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.

Input: Consider Input: Context: Scutellaria barbata D.Don has been applied to treat cancers, inflammation and urinary disease. However, its antitumor mechanism still remains unclear.', 'With methylene chloride fraction of Herba Scutellariae barbatae (MCSB), apoptosis-related experiments were carried out on human U937 leukemia cells by (a) 2,3-bis[2-4-nitro-5-sulphophenyl]2H-tetrazolium-5-carboxanilide (XTT) assay for cytotoxicity; (b) terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL) assay for morphological changes; (c) cell cycle analysis; (d) Western blot analysis of poly(ADP-ribose) polymerase (PARP), caspase-8, caspase-9, caspase-3 and Bax, Bcl-2 and cytochrome c expressions for apoptosis signaling pathway.', 'MCSB inhibited the proliferation of human U937 leukemia cells in a dose-dependent manner (IC50 = approximately 10 microg/ml). MCSB dose-dependently increased the sub-G1 DNA contents by cell cycle analysis. DNA fragments indicating induction of apoptosis were observed in MCSB-treated U937 cells by TUNEL assay. Caspase-9 and caspase-3 were activated while caspase-8 was intact by MCSB. Similarly, MCSB effectively cleaved PARP, increased the ratio of Bax/Bcl-2 and released the cytochrome c from mitochondria during apoptosis in U937 cells.
Answer: Our results suggest that MCSB can induce apoptosis via the mitochondria-mediated signaling pathway.

Output: Does methylene chloride fraction of Scutellaria barbata induce apoptosis in human U937 leukemia cells via the mitochondrial signaling pathway?


Input: Consider Input: Context: To investigate the recent incidence of T1D in a US Midwestern county to determine whether this increase has been sustained and compare it with the incidence of celiac disease (CD) and also investigate the prevalence of CD, an associated autoimmune disease, within the cohort.', 'A broad search strategy was used to identify all incident cases of T1D in Olmsted County, Minnesota, between January 1, 1994, and December 31, 2010, using the Rochester Epidemiology Project. Diagnosis and residency status were confirmed through the medical record. Incidence rates were directly standardized to the 2010 US population. Poisson regression was used to test for a change in incidence rate. Clinical charts were reviewed to confirm case status.', 'There were 233 incident cases of T1D. Directly adjusting for age and sex with respect to the 2010 US white population, the overall annual incidence of T1D was 9.2 (95% CI, 8.0-10.4) per 100,000 people per year among all ages and 19.9 (95% CI, 16.6-23.2) per 100,000 people per year for those younger than 20 years. There was no significant increase in the incidence of T1D over time (P=.45). Despite the overall stability in annual incidence, there was an initial increasing trend followed by a plateau. Of the 109 patients with T1D (47%) tested for CD, 12% (13) had biopsy-proven CD.
Answer: The incidence of T1D has stopped increasing in Olmsted County, Minnesota, in the most recent decade. Further studies are needed to confirm this finding and explore reasons for this plateau.

Output: Is incidence of Type 1 Diabetes Increasing in a Population-Based Cohort in Olmsted County , Minnesota , USA?


Input: Consider Input: Context: Coxsackie and adenovirus receptor is a high affinity receptor for adenovirus type 5. To our knowledge the expression profile of coxsackie and adenovirus receptor in renal cancer has not been described. We evaluated the expression of coxsackie and adenovirus receptor in human renal cancer specimens and determined whether the histone deacetylase inhibitor FK-228 (Astelas Pharmaceutical, Osaka, Japan) increases the efficiency of adenoviral infections in renal carcinoma cells in vivo and in vitro.', 'We used randomly selected renal cancer specimens. Specimens were analyzed for coxsackie and adenovirus receptor expression using reverse transcriptase-polymerase chain reaction and immunohistochemistry. In vitro experiments on cytotoxicity were performed to determine a nontoxic dose of FK-228 for renal cancer cells. The level of coxsackie and adenovirus receptor expression was determined by fluorescence activated cell scanning and/or reverse transcriptase-polymerase chain reaction in FK-228 treated renal cancer cells. The effect in vivo on adenoviral gene expression was investigated in athymic mice.', 'In several human renal cancer specimens a loss of or decreased coxsackie and adenovirus receptor expression was detected by reverse transcriptase-polymerase chain reaction based analysis and immunohistochemistry. The nontoxic dose of FK-228 for renal carcinoma cells was 0.5 ng/ml. Treatment of cancer cells with 0.5 ng/ml FK-228 increased levels of coxsackie and adenovirus receptor RNA and acetylated histone H3. This increase was associated with an approximately 10-fold increase in adenoviral infection, as evidenced by increased transgene expression from a beta-galactosidase containing adenoviral vector. Intravenous administration of FK-228 enhanced coxsackie and adenovirus receptor expression in athymic mice. The combination of beta-galactosidase adenovirus and FK-228 was significantly more effective than adenovirus only in A498 cells 3 weeks after treatment in vivo. The combination of p21 adenovirus and FK-228 resulted in significant tumor inhibition in vitro and in vivo.
Answer: In human renal cancer specimens a loss of or decrease in coxsackie and adenovirus receptor expression may be an early event in renal cancer progression. Pretreatment with FK-228 may increase tumor cell sensitivity to adenoviral gene therapy vectors.


Output: Does a histone deacetylase inhibitor enhance adenoviral infection of renal cancer cells?