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: Innate immune protein C1q plays a dual role in the chronic inflammatory disease of atherosclerosis. Complement activation via C1q exacerbates pathology in the atherosclerotic lesion in later stages of the disease. However, in early stages of disease C1q is protective. We hypothesize that complement-independent activities of C1q are involved in reprogramming macrophage inflammatory polarization.', 'The influence of C1q on macrophage inflammatory responses during clearance of oxLDL was examined. Changes in cytokines at the gene and protein level were measured by quantitative PCR and ELISA assay.', 'C1q modulated cytokine expression in Raw264.7 macrophages during ingestion of oxLDL. Levels of pro-inflammatory cytokines IL-1β and IL-6 were downregulated by C1q, whereas levels of the anti-inflammatory cytokine IL-10 were increased. In addition, data from an NFκB-luciferase gene reporter assay suggest that C1q suppresses activation of NFκB during lipoprotein clearance in macrophages, providing one mechanism by which C1q downregulates pro-inflammatory cytokine production.
Answer: C1q-polarization of macrophages toward an anti-inflammatory (M2-like) phenotype may be important in dampening inflammation in the early atherosclerotic lesion. Further investigation of molecular pathways targeted by C1q may provide novel therapeutic targets for this disease.

Output: Does complement protein C1q promote macrophage anti-inflammatory M2-like polarization during the clearance of atherogenic lipoproteins?


Input: Consider Input: Context: High sensitivity C-reactive protein (hsCRP) is more sensitive than standard C-reactive protein (CRP) assay in evaluating the risk of coronary heart disease and other atherosclerotic events. By this time, there are several reports that type 2 diabetic subjects have higher serum levels of hsCRP than those of non-diabetic subjects. However, there are few reports about factors which have influence upon the level of serum hsCRP in type 2 diabetic subjects. We had evaluated the association of serum hsCRP level with risk factors of cardiovascular diseases and carotid intima-media thickness (IMT) in type 2 diabetic subjects.', 'One hundred and five patients (59 men and 46 women) with type 2 diabetes were recruited. Subjects with severe cardiovascular diseases were excluded. All subjects were undergone carotid ultrasonography for evaluation of carotid IMT. Serum hsCRP concentrations were measured.', 'Serum hsCRP level was correlated with mean left IMT (r = 0.366, P = 0.003), maximal left IMT (r = 0.370, P = 0.002), mean right IMT (r = 0.281, P = 0.023) and maximal right IMT (r = 0.370, P = 0.002), body mass index (r = 0.377, P < 0.001), waist circumference (r = 0.342, P < 0.001), waist-hip ratio (r = 0.229, P = 0.020), serum total cholesterol (r = 0.202, P = 0.024), serum triglyceride (r = 0.292, P = 0.022) and serum low-density lipoprotein (r = 0.133, P = 0.044).
Answer: Our result shows that serum hsCRP level is correlated with carotid IMT and the risk factors of cardiovascular diseases and may be useful to predict accelerated atherosclerotic process in type 2 diabetic subjects.

Output: Is serum high sensitivity C-reactive protein associated with carotid intima-media thickness in type 2 diabetes?


Input: Consider Input: Context: To test the role of mast cells in gut inflammation and colitis using interleukin (IL)-10-deficient mice as an experimental model.', 'Mast cell-deficient (Kit (W-sh/W-sh) ) mice were crossbred with IL-10-deficient mice to obtain double knockout (DKO) mice. The growth, mucosal damage and colitis status of DKO mice were compared with their IL-10-deficient littermates.', 'DKO mice exhibited exacerbated colitis compared with their IL-10-deficient littermates, as shown by increased pathological score, higher myeloperoxidase content, enhanced Th1 type pro-inflammatory cytokines and inflammatory signaling, elevated oxidative stress, as well as pronounced goblet cell loss. In addition, deficiency in mast cells resulted in enhanced mucosal damage, increased gut permeability, and impaired epithelial tight junctions. Mast cell deficiency was also linked to systemic inflammation, as demonstrated by higher serum levels of tumor necrosis factor α and interferon γ in DKO mice than that in IL-10-deficient mice.
Answer: Mast cell deficiency in IL-10-deficient mice resulted in systematic and gut inflammation, impaired gut barrier function, and severer Th1-mediated colitis when compared to mice with only IL-10-deficiency. Inflammation and impaired gut epithelial barrier function likely form a vicious cycle to worsen colitis in the DKO mice.


Output: Does mast cell deficiency exacerbate inflammatory bowel symptoms in interleukin-10-deficient mice?