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Abstract: Introduction: Cytogenetically normal acute myeloid leukemia (CN‐AML), which accounted for nearly half of total AML patients, is a highly heterogeneous subset of AML. The specific genetic profile and the ethnic features of CN‐AML are worth to be studied. Methods: Using deep sequencing technology, we detected the mutation pattern of 39 genes in 152 Chinese CN‐AML patients and analyzed their clinical features. Results: A total of 503 mutations of 39 genes were identified in 145 (95.4%) patients, with the median number of 3 mutations per case. Nine genes (NPM1, CEBPA, DNMT3A, GATA2, NRAS, TET2, FLT3, IDH2, and WT1) mutated in more than 10% patients. Function groups of myeloid transcription factors, activated signaling, and DNA methylation were most affected. The distribution of variant allele frequencies (VAF) of recurrent genes was different among functional groups. High mutation rates of CEBPA and GATA2 together with the low frequency of FLT3‐ITD mutation seemed to be the distinct characteristics of Chinese patients. Furthermore, CEBPAbi and GATA2 were found to mutate most in M2 subtype, while NPM1 and DNMT3A mutated more in M4 and M5. The prognostic analysis identified CEBPAmo mutation as an inferior factor. FLT3‐ITD, TP53, DNMT3A, CEBPAmo, and WT1 mutations were selected as high‐risk markers to identify the CN‐AML patients with poor prognosis. Conclusion: Our study provided the valuable information of ethnic genetic characteristics and the clinical relevance of Chinese CN‐AML patients. [ABSTRACT FROM AUTHOR]

Background The proportion of oesophageal adenocarcinoma that is detected concurrently with initial Barrett's oesophagus diagnosis is not well studied. Aim To compare the proportion of prevalent adenocarcinoma vs. incident adenocarcinoma found during surveillance of Barrett's. Methods We performed a systematic search of MEDLINE, EMBASE and Web of Science (from their inception to 31 May 2015) for cohort studies in adults with Barrett's (nondysplastic Barrett's ± Barrett's with low-grade dysplasia) with minimum average follow-up of 3 years, and providing numbers of prevalent adenocarcinoma detected (concurrently with Barrett's diagnosis and up to 1 year afterwards) vs. incident adenocarcinoma detected (greater than 1 year after Barrett's diagnosis). Pooled weighted proportions of prevalent and incident adenocarcinoma were calculated, using a random effects model. Results On meta-analysis of 13 studies reporting on 603 adenocarcinomas in 9657 Barrett's patients, 85.1% of adenocarcinomas were classified as prevalent [95% confidence interval ( CI), 78.1-90.2%) and 14.9% as incident (95% CI, 9.8-21.9%), with substantial heterogeneity ( I2 = 66%). Among nine studies reporting on 787 high-grade dysplasia and oesophageal adenocarcinomas in 8098 Barrett's patients, the proportion of prevalent high-grade dysplasia-oesophageal adenocarcinoma was similar at 80.5% (95% CI, 68.1-88.8%, I2 = 87%). These results remained stable across multiple subgroup analyses including study quality, setting, duration of follow-up and presence of baseline dysplasia. Conclusions In our meta-analysis, four of five patients diagnosed with adenocarcinoma or high-grade dysplasia at index endoscopy or within 1 year of Barrett's follow-up were considered to be prevalent cases. Continued efforts are needed to identify patients with Barrett's before the development of adenocarcinoma. [ABSTRACT FROM AUTHOR]

Background In 2002, a U.S. Multi-Society Task Force on Colorectal Cancer recommended that the withdrawal phase for colonoscopy should average at least 6–10 min. This was based on 10 consecutive colonoscopies by two endoscopists with different adenoma miss rates. Aims To characterize the relationship between endoscopist withdrawal time and polyp detection at colonoscopy, and to determine the withdrawal time that corresponds to the median polyp detection rate. Design Procedural data from out-patient colonoscopies performed at the Mayo Clinic, Rochester during 2003 were reviewed. Endoscopists were characterized by their mean withdrawal time for a negative procedure and individual polyp detection rate. Results A total of 10 955 colonoscopies performed by 43 endoscopists were analysed. Median withdrawal time was 6.3 min (range: 4.2–11.9); polyp detection rate was 44.0% (all polyps), 29.8% (≤5 mm), 5.9% (6–9 mm), 6.7% (10–19 mm), 2.1% (≥20 mm). Longer withdrawal time was associated with higher polyp detection rate ( r = 0.76; P < 0.0001); this relationship weakened for larger polyps ( r = 0.19 for polyps 6–9 mm, r = 0.28 for polyps 10–19 mm, r = 0.02 for polyps ≥20 mm). Overall median polyp detection rate corresponded to a withdrawal time of 6.7 min. Conclusion Our findings support a colonoscopy withdrawal time of at least 7 min, which correlates with higher colon polyp detection rates. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the study "Necrotic and Apoptotic Neuronal Death: From Calcium, Cytochrome C to Proteases," by K.K.W. Wang, which will be presented at the 30th annual meeting of the American Society for Neurochemistry, to be held from March 14-17, 1999 in New Orleans, Louisiana. The Calcium-dependent cysteine protease is activated by excessive intracellular calcium-overload encountered in neuronal injury.

The article presents an abstract of the study "Caspase-3 and Calpain Activation Following Glucose-Oxygen Deprivation in Mixed Primary Septo-Hippocampal Cell Cultures," by researcher J.K. Newcomb and colleagues, which will be presented at the 30th annual meeting of the American Society for Neurochemistry to be held on March 14-17, 1999 in New Orleans, Louisiana. The study showed that increased duration of oxygen-glucose deprivation is systematically associated with cell injury.

The article presents an abstract of the study "Novel Characteristics of Glutamate Induced Cell Death in Primary Septo-Hippocampal Cultures: Relationship to Calpain and Caspase-3 Activation," which will be presented at the 30th annual meeting of the American Society for Neurochemistry, to be held from March 14-17, 1999 in New Orleans, Louisiana. It was observed that glutamate does not produce phenotypic profiles characteristic of necrotic or apoptotic cell death.