Books: 'GBS met' – Grafiati

1

Youling, Lin, and Lü Shaolin, eds. Zhongguo mei ceng wa si fen bu te zheng. Beijing: Mei tan gong ye chu ban she, 1998.

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2

Mei ceng qi cang gong cheng. Beijing: Ke xue chu ban she, 2009.

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3

Thieme, Marianne, Monique van Dijk, Claudine Everaert, and Gertjan Zwanikken. Meat the truth. Amsterdam]: Alalena Production, 2008.

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4

Men of honor: American GIs in the Jewish Holocaust. Central Point, Or: Hellgate Press, 2005.

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5

Martínez-Martín, Javier Alberto. Monitoring intra-urban inequalities with GIS-based indicators: With a case study in Rosario, Argentina = Monitoren van ongelijkheid binnen steden met op GIS gebaseerde indicatoren : met een gevalstudie in Rosario, Argentinië. Utrecht]: Utrecht University, 2005.

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6

ill, Chen Xi, ed. Mei ge ren dou hui "pu". Xinbei Shi: You fu wen hua shi ye gu fen you xian gong si, 2016.

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7

Li, Zhonghua. Wa si mei ceng chong ji di ya fang zhi ji shu ji ying yong. Bei jing: Guo fang gong ye chu ban she, 2009.

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8

Mei ceng qi jing ji kai cai zeng chan ji li yan jiu. Beijing: Ke xue chu ban she, 2011.

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9

Pakistan, Oil &. Gas Conference (3rd 2007 Islāmābād Pakistan). Pakistan, a link to meet South Asian energy needs. Karachi: Petroleum Institute of Pakistan, 2007.

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10

Cheng shi mei qi qing bao wang (China), ed. Mei qi gong ye ci hui: Ying Fa De E Han dui zhao. 2nd ed. Beijing: Zhongguo jian zhu gong ye chu ban she, 1986.

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11

Rachlitz, Carl-Otto. Måling af kvælstofilter i køkkener med gaskomfur: Bygas og naturgas : vintermåling. [Copenhagen]: Byggestyrelsen, 1988.

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12

Mei kuang wa si zhi li he li yong xian jin ji shu ji shi fan. Xuzhou Shi: Zhongguo kuang ye da xue chu ban she, 2009.

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13

La condition juridique des pipelines dans le droit de la mer. Paris: Presses universitaires de France, 1990.

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14

Madsen, Henrik Breuning. Jordprofilundersøgelsen: Rapport over pedologiske studier udført i forbindelse med anlæg af hovedtransmissionsledninger for naturgas i Danmark. [Copenhagen]: Landbrugsministeriet, 1. afd. 6. kontor, Arealdatakontoret, 1985.

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15

Thaisetthawatkul, Pariwat, and Eric Logigian. Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy in Pregnancy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190667351.003.0026.

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Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are both immune-mediated diseases of the peripheral nervous system that typically present with symmetric, progressive muscle weakness, areflexia, and sensory symptoms or signs. GBS evolves rapidly with a nadir at 2–4 weeks usually with an antecedent viral illness, while CIDP progresses more slowly over months to years. GBS is sometimes complicated by life-threatening respiratory failure or dysautonomia. Onset of GBS and relapse of CIDP can occur during pregnancy or postpartum. But with appropriate supportive care and immunotherapy, maternal and fetal outcome in both conditions is typically excellent. The exception is fetal outcome in GBS triggered by maternal CMV or Zika infection transmitted to the fetus. Full-term vaginal delivery and regional anesthesia are preferred in maternal GBS and CIDP, but if C-section and general anesthesia are indicated, non-depolarizing agents such as succinylcholine should be avoided.

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16

Le Doare, Kirsty, Christine E. Jones, and Paul T. Heath. Group B Streptococcus (Streptococcus agalactiae). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190604813.003.0019.

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Group B Streptococcus (GBS) is a leading cause of early neonatal infection and neonatal mortality, with long-term adverse neurodevelopmental outcomes in up to 50% of survivors of GBS meningitis. GBS has a likely underappreciated role in causing preterm birth and stillbirth. GBS colonizes the vagina and gastrointestinal tract of the pregnant woman, and transmission to the infant occurs during or just before delivery. Although the majority of these infants do not develop invasive disease, maternal colonization is a prerequisite for early onset disease (0–6 days of life, most commonly associated with sepsis and respiratory distress) and a significant risk factor for late onset disease (7–89 days of life, most commonly associated with sepsis and meningitis). The introduction of intrapartum antibiotic prophylaxis has resulted in significant declines in the incidence of early onset disease but provides no protection against late onset disease.

