Image Restoration Based on Hybrid Ant Colony Algorithm

Image restoration is the process to eliminate or reduce the image quality degradation in the digital image formation, transmission and recording and its purpose is to process the observed degraded image to make the restored result approximate the un-degraded original image. This paper, based on the basic ant colony algorithm and integrating with the genetic algorithm, proposes an image restoration processing method based on hybrid ant colony algorithm. This method transforms the optimal population information of genetic algorithm into the original pheromone concentration matrix of ant colony algorithm and uses it to compute the parameters of degradation function so as to get a precise estimate of the original image. By analyzing and comparing the restoration results, the method of this paper can not only overcome the influence of noises, but it can also make the image smoother with no fringe effects in the edges and excellent visual effects, verifying its practicability

The claudin family of proteins in human malignancy: A clinical perspective

Tight junctions, or zonula occludens, are the most apical component of the junctional complex and provide one form of cell–cell adhesion in epithelial and endothelial cells. Nearly 90% of malignant tumors are derived from the epithelium. Loss of cell–cell adhesion is one of the steps in the progression of cancer to metastasis. At least three main tight junction family proteins have been discovered: occludin, claudin, and junctional adhesion molecule (JAM). Claudins are the most important structural and functional components of tight junction integral membrane proteins, with at least 24 members in mammals. They are crucial for the paracellular flux of ions and small molecules. Overexpression or downregulation of claudins is frequently observed in epithelial-derived cancers. However, molecular mechanisms by which claudins affect tumorigenesis remain largely unknown. As the pivotal proteins in epithelial cells, altered expression and distribution of different claudins have been reported in a wide variety of human malignancies, including pancreatic, colonic, lung, ovarian, thyroid, prostate, esophageal, and breast cancers. In this review, we will give the readers an overall picture of the changes in claudin expression observed in various cancers and their mechanisms of regulation. Downregulation of claudins contributes to epithelial transformation by increasing the paracellular permeability of nutrients and growth factors to cancerous cells. In the cases of upregulation of claudin expression, the barrier function of the cancerous epithelia changes, as they often display a disorganized arrangement of tight junction strands with increased permeability to paracellular markers. Finally, we will summarize the literature suggesting that claudins may become useful biomarkers for cancer detection and diagnosis as well as possible therapeutic targets for cancer treatment

Impurity resonance states in electron-doped high T_c superconductors

Two scenarios, i.e., the anisotropic s-wave pairing (the s-wave scenario) and the d-wave pairing coexisting with antiferromagnetism (the coexisting scenario) have been introduced to understand some of seemingly s-wave like behaviors in electron doped cuprates. We considered the electronic structure in the presence of a nonmagnetic impurity in the coexistence scenario. We found that even if the AF order opens a full gap in quasi-particle excitation spectra, the mid-gap resonant peaks in local density of states (LDoS) around an impurity can still be observed in the presence of a d-wave pairing gap. The features of the impurity states in the coexisting phase are markedly different from the pure AF or pure d-wave pairing phases, showing the unique role of the coexisting AF and d-wave pairing orders. On the other hand, it is known that in the pure s-wave case no mid-gap states can be induced by a nonmagnetic impurity. Therefore we proposed that the response to a nonmagnetic impurity can be used to differentiate the two scenarios.Comment: 5 pages, two-column revtex4, 5 figures, author list correcte

Increased nucleotide polymorphic changes in the 5'-untranslated region of δ-catenin (CTNND2) gene in prostate cancer

Cancer pathogenesis involves multiple genetic and epigenetic alterations, which result in oncogenic changes in gene expression. δ-Catenin (CTNND2) is overexpressed in cancer although the mechanisms of its upregulation are highly variable. Here we report that in prostate cancer the methylation of CpG islands in δ-catenin promoter was not a primary regulatory event. There was also no δ-catenin gene amplification. However, using Single-Strand onformation Polymorphism analysis, we observed the increased nucleotide changes in the 5'-untranslated region of δ-catenin gene in human prostate cancer. At least one such change (-9 G>A) is a true somatic point mutation associated with a high Gleason score, poorly differentiated prostatic adenocarcinoma. Laser capture microdissection coupled with PCR analyses detected the mutation only in cancerous but not in the adjacent benign prostatic tissues. Using chimeric genes encoding the luciferase reporter, we found that this mutation, but not a random mutation or a mutation that disrupts an upstream open reading frame, resulted in a remarkably higher expression and enzyme activity. This mutation did not affect transcriptional efficiency, suggesting that it promotes δ-catenin translation. This is the first report of δ-catenin gene mutation in cancer and supports the notion that multiple mechanisms contribute to its increased expression in carcinogenesis. Originally published ncogene, Vol. 28, No. 4, Jan 200

Method of detecting cancer using delta-catenin

The present invention provides a method for detecting or screening for the presence of cancer in a subject. The method comprises obtaining, providing or collecting a tissue or fluid sample (such as a urine sample) from said subject, and then determining the presence or absence of delta-catenin in said sample, or increased levels of delta-catenin in said sample as compared to a normal or control subject. The presence of delta-catentin in said sample, or increased levels of delta-catenin in said sample, indicating said subject is afflicted with or at least at risk of developing cancer