Platelet Factor
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Diagnosing Platelet Secretion Disorders: Examples Cases
Diagnosing platelet secretion disorders: examples cases Martina Daly Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield Disclosures for Martina Daly In compliance with COI policy, ISTH requires the following disclosures to the session audience: Research Support/P.I. No relevant conflicts of interest to declare Employee No relevant conflicts of interest to declare Consultant No relevant conflicts of interest to declare Major Stockholder No relevant conflicts of interest to declare Speakers Bureau No relevant conflicts of interest to declare Honoraria No relevant conflicts of interest to declare Scientific Advisory No relevant conflicts of interest to declare Board Platelet granule release Agonists (FIIa, Collagen, ADP) Signals Activation Shape change Membrane fusion Release of granule contents Platelet storage organelles lysosomes a granules Enzymes including cathepsins Adhesive proteins acid hydrolases Clotting factors and their inhibitors Fibrinolytic factors and their inhibitors Proteases and antiproteases Growth and mitogenic factors Chemokines, cytokines Anti-microbial proteins Membrane glycoproteins dense (d) granules ADP/ATP Serotonin histamine inorganic polyphosphate Platelet a-granule contents Type Prominent components Membrane glycoproteins GPIb, aIIbb3, GPVI Clotting factors VWF, FV, FXI, FII, Fibrinogen, HMWK, FXIII? Clotting inhibitors TFPI, protein S, protease nexin-2 Fibrinolysis components PAI-1, TAFI, a2-antiplasmin, plasminogen, uPA Other protease inhibitors a1-antitrypsin, a2-macroglobulin -
WHITE BLOOD CELLS Formation Function ~ TEST YOURSELF
Chapter 9 Blood, Lymph, and Immunity 231 WHITE BLOOD CELLS All white blood cells develop in the bone marrow except Any nucleated cell normally found in blood is a white blood for some lymphocytes (they start out in bone marrow but cell. White blood cells are also known as WBCs or leukocytes. develop elsewhere). At the beginning of leukopoiesis all the When white blood cells accumulate in one place, they grossly immature white blood cells look alike even though they're appear white or cream-colored. For example, pus is an accu- already committed to a specific cell line. It's not until the mulation of white blood cells. Mature white blood cells are cells start developing some of their unique characteristics larger than mature red blood cells. that we can tell them apart. There are five types of white blood cells. They are neu- Function trophils, eosinophils, basophils, monocytes and lymphocytes (Table 9-2). The function of all white blood cells is to provide a defense White blood cells can be classified in three different ways: for the body against foreign invaders. Each type of white 1. Type of defense function blood cell has its own unique role in this defense. If all the • Phagocytosis: neutrophils, eosinophils, basophils, mono- white blood cells are functioning properly, an animal has a cytes good chance of remaining healthy. Individual white blood • Antibody production and cellular immunity: lympho- cell functions will be discussed with each cell type (see cytes Table 9-2). 2. Shape of nucleus In providing defense against foreign invaders, the white • Polymorphonuclear (multilobed, segmented nucleus): blood cells do their jobs primarily out in the tissues. -
Chapter 18 *Lecture Powerpoint the Circulatory System: Blood
