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Factor XIII and Fibrin Clot Properties in Acute Venous Thromboembolism
International Journal of Molecular Sciences Review Factor XIII and Fibrin Clot Properties in Acute Venous Thromboembolism Michał Z ˛abczyk 1,2 , Joanna Natorska 1,2 and Anetta Undas 1,2,* 1 John Paul II Hospital, 31-202 Kraków, Poland; [email protected] (M.Z.); [email protected] (J.N.) 2 Institute of Cardiology, Jagiellonian University Medical College, 31-202 Kraków, Poland * Correspondence: [email protected]; Tel.: +48-12-614-30-04; Fax: +48-12-614-21-20 Abstract: Coagulation factor XIII (FXIII) is converted by thrombin into its active form, FXIIIa, which crosslinks fibrin fibers, rendering clots more stable and resistant to degradation. FXIII affects fibrin clot structure and function leading to a more prothrombotic phenotype with denser networks, characterizing patients at risk of venous thromboembolism (VTE). Mechanisms regulating FXIII activation and its impact on fibrin structure in patients with acute VTE encompassing pulmonary embolism (PE) or deep vein thrombosis (DVT) are poorly elucidated. Reduced circulating FXIII levels in acute PE were reported over 20 years ago. Similar observations indicating decreased FXIII plasma activity and antigen levels have been made in acute PE and DVT with their subsequent increase after several weeks since the index event. Plasma fibrin clot proteome analysis confirms that clot-bound FXIII amounts associated with plasma FXIII activity are decreased in acute VTE. Reduced FXIII activity has been associated with impaired clot permeability and hypofibrinolysis in acute PE. The current review presents available studies on the role of FXIII in the modulation of fibrin clot properties during acute PE or DVT and following these events. -
(Apis Mellifera) ELISABETH P
J. Insect Ph.vsiol. Vol. 42, No. 9, pp. 823-828, 1996 Pergamon Copyright 0 1996 Elsevier Science Ltd Printed in Great Britain. All rights reserved PII: SOO22-1910(96)00045-5 0022-1910196 $15.00 + 0.00 Effects of Two Proteinase Inhibitors on the Digestive Enzymes and Survival of Honey Bees (Apis mellifera) ELISABETH P. J. BURGESS,*1 LOUISE A. MALONE,* JOHN T. CHRlSTELLERt Received I1 December 1995; revised und accepted 1 March 1996 Two endopeptidase inhibitors, BPTI (bovine pancreatic trypsin inhibitor) and SBTI (Kunitz soybean trypsin inhibitor), were found to significantly reduce the longevity of adult honey bees (&is mellifera L.) fed the inhibitors ad lib in sugar syrup at l.O%, 0.5% or O.l%, but not at 0.01% or 0.001% (w:v). Bees were taken from frames at emergence, kept in cages at 33”C, and provided with a pollen/protein diet, water and syrup. In vivo activity levels of three midgut endopeptidases (trypsin, chymotrypsin and elastase) and the exopeptidase leucine aminopeptidase (LAP) were determined in bees fed either BPTI or SBTI at l.O%, 0.3% or 0.1% (w:v) at two time points: the 8th day after emergence and when 75% of bees had died. LAP activity levels increased significantly in bees fed with either inhibitor at all concen- trations. At day 8, bees fed BPTI at all concentrations had significantly reduced levels of trypsin, chymotrypsin and elastase. At the time of 75% mortality, bees fed BPTI at each concentration had reduced trypsin levels, but only those fed the inhibitor at the highest dose level had reduced chymotrypsin or elastase activity. -
Ilamycin C Induces Apoptosis and Inhibits Migration and Invasion In
Xie et al. Journal of Hematology & Oncology (2019) 12:60 https://doi.org/10.1186/s13045-019-0744-3 RESEARCH Open Access Ilamycin C induces apoptosis and inhibits migration and invasion in triple-negative breast cancer by suppressing IL-6/STAT3 pathway Qing Xie1†, Zhijie Yang2†, Xuanmei Huang1, Zikang Zhang1, Jiangbin Li1, Jianhua Ju2*, Hua Zhang1* and Junying Ma2* Abstract Background: Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor prognosis, and its treatment remains a challenge due to few targeted medicines and high risk of relapse, metastasis, and drug resistance. Thus, more effective drugs and new regimens for the therapy of TNBC are urgently needed. Ilamycins are a kind of