Reproductive Health Guideline Appendix 3 – Search Strategies

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Reproductive Health Guideline Appendix 3 – Search Strategies

SUPPLEMENTARY APPENDIX 3: Search Strategies 2020 American College of Rheumatology Guideline for the Management of Reproductive Health in Rheumatic and Musculoskeletal Diseases All searches initially run on 11/8/2017 and updated on 5/8/2018. Searches run from database inception to 5/8/2018. PUBMED Syntax Guide for PubMed [MeSH] = Medical Subject Heading [Text Word] = Includes all words and numbers in the title, abstract, other abstract, MeSH terms, MeSH Subheadings, Publication Types, Substance Names, Personal Name as Subject, Corporate Author, Secondary Source, Comment/Correction Notes, and Other Terms - typically non-MeSH subject terms (keywords)…assigned by an organization other than NLM [MeSH subheading] = a Medical Subject [Title/Abstract] = Includes words in the title Heading subheading, e.g.

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The Effects of Targeted Deletion of the Aromatase Enzyme on Prostatic Contractile Responses to Noradrenaline in Mice
495 The effects of targeted deletion of the aromatase enzyme on prostatic contractile responses to noradrenaline in mice Katherine T Gray, Jennifer L Short, Evan R Simpson1 and Sabatino Ventura Prostate Research Co-operative, Victorian College of Pharmacy, Monash University, 381 Royal Parade, Parkville, Victoria 3052, Australia 1Prince Henry’s Institute of Medical Research, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia (Correspondence should be addressed to S Ventura; Email: [email protected]) Abstract This investigation aimed to see whether a change in the concentration-dependent contractions. Prazosin (0.3 mM) oestrogen to androgen ratio alters prostate contractility. Isolated attenuated the responses induced by noradrenaline and EFS in organ bath studies using prostates from aromatase knockout all mice (P%0.019, nZ5–7), while cocaine (10 mM) attenuated (ArKO) mice which were homozygous (ArKOK/K)and the responses evoked by tyramine (P!0.001, nZ6). There were heterozygous (ArKOC/K) for the disrupted aromatase cyp19 no genotype differences in EFS- and noradrenaline-induced gene and wild-type littermates (ArKOC/C) were conducted. responses (PR0.506, nZ10–13). Prostates from ArKOK/K The distribution of noradrenergic nerves was visualized using and ArKOC/K mice were more sensitive to tyramine than the sucrose–potassium phosphate–glyoxylic acid method. prostates from ArKOC/C mice (P!0.001, nZ11–13). Dense ArKOK/K mice had increased prostate weights compared adrenergic innervation of the prostate was similar in all mice. with ArKOC/C mice. Frequency–response curves to electrical These results suggest that although the absence of aromatase ﬁeld stimulation (EFS; 0.5 ms pulse duration, 60 V,0.1–20 Hz) increases prostatic growth, this translates only to a subtle and yielded frequency-dependent contractions, while noradrenaline selective increase in contractility in mature mice.
