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.
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Question: Context: Mast cells play a central role in allergic and inflammatory diseases. Several reports indicated role of peroxisome proliferator-activated receptor gamma (PPARgamma) on mast cell function. However, there is no report about the role of PPARgamma on differentiation of mast cells from the progenitors. In this study, we investigated the role of PPARgamma in regulating bone marrow-derived mast cell maturation and the therapeutic implications for mast cell-related diseases such as atopic or contact dermatitis.', 'We used in vitro cell culture system for mast cell differentiation from bone marrow-progenitors using specific ligands and lentiviral-mediated short hairpin RNA of PPARgamma, and in vivo murine dermatitis models.', 'Activation of PPARgamma inhibited the maturation of bone marrow progenitors into connective tissue-type mast cells (CTMCs) through up-regulation of GATA-4 and GATA-6 resulting in a decrease in expression of histidine decarboxylase and mast cell histamine content. In comparison, the differentiation of bone marrow progenitors into CTMCs was significantly accelerated by the knockdown of PPARgamma expression by lentiviral-mediated short hairpin RNA. Peroxisome proliferator-activated receptor gamma ligand administration to mice inhibited the maturation of mast cells resulting in attenuation of atopic and contact dermatitis via diminishment of the number of mature mast cells.\Question: Does activation of peroxisome proliferator-activated receptor gamma suppress mast cell maturation involved in allergic diseases?

Answer: Our results indicate that PPARgamma is one of master regulators on mast cell maturation and potentially useful for the therapy in various disorders involving mast cell activation.

Question: 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 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 = 0.03, p = 0.22).\Question: Does benchmarking trauma centers on mortality alone reflect quality of care : implications for pay-for-performance?

Answer: 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.

Question: Context: -Colorectal carcinoma is the third most common cause of cancer death in males and females in the United States. Rectal adenocarcinoma can have distinct therapeutic and surgical management from colonic adenocarcinoma owing to its location and anatomic considerations.', '-To determine the oncologic driver mutations and better understand the molecular pathogenesis of rectal adenocarcinoma in relation to colon adenocarcinoma.', '-Next-generation sequencing was performed on 20 cases of primary rectal adenocarcinoma with a paired lymph node or solid organ metastasis by using an amplicon-based assay of more than 2800 Catalogue of Somatic Mutations in Cancer (COSMIC)-identified somatic mutations.', '-Next-generation sequencing data were obtained on both the primary tumor and metastasis from 16 patients. Most rectal adenocarcinoma cases demonstrated identical mutations in the primary tumor and metastasis (13 of 16, 81%). The mutations identified, listed in order of frequency, included TP53, KRAS, APC, FBXW7, GNAS, FGFR3, BRAF, NRAS, PIK3CA, and SMAD4.\Question: Does next-Generation Sequencing of Matched Primary and Metastatic Rectal Adenocarcinomas demonstrate Minimal Mutation Gain and Concordance to Colonic Adenocarcinomas?

Answer:
-The somatic mutations identified in our rectal adenocarcinoma cohort showed a strong correlation to those previously characterized in colonic adenocarcinoma. In addition, most rectal adenocarcinomas harbored identical somatic mutations in both the primary tumor and metastasis. These findings demonstrate evidence that rectal adenocarcinoma follows a similar molecular pathogenesis as colonic adenocarcinoma and that sampling either the primary or metastatic lesion is valid for initial evaluation of somatic mutations and selection of possible targeted therapy.