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.

[Q]: Expression of CINCs was regulated differentially in lipopolysaccharide-stimulated rat macrophages. We examined whether the expression of CINCs in lipopolysaccharide-stimulated rat macrophages is similarly inhibited by anti-inflammatory drugs.', 'Rat peritoneal macrophages were stimulated by lipopolysaccharide in the presence of anti-inflammatory steroids (dexamethasone, prednisolone and hydrocortisone) or non-steroidal anti-inflammatory drugs (indomethacin and piroxicam). The production and mRNA expression of three types of CINCs were measured using enzyme-linked immunosorbent assay and northern hybridization.', 'Anti-inflammatory steroids; dexamethasone, prednisolone and hydrocortisone, dose-dependently inhibited the production of CINC-1, -2 and -3, whose inhibitory patterns were similar to each other. Furthermore mRNA expression of each CINC was inhibited by dexamethasone in a dose-dependent manner. In contrast, non-steroidal anti-inflammatory drugs, indomethacin and piroxicam were without effect. Expression of each CINC was regulated differently; the production of CINC-1 reached a maximum at 12 h and then slightly decreased after lipopolysaccharide stimulation, whereas that of CINC-2 and CINC-3 increased up to 24 h. Dexamethasone inhibited the CINCs production and mRNA expression at 9 h after lipopolysaccharide stimulation.
[A]: Is the expression of three types of CINCs by lipopolysaccharide-stimulated rat macrophages inhibited similarly by anti-inflammatory steroids?


[Q]: There is no consensus about the ideal method for diagnosis in patients who have already undergone endoscopic ultrasound fine needle aspiration (EUS-FNA), and the inconclusive material is often obtained. The aim was to evaluate the diagnostic yield of the second EUS-FNA of pancreatic lesions.', 'A retrospective analysis of prospectively collected data of patients with EUS-FNA of pancreatic lesions is performed. All patients who underwent more than one EUS-FNA for the evaluation of suspected pancreatic cancer over a 7-year period were included in the analysis.', 'A total of 296 EUS-FNAs of the pancreas were performed in 257 patients. The diagnostic yield with the first EUS-FNA was 78.6% (202/257). Thirty-nine (13.3%) FNAs were repeated in 34 patients; 17 (50%) patients were women. The mean ± standard deviation (SD) age was 58.8 ± 16.1 years. The location of the lesions in the pancreatic gland, from which the second biopsies were taken, was head of the pancreas, n = 28 (82.4%), body of the pancreas, n = 3 (8.8%), and tail, n = 3 (8.8%). The mean ± SD of the size of the lesion was 36.3 ± 14.6 mm. The second EUS-FNA was more likely to be positive for diagnosis in patients with an "atypical" histological result in the first EUS-FNA (odds ratio [OR]: 4.04; 95% confidence interval [CI]: 0.9-18.3), in contrast to patients with a first EUS-FNA reported as "normal" (OR: 0.21; 95% CI: 0.06-0.71). Overall, the diagnostic yield of the second EUS-FNA was 58.8% (20/34) with an increase to 86.3% overall (222/257).
[A]: Is repeat endoscopic ultrasound fine needle aspiration after a first negative procedure useful in pancreatic lesions?


[Q]: To elucidate the importance of hepatitis C Virus (HCV) genotype in HIV disease progression.', 'This study was conducted among 126 HIV/HCV co-infected drug users with a known interval of HIV seroconversion whose HCV genotype was known early in HIV infection. Both clinical progression (to AIDS) and immunological progression (to a CD4+ T-cell count of 200 x 10(6) cells/l) by HCV genotype were studied using Cox proportional hazards analysis.', 'The median duration of follow-up was 7.3 years [interquartile range (IQR), 4.6-10.1 years]. The majority of the HCV infections concerned genotype 1 and genotype 3; The distribution was: HCV type 1: 48%, HCV type 3: 34%, HCV type 4: 13%, multiple HCV types: 5%. Concurrent multiple infections consisted of HCV genotypes 1b+3a, 1b+4 and 3a+4. HCV genotype 1 and multiple HCV genotype infections were associated with faster immunological progression [hazard ratio (HR), 2.02; 95% confidence interval (CI), 1.04-3.92 and HR, 2.74; 95% CI, 0.95-7.90, respectively]. Multiple HCV genotype infection was also associated with faster clinical progression (HR, 3.36; 95% CI, 0.82-13.79). These hazard ratios increased further and were all significant when analyses were limited to data in the pre-HAART era (HR, 3.92; 95% CI, 1.51-10.20; HR, 4.38; 95% CI, 1.04-18.40 and HR, 6.54; 95% CI, 1.39-30.76, respectively).
[A]:
Is infection with concurrent multiple hepatitis C virus genotypes associated with faster HIV disease progression?