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.

Input: Consider Input: The human immunodeficiency virus Vif protein overcomes the inhibitory activity of the APOBEC3G cytidine deaminase by prohibiting its packaging into virions. Inhibition of APOBEC3G encapsidation is paralleled by a reduction of its intracellular level presumably caused by the Vif-induced proteasome-dependent degradation of APOBEC3G.', 'In this report we employed confocal microscopy to study the effects of Vif on the expression of APOBEC3G on a single cell level. HeLa cells dually transfected with Vif and APOBEC3G expression vectors revealed efficient co-expression of the two proteins. Under optimal staining conditions approximately 80% of the transfected cells scored double-positive for Vif and APOBEC3G. However, the proportion of double-positive cells observed in identical cultures varied dependent on the fixation protocol and on the choice of antibodies used ranging from as low as 40% to as high as 80% of transfected cells. Importantly, single-positive cells expressing either Vif or APOBEC3G were observed both with wild type Vif and a biologically inactive Vif variant. Thus, the lack of APOBEC3G in some Vif-expressing cells cannot be attributed to Vif-induced degradation of APOBEC3G. These findings are consistent with our results from immunoblot analyses that revealed only moderate effects of Vif on the APOBEC3G steady state levels. Of note, viruses produced under such conditions were fully infectious demonstrating that the Vif protein used in our analyses was both functional and expressed at saturating levels.

Output: Does production of infectious human immunodeficiency virus type 1 require depletion of APOBEC3G from virus-producing cells?


Input: Consider Input: ID4 gene is a member of the inhibitor of DNA binding (ID) family proteins that inhibit DNA binding of basic helix-loop-helix transcription factors. The epigenetic inactivation of ID4 gene on colorectal cancer (CRC) development and its clinical significance was assessed.', 'In CRC cell lines, ID4 methylation status of the promoter region was assessed by methylation-specific PCR and bisulfite sequencing. The mRNA expression level was assessed by quantitative real-time reverse transcription-PCR. The methylation status of 9 normal epithelia, 13 adenomas, 92 primary CRCs, and 26 liver metastases was assessed by methylation-specific PCR. ID4 protein expression was assessed by immunohistochemistry analysis of tissue specimen.', 'CRC cell lines were shown to be hypermethylated, and mRNA expression was suppressed and could be restored by 5-aza-cytidine treatment. In clinical specimens from normal epithelia, adenomas, primary CRCs, and liver metastases, the frequency of ID4 hypermethylation was 0 of 9 (0%), 0 of 13 (0%), 49 of 92 (53%), and 19 of 26 (73%), respectively, with a significant elevation according to CRC pathological progression. Methylation status of primary CRCs significantly correlated with histopathological tumor grade (P = 0.028). Immunohistochemistry analysis showed ID4 expression of normal colon epithelia, adenomas, and unmethylated primary CRCs but not hypermethylated CRC specimens. Among 76 American Joint Committee on Cancer stage I to IV patients who had undergone curative surgical resection, overall survival was significantly poorer in patients with hypermethylated ID4 bearing tumors (P = 0.0066).

Output: Does epigenetic inactivation of ID4 in colorectal carcinomas correlate with poor differentiation and unfavorable prognosis?


Input: Consider Input: There is a need in urological practice to identify new bladder cancer molecular markers to further develop noninvasive diagnostic tests. We analyzed bladder cancer gene expression profiles to determine the relevant differentially expressed genes and whether this differential expression is maintained in urine samples.', 'We collected 55 tissue specimens from a total of 43 patients with bladder cancer and 12 controls, and 49 urine samples from bladder washings from a total of 36 patients with bladder cancer and 13 controls between September 2003 and December 2004. DNA microarrays (GeneChip Human Genome U133 Plus 2.0 Array) were used to identify differentially expressed genes at 3 bladder cancer stages. Selected differentially expressed genes were validated in an independent set of bladder washings by quantitative reverse transcriptase-polymerase chain reaction.', 'Unsupervised cluster analysis of DNA microarray data showed a clear distinction in control vs tumor samples and low vs high grade tumors. Genes with at least 2-fold differential expression in controls vs tumors (2,937 probe sets or 2,295 genes) and in low vs high grade tumors (674 probe sets or 530 genes) were identified and ranked. Gene expression measurements in bladder washings of the 6 most differentially expressed genes in controls vs tumors were confirmed for the 2 over expressed genes tested by quantitative reverse transcriptase-polymerase chain reaction. All 8 selected differentially expressed genes in low vs high grade tumors were confirmed in bladder washing samples.


Output: Does dNA microarray expression profiling of bladder cancer allow identification of noninvasive diagnostic markers?