30 research outputs found
Conjectures on exact solution of three - dimensional (3D) simple orthorhombic Ising lattices
We report the conjectures on the three-dimensional (3D) Ising model on simple
orthorhombic lattices, together with the details of calculations for a putative
exact solution. Two conjectures, an additional rotation in the fourth curled-up
dimension and the weight factors on the eigenvectors, are proposed to serve as
a boundary condition to deal with the topologic problem of the 3D Ising model.
The partition function of the 3D simple orthorhombic Ising model is evaluated
by spinor analysis, by employing these conjectures. Based on the validity of
the conjectures, the critical temperature of the simple orthorhombic Ising
lattices could be determined by the relation of KK* = KK' + KK'' + K'K'' or
sinh 2K sinh 2(K' + K'' + K'K''/K) = 1. For a simple cubic Ising lattice, the
critical point is putatively determined to locate exactly at the golden ratio
xc = exp(-2Kc) = (sq(5) - 1)/2, as derived from K* = 3K or sinh 2K sinh 6K = 1.
If the conjectures would be true, the specific heat of the simple orthorhombic
Ising system would show a logarithmic singularity at the critical point of the
phase transition. The spontaneous magnetization and the spin correlation
functions of the simple orthorhombic Ising ferromagnet are derived explicitly.
The putative critical exponents derived explicitly for the simple orthorhombic
Ising lattices are alpha = 0, beta = 3/8, gamma = 5/4, delta = 13/3, eta = 1/8
and nu = 2/3, showing the universality behavior and satisfying the scaling
laws. The cooperative phenomena near the critical point are studied and the
results obtained based on the conjectures are compared with those of the
approximation methods and the experimental findings. The 3D to 2D crossover
phenomenon differs with the 2D to 1D crossover phenomenon and there is a
gradual crossover of the exponents from the 3D values to the 2D ones.Comment: 176 pages, 4 figure
Macrostructural Alterations of Subcortical Grey Matter in Psychogenic Erectile Dysfunction
Psychogenic erectile dysfunction (ED) has been defined as the persistent inability to attain and maintain an erection sufficient to permit sexual performance. It shows a high incidence and prevalence among men, with a significant impact on the quality of life. Few neuroimaging studies have investigated the cerebral basis of erectile dysfunctions observing the role played by prefrontal, cingulate, and parietal cortices during erotic stimulation. In spite of the well-known involvement of subcortical regions such as hypothalamus and caudate nucleus in male sexual response, and the key role of nucleus accumbens in pleasure and reward, poor attention was paid to their role in male sexual dysfunction. In this study, we determined the presence of grey matter (GM) atrophy patterns in subcortical structures such as amygdala, hippocampus, nucleus accumbens, caudate nucleus, putamen, pallidum, thalamus, and hypothalamus in patients with psychogenic ED and healthy men. After Rigiscan evaluation, urological, general medical, metabolic and hormonal, psychological and psychiatric assessment, 17 outpatients with psychogenic ED and 25 healthy controls were recruited for structural MRI session. Significant GM atrophy of nucleus accumbens was observed bilaterally in patients with respect to controls. Shape analysis showed that this atrophy was located in the left medial-anterior and posterior portion of accumbens. Left nucleus accumbens volumes in patients correlated with low erectile functioning as measured by IIEF-5 (International Index of Erectile Function). In addition, a GM atrophy of left hypothalamus was also observed. Our results suggest that atrophy of nucleus accumbens plays an important role in psychogenic erectile dysfunction. We believe that this change can influence the motivation-related component of sexual behavior. Our findings help to elucidate a neural basis of psychogenic erectile dysfunction
Pan-cancer analysis of whole genomes
Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe