A Q-Ising model application for linear-time image segmentation

A computational method is presented which efficiently segments digital grayscale images by directly applying the Q-state Ising (or Potts) model. Since the Potts model was first proposed in 1952, physicists have studied lattice models to gain deep insights into magnetism and other disordered systems. For some time, researchers have realized that digital images may be modeled in much the same way as these physical systems (i.e., as a square lattice of numerical values). A major drawback in using Potts model methods for image segmentation is that, with conventional methods, it processes in exponential time. Advances have been made via certain approximations to reduce the segmentation process to power-law time. However, in many applications (such as for sonar imagery), real-time processing requires much greater efficiency. This article contains a description of an energy minimization technique that applies four Potts (Q-Ising) models directly to the image and processes in linear time. The result is analogous to partitioning the system into regions of four classes of magnetism. This direct Potts segmentation technique is demonstrated on photographic, medical, and acoustic images.Comment: 7 pages, 8 figures, revtex, uses subfigure.sty. Central European Journal of Physics, in press (2010

Interface relaxation in electrophoretic deposition of polymer chains: Effects of segmental dynamics, molecular weight, and field

Using different segmental dynamics and relaxation, characteristics of the interface growth is examined in an electrophoretic deposition of polymer chains on a three (2+1) dimensional discrete lattice with a Monte Carlo simulation. Incorporation of faster modes such as crankshaft and reptation movements along with the relatively slow kink-jump dynamics seems crucial in relaxing the interface width. As the continuously released polymer chains are driven (via segmental movements) and deposited, the interface width $W$ grows with the number of time steps $t$, $W \propto t^{\beta},$ ($\beta \sim 0.4$--$0.8)$, which is followed by its saturation to a steady-state value $W_s$. Stopping the release of additional chains after saturation while continuing the segmental movements relaxes the saturated width to an equilibrium value ($W_s \to W_r$). Scaling of the relaxed interface width $W_r$ with the driving field $E$, $W_r \propto E^{-1/2}$ remains similar to that of the steady-state $W_s$ width. In contrast to monotonic increase of the steady-state width $W_s$, the relaxed interface width $W_r$ is found to decay (possibly as a stretched exponential) with the molecular weight.Comment: 5 pages, 7 figure

Isoform-specific upregulation of palladin in human and murine pancreas tumors.

Pancreatic ductal adenocarcinoma (PDA) is a lethal disease with a characteristic pattern of early metastasis, which is driving a search for biomarkers that can be used to detect the cancer at an early stage. Recently, the actin-associated protein palladin was identified as a candidate biomarker when it was shown that palladin is mutated in a rare inherited form of PDA, and overexpressed in many sporadic pancreas tumors and premalignant precursors. In this study, we analyzed the expression of palladin isoforms in murine and human PDA and explored palladin's potential use in diagnosing PDA. We performed immunohistochemistry and immunoblot analyses on patient samples and tumor-derived cells using an isoform-selective monoclonal antibody and a pan-palladin polyclonal antibody. Immunoblot and real-time quantitative reverse transcription-PCR were used to quantify palladin mRNA levels in human samples. We show that there are two major palladin isoforms expressed in pancreas: 65 and 85-90 kDa. The 65 kDa isoform is expressed in both normal and neoplastic ductal epithelial cells. The 85-90 kDa palladin isoform is highly overexpressed in tumor-associated fibroblasts (TAFs) in both primary and metastatic tumors compared to normal pancreas, in samples obtained from either human patients or genetically engineered mice. In tumor-derived cultured cells, expression of palladin isoforms follows cell-type specific patterns, with the 85-90 kDa isoform in TAFs, and the 65 kDa isoform predominating in normal and neoplastic epithelial cells. These results suggest that upregulation of 85-90 kDa palladin isoform may play a role in the establishment of the TAF phenotype, and thus in the formation of a desmoplastic tumor microenvironment. Thus, palladin may have a potential use in the early diagnosis of PDA and may have much broader significance in understanding metastatic behavior