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.

[EX Q]: Context: We have previously demonstrated that hypertonic saline (HS) resuscitation decreased inflammation and mucosal injury after mesenteric ischemia/reperfusion (I/R). In contrast to I/R cell necrosis, apoptosis provides controlled cell death that minimizes inflammation. We therefore hypothesized that HS resuscitation after mesenteric I/R would induce apoptosis and decrease mucosal injury.', "Rats underwent 60 minutes of superior mesenteric artery occlusion (SMAO) and then received no resuscitation or resuscitation with 4 mL/kg of HS, 4 mL/kg of lactated Ringer's (LR) solution (equal volume), or 32 mL/kg of LR solution (equal salt load). Rats were killed at 6 hours of reperfusion, and ileum was harvested for analysis. DNA fragmentation (apoptosis) was assessed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) and mucosal injury by histology (Chiu score 0-5). Caspase-3 (proapoptotic mediator) and Bcl-xL (antiapoptotic mediator) protein expression were analyzed by Western immunoblot.", 'SMAO with no resuscitation, SMAO with 4 mL/kg of LR, and SMAO with 32 mL/kg of LR increased apoptosis (quantitated by TUNEL) and I/R-induced mucosal injury (quantitated by Chiu score). This was associated with an increase to similar levels in both proapoptotic caspase-3 and antiapoptotic Bcl-xL protein expression. Moreover, SMAO with 4 mL/kg of HS further increased apoptosis but decreased mucosal injury. This was associated with a differential expression of proapoptotic caspase-3 over antiapoptotic Bcl-xL.\Question: Does hypertonic saline resuscitation after mesenteric ischemia/reperfusion induce ileal apoptosis?
[EX A]: HS resuscitation after mesenteric I/R significantly increased ileal mucosal apoptosis while decreasing mucosal injury and may represent a novel mechanism by which HS resuscitation after mesenteric I/R reduces inflammation and imparts protection to the gut.

[EX Q]: Context: Re-stenosis after percutaneous coronary angioplasty (PTCA) is related to clinical and angiographic features.', 'To describe the clinical and angiographic characteristic of our patients with coronary cardiopathy subjected to PTCA and the predictor factors for re-stenosis.', 'We gathered the clinical and angiographic characteristics of all patients who underwent a successful PTCA of a native coronary artery. All patients had a clinical assessment one year after the procedure. Patients were classified in Group 1, if they did not have angina or coronary events after the angioplasty or Group 2, if they had angina or a coronary event after the procedure. Only Group 2 patients were subjected to a coronary angiogram.', 'We collected 383 PTCA procedures. Follow up information was obtained in 92.2%. Three hundred forty two patients (89.3%) were assessed one year the procedure. Nine patients (2.3%) died of a cardiovascular cause. Ninety patients (26.3%) were classified in Group 2. In 65 patients, angiographic re-stenosis was demonstrated (19%). Re-stenosis occurred in 36 and 13% of patients with an without Diabetes Mellitus, respectively (p <0.01). The other clinical predictor variables were a history of myocardial infarction (p =0.007), obesity (p =0.041) and hypercholesterolemia (p =0.050). None of the angiographic characteristics predicted restenosis. Stents were protective factors against restenosis (15.6% in stented lesions vs 25.4% in nonstented; p =0.01).\Question: Do [ One year follow up of successful coronary angioplasty in non selected patients ]?
[EX A]: Re-stenosis after angioplasty occurred in 19% of our patients with angina or coronary events. The clinical variables associated with a higher risk of re-stenosis were diabetes (the main risk factor), previous myocardial infarction, obesity and hypercholesterolemia. Angiographic variables were not associated with re-stenosis. The use of stents decreases the incidence of re-stenosis in all groups).

[EX Q]: Context: There is no reliable serum marker available to monitor incipient pancreas or islet-cell rejection. We tested the hypothesis that quantification of donor-specific genomic DNA in serum (from tissue damage) can serve as a marker of rejection.', 'Using a recently developed panel of HLA-specific quantitative PCR assays (Q-PCR), we tested 158 sera from 42 pancreas-kidney transplant recipients. Temporally related biopsies for 65 sera permitted analysis for correlation of donor DNA concentrations with rejection.', 'Donor DNA concentrations were higher in sera from recipients who had experienced allograft rejection (n = 31) than from those who had not (n = 34). Median concentrations, expressed as the genome-equivalent (gEq) number of donor cells per 10(6) host cells, were 2613 and 59 gEq/10(6), respectively (P = 0.03).\Question: Do soluble donor DNA concentrations in recipient serum correlate with pancreas-kidney rejection?
[EX A]:
Q-PCR for donor-specific genetic polymorphisms merits further investigation as a noninvasive approach to monitor pancreas-kidney as well as other types of allograft rejection.