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Priera

Category: Other

Description

Hyaluronic Acid provides support for healthy joint function and maintaining joint shock absorption and cushioning. It works by acting as a cushion and lubricant in the joints and other tissues. In addition, it might affect the inflammatory response of the body.

Active Ingredient: hyaluronic acid

Hyaluronic Acid (Priera) as known as: Adant, Admac, Altergen, Amo vitrax, Amvisc, Arhealo, Artelac, Artflex, Arthrease, Artroject, Artz, Artzal, Athlikan, Atopiclair, Biolan, Biolon, Bionect, Bonal, Condrox, Connettivina, Corpus vitreum, Curavisc, Curiosin, Cystistat, Discovisc, Dropstar, Dropyal, Duovisc, Durolane, Endogel, Enhance, Equinate, Equron, Euflexxa, Exoline, Eyecare, Eyecon, Eyestil, Fermathron, Fermavisc, Gelbag, Gelclair, Gengigel, Genteal ha, Gonilert, Griolon, Halo, Halonix, Harison, Healon, Hialid, Hikamilon, Hivisco, Husren, Hy-drop, Hya-ject, Hya-ophtal, Hyabak, Hyaguard, Hyal, Hyal-system, Hyalart, Hyalastine, Hyalectine, Hyalein, Hyalgan, Hyalistil, Hyalomb, Hyalona, Hyalonsan, Hyaloph, Hyalos, Hyalovet, Hyalubrix, Hyaludermin, Hyalulod, Hyaluope, Hyalur, Hyaluron hexal, Hyaluronate, Hyalutowa, Hyasol, Hycosan, Hylan, Hylartil, Hylartin, Hylatril, Hylnate, Hylo-care, Hylo-care nasenspray, Hylo-comod, Hylo-lasop, Hylo-parin, Hylo-vision, Hyonate, Hysan, Hysan-baby, Hyvisc, Ial, Ialugen, Ialurex, Intragel, Irilens, Juvederm, Lacrycon, Lagricel, Lagricel ofteno, Laservis, Legend, Lghyal, Lumisteron, Lydium, Maxiostenil, Megacrom, Miniostenil, Monovisc, Neovisc, Nicozet, Nidelon, Nv halo, Oculocrom, Opegan, Opelead, Opelead hv, Ophtalin, Ophthalin, Orthovisc, Osflex, Oxyal, Phosbiron, Piones, Polireumin, Priera, Provisc, Sanorine, Sifi, Sinovial, Solpent, Sportvis, Suplasyn, Suprahyal, Suvenyl, Synacid, Synocrom, Synopsis, Synvisc, Tearbalance, Twinvisc, Unihylon, Viscoat, Viscoking, Viscoseal, Visiol, Vislube, Vismed, Visthesia, Vitadrop, Vitrax, Xclair, Xidan edo, Zonaker

Chronic Diseases Summit (3-4 April 2014) - European Commission

European Commission
Public health
Chronic Diseases Summit (3-4 April 2014) Brussels, 3-4 April 2014 About the Conference

This first EU summit on chronic diseases discussed medical, social and economic benefits of sustainable investments in health, ways to reduce the burden of chronic diseases, and how to strengthen the prevention and management of chronic diseases, with a focus on EU added value and action.

Objectives

The first EU summit on chronic diseases brought together key policymakers, stakeholders and interest groups to explore ways to address chronic diseases effectively in the EU and to develop recommendations along the following questions:

  1. How does the expanding burden of chronic diseases affect the quality of life of citizens, the competitiveness of economies and the cohesion of societies and what can the EU do about it?
  2. How can the pressure of the expanding burden of chronic diseases on health systems be reduced and how can available resources be invested in the most efficient way?
  3. Which prevention measures are the most cost-effective in the short and in the long term, and how could they be implemented? How should the EU and its Member States promote their implementation? Which risk factors need to be addresses more efficiently?
  4. How do the health and care systems need to change to respond to the ageing challenge and growing phenomena of frailty and multi-morbidity?
  5. How to best reach, include and empower the most vulnerable and marginalised people successfully in prevention and care strategies?
  6. How could the European Union support Member States’ attempts towards containing the chronic disease burden? Which EU action would provide most added value – in economic, social and political terms?

The summit will develop Conference conclusions and a set of policy recommendations for action clarifying on how the medical, social and economic burden of chronic diseases should be tackled in the European Union now and in the years to come.

Participants

The number of participants was around 450. The conference brought together representatives of Member States, non-governmental organisations and other relevant stakeholders, professional groups, business operators, academics, and EU institutions.

Video recordings

The Conference was broadcast online:

Watch the video recordings.

