instruction:
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.
question:
To examine whether trichostatin A (TSA), a histone deacetylase inhibitor (HDACI), can induce up-regulation of peroxisome proliferator-activating receptor gamma (PPAR gamma) and to see whether LG100268, a retinoid X receptor (RXR) ligand, can inhibit proliferation of endometriotic cells alone or in synergy with ciglitazone, a PPAR gamma agonist.', 'One endometrial stromal cell line and two endometriotic cell lines used as a model system: Western blot analysis to determine whether TSA can up-regulate PPAR gamma expression, and MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) proliferation assay to see whether ciglitazone and LG100268 have any antiproliferative effects individually or jointly.', 'Academic.', 'None.', 'Culture of immortalized endometrial and endometriotic cell lines with TSA, or ciglitazone or LG100268.', 'PPAR gamma protein expression levels in cells treated with or without TSA, and number of viable cells treated with or without ciglitazone, LG100268, or both.', 'The TSA treatment resulted in up-regulation of PPAR gamma expression in all cell lines in a dose-dependent fashion. Both ciglitazone and LG100268 inhibited proliferation in a dose-dependent manner, and the antiproliferative effects appeared to be synergistic. In addition, endometriotic cells were more sensitive than endometrial stromal cells to LG100268 treatment.
answer:
Do peroxisome proliferator-activated receptor-gamma and retinoid X receptor agonists synergistically suppress proliferation of immortalized endometrial stromal cells?


question:
The objective of this study is to characterize differential proteomic expression among well-differentiation and poor-differentiation colorectal carcinoma tissues and normal mucous epithelium.', 'The study is based on quantitative 2-dimensional gel electrophoresis and analyzed by PDquest.', 'Excluding redundancies due to proteolysis and posttranslational modified isoforms of over 600 protein spots, 11 proteins were revealed as regulated with statistical variance being within the 95th confidence level and were identified by peptide mass fingerprinting in matrix assisted laser desorption/ionization time-of-flight mass spectrometry. Progression-associated proteins belong to the functional complexes of tumorigenesis, proliferation, differentiation, metabolism, and the regulation of major histocompatibility complex processing and other functions. Partial but significant overlap was revealed with previous proteomics and transcriptomics studies in CRC. Among various differentiation stage of CRC tissues, we identified calreticulin precursor, MHC class I antigen (human leukocyte antigen A ), glutathione S-transferase pi1, keratin 8, heat shock protein 27, tubulin beta chain, triosephosphate, fatty acid-binding protein, hemoglobin (deoxy) mutant with val b 1 replaced by met (HBB), and zinc finger protein 312 (FEZF2).
answer:
Does proteomic analysis reveal novel proteins associated with progression and differentiation of colorectal carcinoma?


question:
To study the outcome of EEG from patients with Chiari I malformations and nonspecific EEG abnormalities, after posterior fossa decompression and CSF flow normalization.', "Three 'apparently asymptomatic' children who had been diagnosed with Arnold-Chiari type 1 EEG abnormalities and who exhibited (a) a wide range of abnormalities according to common anatomical Chiari MRI classifications (Elster AD, Chen MY. Chiari I malformations: clinical and radiologic reappraisal. Radiology 1992;183:347-53), (b) a lack of specific, clinical signs of increased intracranial pressure, and (c) apparently unrelated, EEG-nonspecific abnormalities (focal intermittent rhythmic delta activity (IRDA)--solely in patients 1 and 3, and with focal IRDA plus spikes and spike waves of high voltage in patient 2). Standard EEGs were recorded before surgery and within one month of surgery, which was performed in conjunction with intraoperative echo-Doppler ultrasonography to control CSF flow. Subsequent EEGs and clinical follow-ups were performed within 6-12 months of surgery.", 'In all patients, intraoperative echo-Doppler ultrasonographic control demonstrated poor CSF flow, which was completely restored by posterior fossa decompression. In all patients, the EEG abnormalities disappeared within one month of surgery and the EEGs were normal at follow-up.
answer:

Does surgery remove EEG abnormalities in patients with Chiari type I malformation and poor CSF flow?