cyclic peptides and produced by Streptomyces atratus and Streptomyces islandicus with effective anti-tuberculosis activity. Ilamycin C is a novel compound isolated from the deep South China Sea- derived Streptomyces atratus SCSIO ZH16 and exhibited a strong cytotoxic activity against several cancers including breast cancer cell line MCF7. However, the cytotoxic activity of Ilamycin C to TNBC cells and a detailed antitumor mechanism have not been reported. Methods: CCK-8 assays were used to examine cell viability and cytotoxic activity of Ilamycin C to TNBC, non-TNBC MCF7, and nonmalignant MCF10A cells. EdU assays and flow cytometry were performed to assess cell proliferation and cell apoptosis. Transwell migration and Matrigel invasion assays were utilized to assess the migratory and invading capacity of TNBC cells following the treatment of Ilamycin C. The expressions of proteins were detected by western blot. Results: In this study, we found that Ilamycin C has more preferential cytotoxicity in TNBC cells than non-TNBC MCF7 and nonmalignant MCF10A cells. -
Nitrate Prodrugs Able to Release Nitric Oxide in a Controlled and Selective
Europäisches Patentamt *EP001336602A1* (19) European Patent Office Office européen des brevets (11) EP 1 336 602 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.7: C07C 205/00, A61K 31/00 20.08.2003 Bulletin 2003/34 (21) Application number: 02425075.5 (22) Date of filing: 13.02.2002 (84) Designated Contracting States: (71) Applicant: Scaramuzzino, Giovanni AT BE CH CY DE DK ES FI FR GB GR IE IT LI LU 20052 Monza (Milano) (IT) MC NL PT SE TR Designated Extension States: (72) Inventor: Scaramuzzino, Giovanni AL LT LV MK RO SI 20052 Monza (Milano) (IT) (54) Nitrate prodrugs able to release nitric oxide in a controlled and selective way and their use for prevention and treatment of inflammatory, ischemic and proliferative diseases (57) New pharmaceutical compounds of general effects and for this reason they are useful for the prep- formula (I): F-(X)q where q is an integer from 1 to 5, pref- aration of medicines for prevention and treatment of in- erably 1; -F is chosen among drugs described in the text, flammatory, ischemic, degenerative and proliferative -X is chosen among 4 groups -M, -T, -V and -Y as de- diseases of musculoskeletal, tegumental, respiratory, scribed in the text. gastrointestinal, genito-urinary and central nervous sys- The compounds of general formula (I) are nitrate tems. prodrugs which can release nitric oxide in vivo in a con- trolled and selective way and without hypotensive side EP 1 336 602 A1 Printed by Jouve, 75001 PARIS (FR) EP 1 336 602 A1 Description [0001] The present invention relates to new nitrate prodrugs which can release nitric oxide in vivo in a controlled and selective way and without the side effects typical of nitrate vasodilators drugs. -
The National Drugs List
^ ^ ^ ^ ^[ ^ The National Drugs List Of Syrian Arab Republic Sexth Edition 2006 ! " # "$ % &'() " # * +$, -. / & 0 /+12 3 4" 5 "$ . "$ 67"5,) 0 " /! !2 4? @ % 88 9 3: " # "$ ;+<=2 – G# H H2 I) – 6( – 65 : A B C "5 : , D )* . J!* HK"3 H"$ T ) 4 B K<) +$ LMA N O 3 4P<B &Q / RS ) H< C4VH /430 / 1988 V W* < C A GQ ") 4V / 1000 / C4VH /820 / 2001 V XX K<# C ,V /500 / 1992 V "!X V /946 / 2004 V Z < C V /914 / 2003 V ) < ] +$, [2 / ,) @# @ S%Q2 J"= [ &<\ @ +$ LMA 1 O \ . S X '( ^ & M_ `AB @ &' 3 4" + @ V= 4 )\ " : N " # "$ 6 ) G" 3Q + a C G /<"B d3: C K7 e , fM 4 Q b"$ " < $\ c"7: 5) G . HHH3Q J # Hg ' V"h 6< G* H5 !" # $%" & $' ,* ( )* + 2 ا اوا ادو +% 5 j 2 i1 6 B J' 6<X " 6"[ i2 "$ "< * i3 10 6 i4 11 6! ^ i5 13 6<X "!# * i6 15 7 G!, 6 - k 24"$d dl ?K V *4V h 63[46 ' i8 19 Adl 20 "( 2 i9 20 G Q) 6 i10 20 a 6 m[, 6 i11 21 ?K V $n i12 21 "% * i13 23 b+ 6 i14 23 oe C * i15 24 !, 2 6\ i16 25 C V pq * i17 26 ( S 6) 1, ++ &"r i19 3 +% 27 G 6 ""% i19 28 ^ Ks 2 i20 31 % Ks 2 i21 32 s * i22 35 " " * i23 37 "$ * i24 38 6" i25 39 V t h Gu* v!* 2 i26 39 ( 2 i27 40 B w< Ks 2 i28 40 d C &"r i29 42 "' 6 i30 42 " * i31 42 ":< * i32 5 ./ 0" -33 4 : ANAESTHETICS $ 1 2 -1 :GENERAL ANAESTHETICS AND OXYGEN 4 $1 2 2- ATRACURIUM BESYLATE DROPERIDOL ETHER FENTANYL HALOTHANE ISOFLURANE KETAMINE HCL NITROUS OXIDE OXYGEN PROPOFOL REMIFENTANIL SEVOFLURANE SUFENTANIL THIOPENTAL :LOCAL ANAESTHETICS !67$1 2 -5 AMYLEINE HCL=AMYLOCAINE ARTICAINE BENZOCAINE BUPIVACAINE CINCHOCAINE LIDOCAINE MEPIVACAINE OXETHAZAINE PRAMOXINE PRILOCAINE PREOPERATIVE MEDICATION & SEDATION FOR 9*: ;< " 2 -8 : : SHORT -TERM PROCEDURES ATROPINE DIAZEPAM INJ. -
