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A Heterozygous Variant in the Human Cardiac Mir-133 Gene, MIR133A2, Alters Mirna Duplex Processing and Strand Abundance
Ohanian et al. BMC Genetics 2013, 14:18 http://www.biomedcentral.com/1471-2156/14/18 RESEARCH ARTICLE Open Access A heterozygous variant in the human cardiac miR-133 gene, MIR133A2, alters miRNA duplex processing and strand abundance Monique Ohanian1†, David T Humphreys2,3†, Elizabeth Anderson4, Thomas Preiss5 and Diane Fatkin1,2,3,6* Abstract Background: MicroRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression. Sequential cleavage of miRNA precursors results in a ~22 nucleotide duplex of which one strand, the mature miRNA, is typically loaded into the RNA-induced silencing complex (RISC) while the passenger strand is degraded. Very little is known about how genetic variation might affect miRNA biogenesis and function. Results: We re-sequenced the MIR1-1, MIR1-2, MIR133A1, MIR133A2, and MIR133B genes, that encode the cardiac- enriched miRNAs, miR-1 and miR-133, in 120 individuals with familial atrial fibrillation and identified 10 variants, including a novel 79T > C MIR133A2 substitution. This variant lies within the duplex at the 30 end of the mature strand, miR-133a-3p, and is predicted to prevent base-pairing and weaken thermostability at this site, favoring incorporation of the passenger strand, miR-133a-5p, into RISC. Genomic DNA fragments containing miR-133a-2 precursor sequences with 79T and 79C alleles were transfected into HeLa cells. On Northern blotting the 79T allele showed strong expression of miR-133a-3p with weak expression of miR-133a-5p. In contrast, the 79C allele had no effect on miR-133a-3p but there was a significant increase (mean 3.6-fold) in miR-133a-5p levels. -
Identification of Molecules Relevant for the Invasiveness of Fibrosarcomas and Melanomas
Helsinki University Biomedical Dissertations No. 148 IDENTIFICATION OF MOLECULES RELEVANT FOR THE INVASIVENESS OF FIBROSARCOMAS AND MELANOMAS Pirjo Nummela Department of Pathology Haartman Institute Faculty of Medicine and Division of Biochemistry Department of Biosciences Faculty of Biological and Environmental Sciences University of Helsinki Finland Academic dissertation To be presented for public examination with the permission of the Faculty of Biological and Environmental Sciences of the University of Helsinki in the Lecture Hall 2 of Haartman Institute (Haartmaninkatu 3, Helsinki), on 13.5.2011 at 12 o’clock noon. Helsinki 2011 Supervisor Docent Erkki Hölttä, M.D., Ph.D. Department of Pathology Haartman Institute University of Helsinki Thesis committee Docent Jouko Lohi, M.D., Ph.D. Department of Pathology Haartman Institute University of Helsinki and Pirjo Nikula-Ijäs, Ph.D. Division of Biochemistry Department of Biosciences University of Helsinki Reviewers Professor Veli-Matti Kähäri, M.D., Ph.D. Department of Dermatology University of Turku and Turku University Hospital and Docent Jouko Lohi, M.D., Ph.D. Opponent Professor Jyrki Heino, M.D., Ph.D. Department of Biochemistry and Food Chemistry University of Turku Custos Professor Kari Keinänen, Ph.D. Division of Biochemistry Department of Biosciences University of Helsinki ISBN 978-952-92-8821-2 (paperback) ISBN 978-952-10-6924-6 (PDF) ISSN 1457-8433 http://ethesis.helsinki.fi Helsinki University Print Helsinki 2011 To Juha, Joona, and Joel TABLE OF CONTENTS LIST OF ORIGINAL PUBLICATIONS -
Q# Introduction
Introduction to Q# Q# (Q-sharp) is a domain-specific and open-sourced programming language, part of Microsoft's Quantum Development Kit (QDK), used for expressing quantum algorithms. It is to be used for writing subroutines that execute on an adjunct quantum processing unit (QPU), under the control of a classical host program and computer. Q# can be installed on Windows 10, OSX and Linux. The instructions to install Q# can be found in the online documentation here. If you prefer not to install Q# on your local computer, you can use one of the machines in CSE’s Virtual Lab found here. The Windows 10 machines already have .Net Core