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Supplementary Appendix 1. Search Strategy for the Systematic Review and Meta-Analysis
BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) Thorax Supplementary Appendix 1. Search strategy for the systematic review and meta-analysis # COVID-19 AND (ACEI or ARB) Pubmed #1. COVID-19 ((((novel[Title/Abstract]) AND (((corona[Title/Abstract]) AND virus[Title/Abstract]) OR (coronavirus[Title/Abstract]))) OR ((COVID[Title/Abstract]) OR (COVID-19[Title/Abstract]) OR (nCoV[Title/Abstract]) OR (2019-nCoV[Title/Abstract]) OR (Novel Coronavirus Pneumon.ia[Title/Abstract]) OR (NCP[Title/Abstract]) OR (severe acute respiratory infection[Title/Abstract]) OR (SARI[Title/Abstract]) OR (SARS-CoV-2[Title/Abstract]))) #2. ARB (("Angiotensin Receptor Antagonists"[Mesh]) OR (((angiotensin receptor blocker[Title/Abstract]) OR angiotensin receptor blockers[Title/Abstract]) OR ARB.*[Title/Abstract]) OR (((angiotensin[Title/Abstract]) AND receptor[Title/Abstract]) AND (antagonist.*[Title/Abstract] OR inhibitor.*[Title/Abstract] OR blocker.*[Title/Abstract]))) OR (ARB[Title/Abstract]) OR (olmesartan[Title/Abstract]) OR (valsartan[Title/Abstract]) OR (eprosartan[Title/Abstract]) OR (irbesartan[Title/Abstract]) OR (candesartan[Title/Abstract]) OR (losartan[Title/Abstract]) OR (telmisartan[Title/Abstract]) OR (azilsartan[Title/Abstract]) OR (tasosartan[Title/Abstract]) OR (embusartan[Title/Abstract]) OR (forasartan[Title/Abstract]) OR (milfasartan[Title/Abstract]) OR (saprisartan[Title/Abstract]) OR (zolasartan[Title/Abstract])
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New Rules Pertaining to the Banning of Anabolic Steroids in the Western Australian Harness Racing Industry to Be Introduced 1St September 2014
NEW RULES PERTAINING TO THE BANNING OF ANABOLIC STEROIDS IN THE WESTERN AUSTRALIAN HARNESS RACING INDUSTRY TO BE INTRODUCED 1ST SEPTEMBER 2014 Notice is hereby given that the Board of Racing and Wagering WA have resolved that the RWWA Rules of Harness Racing 2004 be amended. In accordance with section 45 (1) (b) of the Racing and Wagering Western Australia Act 2003 the Board of Racing and Wagering WA on the 10th April 2014 resolved that these amendments be adopted accordingly into the RWWA Rules of Harness Racing. The Harness Racing Board had advised of these amendments and the RWWA Board has determined that these amendments will come into effect on 1st September 2014. The details of the relevant rules pertaining to this ban of anabolic steroids for reference can be found following this advice. There are many implications arising from the introduction of these rules, and to assist trainers and veterinarians to comply with the new rules the following explanatory statement has been prepared. Which steroids are banned under these rules? The new rules ban the use of "anabolic androgenic steroids" in Standardbred horses at any time from birth until retirement. "Anabolic androgenic steroids" include those that are currently registered in Australia by the APVMA for use in horses, such as boldenone, ethylestrenol (in Nitrotain), methandriol, nandrolone, stanozolol and testosterone. Exogenous anabolic androgenic steroids that are banned also include but are not limited to those listed in the WADA prohibited list, such as 1-androstenediol; 1-androstenedione;
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Azathioprine in Connective Tissue Disease-Associated Interstitial Lung Diseases
Disease ng s u & Aldehaim et al., Lung Dis Treat 2019, 5:1 L T f r o e a l t DOI: 10.4172/2472-1018.1000132 a m n r e u n o t J Journal of Lung Diseases & Treatment ISSN: 2472-1018 Research Article Open Access Azathioprine in Connective Tissue Disease-Associated Interstitial Lung Diseases. How Valuable? Aldehaim AY1*, AboAbat A1,2 and Alshabanat A1,3 1Department of Medicine, King Saud University, Riyadh, Saudi Arabia 2Department of Medicine, University of Toronto, Toronto, Canada 3Department of Medicine, McMaster University, Hamilton, Canada Abstract Objective: To systematically review the use of azathioprine as a treatment for connective tissue disease- associated interstitial lung disease (CTD-ILD) in terms of effectiveness and safety. Materials and methods: A literature search was performed using the PubMed, EMBASE, CINAHL, Cochrane, and Scopus databases. The search was restricted to articles published in English from 1950 to March 2018 that examined the use of azathioprine in patients with CTD-ILD and determined its effects on a primary or secondary endpoint. This review included studies that measured the impacts of azathioprine in terms of effectiveness and safety. Results: The search identified 15 studies with a total of 424 subjects. Two hundred twenty patients received azathioprine. A majority of the studies failed to provide clear evidence for the effectiveness of azathioprine. The reported adverse events were: death 4.5% (n=10), infection 1.3% (n=3), myelosuppression 0.9% (n=2), and malignancy 0.45% (n=1). The rate of azathioprine discontinuation due to treatment failure was 2.7% (n=6).