Factor XIII Deficiency
Factor XIII deficiency Information for families Great Ormond Street Hospital for Children NHS Foundation Trust 2 Factor XIII deficiency is a type of clotting disorder. A specific protein is missing from the blood so that injured blood vessels cannot heal in the usual way. This information sheet from Great Ormond Street Hospital (GOSH) explains the causes, symptoms and treatment of Factor XIII deficiency and where to get help. What is a clotting disorder? A clotting (or coagulation) disorder is a on in order. When all of the factors are turned medical condition where a specific protein on, the blood forms a clot which stops the is missing from the blood. injury site bleeding any further. Blood is made up of different types of There are a number of coagulation factors cells (red blood cells, white blood cells and circulating in the blood, lying in wait to be platelets) all suspended in a straw-coloured turned on when an injury occurs. If any one liquid called plasma. Platelets are the cells of the factors is missing from the body, the responsible for making blood clot. When complicated chemical reaction described a blood vessel is injured, platelets clump above will not happen as it should. This can together to block the injury site. They also lead to blood loss, which can be severe and start off a complicated chemical reaction to life-threatening. Each coagulation factor form a mesh made of a substance called fibrin. is given a number from I to XIII – they are This complicated chemical reaction always always written as Roman numerals – and follows a strict pattern – with each clotting the effects of the missing factor will vary. -
Pfeiffer Syndrome Type II Discovered Perinatally
Diagnostic and Interventional Imaging (2012) 93, 785—789 CORE Metadata, citation and similar papers at core.ac.uk Provided by Elsevier - Publisher Connector LETTER / Musculoskeletal imaging Pfeiffer syndrome type II discovered perinatally: Report of an observation and review of the literature a,∗ a a a H. Ben Hamouda , Y. Tlili , S. Ghanmi , H. Soua , b c b a S. Jerbi , M.M. Souissi , H. Hamza , M.T. Sfar a Unité de néonatologie, service de pédiatrie, CHU Tahar Sfar, 5111 Mahdia, Tunisia b Service de radiologie, CHU Tahar Sfar, 5111 Mahdia, Tunisia c Service de gynéco-obstétrique, CHU Tahar Sfar, 5111 Mahdia, Tunisia Pfeiffer syndrome, described for the first time by Pfeiffer in 1964, is a rare hereditary KEYWORDS condition combining osteochondrodysplasia with craniosynostosis [1]. This syndrome is Pfeiffer syndrome; also called acrocephalosyndactyly type 5, which is divided into three sub-types. Type I Cloverleaf skull; is the classic Pfeiffer syndrome, with autosomal dominant transmission, often associated Craniosynostosis; with normal intelligence. Types II and III occur as sporadic cases in individuals who have Syndactyly; craniosynostosis with broad thumbs, broad big toes, ankylosis of the elbows and visceral Prenatal diagnosis abnormalities [2]. We report a case of Pfeiffer syndrome type II, discovered perinatally, which is distinguished from type III by the skull appearing like a cloverleaf, and we shall discuss the clinical, radiological and evolutive features and the advantage of prenatal diagnosis of this syndrome with a review of the literature. Observation The case involved a male premature baby born at 36 weeks of amenorrhoea with multiple deformities at birth. The parents were not blood-related and in good health who had two other boys and a girl with normal morphology. -
Thromboxane A2 Receptor Antagonist SQ29548 Attenuates SH‑SY5Y Neuroblastoma Cell Impairments Induced by Oxidative Stress
