Duodenal neuroendocrine neoplasms (D-NEN) is a kind of heterogeneous tumor originated from neuroendocrine cells. With the continuous progress of diagnostic technology, more and more examination methods and treatment methods are applied. This article reviews the characteristics, classification, imaging applications, biochemical markers' monitoring and treatment of D-NEN.

OBJECTIVES: To investigate the clinical characteristics of patients with listeriosis and to provide a basis for diagnosis, treatment, prevention and control of hospital infection. METHODS: A total of 10 inpatients, who suffered from the listeriosis in Xiangya Hospital, Central South University from January 2013 to June 2019, were retrospectively collected for this study. The characteristics of the patients' age, gander, basic information, case type, clinical manifestations, first consultation department, days of diagnosis, infection indicator, specimen type, results of drug sensitivity, treatment plan, hospital infection or not, outcome, follow-up data were analyzed. RESULTS: Two cases were pregnant women and other were non-pregnant adults among 10 patients with listeriosis. Among them, there were 3 cases with hospital acquired infection. The age of patient onset was 27-71 years old, and the time from onset to diagnosis was 5-36 days. Five cases had fever, and other 5 cases had not fever. There were headache, fatigue, local pain, and other specialized symptoms in the 10 patients.The white blood cell count,the neutrophil ratio, the inflammatory index C-reactive protein, the procalcitonin were all increased, and the erythrocyte sedimentation was accelerated in the 10 patients.All the patients were sensitive to ampicillin, penicillin G, meropenem, and compound sinomine. CONCLUSIONS Listeriosis often affects the patients with low immunity, which often leads to misdiagnosis or missed diagnosis in clinic.So early prevention, early diagnosis, and early treatment can reduce mortality; it is important for departments of nosocomial infection management to manage patients' diet for avoiding outbreaks of listeriosis in hospital.
Adult ; Aged ; Female ; Humans ; Listeria monocytogenes ; Listeriosis/epidemiology* ; Meropenem ; Middle Aged ; Pregnancy ; Pregnancy Complications, Infectious ; Retrospective Studies

AIM: To investigate the effect of atorvastatin ( AT) on the release of endothelial microparticles (EMP) and myocardial apoptosis in the rats with myocardial infarction .METHODS: SD male rats (n=24) were ran-domly divided into 3 groups:sham operation ( sham) group , myocardial infarction ( MI) group and MI+AT group.The rat model of acute myocardial infarction was prepared by coronary artery ligation .At 2 h and 24 h after modeling , the pe-ripheral blood was collected to detect creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT).The circulating levels of EMP were measured by flow cytometry .The myocardial apoptosis was detected by terminal deoxynucleotidyl transferase -mediated dUTP nick end labeling (TUNEL) assay.RESULTS: At 2 h after modeling, the level of CK-MB was signifi-cantly increased in MI group compared with sham group , and the level of EMP and the myocardial apoptotic rate were sig-nificantly increased in MI group and MI +AT group compared with sham group .At 24 h after modeling , the level of EMP was significantly increased in MI group compared with sham group .The levels of CK-MB, cTnT, EMP and the myocardial apoptotic rate were significantly decreased in MI +AT group compared with MI group .Moreover , the level of CK-MB in MI group was significantly increased at 24 h compared with that at 2 h after modeling .The levels of CK-MB, cTnT and EMP were significantly decreased in MI +AT group at 24 h compared with those at 2 h after modeling .CONCLUSION: Ator-vastatin may reduce the level of EMP and the myocardial apoptotic rate in the rats with acute myocardial infarction , indica-ting that atorvastatin plays a role in protecting endothelium .

Amyloid Neuropathies, Familial ; genetics ; Cardiomyopathies ; Humans ; Mutation

OBJECTIVETo detect pathogenic mutations in Marfan syndrome (MFS) using an Ion Torrent Personal Genome Machine (PGM) and to validate the result of targeted next-generation semiconductor sequencing for the diagnosis of genetic disorders.

METHODSPeripheral blood samples were collected from three MFS patients and a normal control with informed consent. Genomic DNA was isolated by standard method and then subjected to targeted sequencing using an Ion Ampliseq(TM) Inherited Disease Panel. Three multiplex PCR reactions were carried out to amplify the coding exons of 328 genes including FBN1, TGFBR1 and TGFBR2. DNA fragments from different samples were ligated with barcoded sequencing adaptors. Template preparation and emulsion PCR, and Ion Sphere Particles enrichment were carried out using an Ion One Touch system. The ion sphere particles were sequenced on a 318 chip using the PGM platform. Data from the PGM runs were processed using an Ion Torrent Suite 3.2 software to generate sequence reads. After sequence alignment and extraction of SNPs and indels, all the variants were filtered against dbSNP137. DNA sequences were visualized with an Integrated Genomics Viewer. The most likely disease-causing variants were analyzed by Sanger sequencing.

RESULTSThe PGM sequencing has yielded an output of 855.80 Mb, with a > 100 × median sequencing depth and a coverage of > 98% for the targeted regions in all the four samples. After data analysis and database filtering, one known missense mutation (p.E1811K) and two novel premature termination mutations (p.E2264X and p.L871FfsX23) in the FBN1 gene were identified in the three MFS patients. All mutations were verified by conventional Sanger sequencing.

CONCLUSIONPathogenic FBN1 mutations have been identified in all patients with MFS, indicating that the targeted next-generation sequencing on the PGM sequencers can be applied for accurate and high-throughput testing of genetic disorders.

Base Sequence ; Computational Biology ; Fibrillin-1 ; Fibrillins ; Genomics ; High-Throughput Nucleotide Sequencing ; methods ; Humans ; Marfan Syndrome ; diagnosis ; genetics ; Microfilament Proteins ; genetics ; Mutation ; Semiconductors