Presentations

Other articles

Animal and plant health

Animal and plant health Display type: News story From: Veterinary Medicines Directorate Updated: 25 April 2016
  • Display type: News story From: Department for Environment, Food & Rural Affairs Updated: 22 April 2016
  • Display type: Detailed guide From: Department for Environment, Food & Rural Affairs and 1 others Updated: 20 April 2016
  • Display type: Guidance From: Department for Environment, Food & Rural Affairs and 1 others Updated: 19 April 2016
  • Display type: Detailed guide From: Veterinary Medicines Directorate Updated: 18 April 2016
  • Display type: Collection From: Department for Environment, Food & Rural Affairs and 1 others Updated: 15 April 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 15 April 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs Updated: 15 April 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 15 April 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 8 April 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 6 April 2016
  • Display type: Policy paper From: Department for Environment, Food & Rural Affairs Updated: 5 April 2016
  • Display type: Guidance From: Department for Environment, Food & Rural Affairs Updated: 5 April 2016
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  • Display type: Guidance From: Veterinary Medicines Directorate Updated: 1 April 2016
  • Display type: Detailed guide From: Veterinary Medicines Directorate Updated: 31 March 2016
  • Display type: Detailed guide From: Veterinary Medicines Directorate Updated: 31 March 2016
  • Display type: Detailed guide From: Department for Environment, Food & Rural Affairs and 1 others Updated: 31 March 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 24 March 2016
  • Display type: Form From: Centre for Environment, Fisheries and Aquaculture Science Updated: 22 March 2016
  • Display type: Policy paper From: Department for Environment, Food & Rural Affairs and 1 others Updated: 17 March 2016
  • Display type: Guidance From: Department for Environment, Food & Rural Affairs Updated: 8 March 2016
  • Display type: Form From: Centre for Environment, Fisheries and Aquaculture Science Updated: 24 February 2016
  • Display type: Speech From: Department for Environment, Food & Rural Affairs Updated: 23 February 2016
  • Display type: Transparency data From: Centre for Environment, Fisheries and Aquaculture Science Updated: 23 February 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 19 February 2016
  • Display type: Detailed guide From: Department for Environment, Food & Rural Affairs Updated: 19 February 2016
  • Display type: Consultation outcome From: Department for Environment, Food & Rural Affairs Updated: 19 February 2016
  • Display type: Consultation outcome From: Department for Environment, Food & Rural Affairs Updated: 19 February 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 12 February 2016
  • Display type: News story From: Department for Environment, Food & Rural Affairs and 1 others Updated: 12 February 2016
  • Display type: Collection From: Veterinary Medicines Directorate Updated: 26 January 2016
  • Display type: Notice From: Veterinary Medicines Directorate Updated: 26 January 2016
  • Display type: Research and analysis From: Veterinary Medicines Directorate Updated: 25 January 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 21 January 2016
  • Display type: Research and analysis From: Department for Environment, Food & Rural Affairs and 1 others Updated: 19 January 2016
  • Display type: Collection From: Department for Environment, Food & Rural Affairs and 4 others Updated: 31 December 2015
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    A Basic Guide to Pests and Diseases That Affect Bonsai

    A Basic Guide to Pests and Diseases That Affect Bonsai

    "Upon finding that I work as a professional bonsai artist, many people will remark that they once had a bonsai, but it died and with some regret, they gave up".

    Based on the Bonsai Basics section of the hugely successful Bonsai4me.com website and an e-book of the same name, 'Bonsai Basics: The Foundations of Bonsai', written and developed over the past 15 years is out now!

    All copies are signed by the author.

    Most species of shrubs or trees commonly used for bonsai cultivation rarely succumb to disease if looked after carefully and given the correct environment to grow in.

    Bugs can attack trees randomly though you quickly learn which are likely to become infested at a moments' notice! Healthy and vigorous trees are unlikely to be attacked, they will also be better equiped to survive if there are attacks from bugs and diseases. Trees in poor health or trees that are under stressful growing conditions will be more affected by any external attack on its weakened defences.

    Precautions, such as regular spraying with systemic insecticides and fungicides, can be useful though should not be relied upon. Systemic remedies work by being sprayed onto the foliage, which digests the treatment into the sap stream of the plant where it is distributed throughout the entire plant. Attacks of fungi or bugs are quelled when they attack the plant and are exposed to the treated sap.

    However, systemic treatments are not 100% effective, regular spraying is expensive, environmentally unsound; repeated use can also reduce the effectiveness of treatments when they are actually needed. In my opinion, it is far better to use systemic insecticides or fungicides only on trees that are known to suffer problems at certain times of the year.

    Primarily, try to identify what has happened to your tree. Has it lost foliage? Do any of the leaves have discolouration or holes? Closely examine the tree and the foliage, is there any evidence of pests either on the tree itself, on the surface of the compost or around the surface on which the pot itself is standing. Secondly, once (hopefully) the pest or disease is identified and dealt with, it is important to identify if there is any way that you could prevent re-occurrence in the future. Some problems such as caterpillars and aphids are difficult to guard against, although you should be able to anticipate which trees in your collection are more likely to be attacked.

    Yellowing Leaves/Dropping Leaves

    There are only 3 ways that a healthy tree with healthy foliage will suddenly lose leaves or have leaves that suddenly turn dry and crispy (over just 2 or 3 days):

    Frost. a tropical and subtropical species being exposed to frost.

    Poison. the bonsai is exposed to a poisonous chemical either in the soil or the air (directly onto the foliage). Though very rare, it isn't unknown for a tree to be badly affected when accidentally exposed to drifting spray from weedkiller use.

    Yellowing leaves and/or dropping leaves can occur for a number of different reasons;

    Chlorosis is caused by a mineral deficiency and is due to a lack of magnesium, manganese or iron. It usually only affects acid-loving species such as Azaleas. Administer a liquid fertiliser that contains trace mineral elements easily available at all garden centres. Acid-loving species such as Azaleas can (and should) be fed ericaceous-fertilizers that contain easily-absorbed sequestered iron on a routine basis.

