Carburisation of sintered iron compacts in CH_4+ cracked NH_3 atmospheres

26.00; Translated from Czech. (Kovove Mater. 1990 v. 28(1) p. 37-46)SIGLEAvailable from British Library Document Supply Centre- DSC:9023.19(VR-Trans--4644)T / BLDSC - British Library Document Supply CentreGBUnited Kingdo

Human mesenchymal stem cell-derived iron oxide exosomes allow targeted ablation of tumor cells via magnetic hyperthermia

U Altanerova,1 M Babincova,2 P Babinec,2 K Benejova,1 J Jakubechova,1 V Altanerova,1 M Zduriencikova,3 V Repiska,4 C Altaner1,3 1Stem Cell Preparation Department, St Elisabeth Cancer Institute, Bratislava, Slovakia; 2Department of Nuclear Physics and Biophysics, Comenius University, Bratislava, Slovakia; 3Cancer Research Institute, Biomedical Center, Slovak Academy of Sciences, Bratislava, Slovakia; 4Institute of Medical Biology, Genetics and Clinical Genetics, Faculty of Medicine, Comenius University in Bratislava, Slovakia Abstract: Magnetic hyperthermia, or the heating of tissues using magnetic materials, is a promising approach for treating cancer. We found that human mesenchymal stem cells (MSCs) isolated from various tissues and MSCs expressing the yeast cytosine deaminase::uracil phosphoribosyl transferase suicide fusion gene (yCD::UPRT) can be labeled with Venofer, an iron oxide carbohydrate nanoparticle. Venofer labeling did not affect cell proliferation or the ability to home to tumors. All Venofer-labeled MSCs released exosomes that contained iron oxide. Furthermore, these exosomes were efficiently endocytosed by tumor cells. Exosomes from Venofer-labeled MSCs expressing the yCD::UPRT gene in the presence of the prodrug 5-fluorocytosine inhibited tumor growth in a dose-dependent fashion. The treated tumor cells were also effectively ablated following induction of hyperthermia using an external alternating magnetic field. Cumulatively, we found that magnetic nanoparticles packaged into MSC exosomes are efficiently endocytosed by tumor cells, facilitating targeted tumor cell ablation via magnetically induced hyperthermia. Keywords: mesenchymal stem cells, iron oxide labeling, Venofer, yCD::UPRT-exosomes, yCD::UPRT-MSCs/Fe exosomes, magnetic hyperthermi

Identification of 13 novel NLRP7 mutations in 20 families with recurrent hydatidiform mole; missense mutations cluster in the leucine-rich region

Background: NLRP7 (NALP7) has recently been identified as the causative gene for familial recurrent hydatidiform mole (FRHM), a rare autosomal recessive condition in which affected women have recurrent molar pregnancies of diploid biparental origin. To date only a small number of affected families have been described. Our objectives were to investigate the diversity of mutations and their localisation to one or both isoforms of NLRP7, by screening a large series of women with FRHM and to examine the normal expression of NLRP7 in ovarian tissue.Methods: Fluorescent microsatellite genotyping of molar tissue was used to establish a diagnosis of FRHM. Twenty families were subsequently screened for mutations in NLRP7 using DNA sequencing. Expression of NLRP7 in the ovary was examined by immunohistochemical staining.Results: 16 different mutations were identified in the study, 13 of which were novel. Missense mutations were found to be present in transcript variant 2 of NLRP7 and cluster in the leucine-rich region (LRR). A man with two affected sisters and homozygous for the p.R693P mutation had normal reproductive outcomes. In the normal human ovary, NLRP7 expression is confined to the oocytes and present at all stages from primordial to tertiary follicles.Conclusion: 13 novel mutations in NLRP7 were identified. We confirm that mutations in NLRP7 affect female but not male reproduction, and provide evidence that transcript variant 2 of NLRP7 is the important isoform in this condition. The mutation clustering seen confirms that the LRR is critical for normal functioning of NLRP7