The Role of Somatostatin Receptor Scintigraphy on the Diagnosis of Desmoid Tumors

Background. Magnetic resonance imaging is considered as imaging modality of choice in diagnosis of desmoid tumors, though even this technique can lack the ability to distinguish aggressive fibromatosis from other benign or malignant soft tissue tumors. The aim of this study was to investigate if desmoid tumors would show an adequate tracer uptake in somatostatin receptor scintigraphy and moreover to correlate these results with immunohistochemical staining. Patients and Methods. Thirteen patients with desmoid tumors were examined with somatostatin receptor scintigraphy. Additionally, seven of these patients have been tested for the immunohistochemical expression of somatostatin receptor subtype 2A. The results of somatostatin receptor scintigraphy and the results of immunohistochemical staining (somatostatin receptor subtype 2A) were evaluated and correlated. Results. Somatostatin receptor scintigraphy revealed that eight of 13 affected patients (62%) showed an enhanced tracer uptake. On the other hand, the correlation between the results of somatostatin receptor scintigraphy and immunohistochemical investigations was poor (two out of seven cases). Conclusion. The current study demonstrated that desmoid tumors frequently express somatostatin receptor subtype 2, while immunohistochemical investigations did not correlate with these findings. This may likely be due to lack of standardization of this technique and also due to heterogeneous receptor distribution within the tumors

Entrained flow gasification. Part 3: Insight into the injector near-field by Large Eddy Simulation with detailed chemistry

Entrained flow gasification is a promising process for the conversion of low-grade feedstock, e.g. highly viscous slurries and suspensions with a significant content of solid particles, to high quality fuels. A major scientific challenge is the prediction of the physical and chemical phenomena occurring in such high-temperature and high-pressure multiphase flow systems. In this context, this article is the sequel to “Entrained flow gasification. Part 1: Gasification of glycol in an atmospheric-pressure experimental rig” and “Entrained flow gasification. Part 2: Mathematical modeling of the gasifier using RANS method”. The same strategy as in the first two parts was followed. In order to reduce complexity, this study focused on a two-phase (gas and liquid) flow system with a model fuel (mono-ethylene glycol) under the simplified conditions provided by the atmospheric lab-scale gasifier REGA. Using the experimental data set provided in Part 1 of the coordinated papers for validation purposes, the main focus of this study was on the detailed understanding of the near injector region of the entrained flow gasifier REGA. The unsteady flow and the chemical conversion in the gasifier were investigated by means of Large Eddy Simulations with a detailed chemistry solver including 44 individual species and a direct calculation of 329 chemical reactions. The dispersed phase was solved by Lagrangian Particle Tracking. Downstream comparisons with experimental data showed a reasonable agreement concerning temperature and species profiles. The analysis of the injector near-field revealed that the high temperature reaction zone close to the injector could not be explained by a direct reaction of the fuel with the oxidizer. Instead, carbon monoxide and hydrogen mainly formed on the axis were transported upstream by the recirculation zone. The reaction of CO and H2 with the oxygen stabilized the flame. The heat release from this reactions supported the vaporization and decomposition of fuel as well as the downstream gasification reactions

Anti-CD3 antibody treatment reduces scar formation in a rat model of myocardial infarction