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Predictive QSAR Tools to Aid in Early Process Development of Monoclonal Antibodies
Predictive QSAR tools to aid in early process development of monoclonal antibodies John Micael Andreas Karlberg Published work submitted to Newcastle University for the degree of Doctor of Philosophy in the School of Engineering November 2019 Abstract Monoclonal antibodies (mAbs) have become one of the fastest growing markets for diagnostic and therapeutic treatments over the last 30 years with a global sales revenue around $89 billion reported in 2017. A popular framework widely used in pharmaceutical industries for designing manufacturing processes for mAbs is Quality by Design (QbD) due to providing a structured and systematic approach in investigation and screening process parameters that might influence the product quality. However, due to the large number of product quality attributes (CQAs) and process parameters that exist in an mAb process platform, extensive investigation is needed to characterise their impact on the product quality which makes the process development costly and time consuming. There is thus an urgent need for methods and tools that can be used for early risk-based selection of critical product properties and process factors to reduce the number of potential factors that have to be investigated, thereby aiding in speeding up the process development and reduce costs. In this study, a framework for predictive model development based on Quantitative Structure- Activity Relationship (QSAR) modelling was developed to link structural features and properties of mAbs to Hydrophobic Interaction Chromatography (HIC) retention times and expressed mAb yield from HEK cells. Model development was based on a structured approach for incremental model refinement and evaluation that aided in increasing model performance until becoming acceptable in accordance to the OECD guidelines for QSAR models.
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Future Research Needs Paper Number 8 Future Research Needs for Angiotensin Converting Enzyme Inhibitors or Angiotensin II Receptor Blockers Added to Standard Medical Therapy for Treating Stable Ischemic Heart Disease This report is based on research conducted by the Duke Evidence-based Practice Center (EPC) under contract to the Agency for Healthcare Research and Quality (AHRQ), Rockville, MD (Contract No. 290-2007-10066-I). The findings and conclusions in this document are those of the author(s), who are responsible for its contents; the findings and conclusions do not necessarily represent the views of AHRQ. Therefore, no statement in this report should be construed as an official position of AHRQ or of the U.S. Department of Health and Human Services. The information in this report is intended to help health care researchers and funders of research make well-informed decisions in designing and funding research and thereby improve the quality of health care services. This report is not intended to be a substitute for the application of scientific judgment. Anyone who makes decisions concerning the provision of clinical care should consider this report in the same way as any medical research and in conjunction with all other pertinent information, i.e., in the context of available resources and circumstances. This report may be used, in whole or in part, as the basis for research design or funding opportunity announcements. AHRQ or U.S. Department of Health and Human Services endorsement of such derivative products may not be stated or implied. This information does not represent and should not be construed to represent a determination or policy of the Agency for Healthcare Research and Quality or the U.S.
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Role of Thrombin and Thromboxane A2 in Reocclusion Following Coronary
Proc. Natl. Acad. Sci. USA Vol. 86, pp. 7585-7589, October 1989 Medical Sciences Role of thrombin and thromboxane A2 in reocclusion following coronary thrombolysis with tissue-type plasminogen activator (thrombolytic therapy/coronary thrombosis/platelet activation/reperfusion) DESMOND J. FITZGERALD*I* AND GARRET A. FITZGERALD* Divisions of *Clinical Pharmacology and tCardiology, Vanderbilt University, Nashville, TN 37232 Communicated by Philip Needleman, June 28, 1989 (receivedfor review April 12, 1989) ABSTRACT Reocclusion of the coronary artery occurs against the prothrombinase formed on the platelet surface after thrombolytic therapy of acute myocardlal infarction (13) and the neutralization ofheparin by platelet factor 4 (14) despite routine use of the anticoagulant heparin. However, and thrombospondin (15), proteins released by activated heparin is inhibited by platelet activation, which is greatly platelets. enhanced in this setting. Consequently, it is unclear whether To address the role of thrombin during coronary throm- thrombin induces acute reocclusion. To address this possibility, bolysis, we have examined the effect of a specific thrombin we examined the effect of argatroban {MCI9038, (2R,4R)- inhibitor, argatroban {MCI9038, (2R,4R)-4-methyl-1-[N-(3- 4-methyl-l-[Na-(3-methyl-1,2,3,4-tetrahydro-8-quinolinesulfo- methyl-1,2,3,4-tetrahydro-8-quinolinesulfonyl)-L-arginyl]-2- nyl)-L-arginyl]-2-piperidinecarboxylic acid}, a specific throm- piperidinecarboxylic acid} on the response to tissue plasmin- bin inhibitor, on the response to tissue-type plasminogen ogen activator (t-PA) in a closed-chest canine model of activator in a dosed-chest canine model of coronary thrombo- coronary thrombosis. MCI9038, an argimine derivative which sis. MCI9038 prolonged the thrombin time and shortened the binds to a hydrophobic pocket close to the active site of time to reperfusion (28 + 2 min vs.
