Background Total parenteral nutrition (TPN) as a traditional mode of treatment in severe acute pancreatitis was still used widely in clinical work. In addition, enteral nutrition treatment methods have developed; early enteral nutrition has already been highlighted for severe acute pancreatitis, but the therapeutic risks versus benefits need to be studied. Aims and Objective To compare total parenteral nutrition with total enteral nutrition (TEN) in patients with severe acute pancreatitis by performing a meta-analysis. Materials and Methods Electronic databases including PubMed, EMBASE, Science Citation Index, were searched to find relevant randomized controlled trials. Two reviewers independently identified relevant trials evaluating the effect of total parenteral nutrition and early enteral nutrion. Outcome measures were the mortality, hospital length of stay, infectious complications, duration of nutrition, organ failure and surgical inter- p=0.22,)] and as for duration of nutrition [p=0.72, 95%CI -1.50(-9.56-6.56)] there was not enough data to compare the differences. Conclusion Total enteral nutritional support is associated with lower mortality, fewer infectious complications, decreased organ failure and surgical intervention rate compared to parenteral nutritional support.

Frameshift mutations in the TTN gene encoding titin are a major cause for inherited forms of dilated cardiomyopathy (DCM), a heart disease characterized by ventricular dilatation, systolic dysfunction, and progressive heart failure. To date, there are no specific treatment options for DCM patients but heart transplantation. Here, we show the beneficial potential of reframing titin transcripts by antisense oligonucleotide (AON)-mediated exon skipping in human and murine models of DCM carrying a previously identified autosomal-dominant frameshift mutation in titin exon 326. Correction of TTN reading frame in patient-specific cardiomyocytes derived from induced pluripotent stem cells rescued defective myofibril assembly and stability and normalized the sarcomeric protein expression. AON treatment in Ttn knock-in mice improved sarcomere formation and contractile performance in homozygous embryos and prevented the development of the DCM phenotype in heterozygous animals. These results demonstrate that disruption of the titin reading frame due to a truncating DCM mutation can be restored by exon skipping in both patient cardiomyocytes in vitro and mouse heart in vivo, indicating RNA-based strategies as a potential treatment option for DCM.

Translational perspectiveCardiomyocytes (CMs) generated from human induced pluripotent stem cells are an evolving platform to understand molecular disease mechanism and evaluate cardiovascular drugs. A major limitation of this system is that they represent a heterogeneous mix of ventricular-, atrial-, and nodal-like CMs. By expressing a voltage-sensitive fluorescent protein under the control of lineage-specific promoters, we developed a convenient system allowing high-throughput subtype-specific optical action potential (AP) imaging in these cells. This enables not only quantification of electrical phenotypes in patient-specific CMs but also subtype-specific investigation of drug effects, which may aid both drug development and safety pharmacology in the cardiovascular field.