Chapter 18 *Lecture PowerPoint The Circulatory System: Blood *See separate FlexArt PowerPoint slides for all figures and tables preinserted into PowerPoint without notes. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Introduction • Many myths about blood – Mysterious ―vital force‖ – Drained ―bad-blood‖ for medical reasons – Hereditary traits were once thought to be transmitted through blood • Blood cells were seen with the first microscopes • Hematology—the study of blood • Recent developments in this field help save lives 18-2 Introduction • Expected Learning Outcomes – Describe the functions and major components of the circulatory system. – Describe the components and physical properties of blood. – Describe the composition of blood plasma. – Explain the significance of blood viscosity and osmolarity. – Describe in general terms how blood is produced. 18-3 Functions of the Circulatory System • Circulatory system consists of the heart, blood vessels, and blood • Cardiovascular system refers only to the heart and blood vessels • Hematology—the study of blood • Functions of circulatory system – Transport • O2, CO2, nutrients, wastes, hormones, and stem cells – Protection • Inflammation, limit spread of infection, destroy microorganisms and cancer cells, neutralize toxins, and initiate clotting – Regulation • Fluid balance, stabilizes pH of ECF, and temperature control 18-4 Components and General Properties of Blood • Adults have 4 to 6 L of blood • A liquid connective tissue consisting of -
Impaired Production and Increased Apoptosis of Neutrophils in Granulocyte Colony-Stimulating Factor Receptor–Deficient Mice
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Immunity, Vol. 5, 491±501, November, 1996, Copyright 1996 by Cell Press Impaired Production and Increased Apoptosis of Neutrophils in Granulocyte Colony-Stimulating Factor Receptor±Deficient Mice Fulu Liu, Huai Yang Wu, Robin Wesselschmidt, decrease in granulocytic precursors in their bone mar- Tad Kornaga, and Daniel C. Link row (Lieschke et al., 1994). Division of Bone Marrow Transplantation In addition to its effect on granulopoiesis, G-CSF may and Stem Cell Biology also contribute to the regulation of multipotential hema- Department of Medicine topoietic progenitors. The administration of large doses Washington University Medical School of G-CSF is associated with a dramatic increase in the St. Louis, Missouri 63110-1093 levels of hematopoietic stem cells and progenitor cells in the peripheral blood (Bungart et al., 1990; de Haan et al., 1995). In vitro, direct effects of G-CSF on primitive progenitor cells have been demonstrated. G-CSF is able Summary to stimulate the formation of granulocyte/macrophage colonies (CFU-GM) from purified CD34-positiveprogeni- We have generated mice carrying a homozygous null tors (Haylock et al., 1992). Furthermore, like interleu- mutation in the granulocyte colony-stimulating factor kin-6 (IL-6), G-CSF exhibits synergistic activity with IL-3 receptor (G-CSFR) gene. G-CSFR-deficient mice have to support murine multipotential blast cell colony forma- decreased numbers of phenotypically normal circulat- tion in cultures of spleen cells from 5-fluorouracil- ing neutrophils. Hematopoietic progenitors are de- treated mice (Ikebuchi et al., 1988). -
Alterations in Platelet Alpha-Granule Secretion and Adhesion on Collagen Under Flow in Mice Lacking the Atypical Rho Gtpase Rhobtb3
cells Article Alterations in Platelet Alpha-Granule Secretion and Adhesion on Collagen under Flow in Mice Lacking the Atypical Rho GTPase RhoBTB3 Martin Berger 1,2, David R. J. Riley 1, Julia Lutz 1, Jawad S. Khalil 1, Ahmed Aburima 1, Khalid M. Naseem 3 and Francisco Rivero 1,* 1 Centre for Atherothrombosis and Metabolic Disease, Hull York Medical School, Faculty of Health Sciences, University of Hull, HU6 7RX Hull, UK; [email protected] (M.B.); [email protected] (D.R.J.R.); [email protected] (J.L.); [email protected] (J.S.K.); [email protected] (A.A.) 2 Department of Internal Medicine 1, University Hospital, RWTH Aachen, 52074 Aachen, Germany 3 Leeds Institute for Cardiovascular and Metabolic Medicine, University of Leeds, LS2 9NL Leeds, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-1482-466433 Received: 8 January 2019; Accepted: 7 February 2019; Published: 11 February 2019 Abstract: Typical Rho GTPases, such as Rac1, Cdc42, and RhoA, act as molecular switches regulating various aspects of platelet cytoskeleton reorganization. The loss of these enzymes results in reduced platelet functionality. Atypical Rho GTPases of the RhoBTB subfamily are characterized by divergent domain architecture. One family member, RhoBTB3, is expressed in platelets, but its function is unclear. In the present study we examined the role of RhoBTB3 in platelet function using a knockout mouse model. We found the platelet count, size, numbers of both alpha and dense granules, and surface receptor profile in these mice were comparable to wild-type mice. -
