In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: Hypercontracture is an important mechanism of myocyte death during reperfusion. cGMP modulates the sensitivity of contractile myofilaments to Ca2+, and increasing cGMP concentration during the last minutes of anoxia prevents reoxygenation-induced hypercontracture in isolated cardiomyocytes. The purpose of this study was to determine whether stimulation of particulate guanylyl cyclase with the natriuretic peptide urodilatin, given at the time of reperfusion, reduces myocardial necrosis in the rat heart submitted to transient ischemia.', 'Isolated rat hearts (n = 38) were submitted to either 40 or 60 min of no-flow ischemia and 2 h of reperfusion, and were allocated to receive or not receive 0.05 microM urodilatin during the first 15 min of reperfusion or non-reperfusion treatment.', 'A marked reduction in myocardial cGMP concentration was observed in control hearts during reperfusion after 40 or 60 min of ischemia. Urodilatin significantly attenuated cGMP depletion during initial reperfusion, markedly improved contractile recovery after 40 min of ischemia (P < 0.0309), and reduced reperfusion-induced increase in left ventricular end-diastolic pressure (P = 0.0139), LDH release (P = 0.0263), and contraction band necrosis (P = 0.0179) after 60 min of ischemia. The beneficial effect of urodilatin was reproduced by the membrane permeable cGMP analog 8-Bromo-cGMP.\Question: Does urodilatin limit acute reperfusion injury in the isolated rat heart?

A: These results indicate that reduced cGMP concentration may impair myocyte survival during reperfusion. Stimulation of particulate guanylyl cyclase may appear as a new strategy to prevent immediate lethal reperfusion injury.
****
Q: Context: To evaluate the relationship between pro-atherogenic biomarkers and epicardial adipose tissue (EAT) thickness in patients with cardiovascular risk factors.', 'Plasma nitric oxide (NO), soluble intercellular adhesion molecule-1 and malondialdehyde (MDA) levels, EAT thickness, flow-mediated dilation (FMD) and carotid intima media thickness (CIMT) were determined in patients aged >18 years who were referred for echocardiography for heart ischemia or non-ischemic diseases. Cardiovascular risk factors (Framingham score [FS]20) were weighted.', 'Hypertension, dyslipidaemia and type 2 diabetes mellitus were prevalent (55% of 40 patients). Patients with FS20 (n=21) showed significantly higher EAT and CIMT values. Globally, MDA, CIMT, age, waist circumference, high-density lipoprotein cholesterol (HDL-C) and FS were associated with EAT thickness. EAT was significantly associated with NO in patients with FS20. Significant differences in EAT thickness were found between patients stratified by NO value, FMD, age, smoking status, dyslipidaemia, type 2 diabetes mellitus and FS. An EAT-associated atherogenic risk (CIMT1mm) model was statistically significant when MDA and type 2 diabetes mellitus were included.\Question: Are pro-atherogenic mediators and subclinical atherogenesis related to epicardial adipose tissue thickness in patients with cardiovascular risk?

A: EAT thickness was associated with MDA, CIMT, age, waist circumference, HDL-C and FS globally, but with NO only in patients with FS20. EAT may be used to identify vascular damage stage, possibly influenced by MDA and type 2 diabetes mellitus.
****
Q: Context: Our previous work demonstrated altered messenger RNA expression of integrin -5 and -8, using an in silico analysis of publically available data from patients with biliary atresia (BA); however, we were unable to demonstrate statistically significant differences in protein expression because of sample size. In the present study, we repeated the analysis of liver fibrosis and protein expression of the integrins in a larger cohort of patients with BA and compared them with patients undergoing liver biopsy for other diagnoses, with the hypothesis that 1 of the integrins would be differentially expressed.', 'Liver specimens were obtained at 2 collaborating institutions. Samples from infants with BA (n = 23) were compared with samples from those who underwent liver biopsy for neonatal hepatitis (n = 9). All of the specimens were analyzed by 2 pathologists (C.R. and R.A.), who were blinded to the diagnoses. Standard Ishak scoring was performed to evaluate fibrosis and inflammation, and immunohistochemical (IHC) positivity was graded from 0 to 4. Comparisons between the IHC positivity and Ishak scoring for the BA and control groups were performed using the Student t test with P < 0.01 considered significant because of the multiple comparisons. Interobserver variability was assessed by intraclass correlation (ICC).', 'Pooled analysis from specimens from patients with BA showed significantly more fibrosis than controls based on Ishak scores (3.21 1.82 vs 1.17 1.00, P < 0.005). IHC evaluation showed increased integrin 8 protein expression when compared with controls (2.67 0.81 vs 1.72 0.62, P < 0.005); however, there were no significant differences in integrin 5 (1.93 0.84 vs 1.50 0.90, P = 0.23) or integrin 6 (0.85 1.20 vs 0.94 0.85, P = 0.82) expression. These data were confirmed on individual analysis. Interobserver agreement was fair for integrin 5 (ICC 0.52), good for integrin 6 (ICC 0.72), and excellent for integrin 8 (ICC 0.79) and fibrosis (ICC 0.89).\Question: Is integrin -8 , but not -5 or -6 , protein expression increased in livers of children with biliary atresia?

A:
Our data show that integrin 8, but not integrin 5 or integrin 6, protein expression is increased in liver specimens of patients with BA. These data support the mounting evidence that transforming growth factor- (TGF-) activation is responsible for the fibrosis found in BA. Anti-integrin 8 or more global integrin blocking strategies may be therapeutic options in BA, but further work is clearly needed.
****