紫杉醇纳米递药系统研究进展

紫杉醇通过稳定微管而诱导细胞有丝分裂停止,为一疗效确切的抗癌药物,但其水溶性较差,有骨髓抑制、神经毒性和肌肉毒性等副作用。纳米载体作为一种新的药物运输工具,具有靶向性、缓释性及降低药物毒副作用方面等优点,对于紫杉醇的运输非常有效。综述近年来紫杉醇纳米运输的研究进展,为新药开发提供参考。     

苦马豆素国内外研究进展

苦马豆素作为疯草毒性的主要成分，文中阐述了其物理化学特性，来源，临床症状，致病机理。但随着科学家对它的研究，发现了其抑制肿瘤细胞生长与免疫调节的作用，并作为一种新型的抗癌药物，对其进行了分离纯化与合成。     

农药细胞毒性及其机理的研究现状

对农药毒性研究中常用的细胞模型进行了综述,结合细胞毒性的评价方法和细胞毒性的可能机理,提出了今后在对农药体外毒性研究中所需考虑的一些诸如模型选择、浓度选择、机理阐释等关键问题。     

紫杉醇提取及分离纯化技术研究进展

紫杉醇是从红豆杉属植物分离出来的一种具有独特抗癌机制的二萜类化合物,紫杉醇因其独特的抗癌机理及其显著疗效而倍受重视.目前紫杉醇主要来自于红豆杉属植物中,提取和分离纯化技术是从红豆杉属植物中获得紫杉醇必须的技术手段.在此较为全面地论述了近年来国内外紫杉醇的提取纯化技术.     

紫杉属树木培育技术及紫杉醇的开发利用问题

综合分析了紫杉属植物的生物生态学特性，繁殖培育技术，并对紫杉植物的化学成分，生理活性进行了研究；对紫杉醇的结构，抗癌作用机理及其人临床应用做了较详尽的论述，最后对紫杉醇药物的开发对策进行了探讨。     

水体铜对水生动物毒性的研究进展

介绍了水生动物对水体铜的吸收、富集和排放过程,以及水体铜对水生动物的毒性机理,如组织毒性,生长、发育、遗传毒性,血液生理生化毒性;并指出了国内关于水体铜毒性研究的不足之处。     

天然药物紫杉醇的研究与开发

阐述了天然抗癌新药紫衫醇的作用机理及生产途径,探讨了紫杉醇生产、应用研究存在的问题及发展前景。     

紫杉醇的提取与纯化技术探析

紫杉醇是从红豆杉科红豆杉属植物分离出来的一种具有独特抗肿瘤机理的二萜类化合物,目前仅能采自于红豆杉属植物中,提取和分离纯化技术是获得紫杉醇所必须的技术手段。紫杉醇的提取方法有液液萃取法、固相萃取法、超临界流体萃取法、柱切换技术、层析法。通常获得高纯度的的紫杉醇纯化处理方法有碱性氧化铝作柱层析、反相层析法、色谱法、细胞生物学法。     

多西他赛治疗乳腺癌30例毒副反应护理

多西他赛是紫杉醇类抗肿瘤药，通过加强微管蛋白聚合作用和抑制微管解聚作用，导致形成稳定的非功能性微管束，破坏肿瘤细胞的有丝分裂，诱导肿瘤细胞的凋亡。我院肿瘤科于2003年7月～2005年7月对30例乳腺癌患者应用多西他赛化疗，对出现的毒副反应采取针对性护理，取得了较好疗效，现将护理体会总结如下。     

氟对精子毒性作用的研究进展

氟是一种全身性毒物,除累及牙齿、骨骼外,还对非骨相的多种组织和器官有损害作用,氟对生殖系统的损伤作用已经引起了广泛的关注。从氟对动物精子及人类精子的毒性作用入手,探讨了氟对精子的毒性作用机理,以期人们能更深入地研究氟的生殖毒性机理。     

Study on the Antitumor Effects of Low—energy Laser Irradiation Combined with Cyclophosphamide

1　Introduction　　 Surgery,irradiation and chemical treatment are three main therapies in treating cancers,and thesethree treatments usually combined together to obtain better effects,but irradiation and chemical treatmentcan cause immunosuppressive effects.The relationship between tumor,body,irradiation and chemical treat-ment is very complicated.How to protect immunity of the body and kill tumor at the most has become akey problem in treating malignanttumor.It was proved that proper dosages…     

抗肿瘤DNA疫苗

抗肿瘤DNA疫苗是一种调解免疫功能的基因治疗苗,它包括含有免疫刺激序列的质粒载体,肿瘤特异性抗原和肿瘤相关抗原表位。DC细胞将同时以抗原表位与MHC-I类分子形成复合物和与MHC-II分子形成复合物途径加工,提呈。活化CD4+和CD8+T细胞,同时产生抗肿瘤免疫和治疗作用。     

鸡球虫的发育及侵入机理

对鸡球虫的发育过程、影响发育的因素和鸡球虫侵入机体细胞的机理进行了综述。着重介绍了球虫侵入的特异性 ,球虫的侵入过程和球虫孢子的移行     

CD40 agonists alter tumor stroma and show efficacy against pancreatic carcinoma in mice and humans

Immunosuppressive tumor microenvironments can restrain antitumor immunity, particularly in pancreatic ductal adenocarcinoma (PDA). Because CD40 activation can reverse immune suppression and drive antitumor T cell responses, we tested the combination of an agonist CD40 antibody with gemcitabine chemotherapy in a small cohort of patients with surgically incurable PDA and observed tumor regressions in some patients. We reproduced this treatment effect in a genetically engineered mouse model of PDA and found unexpectedly that tumor regression required macrophages but not T cells or gemcitabine. CD40-activated macrophages rapidly infiltrated tumors, became tumoricidal, and facilitated the depletion of tumor stroma. Thus, cancer immune surveillance does not necessarily depend on therapy-induced T cells; rather, our findings demonstrate a CD40-dependent mechanism for targeting tumor stroma in the treatment of cancer.     

