Mechanical oscillations of magnetic strips under the influence of external field

This is the final version of the article. Available from EDP Sciences via the DOI in this record.JEMS 2012 – Joint European Magnetic SymposiaBy application of a magnetic field on an amorphous metallic strip, the orientation of magnetization of Weiss domains can be changed. When the strip changes its length, this effect is called magnetostriction. We simulate this effect using a finite element method. In particular we calculate the change of the mechanical resonance frequency of a magnetic platelet as a function of the applied field. This gives a quantitative model of the influence of the applied magnetic field on the effective Young's Modulus of the material. © 2013 Owned by the authors, published by EDP Sciences

Macrophage-Related Interaction Pathways in Tumor Stroma

Cancer is a leading cause of death in developed countries. Within the adult population, epithelial cancers are—with 83%—the most frequent cancer types (1). The deadliest cancers are in men those of lung, colon and prostate, and in women, those of breast, colon and lung (2). Based on observations in the early twentieth century that some cancers are familial, scientists began to search for genetic changes that might underlie cancer development. Dominant gain-of-function and recessive loss-of-function alterations in critical gatekeeper genes, e.g., oncogenes and tumor-suppressor genes, have been identified and characterized during the last decades. Tumorigenesis is now recognized as a multistep process during which cancer cells accumulate multiple and sequential genetic alterations affecting intrinsic cellular programs, such as cell proliferation, cell death, differentiation, metabolism, and cell adhesion (3, 4). During the last two decades it has been increasingly recognized that the surrounding tissue, or so-called tumor stroma, plays an important part in neoplastic growth (5, 6). Thus, tumors are regarded as complex organs consisting of two distinct but interdependent compartments: the tumor epithelial cells themselves and the stroma in which they disperse. During the neoplastic process somatic genetic alterations occur in both, tumor cells and stromal cells—also referred to as tumor stroma co-evolution (7). Stromal cells are a heterogeneous mixture of different cell lineages. It is believed, that tumorigenesis cannot proceed without active cooperation from the stroma. This cooperation influences tumor establishment, progression and dissemination (5). When viewed from this perspective, the biology of a tumor can only be understood by studying the cancer cells themselves as well as the ‘‘tumor microenvironment’’ that they construct during the multistep tumorigenesis

YangZheng XiaoJi exerts anti-tumour growth effects by antagonising the effects of HGF and its receptor, cMET, in human lung cancer cells

BACKGROUND: Hepatocyte growth factor (HGF) is a cytokine that has a profound effect on cancer cells by stimulating migration and invasion and acting as an angiogenic factor. In lung cancer, the factor also plays a pivotal role and is linked to a poor outcome in patients. In particular, HGF is known to work in combination with EGF on lung cancer cells. In the present study, we investigated the effect of a traditional Chinese medicine reported in cancer therapies, namely YangZheng XiaoJi (YZXJ) on lung cancer and on HGF mediated migration and invasion of lung cancer cells. METHODS: Human lung cancer cells, SKMES1 and A549 were used in the study. An extract from the medicine was used. Cell migration was investigated using the EVOS and by ECIS. Cell–matrix adhesion and in vitro invasion were assessed. In vivo growth of lung cancer was tested using an in vivo xenograft tumour model and activation of the HGF receptor in lung tumours by an immunofluorescence method. RESULTS: Both lung cancer cells increased their migration in response to HGF and responded to YZXJ by reducing their speed of migration. YZXJ markedly reduced the migration and in vitro invasiveness induced by HGF. It worked synergistically with PHA665752 and SU11274, HGF receptor inhibitors on the lung cancer cells both on HGF receptor activation and on cell functions. A combination of HGF and EGF resulted in a greater increase in cell migration, which was similarly inhibited by YZXJ, and in combination with the HGF receptor and EGF receptor inhibitors. In vivo, YZXJ reduced the rate of tumour growth and potentiated the effects of PHA665752 on tumour growth. It was further revealed that YZXJ significantly reduced the degree of phosphorylation of the HGF receptor in lung tumours. CONCLUSION: YZXJ has a significant role in reducing the migration, invasion and in vivo tumour growth of lung cancer and acts to inhibit the migratory and invasive effects induced by HGF and indeed by HGF/EGF. This effect is likely attributed to the inhibition of the HGF receptor activation. These results indicate that YZXJ has a therapeutic role in lung cancer and that combined strategy with methods to block HGF and EGF should be considered. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12967-015-0639-1) contains supplementary material, which is available to authorized users

HGF induces novel EGFR functions involved in resistance formation to tyrosine kinase inhibitors

The epidermal growth factor receptor (EGFR) is overexpressed and activated in many human cancers and predicts poor patient prognosis. Targeting the kinase domain with specific EGFR tyrosine kinase inhibitors (TKIs) like gefitinib and erlotinib has been used in anticancer treatments. However, patient response rates in different human cancers were initially low. Only a subgroup of nonsmall- cell lung cancer (NSCLC) patients harboring EGFR-activating mutations responds to EGFR TKI treatment, but most of these responders relapse and acquire resistance. Recent clinical studies have demonstrated that MET proto-oncogene overexpression correlates with resistance to EGFR TKI treatment. Similarly to MET overexpression, the tumor microenvironment-derived ligand hepatocyte growth factor (HGF) was shown to activate Met and thereby induce short-term resistance to EGFR TKI treatment in gefitinib-sensitive NSCLC cell lines in vitro. However, only little is known about the HGF/Met-induced EGFR TKI resistance mechanism in other human cancer types. Therefore, in order to develop possible new anticancer strategies for diverse human cancers, we screened 12 carcinoma cell lines originating from the breast, kidney, liver and tongue for HGF-induced EGFR tyrosine kinase (TK)-inhibition. In addition, in order to advance our understanding of a TK-inactive EGFR, we used EGFR co-immunoprecipitation, followed by mass spectrometry to identify novel HGF-induced EGFR binding partners, which are potentially involved in tyrosine kinase-independent EGFR signaling mechanisms. Here we show for the first time that HGF-induced EGFR TK-inhibition is a very common mechanism in human cancers, and that the kinase-inactive EGFR directly interacts with and stabilizes several cancer-relevant proteins, including the receptor tyrosine kinases Axl and EphA2, and the CUB domain-containing protein-1. This study has strong implications for the development of new anticancer strategie

Fast stray field computation on tensor grids

AbstractA direct integration algorithm is described to compute the magnetostatic field and energy for given magnetization distributions on not necessarily uniform tensor grids. We use an analytically-based tensor approximation approach for function-related tensors, which reduces calculations to multilinear algebra operations. The algorithm scales with N4/3 for N computational cells used and with N2/3 (sublinear) when magnetization is given in canonical tensor format. In the final section we confirm our theoretical results concerning computing times and accuracy by means of numerical examples