Predicting postoperative vomiting for orthopedic patients receiving patient-controlled epidural analgesia with the application of an artificial neural network.

Patient-controlled epidural analgesia (PCEA) was used in many patients receiving orthopedic surgery to reduce postoperative pain but is accompanied with certain incidence of vomiting. Predictions of the vomiting event, however, were addressed by only a few authors using logistic regression (LR) models. Artificial neural networks (ANN) are pattern-recognition tools that can be used to detect complex patterns within data sets. The purpose of this study was to develop the ANN based predictive model to identify patients with high risk of vomiting during PCEA used. From January to March 2007, the PCEA records of 195 patients receiving PCEA after orthopedic surgery were used to develop the two predicting models. The ANN model had a largest area under curve (AUC) in receiver operating characteristic (ROC) curve. The areas under ROC curves of ANN and LR models were 0.900 and 0.761, respectively. The computer-based predictive model should be useful in increasing vigilance in those patients most at risk for vomiting while PCEA is used, allowing for patient-specific therapeutic intervention, or even in suggesting the use of alternative methods of analgesia.

Nucleolin is important for Epstein-Barr virus nuclear antigen 1-mediated episome binding, maintenance, and transcription.

Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) is essential for EBV episome maintenance, replication, and transcription. These effects are mediated by EBNA1 binding to cognate oriP DNA, which comprise 20 imperfect copies of a 30-bp dyad symmetry enhancer and an origin for DNA replication. To identify cell proteins essential for these EBNA1 functions, EBNA1 associated cell proteins were immune precipitated and analyzed by liquid chromatography-tandem mass spectrometry. Nucleolin (NCL) was identified to be EBNA1 associated. EBNA1's N-terminal 100 aa and NCL's RNA-binding domains were critical for EBNA1/NCL interaction. Lentivirus shRNA-mediated NCL depletion substantially reduced EBNA1 recruitment to oriP DNA, EBNA1-dependent transcription of an EBV oriP luciferase reporter, and EBV genome maintenance in lymphoblastoid cell lines. NCL RNA-binding domain K429 was critical for ATP and EBNA1 binding. NCL overexpression increased EBNA1 binding to oriP and transcription, whereas NCL K429A was deficient. Moreover, NCL silencing impaired lymphoblastoid cell line growth. These experiments reveal a surprisingly critical role for NCL K429 in EBNA1 episome maintenance and transcription, which may be a target for therapeutic intervention.