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.
--------
Question: Context: Objective analysis of surgical skill is necessary. A novel method of assessment using simple error analysis in synthetic models is examined for construct validity.', 'Two examination protocols were devised using synthetic models. These contained either a purpose made error or were representative of good surgical practice. Protocol one contained models of skin closure and minor operations. Protocol two in addition more complex procedures. Face validity was established by the approval of senior surgeons. Junior surgeons were recruited to undertake the assessment. A p value of less than 0.05 was deemed to be significant.', 'Eighty-nine surgeons were recruited. Both protocol one and two were able to discriminate between groups at statistically significant levels.\Question: Is the surgical error examination a novel method for objective technical knowledge assessment?

Answer: Construct validity has been established by showing that error analysis is able to distinguish surgeons with varying levels of experience.


Question: Context: The purpose of this study was to investigate the ability of neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, and their combination in predicting the duration and severity of acute kidney injury (AKI) after cardiac surgery in adults.', 'Using data from a prospective observational study of 100 adult cardiac surgical patients, we correlated early postoperative concentrations of plasma NGAL and serum cystatin C with the duration (time during which AKI persisted according to the Acute Kidney Injury Network criteria) and severity of AKI (change in serum creatinine) and with length of stay in intensive care.', 'We found a mean AKI duration of 67.2 +/- 41.0 hours which was associated with prolonged hospitalization (p < 0.001). NGAL, cystatin C, and their combination on arrival in intensive care correlated with subsequent AKI duration (all p < 0.01) and severity (all p < 0.001). The area under the receiver operating characteristic curve for AKI prediction was 0.77 (95% confidence interval: 0.63 to 0.91) for NGAL and 0.76 (95% confidence interval: 0.61 to 0.91) for cystatin C on arrival in intensive care. Both markers also correlated with length of stay in intensive care (p = 0.037; p = 0.001). Neutrophil gelatinase-associated lipocalin and cystatin C were independent predictors of AKI duration and severity and of length of stay in intensive care (all p < 0.05). The value of cystatin C on arrival in intensive care appeared to be due to a carry-over effect from preoperative values.\Question: Do novel biomarkers early predict the severity of acute kidney injury after cardiac surgery in adults?

Answer: Immediately postoperatively, NGAL and cystatin C correlated with and were independent predictors of duration and severity of AKI and duration of intensive care stay after adult cardiac surgery. The combination of both renal biomarkers did not add predictive value.


Question: Context: Evidence suggests that induction of heme oxygenase-1 (HO-1) inhibits proliferation of vascular smooth muscle cells and intimal thickening after arterial injury, and therapeutic molecules induce HO-1. Probucol is the only oral drug that inhibits restenosis in humans and intimal thickening in animals, although its underlying mechanism remains unclear.', 'Aortas were harvested from New Zealand White rabbits fed normal or 0.75% (wt/wt) probucol-fortified chow, with or without endothelial denudation of the abdominal aorta on day 21, and analyzed for heme oxygenase and apoptosis. Uninjured aortas were harvested on day 21 and balloon-injured aortas on days 22 and 25. Probucol significantly increased mRNA of HO-1 assessed by real-time PCR and HO activity in aortas at all time points. Probucol also enhanced apoptosis of medial cells in the injured aorta, as evidenced by the TUNEL assay. Furthermore, probucol (100 micromol/L) increased HO-1 mRNA and HO activity when added to rabbit aortic smooth muscle cells (RASMCs) cultured in serum-free medium for 24 hours. Induction of HO-1 mRNA was inhibited by actinomycin D and was associated with inhibition of RASMC proliferation. This probucol-induced increase in HO-1 mRNA and inhibition of RASMC proliferation was prevented by the HO inhibitor Sn(IV) protoporphyrin or transfection with small interference RNA (siRNA) to knockdown HO-1, but not by inactive Cu(II) protoporphyrin or scrambled siRNA.\Question: Does probucol protect against smooth muscle cell proliferation by upregulating heme oxygenase-1?

Answer:
Probucol induces HO-1, and this contributes to the inhibition of vascular SMC proliferation. This novel finding may explain how probucol inhibits restenosis and highlights HO-1 as a target for therapeutic intervention against occlusive vascular disease.