Given a passage, 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.

Example Input: Recently we have shown that the imunoglobulins G from blood serum of some multiple sclerosis patients are capable of cleaving histone H1.', 'To check whether histone H1-hydrolyzing abzymes could be detected not only in blood plasma of autoimmune patients, but also during cancer development, particularly during the onset of multiple myeloma.', "Immunoglobulines were isolated from blood serum of multiple myeloma patients (n = 11) by precipitation with 50% ammonium sulfate and tested for proteolytic activity toward linker and core calf thymus histones. Antibody preparations able to cleaved histone H1 were subjected to affinity chromatography on histone H1-Sepharose with following analysis of chromatographic fractions' protease activity. To prove that antibody molecules are responsible for hydrolysis of histone H1, gel filtration at acidic pH with subsequent examination of protease activity of chromatographic fractions (pH-shock analysis) was used.", 'It was found that 3 of 11 antibody preparations are capable of hydrolyzing calf thymus histone H1 but not core histones. It was shown that histone H1-hydrolysing activity of 2 proteolytically active antibody preparations is associated with IgGs that possess affinity towards histone H1. pH-shock analysis proved that protease activity towards histone H1 is intrinsic property of IgG molecules.
Example Output: Are blood serum immunoglobulins of patients with multiple myeloma capable of hydrolysing histone H1?

Example Input: To investigate the mechanisms of anti-atherosclerotic action of ezetimibe in rat vascular smooth muscle cells (VSMCs) in vitro.', 'VSMCs of SD rats were cultured in the presence of Chol:MCD (10 g/mL) for 72 h, and intracellular lipid droplets and cholesterol levels were evaluated using Oil Red O staining, HPLC and Enzymatic Fluorescence Assay, respectively. The expression of caveolin-1, sterol response element-binding protein-1 (SREBP-1) and ERK1/2 were analyzed using Western blot assays. Translocation of SREBP-1 and ERK1/2 was detected with immunofluorescence.', 'Treatment with Chol:MCD dramatically increased the cellular levels of total cholesterol (TC), cholesterol ester (CE) and free cholesterol (FC) in VSMCs, which led to the formation of foam cells. Furthermore, Chol:MCD treatment significantly decreased the expression of caveolin-1, and stimulated the expression and nuclear translocation of SREBP-1 in VSMCs. Co-treatment with ezetimibe (3 mol/L) significantly decreased the cellular levels of TC, CE and FC, which was accompanied by elevation of caveolin-1 expression, and by a reduction of SREBP-1 expression and nuclear translocation. Co-treatment with ezetimibe dose-dependently decreased the expression of phosphor-ERK1/2 (p-ERK1/2) in VSMCs. The ERK1/2 inhibitor PD98059 (50 mol/L) altered the cholesterol level and the expression of p-ERK1/2, SREBP-1 and caveolin-1 in the same manner as ezetimibe did.
Example Output: Does ezetimibe suppress cholesterol accumulation in lipid-loaded vascular smooth muscle cells in vitro via MAPK signaling?

Example Input: Congenital factor VII (FVII) and factor X (FX) deficiencies belong to the group of rare bleeding disorders which may occur in separate or combined forms since both the F7 and F10 genes are located in close proximity on the distal long arm of chromosome 13 (13q34). We here present data of 192 consecutive index cases with FVII and/or FX deficiency. 10 novel and 53 recurrent sequence alterations were identified in the F7 gene and 5 novel as well as 11recurrent in the F10 gene including one homozygous 4.35kb deletion within F7 (c.64+430_131-6delinsTCGTAA) and three large heterozygous deletions involving both the F7 and F10 genes. One of the latter proved to be cytogenetically visible as a chromosome 13q34 deletion and associated with agenesis of the corpus callosum and psychomotor retardation.
Example Output:
Do large deletions play a minor but essential role in congenital coagulation factor VII and X deficiencies?