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.

Q: 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?

A: 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.
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Q: Context: Ingested proteins are known to stimulate a rise in insulin and glucagon concentrations. In our effort to explain this effect, we have begun to measure the effect of individual amino acids.', 'The objectives were to determine the effect of lysine ingestion on insulin and glucagon concentrations and whether the effect is moderated by glucose ingestion.', 'Thirteen healthy subjects were studied on 4 occasions. Water, 25 g glucose, 1 mmol lysine/kg lean body mass, or lysine plus glucose was given on separate occasions at 0800 after a 12-h fast. Serum lysine, glucose, insulin, and glucagon were measured during a 2.5-h period. The amount of lysine provided was equivalent to that present in a 672-g (24-oz) steak.', 'Lysine ingestion resulted in an approximately 3-fold increase in lysine concentration and in a small decrease in glucose concentration. When lysine was ingested with glucose, the 2.5-h glucose area response decreased by 44% (P < 0.02). Lysine alone increased the insulin area response modestly; the insulin increase when lysine was ingested with glucose was similar to that when only glucose was ingested. Lysine stimulated an increase in glucagon (P < 0.02), whereas glucose decreased glucagon.\Question: Does lysine ingestion markedly attenuate the glucose response to ingested glucose without a change in insulin response?

A: Lysine ingestion results in a small decrease in serum glucose and an increase in glucagon and insulin concentrations. Lysine ingested with glucose dramatically attenuated the glucose-stimulated glucose response, but there was no change in insulin response. Whether similar effects will be observed with more physiologic doses of lysine remains to be determined.
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Q: Context: HIV patients exposed to abacavir have an increased risk of myocardial infarction, with contradictory results in the literature. The aim of our study was to determine whether abacavir has a direct effect on platelet activation and aggregation using platelets from healthy donors and from HIV-infected patients under therapy with an undetectable viral load.', 'Platelet-rich plasma (PRP) or whole blood from healthy donors was treated with abacavir (5 or 10 μg/mL) or its active metabolite carbovir diphosphate. Experiments were also performed using blood of HIV-infected patients (n\u200a=\u200a10) with an undetectable viral load. Platelet aggregation was performed on PRP by turbidimetry and under high shear conditions at 4000 s', 'Abacavir and carbovir diphosphate significantly increased the aggregation of platelets from healthy donors induced by collagen at 2 μg/mL (P\u200a=\u200a0.002), but not at 0.5 μg/mL. No effect of abacavir or carbovir diphosphate was observed on platelet aggregation induced by other physiological agonists or by high shear stress, or on thrombin generation. Pretreatment of blood from HIV-infected patients with abacavir produced similar results.\Question: Does abacavir have no prothrombotic effect on platelets in vitro?

A:
Our results suggest that abacavir does not significantly influence platelet activation in vitro when incubated with platelets from healthy donors or from HIV-infected patients. It is, however, not excluded that a synergistic effect with other drugs could promote platelet activation and thereby play a role in the pathogenesis of myocardial infarction.
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