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.

[Q]: Alcoholic liver disease (ALD) ranges from fatty liver to inflammation and cirrhosis. miRNA-155 is an important regulator of inflammation. In this study, we describe the in vivo role of miR-155 in ALD.', 'Wild-type (WT) (C57/BL6J) or miR-155 knockout (KO) and TLR4 KO mice received Lieber DeCarli diet for 5weeks. Some mice received corn oil or CCl4 for 2 or 9weeks.', 'We found that miR-155 KO mice are protected from alcohol-induced steatosis and inflammation. The reduction in alcohol-induced fat accumulation in miR-155 KO mice was associated with increased peroxisome proliferator-activated receptor response element (PPRE) and peroxisome proliferator-activated receptors (PPAR)α (miR-155 target) binding and decreased MCP1 production. Treatment with a miR-155 inhibitor increased PPARγ expression in naïve and alcohol treated RAW macrophages. Alcohol increased lipid metabolism gene expression (FABP4, LXRα, ACC1 and LDLR) in WT mice and this was prevented in KO mice. Alcohol diet caused an increase in the number of CD163(+) CD206(+) infiltrating macrophages and neutrophils in WT mice, which was prevented in miR-155 KO mice. Kupffer cells isolated from miR-155 KO mice exhibited predominance of M2 phenotype when exposed to M1 polarized signals and this was due to increased C/EBPβ. Pro-fibrotic genes were attenuated in miR-155 KO mice after alcohol diet or CCl4 treatment. Compared to WT mice, attenuation in CCl4 induced hydroxyproline and α-SMA was observed in KO mice. Finally, we show TLR4 signaling regulates miR-155 as TLR4 KO mice showed no induction of miR-155 after alcohol diet.
[A]: 1


[Q]: To investigate if diabetic patients without diabetic retinopathy despite long disease duration have different human leukocyte antigen (HLA) status vs those with an early onset of retinopathy.', 'Retrospective, nonrandomized, masked comparative study. Type 1 diabetic patients with a disease onset before age 30 were recruited to the study. The study population consisted of two groups of diabetic patients: those with normal retinopathy course (retinopathy developed during the first 20 years of diabetes onset) (23 patients) and those with postponed retinopathy (no obvious retinopathy in spite of passing 20 years of diabetes) (19 patients). These groups were matched with regard to level of glycemic control, blood pressure, and lipid profile. A group of 23 healthy patients served as controls. HLA-DQB1 typing of blood samples was done using a polymerase chain reaction with sequence-specific primer (PCR-SSP) method.', 'HLA-DQB1*0201/HLA-DQB1*0501 and HLA-DQB1*0201/HLA-DQB1*0504 haplotypes were more common among type 1 diabetic patients with normal retinopathy course than those with postponed retinopathy (26.1% vs 0.0%; p=0.019). HLA-DQB1*0301 and HLA-DQB1*0304 were less common among those diabetic patients with normal retinopathy course than those with a postponed retinopathy (63.2% vs 34.8%; p=0.067).
[A]: 1


[Q]: High dose melphalan (HDM) and autologous stem cell transplantation (ASCT) retains a central role in the treatment of myeloma. The aim of this study was to determine whether HDM exposure (area under the concentration vs. time curve, AUC), is significantly associated with transplant outcomes.', 'Melphalan concentrations were measured in six to 11 plasma samples collected after HDM (median 192\xa0mg\xa0m(-) (2) ) to determine melphalan AUC for a total of 114 patients. Binary logistic regression was used to assess whether melphalan AUC was associated with severe (≥ grade 3) oral mucositis. Multivariate Cox regression was used to assess whether melphalan AUC was significantly associated with time to progression, progression-free survival and overall survival (OS).', 'Melphalan AUC ranged from 4.9 to 24.6\xa0mg\xa0l(-1) \xa0h, median 12.84\xa0mg\xa0l(-1) h. Melphalan AUC above the median was a risk factor for severe mucositis (HR 1.21, 95% CI 1.06, 1.38, P\xa0=\xa00.004) but was also associated with significantly improved overall survival (OS) (HR 0.40, 95% CI 0.20, 0.81, P\xa0=\xa00.001), with an estimated median survival of 8.50\xa0years vs. 5.38\xa0years for high vs. low AUC groups. Multivariate analysis did not identify melphalan AUC as being significantly associated with time to progression or progression-free survival.
[A]:
1