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.

[EX Q]: Context: The aim of this study was to evaluate and compare microwave disinfection with chemical disinfection of dental gypsum casts.', 'A total of 120 casts were prepared from a silicone mold using Type III dental stone. Of the 120 casts, 60 casts were contaminated with 1 ml suspension of Staphylococcus aureus and 60 casts were contaminated with 1 ml suspension of Pseudomonas aeruginosa. Then, the casts were disinfected with microwave irradiation and chemical disinfection using the microwave oven and 0.5% sodium hypochlorite. Bacteriologic procedures were performed; the cfu/ml for each cast was calculated as a weighted mean. The results were analyzed using Kruskal-Wallis test and Mann-Whitney test.', 'The untreated casts showed Brain heart infusion broth counts of 106 log cfu/ml compared to irradiated and chemically disinfected casts, in which 105 log reduction of cfu/ml was seen. These results satisfied the requirements of current infection control guidelines for the dental laboratory. The results obtained for chemical disinfection were in equivalence with microwave disinfection.\Question: Does evaluation and comparison of high-level microwave oven disinfection with chemical disinfection of dental gypsum cast?
[EX A]: Within the limitation of this in vitro study, it was found that microwave disinfection of casts for 5 min at 900 W gives high-level disinfection that complies with the current infection control guidelines for the dental laboratory and microwave disinfection method is an effective and validated method as chemical disinfection. How to cite the article: Meghashri K, Kumar P, Prasad DK, Hegde R. Evaluation and comparison of high-level microwave oven disinfection with chemical disinfection of dental gypsum casts. J Int Oral Health 2014;6(3):56-60 .

[EX Q]: Context: To evaluate the effects of COX-1 and/or COX-2 inhibition in a model of chronic esophagitis in rabbits.', 'Both high- and low-grade esophagitis were induced in rabbits by the perfusion of acidified pepsin. Rabbits were treated with either a selective COX-2 inhibitor (DFU[3-(3-Fluorophenyl)-4-(4-Methanesulfonyl)-5,5-Dimethyl-5H-Furan-2-One];30 mg/Kg/day), a nonspecific COX inhibitor (indomethacin; 2 mg/Kg/day), or a COX-1 preferential inhibitor (piroxicam; 2 mg/Kg/12 h).', 'Prostaglandins are derived from COX-1 activity in the normal esophagus. Both low- and high-grade esophagitis are associated with a progressive increase of COX activity, which is partially dependent on the COX-2 isoform. DFU reduced muscosal damage in both models of esophagitis. However, indomethacin did not affect significantly mucosal damage, and piroxicam increased damage in low-grade esophagitis.\Question: Is selective COX-2 inhibition associated with decreased mucosal damage induced by acid and pepsin in rabbit esophagitis?
[EX A]: COX-1 activity is constitutive in the rabbit esophageal mucosa, but both COX-2 and COX-1 activity are increased under the impact of acidified pepsin. Treatment with the COX-2 inhibitor DFU is associated with improvement of mucosal damage, which may have therapeutic implications.

[EX Q]: 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-1 and IL-6 were downregulated by C1q, whereas levels of the anti-inflammatory cytokine IL-10 were increased. In addition, data from an NFB-luciferase gene reporter assay suggest that C1q suppresses activation of NFB during lipoprotein clearance in macrophages, providing one mechanism by which C1q downregulates pro-inflammatory cytokine production.\Question: Does complement protein C1q promote macrophage anti-inflammatory M2-like polarization during the clearance of atherogenic lipoproteins?
[EX A]:
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.