极低频磁场对激动剂诱发钙振荡的影响

从激动剂诱发钙振荡的非线性动力学模型出发, 通过数值计算分析极低频磁场对胞内游离钙离子浓度［Ｃａ２ ＋ ］ｉ 的影响。研究结果表明：只有当外加磁场的频率与胞内钙振荡的特征频率相近时,极低频磁场才会对该细胞的［Ｃａ２ ＋］ｉ 产生影响;由于激动剂诱发钙振荡的动力学模型中的许多参数是因细胞而异的,因此极低频磁场对［Ｃａ２ ＋ ］ｉ 的影响具有显著的个体差异     

磁场对肿瘤细胞的抑制作用

目的 :用磁场进行小鼠荷瘤和人体的离体癌细胞抑制试验。方法 :用装备有NdFeB永磁材料的仪器产生非均匀磁场 (磁通密度为 0 .2 0T ,梯度为 0 .0 7T/cm)对荷瘤小鼠和人体的离体癌细胞每天作用0 .5小时 ,1 2天后解剖检查试验结果。结果 :磁场对荷瘤小鼠的癌细胞抑止率达 61 % (p <0 .0 0 2 ) ,胸腺平均比化疗组重 8mg(p <0 .0 1 ) ,癌组织的纤维包膜是对照组的 2～ 3倍。谷丙转氨酶 (SGPT)低于化疗组的平均值 (p <0 .0 0 1 ) ,肝、心肌细胞无损伤 ;白细胞 (WBC)高于化疗组的平均值 (p <0 .0 2 ) ,免疫功能提高 ;血红蛋白 (Hb)低于化疗组的平均值 (p <0 .0 5 ) ,局部缺氧 ,癌细胞呈片状坏死 ,部分癌组织呈孤岛状。磁疗组无明显毒副作用反应。重复性实验结果相近。小鼠和人体离体癌细胞实验显著性检验无显著性意义。结论 :磁场在一定的梯度范围是可以有效的抑制小鼠肿瘤的生长。     

磁场对肿瘤细胞抑制作用的试验与分析

目的:用磁场进行小鼠荷瘤和人体的离体癌细胞抑制试验。方法:用装备有NdFeB永磁材料的仪器产生非均匀磁场(磁通密度为0.20T,梯度为0.07T/cm)对荷瘤小鼠和人体的离体癌细胞每天照射0.5小时,12天后解剖检查试验结果。结果:磁场对荷瘤小鼠的癌细胞抑止率达61%(P<0.002),胸腺平均比化疗组重8mg(P<0.01),癌组织的纤维包膜是对照组的2～3倍。谷丙转氨酶(SGPT)低于化疗组的平均值(P<0.001),肝、心肌细胞无损伤;白细胞(WBC)高于化疗组的平均值(P<0.02),免疫功能提高;血红蛋白(Hb)低于化疗组的平均值(P<0.05),局部缺氧,癌细胞呈片状坏死,部分癌组织呈孤岛状。磁疗组无明显毒副作用反应。重复性实验结果相近。小鼠和人体离体癌细胞实验显著性检验无显著性意义。结论:磁场在一定的梯度范围是可以有效的抑制小鼠肿瘤的生长。     

电场和磁场响应的智能高分子材料

过去的几年里,人们开始对新型智能材料的开发产生了极大的兴趣。这些新型的智能材料包括生物材料、自组装材料、复集合流体材料以及高分子凝胶等;但是人们发现还没有哪种智能材料能像高分子凝胶智能材料那样可以对多重的外场刺激产生响应。这些外场刺激通常包括温度、溶剂、pH值、离子、分子、光、电、磁等。同时这种材料对外场响应时可以产生多种变化,包括体积的膨胀收缩、力学性能的变化、光电性质的变化等。在过去的时间里,人们已经在智能高分子凝胶领域取得了重要的进展。具有电磁响应的胶体粒子能够与高分子凝胶形成复合物。这些胶体粒子可以使高分子凝胶在外场刺激时发生形变。当施加电场或磁场时,高分子凝胶的形状发生变化,当撤去外场时,形状回复原样。基于这些特点,电磁响应的智能材料可以用来设计成新型的驱动器、阀、马达,以及药物输运装置。     