SDK, Visual Studio and VS Code installed to get your started, you should still install the Q# extension to get syntax- highlighting, code complete, etc. To get help with Q# and the QDK, feel free to ask questions on our messages board, come to office hours as posted on the calendar, or ask in stackoverflow. The Q# team is constantly monitoring any questions posted there with the "q#" tag. Writing Q# programs. Operations and functions are the basic unit of execution in Q#. They are roughly equivalent to a function in C or C++ or Python, or a static method in C# or Java. A Q# operation is a quantum subroutine. That is, it is a callable routine that contains quantum operations. A Q# function is a classical subroutine used within a quantum algorithm. It may contain classical code but no quantum operations. Specifically, functions may not allocate or borrow qubits, nor may they call operations. -
The Role of TGFβ Type III Receptor in Lung Cancer Cell Migration And
Western University Scholarship@Western Electronic Thesis and Dissertation Repository 6-26-2018 1:00 PM The role of TGFβ type III receptor in lung cancer cell migration and invasion Anthony Ziccarelli The University of Western Ontario Supervisor Di Guglielmo, John The University of Western Ontario Graduate Program in Physiology and Pharmacology A thesis submitted in partial fulfillment of the equirr ements for the degree in Master of Science © Anthony Ziccarelli 2018 Follow this and additional works at: https://ir.lib.uwo.ca/etd Recommended Citation Ziccarelli, Anthony, "The role of TGFβ type III receptor in lung cancer cell migration and invasion" (2018). Electronic Thesis and Dissertation Repository. 5454. https://ir.lib.uwo.ca/etd/5454 This Dissertation/Thesis is brought to you for free and open access by Scholarship@Western. It has been accepted for inclusion in Electronic Thesis and Dissertation Repository by an authorized administrator of Scholarship@Western. For more information, please contact [email protected]. i Abstract Metastasis is responsible for 90% of cancer-related deaths. An important early step in the metastatic process is epithelial-to-mesenchymal transition (EMT) of tumor cells. Stimulated by TGFβ signaling, cells that undergo EMT have increased migratory and invasive potential, resulting in metastasis and the development of tumors at a secondary site. The TGFβ type 3 receptor (TβR3) has been implicated in modulating TGFβ signaling, yet its functional outcomes remain unclear. My findings demonstrated that TβR3 silencing does not alter TGFβ-dependent Smad2 phosphorylation in neither H1299, not A549 non- small cell lung carcinoma cells but reduces Smad2 expression in H1299 cells. -
Targeting the Phosphatidylinositide-3 Kinase Pathway and the Mitogen
Targeting the Phosphatidylinositide-3 Kinase Pathway and the Mitogen-Activated-Protein Kinase Pathway through Thymosin-β4, Exercise, and Negative Regulators to Promote Retinal Ganglion Cell Survival or Regeneration by Mark Magharious A thesis submitted in conformity with the requirements for the degree of Master of Science Rehabilitation Sciences Institute University of Toronto © Copyright by Mark Magharious 2015 Targeting the Phosphatidylinositide-3 Kinase Pathway and the Mitogen-Activated-Protein Kinase Pathway through Thymosin-β4, Exercise, and Negative Regulators to Promote Retinal Ganglion Cell Survival or Regeneration Mark Magharious Master of Science Rehabilitation Sciences Institute University of Toronto 2015 Abstract The phosphatidylinositide-3 kinase (PI3K) and mitogen-activated-protein kinase (MAPK) pathways mediate cellular survival in the presence of apoptotic stimuli. These pathways are known to promote the survival of injured retinal ganglion cells (RGCs), central nervous system neurons that project visual information from the retina to the brain. Injury to the optic nerve triggers apoptosis of RGCs. This work demonstrates that Thymosin-β4, a peptide involved in actin sequestration, both enhances RGC survival after injury and increases axonal regeneration. Moreover, Thymosin-β4 modulates the PI3K and MAPK pathways. In addition, this study demonstrates that exercise reduces apoptosis of injured RGCs, and explores the function of the PI3K and MAPK pathways in this process. Finally, small peptides are used to interfere with the functions of PTEN, a negative regulator of the PI3K pathway, as well as Erbin and BCR, negative regulators in the MAPK pathway. These peptides enhance RGC survival and axonal regeneration after injury. ii Acknowledgments I would like to take this opportunity to recognize all those who helped me through the process of researching and writing this thesis. -
