to provide direct evidence that adenosine is able to release norepinephrine in spinal cord dorsal horns in living animals. However, this effect was only seen in animals after spinal nerve ligation. These data are consistent with behavioral studies demonstrating that adenosine's antinociceptive effects in rats after spinal nerve ligation is totally dependent on intact spinal noradrenergic terminals and can be blocked by spinal alpha 2-adrenergic receptor antagonists.

Example Input: Context: Ideally, preoxygenation is performed using a tight fitting mask either by breathing normally for three to five minutes or with four to eight vital capacity (VC) breaths in 0.5 to one minute, but in practice leaks are frequent and sometimes unavoidable. This study was designed to determine which breathing method provided the best oxygenation in the presence of leak.', 'Twenty volunteers were instructed to breathe from a circle circuit supplied with 6 L x min(-1) of fresh oxygen. Each subject was tested under four situations selected in random order: 1) normal breathing for three minutes without leak; 2) normal breathing for three minutes with a leak; 3) four VCs in 30 sec without a leak; and 4) four VCs in 30 sec with a leak. The leak was created by a piece of size 18 French nasogastric tube, 5 cm long, taped under the face mask. Inspired and expired O(2) and CO(2) were sampled at the nostrils.', 'In the absence of a leak, the end-tidal oxygen fraction (F(EO(2)) was greater after three minutes of tidal breathing (89 +/- 3%; mean +/- SD) in comparison with the response to four VCs (76 +/- 7%; P < 0.001). Introduction of a leak decreased the F(EO(2)) significantly (P < 0.001). With a leak, the F(EO(2)) was similar with normal breathing (61 +/- 8%) and after four VCs (59 +/- 11%).\Question: Is when a leak unavoidable , preoxygenation is equally ineffective with vital capacity or tidal volume breathing?
Example Output:
Preoxygenation with tidal volume breathing for three minutes yields higher F(EO(2)) in comparison to four VCs. If a small leak (4 mm internal diameter) is introduced, the F(EO(2)) decreases significantly with both breathing methods to approximately 60%.