Книги з теми "Inflammatory component"

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1

Zhou, Jiaju. Zhong yao kang yan huo xing cheng fen: Anti-inflammatory active components in TCM. 8th ed. Beijing: Ke xue chu ban she, 2012.

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2

Klingenberg, Roland, and Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.

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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α‎ and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
3

Freer, Phoebe E. Skin Lesions. Edited by Christoph I. Lee, Constance D. Lehman, and Lawrence W. Bassett. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190270261.003.0050.

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Skin lesions are commonly seen on breast imaging. Often, a raised skin lesion is encountered incidentally during screening mammography and can be mistaken for a mass within the breast parenchyma. In most cases, lesions confined within the dermis are benign. Occasionally, focal skin involvement may be the presenting sign of a breast cancer that is either locally extensive to the skin or has an inflammatory component. This chapter reviews the key imaging and clinical features of skin lesions that may be encountered either incidentally on breast imaging or on diagnostic imaging as an area of patient concern. Imaging features of skin lesions, the differential diagnoses, and further management will be reviewed. Topics discussed include benign epithelial cysts (i.e., sebaceous cyst and epidermal inclusion cysts), seborrheic keratosis, keloid and dermal nevi, cellulitis, and inflammatory and locally advanced breast cancers.
4

Machado, Pedro M. Inclusion body myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.

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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.
5

Laffey, John G., and Brian P. Kavanagh. Hypercapnia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0086.

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Hypercapnia is a central component of current ‘protective’ ventilator management. Hypercapnia, and the associated acidosis, has potentially important biologic effects on immune responses, injury and repair. Arterial carbon dioxide tension PaCO2 is tightly governed under physiological conditions and small elevations rapidly increase spontaneous minute ventilation. In the mechanically-ventilated patient, elevated PaCO2 usually reflects reduced elimination. This can be because tidal volume or respiratory rate delivered by the ventilator are reduced, or because of the diseased lung per se. Hypercapnia has many effects that are clinically obvious, but research over the last decade reveals important consequences on inflammatory and cellular mechanisms that are not apparent at the bedside.
6

Hahn, Robert G. Intravenous fluids in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0020.

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Infusion fluids may be regarded as drugs in the perioperative setting. The therapeutic effects of crystalloid solutions are strongly related to the administered volume, while fluids of the colloid type may also improve microcirculation and have anti-inflammatory properties. The anaesthetist should be able to handle all available infusion fluids and be aware of their benefits, limitations, and risks. Fluid administration programmes for surgery are traditionally based on a balance method in which perceived and measured losses are continuously replaced. Two outcome-guided approaches—restrictive and goal-directed fluid therapy—have been added in recent years. The latter places all patients on the top of the Frank–Starling curve by titrating repeated bolus infusions of colloid fluid while observing the stroke volume response. Areas where special consideration should be given to fluid therapy include burn injury, children, day surgery, endoscopic surgery, neurosurgery, induction of spinal and epidural anaesthesia, and in septic and trauma-related shock. As volume is the key component of infusion fluids, kinetic analysis of their disposition is based on their dilution effect on components already present in the blood, usually haemoglobin.
7

Lalvani, Ajit, and Katrina Pollock. Defences against infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0303.

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The immune system is classified into a series of component parts, each specialized to defend the host against infection. Cells of the innate immune system are distributed throughout the body, in the tissues, and in the circulation, to defend against the first signs of danger, combining the acute inflammatory response with the ability to kill and remove invading pathogens. Monocytes, macrophages, and neutrophils phagocytose and kill exogenous and endogenous targets, using both oxygen-dependent and oxygen-independent mechanisms. The adaptive immune system creates a structurally specific and prolonged response, mediated by lymphocytes to clear infection and generate immunological memory. In this chapter, the functions of the innate and adaptive immune system are reviewed, together with the clinical features and investigation of acquired and inherited immune deficiencies.
8

Eisen, Andrew. Motor neurone disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0009.

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In this chapter, the following ten key events in motor neurone disease, also known as amyotrophic lateral sclerosis (ALS), are considered: the first description of ALS by Cruveilhier; discovery of the first SOD1 mutation; use of the ALSFRS (functional rating scale) for determining therapeutic trial outcomes; the contentious issue of establishing the site of onset of ALS; clinical, pathological, and molecular evidence indicating that frontotemporal dementia and ALS are closely related; demonstration that ALS bears some resemblance to the transmissible spongiform encephalopathies; use of Riluzole as the approved therapy for ALS; the major inflammatory component of ALS; a Guamanian disorder that is biochemically and ultrastructurally similar to that of Alzheimer’s disease; and awareness that the true onset of ALS is unknown but certainly precedes clinical onset by years or decades.
9

Patel, Mayur B., and Pratik P. Pandharipande. Analgesics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0043.

