University of Houston

Abstract: How people intentionally change addictive behaviors with and without treatment is not well understood by behavioral scientists. This article summarizes research on self-initiated and professionally facilitated change of addictive behaviors using the key transtheoretical constructs of stages and processes of change. Modification of addictive behaviors involves progression through five stages—precontemplation, contemplation, preparation, action, and maintenance—and individuals typically recycle through these stages several times before termination of the addiction. Multiple studies provide strong support for these stages as well as for a finite and common set of change processes used to progress through the stages. Research to date supports a transtheoretical model of change that systematically integrates the stages with processes of change from diverse theories of psychotherapy.

Abstract: To characterize somatic alterations in colorectal carcinoma, we conducted a genome-scale analysis of 276 samples, analysing exome sequence, DNA copy number, promoter methylation and messenger RNA and microRNA expression. A subset of these samples (97) underwent low-depth-of-coverage whole-genome sequencing. In total, 16% of colorectal carcinomas were found to be hypermutated: three-quarters of these had the expected high microsatellite instability, usually with hypermethylation and MLH1 silencing, and one-quarter had somatic mismatch-repair gene and polymerase e (POLE) mutations. Excluding the hypermutated cancers, colon and rectum cancers were found to have considerably similar patterns of genomic alteration. Twenty-four genes were significantly mutated, and in addition to the expected APC, TP53, SMAD4, PIK3CA and KRAS mutations, we found frequent mutations in ARID1A, SOX9 and FAM123B. Recurrent copy-number alterations include potentially drug-targetable amplifications of ERBB2 and newly discovered amplification of IGF2. Recurrent chromosomal translocations include the fusion of NAV2 and WNT pathway member TCF7L1. Integrative analyses suggest new markers for aggressive colorectal carcinoma and an important role for MYC-directed transcriptional activation and repression.

Abstract: A stable and reproducible superconductivity transition between 80 and 93 K has been unambiguously observed both resistively and magnetically in a new Y-Ba-Cu-O compound system at ambient pressure. An estimated upper critical field H c2(0) between 80 and 180 T was obtained.

Abstract: Considerable confusion surrounds the longstanding question of what constitutes a vortex, especially in a turbulent flow. This question, frequently misunderstood as academic, has recently acquired particular significance since coherent structures (CS) in turbulent flows are now commonly regarded as vortices. An objective definition of a vortex should permit the use of vortex dynamics concepts to educe CS, to explain formation and evolutionary dynamics of CS, to explore the role of CS in turbulence phenomena, and to develop viable turbulence models and control strategies for turbulence phenomena. We propose a definition of a vortex in an incompressible flow in terms of the eigenvalues of the symmetric tensor ${\bm {\cal S}}^2 + {\bm \Omega}^2$ are respectively the symmetric and antisymmetric parts of the velocity gradient tensor ${\bm \Delta}{\bm u}$. This definition captures the pressure minimum in a plane perpendicular to the vortex axis at high Reynolds numbers, and also accurately defines vortex cores at low Reynolds numbers, unlike a pressure-minimum criterion. We compare our definition with prior schemes/definitions using exact and numerical solutions of the Euler and Navier–Stokes equations for a variety of laminar and turbulent flows. In contrast to definitions based on the positive second invariant of ${\bm \Delta}{\bm u}$ or the complex eigenvalues of ${\bm \Delta}{\bm u}$, our definition accurately identifies the vortex core in flows where the vortex geometry is intuitively clear.

Abstract: A catalogue of molecular aberrations that cause ovarian cancer is critical for developing and deploying therapies that will improve patients' lives. The Cancer Genome Atlas project has analysed messenger RNA expression, microRNA expression, promoter methylation and DNA copy number in 489 high-grade serous ovarian adenocarcinomas and the DNA sequences of exons from coding genes in 316 of these tumours. Here we report that high-grade serous ovarian cancer is characterized by TP53 mutations in almost all tumours (96%); low prevalence but statistically recurrent somatic mutations in nine further genes including NF1, BRCA1, BRCA2, RB1 and CDK12; 113 significant focal DNA copy number aberrations; and promoter methylation events involving 168 genes. Analyses delineated four ovarian cancer transcriptional subtypes, three microRNA subtypes, four promoter methylation subtypes and a transcriptional signature associated with survival duration, and shed new light on the impact that tumours with BRCA1/2 (BRCA1 or BRCA2) and CCNE1 aberrations have on survival. Pathway analyses suggested that homologous recombination is defective in about half of the tumours analysed, and that NOTCH and FOXM1 signalling are involved in serous ovarian cancer pathophysiology.