Search

8th World Conference on Photovoltaic Energy Conversion; 399-401, In this work, ultrathin GaAs solar cells are presented with a rough backscattering structure based on lattice mismatched gallium phosphide, grown with MOCVD. This way, a simple and reproducible light-trapping scheme is introduced with low parasitic absorption and full compatibility with hydrofluoric acid-based epitaxial lift-off. Solar cells with two different GaP surface morphologies are demonstrated and shown to be compatible with epitaxial lift-off without any complications or performance loss. An increase in short-circuit current density of up to 9% is observed, a direct result of the increased photon absorption induced by the scattering of the rough GaP texture.

Background Despite advances in chemotherapy, prognosis of ovarian cancer remains poor. Antigen-specific active immunotherapy aims to induce a tumour-antigen-specific anti-tumour immune responses as an alternative treatment for ovarian cancer. Objectives To assess feasibility of antigen-specific active immunotherapy for ovarian cancer. Primary outcomes are clinical efficacy and antigen-specific immunogenicity with carrier-specific immunogenicity and side-effects as secondary outcomes. Search strategy A systematic search of the Cochrane Central Register of Controlled Trials (CENTRAL) Issue 3, 2009, Cochrane Gynaecological Cancer Group Specialized Register, MEDLINE and EMBASE databases and clinicaltrials.gov was performed (1966 to July 2009). Hand searches were conducted of the proceedings of relevant annual meetings (1996 to July 2009). Selection criteria Randomised controlled trials (RCTs), as well as non-randomised non-controlled studies that included patients with epithelial ovarian cancer, irrespective of stage of disease, and treated with antigen-specific active immunotherapy, irrespective of type of vaccine, antigen used, adjuvant used, route of vaccination, schedule, and reported clinical or immunological outcomes. Data collection and analysis Data extraction was performed independently by two review authors. Risk of bias was evaluated with the Delphi-list for RCTs or a selection of quality domains pivotal to the assessment of non-RCTs and deemed best applicable to the non-randomised non-controlled studies. Main results Thirty-six studies were included. Response definitions showed substantial variation between trials, which makes comparison of trial results unreliable. Information on adverse events was frequently limited. Furthermore, reports of both RCTs and non-RCTs frequently lacked information necessary to assess risk of bias. Serious biases in these trials can thus not be ruled out. The largest body of evidence is currently available for CA-125 targeted antibody therapy (15 studies: 1505 patients). Non-RCTs of this CA-125 targeted antibody therapy suggest increased survival in humoral and/ or cellular responders. However, three large randomised placebo-controlled trials did not show any clinical benefit despite induction of immune responses in approximately 60% of patients. Other small studies targeting many different tumour antigens showed promising immunological results. As these strategies have not yet been tested in RCTs, no reliable inferences about clinical efficacy can be made. Given the promising immunological results, limited side effects and toxicity exploration of clinical efficacy in large well-designed RCTs may be worthwhile. Authors' conclusions We conclude that despite promising immunological responses no clinically effective antigen-specific active immunotherapy is yet available for ovarian cancer. Furthermore, the adoption of guidelines to ensure uniformity in trial conduct, response definitions and trial reporting is recommended to improve quality and comparability of immunotherapy trials.

Reconstituted influenza virus envelopes (virosomes) represent efficient influenza vaccines inducing high antibody titers upon intramuscular adminsitration. Virosomes are reconstituted viral envelopes which retain the cell entry and membrane fusion characteristics of native influenza virus. Here, we show that virosomes, by virtue of their membrane fusion activity, have the capacity to deliver a virosome-encapsulated protein antigen (ovalbumin, OVA) to the cytosol of cultured murine bone-marrow-derived dendritic cells (DCs) and thus to the MHC class I presentation pathway. Accordingly, immunization of mice with OVA-containing virosomes resulted in efficient priming of an OVA-specific class I MHC-restricted cytotoxic T lymphocyte (CTL) response. These results indicate that virosomes have the capacity to prime a broad immune response, inducing not only humoral but also cellular immunity.

This study investigates whether and to what extent cyclooxygenase type-2 (COX-2) and inducible nitric oxide-synthase (iNOS), both known to have an immunosuppressive effect, are expressed in human ovarian tumors. Because COX-2 and iNOS can be expressed by activated macrophages, the presence of tumor-associated macrophages and the expression of COX-2 and iNOS by these tumor-associated macrophages were determined. The results obtained may provide insight into the function of COX-2 and iNOS expression by tumors. The expression of COX-2 and iNOS in tumor cells and macrophages was assessed in 18 malignant, 15 borderline, and 14 benign human ovarian tumors by immunohistochemical staining of frozen tissue sections. The intra- and peritumoral macrophages were stained using an anti-CD68 monoclonal antibody. Most of the malignant tumors (15 of 18), 10 of 15 borderline, and 9 of 14 benign tumors showed COX-2 expression in the epithelial cells, a result which indicates that COX-2 expression is not exclusive to malignancy. In addition, COX-2 staining was more intense in the epithelial cells of benign and borderline tumors than in malignant tumors. Weak iNOS staining was observed in 5 of 18 malignant, 4 of 15 borderline, and 5 of 14 benign tumors. The number of tumor-associated macrophages varied widely between the different tumors. The highest number of tumor-associated macrophages ( greater than or equal to 20/0.125 mm(2)) was observed in malignant tumors, whereas low to moderate intra- and peritumoral macrophage infiltration (5-20/0.125 mm(2)) was observed in the borderline and benign tumors. COX-2-positive tumor-associated macrophages were found in 3 of 18 malignant tumors, 7 of 15 borderline tumors, and 1 of 14 benign tumors. The number of COX-2-positive tumor-associated macrophages ranged from 3 to 30% of the total macrophage population. Some malignant (4 of 18), borderline (5 of 15), and benign (2 of 14) tumors contained iNOS-positive macrophages. Notable was that COX-2- and iNOS-positive macrophages were predominantly located in the tumor stroma, the regions between tumor and stroma, and in the lumina of the tumor when located in the tumor tissue. These data indicate that not only malignant but also borderline and benign ovarian tumors can exhibit increased levels of COX-2 and iNOS expression. In addition, a small proportion of the tumor-associated macrophages found in malignant, borderline, and benign tumors seems to be in an activated state, judged by their iNOS and COX-2 expression. This subpopulation of tumor-associated macrophages was invariably located in the tumor stroma or in the lumina of the tumor, specifically suggesting that macrophages outside the tumor can be tumor cytotoxic.