Automatic System for Differential Blood Counting
ISSN (Print) : 2320 – 3765 ISSN (Online): 2278 – 8875 International Journal of Advanced Research in Electrical, Electronics and Instrumentation Engineering (An ISO 3297: 2007 Certified Organization) Vol. 5, Issue 4, April 2016 Automatic System for Differential Blood Counting 1 2 Manisha Shirvoikar , Dr.H.G.Virani PG Student [ECI], Dept. of ETC, Goa College of Engineering, Ponda, Goa, India1 Professor & Head of Department, Dept. of ETC, Goa College of Engineering, Ponda, Goa, India2 ABSTRACT: For detecting various diseases, Doctor first suggests the patient to undergo blood test which is used as a health indicator. Differential Blood Count (DBC) provides haematologist with valuable information about health of the patient. DBC determines the percentage of types of WBC this is important because it give exact count of five types of WBC such as neutrophil, lymphocyte, monocyte, eosinophil and basophile. Increase or decrease of DBC than the ideal count indicated that our body is not healthy. Precise counting of type of WBC is very important. Manual counting of White blood cells is time consuming and can lead to human error with increase in number of samples. Automatic cell counter sometimes misclassifies the cells having different morphology. Even they are very expensive and unaffordable by remote area health centres and hospitals. These problems are overcome by developing a system which is image based, cost effective, fast and accurate which has the capability to identify, classify the different type of white blood cell and perform DBC. Implementation is done using MATLABR2014b. KEYWORDS: MATLAB, peripheral blood smear, RBC, Thresholding, WBC, DBC. I.INTRODUCTION Total volume of blood in human is 5-6 litres i.e 8% of body weight or 80 mL/kg body weight. -
Nihms124287.Pdf (2.042Mb)
Intragranular Vesiculotubular Compartments are Involved in Piecemeal Degranulation by Activated Human Eosinophils The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Melo, Rossana C.N., Sandra A.C. Perez, Lisa A. Spencer, Ann M. Dvorak, and Peter F. Weller. 2005. “Intragranular Vesiculotubular Compartments Are Involved in Piecemeal Degranulation by Activated Human Eosinophils.” Traffic 6 (10) (July 28): 866–879. doi:10.1111/j.1600-0854.2005.00322.x. Published Version doi:10.1111/j.1600-0854.2005.00322.x Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:28714144 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA NIH Public Access Author Manuscript Traffic. Author manuscript; available in PMC 2009 July 24. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Traffic. 2005 October ; 6(10): 866±879. doi:10.1111/j.1600-0854.2005.00322.x. Intragranular Vesiculotubular Compartments are Involved in Piecemeal Degranulation by Activated Human Eosinophils Rossana C.N. Melo1,2, Sandra A.C. Perez2, Lisa A. Spencer2, Ann M. Dvorak3, and Peter F. Weller2,* 1Laboratory of Cellular Biology, Department of Biology, Federal University of Juiz de Fora, UFJF, Juiz de Fora, MG, Brazil 2Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA 3Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA Abstract Eosinophils, leukocytes involved in allergic, inflammatory and immunoregulatory responses, have a distinct capacity to rapidly secrete preformed granule-stored proteins through piecemeal degranulation (PMD), a secretion process based on vesicular transport of proteins from within granules for extracellular release. -
The Endogenous Antimicrobial Cathelicidin LL37 Induces Platelet Activation and Augments Thrombus Formation
