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.

The objective in lung transplantation is to prolong life, but the survival effect in patients with chronic obstructive pulmonary disease (COPD) or alpha1-anti-trypsin deficiency emphysema is still unresolved. This study assesses the impact of diagnosis, single-lung transplantation (SLT) vs bilateral lung transplantation (BLT) and timing of transplantation on survival in a national cohort.', 'In 219 consecutive patients accepted onto the lung transplantation waiting list in Norway, 1990 to 2003, we assessed predictors of death: (1) on the waiting list; (2) <or=90 days after transplantation; and (3) >90 days after transplantation. For each period we used Cox regression, including age, gender, diagnosis, baseline pulmonary function tests, cardiac catheterization data, exercise capacity and transplant type, as potential predictors. Survival benefit was assessed graphically by combining adjusted survival curves after transplantation with the curve for those waiting, modeling transplantation after 6, 12 or 24 months.', 'Mean patient age was 49 years (SD 10), with 55% women. High forced expiratory volume in 1 second (FEV(1)) percentage predicted death on the waiting list. Diagnoses other than COPD/emphysema and receiving SLT were associated with death <or=90 days after transplantation. Only low forced vital capacity (FVC) percentage predicted death >90 days after transplantation. In COPD/emphysema, there was no clear survival benefit from BLT or SLT. For patients in the "Other" group, the data suggest a survival benefit from BLT.
Is lung transplantation in patients with chronic obstructive pulmonary disease in a national cohort without obvious survival benefit?

GM-CSF has broad clinical applicability as a potent myelopoietic stimulator. However, its function is not restricted to the myelopoietic system and several observations suggest that GM-CSF may interfere with the hemostatic balance. In order to assess whether GM-CSF has any influence on hemostasis, we evaluated some coagulative and fibrinolytic parameters in patients treated with GM-CSF following chemotherapy.', 'Fibrinolytic activity (FA), fibrinogen and D-dimer were evaluated before and after high-dose cyclophosphamide in 6 patients additionally treated with GM-CSF and in 5 control patients; moreover, tissue plasminogen activator (tPA) was assayed in those treated with GM-CSF. Comparative in vitro analysis was performed on cultured endothelial cells before and after exposure to GM-CSF.', 'Control patients showed a significant decrease in plasma FA after chemotherapy compared to basal values (FA/mm2: 15.6 +/- 2.1 at day + 2 and 20.8 +/- 19 at day + 4 vs. 103.8 +/- 64.2 at day 0; p < 0.005); conversely, no FA reduction was observed in GM-CSF-treated subjects. In this latter group a marked increase in tPA antigen was seen, consistent with enhanced FA. No significant changes in plasma D-dimer and fibrinogen values were detected in the two groups. tPA, urokinase-type plasminogen activator, PAI-1 and procoagulant activity were evaluated in vitro on cultured human endothelial cells and found to be unchanged following GM-CSF addition.
Is reduction of plasma fibrinolytic activity following high-dose cyclophosphamide neutralized in vivo by GM-CSF administration?

There is evidence that melatonin plays a role in the regulation of GH secretion. The aim of this study was to investigate the neuroendocrine mechanisms by which melatonin modulates GH secretion. Thus we assessed the effect of oral melatonin on the GH responses to GHRH administration and compared the effects of melatonin with those of pyridostigmine, a cholinergic agonist drug which is likely to suppress hypothalamic somatostatin release.', 'The study consisted of four protocols carried out during the afternoon hours. Study 1: oral melatonin (10 mg) or placebo were administered 60 minutes prior to GHRH (100 micrograms i.v. bolus). Study 2: GHRH (100 micrograms i.v. bolus) or placebo were administered at 0 minutes; oral melatonin or placebo were given at 60 minutes and were followed by a second GHRH stimulus (100 micrograms i.v. bolus) at 120 minutes. Study 3: placebo; oral melatonin (10 mg); oral pyridostigmine (120 mg); melatonin (10 mg) plus pyridostigmine (120 mg) were administered on separate occasions. Study 4: placebo; oral melatonin (10 mg); oral pyridostigmine (120 mg); melatonin (10 mg) plus pyridostigmine (120 mg) were administered on separate occasions 60 minutes prior to a submaximal dose (3 micrograms i.v. bolus) of GHRH.', 'Four groups of eight normal male subjects, ages 22-35 years, were randomly assigned to each protocol.', 'Growth hormone was measured by RIA at 15-minute intervals.', 'Oral melatonin administration had a weak stimulatory effect on GH basal levels. Prior melatonin administration approximately doubled the GH release induced by supramaximal (100 micrograms) or submaximal (3 micrograms) doses of GHRH. Melatonin administration restored the GH response to a second GHRH challenge, given 120 minutes after a first GHRH i.v. bolus. The GH releasing effects of pyridostigmine, either alone or followed by GHRH, were greater than those of melatonin. However, the simultaneous administration of melatonin and pyridostigmine was not followed by any further enhancement of GH release, either in the absence or in the presence of exogenous GHRH.

Does melatonin stimulate growth hormone secretion through pathways other than the growth hormone-releasing hormone?