    Die-back and yellowing leaves nearly always end up dying and falling off the tree unless the cause is Chlorosis, this is likely to be dieback of the foliage. Die-back of large areas of the tree can occur when a tree is traumatised for some reason and the tree responds by dropping any foliage that is not required for its survival. The cause is often due to damage to the rootsystem by root rot through over-watering or lack of watering which has allowed the root system to dry out. Some species (particularly tropical indoor varieties) can also become stressed by moving a tree to a new position, and they will loose their foliage. (See sections on root rot and underwatering.)

    ©Harry Harrington 2016. All articles and images by Harry Harrington unless otherwise indicated. Use of Text or Images contained within this website is strictly prohibited without the express permission of Harry Harrington.

    Ischemic heart disease

    Metlyaeva N.A. Lartsev M.A. Shcherbatykh O.V. Bushmanov A.Yu. Krasnyuk V.I. - Saratov Journal of Medical Scientific Research. 2014

    Purpose: assessment the heavy psychosomatic and all-somatic cardiovascular and cerebrovascular pathology of patient, transferred an acute I degree radiation sickness, from the general evenly gamma-beta radiation. Conclusions. The subdepressive and.

    Purpose: assessment the heavy psychosomatic and all-somatic cardiovascular and cerebrovascular pathology of patient, transferred an acute I degree radiation sickness, from the general evenly gamma-beta radiation. Conclusions. The subdepressive and disturbing-depressive syndrome of patient, transferred an acute radiation sickness (ARS) of I degree, from the general evenly gamma-beta radiation, was independent risk factor of development of multifocal atherosclerosis; Features of development of all-somatic and psychosomatic pathology of patient are based on a combination of genetic prerequisites, environment influences (the stress caused by accident on the ChNPP) and social factors, influencing on him during a course of life, especially during early socialization. Thus at development of psychosomatic frustration the combination of feature of the mental reaction connected with the personal characteristic and special relationship between mental (stress) and physiological (somatic) by aspects of reaction which led to metabolism violation, to aging, decrease in adaptation opportunities of an organism and development age — dependent pathology took place.
    Metlyaeva N.A. Lartsev M.A. Shcherbatykh O.V. Bushmanov A.Yu. Krasnyuk V.I. Multifocal atherosclerosis in patient after acute first degree radiation sickness. // Saratov Journal of Medical Scientific Research, Vol. 10, Issue 4, 2014, pp. 862-867

    The aim of the article is to study the relation of chronic heart failure, cognitive disturbances and changes in white matter of brain. Material et methods: Cognitive tests, echocardiography, MRI of brain and measurement of NT-proBNP in venous.

    The article considers quality of life as an evaluation category of state of a subject in conditions of illness. The results of the research of quality of life relevant to health in patients with coronary heart disease are given in the work.

    Purpose: the study of interrelation between characteristics of psychological profile of elderly patients, level of stress hormones in blood serum and character of IHD course. Materials and Methods. The level of catecholamines and cortisol in blood.

    Chelnokova N.O. Golyadkina A.A. Schuchkina O.A. - Saratov Journal of Medical Scientific Research. 2011

    The review presents the features of modern viewpoints on the theory of atherosclerosis pathogenesis. The possibilities of mathematical modelling of hemodynamics in coronary arteries in consideration of their morphological parameters and.

    The review presents the features of modern viewpoints on the theory of atherosclerosis pathogenesis. The possibilities of mathematical modelling of hemodynamics in coronary arteries in consideration of their morphological parameters and relationship with myocardium are described
    Chelnokova N.O. Golyadkina A.A. Schuchkina O.A. Clinicopathologic basis of hemodynamics modelling in the system of coronary arteries in consideration of its interaction with myocardium (review) // Saratov Journal of Medical Scientific Research, Vol. 7, Issue 4, 2011, pp. 762-768

    Anemic syndrome of different severity often accompanies ischemic heart disease (IHD) and chronic heart failure (CHF). Anemia has association with unfavorable prognosis in patients with all forms of CVD — acute and chronic. In this article the.

    Vardosanidze S.L. Galstyan A.S. - Saratov Journal of Medical Scientific Research. 2010

    158 patients with ischemic heart disease (IHD) have been understudy during the period of 12 months in out-patient conditions. After completion of the primary examination all the patients of basic group (118 patients) received clinical way method.

    158 patients with ischemic heart disease (IHD) have been understudy during the period of 12 months in out-patient conditions. After completion of the primary examination all the patients of basic group (118 patients) received clinical way method of treatment. Patients of the comparison group (40 patients) after provided treatment were cared by their local therapeutists (cardiologists). The findings proved the fact that treatment of patients after cardiosurgery by clinical way method in out-patient conditions enabled to raise patient motivation to treatment, thereby assisting them to feel better, promoting normalization of arterial pressure data. The research results stated that clinical way method of treatment may be considered as rational and effective
    Vardosanidze S.L. Galstyan A.S. Clinical way method in treatment of out-patients with ischemic heart disease after cardiosurgery // Saratov Journal of Medical Scientific Research, Vol. 6, Issue 4, 2010, pp. 824-828

    The article presents the results of studies of life quality of patients with ischemic heart disease and old myocardial infarction. The life quality is considered as an independent and objective multifactor indicator reflecting the status of this.

