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.
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Question: To evaluate whether genotypes of interleukin (IL)-6 gene promoter positions -174 and -572 are associated with histologic chorioamnionitis and neonatal inflammatory disease in preterm infants.', 'DNA from very low birth weight or very preterm infants (n = 107) was genotyped for IL-6-174 and -572 polymorphisms (GG/GC/CC). The placentas were analyzed for histological inflammatory findings. Data on neonatal inflammatory diseases, including chronic lung disease (CLD), necrotizing enterocolitis (NEC), and septicemia, were collected using the definitions of the Vermont Oxford Network database.', 'In univariate analyses, the IL-6-174 GG genotype was associated with a higher incidence of histologic chorioamnionitis. In multivariate analyses, the -174 GG and -572 GC genotypes were correlated with histologic chorioamnionitis (P = .039 and .009, respectively). Gestational age was not associated with genotype polymorphisms. IL-6-174 genotypes were not associated with CLD and/or NEC, but the CC genotype was correlated with septicemia in both univariate and multivariate analyses (P = .027). IL-6-572 genotypes were not associated with neonatal inflammatory disease.

Answer: 1


Question: The apoptosis inhibitor-5 (API5), anti-apoptosis protein, is considered a key molecule in the tumor progression and malignant phenotype of tumor cells. Here, we investigated API5 expression in cervical cancer, its clinical significance, and its relationship with phosphorylated extracellular signal-regulated kinase 1 and 2 (pERK1/2) in development and progression of cervical cancer.', 'API5 effects on cell growth were assessed in cervical cancer cell lines. API5 and pERK1/2 immunohistochemical staining were performed on a cervical cancer tissue microarray consisting of 173 primary cervical cancers, 306 cervical intraepithelial neoplasias (CINs), and 429 matched normal tissues.', 'API5 overexpression promoted cell proliferation and colony formation in CaSki cells, whereas API5 knockdown inhibited the both properties in HeLa cells. Immunohistochemical staining showed that API5 expression increased during the normal to tumor transition of cervical carcinoma (P\u2009<\u20090.001), and this increased expression was significantly associated with tumor stage (P\u2009=\u20090.004), tumor grade (P\u2009<\u20090.001), and chemo-radiation response (P\u2009=\u20090.004). API5 expression levels were positively associated with pERK1/2 in cervical cancer (P\u2009<\u20090.001) and high grade CIN (P\u2009=\u20090.031). In multivariate analysis, API5+ (P\u2009=\u20090.039) and combined API5+/pERK1/2+ (P\u2009=\u20090.032) were independent prognostic factors for overall survival.

Answer: 0


Question: Using publicly available data from inbred mouse strains, we conducted a genome-wide association study to identify loci that accounted for liver-related phenotypes between C57BL/6J and A/J mice fed a Paigen diet. We confirmed genome-wide significant associations for hepatic cholesterol (chromosome 10A2) and serum total bile acid concentration (chromosome 12E) and identified a new locus for liver inflammation (chromosome 7C). Analysis of consomic mice confirmed that chromosome 12 A/J alleles accounted for the variance in serum total bile acid concentrations and had pleiotropic effects on liver mass, serum cholesterol, and serum alanine aminotransferase activity. Using an affected-only haplotype analysis among strains, we refined the chromosome 12E signal to a 1.95 Mb linkage disequilibrium block containing only one gene, sel-1 suppressor of lin-12-like (Sel1l). RNA sequencing and immunoblotting demonstrated that the risk allele locally conferred reduced expression of SEL1L in liver and distantly down-regulated pathways associated with hepatocyte nuclear factor 1 homeobox A (Hnf1a) and hepatocyte nuclear factor 4A (Hnf4a), known modifiers of bile acid transporters and metabolic traits. Consistent with these data, knockdown of SEL1L in HepG2 cells resulted in reduced HNF1A and HNF4A and increased bile acids in culture media; it further captured multiple molecular signatures observed in consomic mouse livers with reduced SEL1L. Finally, dogs harboring a SEL1L mutation and Sel1l(+/-) mice fed a Paigen diet had significantly increased serum total bile acid concentrations, providing independent confirmation linking SEL1L to bile acid metabolism.

Answer:
0