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17

Centre for Environment and Development for the Arab Region and Europe., ed. CEDARE GIS meta data. [Cairo?]: The Centre, 2002.

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18

Chase, James Hadley. Gas chamber men maut. 1990.

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19

Miller, Aaron E., and Teresa M. DeAngelis. Acute Inflammatory Demyelinating Polyneuropathy (Guillain-Barré Syndrome). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0024.

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Acute inflammatory demyelinating polyneuropathy (AIDP), also known as Guillain-Barré syndrome (GBS), is a common acute neurological presentation encountered in both the outpatient setting and hospital wards. The hallmark of the disorder is the development of ascending motor paralysis with loss of deep tendon reflexes. In this chapter, we outline the classical clinical and laboratory findings in GBS as well as critical therapeutic and supportive measures along with prognosis.

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20

Arbeidsinspectie, Netherlands, ed. Gevarenzone-indeling met betrekking tot gasontploffingsgevaar. Den Haag: Arbeidsinspectie, 1992.

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21

Kaplan, Tamara, and Tracey Milligan. Demyelinating Diseases 2: NMO, ADEM, GBS, CIDP (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190650261.003.0014.

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The video in this chapter explores demyelinating diseases, and focuses on neuromyelitis optica (NMO), acute disseminated encephalomyelitis (ADEM), Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), including their symptoms, causes, and diagnostic tests.

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22

de Min, Erik. De geoïde voor Nederland. Nederlandse Commissie voor Geodesie, 1996. http://dx.doi.org/10.54419/g3ej06.

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De combinatie van GPS-metingen met geoïdehoogteverschillen levert orthometrische hoogteverschillen op die kunnen worden gebruikt als controle op, of vervanging van waterpasmetingen. Omdat voor deze orthometrische hoogten (NAP-hoogten) voor veel toepassingen een cm-precisie gewenst is, dient ook de geoïde op dit precisie-niveau bekend te zijn. Om de geoïde zo precies te bepalen is een drietal zaken van belang: om te beginnen de dichtheid en kwaliteit van de beschikbare zwaartekrachtdata, daarnaast de kwaliteit van de theoretische oplossing van het randvoorwaardeprobleem voor de bepaling van de geoïde, en bovendien is, voor de praktische geoïdeberekening, de kwaliteit van de rekenmethoden, uit eerder genoemde theoretische oplossing, van belang. De beschrijving van deze probleemgebieden komt in dit proefschrift aan de orde, met als doel de daadwerkelijke geoïdeberekening voor Nederland. Allereerst richten we ons op de techniek van geoïdebepaling met behulp van de Stokes oplossing voor het randvoorwaardeprobleem. Hier worden de numerieke integratie van Stokes formule en de kleinste-kwadraten collocatiemethode beschreven en met elkaar vergeleken. Er wordt getoond dat beide methoden voor praktische berekeningen niet dezelfde resultaten opleveren. Voor de bepaling van empirische covariantiefuncties, die nodig zijn voor collocatie en foutberekeningen, wordt een nieuwe techniek voorgesteld. De praktische geoïdeberekening zal worden uitgevoerd door een combinatie van globale zwaartekrachtinformatie uit een geopotentiaalmodel en regionale zwaartekrachtmetingen en gemiddelde zwaartekrachtwaarden. De verschillende mogelijkheden van combineren via kernfunctiemodificaties worden daartoe op een originele manier geïntroduceerd. Tevens wordt een formele foutvoortplanting van zwaartekrachtdata naar geoïdehoogte(verschillen) behandeld. Vervolgens worden de data behandeld die beschikbaar zijn voor de geoïdebepaling voor Nederland. Aan het nieuw gemeten zwaartekrachtnet voor Nederland wordt uitgebreid aandacht geschonken, waarna een analyse en vergelijking volgen van de beschikbare (oude en nieuwe) zwaartekrachtdatasets. Daarna wordt beschreven hoe uit de gemeten puntzwaartekrachtwaarden optimaal de gemiddelde blokwaarden kunnen worden bepaald, en hoe de foutberekening daarbij verloopt. Ten slotte wordt de overige informatie beschreven die van belang is voor de geoïdeberekening: het geopotentiaalmodel, geoïdehoogten uit de combinatie van GPS- en waterpasmetingen, en schietloodafwijkingen. Deze laatste twee leveren onafhankelijke geoïde-informatie. Op basis van de beschikbare zwaartekrachtdata worden diverse geoetests gedaan. Hierbij wordt ingegaan op de invloed van predictie-parameters van gemiddelde zwaartekrachtblokwaarden, de verschillende kernfunctiemodificaties en de evaluatietechnieken. Tevens wordt een vergelijking met onafhankelijke geoïde-informatie uitgevoerd. Alvorens de geoïdeberekening te kunnen uitvoeren wordt de kwaliteit van de Stokes oplossing voor geoïdebepaling nader bestudeerd, waarbij we ons richten op de Nederlandse situatie. We kijken naar een betere oplossing voor het randvoorwaardeprobleem door Molodenskii, en naar de invloed van atmosfeeraantrekking en ellipsoïdische correcties. Hieruit blijkt dat het voor Nederland mogelijk moet zijn om cm-precisie te bereiken voor geoïdehoogteverschillen. Het proefschrift wordt afgesloten met de beschrijving van de daadwerkelijke geoïdeberekening voor Nederland. De procedure die is gevolgd is een combinatie van de methoden van Meissl en Wong&Gore met L = 32. Er wordt gebruik gemaakt van het OSU91A geopotentiaalmodel en de nieuwe Nederlandse data en overige Europese data in een gebied van 5o rondom Nederland, waarmee 3'x5' gemiddelde waarden zijn bepaald. Tevens is de formele foutvoortplanting uitgevoerd. Vervolgens wordt een vergelijking met GPS- en waterpasmetingen, en met schietloodafwijkingen gemaakt. Hiermee wordt een correctievlak bepaald om tot de best mogelijke geoïde voor Nederland te komen. Tenslotte wordt de berekende WGS84-geoïde ook getransformeerd naar het lokale Nederlandse Bessel-referentiesysteem. Het blijkt dat de geoïde binnen Nederland met een precisie van 1 tot enkele cm is bepaald.