Sized Neuropeptides
M ETHODS IN MOLECULAR BIOLOGY™ Series Editor John M. Walker School of Life Sciences University of Hertfordshire Hatfield, Hertfordshire, AL10 9AB, UK For further volumes: http://www.springer.com/series/7651 Neuropeptides Methods and Protocols Edited by Adalberto Merighi Dipartimento di Morfofisiologia Veterinaria, Università degli Studi di Torino, Grugliasco, TO, Italy; Istituto Nazionale di Neuroscienze (INN), Università degli Studi di Torino, Grugliasco, TO, Italy Editor Adalberto Merighi Dipartimento di Morfofisiologia Veterinaria Università degli Studi di Torino and Istituto Nazionale di Neuroscienze (INN) Università degli Studi di Torino Grugliasco, TO, Italy [email protected] Please note that additional material for this book can be downloaded from http://extras.springer.com ISSN 1064-3745 e-ISSN 1940-6029 ISBN 978-1-61779-309-7 e-ISBN 978-1-61779-310-3 DOI 10.1007/978-1-61779-310-3 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2011936011 © Springer Science+Business Media, LLC 2011 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Humana Press, c/o Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. -
Pyrevit Documentation Release 4.7.0-Beta
pyRevit Documentation Release 4.7.0-beta eirannejad May 15, 2019 Getting Started 1 How To Use This Documents3 2 Create Your First Command5 3 Anatomy of a pyRevit Script 7 3.1 Script Metadata Variables........................................7 3.2 pyrevit.script Module...........................................9 3.3 Appendix A: Builtin Parameters Provided by pyRevit Engine..................... 12 3.4 Appendix B: System Category Names.................................. 13 4 Effective Output/Input 19 4.1 Clickable Element Links......................................... 19 4.2 Tables................................................... 20 4.3 Code Output............................................... 21 4.4 Progress bars............................................... 21 4.5 Standard Prompts............................................. 22 4.6 Standard Dialogs............................................. 26 4.7 Base Forms................................................ 35 4.8 Graphs.................................................. 37 5 Keyboard Shortcuts 45 5.1 Shift-Click: Alternate/Config Script................................... 45 5.2 Ctrl-Click: Debug Mode......................................... 45 5.3 Alt-Click: Show Script file in Explorer................................. 46 5.4 Ctrl-Shift-Alt-Click: Reload Engine................................... 46 5.5 Shift-Win-Click: pyRevit Button Context Menu............................. 46 6 Extensions and Commmands 47 6.1 Why do I need an Extension....................................... 47 6.2 Extensions............................................... -
2009 Door County Folk Festival Syllabus.Pdf
30th Annual Door County Folk Festival Get Your Foot in the Door! Wednesday – Sunday, July 8 – 12, 2009 Sister Bay, Ephraim and Baileys Harbor, Wisconsin http://www.dcff.net/[email protected]/(773-463-2288) DCFF Home Dance Syllabus Advance Regular Discount Price On Paper $19.00 $22.00 OnCD $8.00 $11.00 2009 Door County Folk Festival (DCFF), Wisconsin 2009 Door County Folk Festival Schedule v11 (Subject to Change - Changes Marked with +) Get Your Foot in the Door! Wednesday - Sunday, July 8-12, 2009 - Sister Bay, Ephraim and Baileys Harbor, Wisconsin DCFF Home Phone: (773)-463-2288 or (773)-634-9381 [email protected] Wednesday Start End Where Event Who