Resident pulmonary lymphocytes expressing the gamma/delta T-cell receptor

The biological role of cells bearing the gamma delta T-cell antigen receptor (TCR) is as yet unclear. Although there are indications that some gamma delta+ cells can mediate cytotoxicity, their antigen-related functions have not yet been defined. In the mouse, gamma delta+ cells constitute 1-3% of T cells in lymphoid organs. Intestinal intraepithelial lymphocytes (IELs) and dendritic epidermal cells (DECs) also appear to carry the gamma delta TCR. The strategic locations of DECs and IELs have led to the suggestion that gamma delta+ cells could constitute a first line of defence in the vicinity of large surfaces of contact with the environment. We report here that an estimated 8-20% of resident pulmonary lymphocytes (RPLs) are CD3+ alpha beta TCR-, and presumably gamma delta TCR+. Furthermore, mice exposed to aerosols containing a Mycobacterium tuberculosis extract have an increased number of activated CD3+ alpha beta-TCR- pulmonary T cells which can be propagated in vitro.     

太阳能电池最大功率跟踪控制的研究(英文)

光伏电池输出功率随外部环境和负载的变化而变化,要提高光伏发电系统的输出效率须采用有效的最大功率点跟踪算法.针对光伏电池的非线性特性,提出了一个基于增量电导法、以升降压斩波器为核心的光伏能量转换系统.经PSIM和LabVIEW软件仿真证实,该方法能使系统稳定工作在最大功率点,同时能对外界环境的变化做出快速反应.     

Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia

Despite intense investigation, mechanisms that facilitate the emergence of the pre-eclampsia phenotype in women are still unknown. Placental hypoxia, hypertension, proteinuria and oedema are the principal clinical features of this disease. It is speculated that hypoxia-driven disruption of the angiogenic balance involving vascular endothelial growth factor (VEGF)/placenta-derived growth factor (PLGF) and soluble Fms-like tyrosine kinase-1 (sFLT-1, the soluble form of VEGF receptor 1) might contribute to some of the maternal symptoms of pre-eclampsia. However, pre-eclampsia does not develop in all women with high sFLT-1 or low PLGF levels, and it also occurs in some women with low sFLT-1 and high PLGF levels. Moreover, recent experiments strongly suggest that several soluble factors affecting the vasculature are probably elevated because of placental hypoxia in the pre-eclamptic women, indicating that upstream molecular defect(s) may contribute to pre-eclampsia. Here we show that pregnant mice deficient in catechol-O-methyltransferase (COMT) show a pre-eclampsia-like phenotype resulting from an absence of 2-methoxyoestradiol (2-ME), a natural metabolite of oestradiol that is elevated during the third trimester of normal human pregnancy. 2-ME ameliorates all pre-eclampsia-like features without toxicity in the Comt(-/-) pregnant mice and suppresses placental hypoxia, hypoxia-inducible factor-1alpha expression and sFLT-1 elevation. The levels of COMT and 2-ME are significantly lower in women with severe pre-eclampsia. Our studies identify a genetic mouse model for pre-eclampsia and suggest that 2-ME may have utility as a plasma and urine diagnostic marker for this disease, and may also serve as a therapeutic supplement to prevent or treat this disorder.