The endogenous antimicrobial cathelicidin LL37 induces platelet activation and augments thrombus formation Article Published Version Salamah, M. F., Ravishankar, D., Kodji, X., Moraes, L. A., Williams, H. F., Vallance, T. M., Albadawi, D. A., Vaiyapuri, R., Watson, K., Gibbins, J. M., Brain, S. D., Perretti, M. and Vaiyapuri, S. (2018) The endogenous antimicrobial cathelicidin LL37 induces platelet activation and augments thrombus formation. Blood Advances, 2 (21). pp. 2973-2985. ISSN 2473-9529 doi: https://doi.org/10.1182/bloodadvances.2018021758 Available at http://centaur.reading.ac.uk/79972/ It is advisable to refer to the publisher’s version if you intend to cite from the work. See Guidance on citing . To link to this article DOI: http://dx.doi.org/10.1182/bloodadvances.2018021758 Publisher: American Society of Hematology All outputs in CentAUR are protected by Intellectual Property Rights law, including copyright law. Copyright and IPR is retained by the creators or other copyright holders. Terms and conditions for use of this material are defined in the End User Agreement . www.reading.ac.uk/centaur CentAUR Central Archive at the University of Reading Reading’s research outputs online REGULAR ARTICLE The endogenous antimicrobial cathelicidin LL37 induces platelet activation and augments thrombus formation Maryam F. Salamah,1 Divyashree Ravishankar,1,* Xenia Kodji,2,* Leonardo A. Moraes,3,* Harry F. Williams,1 Thomas M. Vallance,1 Dina A. Albadawi,1 Rajendran Vaiyapuri,4 Kim Watson,5 Jonathan M. Gibbins,5 Susan D. Brain,2 Mauro Perretti,6 -
Β-Adrenergic Modulation in Sepsis Etienne De Montmollin, Jerome Aboab, Arnaud Mansart and Djillali Annane
Available online http://ccforum.com/content/13/5/230 Review Bench-to-bedside review: β-Adrenergic modulation in sepsis Etienne de Montmollin, Jerome Aboab, Arnaud Mansart and Djillali Annane Service de Réanimation Polyvalente de l’hôpital Raymond Poincaré, 104 bd Raymond Poincaré, 92380 Garches, France Corresponding author: Professeur Djillali Annane, [email protected] Published: 23 October 2009 Critical Care 2009, 13:230 (doi:10.1186/cc8026) This article is online at http://ccforum.com/content/13/5/230 © 2009 BioMed Central Ltd Abstract in the intensive care setting [4] – addressing the issue of its Sepsis, despite recent therapeutic progress, still carries unaccep- consequences in sepsis. tably high mortality rates. The adrenergic system, a key modulator of organ function and cardiovascular homeostasis, could be an The present review summarizes current knowledge on the interesting new therapeutic target for septic shock. β-Adrenergic effects of β-adrenergic agonists and antagonists on immune, regulation of the immune function in sepsis is complex and is time cardiac, metabolic and hemostasis functions during sepsis. A dependent. However, β activation as well as β blockade seems 2 1 comprehensive understanding of this complex regulation to downregulate proinflammatory response by modulating the β system will enable the clinician to better apprehend the cytokine production profile. 1 blockade improves cardiovascular homeostasis in septic animals, by lowering myocardial oxygen impact of β-stimulants and β-blockers in septic patients. consumption without altering organ perfusion, and perhaps by restoring normal cardiovascular variability. β-Blockers could also β-Adrenergic receptor and signaling cascade be of interest in the systemic catabolic response to sepsis, as they The β-adrenergic receptor is a G-protein-coupled seven- oppose epinephrine which is known to promote hyperglycemia, transmembrane domain receptor. -
Digitalcommons@UNMC Granulocytopenia
