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.

Ex Input:
Context: Surfactant protein A (SP-A) is a C-type lectin involved in surfactant homeostasis as well as host defense in the lung. We have recently demonstrated that SP-A enhances the killing of bacillus Calmette-Guerin (BCG) by rat macrophages through a nitric oxide-dependent pathway. In the current study we have investigated the role of tyrosine kinases and the downstream mitogen-activated protein kinase (MAPK) family, and the transcription factor NFkappaB in mediating the enhanced signaling in response to BCG in the presence of SP-A.', 'Human SP-A was prepared from alveolar proteinosis fluid, and primary macrophages were obtained by maturation of cells from whole rat bone marrow. BCG-SP-A complexes were routinely prepared by incubation of a ratio of 20 microg of SP-A to 5 x 105 BCG for 30 min at 37 degrees C. Cells were incubated with PBS, SP-A, BCG, or SP-A-BCG complexes for the times indicated. BCG killing was assessed using a 3H-uracil incorporation assay. Phosphorylated protein levels, enzyme assays, and secreted mediator assays were conducted using standard immunoblot and biochemical methods as outlined.', 'Involvement of tyrosine kinases was demonstrated by herbimycin A-mediated inhibition of the SP-A-enhanced nitric oxide production and BCG killing. Following infection of macrophages with BCG, the MAPK family members ERK1 and ERK2 were activated as evidence by increased tyrosine phosphorylation and enzymatic activity, and this activation was enhanced when the BCG were opsonized with SP-A. An inhibitor of upstream kinases required for ERK activation inhibited BCG- and SP-A-BCG-enhanced production of nitric oxide by approximately 35%. Macrophages isolated from transgenic mice expressing a NFkappaB-responsive luciferase gene showed increased luciferase activity following infection with BCG, and this activity was enhanced two-fold in the presence of SP-A. Finally, lactacystin, an inhibitor of IkappaB degradation, reduced BCG- and SP-A-BCG-induced nitric oxide production by 60% and 80% respectively.
Answer: These results demonstrate that BCG and SP-A-BCG ingestion by macrophages is accompanied by activation of signaling pathways involving the MAP kinase pathway and NFkappaB.

Ex Output:
Are mitogen-activated protein kinases and NFkappaB involved in SP-A-enhanced responses of macrophages to mycobacteria?

Ex Input:
Context: Although diabetic patients often have gastrointestinal complications, the gastric mucosal function in diabetes has not been well documented.', 'To investigate the effect of fasting on the gastric mucosa in C57BL/KsJ-db +/+ db (db/db) mice, genetically non-insulin-dependent diabetic animals.', 'Blood glucose levels, gastric mucosal morphology, and the amount of gastric mucin were examined before and after 18 h of fasting with free access to water in db/db mice and their non-diabetic littermates (db/m).', 'Although 18 h of fasting reduced the blood glucose levels of both db/db and db/m mice, fasting decreased the amount of gastric adherent mucin and caused haemorrhagic gastric lesions only in db/db mice. After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice. The above fasting-induced gastric damage such as haemorrhagic lesions, loss of the mucin, and the increased sensitivity to ethanol worsened as the duration of diabetes became longer. Glucose ingestion in drinking water during the fasting counteracted the fall in blood glucose and prevented the decrease in the amount of gastric mucin and the formation of gastric mucosal lesions in db/db mice.
Answer: These findings indicate that fasting-induced glucose deficit causes gastric mucosal lesions and increases the susceptibility of gastric mucosa to noxious agents owing to the loss of mucus glycoprotein in db/db mice. Prolonged diabetes is likely to augment the severity of fasting-induced impairment of the gastric mucosal function.

Ex Output:
Does fasting induce impairment of gastric mucosal integrity in non-insulin-dependent diabetic ( db/db ) mice?

Ex Input:
Context: Selenium is an essential mineral for immunological function, performing crucial functions at the cellular level. This micronutrient has been determined to be frequently deficient in HIV infected patients, with correlations between reduced immunological function and greater susceptibility to opportunistic infections. Our aim was to evaluate the influence of time of exposure to antiretroviral therapy (ART) on the biochemical profile of selenium in HIV-infected patients.', 'We performed a cross-sectional study on 50 HIV-positive men with different quantitations of viral load and CD4+ T cells, who were either receiving or not receiving ART. Dual energy X-ray absorptiometry (DXA) to determine body composition, biochemical analysis of selenium and albumin, anthropometric measurements were performed. The subjects were divided into groups according to the use of ART or not: The Control Group (CG) was 10 treatment-naive volunteers, Group G < 2 was 20 volunteers on ART for less than 2 years, and Group G > 2 was 20 volunteers on ART for >2 years.', 'The body mass index showed that all subjects were of normal weight. The group with a longer time of exposure to ART (G > 2) had undetectable viremia and a higher CD4+ T cell count: 593.1 234.6 mm(3). Selenium values (g/L) were 55.9 11.9 for CG, 52.1 10.5 for G < 2, and 66.9 20.8 for G > 2, with a significant difference between groups G < 2 and G > 2 (p < 0.05), and only G > 2 showed normal selenium values.
Answer: Most of the men studied showed selenium deficiency, except for the subjects with a longer exposure to antiretroviral treatment. Thus, an adequate selenium concentration is related to better control of virology and of immunologic function.

Ex Output:
Does a longer time of exposure to antiretroviral therapy improve selenium levels?