DC和AC磁场混合作用下的离子运动

本文研讨了在微弱ＤＣ磁场和频率非常低的ＡＣ磁场并行作用下,位于大分子内部的离子运动情况。主要焦点是大分子中磁场对离子热运动的影响,通过一些离散频率的分析揭示了热运动的共振效应。指出当ＤＣ和ＡＣ磁场施加或切断时离子热运动能量将发生变化,如果大分子周围的媒介质的粒子能充分阻止瞬间接触,就会引起大分了子量子态的变化。     

脉冲电场和磁场对高血粘和高凝血影响的比较研究

比较研究脉冲电场和脉冲磁场对高血粘和高凝血的影响,探寻降低血液粘度,抑制凝血过快、过强的物理方法.每份血样等分9份,1份作对照,对另外8份分别作不同的脉冲电场或磁场处理.结果显示不同上升沿速率的脉冲电场和磁场对高血粘和高凝血的影响程度不同,上升沿速率为2.5 × 105T s-1的脉冲磁场使全血表观粘度η降低(P＜0.01)、复钙凝血时间tr变长(P＜0.01),血块的最大剪切应力τax变小(P＜0.01).脉冲磁场作用能改善高血粘和高凝血状况.     

极低频磁场对大鼠急性和慢性关节炎影响的研究

目的：探讨极低频磁场对大鼠急性和慢性关节炎模型的影响。方法：大鼠足内皮下注射角叉菜胶建立急性关节炎模型,磁场分别暴露6h和8h,注射弗氏完全佐剂建立慢性关节炎模型,磁场暴露7d,每天6h,观察炎症肿胀和炎性细胞因子的改变情况。结果：急性和慢性关节炎大鼠经过不同时间的磁场暴露后,踝关节和足垫肿胀均有不同程度的减轻,急性模型暴露6h和慢性模型血清和关节液的细胞因子均无改变,急性模型暴露8h血清IL-6,关节浸液IL-6和TNF-α均比对照组降低,其余指标无变化,但是有下降的趋势。结论：极低频磁场对急性和慢性关节炎肿胀有抑制作用,每天暴露8h可以部分抑制细胞因子的产生,但其详细机制还有待于进一步研究。     

细胞离子在振荡电磁场作用下的受力模型分析

本文通过生物细胞模型,研究振荡电场、振荡磁场以及振荡磁场产生的感应电场对细胞离子的作用机理。模型分析结果表明,电场力和罗仑兹力对细胞膜两侧的自由离子将产生加速度,振荡离子将产生周期性电位移。该模型同时也解释了脉冲电磁场比同参教的连续场产生更多的生物效应,以及连续场在开始施加和切除时的效应最大。     

磁场的生物学效应及最新进展

伴随科技的发展,磁场与人类的关系越来越密切。然而目前人们对磁场如何影响机体结构和(或)功能还未达成共识,其中磁场在致癌或抑癌方面的作用受到人们的广泛关注。但是关于磁场对机体的作用的研究还处在比较初始的阶段,并且目前的研究结果仍然存在许多的不同与矛盾。由于研究人员对磁场强度、照磁量的确定方法不一,使实验结果的可比性下降。本文从目前电磁场,静磁场,以及磁场作用机制等方面就磁场与机体作用最新的研究结果进行综述,探讨磁场在癌症发生发展过程中的作用,寻找治疗癌症的新思路。     

Theoretical evaluation of cell membrane ion channel activation by applied magnetic fields

This letter re-examines a recently published calculation of the forces exerted on a membrane ion channel by a cation passing through in the presence of an externally applied magnetic field. We show here, in contradiction to the originally published calculation, that the forces generated due to the Lorentz force of the magnetic field on the cation are negligible compared with the forces required to activate an ion channel protein conformation change associated with the gating of the channel. Received: 11 August 1998 / Revised version: 25 October 1998 / Accepted: 11 November 1998     