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Stroke Prevention in Chronic Kidney Disease Disclosures
5/18/2020 Controversies: Stroke Prevention in Chronic Kidney Disease Wei Ling Lau, MD FASN FAHA FACP Assistant Professor, Nephrology University of California, Irvine Visiting Fellow at OptumLabsCOPY Disclosures • Prior or current research funding from NIH, AHA, Sanofi, ZS Pharma, and Hub Therapeutics. • Associate Medical Director for home peritoneal dialysis at Fresenius University Dialysis Center of Orange. • Has beenNOT on Fresenius medical advisory board for Velphoro. • No conflicts of interest relevant to the current talk. Controversies: Stroke prevention in CKD Wei Ling Lau, MD DO 1 5/18/2020 Stroke Prevention in CKD • Blood pressure targets • Antiplatelet agents • Statins • Anticoagulation Controversies: Stroke prevention in CKD Wei Ling Lau, MD COPY BP TARGETS Data is limited, as patients with CKD were historically excluded from clinical trials NOT Whelton 2017 ACC/AHA hypertension guidelines [Hypertension 2018] Controversies: Stroke prevention in CKD Wei Ling Lau, MD DO 2 5/18/2020 Systolic Blood Pressure Intervention Trial SPRINT: BP lowering to <120 vs <140 mmHg significantly lowered rate of CVD composite primary outcome; no clear effect on stroke Controversies: Stroke prevention in CKD The SPRINT Research Group. N Engl J Med 2015 p2103 Wei Ling Lau, MD COPY SPRINT subgroup analysis: CKD • Patients with CKD stage 3‐4 (eGFR of 20 to <60) comprised 28% of the SPRINT study population • Intensive BP management seemed to provide the same benefits for reduction in the CVD composite primary outcomeNOT – but did not impact stroke Controversies: Stroke prevention in CKD Cheung 2017 J Am Soc Nephrol p2812 Wei Ling Lau, MD DO 3 5/18/2020 The hazard of incident stroke associated with systolic BP (SBP) and chronic kidney disease (CKD)BP using and an unadjusted stroke model risk: that contained J‐shaped dummy variables association for CKD and BP groups (A) and a fully adjusted model that contained dummy variables for CKD and BP grou..
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Endocrine Disrupting Compounds and Prostate Cell Proliferation
Review Article Clinics in Oncology Published: 18 Oct, 2016 Endocrine Disrupting Compounds and Prostate Cell Proliferation Joubert Banjop Kharlyngdoh and Per-Erik Olsson* Department of Biology, Örebro University, Sweden Abstract Epidemiological, in vitro and animal studies have indicated that Endocrine Disrupting Compounds (EDCs) influence the normal growth and development of the prostate as well as development and progression of prostate cancer. This has been linked to an increased presence of environmental chemicals that interfere with hormonal signaling. Many of these effects appear to be associated with interferences with steroid hormone receptor signaling or by affecting steroidogenesis. Currently, there is abundant evidence from epidemiological studies linking pesticides and EDCs with elevated prostate cancer risk. Bisphenol-A, a known EDC, has been shown to promote induction of Prostate Specific Antigen (PSA), which is a biomarker for prostate cancer, in the LNCaP human prostate carcinoma cells, and to increase prostate carcinogenesis in animal models. Our research has focused on AR signaling and identification of novel androgenic and anti-androgenic EDCs. Using prostate cancer cell lines we have shown that the AR agonist, TBECH, and antagonist ATE, which is also a partial ART877A agonist, induce PSA expression. With the increasing presence of these EDCs in indoor and outdoor air, follows an increased risk of disturbed prostate development, regulation and function. Hence, identification of the contribution of EDCs to prostate cancer
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Classification Decisions Taken by the Harmonized System Committee from the 47Th to 60Th Sessions (2011
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