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.

[Q]: Context: To assess the effect of six different enteral diets on the gut barrier.', 'Laboratory study.', 'University hospital, Germany.', '70 Specific pathogen free female Crl:CDR BR rats.', 'For 7 days, 6 groups of rats were fed orally with standard chow (n = 15); total parenteral nutrition solution (oral TPN, n = 15); elemental diet (ED, n = 10); nutrient-defined diet (NDD, n = 10); or the NDD supplemented with uracil (NDD+uracil, n = 10), or fibre (NDD+fibre, n = 10).', 'Bacterial translocation to mesenteric lymph nodes, numbers of Gram negative enterobacteria and total aerobic bacteria in the caecum, and intestinal concentrations of secretory IgA.', 'The incidence of bacterial translocation was significantly increased in the groups given oral TPN, ED, NDD, and NDD+uracil compared with the group given chow. Only NDD+fibre resulted in a similar degree of translocation to that in the chow group. All groups in which there was increased translocation had a highly significant overgrowth of aerobic bacteria in the caecum, mainly by Gram negative enteric organisms. The secretory IgA concentration was reduced in the group that had been given oral TPN, and that in the ED and NDD+uracil groups was similar to that in the chow group. NDD and NDD+fibre were associated with higher intestinal concentrations of secretory IgA than chow.\Question: Is fibre an essential ingredient of enteral diets to limit bacterial translocation in rats?
[A]: Fibre-free enteral diets do not protect the gut antimicrobial barrier whatever else is in them. The superiority of early enteral as opposed to parenteral nutrition after injury may, therefore, not be the result of a specific protective effect on the gut barrier. The supplementation of commercial enteral diets with bulk fibre should be tested in clinical trials.


[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?
[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.


[Q]: Context: To investigate cellular immune responses to streptococcal antigens in patients with psoriatic arthritis (PsA). To specifically examine responses of the gamma delta + T cell subset.', 'Proliferation of PsA synovial fluid lymphocytes (SFL) and peripheral blood lymphocytes (PBL) cultured with streptococcal antigen was measured using a 3H thymidine (3HTdr) uptake assay system. gamma delta + T cells from PsA PBL and SFL were phenotyped by flow cytometry. Following culture with streptococcal antigen, gamma delta + enriched SFL were sorted by automated flow cytometry and 3HTdr uptake measured.', 'Patients with PsA and the control group did not differ significantly in their PBL responses to 2 strains of streptococci, one of which was isolated from a patient with guttate psoriasis (Strep 1) and the other from a patient with rheumatic fever (Strep 2). There was also no difference in their responses to a cell wall preparation derived from the former strain. SFL from 8 of 9 patients with PsA responded to both streptococcal strains as did SFL from 3 patients with rheumatoid arthritis (RA). gamma delta + SFL from 7 patients with PsA 3 patients with RA responded only to the psoriasis associated strain.\Question: Do gamma delta + T cells from patients with psoriatic and rheumatoid arthritis respond to streptococcal antigen?
[A]:
PsA PBL and SFL responded to stimulation by streptococcal antigen but this reactivity was not disease specific. We have demonstrated that gamma delta + T cells from PsA SF proliferated when cultured with a psoriasis associated strain of streptococcus (Strep 1). However, RA gamma delta + SFL responded similarly suggesting that gamma delta + T cell reactivity to streptococcal antigen may be a feature of inflammatory arthritis.