Transition to turbulence in a crossed‐field gap

The transition from laminar to turbulent behavior of the electron sheath in a cross‐field gap is examined for the regime B≳BH, where B is the external magnetic field and BH is the Hull cutoff value. An analytic expression is presented for the critical emitted current beyond which laminar solutions cease to exist. A one‐dimensional particle code is used to corroborate the analytic theory. This code shows several interesting properties when the emitted current exceeds the critical value. Chief among them is the presence of a turbulent microsheath near the cathode surface. The electrostatic potential in the gap’s vacuum region is found to oscillate at a frequency that is quite insensitive to the emitted current and to the electrons’ emission velocity. © 1994 American Institute of Physics.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71334/2/PHPAEN-1-12-3725-1.pd

Erratum: ‘‘Transition to turbulence in a crossed‐field gap’’ [Phys. Plasmas 1, 3725 (1994)]

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/70343/2/PHPAEN-3-11-4293-1.pd

Limiting current in a crossed‐field gap

An analytic theory is presented that yields the maximum transmittable current across an anode–cathode gap that is embedded in an arbitrary transverse magnetic field (B). The limiting current is found to be relatively insensitive to B for all B<BH, where BH is the Hull cutoff magnetic field required for magnetic insulation. The classical Child–Langmuir solution is recovered in the limit B→0.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71084/2/PFBPEI-5-12-4486-1.pd

Resistive destabilization of cycloidal electron flow and universality of (near‐) Brillouin flow in a crossed‐field gap

It is shown that a small amount of dissipation, caused by current flow in a lossy external circuit, can produce a disruption of steady‐state cycloidal electron flow in a crossed‐field gap, leading to the establishment of a turbulent steady state that is close to, but not exactly, Brillouin flow. This disruption, which has nothing to do with a diocotron or cyclotron instability, is fundamentally caused by the failure of a subset of the emitted electrons to return to the cathode surface as a result of resistive dissipation. This mechanism was revealed in particle simulations, and was confirmed by an analytic theory. These near‐Brillouin states differ in several interesting respects from classic Brillouin flow, the most important of which is the presence of a microsheath and a time‐varying potential minimum very close to the cathode surface. They are essentially identical to that produced when (i) injected current exceeds a certain critical value [P. J. Christenson and Y. Y. Lau, Phys. Plasmas 1, 3725 (1994)] or (ii) a small rf electric field is applied to the gap [P. J. Christenson and Y. Y. Lau, Phys. Rev. Lett. 76, 3324 (1996)]. It is speculated that such near‐Brillouin states are generic in vacuum crossed‐field devices, due to the ease with which the cycloidal equilibrium can be disrupted. Another novel aspect of this paper is the introduction of transformations by which the nonlinear, coupled partial differential equations in the Eulerian description (equation of motion, continuity equation, Poisson equation, and the circuit equation) are reduced to an equivalent system of very simple linear ordinary differential equations. © 1996 American Institute of Physics.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71350/2/PHPAEN-3-12-4455-1.pd

Pre-primary education in Hong Kong : the evolution of governance and policy tools

published_or_final_versionPolitics and Public AdministrationMasterMaster of Public Administratio

The Effect of LXR Activators on AP-1 Proteins in Keratinocytes

Oxysterols, via activation of liver X receptor (LXR), regulate keratinocyte differentiation by stimulating transglutaminase cross-linking of several constituent proteins leading to the formation of the cornified envelope. We previously reported that oxysterols increase the expression of one of these cross-linked proteins, involucrin, and that this effect can be abolished by mutations of the distal activator protein (AP)-1 response element in the involucrin promoter. Furthermore, oxysterols increase AP-1 binding in an electrophoretic gel mobility shift assay and increase the expression of an AP-1 reporter. In this study, we describe the individual components of the AP-1 complex that are involved in the oxysterol-mediated AP-1 activation and stimulation of keratinocyte differentiation. We identified Fra-1 within the AP-1 DNA binding complex by supershift analysis of nuclear extracts from oxysterol-treated, cultured keratinocytes and confirmed that oxysterol treatment increased the levels of Fra-1 by western blot analysis. Additionally, on Western and Northern analysis, oxysterol treatment increased two other AP-1 proteins, Jun-D and c-Fos, whereas Fra-2, Jun-B, and c-Jun were not changed. Similar alterations in AP-1 proteins occurred when 25-OH-cholesterol or non-steroidal LXR agonists (GW3965, TO-901317) were used. These results indicate that oxysterols induce specific AP-1 proteins, thereby activating involucrin, one of the genes required for epidermal differentiation

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment