TASK DEFINITION: Given a passage classify if the passage has a definite objective/aim/goal or not. Output '1' if the passage has a defininte objective/aim/goal and output '0' if the passage does not have a definite objective/aim/goal.
PROBLEM: Human hepatocellular carcinoma (HCC) heterogeneity promotes recurrence and resistance to therapies. Recent studies have reported that HCC may be derived not only from adult hepatocytes and hepatoblasts but also hepatic stem/progenitors. In this context, HepaRG cells may represent a suitable cellular model to study stem/progenitor cancer cells and the retrodifferentiation of tumor-derived hepatocyte-like cells. Indeed, they differentiate into hepatocyte- and biliary-like cells. Moreover, tumor-derived HepaRG hepatocyte-like cells (HepaRG-tdHep) differentiate into both hepatocyte- and biliary-like cells through a hepatic progenitor. In this study we report the mechanisms and molecular effectors involved in the retrodifferentiation of HepaRG-tdHep into bipotent progenitors. Gene expression profiling was used to identify genomic changes during the retrodifferentiation of HepaRG-tdHep into progenitors. We demonstrated that gene expression signatures related to a poor-prognosis HCC subclass, proliferative progenitors, or embryonic stem cells were significantly enriched in HepaRG progenitors derived from HepaRG-tdHep. HepaRG-tdHep retrodifferentiation is mediated by crosstalk between transforming growth factor beta 1 (TGF1) and inflammatory cytokine pathways (e.g., tumor necrosis factor alpha [TNF] and interleukin 6 [IL6]). Signatures related to TNF, IL6, and TGF activation pathways are induced within the first hour of retrodifferentiation. Moreover, specific activation or inhibition of these signaling pathways allowed us to determine that TNF and IL6 contribute to the loss of hepatic-specific marker expression and that TGF1 induces an epithelial-to-mesenchymal transition of HepaRG-tdHep. Interestingly, the retrodifferentiation process is blocked by the histone deacetylase inhibitor trichostatin A, opening new therapeutic opportunities.

SOLUTION: 0

PROBLEM: We reviewed our experience with preoperative chemoradiotherapy in patients with adenocarcinoma of the distal esophagus and pretreatment endoscopic ultrasonography-identified celiac adenopathy.', 'One hundred eighty-six patients with adenocarcinoma of the distal esophagus were staged with endoscopic ultrasonography before treatment from 1997 through 2004. All patients were treated with concurrent chemoradiotherapy (CRT group) and surgical intervention or induction chemotherapy followed by concurrent chemoradiotherapy (C-->CRT group) and surgical intervention. Survival analysis (excluding operative mortality) evaluated various pretreatment factors.', 'Multivariable Cox regression analysis showed that pretreatment endoscopic ultrasonography-identified celiac adenopathy was a significant predictor of decreased long-term survival (P = .03). Median and 3-year survivals were 49 months and 54% in the endoscopic ultrasonography-identified cN0 M0 group (n = 65), 45 months and 56% in the endoscopic ultrasonography-identified cN1 M0 group (n = 96), and 19 months and 12% in the endoscopic ultrasonography-identified celiac adenopathy (cM1a) group (n = 18; P = .03). Increased systemic relapse was noted in the endoscopic ultrasonography-identified cM1a group (44% vs 22%, P = .07). The only factor associated with increased survival in the endoscopic ultrasonography-identified cM1a group (27 vs 15 months, P = .02) was the addition of induction chemotherapy before concurrent chemoradiotherapy and surgical intervention.

SOLUTION: 1

PROBLEM: Study the prevalence and correlates of ADHD symptoms in the National Health Interview Survey (NHIS).', 'NHIS includes 10,367 children ages 4 to 17. Parents report lifetime diagnosis of ADHD and complete the Strengths and Difficulties Questionnaire (SDQ). Prevalences of clinically significant ADHD and comorbid symptoms by race and ethnicity, gender, and age are presented.', 'Prevalence of clinically significant SDQ ADHD symptoms is 4.19% (males) and 1.77% (females). Male prevalence by race is 3.06% for Hispanics, 4.33% for Whites, and 5.65% for Blacks. Significant differences in prevalence occur across gender (p < .01) and among males across race (p < .01), age (p < .01), and income (p < .02). In the full sample, 6.80% of males and 2.50% of females have a parent-reported lifetime ADHD diagnosis but are negative for SDQ ADHD. Likewise, 1.59% of males and 0.81% of females are positive for SDQ ADHD but negative for parent report of ADHD diagnosis. SDQ ADHD positive children have substantially higher proportions of elevated scores on other SDQ subscales.

SOLUTION:
1