Novel selective emitter process using non-acidic etch-back for inline-diffused silicon wafer solar cells

10.1016/j.renene.2013.11.062Renewable Energy6669-7

Single Print Metal Stencils for High-efficiency PERC Solar Cells

Industrial silicon solar cells like Passivated Emitter and Rear Cells (PERC) typically apply a screen-printed (Ag) front contact with a single print process using a mesh screen. It has been shown that using stencils instead of screens improves the finger profile leading to slightly higher cell conversion efficiencies. However, so far stencil printing required an extra printing step for the busbars since conventional stencils do not support H-pattern designs. In this paper, we evaluate a novel "single print" stencil from ASM AE that allows to print busbars and fingers in a single print step. We apply the novel single print stencil to high-efficiency PERC solar cells and compare it to today's industrial screen printing processes (single print and dual print) as well as to a high performance dual-printed front side grid applying a stencil for the fingers and a screen for the busbars. The printed finger width ranges from 35.8 ± 2.3μm for 30μm stencil opening to 46.7 ± 3.4μm for 40μm screen opening which leads to an 0.5%abs increased metallized area on the front side of the screen printed fingers compared to the stencil printed fingers. The resulting average finger height is 22.3μm for the stencil groups and 11.9μm for the screen printed Ag finger which leads to a difference in the finger line resistance and an additional series resistance contribution for the screen-printed cells of 0.05Ωcm2. We achieve almost identical PERC cell efficiencies with the single print stencil and the dual print stencil process obtaining best values up to 21.1% and average values of 21.0%. In contrast, both screen printed groups achieve 0.2%abs lower average conversion efficiencies mostly due to the lower Jsc and FF. The advantage of the dual print process compared to single print is shown in the increased Voc by 1 to 2mV due to the used non-firing through Ag busbar paste. With these results we demonstrate that the single print stencil process saves two process steps compared to dual print using a stencil while obtaining the same PERC cell performance with an efficiency gain of 0.2%abs compared to today's industrial screen print processes

18.7% Efficient inline-diffused screen-printed silicon wafer solar cells with deep homogeneous emitter etch-back

10.1016/j.solmat.2013.06.046Solar Energy Materials and Solar Cells117412-420SEMC

Two different regulatory T cell populations that promote corneal allograft survival. Invest Ophthalmol Vis Sci 51

PURPOSE. To compare and contrast the T regulatory cells (Tregs) induced by anterior chamber (AC) injection of antigen with those induced by orthotopic corneal allografts. METHODS. Anterior chamber-associated immune deviation (ACAID) Tregs were induced by injecting C57BL/6 spleen cells into the AC of BALB/c mice. Delayed-type hypersensitivity responses to C57BL/6 alloantigens were evaluated by a conventional ear swelling assay. Corneal allograft Tregs were induced by applying orthotopic C57BL/6 corneal allografts onto BALB/c hosts. The effects of anti-CD25, anti-CD8, anti-interferon-␥ (IFN-␥), anti-IL-17A, or cyclophosphamide treatments on corneal allograft survival and ACAID were evaluated. RESULTS. Administration of either anti-CD25 or anti-IFN-␥ antibodies prevented the expression of ACAID and abolished the immune privilege of corneal allografts. By contrast, in vivo treatment with anti-CD8 antibody abrogated ACAID but had no effect on corneal allograft survival. Further discordance between ACAID and corneal allograft survival emerged in experiments in which the induction of allergic conjunctivitis or the administration of anti-IL-17A abolished the immune privilege of corneal allografts but had no effect on the induction or expression of ACAID. CONCLUSIONS. Although orthotopic corneal allografts are strategically located for the induction of ACAID by the sloughing of corneal cells into the AC, the results reported here indicate that the Tregs induced by orthotopic corneal allografts are remarkably different from the Tregs that are induced by AC injection of alloantigen. Although both of these Treg populations promote corneal allograft survival, they display distinctly different phenotypes. (Invest Ophthalmol Vis Sci. 2010;51:6566 -6574) DOI:10.1167/iovs.10-6161 C orneal transplantation has been performed successfully on humans for over 100 years and on animals since 1837. 1,2 Corneal transplants are routinely performed without HLA typing or the use of systemic immunosuppressive drugs. Patients who require corneal transplants because of developmental anomalies of the cornea, which are not associated with inflammation of the ocular surface, have exceptionally high success rates that often reach 90%. 3 This apparent defiance of the laws of transplantation was recognized over 50 years ago in animal studies by Billingham and Medawar. 4, 5 The immune privilege of corneal allografts can be defined mathematically if one considers the fate of corneal allografts in rodents that receive corneal allografts that are mismatched at the entire major histocompatibility complex and multiple minor loci. In rat and mouse models of penetrating keratoplasty, 50% of such corneal allografts survive long term. 6 -8 By contrast, skin and heart allografts undergo 100% immune rejection in such hosts. Three basic factors contribute to the immune privilege of corneal allografts: the blockade in the induction of the immune response to the alloantigens expressed on the corneal allograft, the generation of T regulatory cells (Tregs) that suppress the allodestructive immune responses against the donor alloantigens, and the expression of apoptosis-inducing molecules on the cell membranes of corneal cells that delete alloreactive T cells at the graft/host interface. Antigens introduced into the AC elicit a unique form of systemic immune tolerance termed anterior chamber-associated immune deviation (ACAID), which culminates in the antigen-specific suppression of delayed-type hypersensitivity (DTH). 9 -11 Orthotopic corneal allografts are placed directly over the AC of the eye, and it has been proposed that this juxtapositioning of the orthotopic corneal allograft with the AC facilitates the sloughing or shedding of corneal alloantigens into the AC, which in turn would induce ACAID. 10 Several observations support this hypothesis. Rodents with long-term clear corneal allografts display an antigen-specific suppression of DTH responses that resembles the suppression of DTH found in ACAID. 10 -12 Moreover, manipulations that inhibit the induction of ACAID, such as splenectomy, ablation of NK T cell or ␥␦ T cell populations, invariably lead to an increased tempo and incidence of corneal allograft rejection