Given a passage with a context and an answer, 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.

Input: Consider Input: Context: Bradykinin is a neuropeptide released after tissue damage which plays an important role in inflammatory pain. The up-regulation of the bradykinin B1 receptor in response to inflammation makes it an attractive target for drug development. Aim was to investigate if the selective B1 receptor antagonist BI113823 reduces inflammation-induced mechanical hyperalgesia and if the effect is mediated via peripheral and/or spinal B1 receptor antagonism.', "Electrophysiological recordings of peripheral afferents and spinal neurons were combined with behavioural experiments to better understand the underlying mechanisms of B1 receptor antagonism. Experiments were performed 24\u2009h after injection of complete Freund's adjuvant (CFA) or saline into the paw of Wistar rats. A gene expression analysis for the B1 receptor was performed in different tissues. BI113823 was administered orally or intrathecally to assess effects on CFA-induced hyperalgesia. Peripheral afferents of the saphenous nerve as well as spinal wide dynamic range (WDR) and nociceptive-specific (NS) neurons were recorded, and mechanosensitivity was measured before and after BI113823 administration.", 'BI113823 reduced CFA-induced mechanical hyperalgesia when administered orally or intrathecally. An increased B1 receptor gene expression was found in peripheral and spinal neural tissue. BI113823 significantly reduced mechanosensitivity of peripheral afferents and spinal NS neurons, but had no effect on WDR neurons.
Answer: The selective bradykinin B1 receptor antagonist BI113823 reduces CFA-induced mechanical hyperalgesia which is mediated via antagonism of peripheral as well as spinal bradykinin B1 receptors. The selective modulation of CFA-sensitized spinal NS neurons by BI113823 could be a promising property for the treatment of inflammatory pain.

Output: Does the bradykinin B1 receptor antagonist BI113823 reverse inflammatory hyperalgesia by desensitization of peripheral and spinal neurons?


Input: Consider Input: Context: To investigate the effect of the X-linked immunodeficiency (Xid) B cell defect on the response to the cockroach allergen in mice.', 'Two cockroach allergen immunization and challenge protocols were employed to sensitize CBA/J wild-type and CBA/CaHN-btk(-/-)xid/J (Xid) mice. Blood and tissue samples were collected 24 and 48 hrs after the last intratracheal antigen challenge and were analyzed for several parameters of allergic inflammation.', 'Nearly equivalent amounts of serum IgE were detected in Xid and CBA/J mice after short-term antigen challenge despite the B cell deficiency in Xid mice. A decreased concentration of IgE was detected in CBA/J mice after repeated allergen challenges but not in the Xid mice. Correlating with the discrepancy in serum IgE levels, higher levels of IL-13, IL-5, IL-10 and CCL5 were measured in whole lung homogenates from allergen-challenged Xid mice compared to CBA/J mice. In addition, draining lymph node cells from Xid mice expressed elevated levels of IL-4, IL-5, IL-10 and IFNgamma mRNA compared to cells from CBA/J mice after in vitro culture with cockroach antigen. An increase in lung inflammation, interstitial eosinophilia and mucus production was also observed in allergen-challenged Xid mice. CD95L expression increased on B-1a cells following allergen challenge, which was accompanied by an increase in lung CD4(+) Th cell apoptosis in wild-type CBA/J mice. In contrast, Xid mice did not have an increase in CD4(+) T cell apoptosis following allergen challenge.
Answer: These data suggest a regulatory role for B-1a cells in reducing cytokine production, pulmonary inflammation, and CD4(+) T cell survival during cockroach allergen-induced airway inflammation.

Output: Does deficiency of regulatory B cells increase allergic airway inflammation?


Input: Consider Input: Context: Evidence remains inconclusive as to whether eradication of Helicobacter pylori prevents ulcer relapse after simple closure of a perforated duodenal ulcer. This study was conducted to determine the effect of H. pylori eradication using a quadruple drug regimen along with a probiotic on ulcer recurrence after perforation closure.', 'A total of 93 patients who had presented with perforated duodenal ulcer and had a simple closure of a duodenal perforation comprised the study group. Three months postoperatively, patients who were found to be positive for H. pylori infection (n = 60) were administered quadruple therapy consisting of omeprazole, clarithromycin, amoxicillin and colloidal bismuth subcitrate for 10 days along with the probiotic Lactobacillus sporogenes for 14 days. Diagnosis of H. pylori was carried out by urease test and histology. Patients were followed for 18 months. Recurrence of ulcer was analyzed for correlation with H. pylori status.', 'Of 60 patients who received H. pylori eradication therapy, 53 were available for subsequent follow up. H. pylori eradication was achieved in 43/53 (81.1%) patients. The ulcer recurrence in the eradicated group was 18.6% (8/43) compared to 70% (7/10) in the noneradicated group (P = 0.003).
Answer: Eradication of H. pylori significantly reduces the relapse of duodenal ulcer after simple closure of perforation. Anti H. pylori therapy must be recommended for all H. pylori positive patients after simple closure of a perforated duodenal ulcer.


Output: Does helicobacter pylori eradication prevent recurrence after simple closure of perforated duodenal ulcer?