instruction:
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.
question:
Context: To determine whether tissue factor (TF) contributes to the progression of atherosclerotic lesions in mice.', 'We determined the effect of a 50% reduction of TF levels in all cells on atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice. No differences were observed in the extent of atherosclerosis in apoE(-/-)/TF(+/+) and apoE(-/-)/TF(+/-) mice fed regular chow for 34 weeks. Atherosclerosis could not be analyzed in apoE(-/-) mice expressing low levels of TF because of premature death of these mice. Macrophages are a major source of TF in atherosclerotic plaques. Therefore, in a second series of experiments, we investigated the effect on atherosclerosis of selectively reducing hematopoietic cell-derived TF by transplanting bone marrow from mice expressing low levels of TF into low-density lipoprotein receptor deficient (LDLR(-/-)) mice. Atherosclerosis within the arterial tree and aortic root were similar in LDLR(-/-) mice with low-TF bone marrow compared with control bone marrow (TF(+/+) or TF(+/-)) after 4 and 16 weeks on an atherogenic diet. Furthermore, the cellular composition of the aortic root lesions was similar between the 2 groups.
Answer: Our data indicate that either a 50% reduction of TF in all cells or a selective reduction in hematopoietic cell-derived TF does not affect the development of atherosclerotic lesions in mice.
answer:
Is atherosclerosis in mice affected by a reduction in tissue factor expression?

question:
Context: Prostaglandin D2 (PGD2) and cysteinyl leukotrienes (cysLTs) are lipid mediators derived from mast cells, which activate TH2 cells. The combination of PGD2 and cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine production. However, the synergistic interaction of cysLTs with PGD2 in promoting TH2 cell activation is still poorly understood. The receptors for these mediators are drug targets in the treatment of allergic diseases, and hence understanding their interaction is likely to have clinical implications.', 'We aimed to comprehensively define the roles of PGD2, LTE4, and their combination in activating human TH2 cells and how such activation might allow the TH2 cells to engage downstream effectors, such as neutrophils, which contribute to the pathology of allergic responses.', 'The effects of PGD2, LTE4, and their combination on human TH2 cell gene expression were defined by using a microarray, and changes in specific inflammatory pathways were confirmed by means of PCR array, quantitative RT-PCR, ELISA, Luminex, flow cytometry, and functional assays, including analysis of downstream neutrophil activation. Blockade of PGD2 and LTE4 was tested by using TM30089, an antagonist of chemoattractant receptor-homologous molecule expressed on TH2 cells, and montelukast, an antagonist of cysteinyl leukotriene receptor 1.', 'PGD2 and LTE4 altered the transcription of a wide range of genes and induced diverse functional responses in TH2 cells, including cell adhesion, migration, and survival and cytokine production. The combination of these lipids synergistically or additively enhanced TH2 responses and, strikingly, induced marked production of diverse nonclassical TH2 inflammatory mediators, including IL-22, IL-8, and GM-CSF, at concentrations sufficient to affect neutrophil activation.
Answer: PGD2 and LTE4 activate TH2 cells through different pathways but act synergistically to promote multiple downstream effector functions, including neutrophil migration and survival. Combined inhibition of both PGD2 and LTE4 pathways might provide an effective therapeutic strategy for allergic responses, particularly those involving interaction between TH2 cells and neutrophils, such as in patients with severe asthma.
answer:
Do prostaglandin D2 and leukotriene E4 synergize to stimulate diverse TH2 functions and TH2 cell/neutrophil crosstalk?

question:
Context: Hyperhomocysteinemia, increased oxidative stress, and decreased antioxidant defense function have been found to be associated with the risk of chronic kidney disease (CKD). Deficiencies of folate and vitamin B-6 (pyridoxal 5'-phosphate, PLP) may cause hyperhomocysteinemia and increased oxidative stress. The purpose of this study was to determine the associations among homocysteine, folate, PLP, oxidative stress indicator, and antioxidant capacities in patients with stage 2 to 3 CKD, and to further analyze these relationships with respect to risk for CKD.", 'Ninety-seven patients with CKD and 135 healthy subjects were recruited.', 'Patients with CKD had significantly higher levels of malondialdehyde and total antioxidant capacities, but had significantly lower antioxidant enzyme activities compared with healthy subjects. Serum folate but not plasma PLP was significantly negatively associated with plasma homocysteine. There were no significant associations of homocysteine, PLP, and folate with oxidative stress indicator and antioxidant capacities. High homocysteine (odds ratio [OR] = 1.11; 95% confidence interval [CI], 1.02-1.22) and malondialdehyde (OR = 34.24; 95% CI, 4.44-264.40) level increased the risk of CKD, whereas high plasma PLP (OR = 0.98; 95% CI, 0.97-0.99) and superoxide dismutase activity (OR = 0.82; 95% CI, 0.74-0.91) decreased the risk of CKD after adjusting all potential confounders.
Answer: High homocysteine, low PLP, increased oxidative stress, and decreased antioxidant enzyme activity (superoxide dismutase activity) were independent contributing factors in the development of early stage CKD.
answer:
Are high homocysteine , low vitamin B-6 , and increased oxidative stress independently associated with the risk of chronic kidney disease?