Cardiac hypertrophy, acting as a pathologic process of chronic hypertension and coronary disease, and its underlying mechanisms still need to be explored. Long non-coding RNA (LncRNA) potassium voltage-gated channel subfamily Q member 1 Transcript 1 (KCNQ1OT1) has been implicated in myocardial infarction. However, its role in cardiac hypertrophy remains reported.

To explore the regulated effect of lncRNAKCNQ1OT1 and miR-301b in cardiac hypertrophy, gain-and-lose function assays were tested. The expression of lncRNAKCNQ1OT1 and miR-301b were tested by quantitative real time polymerase chain reaction (qRT-PCR). The levels of transcription factor 7 (Tcf7), Proto-oncogene c-myc (c-myc), Brainnatriureticpeptide (BNP) and β-myosin heavy chain (β-MHC) were detected by Western blot. Additionally, luciferase analysis revealed interaction between lncRNAKCNQ1OT1, BNPβ-MHCmiR-301b, and Tcf7.

LncRNAKCNQ1OT1 overexpression significantly induced cardiac hypertrophy. Furthermore, lncRNAKCNQ1OT1 acts as a sponge for microRNA-301b, which exhibited lower expression in cardiac hypertrophy model, indicating an anti-hypertrophic role. Furthermore, the BNP and β-MHC expression increased, as well as cardiomyocyte surface area, with Ang II treatment, while the effect was repealed by miR-301b. Moreover, the protein expression of Tcf7 was inversely regulated by miR-301b and Antisense miRNA oligonucleotides (AMO)-301b.

Our study has shown that overexpression of lncRNAKCNQ1OT1 could promote the development of cardiac hypertrophy by regulating miR-301b and Tcf7. Therefore, inhibition of lncRNAKCNQ1OT1 might be a potential therapeutic strategy for cardiac hypertrophy.

Enterococcal bloodstream infections (BSIs) cause morbidity and mortality in children. This study aims to describe the epidemiological characteristics of enterococcal BSI, to determine the risk factors for vancomycin-resistant Enterococcus (VRE) BSI, and to compare outcomes of VRE BSI and vancomycin-susceptible Enterococcus (VSE) BSI in this population.

A retrospective cohort study at a 418-bed tertiary care children's hospital in Philadelphia, Pennsylvania, examined the epidemiological characteristics of children hospitalized with enterococcal BSI during the period from 2001 through 2006. A nested case-control study compared patients with VRE BSI with control patients with VSE BSI. Analysis included regression modeling to identify independent risk factors for VRE BSI.

We identified 339 patients with enterococcal BSI during the study period, including 39 patients with VRE infection. Fifty-three patients (16%) died before hospital discharge. Risk factors for VRE included long-term receipt of mechanical ventilation (adjusted odds ratio [OR], 5.40 [95% confidence interval {CI}, 1.28-6.48]), receipt of immunosuppressive medications during the preceding 30 days (adjusted OR, 2.88 [95% CI, 1.40-20.78]), use of vancomycin during the 2 weeks before onset of bacteremia (adjusted OR per day of vancomycin use, 1.25 [95% CI, 1.14-1.38]), and older age (adjusted OR, 1.08 [95% CI, 1.03-1.14]). VRE BSI was not associated with an increased length of stay after onset of bacteremia (0.77 days [95% CI, 0.55-1.07 days]). Mortality was higher for VRE BSI, but the difference was not statistically significant (adjusted OR, 1.94 [95% CI, 0.78-4.8]).

Most enterococcal BSI in children was caused by VSE. Risk factors for VRE BSI included receipt of vancomycin, long-term receipt of mechanical ventilation, immunosuppression, and older age. Differences in length of stay and mortality were not detected.