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.

Q: Context: Endoplasmic reticulum (ER) stress is induced in many forms of chronic liver disease and may promote the development of hepatocellular carcinoma. The activator protein 1 (AP-1) complex is a transcription factor that promotes hepatic carcinogenesis in response to cellular stress. The aim of this study was to determine the role of ER stress in the regulation of the hepatic AP-1 complex.', 'Human hepatocellular carcinoma (HepG2) cells and C57BL/6J mice were subjected to pharmacologic ER stress and the expression of AP-1-associated genes and proteins was assessed. To determine the role of MAPK signaling in ER stress-induced AP-1 activation, ER stress was induced in JNK- and ERK-inhibited HepG2 cells.', 'Induction of ER stress promoted the activation of both Jun- and Fos-related genes and proteins of the AP-1 complex in HepG2 cells and murine liver. Inhibition of ERK phosphorylation in HepG2 cells completely prevented ER stress-induced activation of the fos-related components of AP-1 whereas activation of Jun-related components was only partially attenuated. Conversely, inhibition of JNK phosphorylation in HepG2 cells reduced ER stress-induced activation of Jun-related components but did not prevent activation of fos-related components.
Answer: ER stress activates the hepatic AP-1 complex via MAPK-dependent signaling pathways. ER stress-induced activation of Fos-related components is dependent primarily on ERK activation whereas ER stress-induced activation of Jun-related components is dependent primarily on JNK activation, although there is interplay between these regulatory pathways. These data implicate a novel signaling pathway by which sustained ER stress, as observed in many chronic liver diseases, may promote hepatic carcinogenesis.

A: Does endoplasmic reticulum stress activate the hepatic activator protein 1 complex via mitogen activated protein kinase-dependent signaling pathways?
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Q: 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.

A: Does methylene chloride fraction of Scutellaria barbata induce apoptosis in human U937 leukemia cells via the mitochondrial signaling pathway?
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Q: Context: Longer-term tuberculosis (TB) drug resistance surveillance among children is rare. We determined the prevalence of drug resistance among children with culture-confirmed TB from 2011 to 2013, compared these results with four previous consecutive 2-year periods and documented other mycobacterial isolates identified.', "Surveillance study of mycobacterial culture in all children aged <13 years conducted from March 2011 to February 2013 at the Tygerberg Children's Hospital, Cape Town, South Africa. Drug susceptibility testing against isoniazid (INH) and rifampicin (RMP) was performed using line-probe assay (GenoType(®) MTBDRplus). Clinical data were obtained through folder review.", 'Of 381 children, 323 (84.8%; 324 episodes) had Mycobacterium tuberculosis, 46 (12.1%) had M. bovis bacille Calmette-Guérin and 12 (3.1%) had non-tuberculous mycobacteria isolated. Forty-one (12.7%) children had M. tuberculosis resistant to INH and/or RMP; 15 (4.7%) had multidrug-resistant TB (MDR-TB). The prevalence of INH mono- or polyresistance remained stable; however, RMP monoresistance increased (0/313 in 2003-2005 vs. 6/324, 1.9%, in 2011-2013; P = 0.041); MDR-TB prevalence has declined significantly, from 26/292 (8.9%) in 2007-2009 to 15/324 (4.7%) in 2011-2013 (OR 0.50, 95%CI 0.24-0.99). The prevalence of human immunodeficiency virus co-infection has decreased significantly, from a peak of 29% to 15.3%.
Answer: There has been a significant reduction in bacteriologically confirmed MDR-TB cases. The increase in RMP monoresistance has important implications for treatment.

A:
Does surveillance provide insight into epidemiology and spectrum of culture-confirmed mycobacterial disease in children?
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