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 Input:
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?

Ex Output:
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.

Ex Input:
Context: In HIV patients, disorders in glucose metabolism seem to be side effects of highly active antiretroviral therapy (HAART) which may be favoured by obesity, abdominal fat accumulation and familial disposition for diabetes mellitus (DM). The aim of our study was to identify patients at high risk for abnormalities in glucose metabolism taking into account HAART, familial disposition for DM and anthropometric parameters.', 'Plasma glucose, insulin, c-peptide and insulin resistance (homeostasis model assessment, HOMA) were determined in 44 HIV patients [16 without HAART, 19 with protease inhibitors (PI), 9 without PI (non-PI)] and in 11 healthy subjects. Glucose tolerance was determined by standard procedures. Body mass index (BMI), triceps skin fold thickness and waist circumference were measured and the waist-to-hip-ratio was calculated. Familial disposition for DM was assessed by questionnaire.', 'Impaired fasting glucose was observed in 28% of HAART-treated patients (21% with PI, 7% non-PI), in 13% of HAART-naive but none in healthy controls. 58% of PI, 44% of non-PI, 38% of HAART-naive and none of healthy controls had a HOMA-index > 2.5 which indicates insulin resistance. HAART-treated patients had significantly higher fasting glucose levels (PI: 97 +/- 11 mg/dL, p = 0.048; non-PI: 109 +/- 58 mg/dL, p = 0.009) compared to healthy controls (72 +/- 8 mg/dL). HOMA-Index was higher in PI treated patients (3.74 +/- 3.08) than in HIV negative controls (0.95 +/- 0.28, p = 0.018). The duration of HAART (p = 0.045), overweight and familial disposition for DM (p = 0.017) significantly affected fasting glucose among PI users. Waist circumference affected c-peptide (p = 0.046) concentration in these patients.\Question: Are overweight HIV patients with abdominal fat distribution treated with protease inhibitors at high risk for abnormalities in glucose metabolism - a reason for glycemic control?

Ex Output:
HIV patients on long-term PI therapy with overweight and familial disposition for DM are at high risk to develop abnormalities of glucose metabolism. Thus, measurements of HOMA-Index, BMI and waist circumference should be routinely done especially in PI medicated patients.

Ex Input:
Context: R136K is a mutation of fibroblast growth factor-1 (FGF-1) in which arginine replaces lysine at the primary thrombin cleavage site. This may be important in vivo in inducing endothelial cell (EC) migration and coverage of arterial injury sites by allowing R136K to be used in a fibrin glue delivery system, without thrombin-induced degradation, in the absence of heparin. The objectives of this study were to determine whether R136K, with and without heparin, can induce migration of EC and smooth muscle cells (SMC) through fibrin glue, and to compare these results with those of wild-type FGF-1; and to determine the resistance of R136K to thrombin-induced degradation versus FGF-1.', 'The dose-response migration through fibrin glue induced by wild-type FGF-1 and the R136K mutant in the presence and absence of heparin was tested with EC and SMC. Migration was tested with 50, 100, and 200 ng/mL of both FGF-1 and R136K, either with or without 5 U/mL of heparin. Migration of EC was also assessed after growth inhibition with mitomycin C. A novel modified Boyden chamber-type migration assay using fibrin glue on the upper surface of the chamber filter was used to test migration. The fluorescent marker calcein was used to identify those cells that had migrated through the fibrin glue and were embedded in the filter. Molecular degradation by thrombin was assessed with sodium dodecylsulfate polyacrylamide gel electrophoresis.', 'For EC, R136K in the absence of heparin induced significantly more migration than did FGF-1 at 50 (P <.002), 100 (P <.0001), and 200 (P <.0001) ng/mL. In the presence of heparin, a chemotactic response of EC to cytokine was seen at all doses, with no significant difference between FGF-1 and R136K. A dose-dependent difference was noted in this group between the 100 and 200 ng/mL concentrations of cytokine (for FGF-1, P <.0001; for R136K, P <.0001). SMC showed no difference in migration with FGF-1, R136K, or negative control at any dose in the presence or absence of heparin. Gel electrophoresis demonstrated that R136K was more resistant to thrombin degradation than was FGF-1.\Question: Does r136K fibroblast growth factor-1 mutant induce heparin-independent migration of endothelial cells through fibrin glue?

Ex Output:
Site-directed mutagenesis of FGF-1 to R136K enables induction of heparin-independent migration of EC through fibrin glue at an optimal concentration of 100 ng/mL. Neither FGF-1 nor R136K elicits SMC migration through fibrin glue. The ability of R136K to induce EC migration through fibrin glue in the absence of heparin may prove useful in vivo by inducing EC migration and coverage of arterial injury sites, thus potentially reducing thrombogenicity and intimal hyperplasia.