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.

[EX Q]: Hepatocyte nuclear factor 4 (HNF4) is a liver enriched transcription factor and is indispensable for liver development. However, the role of HNF4 in hepatocellular carcinoma (HCC) progression remains to be elucidated. We report that reduced HNF4 expression correlated well with the aggressive clinicopathological characteristics of HCC and predicted poor prognosis of patients. HNF4 levels were even lower in metastatic HCCs, and ectopic HNF4 expression suppressed the metastasis of hepatoma cells both in vitro and in vivo. Forced HNF4 expression attenuated the expression and nuclear translocation of RelA (p65) and impaired NF-B activation through an IKK-independent mechanism. Blockage of RelA robustly attenuated the suppressive effect of HNF4 on hepatoma cell metastasis. MicroRNA (miR)-7 and miR-124 were transcriptionally up-regulated by HNF4, which repressed RelA expression by way of interaction with RelA-3' untranslated region (UTR). In addition, nuclear factor kappa B (NF-B) up-regulated the expression of miR-21 in hepatoma cells, resulting in decreased HNF4 levels through down-regulating HNF4-3'UTR activity.
[EX A]: Does hepatocyte nuclear factor 4-nuclear factor-B feedback circuit modulate liver cancer progression?

[EX Q]: Effective therapeutic interventions for chronic, idiopathic lung diseases remain elusive. Normalized T-cell function is an important contributor to spontaneous resolution of pulmonary sarcoidosis. Up-regulation of inhibitor receptors, such as programmed death-1 (PD-1) and its ligand, PD-L1, are important inhibitors of T-cell function.', 'To determine the effects of PD-1 pathway blockade on sarcoidosis CD4(+) T-cell proliferative capacity.', 'Gene expression profiles of sarcoidosis and healthy control peripheral blood mononuclear cells were analyzed at baseline and follow-up. Flow cytometry was used to measure ex vivo expression of PD-1 and PD-L1 on systemic and bronchoalveolar lavage-derived cells of subjects with sarcoidosis and control subjects, as well as the effects of PD-1 pathway blockade on cellular proliferation after T-cell receptor stimulation. Immunohistochemistry analysis for PD-1/PD-L1 expression was conducted on sarcoidosis, malignant, and healthy control lung specimens.', 'Microarray analysis demonstrates longitudinal increase in PDCD1 gene expression in sarcoidosis peripheral blood mononuclear cells. Immunohistochemistry analysis revealed increased PD-L1 expression within sarcoidosis granulomas and lung malignancy, but this was absent in healthy lungs. Increased numbers of sarcoidosis PD-1(+) CD4(+) T cells are present systemically, compared with healthy control subjects (P < 0.0001). Lymphocytes with reduced proliferative capacity exhibited increased proliferation with PD-1 pathway blockade. Longitudinal analysis of subjects with sarcoidosis revealed reduced PD-1(+) CD4(+) T cells with spontaneous clinical resolution but not with disease progression.
[EX A]: Does blockade of the programmed death-1 pathway restore sarcoidosis CD4 ( + ) T-cell proliferative capacity?

[EX Q]: Cape Town, South Africa.', 'To evaluate anti-tuberculosis treatment outcomes and rate of antiretroviral therapy (ART) initiation using weekly community-based adherence support compared to daily directly observed therapy (DOT).', 'This was a retrospective analysis comparing two cohorts treated for tuberculosis (TB) in 70 TB clinics during 6-month periods before and after the introduction of a new adherence model comprising treatment literacy sessions during 2 weeks of DOT, followed by weekly home visits by community care workers to eligible patients managing their own treatment. Odds ratios (ORs) of treatment success and ART initiation were calculated using multivariable random effects logistic regression models. Hazard ratios (HRs) of default and death were calculated using multivariable random effects Cox regression models.', 'The pre-intervention cohort comprised 11896 patients with TB and the post-intervention cohort 11314. There was no difference in pre- and post-intervention anti-tuberculosis treatment success rates (respectively 82.8% and 82.5%, adjusted OR [aOR] 1.02, 95%CI 0.89-1.17, P = 0.76) nor an increased hazard of death (adjusted HR [aHR] 0.98, 95%CI 0.80-1.21, P = 0.87) or default (aHR 0.97, 95%CI 0.81-1.15, P = 0.69). The ART initiation rate increased from 67% to 74% (aOR 1.43; 95%CI 1.01-1.85, P < 0.01).
[EX A]:
Does an integrated community TB-HIV adherence model provide an alternative to DOT for tuberculosis patients in Cape Town?