Among the various organic photovoltaic devices, the conjugated polymer/fullerene approach has drawn the most research interest. The performance of these types of solar cells is greatly determined by the nanoscale morphology of the two components (donor/acceptor) and the molecular orientation/crystallinity in the photoactive layer. A vertically bicontinuous and interdigitized heterojunction between donor and acceptor has been regarded as one of the ideal structures to enable both efficient charge separation and transport. Synergistic control of polymer orientation in the nanostructured heterojunction is also critical to improve the performance of polymer solar cells. Nanoimprint lithography has emerged as a new approach to simultaneously control both the heterojunction morphology and polymer chains in organic photovoltaics. Currently, in the area of nanoimprinted polymer solar cells, much progress has been achieved in the fabrication of nanostructured morphology, control of molecular orientation/crystallinity, deposition of acceptor materials, patterned electrodes, understanding of structure-property correlations, and device performance. This review article summarizes the recent studies on nanoimprinted polymer solar cells and discusses the outstanding challenges and opportunities for future work.

We demonstrate the fabrication of poly(3,4-ethylenedioxythiophene) poly(styrenesulfonate) (PEDOT:PSS) nanogratings by a dehydration-assisted nanoimprint lithographic technique. Dehydration of PEDOT:PSS increases its cohesion to protect the nanostructures formed by nanoimprinting during demolding, resulting in the formation of high quality nanogratings of 60 nm in height, 70 nm in width and 70 nm in spacing (aspect ratio of 0.86). PEDOT:PSS nanogratings are used as hole transport and an electron blocking layer in blended poly(3-hexylthiophene-2,5-diyl) (P3HT):[6,6]-penyl-C61-butyric-acid-methyl-ester (PCBM) organic photovoltaic devices (OPV), showing enhancement of photocurrent and power efficiency in comparison to OPV devices with non-patterned PEDOT:PSS films.

We report here the results of our evaluation of virus inactivation during the manufacturing steps of two intravenous immunoglobulin (IGIV) preparations. Virus inactivation and/or removal by processing steps, such as ethanol fractionation and polyethylene glycol precipitation, and deliberate virucidal steps, such as solvent/detergent treatment and pasteurization, were tested on a variety of human pathogenic and experimental model viruses, including human immunodeficiency, Hepatitis C, Mumps, Vaccinia, Chikungunya, Vesicular Stomatitis, Sindbis, and ECHO viruses. All viruses were successfully inactivated and/or eliminated by the processing steps studied. In some cases, however, multiple steps were required. We conclude that the incorporation of steps deliberately designed to inactivate or remove viruses during the production of IGIV provides an extra measure of viral safety.

Hepatocellular carcinoma (HCC) relies on angiogenesis for growth and metastasis. Leukocyte cell-derived chemotaxin 2 (LECT2) is a cytokine and preferentially expressed in the liver. Previous studies have found that LECT2 targets to both immune and tumor cells to suppress HCC development and vascular invasion. Although LECT2 did not affect HCC cells growth in vitro, it still suppressed HCC xenografts growth in immune-deficient mice, suggesting other cells such as stroma cells may also be targeted by LECT2. Here, we sought to determine the role of LECT2 in tumor angiogenesis in HCC patients. We found that LECT2 expression inhibited tumor growth via angiogenesis in the HCC xenograft model. Specifically, we demonstrated that recombinant human LECT2 protein selectively suppressed vascular endothelial growth factor (VEGF)165-induced endothelial cell proliferation, migration, and tube formation in vitro and in vivo. Mechanistically, LECT2 reduced VEGF receptor 2 tyrosine phosphorylation and its downstream extracellular signal-regulated kinase and AKT phosphorylation. Furthermore, LECT2 gene expression correlated negatively with angiogenesis in HCC patients. Taken together, our findings demonstrate that LECT2 inhibits VEGF165-induced HCC angiogenesis through directly binding to VEGFR2 and has broad applications in treating VEGF-mediated solid tumors.