    The article presents the research results on the correlation between anemic syndrome and main risk factors in hospitalized patients with different forms of cardiovascular pathologies. This category of patients is characterized by more severe.

    E.U. Eremina, E.V. Shipalkina - Saratov Journal of Medical Scientific Research. 2008

    The article is devoted to some aspects of influence of digestive apparatus diseases (chronic gastritis, a stomach ulcer, chronic cholecystitis) on clinical course ofischemic heart disease. It is revealed, thatthe patients with clinical.

    The article is devoted to some aspects of influence of digestive apparatus diseases (chronic gastritis, a stomach ulcer, chronic cholecystitis) on clinical course ofischemic heart disease. It is revealed, thatthe patients with clinical symptomatology are typically to have extra cardiac hue of painful heart attacks. The patients with influence ofischemic heartdisease and digestive apparatus disorders have sympathetic overbalance of the vegetative one against the background of the parasympathotonia.
    E.U. Eremina, E.V. Shipalkina SOME ASPECTS OF INFLUENCE OF DIGESTIVE ORGANS DISEASES ON CLINICAL COURSE OF ISCHEMIC HEART DISEASE // Saratov Journal of Medical Scientific Research, Vol. 4, Issue 1, 2008, pp. 122-127

    PRIMER ON THE RHEUMATIC DISEASES

    PRIMER ON THE RHEUMATIC DISEASES Este libro está en oferta. Los libros pueden ponerse en oferta por varios motivos:
    • Llevar demasiado tiempo en nuestro almacén sin venderse.
    • Tratarse de una edición que no es la última, existiendo otra posterior (comprobar Nº de edición y año).
    • Tener algún desperfecto como ligeros golpes (en ningún caso serán defectos que afecten al contenido, como falta de páginas, letra borrosa etc.)
    Existencias limitadas. Se servirán por orden de pedido hasta agotar stock.

    Puede encontrar libros similares en:

    About this textbook

    New and expanded chapters heighten the translational nature of the book
    Color figures depict cutaneous findings and histopathology
    An entire section devoted to juvenile inflammatory arthritis

    Arthritis and other rheumatic diseases are a leading cause of disability and affect more than 46 million Americans (including 300,000 children). The Primer is designed to provide up-to-date information about the major clinical syndromes. It is one of the most prestigious and comprehensive texts on arthritis and related diseases, including osteoarthritis, rheumatoid arthritis, osteoporosis, lupus and more than one hundred others. It offers medical students and physicians a concise description of the current science, diagnosis, clinical consequences, and principles of management.

    Now entering its eighth decade, the 13th Edition of The Primer strongly rejects the notion “If it ain’t broke, don’t fix it”. New and expanded chapters heighten the translational nature of this edition, and color figures depict cutaneous findings and histopathology.

    In view of the recent remarkable strides in understanding and treating rheumatic disease, students, trainees, and practicing clinicians all need a standard textbook that can change with the times and reflect these advances. The Primer continues to fill that need.

    Medical students and physicians

    Foreword by Michael E. Weinblatt
    Preface
    Contributors

    1. Public Health and Arthritis. A Growing Imperative - Patience H. White and Rowland W. Chang

    2. Evaluation of the Patient

    A. History and Physical Examination - David B. Robinson and Hani S. El-Gabalawy
    B. Laboratory Assessment - Kerstin Morehead
    C. Arthrocentesis, Synovial Fluid Analysis, and Synovial Biopsy - Kenneth H. Fye
    D. Imaging of Rheumatologic Diseases - William W. Scott, Jr. William J. Didie, and Laura M. Fayad

    3. Musculoskeletal Signs and Symptoms

    A. Monarticular Joint Disease - H. Ralph Schumacher and Lan X. Chen
    B. Polyarticular Joint Disease - Sterling West
    C. Neck and Back Pain - David Borenstein
    D. Regional Rheumatic Pain Syndromes - Joseph J. Biundo, Jr.
    E. The Fibromyalgia Syndrome - Dina Dadabhoy and Daniel J. Clauw

    4. Molecular and Cellular Basis of Immunity and Immunological Diseases - Kevin Elias, Richard Siegel, and John J. O’Shea

    5. Genetics and Disease - James Kelley and Robert P. Kimberly

    6. Rheumatoid Arthritis

    A. Clinical and Laboratory Manifestations
    B. Epidemiology, Pathology, and Pathogenesis - Jean-Marc Waldenburger and Gary S. Firestein
    C. Treatment and Assessment - Alyce M. Oliver and E. William St. Clair

    7. Juvenile Idiopathic Arthritis

    A. Clinical Features - Daniel J. Lovell
    B. Pathology and Pathogenesis - Patricia Woo
    C. Treatment and Assessment - Philip J. Hashkes and Ronald M. Laxer
    D. Special Considerations - Carol B. Lindsley

    8. Psoriatic Arthritis

    A. Clinical Features - Dafna D. Gladman
    B. Pathology and Pathogenesis - Christopher Ritchlin
    C. Treatment and Assessment - Philip J. Mease

    9. Ankylosing Spondylitis

    A. Clinical Features - Désirée Van der Heijde
    B. Pathology and Pathogenesis - Juergen Braun
    C. Treatment and Assessment - John C. Davis, Jr.

