OBJECTIVE Long non-coding RNAs (lncRNAs) are currently consider to have vital and wide range of biological functions, but the molecular mechanism underlying triglycerides metabolism remains poorly understood. This study aims to identify novel lncRNAs differentially expressed in rat liver with hypertriglyceridemia and elucidated the function role in TG metabolism. METHODS Differentially expression of lncRNAs in rat liver with hypertriglyceridemia were identified by transcriptome sequencing and validated by real-time PCR. The role of lnc19959.2 in triglyceride metabolism was assessed both in vitro and in vivo. RNA Pull down and RIP assays were conducted to evaluate the interactions between lnc19959.2 and its target proteins. ChIP and Dual report assays were performed to detects the interactions between transcription factors and promoter of its target genes. RESULTS We identified a novel lncRNA, lnc19959.2 was up regulated in rat liver with hypertriglyceridemia. Knockdown of lnc19959.2 has profound TG lowering effects in vitro and in vivo. Subsequently genome-wide analysis identified that knockdown of lnc19959.2 caused deregulation of many genes during TG homeostasis. Further mechanism studies revealed that lnc19959.2 up-regulate ApoA4 expression via ubiquitinated transcription inhibitor factor Purb, while specifically interacted to hnRNPA2B1 to down-regulate expression of Cpt1a, Tm7sf2 and Gpam, respectively. In the upstream pathway, palmitate acid up-regulated CCAAT/Enhancer-Binding Protein Beta (Cebpb) and facilitated its binding to promoter of lnc19959.2, which resulted in significant promotion of lnc19959.2 transcriptional activity. CONCLUSION Our findings provide novel insights of a new layer regulatory complexity of a lncRNA that modulating triglyceride homeostasis by a novel lncRNA lnc19959.2. BACKGROUND & AIMS Dietary therapies based on exclusion of usual dietary elements induce remission in children with Crohn's disease (CD), whereas re-exposure induces rebound inflammation. We investigated whether a short trial of dietary therapy, to identify patients with and without a rapid response or remission on the diet (DiRe), can be used to predict success or failure of long-term dietary therapy. METHODS We collected data from the multicenter randomized trial of the CD exclusion diet (CDED). We analyzed data from 73 children with mild to moderate CD (mean age, 14.2±2.7 y) randomly assigned to groups given either exclusive enteral nutrition (EEN, n=34) or the CDED with 50% (partial) enteral nutrition (n=39).  https://www.selleckchem.com/products/Erlotinib-Hydrochloride.html  Patients were examined at baseline and at weeks 3 and 6 of the diet. Remission was defined as CD activity index scores below 10 and response was defined as a decrease in score of 12.5 points or clinical remission. Inflammation was assessed by measurement of C-reactive protein. RESULTS At week 3 of the diet, 82% of patients in the CDED group and 85% of patients in the EEN group had a DiRe. Median serum levels of C-reactive protein had decreased from 24 mg/L at baseline to 5.0 mg/L at week 3 (P less then .001). Among the 49 patients in remission at week 6, 46 patients (94%) had a DiRe and 81% were in clinical remission by week 3. In multivariable analysis, remission at week 3 increased odds of remission by week 6 (odds ratio, 6.37; 95% CI, 1.6-25; P=.008) whereas poor compliance reduced odds of remission at week 6 (odds ratio, 0.75; 95% CI, 0.012-0.46; P=.006). CONCLUSIONS For pediatric patients with active CD, dietary therapies (CDED and EEN) induce a rapid clinical response (by week 3). Identification of patients with and without a rapid response to diet might help identify those who, with compliance, will be in clinical remission by week 6 of the diet. ClinicalTrials.gov no NCT01728870. The renin-angiotensin system (RAS) is crucial for the physiology and pathology of all the organs. Angiotensin-converting enzyme 2 (ACE2) maintains the homeostasis of RAS as a negative regulator. Recently, ACE2 was identified as the receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the coronavirus that is causing the pandemic of Coronavirus disease 2019 (COVID-19). Since SARS-CoV-2 must bind with ACE2 before entering the host cells in humans, the distribution and expression of ACE2 may be critical for the target organ of the SARS-CoV-2 infection. Moreover, accumulating evidence has demonstrated the implication of ACE2 in the pathological progression in tissue injury and several chronic diseases, ACE2 may also be essential in the progression and clinical outcomes of COVID-19. Therefore, we summarized the expression and activity of ACE2 in various physiological and pathological conditions, and discussed its potential implication in the susceptibility of SARS-CoV-2 infection and the progression and prognosis of COVID-19 patients in the current review. BACKGROUND Positive T wave in lead aVR (TaVR) has been associated with increased risk of adverse events in patients with various cardiovascular diseases. OBJECTIVE The purpose of this study was to investigate the prevalence and prognostic significance of positive TaVR in patients with hypertrophic cardiomyopathy (HCM). METHODS This study investigated 421 consecutive patients with HCM (177 women; age 51.1 ± 14.9 years). Admission electrocardiogram was examined for the presence of a positive TaVR. The primary endpoint was defined as a composite of major arrhythmic events (MAEs), which included sudden cardiac death, sustained ventricular tachycardia or fibrillation, or appropriate implantable cardioverter-defibrillator therapy. Cardiovascular mortality and all-cause death were evaluated as secondary endpoints. RESULTS During median follow-up period of 6.0 years (interquartile range 4.0-11.6 years), 53 patients (12.6%) experienced the primary endpoint. On multivariable competing analysis, after adjusting for other confounding factors, the presence of positive TaVR was found to be an independent and strong predictor of the primary composite endpoint. Time-dependent receiver operating characteristic analysis, net reclassification index, and integrated discrimination improvement showed that the addition of positive TaVR to conventional HCM risk factors improved prediction of arrhythmic events. However, in subgroup analysis, a positive TaVR lost statistical significance in patients with apical HCM but remained significant in patients with all other hypertrophy patterns. CONCLUSION Positive TaVR is associated with MAE in HCM patients, independent of and incremental to traditional risk factors.