Physics of ion beam cancer therapy: a multi-scale approach

We propose a multi-scale approach to understand the physics related to ion-beam cancer therapy. It allows the calculation of the probability of DNA damage as a result of irradiation of tissues with energetic ions, up to 430 MeV/u. This approach covers different scales, starting from the large scale, defined by the ion stopping, followed by a smaller scale, defined by secondary electrons and radicals, and ending with the shortest scale, defined by interactions of secondaries with the DNA. We present calculations of the probabilities of single and double strand breaks of DNA, suggest a way to further expand such calculations, and also make some estimates for glial cells exposed to radiation.Comment: 18 pag,5 fig, submitted to PR

Annual Report on Contract AEC AT(11-1) 34 p107B

Work that has been carried out in several areas of High Energy Physics is described. Visual techniques are used. For the study of the three-pion decay of the K/sup +/ meson, bubble chamber and emulsion methods are used to complement each other, particularly for the tau' mode. Several separate bubble chamber experiments in ..pi../sup +/p, anti pp and K/sup -/p interactions are also described, and the large effort devoted to computer reprogramming for the data analysis indicated. Two emulsion research projects are also described which have for their purpose the study of electromagnetic processes induced by 16 BeV electrons and the study of hypernuclei by K/sup -/ mesons. For the latter work high speed computer methods have been successfully applied to the analysis of the product hypernuclei. These programs of work have not been under way long enough for the main results yet to be available, but some preliminary data have been published and several reports on data analysis and related subjects have been prepared

Data for Elementary-Particle Physics

These data are provided: Masses and .Mean Lives of Elementary Particles; Atomic and Nuclear Properties of Materials; Particle Scattering; Atomic and Nuclear Constants; Particle Decay and Reaction Dynamics; Tentative Data on Strongly lnteracting Particles and Resonances; and Clebsch-Gordan Coefficients and Spherical Harmonics

Nonlinear energy-loss straggling of protons and antiprotons in an electron gas

The electronic energy-loss straggling of protons and antiprotons moving at arbitrary nonrelativistic velocities in a homogeneous electron gas are evaluated within a quadratic response theory and the random-phase approximation (RPA). These results show that at low and intermediate velocities quadratic corrections reduce significantly the energy-loss straggling of antiprotons, these corrections being, at low-velocities, more important than in the evaluation of the stopping power.Comment: 4 pages, 3 figures, to appear in Phys. Rev.

Single-cell transcriptomics uncovers distinct molecular signatures of stem cells in chronic myeloid leukemia

Recent advances in single-cell transcriptomics are ideally placed to unravel intratumoral heterogeneity and selective resistance of cancer stem cell (SC) subpopulations to molecularly targeted cancer therapies. However, current single-cell RNA-sequencing approaches lack the sensitivity required to reliably detect somatic mutations. We developed a method that combines high-sensitivity mutation detection with whole-transcriptome analysis of the same single cell. We applied this technique to analyze more than 2,000 SCs from patients with chronic myeloid leukemia (CML) throughout the disease course, revealing heterogeneity of CML-SCs, including the identification of a subgroup of CML-SCs with a distinct molecular signature that selectively persisted during prolonged therapy. Analysis of nonleukemic SCs from patients with CML also provided new insights into cell-extrinsic disruption of hematopoiesis in CML associated with clinical outcome. Furthermore, we used this single-cell approach to identify a blast-crisis-specific SC population, which was also present in a subclone of CML-SCs during the chronic phase in a patient who subsequently developed blast crisis. This approach, which might be broadly applied to any malignancy, illustrates how single-cell analysis can identify subpopulations of therapy-resistant SCs that are not apparent through cell-population analysis

The Antiproton-Nucleon Annihilation Process (AntiprotonCollaboration Experiment)

In the exposure to a 7 0 0-MeV/c negative particle beam, 35 antiproton stars have been found. Of these antiprotons, 21 annihilate in flight and three give large-angle scatters ( {Theta} > 15 , T{sub P-} > 50 Mev), while 14 annihilate at rest. From the interactions in flight we obtain the total c r o s s section for antiproton interactio

Antiproton stopping power in hydrogen below 120 keV and the Barkas effect

The simultaneous measurement of the spatial coordinates and times of p¯s annihilating at rest in a H2 target at very low density ρ (ρ/ρ0<10-2, ρ0 being the STP density) gives the possibility of evaluating the behavior of the p¯ stopping power in H2 at low energies (below 120 keV). It is different from that of protons (the Barkas effect). Moreover, it is shown that a rise at low-energy values (≲1 keV) is needed to agree with experimental data

Imprinted Gene Expression and Function of the Dopa Decarboxylase Gene in the Developing Heart

Dopa decarboxylase (DDC) synthesizes serotonin in the developing mouse heart where it is encoded by Ddc_exon1a, a tissue-specific paternally expressed imprinted gene. Ddc_exon1a shares an imprinting control region (ICR) with the imprinted, maternally expressed (outside of the central nervous system) Grb10 gene on mouse chromosome 11, but little else is known about the tissue-specific imprinted expression of Ddc_exon1a. Fluorescent immunostaining localizes DDC to the developing myocardium in the pre-natal mouse heart, in a region susceptible to abnormal development and implicated in congenital heart defects in human. Ddc_exon1a and Grb10 are not co-expressed in heart nor in brain where Grb10 is also paternally expressed, despite sharing an ICR, indicating they are mechanistically linked by their shared ICR but not by Grb10 gene expression. Evidence from a Ddc_exon1a gene knockout mouse model suggests that it mediates the growth of the developing myocardium and a thinning of the myocardium is observed in a small number of mutant mice examined, with changes in gene expression detected by microarray analysis. Comparative studies in the human developing heart reveal a paternal expression bias with polymorphic imprinting patterns between individual human hearts at DDC_EXON1a, a finding consistent with other imprinted genes in human