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23

Arbeidsinspectie, Netherlands, ed. Gevarenzone-indeling met betrekking tot gasontstekingsgevaar. Voorburg: Directoraat-Generaal van de Arbeid van het Ministerie van Sociale Zaken en Werkgelegenheid, 1989.

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24

Robb, Laurence, and Andrew Mitchell. Mineral Deposits of Myanmar (Burma). Society of Economic Geologists, 2021. http://dx.doi.org/10.5382/gb.62.

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Myanmar is richly endowed in natural resources that include tin, tungsten, copper, gold, zinc, lead, nickel, and silver, as well as gemstones. The material covered over a nine-day field trip explores the country’s complex geology, which reflects a collisional history stretching from the Late Triassic to at least Miocene, sited at the eastern end of the India-Asia suture. The country can be divided into three principal metallotects: the Wuntho-Popa magmatic arc, with granites and associated porphyry-type and epithermal Cu-Au mineralization; the Slate Belt (also called the Mogok-Mandalay-Mergui Belt), with multiple precollisional I-type and postcollisional S-type crustal melt granites that host significant tin-tungsten mineralization, and which also are host to a number of orogenic gold deposits; and the Shan Plateau with massive sulfide-type and also MVT-style lead-zinc-silver deposits.

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25

Kreit, John W. Gas Exchange. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0002.

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Gas Exchange explains how four processes—delivery of oxygen, excretion of carbon dioxide, matching of ventilation and perfusion, and diffusion—allow the respiratory system to maintain normal partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) in the arterial blood. Partial pressure is important because O2 and CO2 molecules diffuse between alveolar gas and pulmonary capillary blood and between systemic capillary blood and the tissues along their partial pressure gradients, and diffusion continues until the partial pressures are equal. Ventilation is an essential part of gas exchange because it delivers O2, eliminates CO2, and determines ventilation–perfusion ratios. This chapter also explains how and why abnormalities in each of these processes may reduce PaO2, increase PaCO2, or both.

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26

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Disorders of peripheral nerves and motor neuron disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0007.

