Application of omental interposition to reduce pancreatic fistula and related complications in pancreaticoduodenectomy: A propensity score-matched study.

BACKGROUND: The life-threatening complications following pancreatoduodenectomy (PD), intra-abdominal hemorrhage, and postoperative infection, are associated with leaks from the anastomosis of pancreaticoduodenectomy. Although several methods have attempted to reduce the postoperative pancreatic fistula (POPF) rate after PD, few have been considered effective. The safety and short-term clinical benefits of omental interposition remain controversial. AIM: To investigate the safety and feasibility of omental interposition to reduce the POPF rate and related complications in pancreaticoduodenectomy. METHODS: In total, 196 consecutive patients underwent PD performed by the same surgical team. The patients were divided into two groups: An omental interposition group (127, 64.8%) and a non-omental interposition group (69, 35.2%). Propensity score-matched (PSM) analyses were performed to compare the severe complication rates and mortality between the two groups. RESULTS: Following PSM, the clinically relevant POPF (CR-POPF, 10.1% vs 24.6%; P = 0.025) and delayed postpancreatectomy hemorrhage (1.4% vs 11.6%; P = 0.016) rates were significantly lower in the omental interposition group. The omental interposition technique was associated with a shorter time to resume food intake (7 d vs 8 d; P = 0.048) and shorter hospitalization period (16 d vs 21 d; P = 0.031). Multivariate analyses showed that a high body mass index, nonapplication of omental interposition, and a main pancreatic duct diameter < 3 mm were independent risk factors for CR-POPF. CONCLUSION: The application of omental interposition is an effective and safe approach to reduce the CR-POPF rate and related complications after PD.

[Fluorescence emission analysis of caspase-3 activation induced by Xiao-Ai-Ping (XAP) inside living human lung adenocarcinoma cells].

The CCK-8 was used to measure the inhibition effect of Xiao-Ai-Ping (XAP), a traditional medicine, on the human lung adenocarcinoma (ASTC-a-1) cells viability. The ASTC-a-1 cells expressing stably with SCAT3, a fluorescence resonance energy transfer (FRET) plasmid based on the green fluorescent protein mutants (GFPs), was verified using confocal fluorescence scanning microscopy imaging, fluorescence emission spectra and FRET acceptor photobleaching techniques. The caspase-3 activation can be monitored by the fluorescence emission spectra of SCAT3 inside living cells. The cells expressing stably with SCAT3 were cultured with XAP for 96 hours, and the fluorescence emission spectra of the SCAT3 inside living cells were measured at the time of 0, 24, 72, and 96 hours, respectively. Experimental results showed that: (1)XAP inhibited obviously the proliferation of ASTC-a-1 cells and induced the cell death. The inhibition of XAP on the cells was dose-dependent; (2)the SCAT3 inside living cells was cleaved completely 72 hours after the XAP treatment, implying that a great deal of pro-caspase-3 was activated by XAP; (3)24 hours after XAP treatment, the emission spectra of SCAT3 inside living cells cultured in DMEM without XAP for 48 and 72 hours did not change greatly, implying that XAP did not activate obviously caspase-3 within 24 hours.

Taxol induces caspase-independent cytoplasmic vacuolization and cell death through endoplasmic reticulum (ER) swelling in ASTC-a-1 cells.

High concentration of taxol was found to induce programmed cell death (PCD) and cytoplasm vacuolization in human lung adenocarcinoma (ASTC-a-1) cells. To elucidate the relationship between the PCD and cytoplasm vacuolization, confocal fluorescence microscopy was performed on the cytoplasm vacuolization, endoplasmic reticulum (ER) and mitochondria swelling after taxol treatment in living cells. erRFP plasmid was used to probe the ER distribution, and SCAT3 plasmid was used to monitor the caspase-3 activation in living cells. Our results showed that taxol induced concentration-dependent and caspases-independent cytoplasm vacuolization and cell death through ER and mitochondria swelling. Live confocal imaging of ASTC-a-1 cells stably expressing SCAT3 further verified that taxol-induced cytoplasm vacuolization and cell death was caspase-3-independent. In conclusion, we found for the first time that taxol induces a paraptosis-like PCD in the ASTC-a-1 cells by cytoplasm vacuolization due to the swelling of both ER and mitochondria without activating the caspase enzymes.

[Fluorescence analysis of taxol-induced paraptosis-like independent of caspase-3 activation].

In the present report, the authors for the first time described the characteristics of taxol-induced paraptosis-like for the human lung adenocarcinoma cells (ASTC-a-1). CCK-8 was used to assay the inhibition of taxol on the cells viability. Cell viability was inhibited obviously 24 h after taxol treatment. Confocal fluorescence scanning microscope was used to monitor the morphology changes in cells with taxol treatment. Fluorescence resonance energy transfer (FRET) and acceptor photobleaching techniques were used to analyze the caspase-3 activation in the taxol-induced cell swelling and cell dearth. Taxol induced cell swelling, cytoplasmatic vacuolization and cell death without cell shrinkage, an apoptotic feature, and membrane rupture, a necrotic feature. The emission spectra of scat3 inside living cells expressed stably with scat3 were the same for control (without taxol). Further analysis with FRET and acceptor photobleaching techniques showed that the caspase-3 was not activated by taxol for the cytoplastic vacuoliazation cells expressed stably with scat3 plasmid, suggesting that caspase-3 is not involved in the taxol-inducecd cell swelling, cytoplasmatic vacuolization and cell death. These results show that taxol can induce a novel nonapoptotic PCD resembling the paraptosis in ASTC-a-1 cells.