Background:CT portography(CTP)permits comprehensive evaluation of portal vein and its collateral pathways. It is widely used for assessment of portal hypertension in clinical practice. Aims:To assess the value of CTP in esophagogastric varices in cirrhotic patients. Methods:A retrospective cohort study was performed in 143 cirrhotic patients admitted from Jan. 2013 to Sep. 2015 at the Affiliated Hospital of Qingdao University. All patients fulfilled the inclusion criteria and underwent CTP and gastroscopy within 7 days after admission. According to the occurrence of gastrointestinal bleeding at admission,patients were allocated into two groups:bleeding group( n = 70 ) and non-bleeding group( n = 73 ). Consistency of the results of CTP and gastroscopy was analyzed by kappa coefficient;the accuracy of CTP parameters, including diameters of main portal vein(MPV),splenic vein(SPV)and left gastric vein(LGV)for prediction of variceal bleeding was evaluated by ROC curve. Results:CTP and gastroscopy had a good consistency in typing and grading of esophagogastric varices,with the kappa value of 0. 793 and 0. 775,respectively. The diameters of MPV,SPV and LGV were significantly higher in bleeding group than in non-bleeding group(P < 0. 01),and their area under the ROC curve (AUC)in predicting variceal bleeding was 0. 741,0. 627 and 0. 816,respectively. The accuracy of diameter of LGV was superior to that of MPV and SPV. With the cutoff value of 6. 1 mm,the sensitivity and specificity of diameter of LGV were 65. 71% and 84. 93% ,respectively. With the cutoff value of 16. 3 mm,the sensitivity of diameter of MPV was 75. 71% , which was higher than that of LGV and SPV. Conclusions:CTP can be used in clinical diagnosis of esophagogastric varices in cirrhotic patients,and two CTP parameters,the diameters of LGV and MPV,might be helpful for prediction of variceal bleeding.

Many human genetic diseases, including Hutchinson-Gilford progeria syndrome (HGPS), are caused by single point mutations. HGPS is a rare disorder that causes premature aging and is usually caused by a de novo point mutation in the LMNA gene. Base editors (BEs) composed of a cytidine deaminase fused to CRISPR/Cas9 nickase are highly efficient at inducing C to T base conversions in a programmable manner and can be used to generate animal disease models with single amino-acid substitutions. Here, we generated the first HGPS monkey model by delivering a BE mRNA and guide RNA (gRNA) targeting the LMNA gene via microinjection into monkey zygotes. Five out of six newborn monkeys carried the mutation specifically at the target site. HGPS monkeys expressed the toxic form of lamin A, progerin, and recapitulated the typical HGPS phenotypes including growth retardation, bone alterations, and vascular abnormalities. Thus, this monkey model genetically and clinically mimics HGPS in humans, demonstrating that the BE system can efficiently and accurately generate patient-specific disease models in non-human primates.
Animals ; Disease Models, Animal ; Female ; Gene Editing ; Humans ; Lamin Type A/metabolism* ; Macaca fascicularis ; Progeria/pathology*