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This chapter discusses the clinical features and evidence-based drug treatment regimens of polyneuropathies (Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), multifocal motor neuropathy, paraproteinaemic neuropathies, and vasculitic neuropathies), mononeuropathies (Bell’s palsy), systemic conditions with peripheral nerve involvement (Sjögren’s and sarcoidosis), and motor neuron disease (MND).

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27

Paul, Richard, and Paul Grant. Blood gas analysis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0018_update_001.

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Acid-base homeostasis is vital for the maintenance of normal tissue and organ function, as both acidosis and alkalosis can have harmful and potentially life-threatening effects. Arterial blood gas analysis, combined with routine clinical history and examination, can provide useful information for the management of the critically ill cardiac patient. Most acid-base derangements are reversed by treatment of the underlying disease process, rather than simple correction of the abnormal pH, and prognosis is determined by the nature of the underlying disease, rather than the extent of pH value deviation. Within this chapter, a six-step approach is presented for prompt and accurate acid-base interpretation. Water and electrolyte disorders are common in the intensive cardiac care unit, particularly in patients with cardiac failure. Prompt recognition and treatment is required to prevent cardiovascular and neurological compromise. Therapeutic strategies range from simple electrolyte substitution and fluid management to extracorporeal filtration of excess fluid and electrolytes. These are discussed within this chapter.

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28

Ramirez-Valles, Jesus. Social-class Origins and Trajectories. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252036446.003.0002.

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This chapter examines the social-class origins of the Latino GBT activists, the compañeros. It proposes that social-class origins shaped some of these compañeros' life circumstances. That is, the social-class location of the families in which the activists were raised was one factor, if not the most significant, among several. For instance, some of the men who grew up in a poor or working-class environment began working early in their childhood or youth, did not go to college, and emigrated to the United States. As adults, some of them also experienced homelessness and unemployment. Only in very few instances are these Latino GBTs able to change the course set by the social class into which they were born. However, the improvement some of them have made in their social-class standing has been due to their own resiliency or to random events.

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29

Shaibani, Aziz. Dyspnea. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0009.

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The most common causes of dyspnea are not neuromuscular but rather are cardiac and pulmonary. However, dyspnea is an important and serious manifestation of many neuromuscular disorders, and it may compound an underlying pulmonary or cardiac problem. The diaphragm is a skeletal muscle under the control ofperipheral nerves(phrenic nerves) and may be targeted by inflammatory neuropathies such as Guillain-Barrésyndrome(GBS), chronic inflammatory demyelinating polyneuropathy(CIDP), and brachial plexitis, myopathies such as acid maltase deficiency and muscular dystrophies, and neuromuscular disorders such as myasthenia gravis. Periodic measurement of pulmonary function isrecommended in neuromuscular clinics.

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30

Wagner, Peter D. Gas exchange principles in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0075.

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Pulmonary gas exchange in the critically-ill patient is almost always impaired. The reasons are usually multiple and complex, with causes both internal and external to the lung. To understand the relative contributions of these many factors in a given patient requires an understanding of the basic principles of gas exchange. This becomes even more important when a patient’s condition changes quickly, which happens commonly in the critically ill. The purpose of this chapter is to lay out those principles and discuss the several causes of arterial hypoxaemia (and hypercapnia) on the basis of those principles. The key principle that governs gas exchange (in the steady state) is conservation of mass, and writing straightforward mass transport equations that express this principle allows gas exchange to be analysed quantitatively. This chapter is intended to serve as a guide to support appropriate application of tests of pulmonary gas exchange, which are laid out in the chapter that immediately follows it.

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31

Radermacher, Peter, and Claus-Martin Muth. Pathophysiology and management of depth-related disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0351.

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Decompression illness comprises decompression sickness resulting from tissue inert gas super-saturation and pulmonary barotraumas due to alveolar or airway over-distension. Gas bubbles can cause vascular obstruction or tissue compression, resulting in tissue ischaemia and oedema. Interactions between the blood–gas interface and the endothelium will result in further tissue damage, and trigger an inflammatory cascade with capillary leakage and haemoconcentration. Decompression illness may mimic any other emergency pathology and any emergency coinciding with decompression is ‘due to’ decompression. Pulmonary barotrauma-induced arterial gas embolism and decompression sickness can be discriminated according to the onset of symptoms, with gas embolism predominantly developing within a few minutes after or even during decompression. Specific treatment consists of hyperbaric oxygen treatment, using several empirically-derived hyperbaric oxygen treatment schedules. Currently, there is no recognized pharmacological treatment, but fluid resuscitation is useful to counteract haemoconcentration and dehydration. Early treatment initiation is mandatory, and certain technical issues must be considered for the management of critically-ill patients in a hyperbaric chamber.

