Disparities in colon and rectal cancer queried individually between Hispanics and Whites

Background: Colorectal cancer (CRC) is the third most commonly diagnosed cancer and the second leading cause of cancer related deaths in the United States. Racial disparities between Hispanics and Whites exist for incidence of late-onset (LO) CRC. However, not much is known about potential disparities between colon cancer (CC) and rectal cancer (RC) incidence queried individually. Methods: Using the SEER database data from 2000 to 2010, we obtained the national estimates of CC and RC for Hispanics and Whites. We analyzed trends in incidence, mortality, gender and stage of disease for early-onset (EO) (50 years old) CC and RC. Results: In Hispanics, the overall incidence of CC and RC increased by 47% and 52%, respectively; while in Whites, the overall incidence of CC and RC decreased by 13% and 2% respectively. Incidence of EO CC increased in both Hispanics and Whites by 83% and 17%, respectively, and incidence of EO RC also increased for both groups with a 76% increase in Hispanics and a 34% increase in Whites. For LO CC, the incidence increased by 37% in Hispanics while it decreased by 17% in Whites and for LO RC, the trend in incidence increased in Hispanics by 41%, but decreased in Whites by 11%. Conclusions: This study established that the incidence of CC and RC are different and there is racial disparity in incidence between Whites and Hispanics. This study, hopefully, will help in crafting public policy that might help in addressing this disparity.Open Access JournalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

The WW-HECT protein Smurf2 interacts with the Docking Protein NEDD9/HEF1 for Aurora A activation

The multi-functional adaptor protein NEDD9/HEF1/Cas-L regulates cell motility, invasion and cell cycle progression, and plays key roles in cancer progression and metastasis. NEDD9 is localized to the centrosome and is required for activation of Aurora A kinase in mitosis. Here we demonstrate that the HECT-WW protein Smurf2 physically associates with NEDD9 and is required for the stability of NEDD9 protein. Smurf2 depletion results in a marked decrease in NEDD9 protein levels, by facilitating polyubiquitination and proteasomal degradation of NEDD9. Conversely, forced overexpression of Smurf2 results in upregulation of endogenous NEDD9 protein, confirming the role for Smurf2 in NEDD9 stability. Cells with Smurf2 depletion fail to activate Aurora A at the G2/M boundary, leading to a marked delay in mitotic entry. These observations suggest that the stable complex of Smurf2 and NEDD9 is required for timely entry into mitosis via Aurora A activation

Информационная система учета и анализа взаимодействия ВУЗа с потенциальными абитуриентами

Актуальность работы: автоматизация процесса учёта взаимодействия ВУЗа с абитуриентами повысит эффективность профориентационной деятельности технического ВУЗа. Объект исследования: процесс учета и анализа взаимодействия ВУЗа с потенциальными абитуриентами. Целью данной работы является разработка и внедрение Информационной системы учета и анализа взаимодействия ВУЗа с потенциальными абитуриентами. В процессе исследования проводился теоретический анализ, обзор аналогов, проектирование и разработка информационной системы.Relevance of work: automation of process of the accounting of interaction of HEI with entrants will increase efficiency of career guidance of activity of technical HEI. The object of research is the process of the accounting and analysis of interaction of HEI with entrants. The aim of this work is development and implementation of the Information System for accounting and analysis of the interaction of HEI with potential entrants. Theoretical analysis, review of analogues, design and development of an information system were carried out during research

Improved Adhesion, Growth and Maturation of Vascular Smooth Muscle Cells on Polyethylene Grafted with Bioactive Molecules and Carbon Particles

High-density polyethylene (PE) foils were modified by an Ar+ plasma discharge and subsequent grafting with biomolecules, namely glycine (Gly), polyethylene glycol (PEG), bovine serum albumin (BSA), colloidal carbon particles (C) or BSA and C (BSA + C). As revealed by atomic force microscopy (AFM), goniometry and Rutherford Backscattering Spectroscopy (RBS), the surface chemical structure and surface morphology of PE changed dramatically after plasma treatment. The contact angle decreased for the samples treated by plasma, mainly in relation to the formation of oxygen structures during plasma irradiation. A further decrease in the contact angle was obvious after glycine and PEG grafting. The increase in oxygen concentration after glycine and PEG grafting proved that the two molecules were chemically linked to the plasma-activated surface. Plasma treatment led to ablation of the PE surface layer, thus the surface morphology was changed and the surface roughness was increased. The materials were then seeded with vascular smooth muscle cells (VSMC) derived from rat aorta and incubated in a DMEM medium with fetal bovine serum. Generally, the cells adhered and grew better on modified rather than on unmodified PE samples. Immunofluorescence showed that focal adhesion plaques containing talin, vinculin and paxillin were most apparent in cells on PE grafted with PEG or BSA + C, and the fibres containing α-actin, β-actin or SM1 and SM2 myosins were thicker, more numerous and more brightly stained in the cells on all modified PE samples than on pristine PE. An enzyme-linked immunosorbent assay (ELISA) revealed increased concentrations of focal adhesion proteins talin and vinculin and also a cytoskeletal protein β-actin in cells on PE modified with BSA + C. A contractile protein α-actin was increased in cells on PE grafted with PEG or Gly. These results showed that PE activated with plasma and subsequently grafted with bioactive molecules and colloidal C particles, especially with PEG and BSA + C, promotes the adhesion, proliferation and phenotypic maturation of VSMC