Afternoon 12:00pm SBVH Staff Arrives Staff & Volunteers 1:00pm SBVH Setup Begins Staff & Volunteers Evening 6:00pm SBVH Registration Begins Staff & Volunteers 6:30pm 9:00pm BHTH TCE Program - Session 1 - Grades K-5 Sanna Longden 8:00pm 1:00am SBVH 8th of July Party with Recorded Music Forrest Johnson & Other Regional Leaders 1:00am 2:30am SBVH Late Night Party Paul Collins & Company Thursday Start End Where Event Who Morning 9:00am SBVH Setup & Registration Continues Staff & Volunteers 9:00am 12:00pm BHTH TCE Program - Session 2 - Grades K-5 Sanna Longden 10:00am 11:45am SBVH Vintage American Round Dances Paul Collins Afternoon 11:45am 1:15pm Lunch Break 12:00pm 1:00pm SBVH Zumba Latin Dance Workout Session Diane Garvey 1:15pm 3:00pm SBVH Swing Dance - Lindy Hop Workshop Maureen Majeski: Lindy Hop 1:15pm 3:00pm BHTH Regional Greek Folk Dance Workshop Rick King, Dit Olshan, Paul Collins Rick: Vlaha -
Mixed-Signal and Dsp Design Techniques
MIXED-SIGNAL AND DSP DESIGN TECHNIQUES INTRODUCTION SECTION 1 SAMPLED DATA SYSTEMS SECTION 2 ADCs FOR DSP APPLICATIONS SECTION 3 DACs FOR DSP APPLICATIONS SECTION 4 FAST FOURIER TRANSFORMS SECTION 5 DIGITAL FILTERS SECTION 6 DSP HARDWARE SECTION 7 INTERFACING TO DSPs SECTION 8 DSP APPLICATIONS SECTION 9 HARDWARE DESIGN SECTION 10 TECHNIQUES INDEX ANALOG DEVICES TECHNICAL REFERENCE BOOKS PUBLISHED BY PRENTICE HALL Analog-Digital Conversion Handbook Digital Signal Processing Applications Using the ADSP-2100 Family (Volume 1:1992, Volume 2:1994) Digital Signal Processing in VLSI DSP Laboratory Experiments Using the ADSP-2101 ADSP-2100 Family User's Manual PUBLISHED BY ANALOG DEVICES Practical Design Techniques for Sensor Signal Conditioning Practical Design Techniques for Power and Thermal Management High Speed Design Techniques Practical Analog Design Techniques Linear Design Seminar ADSP-21000 Family Applications Handbook System Applications Guide Amplifier Applications Guide Nonlinear Circuits Handbook Transducer Interfacing Handbook Synchro & Resolver Conversion THE BEST OF Analog Dialogue, 1967-1991 HOW TO GET INFORMATION FROM ANALOG DEVICES Analog Devices publishes data sheets and a host of other technical literature supporting our products and technologies. Follow the instructions below for worldwide access to this information. FOR DATA SHEETS U.S.A. and Canada I Fax Retrieval. Telephone number 800-446-6212. Call this number and use a faxcode corresponding to the data sheet of your choice for a fax-on-demand through our automated AnalogFax™ system. Data sheets are available 7 days a week, 24 hours a day. Product/faxcode cross reference listings are available by calling the above number and following the prompts. -
NLRP3 Inflammasome at the Interface of Inflammation, Endothelial
cells Review NLRP3 Inflammasome at the Interface of Inflammation, Endothelial Dysfunction, and Type 2 Diabetes Ilona M. Gora *, Anna Ciechanowska and Piotr Ladyzynski Nalecz Institute of Biocybernetics and Biomedical Engineering, Polish Academy of Sciences, Ks. Trojdena 4, 02-109 Warsaw, Poland; [email protected] (A.C.); [email protected] (P.L.) * Correspondence: [email protected] Abstract: Type 2 diabetes mellitus (T2DM), accounting for 90–95% cases of diabetes, is characterized by chronic inflammation. The mechanisms that control inflammation activation in T2DM are largely unexplored. Inflammasomes represent significant sensors mediating innate immune responses. The aim of this work is to present a review of links between the NLRP3 inflammasome, endothelial dys- function, and T2DM. The NLRP3 inflammasome activates caspase-1, which leads to the maturation of pro-inflammatory cytokines interleukin 1β and interleukin 18. In this review, we characterize the structure and functions of NLRP3 inflammasome as well as the most important mechanisms and molecules engaged in its activation. We present evidence of the importance of the endothelial dysfunction as the first key step to activating the inflammasome, which suggests that suppressing the NLRP3 inflammasome could be a new approach in depletion hyperglycemic toxicity and in averting the onset of vascular complications in T2DM. We also demonstrate reports showing that the expression of a few microRNAs that are also known to be involved in either NLRP3 inflammasome activation or endothelial dysfunction is deregulated in T2DM. Collectively, this evidence suggests that T2DM is an inflammatory disease stimulated by pro-inflammatory cytokines. Finally, studies revealing the role of glucose concentration in the activation of NLRP3 inflammasome are analyzed. -