Modulation of apoptotic signalling by carotenoids in cancer cells

There is a growing body of literature on the role of beta-carotene and other carotenoids in human chronic diseases, including cancer. While epidemiological evidence shows that a high dietary intake of fruits and vegetables rich in carotenoids is associated with a reduced risk for cancer, results from intervention trials indicate that supplemental beta-carotene enhances the risk of developing lung cancer incidence and mortality among smokers. A possible mechanism which can explain the dual role of carotenoids as both beneficial and harmful agents in cancer is that their excess or deficiency may bring about changes in molecular pathways involved in apoptotic signalling. Carotenoid ability in inhibiting or in enhancing apoptosis depends on several factors: carotenoid concentration, concerted action of multiple micronutrients, cell type, and redox status. This review summarizes the available evidence for a modulatory action of carotenoids on apoptosis and focuses on the main molecular pathways involved in this process.     

Epithelial Cell Adhesion Molecule Regulates Tumor Initiation and Tumorigenesis via Activating Reprogramming Factors and Epithelial-Mesenchymal Transition Gene Expression in Colon Cancer

Epithelial cell adhesion molecule (EpCAM) is highly expressed in epithelial-transformed neoplasia and tumor-initiated cells (TICs), but the role that EpCAM plays in the stemness properties of TICs is still unclear. Here we show that EpCAM and reprogramming factors (c-Myc, Oct4, Nanog, and Sox2) were concomitantly elevated in TICs, which were shown to have superior self-renewal, invasiveness, and tumor-initiating abilities. Elevation of EpCAM enhanced tumorsphere formation and tumor initiation. Knockdown of EpCAM inhibited the expressions of reprogramming factors and epithelial-mesenchymal transition genes, thereby suppressing tumor initiation, self-renewal, and invasiveness. In addition, EpCAM, especially intracellular domain of EpCAM (EpICD), bound to and activated the promoter of reprogramming factors. Treatment with the inhibitor of γ-secretase (DAPT) led to the blockage of the expressions of reprogramming factors and epithelial-mesenchymal transition genes, which was accompanied by the reduction of tumor self-renewal and invasion. Furthermore, the increased release of EpEX enhanced production of EpICD and regulated the expression of reprogramming factors. Together, these findings suggest that EpCAM plays an important role in regulating cancer-initiating abilities in TICs of colon cancer. This discovery can be used in the development of new strategies for cancer therapy.     

Stem-like Cancer Cells Are Inducible by Increasing Genomic Instability in Cancer Cells

The existence of cancer stem cells (CSCs) or stem-like cancer cells (SLCCs) is regarded as the cause of tumor formation and recurrence. However, the origin of such cells remains controversial with two competing hypotheses: CSCs are either transformed from tissue adult stem cells or dedifferentiated from transformed progenitor cells. Compelling evidence has determined the chromosomal aneuploidy to be one of the hallmarks of cancer cells, indicating genome instability plays an important role in tumorigenesis, for which CSCs are believed to be the initiator. To gain direct evidence that genomic instability is involved in the induction of SLCCs, we utilized multiple approaches to enhance genomic instability and monitored the percentage of SLCC in cultured cancer cells. Using side population (SP) cells as a marker for SLCC in human nasopharyngeal carcinoma (NPC) and CD133 for human neuroblastoma cells, we found that DNA damage inducers, UV and mitomycin C were capable of increasing SP cells in NPC CNE-2 and neuroblastoma SKN-SH cells. Likewise, either overexpression of a key regulator of cell cycle, Mad2, or knock down of Aurora B, an important kinase in mitosis, or Cdh1, a key E3 ligase in cell cycle, resulted in a significant increase of SP cells in CNE-2. More interestingly, enrichment of SP cells was observed in recurrent tumor tissues as compared with the primary tumor in the same NPC patients. Our study thus suggested that, beside transformation of tissue stem cells leading to CSC generation, genomic instability could be another potential mechanism resulting in SLCC formation, especially at tumor recurrence stage.     

