Analysis of Minimal LDPC Decoder System on a Chip Implementation

This paper presents a practical method of potential replacement of several different Quasi-Cyclic Low-Density Parity-Check (QC-LDPC) codes with one, with the intention of saving as much memory as required to implement the LDPC encoder and decoder in a memory-constrained System on a Chip (SoC). The presented method requires only a very small modification of the existing encoder and decoder, making it suitable for utilization in a Software Defined Radio (SDR) platform. Besides the analysis of the effects of necessary variable-node value fixation during the Belief Propagation (BP) decoding algorithm, practical standard-defined code parameters are scrutinized in order to evaluate the feasibility of the proposed LDPC setup simplification. Finally, the error performance of the modified system structure is evaluated and compared with the original system structure by means of simulation

An Integrated Systems Approach to Deconstructing Glycosylation

Glycosylation involves the post-translational addition of carbohydrates to protein molecules and is an intricate and indispensable biochemical process. Study of this complicated network of interactions is hindered by the lack of a coding template analogous to the genetic code, and by the vast structural complexity inherent to carbohydrate polymers. We use lectins (non-enzymatic carbohydrate-binding proteins of non-immunological origin) as microarray probes to identify carbohydrate features expressed on cellular surfaces. Specifically, we utilized lectin microarray technology to investigate the differences in carbohydrates expressed by the cell lines of the Nation Cancer Institute’s NCI-60 panel. Our investigation identified tissue-specific expression differences in high-mannose N-linked glycans as a result of microRNA-based regulation of key processing enzymes in the N-linked biosynthetic pathway. Thus post-transcriptional regulation at the RNA level affects glycome characteristics

Ubiquitous presence of gluconeogenic regulatory enzyme, fructose-1,6-bisphosphatase, within layers of rat retina

To shed some light on gluconeogenesis in mammalian retina, we have focused on fructose-1,6-bisphosphatase (FBPase), a regulatory enzyme of the process. The abundance of the enzyme within the layers of the rat retina suggests that, in mammals in contrast to amphibia, gluconeogenesis is not restricted to one specific cell of the retina. We propose that FBPase, in addition to its gluconeogenic role, participates in the protection of the retina against reactive oxygen species. Additionally, the nuclear localization of FBPase and of its binding partner, aldolase, in the retinal cells expressing the proliferation marker Ki-67 indicates that these two gluconeogenic enzymes are involved in non-enzymatic nuclear processes

Investigation of the effect of Au2O3 dopant on elastic properties of PbO-B2O3-SeO2: Er2O3 glass ceramics by ultrasonic techniques

Various elastic coefficients of Au2O3 doped PbO-B2O3-SeO2:Er2O3 (PBSE) glass ceramics were evaluated as functions of Au2O3 content using ultrasonic velocity measurements. The elastic coefficients and micro-hardness showed a decreasing tendency with the concentration of Au2O3. Such decrease is attributed to the increasing concentration of gold metallic particles and [SeO3]2- groups that acted as modifiers and induced imperfections in these samples. Obtained results were observed to be consistent with the conclusions drawn from spectroscopic studies that include X-ray photoelectron spectroscopy (XPS), infrared (IR), photoluminescence (PL) and positron annihilation (PAL) spectroscopy studies. Overall, these studies have revealed that even though, the presence of gold metallic particles is preferable for achieving superior luminescence and electrical properties, presence of such particles caused to decrease the elastic coefficients and micro-hardness of these glass ceramics. However, when the concentration of Au2O3 is increased beyond 0.075 mol%, we have observed a slight increase of elastic coefficients and micro-hardness.Comment: 6 pages, 8 figure

Targeting GSK3 and Associated Signaling Pathways Involved in Cancer

Glycogen synthase kinase 3 (GSK-3) is a serine/threonine (S/T) protein kinase. Although GSK-3 originally was identified to have functions in regulation of glycogen synthase, it was subsequently determined to have roles in multiple normal biochemical processes as well as various disease conditions. GSK-3 is sometimes referred to as a moonlighting protein due to the multiple substrates and processes which it controls. Frequently, when GSK-3 phosphorylates proteins, they are targeted for degradation. GSK-3 is often considered a component of the PI3K/PTEN/AKT/GSK-3/mTORC1 pathway as GSK-3 is frequently phosphorylated by AKT which regulates its inactivation. AKT is often active in human cancer and hence, GSK-3 is often inactivated. Moreover, GSK-3 also interacts with WNT/\u3b2-catenin signaling and \u3b2-catenin and other proteins in this pathway are targets of GSK-3. GSK-3 can modify NF-\u3baB activity which is often expressed at high levels in cancer cells. Multiple pharmaceutical companies developed small molecule inhibitors to suppress GSK-3 activity. In addition, various natural products will modify GSK-3 activity. This review will focus on the effects of small molecule inhibitors and natural products on GSK-3 activity and provide examples where these compounds were effective in suppressing cancer growth

Effects of the Mutant TP53 Reactivator APR-246 on Therapeutic Sensitivity of Pancreatic Cancer Cells in the Presence and Absence of WT-TP53

The TP53 tumor suppressor is mutated in ~75% of pancreatic cancers. The mutant TP53 protein in pancreatic ductal adenocarcinomas (PDAC) promotes tumor growth and metastasis. Attempts have been made to develop molecules that restore at least some of the properties of wildtype (WT) TP53. APR-246 is one such molecule, and it is referred to as a mutant TP53 reactivator. To understand the potential of APR-246 to sensitize PDAC cells to chemotherapy, we introduced a vector encoding WT-TP53 into two PDAC cell lines, one lacking the expression of TP53 (PANC-28) and one with a gain-of-function (GOF) mutant TP53 (MIA-PaCa-2). APR-246 increased drug sensitivity in the cells containing either a WT or mutant TP53 protein with GOF activity, but not in cells that lacked TP53. The introduction of WT-T53 into PANC-28 cells increased their sensitivity to the TP53 reactivator, chemotherapeutic drugs, and signal transduction inhibitors. The addition of WT-TP53 to PDAC cells with GOF TP53 also increased their sensitivity to the drugs and therapeutics, indicating that APR-246 could function in cells with WT-TP53 and GOF TP53. These results highlight the importance of knowledge of the type of TP53 mutation that is present in cancer patients before the administration of drugs which function through the reactivation of TP53

Roles of GSK-3 and microRNAs on epithelial mesenchymal transition and cancer stem cells

Various signaling pathways exert critical roles in the epithelial to mesenchymal transition (EMT) and cancer stem cells (CSCs). The Wnt/beta-catenin, PI3K/PTEN/ Akt/mTORC, Ras/Raf/MEK/ERK, hedgehog (Hh), Notch and TP53 pathways elicit essential regulatory influences on cancer initiation, EMT and progression. A common kinase involved in all these pathways is moon-lighting kinase glycogen synthase kinase-3 (GSK-3). These pathways are also regulated by micro-RNAs (miRs). TP53 and components of these pathways can regulate the expression of miRs. Targeting members of these pathways may improve cancer therapy in those malignancies that display their abnormal regulation. This review will discuss the interactions of the multi-functional GSK-3 enzyme in the Wnt/beta-catenin, PI3K/PTEN/Akt/mTORC, Ras/Raf/MEK/ERK, Hh, Notch and TP53 pathways. The regulation of these pathways by miRs and their effects on CSC generation, EMT, invasion and metastasis will be discussed