A novel way to reduce thrombus build‐up in vena cava filters

Objectives and background : The build‐up of thromboses in vena cava filters after deployment presents serious problem to the patients. We proposed a novel way to overcome this problem in a belief that intentionally induced swirling flow can optimize blood flow patterns in Vena cava filters, enhance the stirring motion of flow, in turn accelerate the dissolution of blood clots captured in the filter and facilitate blood to flow pass through the filters. Methods : In this study, we experimentally compared the work efficiency of a vena cava filter under swirling flow condition with that of the same filter under normal flow condition. Results : The results show that when compared to the normal flow, the swirling flow indeed has a significantly beneficial effect on a VCF which can decrease its flow‐out time nearly 40% and reduce clot build‐up in the filter more than 50%. Conclusions : We therefore believe that the design of an ideal VCF should take how to create swirling flow in the filter into the consideration. © 2011 Wiley Periodicals, Inc.     

RKIP regulates CCL5 expression to inhibit breast cancer invasion and metastasis by controlling macrophage infiltration

Accumulating evidence suggests that presence of macrophages in the tumor microenvironment add to the invasive and tumor-promoting hallmarks of cancer cells by secreting angiogenic and growth factors. RKIP is a known metastasis suppressor and interferes with several steps of metastasis. However, the mechanistic underpinnings of its function as a broad metastasis suppressor remain poorly understood. Here, we establish a novel pathway for RKIP regulation of metastasis inhibition through the negative regulation of RANTES/CCL5 thereby limiting tumor macrophage infiltration and inhibition of angiogenesis. Using a combination of loss- and gain-of-function approaches, we show that RKIP hinders breast cancer cell invasion by inhibiting expression of the CC chemokine CCL5 in vitro. We also show that the expression levels of RKIP and CCL5 are inversely correlated among clinical human breast cancer samples. Using a mouse allograft breast cancer transplantation model, we highlight that ectopic expression of RKIP significantly decreases tumor vasculature, macrophage infiltration and lung metastases. Mechanistically, we demonstrate that the inhibition of the CCL5 expression is the cause of the observed effects resulting from RKIP expression. Taken together, our results underscore the significance of RKIP as important negative regulator of tumor microenvironment.     

Increased expression of glutamine transporter SNAT2/SLC38A2 promotes glutamine dependence and oxidative stress resistance,and is associated with worse prognosis in triple-negative breast cancer

Background Glutamine (Gln) is an abundant nutrient used by cancer cells. Breast cancers cells and particularly triple-receptor negative breast cancer (TNBC) are reported to be dependent on Gln to produce the energy required for survival and proliferation. Despite intense research on the role of the intracellular Gln pathway, few reports have focussed on Gln transporters in breast cancer and TNBC.Methods The role and localisation of the Gln transporter SLC38A2/SNAT2 in response to Gln deprivation or pharmacological stresses was examined in a panel of breast cancer cell lines. Subsequently, the effect of SLC38A2 knockdown in Gln-sensitive cell lines was analysed. The prognostic value of SLC38A2 in a cohort of breast cancer was determined by immunohistochemistry.Results SLC38A2 was identified as a strongly expressed amino acid transporter in six breast cancer cell lines. We confirmed an autophagic route of degradation for SLC38A2. SLC38A2 knockdown decreased Gln consumption, inhibited cell growth, induced autophagy and led to ROS production in a subgroup of Gln-sensitive cell lines. High expression of SLC38A2 protein was associated with poor breast cancer specific survival in a large cohort of patients (p = 0.004), particularly in TNBC (p = 0.02).Conclusions These results position SLC38A2 as a selective target for inhibiting growth of Gln-dependent breast cancer cell lines.Subject terms: Breast cancer, Cancer metabolism     

Growth‐promoting effects of low‐level butyl benzyl phthalate exposure on human neuroblastoma SH‐SY5Y cells