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Analgesia is a critical component of intensive care unit (ICU) care. Accordingly, understanding the mechanism, physiological consequences, and assessment of pain is important when caring for the ICU patient. Non-pharmacological approaches should be attempted before supplementing analgesia with pharmacological agents. Pharmacologically-based therapies are divided into regional and systemic therapies. Regional analgesic therapies target specific areas of the body while limiting the systemic effects of intravenous analgesics, but at the risk of invasiveness, local anaesthetic toxicity, and infection of in-dwelling catheters. Systemic analgesic therapy is comprised of two main categories—non-opioids and opioids. Typically, non-opioid analgesics are used as adjunctive therapies and consist of agents such as non-steroidal anti-inflammatory drugs, gabapentinoids, ketamine, or α‎2 agonists. Opioid analgesia in the ICU is commonly infusion-based using fentanyl, hydromorphone, morphine, or recently, remifentanil.
10

Takeshita, Junko, and Joel M. Gelfand. Epidemiology of psoriasis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0002.

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Psoriasis is a common chronic inflammatory disorder of the skin that is associated with multisystem effects. Approximately 125 million people worldwide are affected by psoriasis, nearly one quarter of whom have moderate to severe disease. The majority of patients with psoriasis have a waxing and waning course with variable periods of spontaneous disease improvement or clearance. A rapidly expanding body of epidemiologic literature suggests psoriasis to be associated with a greater comorbid disease burden than patients without psoriasis. In addition to psoriatic arthritis, cardiometabolic diseases, including metabolic syndrome and its component disorders, as well as major adverse cardiovascular events are the most common comorbidities of psoriasis; together they are the primary cause of premature mortality among moderate to severe psoriasis patients. Continued efforts to better understand currently known and identify other emerging comorbidities of psoriasis are critical.
11

Eljaafari, Assia, and Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
12

Bhargava, Pavan, and Peter A. Calabresi. Multiple Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0087.

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Multiple sclerosis is a chronic demyelinating neurological disorder of the brain and spinal cord, with both inflammatory and degenerative components. Current treatment strategies utilize immunomodulatory and immunosuppressive agents to reduce the inflammatory disease activity and retard accumulation of disability. Future challenges for treatment include identifying agents that will promote remyelination and axonal protection to help impact progressive forms of multiple sclerosis. This chapter discusses currently available disease modifying therapies, agents currently in phase 2/3 trials, and future directions in the treatment of multiple sclerosis.
13

Wainger, Brian J. Drug Discovery and Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0117.

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Pain is one of the most common causes of physician visits and disability. Pain has been classified into specific subtypes. We refer to baseline or nociceptive pain as pain that results from an ongoing, high-threshold stimulus acting on an unenhanced somatosensory system. Inflammatory pain refers to pain in the setting of tissue damage and specifically the release of inflammatory molecules that activate and sensitize the nociceptive machinery. Hyperalgesia, or increased pain in response to a noxious stimulus, results from nociceptor sensitization whereas neuropathic pain results from a lesion or disease of the somatosensory system. Pain can have spontaneous, stimulus-independent components as well as evoked components such as hyperalgesia or allodynia, pain that is elicited by a normally innocuous stimulus. This chapter describes the research strategy for discovering new drugs to relieve these different kinds of pain.
14

Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0115_update_002.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local pro-inflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.
15

Gaston, J. S. Hill. Reactive arthritis and enteropathic arthropathy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0115.

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Reactive arthritis (ReA), and enteropathic arthritis secondary to inflammatory bowel disease, are forms of spondyloarthritis, all of which share an association with HLA B27 and can involve both axial and peripheral joints. Genetic studies strongly implicate the cytokines IL-17 and IL-23 in their pathogenesis, and evidence for autoimmunity is lacking. ReA is triggered by particular bacteria, mainly affecting the gut and genitourinary tract, though infections are sometimes asymptomatic. Classically an acute oligo- or monoarthritis with enthesitis occurs, often with inflammatory back pain, though mild polyarthritis can also occur. Septic and crystal-induced arthritis are the principal differential diagnoses. Extra-articular features may aid diagnosis, which otherwise requires laboratory evidence of preceding infection. Bacterial components traffic to the joint (which is nevertheless sterile), and elicit local proinflammatory immune responses. Most ReA is self-limiting, but persistent cases may require disease-modifying anti-rheumatic drugs or even biologics.
16

Haranhalli, Neil, and Jerome J. Graber. Pineal Region Neoplasms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0131.

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Pineal region tumors include a diverse array of neoplasms arising from various components of the pineal gland, including germ cell tumors, germinomas, teratomas, pineocytomas, pineoblastomas, and tumors derived from glial tissues including gliomas, astrocytomas, oligodendrogliomas, and ependymomas. Benign lesions of the pineal gland can include pineal cysts, calcifications and meningiomas. Metastatic tumors can also be found in the pineal region. Numerous infectious and inflammatory conditions can mimic pineal tumors. Most patients present with symptoms of hydrocephalus or Parinaud’s syndrome. Diagnosis often requires biopsy, though some germinomas may be diagnosed based solely on serum and cerebrospinal fluid biomarkers.
17

Pap, Thomas, Adelheid Korb, Marianne Heitzmann, and Jessica Bertrand. Joint biochemistry. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0056.

