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: Some subjects with suspected asthma and a negative exercise challenge test (ECT) demonstrate improved expiratory flow rates after administration of bronchodilators (BD) at the end of the ECT (unpublished observation). This study investigated whether this response predicts the presence of bronchial hyperreactivity (BHR).', 'The study population included 133 young adults (29.4% women) 21.1 +/- 4.2 years of age who underwent ECT and a methacholine challenge test (MCT). A receiver-operator-characteristic curve was used to calculate the optimal cutoff level of the response to BD as a predictor of BHR according to MCT.', 'Using a MCT cutoff level of PC(20) </= 4 mg/mL showed BHR in 12.8% of subjects. Failure to improve FEV(1) by 8% after BD administration predicted the absence of BHR with sensitivity, specificity, and positive and negative predictive values of 76.5%, 68.4%, 25.3%, and 95.5%, respectively. Avoiding MCT in subjects with less than 8% response to BD would have saved 62.5% of the MCTs and would have missed only four (3%) patients with BHR.\Question: Does response to bronchodilators after exercise challenge predict bronchial hyperreactivity?

Ex Output:
BD should be administered routinely after ECT, as the response may be used as a simple, inexpensive tool to predict BHR in young patients and may substantially reduce the number of unnecessary MCTs.


Ex Input:
Context: To systematically review methodological articles which focus on nonpublication of studies and to describe methods of detecting and/or quantifying and/or adjusting for dissemination in meta-analyses. To evaluate whether the methods have been applied to an empirical data set for which one can be reasonably confident that all studies conducted have been included.', 'We systematically searched Medline, the Cochrane Library, and Web of Science, for methodological articles that describe at least one method of detecting and/or quantifying and/or adjusting for dissemination bias in meta-analyses.', 'The literature search retrieved 2,224 records, of which we finally included 150 full-text articles. A great variety of methods to detect, quantify, or adjust for dissemination bias were described. Methods included graphical methods mainly based on funnel plot approaches, statistical methods, such as regression tests, selection models, sensitivity analyses, and a great number of more recent statistical approaches. Only few methods have been validated in empirical evaluations using unpublished studies obtained from regulators (Food and Drug Administration, European Medicines Agency).\Question: Are methods for detecting , quantifying , and adjusting for dissemination bias in meta-analysis described?

Ex Output:
We present an overview of existing methods to detect, quantify, or adjust for dissemination bias. It remains difficult to advise which method should be used as they are all limited and their validity has rarely been assessed. Therefore, a thorough literature search remains crucial in systematic reviews, and further steps to increase the availability of all research results need to be taken.


Ex Input:
Context: The failing heart displays increased glycolytic flux that is not matched by a commensurate increase in glucose oxidation. This mismatch induces increased anaplerotic flux and inefficient glucose metabolism. We previously found adult transgenic mouse hearts expressing the fetal troponin I isoform, (ssTnI) to be protected from ischemia by increased glycolysis. In this study, we investigated the metabolic response of adult mouse hearts expressing ssTnI to chronic pressure overload.', 'At 2 to 3 months of age, ssTnI mice or their nontransgenic littermates underwent aortic constriction (TAC). TAC induced a 25% increase in nontransgenic heart size but only a 7% increase in ssTnI hearts (P<0.05). Nontransgenic TAC developed diastolic dysfunction (65% increase in E/A ratio), whereas the E/A ratio actually decreased in ssTnI TAC. Isolated perfused hearts from nontransgenic TAC mice showed reduced cardiac function and reduced creatine phosphate:ATP (16% reduction), but ssTnI TAC hearts maintained cardiac function and energy charge. Contrasting nontransgenic TAC, ssTnI TAC significantly increased glucose oxidation at the expense of palmitate oxidation, preventing the increase in anaplerosis observed in nontransgenic TAC hearts. Elevated glucose oxidation was mediated by a reduction in pyruvate dehydrogenase kinase 4 expression, enabling pyruvate dehydrogenase to compete against anaplerotic enzymes for pyruvate carboxylation.\Question: Does metabolic efficiency promote protection from pressure overload in hearts expressing slow skeletal troponin I?

Ex Output:

Expression of a single fetal myofilament protein into adulthood in the ssTnI-transgenic mouse heart induced downregulation of the gene expression response for pyruvate dehydrogenase kinase to pressure overload. The consequence of elevated pyruvate oxidation in ssTnI during TAC reduced anaplerotic flux, ameliorating inefficiencies in glucose oxidation, with energetic and functional protection against cardiac decompensation.