Programming with Windows Forms
A P P E N D I X A ■ ■ ■ Programming with Windows Forms Since the release of the .NET platform (circa 2001), the base class libraries have included a particular API named Windows Forms, represented primarily by the System.Windows.Forms.dll assembly. The Windows Forms toolkit provides the types necessary to build desktop graphical user interfaces (GUIs), create custom controls, manage resources (e.g., string tables and icons), and perform other desktop- centric programming tasks. In addition, a separate API named GDI+ (represented by the System.Drawing.dll assembly) provides additional types that allow programmers to generate 2D graphics, interact with networked printers, and manipulate image data. The Windows Forms (and GDI+) APIs remain alive and well within the .NET 4.0 platform, and they will exist within the base class library for quite some time (arguably forever). However, Microsoft has shipped a brand new GUI toolkit called Windows Presentation Foundation (WPF) since the release of .NET 3.0. As you saw in Chapters 27-31, WPF provides a massive amount of horsepower that you can use to build bleeding-edge user interfaces, and it has become the preferred desktop API for today’s .NET graphical user interfaces. The point of this appendix, however, is to provide a tour of the traditional Windows Forms API. One reason it is helpful to understand the original programming model: you can find many existing Windows Forms applications out there that will need to be maintained for some time to come. Also, many desktop GUIs simply might not require the horsepower offered by WPF. -
Deer Thymosin Beta 10 Functions As a Novel Factor for Angiogenesis And
Zhang et al. Stem Cell Research & Therapy (2018) 9:166 https://doi.org/10.1186/s13287-018-0917-y RESEARCH Open Access Deer thymosin beta 10 functions as a novel factor for angiogenesis and chondrogenesis during antler growth and regeneration Wei Zhang1,2†, Wenhui Chu1,2†, Qingxiu Liu1,2†, Dawn Coates3, Yudong Shang1,2 and Chunyi Li1,2* Abstract Background: Deer antlers are the only known mammalian organ with vascularized cartilage that can completely regenerate. Antlers are of real significance as a model of mammalian stem cell-based regeneration with particular relevance to the fields of chondrogenesis, angiogenesis, and regenerative medicine. Recent research found that thymosin beta 10 (TMSB10) is highly expressed in the growth centers of growing antlers. The present study reports here the expression, functions, and molecular interactions of deer TMSB10. Methods: The TMSB10 expression level in both tissue and cells in the antler growth center was measured. The effects of both exogenous (synthetic protein) and endogenous deer TMSB10 (lentivirus-based overexpression) on antlerogenic periosteal cells (APCs; nonactivated antler stem cells with no basal expression of TMSB10) and human umbilical vein endothelial cells (HUVECs; endothelial cells with no basal expression of TMSB10) were evaluated to determine whether TMSB10 functions on chondrogenesis and angiogenesis. Differences in deer and human TMSB10 in angiogenesis and molecular structure were determined using animal models and molecular dynamics simulation, respectively. The molecular mechanisms underlying deer TMSB10 in promoting angiogenesis were also explored. Results: Deer TMSB10 was identified as a novel proangiogenic factor both in vitro and in vivo. Immunohistochemistry revealed that TMSB10 was widely expressed in the antler growth center in situ, with the highest expression in the reserve mesenchyme, precartilage, and transitional zones.