Fractal relationships and spatial distribution of ore body modelling

The nature of spatial distributions of geological variables such as ore grades is of primary concern when modelling ore bodies and mineral resources. The aim of any mineral resource evaluation process is to determine the location, extent, volume and average grade of that resource by a trade off between maximum confidence in the results and minimum sampling effort. The principal aim of almost every geostatistical modelling process is to predict the spatial variation of one or more geological variables in order to estimate values of those variables at locations that have not been sampled. From the spatial analysis of these variables, in conjunction with the physical geology of the region of interest, the location, extent and volume, or series of discrete volumes, whose average ore grade exceeds a specific ore grade cut off value determined\u27 by economic parameters can be determined, Of interest are not only the volume and average grade of the material but also the degree of uncertainty associated with each of these. Geostatistics currently provides many methods of assessing spatial variability. Fractal dimensions also give us a measure of spatial variability and have been found to model many natural phenomenon successfully (Mandelbrot 1983, Burrough 1981), but until now fractal modelling techniques have not been able to match the versatility and accuracy of geostatistical methods. Fractal ideas and use of the fractal dimension may in certain cases provide a better understanding of the way in which spatial variability manifests itself in geostatistical situations. This research will propose and investigate a new application of fractal simulation methods to spatial variability and spatial interpolation techniques as they relate to ore body modelling. The results show some advantages over existing techniques of geostatistical simulation

Electromagnetic Force in Dispersive and Transparent Media

A hydrodynamic-type, macroscopic theory was set up recently to simultaneously account for dissipation and dispersion of electromagnetic field, in nonstationary condensed systems of nonlinear constitutive relations~\cite{JL}. Since it was published in the letter format, some algebra and the more subtle reasonings had to be left out. Two of the missing parts are presented in this paper: How algebraically the new results reduce to the known old ones; and more thoughts on the range of validity of the new theory, especially concerning the treatment of dissipation.Comment: 10 pages, 0 figur

Relativistic ponderomotive force, uphill acceleration, and transition to chaos

Starting from a covariant cycle-averaged Lagrangian the relativistic oscillation center equation of motion of a point charge is deduced and analytical formulae for the ponderomotive force in a travelling wave of arbitrary strength are presented. It is further shown that the ponderomotive forces for transverse and longitudinal waves are different; in the latter, uphill acceleration can occur. In a standing wave there exists a threshold intensity above which, owing to transition to chaos, the secular motion can no longer be described by a regular ponderomotive force. PACS number(s): 52.20.Dq,05.45.+b,52.35.Mw,52.60.+hComment: 8 pages, RevTeX, 3 figures in PostScript, see also http://www.physik.th-darmstadt.de/tqe

Homologous recombination DNA repair defects in PALB2-associated breast cancers

© 2019, The Author(s). Mono-allelic germline pathogenic variants in the Partner And Localizer of BRCA2 (PALB2) gene predispose to a high-risk of breast cancer development, consistent with the role of PALB2 in homologous recombination (HR) DNA repair. Here, we sought to define the repertoire of somatic genetic alterations in PALB2-associated breast cancers (BCs), and whether PALB2-associated BCs display bi-allelic inactivation of PALB2 and/or genomic features of HR-deficiency (HRD). Twenty-four breast cancer patients with pathogenic PALB2 germline mutations were analyzed by whole-exome sequencing (WES, n = 16) or targeted capture massively parallel sequencing (410 cancer genes, n = 8). Somatic genetic alterations, loss of heterozygosity (LOH) of the PALB2 wild-type allele, large-scale state transitions (LSTs) and mutational signatures were defined. PALB2-associated BCs were found to be heterogeneous at the genetic level, with PIK3CA (29%), PALB2 (21%), TP53 (21%), and NOTCH3 (17%) being the genes most frequently affected by somatic mutations. Bi-allelic PALB2 inactivation was found in 16 of the 24 cases (67%), either through LOH (n = 11) or second somatic mutations (n = 5) of the wild-type allele. High LST scores were found in all 12 PALB2-associated BCs with bi-allelic PALB2 inactivation sequenced by WES, of which eight displayed the HRD-related mutational signature 3. In addition, bi-allelic inactivation of PALB2 was significantly associated with high LST scores. Our findings suggest that the identification of bi-allelic PALB2 inactivation in PALB2-associated BCs is required for the personalization of HR-directed therapies, such as platinum salts and/or PARP inhibitors, as the vast majority of PALB2-associated BCs without PALB2 bi-allelic inactivation lack genomic features of HRD

Homologous recombination DNA repair defects in PALB2- associated breast cancers

Abstract: Mono-allelic germline pathogenic variants in the Partner And Localizer of BRCA2 (PALB2) gene predispose to a high-risk of breast cancer development, consistent with the role of PALB2 in homologous recombination (HR) DNA repair. Here, we sought to define the repertoire of somatic genetic alterations in PALB2-associated breast cancers (BCs), and whether PALB2-associated BCs display bi-allelic inactivation of PALB2 and/or genomic features of HR-deficiency (HRD). Twenty-four breast cancer patients with pathogenic PALB2 germline mutations were analyzed by whole-exome sequencing (WES, n = 16) or targeted capture massively parallel sequencing (410 cancer genes, n = 8). Somatic genetic alterations, loss of heterozygosity (LOH) of the PALB2 wild-type allele, large-scale state transitions (LSTs) and mutational signatures were defined. PALB2-associated BCs were found to be heterogeneous at the genetic level, with PIK3CA (29%), PALB2 (21%), TP53 (21%), and NOTCH3 (17%) being the genes most frequently affected by somatic mutations. Bi-allelic PALB2 inactivation was found in 16 of the 24 cases (67%), either through LOH (n = 11) or second somatic mutations (n = 5) of the wild-type allele. High LST scores were found in all 12 PALB2-associated BCs with bi-allelic PALB2 inactivation sequenced by WES, of which eight displayed the HRD-related mutational signature 3. In addition, bi-allelic inactivation of PALB2 was significantly associated with high LST scores. Our findings suggest that the identification of bi-allelic PALB2 inactivation in PALB2-associated BCs is required for the personalization of HR-directed therapies, such as platinum salts and/or PARP inhibitors, as the vast majority of PALB2-associated BCs without PALB2 bi-allelic inactivation lack genomic features of HRD