磁控溅射太阳能电池预镀Mo薄膜及其性能

利用磁控溅射法在玻璃基片上进行了太阳能电池预镀层Mo薄膜的制备,研究了氩气分压、溅射功率、溅射时间等工艺条件对Mo膜性能及厚度的影响,并对Mo膜的物理性能及电学性能进行了研究。结果表明,Mo薄膜的厚度与溅射时间近似的成正比关系,Mo膜的电阻率先降低,并在膜厚为0.3μm处达到最低,而后电阻率逐渐增加。     

磁控溅射太阳能电池预镀Mo薄膜及其性能

利用磁控溅射法在玻璃基片上进行了太阳能电池预镀层Mo薄膜的制备,研究了氩气分压、溅射功率、溅射时间等工艺条件对Mo膜性能及厚度的影响,并对Mo膜的物理性能及电学性能进行了研究.结果表明,Mo薄膜的厚度与溅射时间近似的成正比关系,Mo膜的电阻率先降低,并在膜厚为0.3 μm处达到最低,而后电阻率逐渐增加.     

颗粒蛋白前体缺失型腹膜巨噬细胞的体外炎症应答

探讨颗粒蛋白前体缺失型巨噬细胞的体外炎症反应。选取野生型C57BL/6雄性小鼠6-8周(WT)和PGRN基因敲除雄性小鼠6-8周(KO)为实验动物。向小鼠腹腔内注射1m L6%的淀粉,脱颈法处死小鼠后提取腹膜细胞。用瑞士染色后油镜下观察细胞,用流式细胞仪进行细胞检测,显微镜下观察腹膜巨噬细胞吞噬功能,ELISA法检测腹膜巨噬细胞培养上清中TNF-a和IL-12因子。WT小鼠和PGRN基因敲除KO小鼠腹膜细胞的数目、形态和种类及巨细胞表面标志物和巨噬细胞吞噬功能均无显著性差异(p0.05)。PGRN基因敲除KO小鼠来源腹膜巨噬细胞培养上清中前炎性因子TNF-a和IL-12的含量较WT小鼠明显增高。PGRN对腹膜细胞的数目、形态、种类和巨噬细胞表面标志物没有显著影响,但会使巨噬细胞炎症反应增强。     

Survival of a brown dwarf after engulfment by a red giant star

Many sub-stellar companions (usually planets but also some brown dwarfs) orbit solar-type stars. These stars can engulf their sub-stellar companions when they become red giants. This interaction may explain several outstanding problems in astrophysics but it is unclear under what conditions a low mass companion will evaporate, survive the interaction unchanged or gain mass. Observational tests of models for this interaction have been hampered by a lack of positively identified remnants-that is, white dwarf stars with close, sub-stellar companions. The companion to the pre-white dwarf AA Doradus may be a brown dwarf, but the uncertain history of this star and the extreme luminosity difference between the components make it difficult to interpret the observations or to put strong constraints on the models. The magnetic white dwarf SDSS J121209.31 + 013627.7 may have a close brown dwarf companion but little is known about this binary at present. Here we report the discovery of a brown dwarf in a short period orbit around a white dwarf. The properties of both stars in this binary can be directly observed and show that the brown dwarf was engulfed by a red giant but that this had little effect on it.     

Essential role for Nix in autophagic maturation of erythroid cells

Erythroid cells undergo enucleation and the removal of organelles during terminal differentiation. Although autophagy has been suggested to mediate the elimination of organelles for erythroid maturation, the molecular mechanisms underlying this process remain undefined. Here we report a role for a Bcl-2 family member, Nix (also called Bnip3L), in the regulation of erythroid maturation through mitochondrial autophagy. Nix(-/-) mice developed anaemia with reduced mature erythrocytes and compensatory expansion of erythroid precursors. Erythrocytes in the peripheral blood of Nix(-/-) mice exhibited mitochondrial retention and reduced lifespan in vivo. Although the clearance of ribosomes proceeded normally in the absence of Nix, the entry of mitochondria into autophagosomes for clearance was defective. Deficiency in Nix inhibited the loss of mitochondrial membrane potential (DeltaPsi(m)), and treatment with uncoupling chemicals or a BH3 mimetic induced the loss of DeltaPsi(m) and restored the sequestration of mitochondria into autophagosomes in Nix(-/-) erythroid cells. These results suggest that Nix-dependent loss of DeltaPsi(m) is important for targeting the mitochondria into autophagosomes for clearance during erythroid maturation, and interference with this function impairs erythroid maturation and results in anaemia. Our study may also provide insights into molecular mechanisms underlying mitochondrial quality control involving mitochondrial autophagy.     

