API2-MALT1融合基因变异体在粘膜相关淋巴组织结外边缘区B细胞淋巴瘤中的分布及凋亡的关系

目的探讨API2-MALT1融合基因变异体在粘膜相关淋巴组织结外边缘区B细胞淋巴瘤(extranodal marginal zone B—cell lymphoma of mucosa—associated lymphoid tissue，MALT)中的分布特点及其转录与肿瘤凋亡的关系。方法将逆转录-聚合酶链反应和巢式聚合酶链式反应结合，检测62例不同部位MALT淋巴瘤中API2-MALT1融合基因的多种变异体；通过TdT介导脱氧核苷酸缺口末端标记技术进行肿瘤细胞的原位凋亡检测；通过逆转录-聚合酶链反应和免疫组化染色检测API2的mRNA和蛋白水平。结果62例MALT淋巴瘤中28例检出API2-MALT1融合基因(45．16％)，为变异体A1446-M1123或A1446-M814，但未检出A1446-M541和A1446-M1150。A1446-M1123(18／28)的检出明显多于A1446-M814(10／28)。融和基因转录在甲状腺MALT淋巴瘤中检出最低，在其它部位的分布无差异。在API2-MALT1^ 组(API2-MALT1mRNA表达阳性组)肿瘤凋亡水平明显高于API2-MALT1^-组(API2-MALT1mRNA表达阴性组)，API2的mRNA和蛋白水平低于阴性组。A1446-M1123^ 与A1446-M814^ 病例之间凋亡和API2的变化无差异。结论MALT淋巴瘤中t(11；18)(q21；q21)的发生有部位差异，A1446-M1123可能是中国人MALT淋巴瘤中API2-MALT1融合基因变异体的主要类型。API2-MALT1融合基因转录与MALT淋巴瘤的凋亡水平和API2的变化有关。     

Selenium improves cardiac function by attenuating the activation of NF-kappaB due to ischemia-reperfusion injury

Although selenium, an essential trace element and a component of glutathione peroxidase, is known to protect the heart from ischemia-reperfusion (I/R)-induced injury, the mechanisms of this protection are not fully understood. For this purpose, isolated rat hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion; sodium selenite (25-1,000 nM) was added in the perfusion medium 10 min prior to ischemia, as well as during reperfusion. Selenium caused a dose-dependent improvement in cardiac performance and attenuated the decrease in the ratio of reduced glutathione to oxidized glutathione, as well as the increased level of malondialdehyde in I/R heart. Elevated ratios of nuclear factor-kappaB (NF-kappaB) in particulate and cytosolic fraction and of phosphorylated NF-kappaB and total NF-kappaB in I/R hearts were reduced by selenium. Cardiac dysfunction in hearts perfused with xanthine plus xanthine oxidase mixture, as well as hydrogen peroxide, or subjected to Ca2+ paradox was also attenuated by selenium. These data suggest that selenium protects the heart against I/R injury due to its action on the redox state and deactivation of NF-kappaB in I/R hearts.     

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.     

Differential expression of binding sites for chemokine RANTES on human T lymphocytes

The C-C chemokine RANTES, a T lymphocyte chemoattractant, is considered an important mediator of inflammation, allergy, and host defense against HIV-1 infection. In this study, we investigated the modulation of binding of RANTES to T lymphocytes. Human peripheral blood CD3+ T cells, when freshly isolated from buffy-coat blood, expressed a considerable number of high-affinity binding sites for RANTES. These cells also showed significant chemotactic migration in response to RANTES in vitro. After 6–15 h incubation at 37°C, the binding of RANTES, but not of macrophage inflammatory protein-1α (MIP-1α) or of monocyte chemotactic protein-3 (MCP-3), consistently increased. Scatchard analyses indicated that the number of binding sites for RANTES increased about threefold by 15 h without any change in the affinity. The increase in RANTES binding was no longer detected by 24 h. This increase in the specific binding was mainly attributable to CD4⁺ T cells and was not associated with increased chemotactic activity of these cells in response to RANTES. Incubation with anti-CD3 antibody for 15 h markedly reduced the binding capability of T cells for RANTES and was associated with decreased chemotactic activity. On the other hand, when T cells were incubated with interleukin-2 (IL-2) for 1 week, the specific binding for all three C-C chemokines, RANTES, MIP-1α, and MCP-3 was markedly increased in comparison to cells cultured in the absence of IL-2. These results suggest that the expression of binding sites on T cells for RANTES is differentially modulated, indicating the existence of novel receptors for RANTES that do not bind MIP-1α.     

