Objective
Laparoscopic endoscopic cooperative surgery for duodenal tumors (D‐LECS) has been developed to prevent duodenal leakage by reinforcing the endoscopic submucosal dissection site. However, there has been no prospective trial showing the feasibility of D‐LECS. Herein, we conducted a single‐arm confirmatory trial to evaluate the safety of D‐LECS for non‐ampullary superficial duodenal neoplasms.
Methods
This prospective single‐center single‐arm confirmatory trial analyzed patients with non‐ampullary superficial duodenal neoplasms who underwent D‐LECS. The primary endpoint was the incidence of any postoperative leakage occurring on the duodenal wall within 1 month postoperatively. The planned sample size was 20 patients, considering a threshold of 28% and one‐sided alpha value of 5%.
Results
Between January 2015 and September 2018, 20 eligible patients were enrolled. Sixteen tumors were located in the second portion, three in the first portion, and one in the third portion of the duodenal region. The median operative time was 225 (134–361) min and the median blood loss was 0 (0–150) mL. Curative resection (R0) with negative margins was achieved in 19 cases. One case of postoperative leakage and one case of bleeding of grade 2 according to the Clavien–Dindo classification were observed in this series. The median duration of postoperative hospital stay was 9 (5–12) days. No local recurrence was observed in any patient during the median follow‐up of 15.0 (12.0–38.0) months.
Conclusions
This trial confirmed the safety and feasibility of D‐LECS for non‐ampullary superficial duodenal neoplasms with respect to the low incidence of postoperative duodenal leakage.
We studied the dynamics in the chiral mesogenic phases observed in binary mixtures of 5CB and bent-core molecules by using dynamic light scattering. In the lower-temperature phase, a clear orientational fluctuation was observed, which was not observed in the higher-temperature one. The wave number dependence of the relaxation frequency strongly indicates that nanoscale phase separation occurs and that the fluctuations of 5CB with nematic order are suppressed by the bent-core–rich domains. The spatial heterogeneity of the nematic dynamic motion yields exact information on the characteristic size of the nanostructure, which cannot be obtained by static structural analysis.
BackgroundHepatic fibrosis, which is the excessive accumulation of extracellular matrices (ECMs) produced mainly from activated hepatic stellate cells (HSCs), develops to cirrhosis over several decades. There are no validated biomarkers that can non-invasively monitor excessive production of ECM (i.e., fibrogenesis). Transforming growth factor (TGF)-β, a key driver of fibrogenesis, is produced as an inactive latent complex, in which active TGF-β is enveloped by its pro-peptide, the latency-associated protein (LAP). Thus, active TGF-β must be released from the complex for binding to its receptor and inducing ECM synthesis. We recently reported that during the pathogenesis of liver fibrosis, plasma kallikrein (PLK) activates TGF-β by cleavage between R58 and L59 residues within LAP and that one of its by-products, the N-terminal side LAP degradation products ending at residue R58 (R58 LAP-DPs), can be detected mainly around activated HSCs by specific antibodies against R58 cleavage edges and functions as a footprint of PLK-dependent TGF-β activation. Here, we describe a sandwich enzyme-linked immunosorbent assay (ELISA) that detects the other by-products, the C-terminal side LAP-DPs starting from residue L59 (L59 LAP-DPs). We demonstrated that the L59 LAP-DPs are a potentially novel blood biomarker reflecting hepatic fibrogenesis.ResultsWe established a specific sandwich ELISA to quantify L59 LAP-DPs as low as 2 pM and measured L59 LAP-DP levels in the culture media of a human activated HSC line, TWNT-4 cells. L59 LAP-DPs could be detected in their media, and after treatment of TWNT-4 cells with a TGF-β receptor kinase inhibitor, SB431542, a simultaneous reduction was observed in both L59 LAP-DP levels in the culture media and the mRNA expression levels of collagen type (I) α1. In carbon tetrachloride- and bile duct ligation-induced liver fibrosis models in mice, plasma L59 LAP-DP levels increased prior to increase of hepatic hydroxyproline (HDP) contents and well correlated with α-smooth muscle actin (αSMA) expression in liver tissues. At this time, αSMA-positive cells as well as R58 LAP-DPs were seen in their liver tissues.ConclusionsL59 LAP-DPs reflect PLK-dependent TGF-β activation and the increase in αSMA-positive activated HSCs in liver injury, thereby serving as a novel blood biomarker for liver fibrogenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13069-015-0034-9) contains supplementary material, which is available to authorized users.
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