    10. Reactive and Enteropathic Arthritis - Robert D. Inman

    A. Clinical Features - Paul Dieppe
    B. Pathology and Pathogenesis - Francis Berenbaum
    C. Treatment - Leena Sharma

    A. Clinical Features - N. Lawrence Edwards
    B. Epidemiology, Pathology, and Pathogenesis - Hyon K. Choi
    C. Treatment - Robert A. Terkeltaub

    13. Calcium Pyrophosphate Dihydrate, Hydroxyapatite, and Miscellaneous Crystals - Geraldine McCarthy

    14. Infectious Disorders

    A. Septic Arthritis - George Ho, Jr.
    B. Viral Arthritis - Leonard H. Calabrese
    C. Lyme Disease - Linda K. Bockensted
    D. Mycobacterial, Fungal, and Parasitic Arthritis - Steven R. Ytterberg
    E. Rheumatic Fever - Stanford Shulman and Preeti Jaggi

    15. Systemic Lupus Erythematosus

    A. Clinical and Laboratory Features - Jill P. Buyon
    B. Epidemiology, Pathology, and Pathogenesis - David S. Pisetsky
    C. Treatment and Assessment - Susan Manzi and Amy H. Kao

    16. Antiphospholipid Syndrome - Michelle Petri

    17. Systemic Sclerosis

    A. Clinical Features - Maureen D. Mayes
    B. Epidemiology, Pathology, and Pathogenesis - John Varga
    C. Treatment and Assessment - Maya H. Buch and James R. Seibold

    18. Idiopathic Infl ammatory Myopathies

    A. Clinical Features - Robert L. Wortmann
    B. Pathology and Pathogenesis - Lisa G. Rider and Frederick W. Miller
    C. Treatment and Assessment - Chester V. Oddis

    19. Metabolic Myopathies - Alan N. Baer

    20. Sjögren’s Syndrome - Troy Daniels

    A. Giant Cell Arteritis, Polymyalgia Rheumatica, and Takayasu’s Arteritis - Cornelia M. Weyand and Jörg J. Goronzy
    B. Polyarteritis Nodosa - Keith T. Rott
    C. The Antineutrophil Cytoplasmic Antibody–Associated Vasculitides: Wegener’s Granulomatosis, Microscopic Polyangiitis, and the Churg–Strauss Syndrome - John H. Stone
    D. Immune Complex–Mediated Vasculitis - Philip Seo
    E. Miscellaneous Vasculitis (Behçet’s Disease, Primary Angiitis of the Central Nervous System, Cogan’s Syndrome, and Erythema Elevatum Diutinum) - Kenneth T. Calamia and Carlo Salvarani
    F. Kawasaki’s Disease

    22. Relapsing Polychondritis - Harvinder S. Luthra

    23. Adult-Onset Still’s Disease - John M. Esdaile

    24. Periodic Syndromes - John G. Ryan and Daniel L. Kastner

    25. Less Common Arthropathies

    A. Hematologic and Malignant Disorders - Adel G. Fam
    B. Rheumatic Disease and Endocrinopathies - Peter A. Merkel
    C. Hyperlipoproteinemia and Arthritis - Robert F. Spiera
    D. Neuropathic Arthropathy - Ann K. Rosenthal
    E. Dermatologic Disorders - Jeffrey P. Callen
    F. Hypertrophic Osteoarthropathy - Manuel Martinez-Lavin

    26. Complex Regional Pain Syndrome - Geoffrey Littlejohn

    27. Sarcoidosis - Edward S. Chen

    28. Storage and Deposition Diseases - Duncan A. Gordon

    29. The Amyloidoses - Pasha Sarraf and Jonathan Kay

    30. Neoplasms of the Joint - Andrew J. Cooper, James D. Reeves, and Sean P. Scully

    31. Heritable Disorders of Connective Tissue - Reed Edwin Pyeritz

    32. Bone and Joint Dysplasias - William A. Horton

    33. Osteonecrosis - Thorsten M. Seyler, David Marker, and Michael A. Mont

    34. Paget’s Disease of Bone - Roy D. Altman

    A. Epidemiology and Clinical Assessment - Kenneth G. Saag
    B. Pathology and Pathophysiology - Philip Sambrook
    C. Treatment of Postmenopausal Osteoporosis - Nelson B. Watts

    36. Rehabilitation of Patients with Rheumatic Diseases - Thomas D. Beardmore

    37. Psychosocial Factors in Arthritis - Alex Zautra and Denise Kruszewski

    38. Self-Management Strategies - Teresa J. Brady

    39. Pain Management - John B. Winfi eld

    40. Therapeutic Injections of Joints and Soft Tissues - Juan J. Canoso

    41. Nonsteroidal Anti-Infl ammatory Drugs - Leslie J. Crofford

    42. Glucocorticoids - Frank Buttgereit and Gerd-Rüdiger Burmester

    43. Operative Treatment of Arthritis - Joseph A. Buckwalter and W. Timothy Ballard

    44. Complementary and Alternative Therapies - Erin L. Arnold and William J. Arnold

    Appendix I. Criteria for the Classifi cation and Diagnosis of the Rheumatic Diseases