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32

Lei, Yuan. Humidification, Nebulization, and Gas Filtering. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198784975.003.0006.

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‘Humidification, Nebulization, and Gas Filtering’ describes the therapies, which, while not essential to ventilation, are frequently applied together with it. This chapter provides a comprehensive discussion of these devices, including the clinical needs for them and their operating principles, options, and common complications. It describes the composition and operating principle of active heated humidifiers. Artificial humidification brings with it the additional issue of circuit rainout, which may require that heated wires be added to the breathing circuit. The chapter includes a table for troubleshooting issues related to active humidification. Heat and moisture exchangers or HMEs, an alternative to humidifiers, are also discussed. Finally, the chapter turns to the use of in-line nebulizers or aerosol therapy. The chapter ends with a discussion of respiratory gas filtering, which, for all the benefit a bacteria filter brings, also introduce the risk of occlusion.

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33

Khan, Nayema, and John Pawlowski. Disruption of Diffusion. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0020.

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Adequate gas exchange in the lungs requires a balance between three key processes: ventilation (V), the flow of gas from the environment to the alveoli; perfusion (Q), the circulation to the pulmonary capillary beds; and diffusion of the gas from the alveolar space into the alveolar capillaries. This chapter discusses the management of diseases of the air space, which include secretions, pneumonia, pulmonary edema, and hemoptysis. Collectively these conditions result in the build-up of fluid in the alveolar space and thickening of the alveolar membrane, leading to a mismatch in ventilation and perfusion (V/Q mismatch). Both anesthesia and disease states can adversely affect gas exchange and the chapter discusses strategies to maximize a patient’s pulmonary status in order to minimize perioperative pulmonary complications.

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34

Shaibani, Aziz. Dyspnea. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0009.

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The most common causes of dyspnea are not neuromuscular, but rather cardiac and pulmonary. However, dyspnea is an important and serious manifestation of many neuromuscular disorders, and it may compound an underlying pulmonary or cardiac problem. The diaphragm is a skeletal muscle under the control of a peripheral nerve and may be targeted by inflammatory neuropathies such as Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and brachial plexitis or myopathies such as acid maltase deficiency, muscular dystrophy (MD), and neuromuscular disorders such as myasthenia gravis (MG). Periodic measurement of pulmonary function is a recommended measure in neuromuscular clinics.

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35

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo in later allografts, and in its most extreme form recurs within days. However, inexplicably some subsequent transplants do not provoke aggressive recurrence. Treatment of the most aggressive disease is difficult and in most cases has been ultimately unsuccessful. Lower levels of immune response, marked by linear binding of immunoglobulin-G to GBM without glomerular disease, are not uncommon in Alport patients after transplantation and should not lead to altered treatment. Immunoassays for anti-GBM antibodies can be misleading as in most cases the target of antibodies is the α‎‎‎5 chain of type IV collagen, rather than the α‎‎‎3 chain which is the target in spontaneous anti-GBM disease. Overall the outcome of transplantation in Alport syndrome is better than average. This complication is more likely in patients with partial or total gene deletion rather than point mutations, but no other predictive features have been identified.

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36

Lennon, Rachel, and Neil Turner. The molecular basis of glomerular basement membrane disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0320_update_001.

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The glomerular basement membrane (GBM) is a condensed network of extracellular matrix molecules which provides a scaffold and niche to support the function of the overlying glomerular cells. Within the glomerulus, the GBM separates the fenestrated endothelial cells, which line capillary walls from the epithelial cells or podocytes, which cover the outer aspect of the capillaries. In common with basement membranes throughout the body, the GBM contains core components including collagen IV, laminins, nidogens, and heparan sulphate proteoglycans. However, specific isoforms of these proteins are required to maintain the integrity of the glomerular filtration barrier.Across the spectrum of glomerular disease there is alteration in glomerular extracellular matrix (ECM) and a number of histological patterns are recognized. The GBM can be thickened, expanded, split, and irregular; the mesangial matrix may be expanded and glomerulosclerosis represents a widespread accumulation of ECM proteins associated with loss of glomerular function. Whilst histological patterns may follow a sequence or provide diagnostic clues, there remains limited understanding about the mechanisms of ECM regulation and how this tight control is lost in glomerular disease. Monogenic disorders of the GBM including Alport and Pierson syndromes have highlighted the importance of both collagen IV and laminin isoforms and these observations provide important insights into mechanisms of glomerular disease.