INTERNATIONAL JOURNAL OF MOleCular meDICine 42: 479-488, 2018 Thromboxane A2 receptor antagonist SQ29548 attenuates SH‑SY5Y neuroblastoma cell impairments induced by oxidative stress GAOYU CAI1*, AIJUAN YAN2*, NINGZHEN FU3 and YI FU1 1Department of Neurology, Rui Jin Hospital, Shanghai Jiao Tong University, Shanghai 200025; 2Department of Neurology, Xin Hua Hospital, Shanghai Jiao Tong University, Shanghai 200082; 3Department of Pancreatic Surgery, Rui Jin College of Clinical Medicine, Rui Jin Hospital, Shanghai Jiao Tong University, Shanghai 200025, P.R. China Received September 28, 2017; Accepted March 21, 2018 DOI: 10.3892/ijmm.2018.3589 Abstract. Thromboxane A2 receptor (TXA2R) serves a vital SQ29548, an antagonist of TXA2R, improved the antioxidant role in numerous neurological disorders. Our previous study capacities of SH-SY5Y cells and reduced the cell apoptosis indicated that SQ29548, an antagonist of TXA2R, attenuated through the inhibition of MAPK pathways. the induced neuron damage in cerebral infarction animals; however, the underlying mechanism remains unknown. Introduction Certain studies revealed a new role of TXA2R in the regula- tion of oxidative stress, which is one of the basic pathological Thromboxane A2 receptor (TXA2R), a member of the G processes in neurological disorders. Thus, the present study protein-coupled receptor family (1), is broadly distributed attempted to examine whether the inhibition of TXA2R with in platelets (2), as well as epithelial (3), smooth muscle (4), SQ29548 helped to protect the nerve cells against oxidative glial and nerve cells in the brain (5). TXA2R is regarded as a stress. SQ29548 was utilized as a TXA2R antagonist, and traditional coagulation and inflammation‑associated receptor, relevant assays were performed to detect the cell viability, which is also closely associated with neurological disorders. -
Información Técnica-Científica Internacional. Relación Del Calostro Bovino Y/O Sus Ingredientes Como Suplemento Alimenticio En Diversas Enfermedades
Información técnica-científica internacional. Relación del calostro bovino y/o sus ingredientes como suplemento alimenticio en diversas enfermedades Nota: El calostro bovino no es un medicamento ni está clasificado como tal, tampoco está demostrado medicamente que cure o alivie ninguna enfermedad. El uso y el consumo de calostro bovino es una decisión personal y es responsabilidad de quien lo recomienda y de quien lo usa. Estos trabajos aquí incluidos son responsabilidad exclusiva de (los) autor(es) y son presentados con la única intención de educar y como tópicos de interés general, no es intención de la compañía presentarlos como consejo o soporte médico por lo tanto la compañía Schutze-Segen no es responsable en ningún sentido de su contenido. Alergias LeFranc-Millot C, Vercaigne-Marko D, Wal J. -M, et al. (1996) Comparison of the IgE titers to bovine colostral G immunoglobulins and the F(ab')2 fragments in sera of patients allergic to milk. Int Arch Allergy Immunol. 110:156-162. Savilahti E, Tainio VM, Salmenpera L, Arjomaa P, Kallio M, Perheentupa J, Siimes MA. (1991) Low colostral IgA associated with cow's milk allergy. Acta Pediatr Scan. 80:1207-1213. Selo I, Clement G, Bernard H, et al. (1999) Allergy to bovine B-lactoglobulin: specificity of human IgE to tryptic peptides. Clinical and Experimental Allergy. 29:1055-1063. Delespesse, G. Polypeptide factors from colostrum. US Patent #5,371,073 (1994). IgE (the immunoglobulin involved in allergic response) binding factors (IgE-bf) and IgE suppressor activity (IgE-SF) obtained from colostrum have been successfully used to treat allergies. Collins, AM, et al. -
Development of a Quantitative PCR Assay for the Detection And
bioRxiv preprint doi: https://doi.org/10.1101/544247; this version posted February 8, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Development of a quantitative PCR assay for the detection and enumeration of a potentially ciguatoxin-producing dinoflagellate, Gambierdiscus lapillus (Gonyaulacales, Dinophyceae). Key words:Ciguatera fish poisoning, Gambierdiscus lapillus, Quantitative PCR assay, Great Barrier Reef Kretzschmar, A.L.1,2, Verma, A.1, Kohli, G.S.1,3, Murray, S.A.1 1Climate Change Cluster (C3), University of Technology Sydney, Ultimo, 2007 NSW, Australia 2ithree institute (i3), University of Technology Sydney, Ultimo, 2007 NSW, Australia, [email