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We demonstrate a heating induced aggregation strategy to retard the aggregation of PBDB-T, which promoting the ordering of m-INPOIC. A sequent thermal annealing help to achieve balanced aggregation of donors and acceptors and maximize efficiency.

The molecular aggregation of nonfullerene acceptors (NFA) can significantly affect the light absorption, charge generation, and power conversion efficiency (PCE) of organic solar cells (OSCs). In this work, we demonstrate the regulation of J-aggregation of COi8DFIC NFA toward near-infrared absorption via solvent additives 1,8-diiodooctane (DIO), diphenyl ether (DPE), and 1-chloronaphthalene (CN). Molecular dynamics simulations reveal preferential interaction of DIO with the alkyl side chains of COi8DFIC, endowing side-chains with the flexibility to adjust conformations to promote the formation of “A-to-D” type J-aggregation among the COi8DFIC backbone, resulting in a significant red-shift of absorbance toward the near-infrared region. The enhanced J-aggregation via π–π stacking, evidenced by grazing-incidence wide-angle X-ray scattering, constructs three-dimensional charge transport channels at the molecular level to facilitate charge transport. The presence of 0.5 vol % DIO molecules, which is most effective among all three additives, boosts the maximum achievable PCE of CF cast PTB7-Th:COi8DFIC OSCs from 8.5% to 12.9%. Our results provide a new concept to enhance the efficiency of OSCs via dedicated control of molecular aggregations of nonfullerene acceptors.

Liver re-resection plays a paramount role in treatment of patients with posthepatectomy hepatocellular carcinoma (HCC) recurrence. Laparoscopic liver resection has been a feasible alternative to open surgery. However, whether laparoscopic liver re-resection for posthepatectomy HCC recurrence is better than open liver re-resection remains unknown. From January 2008 to December 2015, 30 patients with recurrent HCC after prior liver resection underwent laparoscopic liver re-resection in our center. To minimize any confounding factors, a propensity score matching study using a patient ratio of 1:1 was conducted to compare the short- and long-term outcomes of patients who underwent laparoscopic or open liver re-resection. With the open surgery group compared laparoscopic group, operative time was 207.50 versus 200.5 min (p= 0.903), blood loss was 400 versus 100 ml (p= 0.000196), blood transfusion rate was 43.3 versus 0.0% (p= 0.000046), complication rates were 30.0 versus 6.7% (p= 0.01), and hospital stay was 13.5 versus 9.5 days (p= 0.000008). The median follow-up was 35 months. The 1-year, 3-year, 5-year disease-free survival rates were 79.0, 51.0, and 31.9%, versus 78.3, 57.4, and 43.0%, respectively (p= 0.474). The 1-year, 3-year, and 5-year overall survival rates were 89.4, 75, and 67.5%, versus 96.7, 85.0, and 74.4%, respectively (p= 0.413). Laparoscopic liver re-resection for patients with posthepatectomy HCC recurrence provided comparable perioperative and oncological outcomes as open liver re-resection and can be a safe alternative to open procedure.

Overexpression of the tumor necrosis factor receptor-associated factor 4 (TRAF4) has been detected in many cancer types and is considered to foster tumor progression. However, the role of TRAF4 in hepatocellular carcinoma (HCC) remains elusive. In this study, we found that TRAF4 was highly expressed in HCC cell lines and HCC tissues compared with normal liver cell lines and adjacent noncancerous tissues. TRAF4 overexpression in HCC tissues was correlated with tumor quantity and vascular invasion. In vitro studies showed that TRAF4 was associated with HCC cell migration and invasion. An in vivo study verified that TRAF4 overexpression facilitated metastasis in nude mice. In addition, overexpressed TRAF4 promoted the phosphorylation of Akt and induced Slug overexpression, leading to downregulated E-cadherin and upregulated vimentin, while silencing TRAF4 moderated the phosphorylation of Akt and repressed the expression of Slug, which resulted in upregulated E-cadherin and downregulated vimentin. These effects were inversed after pretreatment of the PI3K/Akt inhibitor LY294002 or overexpression of constitutively active Akt1. Our study demonstrated that TRAF4 was involved in promoting HCC cell migration and invasion. The process was induced by the EMT through activation of the PI3K/Akt signaling pathway.