    Appendix II. Guidelines for the Management of Rheumatic Diseases

    Appendix III. Supplement and Vitamin and Mineral Guide

    Los precios no incluyen el I.V.A. | ©1998 - 2016 AXON Librería, S. L. | CIF B80790355

    Web www.axon.es | Email se.noxa@noxa | Tel (+34) 91 593 9999 | Fax (+34) 91 448 2188

    Raimundo Lulio 1 - 28010 Madrid - España

    Реферат на тему Diseases

    Diseases – Sex Linked And Sex Influenced Essay, Research Paper

    Diseases: Sex Linked and Sex InfluencedThere are thousands of cases of sex linked and sex influenced diseases worldwide. These diseases can range from a social inconvenience, to a fatal ailment. In sex linked diseases, like Muscular Dystrophy, hemophilia and color blindness, only males are affected. When a man infected with a sex linked disease has children, all his sons are normal, but all of his daughters are carriers. When a carrier woman and an uninfected man have children, half of the sons are normal, and half of the sons are affected; half of the daughters are carriers and half of the daughters are normal. Only males are affected because the sex linked diseases affect the X chromosome. Males have one X chromosome and one Y chromosome, so they need to use that X, whether it is flawed or not. Females on the other hand, have two X chromosomes, so if one is defective, they can use their second X chromosome. Duchenne+s Muscular Dystrophy(DMD) is defined as |a genetic disease characterized by defective muscle cells that can not produce a protein called dystrophinX (Science News 380). In patients of hemophilia, there is a deficiency of a protein needed for blood clotting, causing this hereditary bleeding disorder. In red/green color blindness, the broadest form of color blindness that affects six percent of the population, the cones in the retina that receive green light do not function properly. Unlike sex linked diseases, sex influenced diseases are not reserved solely for the male. However, the diseases occur in males much more frequently than in females. This is because sex influenced diseases occur from imbalances in testosterone, much more highly concentrated in males. Baldness and gout are two diseases that are a result of these hormonal imbalances. Baldness is defined as the lack or loss of hair. Permanent baldness strikes on a hereditary basis because the hormonal imbalances tend to be passed from generation to generation. Gout is a hereditary metabolic disorder that involves recurrent acute attacks of severe inflammation of joints. Sex linked diseases are born when sex genes, that compose two of the 46 chromosomes, are mutated by an error in copying genes in reproduction. One of these sex linked diseases is Duchenne+s Muscular Dystrophy. DMD is a disease that has rightfully been gaining some headlines recently, as the disease is taking the lives of young children. Several cures have been brought up recently in the medical society, but none have paid any dividends. According to the Muscular Dystrophy Association, one in every 2500 boys are infected with muscular dystrophy. The defective gene is found at the top of the X chromosome. This gene is the largest known to exist. In patients of DMD, this gene is either missing or severely mutilated. The symptoms of DMD are fatal. By age eleven, the victims weaken fast. Normally, muscle deterioration begins in the lower legs and then moves up the body of the patient. Generally, victims are in their early twenties when they die from either heart failure or diaphragm failure.(The diaphragm is the muscle that makes breathing possible.) One mother of a Duchenne+s Muscular Dystrophy patient says succinctly, |Eventually these kids get bedridden and then they die.X(Grady 87) It is imperative to find a cure for Duchenne+s Muscular Dystrophy so we can save the lives of thousands of innocent children. One of the major researchers working on a cure for DMD is Dr. Peter K. Law of the Cell Therapy Research Foundation. Law has been in the field for over twenty years and has made many discoveries. In 1972, Law+s doctoral thesis proved that dystrophic muscle cells have abnormal cell membranes. This showed that the disease was caused by a muscle defect, not a nerve defect as was previously thought. Since it was clear that it was a muscle defect, Law tried to transplant both whole and minced muscle into mice. The minced muscle proved to be too damaged to operate, and the whole muscle was so large that it died before an adequate blood and nerve supply was developed. At this point, since the whole muscle was too large but was the only feasible solution, he decided to transplant whole muscles of a baby mouse into an adult mouse. This muscle was not damaged, because it was not minced, and it was not too large, because the baby muscle is considerably smaller than an adult muscle. Not only did the mouse survive, but normal function was restored to diseased adult muscle. Since the transplantation of muscle in mice was so successful, Dr. Law tried to find something along those