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Exosomal noncoding RNAs (ncRNAs) have unique expression profiles reflecting the characteristics of a tumor, and their role in tumor progression and metastasis is emerging. However, the significance of circulating exosomal ncRNAs in the prognosis of hepatocellular carcinoma (HCC) remains to be elucidated. We therefore determined the prognostic significance of circulating exosomal ncRNAs (miRNA-21 and lncRNA-ATB) for human HCC. This prospective study enrolled 79 HCC patients between October 2014 and September 2015. Exosomes were extracted from serum samples using the ExoQuick Exosome Precipitation Solution. To validate the isolation of the exosomes from serum, immunoblotting for exosome markers and characterization of nanoparticle using NanoSight were performed. NcRNAs were isolated from exosomes using the miRNeasy serum/plasma micro kit. Both circulating exosomal miRNA-21 and lncRNA-ATB were related to TNM stage and other prognostic factors, including the T stage and portal vein thrombosis. Multivariate analysis using the Cox regression test identified that both higher miRNA-21 and higher lncRNA-ATB were independent predictors of mortality and disease progression, along with larger tumor size and higher C-reactive protein (all p < 0.05). The overall survival and progression-free survival were significantly lower in patients with higher circulating levels of exosomal miRNA-21 (≥0.09) and lncRNA-ATB (≥0.0016) (log-rank test: p < 0.05). In conclusion, our study has provided strong evidence that circulating exosomal ncRNAs (miRNA-21 and lncRNA-ATB) are novel prognostic markers and therapeutic targets for HCC.

Expression of genes encoding starch-degrading enzymes is regulated by glucose repression in the yeast Saccharomyces cerevisiae. We have identified a transcriptional repressor, Nrg1, in a genetic screen designed to reveal negative factors involved in the expression of STA1, which encodes a glucoamylase. The NRG1 gene encodes a 25-kDa C 2 H 2 zinc finger protein which specifically binds to two regions in the upstream activation sequence of the STA1 gene, as judged by gel retardation and DNase I footprinting analyses. Disruption of the NRG1 gene causes a fivefold increase in the level of the STA1 transcript in the presence of glucose. The expression of NRG1 itself is inhibited in the absence of glucose. DNA-bound LexA-Nrg1 represses transcription of a target gene 10.7-fold in a glucose-dependent manner, and this repression is abolished in both ssn6 and tup1 mutants. Two-hybrid and glutathione S-transferase pull-down experiments show an interaction of Nrg1 with Ssn6 both in vivo and in vitro. These findings indicate that Nrg1 acts as a DNA-binding repressor and mediates glucose repression of the STA1 gene expression by recruiting the Ssn6-Tup1 complex.In yeast, a large number of genes are turned off during growth on glucose (9, 37, 49). These glucose-repressible genes can be divided into three groups: (i) genes for metabolizing other carbon sources; (ii) genes encoding enzymes unique to gluconeogenesis; and (iii) genes involved in the Krebs cycle and in respiration. The Mig1 glucose repressor is a zinc finger protein and binds to the GC-rich motif identified in the promoters of several glucose-repressed genes, including the GAL1, GAL4, SUC2, and MAL genes (10,13,28,29). In the absence of glucose, the Snf1 kinase inhibits the function of Mig1 protein directly or indirectly, leading to derepression of glucose-repressed genes (3, 4). Nuclear translocation of Mig1 is regulated by differential phosphorylation of the protein in response to glucose availability, and recruitment of the general repression complex Ssn6-Tup1 to the DNA-bound Mig1 is required for the repression (5,17,48). Disruption of the MIG1 gene, however, only partially relieves glucose repression of SUC2 and has little or no effect on glucose repression of other genes whose promoters contain the Mig1-binding sites (27,31,37,50), indicating the involvement of other repressors in glucose repression. For instance, Mig2 was recently identified as a second repressor responsible for the remaining glucose repression of SUC2 and contains zinc fingers very similar to those of Mig1 (24).In Saccharomyces cerevisiae var. diastaticus, three unlinked homologous STA genes (STA1, STA2, and STA3) encode glucoamylase isozymes (GAI, GAII, and GAIII), which are responsible for enzymatic degradation of starch to glucose (16,22,25,32,35,47,52). Expression of the STA genes is regulated by complex interactions between positive and negative factors and their cognate elements (1,19,21,33,41). The negative regulation occurs at three different levels: (i) carbon catabolite repression...

In this study, prolonged CIT is identified as a risk factor for BS in DD biliary reconstruction in LDLT.

The preoperative CRP and macroscopic vascular invasion were associated with the aggressiveness of early recurrent HCC.

Droplet-surface interactions are common to a plethora of natural and industrial processes due to their ability to rapidly exchange energy, mass, and momentum. Droplets are particularly of interest due to their large surface-to-volume ratios and hence enhanced transport properties. For example, coalescence-induced droplet jumping on superhydrophobic surfaces has recently received much attention for its potential to enhance heat transfer, anti-icing, and self-cleaning performance by passively shedding microscale water droplets. To study droplet jumping, researchers typically use a two-camera setup to observe the out-of-plane droplet motion, with limited success due to the inability to resolve the depth dimension using two orthogonal cameras. Here we develop a single-camera technique capable of providing three-dimensional (3D) information through the use of focal plane manipulation, termed "focal plane shift imaging" (FPSI). We used FPSI to study the jumping process on superhydrophobic surfaces having a wide range of structure length scales (10 nm < l < 1 μm) and droplet radii (3 μm < R < 160 μm). We benchmarked the FPSI technique and studied the effects of droplet mismatch, multidroplet coalescence, and multihop coalescence on droplet jumping speed. Furthermore, we were able to resolve the full 3D trajectory of multiple jumping events, to show that, unlike previously theorized, the departure angle during droplet jumping is not a function of droplet mismatch or number of droplets coalescing prior to jumping. Rather, angular deviation arises due to in-plane motion postcoalescence governed by droplet pinning. The outcomes of this work both elucidate key fundamental aspects governing droplet jumping and provide a powerful imaging platform for the study of dynamic droplet processes that result in out-of-plane motion such as sliding, coalescence, or impact.

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PD had a greater likelihood of curative resection and R1 resection might have some positive impact. The TNM stage and LVI were independent prognostic factors.