Duke University
Publishes on Cancer Genomics and Diagnostics, Cancer-related Molecular Pathways, Ferroptosis and cancer prognosis. 44 papers and 39.2k citations.
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PURPOSE: Delayed gastric emptying is present in patients with functional dyspepsia (FD), diabetes mellitus, and neurological diseases. Diet may affect gastric emptying symptoms in patients with FD. We sought to determine the extent to which gastric emptying and symptoms of dyspepsia are influenced by caloric content in healthy subjects using ultrasonography. MATERIALS AND METHODS: 32 healthy volunteers were given 2 meals with different caloric content in random order. Gastric emptying was determined using ultrasonography to measure antral area when fasting, and postprandially at intervals of 0, 10, 20, and 30 min. Dyspeptic symptoms including discomfort, nausea, and fullness were graded. RESULTS: The antral area following a high-caloric meal compared to a low-caloric meal was significantly increased at 0, 10, 20, and 30 min (P=0.0203,<0.0001<0.0001,<0.0001, respectively), as was the median fullness (P<0.0048, 0.0001, 0.0009, 0.0001, respectively) measured at the same time points. There was a weak correlation (r2=0.1, P<0.0001) between the antral area and subjective fullness. No differences between gastric emptying in males and females were found. CONCLUSION: The caloric content of a meal influences gastric emptying. Using ultrasonography to measure the antral area helps us to assess gastric emptying and therefore to assess patients with functional dyspepsia.
Oesophageal cancers are prominent worldwide; however, there are few targeted therapies and survival rates for these cancers remain dismal. Here we performed a comprehensive molecular analysis of 164 carcinomas of the oesophagus derived from Western and Eastern populations. Beyond known histopathological and epidemiologic distinctions, molecular features differentiated oesophageal squamous cell carcinomas from oesophageal adenocarcinomas. Oesophageal squamous cell carcinomas resembled squamous carcinomas of other organs more than they did oesophageal adenocarcinomas. Our analyses identified three molecular subclasses of oesophageal squamous cell carcinomas, but none showed evidence for an aetiological role of human papillomavirus. Squamous cell carcinomas showed frequent genomic amplifications of CCND1 and SOX2 and/or TP63, whereas ERBB2, VEGFA and GATA4 and GATA6 were more commonly amplified in adenocarcinomas. Oesophageal adenocarcinomas strongly resembled the chromosomally unstable variant of gastric adenocarcinoma, suggesting that these cancers could be considered a single disease entity. However, some molecular features, including DNA hypermethylation, occurred disproportionally in oesophageal adenocarcinomas. These data provide a framework to facilitate more rational categorization of these tumours and a foundation for new therapies.