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.

Context: Interobserver and intraobserver reliability study of improved method to evaluate radiographs of patients with scoliosis.', 'To determine the reliability of a computer-assisted measurement protocol for evaluating Cobb angle and King et al classification.', 'Evaluation of scoliosis radiographs is inherently unreliable because of technical and human judgmental errors. Objective, computer-assisted evaluation tools may improve reliability.', 'Posteroanterior preoperative radiographic images of 27 patients with adolescent idiopathic scoliosis were each displayed on a computer screen. They were marked 3 times in random sequence by each of 5 evaluators (observers) who marked 70 standardized points on the vertebrae and sacrum in each radiograph. A computer program (Spine 2002;27:2801-5) that identified curves, calculated Cobb angles, and generated the King et al classification automatically analyzed coordinates of these points. The interobserver and intraobserver variability of the Cobb angle and King et al classification evaluations were quantified and compared with values obtained by unassisted observers.', 'Average Cobb angle intraobserver standard deviation was 2.0 degrees for both the thoracic and lumbar curves (range 0.1 to 8.3 degrees for different curves). Interobserver reliability was 2.5 degrees for thoracic curves and 2.6 degrees for lumbar curves. Among the 5 observers, there was an inverse relationship between repeatability and time spent marking images, and no correlation with image quality or curve magnitude. Kappa values for the variability of the King et al classification averaged 0.85 (intraobserver).\Question: Do computer-assisted algorithms improve reliability of King classification and Cobb angle measurement of scoliosis?
Variability of Cobb measurements compares favorably with previously published series. The classification was more reliable than achieved by unassisted observers evaluating the same radiographs. The same principles may be applicable to other radiographic measurement and evaluation procedures.

Context: Trauma centers are currently benchmarked on mortality outcomes alone. However, pay-for-performance measures may financially penalize centers based on complications. Our objective was to determine whether the results would be similar to the current standard method of mortality-based benchmarking if trauma centers were profiled on complications.', 'We analyzed data from the National Trauma Data Bank from 2007 to 2010. Patients 16 years or older with blunt or penetrating injuries and an Injury Severity Score (ISS) of 9 or higher were included. Risk-adjusted observed-to-expected (O/E) mortality ratios for each center were generated and used to rank each facility as high, average, or low performing. We similarly ranked facilities on O/E morbidity ratios defined as occurrence of any major complication. Concordance between hospital performance rankings was evaluated using a weighted κ statistic. Correlation between morbidity- and mortality-based O/E ratios was assessed using Pearson coefficients. Sensitivity analyses were performed to mitigate the competing risk of death for the morbidity analyses.', 'A total of 449,743 patients from 248 facilities were analyzed. The unadjusted morbidity and mortality rates were 10.0% and 6.9%, respectively. No correlation was found between morbidity- and mortality-based O/E ratios (r = -0.01). Only 40% of the centers had similar performance rankings for both mortality and morbidity. Of the 31 high performers for mortality, only 11 centers were also high performers for morbidity. A total of 78 centers were ranked as average, and 11 ranked as low performers on both outcomes. Comparison of hospital performance status using mortality and morbidity outcomes demonstrated poor concordance (weighted κ = 0.03, p = 0.22).\Question: Does benchmarking trauma centers on mortality alone reflect quality of care : implications for pay-for-performance?
Mortality-based external benchmarking does not identify centers with high complication rates. This creates a dichotomy between current trauma center profiling standards and measures used for pay-for-performance. A benchmarking mechanism that reflects all measures of quality is needed.

Context: Adiponectin has been shown to possess potent anti-oxidative properties in various experimental conditions. However, its anti-oxidative effects and underlying mechanisms have not been reported in liver cells. Herein, we investigated the effects of globular adiponectin (gAcrp) on LPS-stimulated reactive oxygen species (ROS) production and its mechanisms underlying in human hepatic cells (HepG2).', 'Intracellular ROS production was determined by fluorescence of 5-chloromethyl-2,7-dichlorodihydrofluorescein diacetate (CM-H2DCFDA). NADPH oxidase-dependent ROS formation was determined by lucigenin-derived chemiluminescence. Messenger RNA expression level of target genes was determined by quantitative RT-PCR and protein expression was measured by Western blot analysis.', 'LPS-induced increase in ROS production was prevented by pretreatment with gAcrp in HepG2 cells. Furthermore, gAcrp treatment suppressed LPS-induced activation of NADPH oxidase and increase in mRNA and protein expression of Nox-4. We also found that adiponectin increased expression of FoxO3A and HO-1 and ablation of either of these genes partially restored suppression of LPS-induced ROS production and NADPH oxidase activation by gAcrp, indicating the vital role of FoxO3A and HO-1 signaling in the inhibition of ROS production and NADPH oxidase activation by gAcrp.\Question: Does globular adiponectin attenuate LPS-induced reactive oxygen species production in HepG2 cells via FoxO3A and HO-1 signaling?

These results suggest that gAcrp prevents LPS-induced ROS production and NADPH oxidase activity in HepG2 cells via FoxO3A and HO-1 signaling-dependent mechanisms. The present study demonstrated a suppressive effect of adiponectin on ROS production in liver cells and presented a novel mechanism underlying suppression of ROS production by adiponectin.