Targeting the Unique Methylation Pattern of Androgen Receptor (AR) Promoter in Prostate Stem/Progenitor Cells with 5-Aza-2′-deoxycytidine (5-AZA) Leads to Suppressed Prostate Tumorigenesis

Androgen receptor (AR) expression surveys found that normal prostate/prostate cancer (PCa) stem/progenitor cells, but not embryonic or mesenchymal stem cells, expressed little AR with high methylation in the AR promoter. Mechanism dissection revealed that the differential methylation pattern in the AR promoter could be due to differential expression of methyltransferases and binding of methylation binding protein to the AR promoter region. The low expression of AR in normal prostate/PCa stem/progenitor cells was reversed after adding 5-aza-2′-deoxycytidine, a demethylating agent, which could then lead to decreased stemness and drive cells into a more differentiated status, suggesting that the methylation in the AR promoter of prostate stem/progenitor cells is critical not only in maintaining the stemness but also critical in protection of cells from differentiation. Furthermore, induced AR expression, via alteration of its methylation pattern, led to suppression of the self-renewal/proliferation of prostate stem/progenitor cells and PCa tumorigenesis in both in vitro assays and in vivo orthotopic xenografted mouse studies. Taken together, these data prove the unique methylation pattern of AR promoter in normal prostate/PCa stem/progenitor cells and the influence of AR on their renewal/proliferation and differentiation. Targeting PCa stem/progenitor cells with alteration of methylated AR promoter status might provide a new potential therapeutic approach to battle PCa because the PCa stem/progenitor cells have high tumorigenicity.     

脑部磁刺激场的理论模型

作为脑部磁刺激研究的一项基础工作,建立了刺激磁场中的球形头模型、对方形线圈在其内产生的时变磁场和感应电场进行了理论研究.导出(?).(?).(?)的解析表达式,分析了场的特性和刺激强度的分布规律.为进一步探索时变磁场对人脑的最佳刺激方式和作用机理提供了初步的理论基础.     

Identification and Isolation of Slow-Dividing Cells in Human Glioblastoma Using Carboxy Fluorescein Succinimidyl Ester (CFSE)

Tumor heterogeneity represents a fundamental feature supporting tumor robustness and presents a central obstacle to the development of therapeutic strategies¹. To overcome the issue of tumor heterogeneity, it is essential to develop assays and tools enabling phenotypic, (epi)genetic and functional identification and characterization of tumor subpopulations that drive specific disease pathologies and represent clinically relevant targets. It is now well established that tumors exhibit distinct sub-fractions of cells with different frequencies of cell division, and that the functional criteria of being slow cycling is positively associated with tumor formation ability in several cancers including those of the brain, breast, skin and pancreas as well as leukemia^2-8. The fluorescent dye carboxyfluorescein succinimidyl ester (CFSE) has been used for tracking the division frequency of cells in vitro and in vivo in blood-borne tumors and solid tumors such as glioblastoma^2,7,8. The cell-permeant non-fluorescent pro-drug of CFSE is converted by intracellular esterases into a fluorescent compound, which is retained within cells by covalently binding to proteins through reaction of its succinimidyl moiety with intracellular amine groups to form stable amide bonds⁹. The fluorescent dye is equally distributed between daughter cells upon divisions, leading to the halving of the fluorescence intensity with every cell division. This enables tracking of cell cycle frequency up to eight to ten rounds of division¹⁰. CFSE retention capacity was used with brain tumor cells to identify and isolate a slow cycling subpopulation (top 5% dye-retaining cells) demonstrated to be enriched in cancer stem cell activity². This protocol describes the technique of staining cells with CFSE and the isolation of individual populations within a culture of human glioblastoma (GBM)-derived cells possessing differing division rates using flow cytometry². The technique has served to identify and isolate a brain tumor slow-cycling population of cells by virtue of their ability to retain the CFSE labeling.