instruction:
Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
question:
P53 is a key protein which controls cell cycle arrest and apoptosis in response to DNA damage. Auto-antibodies against p53 have been detected in some cancer patients and also in patients with autoimmune diseases. In these patients, the main cause of anti-p53 antibody occurrence was considered to be increased intracellular p53 protein in cancer cells and autoreactive lymphocytes, respectively. Intracellular p53 also increases with cardiomyocyte apoptosis during heart failure and autoreactive lymphocytes play a role in the course of idiopathic dilated cardiomyopathy (IDC) and ischemic cardiomyopathy (ICM). Based on these observations, we hypothesized that anti-p53 antibody response may also occur in patients with heart failure due to ICM and IDC.', 'The aim of this study was to evaluate anti-p53 antibodies in the serum of patients with heart failure due to IDC and ICM.', '70 eligible patients with heart failure and severe left ventricular systolic dysfunction (mean fractional shortening 12.03 +/- 3.93%) were included in the study. The aetiology of heart failure was IDC in 26 patients and ICM in 44 patients, according to the angiographic and echocardiographic findings.', 'Anti-p53 antibodies were not detected in any of the patients.
answer:
Do serum anti-p53 antibodies occur in patients with heart failure due to idiopathic dilated and ischemic cardiomyopathies?


question:
The antifibrotic substance pirfenidone and the angiotensin II type I receptor antagonist candesartan cilexetil, given alone and in combination, were tested in rats with chronic anti-glomerular basement membrane glomerulonephritis (anti-GBM GN).', 'Male Wistar rats with anti-GBM GN were treated for 8 weeks with candesartan (4 mg/kg body weight/day), pirfenidone (500 mg/kg body weight/day) or a combination of both drugs. One GN group received no treatment and untreated non-GN-rats were used as controls. Blood pressure and urinary protein excretion were measured after 3 and 7 weeks. Kidney histology was complemented by ultrastructural investigation and by quantification of collagen Ialpha mRNA.', 'The percentage of glomeruli with adsorption droplets in podocytes correlated well with the amount of proteinuria (r = 0.873, P<0.01) and was significantly lowered in rats treated with candesartan (8.3 vs GN 24.6%), pirfenidone (9.8%) and combined treatment (2.6%, P<0.05 vs candesartan alone). A comparable lowering was seen for segmental sclerosis (GN 11%, candesartan 0.7%, P<0.05 vs GN, pirfenidone 1.8%, P = 0.09 vs GN, candesartan/pirfenidone 0.1%, P>0.5 vs candesartan alone). Cortical collagen Ialpha mRNA expression was significantly decreased in all treatment groups. Ultrastructural investigation showed an amelioration of basement membrane alterations and podocyte damage in the treatment groups. Candesartan caused significant blood pressure reduction and the effect was significantly enhanced by combination therapy after 3 weeks. Rats treated with pirfenidone showed blood pressure values similar to control rats.
answer:
Do pirfenidone and candesartan ameliorate morphological damage in mild chronic anti-GBM nephritis in rats?


question:
Acidic fibroblast growth factor (aFGF) has potentially therapeutic uses in some diseases, but the mitogenic activity of aFGF has been found to contribute to several human pathologies, so the extensive applications of wild-type aFGF have been limited. The purpose of the present study was to explore the effects and mechanisms of wild-type (aFGF) and non-mitogenic aFGF on gut ischemia-reperfusion injury in rats.', 'Rat intestinal ischemia-reperfusion injury (I/R) was produced by clamping the superior mesenteric artery (SMA) for 45 min followed by reperfusion. One hundred and fourteen rats were randomly divided into four groups: sham operation (group C, n = 6), intestinal I/R + 0.1 mL saline (group S, n = 36), intestinal I/R + 4 microg/0.1 mL wild-type aFGF (group W, n = 36) and intestinal I/R + 4 microg/0.1 mL modified aFGF (i.e. non-mitogenic aFGF; group M, n = 36). According to different periods after reperfusion, groups S, W and M were further divided into 0.5-, 1-, 2-, 6-, 12- and 24-h subgroups. The contents of D-lactate and nitrite/nitrate were determined, the changes of intestinal histology were analyzed, the protein expressions of caspase-3, extracellular signal-regulated kinase (ERK)1/2, and p38 were detected by western blot, and apoptotic cells were examined by the terminal deoxynucleotidyl transferase (TdT)-mediated dUDP-biotin nick end labeling (TUNEL) assay at 0.5, 1, 2, 6, 12 and 24 h after I/R, respectively.', 'Compared with rats in group S, intestinal histological damage, apoptotic index, d-lactate content and nitrite/nitrate level all decreased significantly in group W and group M rats. However, there was no difference between rats treated with wild-type aFGF and those with non-mitogenic aFGF. The protein expression of caspase-3, ERK1/2, and p38 in saline-treated rats was higher than those in aFGF-treated rats.
answer:

Does non-mitogenic acidic fibroblast growth factor reduce intestinal dysfunction induced by ischemia and reperfusion injury in rats?