TASK DEFINITION: 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.
PROBLEM: Context: Acute kidney injury (AKI) is an established indicator of all-cause mortality in a coronary care unit (CCU), and evaluating the risks of renal dysfunction can guide treatment decisions. In this study we used the Society of Thoracic Surgeons (STS) score to predict the incidence of AKI in CCU patients who had not undergone coronary artery bypass surgery (CABG) after a cardiac angiogram.', 'The study cohort comprised 126 patients diagnosed with 2 or 3 coronary vessels disease who did not receive CABG during their hospital course. This study was performed in the CCU of a tertiary referral university hospital between September 2012 and August 2013. The STS score was evaluated with adjustment in all patients and the outcomes of the risk of mortality, morbidity, or mortality and renal failure were selected for predicting assessment. Furthermore, the performance of the STS scores was compared with that of other scoring systems.', 'A total of 28.5% (36 of 126) of the patients had AKI of varying severity. For predicting AKI, the STS renal failure score was excellent, with areas under the receiver operating characteristic curve of 0.851 0.039, p < 0.001. When compared with other scoring systems, the STS renal failure score demonstrated the highest discriminatory power, the most favorable Youden index, and the highest overall correctness of prediction.\Question: Do society of Thoracic Surgeons score predicts kidney injury in patients not undergoing bypass surgery?

SOLUTION: The STS score is an effective tool for predicting AKI in patients with coronary artery disease who have not undergone CABG. Frequent monitoring of serum creatinine level or early application of AKI biomarkers are warranted for STS renal failure 5.7% or greater.

PROBLEM: Context: Efforts to improve outcomes from acute kidney injury (AKI) have focussed on timely diagnosis and effective delivery of basic patient care. Electronic alerts (e-alerts) for AKI have attracted interest as a tool to facilitate this. Initial feasibility has already been demonstrated; this review will discuss recent advances in alert methodology, implementation beyond single centres and reported effect on outcomes.', 'On-going descriptions of e-alerts highlight increasing variation in both detection algorithms and alert processes. In England, this is being addressed by national rollout of a standardized detection algorithm; recent data have shown this to have good diagnostic performance. In critical care, fully automated detection systems incorporating both serum creatinine and urine output criteria have been developed. A recent randomized trial of e-alerts has also been reported, in which isolated use of a text message e-alert did not affect either clinician behaviour or patient outcome.\Question: Does recent developments in electronic alert for acute kidney injury?

SOLUTION: As e-alerts gain popularity, consideration must be given to both the method of AKI detection and the method by which results are communicated to end-users; these aspects influence the degree of these systems' effectiveness. This approach should be coupled to further work to study the effect on patient outcomes of those interventions that have been demonstrated to influence clinician behaviour.

PROBLEM: Context: Neutrophil infiltration of the postischemic tissue considerably contributes to organ dysfunction on ischemia/reperfusion injury. Beyond its established role in fibrinolysis, tissue-type plasminogen activator (tPA) has recently been implicated in nonfibrinolytic processes. The role of this serine protease in the recruitment process of neutrophils remains largely obscure.', 'Using in vivo microscopy on the postischemic cremaster muscle, neutrophil recruitment and microvascular leakage, but not fibrinogen deposition at the vessel wall, were significantly diminished in tPA(-/-) mice. Using cell transfer techniques, leukocyte and nonleukocyte tPA were found to mediate ischemia/reperfusion-elicited neutrophil responses. Intrascrotal but not intra-arterial application of recombinant tPA induced a dose-dependent increase in the recruitment of neutrophils, which was significantly higher compared with stimulation with a tPA mutant lacking catalytic activity. Whereas tPA-dependent transmigration of neutrophils was selectively reduced on the inhibition of plasmin or gelatinases, neutrophil intravascular adherence was significantly diminished on the blockade of mast cell activation or lipid mediator synthesis. Moreover, stimulation with tPA caused a significant elevation in the leakage of fluorescein isothiocyanate dextran to the perivascular tissue, which was completely abolished on neutrophil depletion. In vitro, tPA-elicited macromolecular leakage of endothelial cell layers was abrogated on the inhibition of its proteolytic activity.\Question: Does tissue plasminogen activator promote postischemic neutrophil recruitment via its proteolytic and nonproteolytic properties?

SOLUTION:
Endogenously released tPA promotes neutrophil transmigration to reperfused tissue via proteolytic activation of plasmin and gelatinases. As a consequence, tPA on transmigrating neutrophils disrupts endothelial junctions allowing circulating tPA to extravasate to the perivascular tissue, which, in turn, amplifies neutrophil recruitment through the activation of mast cells and release of lipid mediators.