Virosomes retain the cell entry, and membrane fusion characteristics of the native virus. Thus, influenza-derived virosomes are taken up by cells via receptor-mediated endocytosis, which directs the particles to the endosomes. Subsequently, the virosomal membrane fuses with the endosomal membrane from within the lumen of the endosomes. The fusion process establishes continuity between the lumen of the virosome, and the cell cytosol. Therefore, protein encapsulated in virosomes will be delivered into the cytosol of the cell as shown here for the A subunit of diphtheria toxin. Antigen-containing virosomes interacting with APCs are expected to introduce part of the antigen into the cell cytosol and, thus, into the MHC class I presentation pathway. Delivery of antigens in vivo indeed results in efficient priming of a class I MHC-restricted CTL response making virosomes a promising vehicle for in vivo targeting.

Background: As a majority of ovarian cancer patients will ultimately develop recurrent disease, there is an urgent need for alternative or additional approaches in the treatment of this cancer. Materials and Methods: The antitumour effect of i.p. administered cisplatin, liposomal muramyltripeptide phosphatidylethanolamine (L-MTP-PE) and granulocyte-macrophage colony-stimulating factor (GM-CSF) were investigated using an ip. growing murine ovarian tumour. Tumour growth was followed by measuring weight and survival of the mice. Results: An i.p. injection of L-MTP-PE in non-tumour bearing mice resulted in an approximately 10-fold increase in the number of peritoneal cells, which were highly cytotoxic. Nonetheless, treatment of mice inoculated with MOT cells with cisplatin, L-MTP-PE and GM-CSF using different treatment schedules did not result in inhibited tumour growth when compared to treatment with cisplatin alone. Conclusion: Although L-MTP-PE showed art enormous increase in peritoneal cells with high tumour cytotoxic capacity, the immunotherapeutic treatment with GM-CSF and L-MTP-PE, aimed at the recruitment and activation of the peritoneal cell population, failed to result in a significant prolongation of survival.

OBJECTIVE: To monitor liver regeneration following partial hepatectomy, liver cell proliferation can be measured by assaying in vivo [H-3]thymidine incorporation into liver cell DNA. We hypothesized that [H-3]thymidine incorporation into whole liver tissue parallels [H-3]thymidine incorporation into liver cell DNA, both in high proliferating and low proliferating liver. STUDY DESIGN: Liver cell proliferation in rats after partial hepatectomy or a sham operation was studied by measuring incorporation of [H-3]thymidine into various fractions of liver tissue on days 1, 2, 3, 4 and 10 after surgery. RESULTS: [H-3]thymidine incorporation into whole with DNA-specific [H-3]thymidine incorporation into regenerating (r > .80, P .69, P

The architecture of the liver constitutes a favorable condition for cell-specific delivery of drugs by means of targeted delivery systems due to the presence of a fenestrated endothelium. This allows access of particulate drug carriers such as liposomes to not only the sinusoidally located Kupffer cells and the endothelial cells but also to the trans-endothelial hepatocytes and stellate cells. Relatively small liposomes are known to accumulate in hepatocytes to much larger extents than larger ones. However, we found that even substantial amounts of relatively large liposomes can be taken up by hepatocytes after i.v, administration, provided they have the proper lipid composition, i.e. containing the negatively charged phospholipid phosphatidylserine (PS) and consisting of fluid-phase lipids. Liposomes containing phosphatidylglycerol (PG) as a negatively charged constituent or PS-containing liposomes consisting of rigid bilayer lipids were shown not to gain access to the hepatocytes. We propose that the mechanism responsible for this transendothelial passage of large fluid-type liposomes involves a PS-specific transient interaction with the endothelial cells followed by a forced squeezing of the fluid liposomes through the fenestrations, possibly mediated by an endothelial cell-surface-located scavenger receptor. An alternative explanation, involving a pharmacological widening effect of the PS on the fenestrations, could be discarded on the basis of experiments in which radiolabeled PG liposomes and nonlabeled PS liposomes were simultaneously injected: under those conditions still no uptake of large PG liposomes by hepatocytes was observed. The endothelial scavenger receptor is able to recognize and internalize PS liposomes in vitro but not in vivo, due to the masking effect of liposome-adsorbed plasma proteins.