姜黄素修饰的纳米金棒抑制胃癌细胞SGC-7901的作用

恶性肿瘤严重威胁着人类的健康。合成了姜黄素修饰的纳米金棒(Cur@Au NRs),并考察其对胃癌细胞(SGC-7901)的作用,采用MTT法测试其对5种肿瘤细胞株的体外增殖活性的影响,同时观察其对SGC-7901形态学的影响;利用实时x CELLigence细胞分析系统(RTCA)检测不同浓度Cur@Au NRs对SGC-7901增殖能力及迁移能力的影响;利用划痕愈合实验及血管形成实验检测Cur@Au NRs对细胞的迁移及血管形成的抑制作用;采用腹腔注射Cur@Au NRs后与正常小鼠内脏组织切片的对比,对其进行毒理学研究。研究结果表明,Cur@Au NRs具有良好的抗肿瘤活性,尤其对SGC-7901,且其IC50值明显低于姜黄素,并且能够抑制SGC-7901的增殖和迁移。毒理学研究表明即使在高剂量下也不具有明显的毒性。     

试验用和临床用紫杉醇诱导肝癌细胞凋亡的比较

[目的]为了探讨试验用和临床用紫杉醇对肝癌HepG2细胞凋亡诱导作用的差异。[方法]用不同浓度的试验用和临床用紫杉醇处理肝癌HepG2培养细胞后,通过显微观察和流式细胞术检测其细胞凋亡。[结果]临床用紫杉醇在终浓度为0.5、1.0和2.0 mg/ml时,24 h非常显著性诱导细胞凋亡,48 h诱导细胞凋亡更剧烈。试验用紫杉醇24 h在终浓度为2.5、5.0和10.0 mg/ml时,非常显著诱导细胞凋亡;当试验用紫杉醇浓度为2.5 mg/ml时,48 h诱导细胞凋亡更剧烈。当试验用紫杉醇浓度为5和10 mg/ml细胞凋亡率逐步变低,可能走向死亡。[结论]在诱导肝癌细胞凋亡中,试验用紫杉醇要比临床所用紫杉醇的浓度要高。     

Cancer immunotherapy: a treatment for the masses

Cancer immunotherapy attempts to harness the exquisite power and specificity of the immune system for the treatment of malignancy. Although cancer cells are less immunogenic than pathogens, the immune system is clearly capable of recognizing and eliminating tumor cells. However, tumors frequently interfere with the development and function of immune responses. Thus, the challenge for immunotherapy is to use advances in cellular and molecular immunology to develop strategies that effectively and safely augment antitumor responses.     

鬼针草90%醇提物对U14荷瘤小鼠的抑瘤效应

以U14细胞株接种小鼠制成荷瘤模型,研究鬼针草90%醇提物对荷瘤小鼠的抑瘤效应.结果表明,90%鬼针草醇提物通过提高机体免疫力抑制小鼠肿瘤生长.     

Treatment of established renal cancer by tumor cells engineered to secrete interleukin-4

The generation of antigen-specific antitumor immunity is the ultimate goal in cancer immunotherapy. When cells from a spontaneously arising murine renal cell tumor were engineered to secrete large doses of interleukin-4 (IL-4) locally, they were rejected in a predominantly T cell-independent manner. However, animals that rejected the IL-4-transfected tumors developed T cell-dependent systemic immunity to the parental tumor. This systemic immunity was tumor-specific and primarily mediated by CD8+ T cells. Established parental tumors could be cured by the systemic immune response generated by injection of the genetically engineered tumors. These results provide a rationale for the use of lymphokine gene-transfected tumor cells as a modality for cancer therapy.     

In vivo administration of anti-CD3 prevents malignant progressor tumor growth

Malignant progressor tumors are only weakly immunogenic and can evade host recognition and rejection. One approach to therapy involves activation of the host antitumor cellular effector mechanisms. Since monoclonal antibodies to CD3 (anti-CD3) can activate T cells in vitro, an attempt was made to determine if tumor immunity could be achieved by the administration of anti-CD3 in vivo. T lymphocytes from mice injected with anti-CD3 showed increased interleukin-2 receptor (IL-2R) expression, increased proliferation to recombinant IL-2 (rIL-2), and enhanced reactivity in both an allogeneic mixed lymphocyte reaction and a mixed lymphocyte tumor culture. Malignant tumor growth in treated mice was also examined. The anti-CD3 treatment prevented tumor outgrowth that would have killed untreated animals and also stimulated an in vivo response against a malignant progressor tumor providing lasting tumor immunity.