Introduction: Antibody treatment with anti-thymocyte globulin (ATG) has been shown to be cardioprotective. We aimed to evaluate which single anti-T-cell epitope antibody alters chemokine expression at a level similar to ATG and identified CD3, which is a T-cell co-receptor mediating T-cell activation. Based on these results, the effects of anti-CD3 antibody treatment on angiogenesis and cardioprotection were tested in vitro and in vivo. Methods: Concentrations of IL-8 and MCP-1 in supernatants of human peripheral blood mononuclear cell (PBMC) cultures following distinct antibody treatments were evaluated by Enzyme-linked Immunosorbent Assay (ELISA). In vivo, anti-CD3 antibodies or vehicle were injected intravenously in rats subjected to acute myocardial infarction (AMI). Chemotaxis and angiogenesis were evaluated using tube and migration assays. Intracellular pathways were assessed using Western blot. Extracellular vesicles (EVs) were quantitatively evaluated using fluorescence-activated cell scanning, exoELISA, and nanoparticle tracking analysis. Also, microRNA profiles were determined by next-generation sequencing. Results: Only PBMC stimulation with anti-CD3 antibody led to IL-8 and MCP-1 changes in secretion, similar to ATG. In a rat model of AMI, systemic treatment with an anti-CD3 antibody markedly reduced infarct scar size (27.8% (Inter-quartile range; IQR 16.2–34.9) vs. 12.6% (IQR 8.3–27.2); p < 0.01). The secretomes of anti-CD3 treated PBMC neither induced cardioprotective pathways in cardiomyocytes nor pro-angiogenic mechanisms in human umbilical vein endothelial cell (HUVECs) in vitro. While EVs quantities remained unchanged, PBMC incubation with an anti-CD3 antibody led to alterations in EVs miRNA expression. Conclusion: Treatment with an anti-CD3 antibody led to decreased scar size in a rat model of AMI. Whereas cardioprotective and pro-angiogenetic pathways were unaltered by anti-CD3 treatment, qualitative changes in the EVs miRNA expression could be observed, which might be causal for the observed cardioprotective phenotype. We provide evidence that EVs are a potential cardioprotective treatment target. Our findings will also provide the basis for a more detailed analysis of putatively relevant miRNA candidates

Aging restricts the ability of mesenchymal stem cells to promote the generation of oligodendrocytes during remyelination.

Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) that leads to severe neurological deficits. Due to their immunomodulatory and neuroprotective activities and their ability to promote the generation of oligodendrocytes, mesenchymal stem cells (MSCs) are currently being developed for autologous cell therapy in MS. As aging reduces the regenerative capacity of all tissues, it is of relevance to investigate whether MSCs retain their pro-oligodendrogenic activity with increasing age. We demonstrate that MSCs derived from aged rats have a reduced capacity to induce oligodendrocyte differentiation of adult CNS stem/progenitor cells. Aging also abolished the ability of MSCs to enhance the generation of myelin-like sheaths in demyelinated cerebellar slice cultures. Finally, in a rat model for CNS demyelination, aging suppressed the capability of systemically transplanted MSCs to boost oligodendrocyte progenitor cell (OPC) differentiation during remyelination. Thus, aging restricts the ability of MSCs to support the generation of oligodendrocytes and consequently inhibits their capacity to enhance the generation of myelin-like sheaths. These findings may impact on the design of therapies using autologous MSCs in older MS patients.The authors would like to thank the following funding agencies for their support: Paracelsus Medical University PMU-FFF Long-Term Fellowship L-12/01/001-RIV (to and Stand-Alone Grant E-12/15/077-RIT (both to F.J.R.); Chilean Comisión Nacional de Investigación Científica y Tecnológica (CONICYT) FONDECYT Program Regular Grant Nº 1161787 (to F.J.R.), Regular Grant Nº 1141015 (to L.F.B.); Chilean CONICYT PCI Program Grant Nº REDES170233 (to F.J.R.), Grant Nº REDES180139 and Grant Nº REDI170037; Chilean CONICYT FONDEFIDeA Program Grant Nº ID17AM0043 (to M.E.S. and F.J.R.); European Union's Seventh Framework Programme (FP7/2007-2013) under grant agreements N HEALTH-F2-2011-278850 (INMiND) and HEALTH-F2-2011-279288 (IDEA). The work in the Küry laboratory was supported by the German Research Foundation (DFG; KU1934/2_1, KU1934/5-1) and the Christiane and Claudia Hempel Foundation for clinical and iBrain. The work in the Franklin laboratory was supported by grants from the UK Multiple Sclerosis Society and the Adelson Medical Research Foundation, and a core support grant from the Wellcome Trust and MRC to the Wellcome-MRC Cambridge Stem Cell Institute. In addition, the present work was supported by the state of Salzburg (to L.A.). We thank Armin Schneider, Sygnis Pharma AG Heidelberg, Germany, for the MBP promoter construct. We disclose any conflict of interest