@article{TranGiaWechBleyetal.2015, author = {Tran-Gia, Johannes and Wech, Tobias and Bley, Thorsten and K{\"o}stler, Herbert}, title = {Model-Based Acceleration of Look-Locker T1 Mapping}, series = {PLoS One}, volume = {10}, journal = {PLoS One}, number = {4}, doi = {10.1371/journal.pone.0122611}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-126436}, pages = {e0122611}, year = {2015}, abstract = {Mapping the longitudinal relaxation time \(T_1\) has widespread applications in clinical MRI as it promises a quantitative comparison of tissue properties across subjects and scanners. Due to the long scan times of conventional methods, however, the use of quantitative MRI in clinical routine is still very limited. In this work, an acceleration of Inversion-Recovery Look-Locker (IR-LL) \(T_1\) mapping is presented. A model-based algorithm is used to iteratively enforce an exponential relaxation model to a highly undersampled radially acquired IR-LL dataset obtained after the application of a single global inversion pulse. Using the proposed technique, a \(T_1\) map of a single slice with 1.6mm in-plane resolution and 4mm slice thickness can be reconstructed from data acquired in only 6s. A time-consuming segmented IR experiment was used as gold standard for \(T_1\) mapping in this work. In the subsequent validation study, the model-based reconstruction of a single-inversion IR-LL dataset exhibited a \(T_1\) difference of less than 2.6\% compared to the segmented IR-LL reference in a phantom consisting of vials with \(T_1\) values between 200ms and 3000ms. In vivo, the \(T_1\) difference was smaller than 5.5\% in WM and GM of seven healthy volunteers. Additionally, the \(T_1\) values are comparable to standard literature values. Despite the high acceleration, all model-based reconstructions were of a visual quality comparable to fully sampled references. Finally, the reproducibility of the \(T_1\) mapping method was demonstrated in repeated acquisitions. In conclusion, the presented approach represents a promising way for fast and accurate \(T_1\) mapping using radial IR-LL acquisitions without the need of any segmentation.}, language = {en} } @article{LapaLinsenmannLueckerathetal.2015, author = {Lapa, Constantin and Linsenmann, Thomas and L{\"u}ckerath, Katharina and Samnick, Samuel and Herrmann, Ken and Stoffer, Carolin and Ernestus, Ralf-Ingo and Buck, Andreas K. and L{\"o}hr, Mario and Monoranu, Camelia-Maria}, title = {Tumor-Associated Macrophages in Glioblastoma Multiforme—A Suitable Target for Somatostatin Receptor-Based Imaging and Therapy?}, series = {PLoS One}, volume = {10}, journal = {PLoS One}, number = {3}, doi = {10.1371/journal.pone.0122269}, url = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125498}, pages = {e0122269}, year = {2015}, abstract = {Background Glioblastoma multiforme (GBM) is the most common primary brain tumor in adults. Tumor-associated macrophages (TAM) have been shown to promote malignant growth and to correlate with poor prognosis. [1,4,7,10-tetraazacyclododecane-NN′,N″,N′″-tetraacetic acid]-d-Phe1,Tyr3-octreotate (DOTATATE) labeled with Gallium-68 selectively binds to somatostatin receptor 2A (SSTR2A) which is specifically expressed and up-regulated in activated macrophages. On the other hand, the role of SSTR2A expression on the cell surface of glioma cells has not been fully elucidated yet. The aim of this study was to non-invasively assess SSTR2A expression of both glioma cells as well as macrophages in GBM. Methods 15 samples of patient-derived GBM were stained immunohistochemically for macrophage infiltration (CD68), proliferative activity (Ki67) as well as expression of SSTR2A. Anti-CD45 staining was performed to distinguish between resident microglia and tumor-infiltrating macrophages. In a subcohort, positron emission tomography (PET) imaging using \(^{68}Ga-DOTATATE\) was performed and the semiquantitatively evaluated tracer uptake was compared to the results of immunohistochemistry. Results The amount of microglia/macrophages ranged from <10\% to >50\% in the tumor samples with the vast majority being resident microglial cells. A strong SSTR2A immunostaining was observed in endothelial cells of proliferating vessels, in neurons and neuropile. Only faint immunostaining was identified on isolated microglial and tumor cells. Somatostatin receptor imaging revealed areas of increased tracer accumulation in every patient. However, retention of the tracer did not correlate with immunohistochemical staining patterns. Conclusion SSTR2A seems not to be overexpressed in GBM samples tested, neither on the cell surface of resident microglia or infiltrating macrophages, nor on the surface of tumor cells. These data suggest that somatostatin receptor directed imaging and treatment strategies are less promising in GBM.}, language = {en} }