Mechanical Structure Design of a 14T Body-Size MRI Magnet

New Radiation Oncology Optimization Principles Based On In-Vivo Predictive Assay and Recent Developments in Molecular Radiation Biology

“…The most recent RHR paper also investigated LDHS and LDA for light ions, demonstrating that it generally peaks for low-LET ions (≈20 eV/nm, [2]: Figure 3), where for reasons related to ion interaction physics, the highest low-energy δ-electron production per unit dose occurs, as the LET is low but sufficient to induce apoptosis, and the ion fluence per unit dose is highest. Thus, apoptosis peaked here (31% measured at 3 Gy of 40 eV/nm B5 + ions ( [1]: Figures 7,11,12,13)), and a clear but small LDHS was observed ([3]: Figure 16, [40]), mainly due to the early dual NHEJ only and HR misrepair (5% at 0.5 Gy, estimated ([1]: Figures 7, 8 and 9b)). The 31% value was not just LDA but mainly serine-46-induced HDA since at high LET, the LDA and HDA regions almost overlap to make an almost straight exponential survival curve (HDA sets in after ≈2+ GyE or 0.7 Gy high LET, as shown in Figure 4).…”

“…Figure 3a [9,10]), developed in collaboration between French and German scientists mainly for brain studies with ≈1 mm resolution (http://phys.org/news/2013-10-world-powerful-mri-online.html [10] and a 14 Tesla system is being developed in China [11]). It should be possible to reduce the aperture somewhat from the present 900 mm of the INUMAC unit and use the latest type of high field strength tolerating windings to get into the 15 to 20 Tesla region with sub mm spectral resolution (cf lower middle insert in Figure 3a and [11]). To further improve the spectral resolution and reconstruction speed, the scanner should use the Fast Padè transform rather than the Fourier transform [4,12].…”

“…This figure illustrates how the TP53 gene works as a complex cellular mastermind and controller by determining how the structure of DNA damage should best be repaired and whether senescence and apoptosis are needed, [1][2][3][30][31][32]. DNA damage by ionizing radiation can induce augmented phosphorylation of three Serine sites (nr 15,20,46) cf [11]) on TP53, following the increase in the extent of damage through some of its key upstream proteins, such as ATM, CHK2, and p38K as well as 53BP1 or BRCA1,2 to signal whether the currently best repair process is going to be NHEJ or HR. Most experimental tumor cell lines suffer from a mutant TP53 gene, making the early/low dose (0.5-1.5 Gy) radiation response more gradual without low-dose LDA and thus no LDHS.…”

“…The linear alignment of the DSB´s on the ion track, and the high density of the DNA damage close to the ion tracks (cf. [3]: Figures 1-5, [23]: Figures 5,[11][12][13] increases the Relative Biological Effectiveness (RBE) in the gross tumor, due to increased probability of severe damage when the cell density is high. However, this is a major disadvantage towards the end of the treatment when the remaining dose is low and very few tumor clonogens are left.…”