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: Recent randomized trials suggest that intensive glycaemic control fails to reduce heart failure-related events in patients with diabetes. The molecular cues underlying persistent myocardial damage despite normoglycaemia restoration remain elusive. MicroRNAs (miRNAs), a class of small non-coding RNAs, orchestrate transcriptional programs implicated in adverse cardiac remodelling. The present study investigates whether miRNAs participate to hyperglycaemic memory in the diabetic heart.', 'miRNA landscape was assessed by Mouse miRNome miRNA PCR Arrays in left ventricular specimens collected from 4-month-old streptozotocin-induced diabetic mice, with or without intensive glycaemic control by slow-release insulin implants. A dysregulation of 316 out of 1008 total miRNAs was observed in the diabetic hearts when compared with controls. Of these, 209 were up-regulated and 107 were down-regulated by >2.0-fold. Interestingly enough, the expression of 268 of those miRNAs remained significantly altered in diabetic mice even after subsequent normoglycaemia. Ingenuity pathway analysis revealed that dysregulated miRNAs were implicated in myocardial signalling networks triggering apoptosis (miR-320b, miR-378, miR-34a), fibrosis (miR-125b, miR-150, miR-199a, miR-29b, miR30a), hypertrophic growth (miR-1, miR-150, miR-199a, miR-133a, miR-214, miR-29a, miR-125b, miR-221, miR-212), autophagy (miR-133a, miR-221, miR-212, miR30a), oxidative stress (miR-221, miR-146a, miR-34a, miR-210, miR-19b, miR-125b, miR27a, miR-155), and heart failure (miR-423, miR-499, miR-199a), respectively.

A: 1
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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
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Q: The aim of this study was to investigate the relationship between intraoperative vasopressin infusion and postoperative cardiac enzymes.', 'A prospective, double-blind, randomized, controlled study.', 'A single tertiary cardiac center.', 'One hundred consecutive patients undergoing cardiac surgery with or without cardiopulmonary bypass.', 'The study was approved by the Institutional Review Board, and patients provided informed consent to participate. Patients were randomized by computer into 2 equal groups: Vasopressin or control. The blinded study included vasopressin administered at a dose of 1.8 U/h or 1.8 mL/h of normal saline, along with catecholamines. The drug was administered continually during surgery while patients needed catecholamines. The intervention was discontinued upon admission to the intensive care unit when information regarding the true character of the drug was reported to the doctor in charge of patients in the intensive care unit by one of the investigators. Primary outcomes were CK-MB and troponin T levels measured at 0, 6, and 12 hours postoperatively.', 'Of the 100 patients, 8 were excluded; the remaining 92 were randomized to either the vasopressin (n = 47) or control (n = 45) group. There were no significant differences in demographic data between the groups. Postoperatively at 0, 6, and 12 hours, there were no differences in CK-MB (U/l) (37.5 ± 57.9 v 32.0 ± 21.5, 29.4 ± 41.1 v 24.4 ± 23.1, and 21.4 ± 21.3 v. 21.8 ± 32.4, respectively) and troponin T (752.4 ± 638.2 v 762.7 ± 557.1, 753.8 ± 507.3 v 777.6 ± 515.0, and 774.6 ± 572.6 v 698.7 ± 540.2, respectively) values.

A:
1
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