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 Q]: Context: Accumulating evidence has indicated that inflammation may act as a potential mechanism underlying post-operative cognitive dysfunction (POCD). High-mobility group box 1 (HMGB1), as a known late mediator of inflammation, is involved in the development of post-operative complications. Thus, we sought to determine the role of HMGB1 in reflecting POCD following major gastrointestinal surgery.', 'Fifty-three elderly patients undergoing gastrointestinal surgery were recruited, and 50 patients completed the study. Serum HMGB1 and interleukin (IL)-6 levels were measured pre-operatively and at 6 h, day 1 and day 3 post-operatively. Neuropsychological tests were administered before and 1 week after surgery. POCD was determined using a Z score 1.96.', 'Seventeen (34%, 17/50) patients developed POCD at 1 week. The POCD group had higher serum HMGB1 levels at day 1 (12.15 3.12 vs. 9.91 3.15 ng/ml, P = 0.021) and day 3 (11.04 2.88 vs. 8.52 3.31 ng/ml, P = 0.011). IL-6 levels at 6 h (51.18 15.22 vs. 39.20 14.32 pg/ml, P = 0.009) and day 1 (41.59 11.08 vs. 33.81 11.42 pg/ml, P = 0.026) were significantly higher in POCD patients. Serum values of IL-6 at 6 h, HMGB1 at day 1 and levels of education showed positive correlations with Z scores. HMGB1 at day 3 and IL-6 at 6 h were independent risk factors.\Question: Does serum high-mobility group box 1 protein correlate with cognitive decline after gastrointestinal surgery?
[EX A]: Serum HMGB1 and IL-6 levels increase significantly after major gastrointestinal surgery in elderly patients and such elevations are associated with the occurrence of cognitive decline after surgery.

[EX Q]: Context: The pulmonary endothelium plays an important role in the metabolism of the amino acid arginine, the exclusive precursor molecule for nitric oxide (NO). Despite decreased circulating arginine levels, endothelial NO production is elevated during endotoxemia. However, the regulation of pulmonary artery endothelial arginine transport has not been studied. We hypothesized that endotoxin stimulates carrier-mediated arginine transport by the pulmonary endothelium.', 'The relative contributions of the various transport systems to total arginine transport by porcine pulmonary artery endothelial cells (PAECs) was determined by assaying the uptake of 3H-L-arginine in the presence or absence of Na+. PAECs were then incubated with various concentrations of Escherichia coli endotoxin, and y(+)-mediated arginine transport was measured at different time points thereafter. Kinetic studies were performed over a range of arginine concentrations to determine changes in transport affinity and maximum rate of metabolism. To address the role of RNA and protein synthesis in the increased transport, uptake was measured after exposure of cells to the transcriptional inhibitor actinomycin D and the protein synthesis inhibitor cycloheximide.', 'Most (75%) of arginine transport by PAECs was mediated by the high-affinity Na(+)-independent transport system y+. Endotoxin stimulated y(+)-mediated arginine transport by PAECs twofold to fivefold, a response that was time and dose dependent. The accelerated transport was detectable within 2 hours and maximal at 12 hours. Kinetic studies revealed that the accelerated arginine transport was the result of a 68% increase in the maximal transport velocity (1519 +/- 65 pmol/mg protein/30 sec in endotoxin-treated cells vs 903 +/- 96 in control cells; p < 0.01) without a change in transport affinity. The endotoxin-mediated increase in arginine uptake was abrogated by actinomycin D and cycloheximide.\Question: Does endotoxin stimulate arginine transport in pulmonary artery endothelial cells?
[EX A]: Endotoxin stimulates Na(+)-independent arginine transport by PAECs through a process that requires de novo RNA and protein synthesis, possibly of the transporter itself. This response may be designed to support arginine-dependent biosynthetic pathways in the lung during septic states.

[EX Q]: Context: Natural history of paediatric-onset ulcerative proctitis (UP) is poorly described. Our aim was to describe the phenotype and disease course of incident UP in a population-based study of paediatric-onset UC.', 'All patients with UC diagnosed <17years from 1988 to 2004, and followed during >2years have been extracted from a population-based registry. UC location was defined according to the Paris classification. Cumulative risks for use of immunosuppressants (IS), anti-tumour necrosis factor alpha (TNF-) therapy, colonic extension and colectomy were described using Kaplan-Meier method. Risk factors for colonic extension were assessed using Cox proportional hazards models.', '158 patients with paediatric-onset UC (91 females) with a median age at diagnosis of 14.5years (Q1: 11.4-Q3: 16.1) have been identified and followed during a median of 11.4years (8.2-15.8). Among them, 25% had UP (E1) at diagnosis and 49% of them presented a colonic extension at maximal follow-up. In these children, the cumulative risk for colonic extension was 10% at 1year, 45% at 5years and 52% at 10years. No parameter at diagnosis was associated with colonic extension in the UP (E1 group). IS use was significantly lower in patients with UP than in those with E2, E3 or E4 location (p=0.049). For the UP cohort, the cumulative risk for colectomy was 3% at 1year, 10% at 5years, 13% at 10years and 13% at 15years. Risks for colonic extension, treatment with anti-TNF- and colectomy did not differ between the E1 group and the E2-E3-E4 group.\Question: Is ulcerative proctitis a frequent location of paediatric-onset UC and not a minor disease : a population-based study?
[EX A]:
UP is frequent in paediatric-onset UC and should not be considered as a minor disease. Compared with more extensive UC locations, risks for colonic extension, anti-TNF- therapy and colectomy were similar in UP, whereas the risk for use of IM was lower.