The purpose of present study was to investigate the impact of butyl benzyl phthalate (BBP) on SH‐SY5Y neuroblastoma cells in vitro. The cell counting kit‐8 was used to measure cell proliferation and flow cytometry was utilized to study cell cycle phases and apoptosis. Western blotting and quantitative real‐time polymerase chain reaction were used to detect levels of aromatase, estrogen receptors (ERs) and some apoptosis and cell cycle‐related genes. Results showed BBP‐stimulated SH‐SY5Y cells in a dose‐dependent manner and produced a reverted U‐shaped dose‐response curve. BBP at lower concentrations (0.01 and 0.1 μm ) significantly induced cell proliferation while inhibited cell growth at 300 μm . The promoting effect of estradiol could be entirely blocked by administration of ICI182 780, a pure antagonist of ERs, while the effect of BBP could be partly blocked. Additionally, we confirmed 0.1 μm BBP‐induced cell proliferation caused the arrest of cells in S phase and inhibited apoptosis, which might be partially explained by the decreased expression of p53, the increased expression of proliferating cell nuclear antigen, Bcl‐2 and cell cycle regulator cyclin‐D1, and the activation of aromatase. The addition of ICI182 780 had no effect on BBP‐induced ERβ mRNA expression, whereas ICI182 780 could effectively counteract the effect of estradiol. Moreover, pretreatment with ICI182 780 could block the induction of aromatase protein expression and activity by BBP, showing an involvement of ERs. Except for the ER pathway, these results showed there might be other pathways involved in promoting the effects of low‐level BBP on SH‐SY5Y cells, which require further investigation.     

Melatonin attenuates postmyocardial infarction injury via increasing Tom70 expression

Mitochondrial dysfunction leads to reactive oxygen species (ROS) overload, exacerbating injury in myocardial infarction (MI). As a receptor for translocases in the outer mitochondrial membrane (Tom) complex, Tom70 has an unknown function in MI, including melatonin‐induced protection against MI injury. We delivered specific small interfering RNAs against Tom70 or lentivirus vectors carrying Tom70a sequences into the left ventricles of mice or to cultured neonatal murine ventricular myocytes (NMVMs). At 48 h post‐transfection, the left anterior descending coronary arteries of mice were permanently ligated, while the NMVMs underwent continuous hypoxia. At 24 h after ischemia/hypoxia, oxidative stress was assessed by dihydroethidium and lucigenin‐enhanced luminescence, mitochondrial damage by transmission electron microscopy and ATP content, and cell apoptosis by terminal deoxynucleotidyl transferase dUTP nick‐end labeling and caspase‐3 assay. At 4 weeks after ischemia, cardiac function and fibrosis were evaluated in mice by echocardiography and Masson's trichrome staining, respectively. Ischemic/hypoxic insult reduced Tom70 expression in cardiomyocytes. Tom70 downregulation aggravated post‐MI injury, with increased mitochondrial fragmentation and ROS overload. In contrast, Tom70 upregulation alleviated post‐MI injury, with improved mitochondrial integrity and decreased ROS production. PGC‐1α/Tom70 expression in ischemic myocardium was increased with melatonin alone, but not when combined with luzindole. Melatonin attenuated post‐MI injury in control but not in Tom70‐deficient mice. N‐acetylcysteine (NAC) reversed the adverse effects of Tom70 deficiency in mitochondria and cardiomyocytes, but at a much higher concentration than melatonin. Our findings showed that Tom70 is essential for melatonin‐induced protection against post‐MI injury, by breaking the cycle of mitochondrial impairment and ROS generation.     

基于医院局域网的知识仓库平台的建立

目的在医院基础网络环境下建立基于Web的医院知识仓库模型,将成熟的商品文献数据库与医院知识仓库等多种不同数据信息集成、传输、存储与管理,为医院临床医疗科研提供信息服务。方法使用SQL Server 2000数据库服务,并结合Datatrans软件系统、CNKI的多媒体知识仓库建库管理系统(KD3.5)和多媒体知识网站管理系统(KW3.5)等工具软件支持,客户端采用IE V6.0或以上浏览器版本,通过Web访问数据库资源。结果利用医院信息系统的基础网络通信资源,有效拓展了医院信息服务功能。结论医院知识仓库平台的建立,促进了图书信息由被动服务向主动服务的转型,在单位时间内,服务对象所获取的信息量成倍增加。     

军医大学学员学习动机、学习态度的调查及对策研究

通过对军医大学本科学员进行问卷调查,以了解本科学员学习动机和学习态度,初步探索了影响学员学习动机和态度的因素,并提出相应的调控策略.为各级部门和学员自身认清教学与学习现状,提高学习目的性、积极性提供参考.本次调查发现,军医大学本科学员学习动机和学习态度总体上较好,但仍存在诸多令人担忧的方面.本研究对此提出了积极的调控对策,以期最大限度帮助学员端正学习态度,促进学员健康成长.