Calculated and Experimental Research of Sheet Resistances of Laser-Doped Silicon Solar Cells

The calculated and experimental research of sheet resistances of crystalline silicon solar cells by dry laser doping is investigated. The nonlinear numerical model on laser melting of crystalline silicon and liquid-phase diffusion of phosphorus atoms by dry laser doping is analyzed by the finite difference method implemented in MATLAB. The melting period and melting depth of crystalline silicon as a function of laser energy density is achieved. The effective liquid-phase diffusion of phosphorus atoms in melting silicon by dry laser doping is confirmed by the rapid decrease of sheet resistances in experimental measurement. The plateau of sheet resistances is reached at around 15 Ω/. The calculated sheet resistances as a function of laser energy density is obtained and the calculated results are in good agreement with the corresponding experimental measurement. Due to the successful verification by comparison between experimental measurement and calculated results, the simulation results could be used to optimize the virtual laser doping parameters.

Experimental study on dendritic cells pulsed with brain tumor stem cells for immunotherapy of glioma

Objective To investigate the effect of dendritic cells pulsed with brain tumor stem cells which are used to treat on intracranial glioma. Methods We obtained murine brain tumor stem cells by grow ing C6 cells in epidermal grow th factor/basic fibroblast grow th factor w ithout serum.Dendritic cells isolated from rat bone marrow w ere pulsed w ith BTSCs. Rat brain

ESTABLISHMENT OF K562/ADM/VER CELL SUBLINE RESISTANT TO VERAPAMIL AND ITS RESISTANT MECHANISM

Objective: To understand whether verapamil (VER) resistance development in the multidrug-resistant cell line and its mechanism. Methods: K562/ADM/VER cell subline resistant to verapamil was established through a gradual increase of VER concentration in the media. MTT method was used to assay resistance to VER, cross resistance to dipyriamole (DPM), cyclosporin A (CsA) in the cells, and HPLC and spectrofluorometer to detect intracellular accumulation of VER or ADM respectively, as well as S-P immunocytochemical technique for detection of genes expression. Results: It were observed that 7.9—fold increase in VER resistance, significantly reduced intracellular accumulation of VER or ADM and also develop across resistance to DPM and CsA in K562/ADM/VER cells, compared with its parent cell, K562/ADM. High-level of p-glycoprotein(pgp), middle-level of p53, p16, was present in two cell lines without expression of GSTPI, C-myc, C-myc, C-fos and C-erbB-2. Bc1–2 protein expression was found only in K562/ADM cells. Conclusion: K562/ADM cells were capable of being induced to develop resistance to VER.

Experimental study of human umbilica cord blood stromal cells transfected with recombinant adenoviral vector co-expressing VCAM-1

This work was funded from National Natural Science Foun-dation of China(No.39770335 and No.30070327)andChongqing Medical Key construction Foundation.Abstract:Ob-jective To establish the experimental foundation for furtherstudying the effect of VCAM-1 gene modified HUCBSCs

Effect of Ligustrazine Nanoparticles Nano Spray on Transforming Growth Factor-β/Smad Signal Pathway of Rat Peritoneal Mesothelial Cells Induced by Tumor Necrosis Factor-α

Objective： To study the effect of ligustrazine nanoparticles nano spray（LNNS） on transforming growth factor β（TGF-β）/Smad signal protein of rat peritoneal mesothelial cells（RPMC） induced by tumor necrosis factor α（TNF-α）, and the anti-adhesion mechanism of LNNS in the abdominal cavity. Methods： The primary culture and subculture of rat peritoneal mesothelial cells（RPMC） was processed by trypsin digestion method in vitro. The third generation was identified for experiment and divided into 5 groups： a blank group： RPMC without treatment; a control group： RPMC stimulated with TNF-α; RPMC treated by a low-dosage LNNS group（2.5 mg/L）; RPMC treated by a medium-dosage LNNS group（5 mg/L）; and RPMC treated by a high-dosage LNNS group（10 mg/L）. Reverse transcription-polymerase chain reaction was applied to test the expression of fibronectin, collagen Ⅰ（COL-Ⅰ）, TGF-β m RNA, and Western blot method to test the Smad protein 7 expression of RPMC. Results： Compared with the blank group, a significant elevation in fibronectin（FN）, COL-Ⅰ and TGF-β m RNA expression of RPMC were observed in the control group（P〈0.05）. Compared with the control group, LNNS suppressed the expressions of FN, COL-Ⅰ and TGF-β m RNA in a concentrationdependent manner（P〈0.05）. The expression of Smad7 protein of RPMC was down-regulated by TNF-α stimulation, and up-regulated with the increase of LNNS dose（P〈0.05）. Conclusions： TNF-α may induce changes in RPMC＇s viability, leading to peritoneal injury. LNNS could reverse the induction of fibrosis related cytokine FN, COL-Ⅰ and TGF-β, up-regulating the expression of Smad7 by TNF-α in RPMC, thus attenuate peritoneal injury by repairing mesothelial cells.

GPR54 deficiency reduces the Treg population and aggravates experimental autoimmune encephalomyelitis in mice

GPR54 is highly expressed in the central nervous system and plays a crucial role in pubertal development. However, GRP54 is also expressed in the immune system, implying possible immunoregulatory functions. Here we investigated the role of GPR54 in T cell and immune tolerance. GPR54 deficiency led to an enlarged thymus, an increased number of thymocytes, and altered thymic micro-architecture starting around puberty, indicating GPR54 function in T-cell development through its regulatory effect on the gonadal system. However, flow cytometry revealed a significant reduction in the peripheral regulatory T cell population and a moderate decrease in CD4 single-positive thymocytes in prepubertal Gpr54^(-/-) mice. These phenotypes were confirmed in chimeric mice with GPR54 deficient bone marrow-derived cells. In addition, we found elevated T cell activation in peripheral and thymic T cells in Gpr54^(-/-) mice. When intact mice were immunized with myelin oligodendrocyte glycoprotein, a more severe experimental autoimmune encephalomyelitis(EAE) developed in the Gpr54^(-/-) mice. Interestingly, aggravated EAE disease was also manifested in castrated and bone marrow chimeric Gpr54^(-/-) mice compared to the respective wild-type control,suggesting a defect in self-tolerance resulting from GPR54 deletion through a mechanism that bypassed sex hormones. These findings demonstrate a novel role for GPR54 in regulating self-tolerant immunity in a sex hormone independent manner.