A population-based surveillance study on severe acute maternal morbidity (near-miss) and adverse perinatal outcomes in Campinas, Brazil: The Vigimoma Project

BACKGROUND: Auditing of sentinel health events based on best-practice protocols has been recommended. This study describes a population-based investigation on adverse perinatal events including severe acute maternal morbidity (near-miss), maternal and perinatal mortality, as a health intervention to help improve the surveillance system. METHODS: From October to December 2005, all cases of maternal death (MD), near-miss (NM), fetal deaths (FD), and early neonatal deaths (END), occurring in Campinas, Brazil, were audited by maternal mortality committees. RESULTS: A total of 4,491 liveborn infants (LB) and 159 adverse perinatal events (35.4/1000 LB) were revised, consisting of 4 MD (89/100.000 LB) and 95 NM (21.1/1000 LB), 23.7 NM for each MD. In addition, 32 FD (7.1/1000 LB) and 28 END (6.2/1000 LB) occurred. The maternal death/near miss rate was 23.7:1. Some delay in care was recognized for 34%, and hypertensive complications comprised 57.8% of the NM events, followed by postpartum hemorrhage. CONCLUSION: Auditing near miss cases expanded the understanding of the spectrum from maternal morbidity to mortality and the importance of promoting adhesion to clinical protocols among maternal mortality committee members. Hypertensive disorders and postpartum hemorrhage were identified as priority topics for health providers training, and organization of care

Non-Invasive Imaging of Cysteine Cathepsin Activity in Solid Tumors Using a 64Cu-Labeled Activity-Based Probe

The papain family of cysteine cathepsins are actively involved in multiple stages of tumorigenesis. Because elevated cathepsin activity can be found in many types of human cancers, they are promising biomarkers that can be used to target radiological contrast agents for tumor detection. However, currently there are no radiological imaging agents available for these important molecular targets. We report here the development of positron emission tomography (PET) radionuclide-labeled probes that target the cysteine cathepsins by formation of an enzyme activity-dependent bond with the active site cysteine. These probes contain an acyloxymethyl ketone (AOMK) functional group that irreversibly labels the active site cysteine of papain family proteases attached to a 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) tag for labeling with 64Cu for PET imaging studies. We performed biodistribution and microPET imaging studies in nude mice bearing subcutaneous tumors expressing various levels of cysteine cathepsin activity and found that the extent of probe uptake by tumors correlated with overall protease activity as measured by biochemical methods. Furthermore, probe signals could be reduced by pre-treatment with a general cathepsin inhibitor. We also found that inclusion of a Cy5 tag on the probe increased tumor uptake relative to probes lacking this fluorogenic dye. Overall, these results demonstrate that small molecule activity-based probes carrying radio-tracers can be used to image protease activity in living subjects

Semaphorin 3A Suppresses Tumor Growth and Metastasis in Mice Melanoma Model

<div><h3>Background</h3><p>Recent understanding on cancer therapy indicated that targeting metastatic signature or angiogenic switch could be a promising and rational approach to combat cancer. Advancement in cancer research has demonstrated the potential role of various tumor suppressor proteins in inhibition of cancer progression. Current studies have shown that axonal sprouting inhibitor, semaphorin 3A (Sema 3A) acts as a potent suppressor of tumor angiogenesis in various cancer models. However, the function of Sema 3A in regulation of melanoma progression is not well studied, and yet to be the subject of intense investigation.</p> <h3>Methodology/Principal Findings</h3><p>In this study, using multiple <em>in vitro</em> and <em>in vivo</em> approaches we have demonstrated that Sema 3A acts as a potent tumor suppressor <em>in vitro</em> and <em>in vivo</em> mice (C57BL/6) models. Mouse melanoma (B16F10) cells overexpressed with Sema 3A resulted in significant inhibition of cell motility, invasiveness and proliferation as well as suppression of <em>in vivo</em> tumor growth, angiogenesis and metastasis in mice models. Moreover, we have observed that Sema 3A overexpressed melanoma clone showed increased sensitivity towards curcumin and Dacarbazine, anti-cancer agents.</p> <h3>Conclusions</h3><p>Our results demonstrate, at least in part, the functional approach underlying Sema 3A mediated inhibition of tumorigenesis and angiogenesis and a clear understanding of such a process may facilitate the development of novel therapeutic strategy for the treatment of cancer.</p> </div