protected] 3Alfred Wegener-Institut Helmholtz-Zentrum fr Polar- und Meeresforschung, Am Handelshafen 12, 27570, Bremerhaven, Germany Abstract Ciguatera fish poisoning is an illness contracted through the ingestion of seafood containing ciguatoxins. It is prevalent in tropical regions worldwide, including in Australia. Ciguatoxins are produced by some species of Gambierdiscus. Therefore, screening of Gambierdiscus species identification through quantitative PCR (qPCR), along with the determination of species toxicity, can be useful in monitoring potential ciguatera risk in these regions. In Australia, the identity, distribution and abundance of ciguatoxin producing Gambierdiscus spp. is largely unknown. In this study we developed a rapid qPCR assay to quantify the presence and abundance of Gambierdiscus lapillus, a likely ciguatoxic species. We assessed the specificity and efficiency of the qPCR assay. The assay was tested on 25 environmental samples from the Heron Island reef in the southern Great Barrier Reef, a ciguatera endemic region, in triplicate to determine the presence and patchiness of these species across samples from Chnoospora sp., Padina sp. -
Treatment Protocol Copyright © 2018 Kostoff Et Al
Prevention and reversal of Alzheimer's disease: treatment protocol Copyright © 2018 Kostoff et al PREVENTION AND REVERSAL OF ALZHEIMER'S DISEASE: TREATMENT PROTOCOL by Ronald N. Kostoffa, Alan L. Porterb, Henry. A. Buchtelc (a) Research Affiliate, School of Public Policy, Georgia Institute of Technology, USA (b) Professor Emeritus, School of Public Policy, Georgia Institute of Technology, USA (c) Associate Professor, Department of Psychiatry, University of Michigan, USA KEYWORDS Alzheimer's Disease; Dementia; Text Mining; Literature-Based Discovery; Information Technology; Treatments Prevention and reversal of Alzheimer's disease: treatment protocol Copyright © 2018 Kostoff et al CITATION TO MONOGRAPH Kostoff RN, Porter AL, Buchtel HA. Prevention and reversal of Alzheimer's disease: treatment protocol. Georgia Institute of Technology. 2018. PDF. https://smartech.gatech.edu/handle/1853/59311 COPYRIGHT AND CREATIVE COMMONS LICENSE COPYRIGHT Copyright © 2018 by Ronald N. Kostoff, Alan L. Porter, Henry A. Buchtel Printed in the United States of America; First Printing, 2018 CREATIVE COMMONS LICENSE This work can be copied and redistributed in any medium or format provided that credit is given to the original author. For more details on the CC BY license, see: http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License<http://creativecommons.org/licenses/by/4.0/>. DISCLAIMERS The views in this monograph are solely those of the authors, and do not represent the views of the Georgia Institute of Technology or the University of Michigan. This monograph is not intended as a substitute for the medical advice of physicians. The reader should regularly consult a physician in matters relating to his/her health and particularly with respect to any symptoms that may require diagnosis or medical attention. -
Airway Inflammation Mitochondrial Dysfunction Increases Allergic
Mitochondrial Dysfunction Increases Allergic Airway Inflammation Leopoldo Aguilera-Aguirre, Attila Bacsi, Alfredo Saavedra-Molina, Alexander Kurosky, Sanjiv Sur and Istvan This information is current as Boldogh of October 1, 2021. J Immunol 2009; 183:5379-5387; Prepublished online 28 September 2009; doi: 10.4049/jimmunol.0900228 http://www.jimmunol.org/content/183/8/5379 Downloaded from References This article cites 61 articles, 11 of which you can access for free at: http://www.jimmunol.org/content/183/8/5379.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 • Fast Publication! 4 weeks from acceptance to publication by guest on October 1, 2021 *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 © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Mitochondrial Dysfunction Increases Allergic Airway Inflammation1 Leopoldo Aguilera-Aguirre,*§ Attila Bacsi,*¶ Alfredo Saavedra-Molina,§ Alexander Kurosky,† Sanjiv Sur,‡ and Istvan Boldogh*2 The prevalence of allergies and asthma among the world’s population has been steadily increasing due to environmental factors.