2450MHz介质复介电常数的测量

目的测量2450MHz频率下蒸馏水和不同浓度NaCl溶液的复介电常数,用以判定系统的可靠性和稳定性.方法根据微扰法得到复介电常数的测量公式,然后通过实验对已知参数的蒸馏水和NaCl溶液进行测量,并计算其复介电常数和电导率,验证计算结果的可靠性和稳定性.结果对计算结果进行统计分析和误差分析,其均值、标准差和变异系数表明,最终结果可与M.I.T标准较好地吻合.结论这种系统可较好地测量2450MHz频率下高损耗介质的复介电常数,测量系统的主要误差是由介质体积的误差引起的,因此精确测量介质体积是测量生物组织等高损耗介质复介电常数的关键.     

Involvement of ERK, p38 and NF-kappaB signal transduction in regulation of TLR2, TLR4 and TLR9 gene expression induced by lipopolysaccharide in mouse dendritic cells

Toll-like receptors (TLR) are sentinel receptors capable of recognizing pathogen-associated molecule patterns (PAMP) such as lipopolysaccharide (LPS) and CpG-containing oligonucleotides (CpG ODN). TLR2 and TLR4 are major receptors for Gram-positive and Gram-negative bacterial cell wall components, respectively. TLR9 is necessary for CpG signalling. LPS or CpG ODN can activate immature dendritic cells (DC) and induce DC maturation characterized by production of cytokines, up-regulation of co-stimulatory molecules, and increased ability to activate T cells. However, little is known regarding the regulation of TLR gene expression in mouse DC. In this study, we investigated the regulation of TLR2, TLR4 and TLR9 gene expression by LPS in murine immature DC. TLR2, TLR4 and TLR9 mRNA were up-regulated following LPS stimulation. The up-regulation of TLR9 expression coincided with significantly increased production of tumour necrosis factor-alpha induced by LPS plus CpG ODN. While inhibition of extracellular signal-related kinase and NF-kappaB activation suppressed the up-regulation of the expression of TLR2, TLR4 and TLR9 mRNA, inhibition of p38 kinase prevented the up-regulation of TLR2 and TLR4 mRNA expression but enhanced the up-regulation of TLR9 expression. These results demonstrated that TLR2, TLR4 and TLR9 gene expression was differently regulated by LPS in mouse immature DC. Up-regulation of TLR2, TLR4 and TLR9 expression by LPS might promote the overall responses of DC to bacteria and help to explain the synergy between LPS and other bacterial products in the induction of cytokine production.     

3～20周人胚和胎儿肾小体的组织发生

应用光、电镜对3～20周22例人胚和胎儿肾小体的组织发生进行了观察.受精后第25天胚肾已有肾小体发生.随着胚龄的增长,肾小体的发生数目增多,肾小体的形成方式是:胚肾内先形成许多厚壁小管,在一部分厚壁小管的诱导下,另一部分厚壁小管的一侧壁呈帽状增厚,分化形成造血干细胞、毛细血管内皮及肾小囊脏层,对侧壁形成肾小囊壁层.即厚壁小管的双侧壁形成肾小体.     

大鼠肝抑素纯化及其生物活性的检测

用ＳｅｐｈａｄｅｃＧ－５凝胶过滤层析法，进一步纯化具肝抑素生物活性的大鼠肝蛋白质粗提品，以分离的大鼠再生肝的肝细胞为靶细胞，体外检测各洗脱峰浓缩物对肝细胞增殖的制率结果证明，Ｅ峰浓缩物的抑制作用最强，其活性比为粗提品的２０倍，ＳＤＳ聚丙烯酰胺电泳图及蛋白质迁移率测定表明，该浓缩物的主要成分为分子量１３．５ｋＤ的多肽。本研究对大鼠肝抑素做了初步纯化，验证了该物质在肝再生中起重要调控作用的生物效应。     

海藻酸钙/聚组氨酸微胶囊的毒性试验研究

为了考察海藻酸钙/聚组氨酸微胶囊的毒性特征,我们利用MTT比色法和小鼠尾静脉注射法,分别考察了该微胶囊的细胞毒性和急性全身毒性。结果表明：微胶囊浓度≤1.0mg/mL时,材料对L929细胞生长无明显抑制作用;微胶囊浸提液即使在高浸提比（10.0mg/mL）下,浸提产物也无细胞毒性作用。急性全身毒性试验结果显示：微胶囊浸提液不引起急性全身毒性反应,表明微胶囊浸提液无有毒的沥滤物和降解产物产生。说明海藻酸钙/聚组氨酸微胶囊无明显毒性。     

4E-binding protein phosphorylation and eukaryotic initiation factor-4E release are required for airway smooth muscle hypertrophy

The molecular mechanisms of airway smooth muscle hypertrophy, a feature of severe asthma, are poorly understood. We previously established a conditionally immortalized human bronchial smooth muscle cell line with a temperature-sensitive SV40 large T antigen. Temperature shift and loss of large T cause G1-phase cell cycle arrest that is accompanied by increased airway smooth muscle cell size. In the present study, we hypothesized that phosphorylation of eukaryotic initiation factor-4E (eIF4E)-binding protein (4E-BP), which subsequently releases eIF4E and initiates cap-dependent mRNA translation, was required for airway smooth muscle hypertrophy. Treatment of cells with chemical inhibitors of PI 3-kinase and mammalian target of rapamycin blocked protein synthesis and cell growth while decreasing the phosphorylation of 4E-BP and increasing the binding of 4E-BP to eIF4E, consistent with the notion that 4E-BP1 phosphorylation and eIF4E function are required for hypertrophy. To test this directly, we infected cells with a retrovirus encoding a phosphorylation site mutant of 4E-BP1 (AA-4E-BP-1) that dominantly inhibits eIF4E. Upon temperature shift, cells infected with AA-4E-BP-1, but not empty vector, failed to undergo hypertrophic growth. We conclude that phosphorylation of 4E-BP, eIF4E release, and cap-dependent protein synthesis are required for hypertrophy of human airway smooth muscle cells.     

重复电刺激前肢神经引起成年大鼠运动皮层的可塑性改变

为了了解成年大鼠运动皮层的功能可塑性，利用皮层内微刺激方法测定ＭＩ代表区并观察重复电刺激前肢神经对ＭＩ代表区的影响。实验组大鼠（９例）持续１．２－２小时的前肢神经电刺激导致前肢运动区与面部触须运动区边界向ＶＩ方向，移动２６３．３±９０．９μｍ并同时伴有运动阈值的改变；ＦＬ内ＭＴ降低５．０±１３．３μＡ，而在ＶＩ内ＭＴ升高９．６±１１．６μＡ对照组大鼠间隔１．５－２小时的两次测定结果，ＦＬ－ＶＩ边界