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37

Kreit, John W. Physiological Assessment of the Mechanically Ventilated Patient. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0009.

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This chapter reviews the tests that can be used to determine the type and severity of respiratory failure and the extent to which one or more of the components of normal ventilation and gas exchange have been compromised by disease. Physiological Assessment of the Mechanically Ventilated Patient describes the bedside procedures, measurements, and calculations that allow the assessment of gas exchange and respiratory mechanics in mechanically ventilated patients. Topics include co-oximetry and pulse oximetry, arterial blood gas measurements, venous admixture and shunt fraction, the dead space to tidal volume ratio, time- and volume-capnography, measurement of peak and plateau pressures, and calculation of respiratory system compliance and resistance.

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38

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.

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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.

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39

Beed, Martin, Richard Sherman, and Ravi Mahajan. Breathing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199696277.003.0003.

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Respiratory failureSevere hypercapniaComplications of mechanical ventilationSevere pneumoniaAspirationInhalational injuryAsthma/severe bronchospasmExacerbation of COPDAir trappingTension pneumothoraxMassive haemothoraxPulmonary haemorrhagePulmonary oedemaAcute respiratory distress syndromePulmonary embolism/fat embolismRespiratory failure occurs when air transfer in and out of the lungs is reduced, or when gas exchange within the lungs fails (due to shunt, VQ mismatch, or poor gas diffusion), resulting in either: ...

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40

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 30-Year-Old Male Requiring Management of Progressive Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0006.

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Management of Guillain-Barré syndrome involves several factors. Pulmonary function tests are important to monitor. Telemetry and blood pressure must be monitored because of the significant risk of autonomic dysfunction. Intravenous immunoglobulin is the immunotherapy of choice for this disease, as it is less complicated to administer than plasma exchange. Supportive management issues to address include deep vein thrombosis prophylaxis, bowel/bladder care as ileus and urinary retention may be develop secondary to dysautonomia, physical/occupational/speech therapy consults, nutrition, and pain control. Gabapentin can also be helpful for GBS-related pain. This chapter discusses an approach to treatment that includes the role of respiratory and autonomic monitoring as well as immunotherapy considerations.

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Shaibani, Aziz. Facial Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0005.

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Unilateral or bilateral facial weakness is an important manifestation of many neuromuscular disorders; some of them are as simple as Bell’s palsy, while others are as serious as Guillain-Barré syndrome (GBS). Facial weakness can be easily mimicked, and therefore, psychogenic etiology should always be kept in mind. Peripheral facial weakness affects all functions and parts, while central weakness may save the upper face and may affect emotional and voluntary functions differentially. Botulinum toxin injection has become a common cause of facial palsy, therefore detailed history is crucial. Examination of the sensory and motor systems is important to define the type and cause. Imaging and electrodiagnostic testing are often needed in the diagnostic process.

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Harrison, Mark. Respiratory physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0033.

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This chapter describes respiratory physiology as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of lung volumes and pressures, lung epithelium, lung compliance, surfactant, airway resistance, gas transfer, gas transport within circulation, control of respiration, and ventilation–perfusion relationship. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.

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Narsinh, Kazim, and Thomas Kinney. Water Seal Technique for Lung Biopsy. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0067.

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Gas embolism is an infrequent but potentially severe complication of percutaneous transthoracic lung biopsy. One potential mechanism for the creation of an arterial gas embolism is the introduction of atmospheric air into the biopsy needle when the tip is located in the pulmonary vein. To minimize the risk of introducing air into a pulmonary vein via the biopsy needle, a “water seal technique” can be used to create a hydrostatic column within the introducer needle before the biopsy needle is inserted. Then, if sufficient negative intrathoracic pressure is generated while the needle tip is in a pulmonary vein, saline will enter the pulmonary vein rather than air. This chapter describes the water seal technique to mitigate the risk of arterial gas embolism during transthoracic lung biopsy.

