Genesis and Morphotectonic Characterisation of Crescent- Shaped feature from Alcock Rise, Andaman Sea

Study of 98 crescent shape depressions over Alcock Rise, Andaman Sea were reported for the first time in between water depth -500 and -2000 m using multibeam swath bathymetry data. These gigantic depressions have crescent length (CL) varies from 600 to 3800 m and width (CW) varies from 200 to 2500 m with an average central depression of 500 m. Detailed parametric characterization reveals that slope and axial ratio of these crescentic structures have no direct relationship with general shape and steepness of their escarpment. Moreover, spatial distribution of these structures show a clustering of elongated crescent with higher crescent length to width ratio in NW margin of Alcock Rise compare to centre. This change in shape from open elliptical to semicircular depression probably suggests that earlier formed open crescents were modified at later stage to semicircular depressions. As observed in the seismic data, the formation of the crescentic depressions were initiated by the normal fault in-association with major dextral transform fault and subsequently its geometry was modified by local transpression along with seismicity induced slumping and bottom current scouring from the weaker zones. So, tectonics and bottom current activity provides simpler explanation for the formation of crescentic structure over Alcock Rise.Keywords: Crescentic depression, Alcock Rise, Swath bathymetry, Bottom current, Normal fault

350 mV, 5 GHz Class-D Enhanced Swing Differential and Quadrature VCOs in 65 nm CMOS

A new enhanced swing class-D VCO which operates from a supply voltage as low as 300 mV is presented. The architectural advantages are described along with an analysis for the oscillation frequency. Prototype differential and quadrature variants of the proposed VCO have been implemented in a 65 nm RF CMOS process with a 5 GHz VCO oscillation frequency. At a 350 mV supply, the measured phase noise performance for the quadrature VCO with a 5% tuning range is -137.1 dBc/Hz at 3 MHz offset with a power dissipation of 2.1 mW from a 0.35 V supply. The highest resulting figure-of-merit (FoM) is 198.3 dBc/Hz.©2015 IEEE. Personal use of this material is permitted. Permission from IEEE must be obtained for all other users, including reprinting/republishing this material for advertising or promotional purposes, creating new collective works for resale or redistribution to servers or lists, or reuse of any copyrighted components of this work in other works

Socio-Economic Burden of Myocardial Infarction Among Cancer Patients

Cancer patients face a higher risk of future myocardial infarction (MI), even after completion of anticancer therapies. MI is a critical source of physical and financial stress in non-cancer patients, but its impacts associated with cancer patients also saddled with the worry (stress) of potential reoccurrence is unknown. Therefore, we aimed to quantify MI's stress and financial burden after surviving cancer and compare to those never diagnosed with cancer. Utilizing cross-sectional national survey data from 2013-2018 derived from publicly available U.S. datasets, the National Health Interview Survey (NHIS), and economic data from the National Inpatient Sample (NIS), we compared the socio-economic outcomes among those with MI by cancer-status. We adjusted for social, demographic, and clinical factors. Overall, 19,504 (10.2%) of the 189,836 NHIS survey responders reported having cancer for more than 1 year. There was an increased prevalence of MI among cancer survivors compared to non-cancer patients (8.8% vs. 3.2%, P0.05). There was no difference in annual residual family income by cancer status; however, 3 lowest deciles of residual income representing 21.1% cancer-survivor with MI had a residual income of <$9,000. Myocardial infarction continues to represent an immense source of financial and perceived stress. In conclusion, although cancer patients face a higher risk of subsequent MI, this does not appear to advance their reported stress significantly

IN-VITRO CYTOTOXICITY ANALYSIS OF TAMOXIFEN CITRATE LOADED CROSS-LINKED GUAR GUM NANOPARTICLES ON JURKAT (HUMAN T-CELL LEUKEMIA) CELL LINE

The present investigation was aimed to study the antiproliferative action of tamoxifen citrate (TMX), a non steroidal antiestrogen, on a human T-cell leukemia cell line, Jurkat, as free drug and TMX loaded guar gum nanoparticles. For this we developed a new formulation containing chemically cross-linked guar gum nanoparticles (GG NPs) loaded with tamoxifen citrate (TMX). Single step (oil in water) emulsion and in-situ polymer cross-linking technique was employed to prepare spherical and smooth surfaced nanoparticles in the size range of 200-300nm. Nanoparticle size and shape was confirmed from observation in transmission electron microscope (TEM) analysis. Cytotoxicity on Jurkat (human T-cell leukemia) cell lines as determined by cell growth inhibition after 48 hrs of incubation indicated that tamoxifen citrate loaded guar gum nanoparticles were as efficient as the free drug when applied to the cancer line. However, the crosslinked guar gum nanoparticles loaded with tamoxifen citrate exhibited sustained release of the drug and delayed apoptosis over a long period of time making it suitable for cancer treatment. Keywords: Nanoparticles, guar gum, tamoxifen citrate, Jurkat (human T-cell leukemia) cell line, cytotoxicity, cell death, WST-1 assay

Sustained proliferation in cancer: mechanisms and novel therapeutic targets

Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression

Activation of Akt Is Essential for the Propagation of Mitochondrial Respiratory Stress Signaling and Activation of the Transcriptional Coactivator Heterogeneous Ribonucleoprotein A2

This article shows that mitochondrial respiratory dysfunction activates a stress signaling that induces Akt1 activation. Akt1 activation occurs through calcineurin-mediated IGF1R/PI3-K pathway. Akt1-mediated phosphorylation of hnRNPA2 is a key requirement for the propagation of stress signaling and activation of nuclear target genes

Analysis of Endocytic Pathways in Drosophila Cells Reveals a Conserved Role for GBF1 in Internalization via GEECs

In mammalian cells, endocytosis of the fluid phase and glycosylphosphatidylinositol-anchored proteins (GPI-APs) forms GEECs (GPI-AP enriched early endosomal compartments) via an Arf1- and Cdc42-mediated, dynamin independent mechanism. Here we use four different fluorescently labeled probes and several markers in combination with quantitative kinetic assays, RNA interference and high resolution imaging to delineate major endocytic routes in Drosophila cultured cells. We find that the hallmarks of the pinocytic GEEC pathway are conserved in Drosophila and identify garz, the fly ortholog of the GTP exchange factor GBF1, as a novel component of this pathway. Live confocal and TIRF imaging reveals that a fraction of GBF1 GFP dynamically associates with ABD RFP (a sensor for activated Arf1 present on nascent pinosomes). Correspondingly, a GTP exchange mutant of GBF1 has altered ABD RFP localization in the evanescent field and is impaired in fluid phase uptake. Furthermore, GBF1 activation is required for the GEEC pathway even in the presence of Brefeldin A, implying that, like Arf1, it has a role in endocytosis that is separable from its role in secretion