lines that would work in a human. He found a solution; myoblasts. A myoblast is a mature muscle cell. It is a long thin fiber that can be more than an inch long. Unlike cells of other types, myoblasts have over 200 nuclei. When they are damaged, the myoblasts call upon a reservoir of satellite cells; small immature cells that nestle inside the muscle fiber+s outer sheath. Satellite cells are the key to muscle repair and regeneration.The satellites leave the fiber, divide and then flatten into spindle shaped forms- the myoblasts. Myoblasts repair muscle cells by fusing with the injured cell and they share their nuclei with the injured cell+s nuclei. When these two myoblasts fuse completely, new cells are formed. In 1970 Law thought of a procedure that would fuse healthy myoblasts with the dystrophic one, hoping that the resulting hybrid would have some function. However, Law had to perfect this procedure. One of the main problems was that when the healthy myoblast cells were fused, the immune system would treat them as alien and attack them. According to Law, another thing they had to do was |… to design and perfect a culture medium to mass-produce myoblasts and weed out other cells.X(Grady 90) Law explains yet another problem encountered,|If you cram too many cells in the same spot, they might not survive.X(Grady 90)While Law was working on his myoblast experiments, another door was opened by the discovery of the exact gene that caused the dystrophy. Many scientists thought that this gene therapy, rather than Law+s cell therapy, was the future. But Law dismissed gene therapy saying, |To me, in reality, that science will not work in our lifetime. First you must make a normal copy of the defective gene, which is enormous, and somehow insert it into a small virus to carry it into the host. Then you must hope that the virus will attack the right cell in the body, get through the cell membrane, break into the nucleus, and splice itself into place inside the cell+s DNA. And then you expect that cell to function as normal? Are you kidding me?X(Grady 91-92) Law also made it clear that in gene therapy you have to replace the exact right nucleus in the exact right gene. In cell therapy, it doesn+t matter which is the exactly right one that needs replacement because all of the cells are being replaced. Just two years after he wrote off the gene therapy, in 1988,when the problems were weeded out, Law injected healthy myoblasts into 19 dystrophic mice. The results of these tests were encouraging; 11 mice fared extremely well, 3 showed moderate improvement and 5 rejected the myoblasts. Another encouraging fact was that the life span was increased from nine months to nineteen months in the mice that fared extremely well. With the success in the mice, Law decided to launch phase I of his human experiments. Each of three boys received four injections of myoblasts from either their brother+s body or their father+s body. In two of the boys, these injections, which were given in the foot, were matched in the other foot by placebo saline solutions so nobody except Law+s assistant would know which foot the real injections were placed. At the end of the experiment, all three boys said that they felt that one foot was stronger than the other. The foot that felt stronger was the same foot that was injected with the myoblasts in all three cases, and all three feelings of greater strength were backed up by muscle strength tests administered by Law. Although the results of Phase I seemed ideal, Law received some criticism from his peers. They said that he rushed too quickly into the human experiments without gaining complete assurance that it would work to perfection. Some scientists were concerned that the myoblast injection would have side-effects. The criticism was not publicized to a wide extent, and it went virtually unnoticed after Law made a statement in which he said, |We have to move the research forward as quickly as possible. These are dying children. We have no time to lose.X(Grady 88) In May 1991, after Phase I was considered to be a success, Law lunched Phase II. As of July 24, 1992 Law had treated the major leg muscle of 32 boys, ages 6 to 14. For this process, Law removes an eraser-sized piece of muscle from either the patients father or brother. Then, he grows the muscle in the lab until he has 5 million myoblasts. At the time of treatment, the patients go under general anesthesia for 10 minutes, and receive 48 injections of myoblasts in 22 muscle groups. All patients take cyclosporin, an immune system suppressive for six months to prevent the boys from rejecting the myoblasts. The muscle strength of each patient is recorded 3 months before treatment, at the time of treatment, and three months after treatment. This test was also successful. Muscle strength was reported to improve in 43% of the muscles by an average of 41% when compared to muscle strength before treatment. 38% of the muscles stopped deteriorating after treatment and 19% completely failed to respond.