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Nasimudeen, Abdul. Normal respiratory function. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0125.

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Respiration has two components: external respiration, which enables the absorption of O2 and the removal of CO2, and internal respiration, which enables the utilization of O2 and production of CO2 and mediates gas exchange between the cells and their fluid medium. This chapter addresses the mechanics of respiration; gas exchange in the lungs; the pulmonary circulation; lung defence mechanisms; and the metabolic and endocrine functions of the lungs.

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45

Associates, Inc Staff Jenson. Natural Gas Requirements for Electric Generation Through 2000: Can the Natural Gas Industry Meet Them? Edison Electric Institute, 1990.

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46

Wagner, Peter D. Gas exchange assessment in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0076.

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Chapter 75 laid out the basic principles that govern pulmonary gas exchange, a step necessary for the appropriate application and interpretation of common clinical tests of gas exchange. The present chapter discusses the several common tests and indices used to analyse and quantify gas exchange abnormalities in critically-ill patients. There is special emphasis on inherent limitations of each technique, as well as on ways to minimize technical and experimental errors when the necessary measurements are made. Limitations and errors are considered to be of major clinical importance because, while the measurements and indices themselves are easy to obtain, and have been in routine use for many years, serious errors of interpretation can occur if the limitations and common errors are not appreciated and allowed for. In particular, it is pointed out that factors external to the lungs can dramatically change arterial oxygenation in the critically-ill patient. This means that not all changes in gas exchange reflect changes in lung pathology. It is not uncommon for arterial PO2 to change without change in lung disease severity when external factors such as metabolic rate, cardiac output, and blood temperature change.

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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0072_update_001.

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Antiglomerular basement membrane (anti-GBM) disease may present as rapidly progressive glomerulonephritis alone, or in the presence of a secondary pulmonary insult (e.g. smoking or other toxicity, or infection) in combination with lung haemorrhage. Rarely it presents as lung disease alone (with haematuria) or as subacute glomerulonephritis. The major differential diagnoses are small vessel vasculitis, which is a more common cause of pulmonary haemorrhage with rapidly progressive glomerulonephritis, and causes of simultaneous pulmonary and renal failure. For most of these, the lung lesion is not pulmonary haemorrhage. The diagnosis often most quickly, most sensitively, specifically and usefully made by renal biopsy, but immunoassays showing a high titre of anti-GBM antibodies in the setting of severe renal disease are also useful. Borderline and even normal anti-GBM titres are not so specific or reliable in some forms of the disease though.

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48

Chambre syndicale de la recherche et de la production du pétrole et du gaz naturel. Comité des techniciens., ed. Circuits eau de mer: Traitements et matériaux. Paris: Editions Technip, 1993.

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49

Joynt, Gavin M., and Gordon Y. S. Choi. Blood gas analysis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0072.

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Arterial blood gases allow the assessment of patient oxygenation, ventilation, and acid-base status. Blood gas machines directly measure pH, and the partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) dissolved in arterial blood. Oxygenation is assessed by measuring PaO2 and arterial blood oxygen saturation (SaO2) in the context of the inspired oxygen and haemoglobin concentration, and the oxyhaemoglobin dissociation curve. Causes of arterial hypoxaemia may often be elucidated by determining the alveolar–arterial oxygen gradient. Ventilation is assessed by measuring the PaCO2 in the context of systemic acid-base balance. A rise in PaCO2 indicates alveolar hypoventilation, while a decrease indicates alveolar hyperventilation. Given the requirement to maintain a normal pH, functioning homeostatic mechanisms result in metabolic acidosis, triggering a compensatory hyperventilation, while metabolic alkalosis triggers a compensatory reduction in ventilation. Similarly, when primary alveolar hypoventilation generates a respiratory acidosis, it results in a compensatory increase in serum bicarbonate that is achieved in part by kidney bicarbonate retention. In the same way, respiratory alkalosis induces kidney bicarbonate loss. Acid-base assessment requires the integration of clinical findings and a systematic interpretation of arterial blood gas parameters. In clinical use, traditional acid-base interpretation rules based on the bicarbonate buffer system or standard base excess estimations and the interpretation of the anion gap, are substantially equivalent to the physicochemical method of Stewart, and are generally easier to use at the bedside. The Stewart method may have advantages in accurately explaining certain physiological and pathological acid base problems.

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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.

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Books on the topic 'GBS met'

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