Selective activation of Lyt 2+ precursor T cells by ligation of the antigen receptor

Resting T lymphocytes may be activated either physiologically, by the specific recognition of antigen in association with molecules encoded by the major histocompatibility complex (MHC), or non-physiologically using mitogens such as concanavalin A (Con A). The former activation process is difficult to analyse because resting precursor T cells specific for a particular antigen-MHC combination can only be isolated in the presence of a large excess of bystander cells of irrelevant specificity; clonal populations of uniform specificity are not useful for studying the activation of naive T cells because there is no reason to believe that such cloned cells ever return to the state of resting precursors. Mitogens may activate a large fraction of resting T cells, but analysis is again complicated because the target molecule(s) of most mitogens is unknown and the relationship of this kind of activation to physiological induction by antigen plus MHC molecules remains unclear. By using a monoclonal antibody specific for the antigen receptors on approximately 25% of all T cells of both Lyt 2+ and Lyt 2- subsets, we have studied the induction of lymphokine responsiveness in resting normal T cells. This antibody, immobilized on Sepharose beads, is sufficient to activate Lyt 2+ T cells, but not Lyt 2- T cells, to clonal expansion in the presence of a mixture of lymphokines (10% rat spleen Con A supernatant). We report here that clonal growth of the T cells obeys single-hit kinetics in limiting-dilution microcultures, suggesting that a single cell type is limiting. We conclude that cytotoxic T-lymphocyte (Tc) precursors require only ligation of the antigen receptor before they become responsive to lymphokines, whereas helper T-lymphocyte (Th) precursors require additional signals.     

Characterization of a common precursor population for dendritic cells

Dendritic cells (DCs) are essential for the establishment of immune responses against pathogens and tumour cells, and thus have great potential as tools for vaccination and cancer immunotherapy trials. Experimental evidence has led to a dual DC differentiation model, which involves the existence of both myeloid- and lymphoid-derived DCs. But this concept has been challenged by recent reports demonstrating that both CD8- and CD8+ DCs, considered in mice as archetypes of myeloid and lymphoid DCs respectively, can be generated from either lymphoid or myeloid progenitors. The issue of DC physiological derivation therefore remains an open question. Here we report the characterization of a DC-committed precursor population, which has the capacity to generate all the DC subpopulations present in mouse lymphoid organs---including CD8- and CD8+ DCs, as well as the B220+ DC subset---but which is devoid of myeloid or lymphoid differentiation potential. These data support an alternative model of DC development, in which there is an independent, common DC differentiation pathway.     

Specific expression of a foreign beta-globin gene in erythroid cells of transgenic mice

The globin gene family represents an attractive system for the study of gene regulation during mammalian development, as its expression is subject to both tissue-specific and temporal regulation. While many aspects of globin gene structure and expression have been described extensively, relatively little is known about the cis-acting DNA sequences involved in the developmental regulation of globin gene expression. To begin to experimentally define these regulatory sequences, we have taken the approach of introducing cloned globin genes into the mouse germ line and examining their expression in the resulting transgenic animals. Here we describe a series of transgenic mice carrying a hybrid mouse/human adult beta-globin gene, several of which express the gene exclusively or predominantly in erythroid tissues. These studies demonstrate that regulatory sequences closely linked to the beta-globin gene are sufficient to specify a correct pattern of tissue-specific expression in a developing mouse, when the gene is integrated at a subset of foreign chromosomal positions.     

BAI1 is an engulfment receptor for apoptotic cells upstream of the ELMO/Dock180/Rac module

Engulfment and subsequent degradation of apoptotic cells is an essential step that occurs throughout life in all multicellular organisms. ELMO/Dock180/Rac proteins are a conserved signalling module for promoting the internalization of apoptotic cell corpses; ELMO and Dock180 function together as a guanine nucleotide exchange factor (GEF) for the small GTPase Rac, and thereby regulate the phagocyte actin cytoskeleton during engulfment. However, the receptor(s) upstream of the ELMO/Dock180/Rac module are still unknown. Here we identify brain-specific angiogenesis inhibitor 1 (BAI1) as a receptor upstream of ELMO and as a receptor that can bind phosphatidylserine on apoptotic cells. BAI1 is a seven-transmembrane protein belonging to the adhesion-type G-protein-coupled receptor family, with an extended extracellular region and no known ligands. We show that BAI1 functions as an engulfment receptor in both the recognition and subsequent internalization of apoptotic cells. Through multiple lines of investigation, we identify phosphatidylserine, a key 'eat-me' signal exposed on apoptotic cells, as a ligand for BAI1. The thrombospondin type 1 repeats within the extracellular region of BAI1 mediate direct binding to phosphatidylserine. As with intracellular signalling, BAI1 forms a trimeric complex with ELMO and Dock180, and functional studies suggest that BAI1 cooperates with ELMO/Dock180/Rac to promote maximal engulfment of apoptotic cells. Last, decreased BAI1 expression or interference with BAI1 function inhibits the engulfment of apoptotic targets ex vivo and in vivo. Thus, BAI1 is a phosphatidylserine recognition receptor that can directly recruit a Rac-GEF complex to mediate the uptake of apoptotic cells.