A new microcellular cytotoxicity test based on calcein AM release

We present a microtest for cell-mediated immunity, based on the use of the Tarasaki tray and calcein AM vital dye. The number of target cells needed has been reduced to 500 per test with a corresponding tenfold reduction in the number of effector cells needed. Results were read at the rate of 1 second per test using a fluorimeter attached to a microscope. Each reaction was also confirmed visually with the use of ethidium bromide as a counterstain for dead cells. The calcein AM dye used to stain the living cells was shown to have a low spontaneous leakage rate—less than 15% in 4 hours at 37°C. Dilutions of targets stained by calcein AM had a linear relationship with measured fluorescence values. NK cells, LAKs, and CTLs were readily detectable by this microtest. Quantitation of killing and kinetic analysis was readily performed with this test system. A significant positive correlation to ⁵¹Cr-release results was found. We conclude that the microtest should find wide application in studies of cell-mediated immunity.     

图书馆无形资产特性研究(上)

以无形资产为切入点．探讨图书馆在网络环境下与各类信息源及用户的辩证关系；以人为本的知识资本运营．无形资产的投入和知识产权保护比以往更加重要；提出社会无形资产概念：甄别信息资源专有权与公有权．论证图书馆社会角色；辨析图书馆知识管理．无形资产评估、立法理念。     

Molecular orientation of ultrahigh molecular weight polyethylene induced by various sliding motions

Wear and wear debris of ultrahigh molecular weight polyethylene (UHMWPE) in joint replacements have been recognized as one of the major contributors to the failure of orthopedic implants. The detailed wear mechanism of polyethylene under biomechanic motions is not well understood. In simulation wear bench tests, it was found that unidirectional sliding produces the least amount of wear, reciprocating motion increases wear significantly, and cross-shear motion (similar to hip and knee joint motion in the human body) produces the highest amount of wear. Conventional wear theories are inadequate to explain this observation. This study utilizes resonant absorption of linearly polarized soft X-rays at a synchrotron radiation beam line to measure the molecular orientation of a UHMWPE surface layer subjected to different wear motions. Carbon-K-edge partial-electron-yield X-ray absorption measurements were done on the worn UHMWPE samples. X-ray absorption measurements show conclusively that the molecular chains of UHMWPE align preferentially parallel to the direction of sliding. Examination under various wear motions showed that unidirectional shear produced the maximum chain orientation, whereas cross-shear wear motions produced the least amount of orientation. When polymeric chains align, the surface layer tends to be more brittle and hard, thus resisting wear. When they do not align, loose chains may be subjected to both Mode I and Mode II fracture, hence increasing the wear rate. This molecular alignment observation may offer an explanation of why different wear motions have different wear characteristics.     

抑癌基因PTEN与食管癌

PTEN是近年发现的一种与细胞信号传导途径有关的具有双特异性磷酸酶活性的新型抑癌基因。研究表明,该基因的突变与人类多种恶性肿瘤的发生发展密切相关。近年来国内外的学者在食管癌组织中发现,虽然该基因发生突变的频率较低,但其蛋白表达却普遍下降,表达程度与食管癌的恶性程度及预后密切相关。因此,PTEN的低表达可能参与了食管癌的发生发展过程。     

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。     

Identification of a frequent variant in ALG6, the cause of Congenital Disorder of Glycosylation-Ic

Congenital Disorder of Glycosylation (CDG) type Ic is caused by mutations in ALG6. This gene encodes an alpha1,3 glucosyltransferase used for synthesis of the lipid linked oligosaccharide (LLO) precursor of the protein N-glycosylation pathway. CDG-Ic patients have moderate to severe psychomotor retardation, seizures, hypotonia, strabismus, and feeding difficulties. We previously identified a typical patient with a heterozygous point mutation, c.391T>C (p.Tyr131His) in ALG6. Using complementation analysis of ALG6-deficient yeast, we show that this alteration is as severe as the most common disease-causing mutation, c998C>T (p. Ala333Val), which occurs in over half of all known CDG-Ic patients. The frequency of c.391T>C (p.Tyr131His) in the US population, is 0.0214, suggesting that homozygotes would occur at a rate of& tilde;1:2,200. We identified one patient with typical CDG-Ic symptoms and a homozygous p.Tyr131His alteration in ALG6. However, in contrast to most CDG patients, her LLO and plasma transferrin glycosylation appeared normal. Thus, it is unclear whether c.391T>C causes CDG-Ic or contributes to the symptoms. Genotyping additional patients with CDG-like symptoms will be required to resolve this issue.