    However, as in Phase I, Law+s success was accompanied with criticism. The major problem his peers had was that there were no controls. Says Robert H. Brown Jr. of Massachusetts General Hospital in Boston during one meeting session, |I am astonished that you haven+t controlled for cyclosporin.(Thompson 473) Law counters, |We have a perfect control, strength before and after transfer on the same muscle.X(Thompson 473) Law also says that the upper body of the patient acts as a control. Law says that another reason he does not use controls is because the saline solution is shown to speed up deterioration, and that would not be ethically correct. His opposition, however says that since he only had two patients with the placebo solution, so those results could not be verified. Another thing that was criticized was the use of muscle strength to measure the effectiveness. The three major components of the criticism is that the children may not be using full exertion, that when you get older your strength gets greater, and third, how do you know dystrophin produced this strength; what about the cyclosporin? The work done by Peter Law has been exemplary. He has found a method for prolonging the life of young DMD patients. Although the way Law went about his trials were controversial, moving as fast as possible is imperative because thousands of children are having their ability to walk, and eventually their lives taken away by this disease. If Law had waited, it may have been too late. Although there is a large controversy concerning Peter Law, the Muscular Dystrophy Association should support him and encourage him to perfect a cure for this disease.Another sex linked diseases that is similar to DMD in makeup, not in symptoms is hemophilia. In hemophiliacs, a protein that clots blood is missing or abnormal due to a gene mutation that was formed in the duplication of sex genes. The protein missing in hemophilia victims is antihemophilic globulin (AHG). Like in all sex linked diseases, only males can show symptoms, and females are the only carriers. The father of a hemophiliac may or may not be infected, but the mother must be a carrier. A hemophiliac has received his mother+s bad X chromosome and his father+s Y. The same couple can also have a normal son who received his mother+s good X and his father+s Y. If the couple has daughters she can receive her father+s X and her mother+s bad X, or mother+s good X. So, the chance of a hemophiliac boy being born when the mother is a carrier is one in four. Therefore the incidence of hemophilia is familial, as in the Russian royal family. In hemophiliacs ,the tendency to bleed becomes noticeable at a young age and leads to severe anemia or even death. Hemophiliacs often have large bruises and soft tissue of the skin from incidents as small as lightly bumping into something. This bruising is much like the bruising of the elderly. Not only will bruises form, but bleeding will often occur for no reason in the mouth, nose and gastrointestinal tract. Once the victim grows out of childhood, hemorrhages in knees. ankles, elbows and other joints occur frequently. These hemorrhages result in swelling which impairs the victim+s function. Hemophilia patients are generally advised to refrain from physical activity. When hemorrhages occur, local application such as thrombin are applied that serve as a blood clotting mechanism, or blood is transfused. A third type of a sex linked disease caused by a defective chromosome is color blindness. Red/green color blindness, the most common type that affects six percent of the population, is caused by defective green cones in the retina. People with red-green color deficiency see blue and orange very clear and bright. Other colors, although different from the colors that normal people see, are always the same to them and suit most victims fine because they have nothing to compare the colors they see to(USA Today 16). Like hemophilia, Duchenne+s Muscular Dystrophy and all sex linked diseases, only males suffer the symptoms, and the females are the carriers. Although color blindness is a disease that affects thousands of people, it is not a life-threatening disease. Most color blind people do not suffer, because they do not know that the color should be different. Few problems, like traffic lights, hinder color blind people, and as Cynthia Bradford, an opthamologist at the University of Oklahoma Health Sciences Center says, |With many people, you might not even know they+re color blind unless they tell youX(USA Today 16)Unlike sex linked diseases, sex influenced diseases do not affect one sex solely. Baldness, the lack or loss of hair, is caused by an imbalance of testosterone. Since it is caused by testosterone, much more concentrated in males, sex influenced diseases are much more common in males.This imbalance causes the destruction of hair follicles which causes the baldness to be permanent. The largest type of baldness is male-pattern baldness that affects forty percent of some male populations(Norton 2:826). Male-pattern baldness is hereditary, and varies in degree from generation to generation. Ironically, people with male pattern baldness have a higher percentage of body hair than most, and those Aborigines with male pattern baldness generally have bald calves as well. Although this disease is not life-threatening, baldness is a social problem. Almost every other man is a victim, and those who do suffer the disease are prejudiced. Solutions, not cures to baldness to exist. The first obvious option is the wig. Secondly, hair transplants are becoming more and more frequent, and topical solutions such as minoxidil have helped to prevent further balding in many cases, and reinitiate hair growth in a much smaller percent of users. The important thing to remember about sex influenced diseases is that they are hereditary, but only to the extent of the amount of testosterone produced. The genes tell the offspring the amount and concentration of testosterone, not whether or not to lose hair. If the amounts of testosterone relayed are not normal, baldness may occur. A second sex influenced disease is gout. Gout is the |hereditary metabolic disorder that is characterized by recurrent acute attacks of severe inflammation in one or more of the extremitiesX(Norton 5:392). This inflammation is caused by an excess deposition of uric acid in and about the joints. Like baldness, this condition strikes men predominantly, but can also be found in women. The exact cause of gout is not yet known, however, it is logical to believe that it is caused by the same hormonal imbalances as baldness, and that is why it is classified as a sex influenced disease. Gout is inborn, however the symptoms do not occur until middle age. Before the attacks, small amount of uric acid build up in the joints. All joints, especially the big toe, are susceptible. Symptoms such as heat, redness of the skin, and extreme tenderness and pain accompany the affected joints. Numerous gout attacks can cause knobby bumps on the affected joints. Acute cases of gout may come and go in a matter of a week for no apparent reason. Some circumstances. however, inhibit the symptoms of gout. These circumstances include: emotional upset, diuresis, surgery, trauma, and the administration of certain drugs. Cochicine is the classic treatment for gout, but new medicines have surfaced recently. Sex linked and sex influenced diseases are a problem that hurts our society. Although many of the diseases are just an inconvenience, others are fatal. There is no fathomable way of preventing any of these diseases, unless genes can be altered. The only medicine to treat theses diseases acts as a suppressant, not as an end to the diseases+s life. Hopefully, cures can be found to save the lives of young, innocent people who are affected with hemophilia, Duchenne+s Muscular Dystrophy and other fatal diseases.

    |Color Blindness Misconceptions.X USA Today 120 (1992):16|Foot Feat: transplant treats dystrophy.X Science News 16 June 1990:380Grady, Denise. |One foot forward.X Discover September 1990:86-93Massie, Robert. and Massie, Suzanne. Journey. New York: Alfred A. Knopf, 1961. Norton, Peter B. |baldness.X The New Encyclopedia Britannica. 1994 ed. Norton, Peter B. |gout.X The New Encyclopedia Britannica. 1994 ed. Norton, Peter B. |hemophilia.X The New Encyclopedia Britannica. 1994 ed. Thompson, Larry. |Cell transplant results under fire.X Science 257 (24 July 1992) 472-474 Diseases: Sex Linked and Sex InfluencedbyRichard NixonHonors BiologyMrs. LindaDecember 19, 1994

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