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1936 Granulocytopenia Howard E. Mitchell University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Mitchell, Howard E., "Granulocytopenia" (1936). MD Theses. 457. https://digitalcommons.unmc.edu/mdtheses/457 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. G PA~lULOCYTOPENI A SENIOR THESIS By Howard E. Mitchell April 17, 1936 TABLE OF CONT'ENTS Introduction Definition • · 1 History . • • • 1 Nomenclature • • • • • 4 ClassificBtion • • • • 6 Physiology • • • • .10 Etiology • • 22 Geographic Distribution • 23 Age, Sex, and R9ce • • ·• 23 Occupation • .. • • • • .. • 23 Ba.cteria • • • • .. 24 Glandu18.r Dysfunction • • • 27 Radiation • • • • 28 Allergy • • • 28 Chemotactic and Maturation Factors • • 28 Chemicals • • • • • 30 Pathology • • • • • 36 Symptoms • • • • • • • 43 DiEtgnosis • • • • • .. • • • • • .. • 4'7 Prognosis 48 '" • • • • • • • • • • • • Treatment • • • • • • • • 49 Non"'specific Therapy • • • • .. 50 Transfusion • • • • .. 51 X-Ray • • • • • • • • • 52 Liver ·Extract • • • • • • • 53 Nucleotides • • • • • • • • • • • 53 General Ca.re • • • • • • • • 57 Conclusion • • • • • • • • • 58 480805 INTHODUCTION Although t~ere is reference in literature of the Nineteenth Century to syndromes similating the disease (granulocytopenia) 9.8 W(~ know it todes, it "vas not un til the year 1922 that Schultz 8ctually described his C8se as a disease entity and by so doing, stimulated the interest of tne medical profession to further in vestigation. -
Monocyte Alterations in Rheumatoid Arthritis Are Dominated by Preterm
Ann Rheum Dis: first published as 10.1136/annrheumdis-2017-211649 on 30 November 2017. Downloaded from Basic and translational research EXTENDED REPORT Monocyte alterations in rheumatoid arthritis are dominated by preterm release from bone marrow and prominent triggering in the joint Biljana Smiljanovic,1 Anna Radzikowska,2 Ewa Kuca-Warnawin,2 Weronika Kurowska,2 Joachim R Grün,3 Bruno Stuhlmüller,1 Marc Bonin,1 Ursula Schulte-Wrede,3 Till Sörensen,1 Chieko Kyogoku,3 Anne Bruns,1 Sandra Hermann,1 Sarah Ohrndorf,1 Karlfried Aupperle,1 Marina Backhaus,1 Gerd R Burmester,1 Andreas Radbruch,3 Andreas Grützkau,3 Wlodzimierz Maslinski,2 Thomas Häupl1 Handling editor Tore K Kvien ABSTRACT of life.1 2 Infiltration of monocytes along with T and Objective Rheumatoid arthritis (RA) accompanies B cells into the joint and production of inflamma- ► Additional material is published online only. To view infiltration and activation of monocytes in inflamed tory mediators characterise the immunopathology please visit the journal online joints. We investigated dominant alterations of RA of this disease. The influence of the monocytic (http:// dx. doi. org/ 10. 1136/ monocytes in bone marrow (BM), blood and inflamed lineage in shaping the immune response is substan- annrheumdis- 2017- 211649). joints. tial and interferes with both the innate and adap- Methods CD14+ cells from BM and peripheral blood tive arm of immunity. Thus, it is not surprising 1Department of Rheumatology and Clinical Immunology, (PB) of patients with RA and osteoarthritis (OA) were that controlling inflammation in disease-modifying Charité Universitätsmedizin, profiled with GeneChip microarrays.D etailed functional antirheumatic drug (DMARD) non-responders Berlin, Germany analysis was performed with reference transcriptomes may be achieved when targeting monocyte-derived 2 Department of Pathophysiology of BM precursors, monocyte blood subsets, monocyte cytokines, tumour necrosis factor (TNF), inter- and Immunology, National activation and mobilisation. -
Of THP-1 Acute Monocytic Leukemia Cells Halt Proliferation and Induce
Human Plasma Membrane-Derived Vesicles Halt Proliferation and Induce Differentiation of THP-1 Acute Monocytic Leukemia Cells This information is current as Ephraim A. Ansa-Addo, Sigrun Lange, Dan Stratton, of September 28, 2021. Samuel Antwi-Baffour, Igor Cestari, Marcel I. Ramirez, Maria V. McCrossan and Jameel M. Inal J Immunol 2010; 185:5236-5246; Prepublished online 4 October 2010; doi: 10.4049/jimmunol.1001656 Downloaded from http://www.jimmunol.org/content/185/9/5236 References This article cites 43 articles, 12 of which you can access for free at: http://www.jimmunol.org/content/185/9/5236.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 28, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Human Plasma Membrane-Derived Vesicles Halt Proliferation and Induce Differentiation of THP-1 Acute Monocytic Leukemia Cells Ephraim A.