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Synovial joints are composed of different morphological structures that have their distinct cellular and biochemical properties. Articular cartilage and synovial membrane are key components of synovial joints and show a number of peculiarities that makes them different from other tissues in our body. An in-depth knowledge of these structural and biochemical peculiarities is not only important for understanding key features of articular function but also provides explanations for important characteristics of both degenerative and inflammatory joint diseases. This chapter reviews the structure and biochemical composition of cartilage and synovium and points to important links between physiology and pathological conditions, particularly arthritis.
18

Dambuza, Ivy M., Jeanette Wagener, Gordon D. Brown, and Neil A. R. Gow. Immunology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0009.

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Advances in modern medicine, such as organ transplantations and the appearance of HIV (human immunodeficiency virus), have significantly increased the patient cohort at risk of developing chronic superficial and life-threatening invasive fungal infections. To tackle this major healthcare problem, there is an urgent need to understand immunity against fungal infections for the purposes of vaccine design or immune-mediated interventions. In this chapter, we give an overview of the components of the innate and adaptive immune system and how they contribute to host defence against fungi. The various cell types contributing to fungal recognition and the subsequent stimulation of phagocytosis, the activation of inflammatory and B- and T-cell responses, and fungal clearance are discussed using the major fungal pathogens as model systems.
19

Gordon-Williams, Richard M., and Anthony H. Dickenson. Pathophysiology of pain in cancer and other terminal illnesses. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0092.

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Cancer pain involves a myriad of peripheral changes in the function of tissue and nerves, at the site of the tumour growth, as well as a number of consequent changes in the processing of pain messages at the spinal cord level with implications for the pain experience at higher centres. This chapter reviews the changes in peripheral pain signalling, notes the likely prevalence of both inflammatory and neuropathic components, and describes the altered events at spinal levels that can come some way towards explaining ongoing pain, hyperalgesia, and allodynias that patients with cancer and other terminal illnesses such as HIV/AIDs experience. Finally, changes induced by cancer at the level of the brain are discussed. The mechanisms of action of therapies, both existing and potential novel approaches, are included at peripheral and central levels.
20

Albert, Tyler J., and Erik R. Swenson. The blood cells and blood count. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0265.

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Blood is a dynamic fluid consisting of cellular and plasma components undergoing constant regeneration and recycling. Like most physiological systems, the concentrations of these components are tightly regulated within narrow limits under normal conditions. In the critically-ill population, however, haematological abnormalities frequently occur and are largely due to non-haematological single- or multiple-organ pathology. Haematopoiesis originates from the pluripotent stem cell, which undergoes replication, proliferation, and differentiation, giving rise to cells of the erythroid, myeloid, and lymphoid series, as well as megakaryocytes, the precursors to platelets. The haemostatic system is responsible for maintaining blood fluidity and, at the same time, prevents blood loss by initiating rapid, localized, and appropriate blood clotting at sites of vascular damage. This system is complex, comprising both cellular and plasma elements, i.e. platelets, coagulation and fibrinolytic cascades, the natural intrinsic and extrinsic pathways of anticoagulation, and the vascular endothelium. A rapid, reliable, and inexpensive method of examining haematological disorders is the peripheral blood smear, which allows practitioners to assess the functional status of the bone marrow during cytopenic states. Red blood cells, which are primarily concerned with oxygen and carbon dioxide transport, have a normal lifespan of only 120 days and require constant erythropoiesis. White blood cells represent a summation of several circulating cell types, each deriving from the hematopoietic stem cell, together forming the critical components of both the innate and adaptive immune systems. Platelets are integral to haemostasis, and also aid our inflammatory and immune responses, help maintain vascular integrity, and contribute to wound healing.
21

Oikonomopoulou, Katerina, and Vinod Chandran. Biomarkers of psoriatic arthritis outcomes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0022.

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Psoriatic arthritis is an inflammatory musculoskeletal disease that occurs in patients suffering from psoriasis. The disease manifests with symptoms affecting the skin, peripheral and axial joints, and periarticular structures. Diagnosis and management of psoriatic arthritis is challenging due to its heterogeneous presentation. However, early diagnosis and subsequent appropriate treatment reduces disease activity, prevents joint damage, and improves long-term outcome. It is hoped that biomarkers for disease progression and activity will aid in cost-effective clinical management of patients. Potential biomarkers under investigation for psoriatic arthritis are disease-related components derived from skin and articular tissues, biological fluids, such as blood and synovial fluid, and arthritis-associated cell populations. Imaging including ultrasound and MRI are also being evaluated as biomarkers for diagnosis, activity and outcome. Despite the challenge of bringing these new markers into the clinic, many of these markers hold promise for the future management of patients with psoriatic arthritis.
22

Afza, Musarrat, Marko Petrovic, and Sam Ghebrehewet. Tuberculosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198745471.003.0012.

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This chapter covers two case studies and scenarios: a case of pulmonary tuberculosis (TB) in a college student; and a case of laboratory-confirmed Mycobacterium bovis in an adult with inflammatory bowel disease. The pulmonary TB case resulted in a wider investigation and contact tracing as the case attended college while symptomatic. The Mycobacterium bovis resulted in wider workplace and hospital contact tracing through convening an Incident Control Team. Background information on the epidemiology and clinical features of TB and the public health response to TB in educational, healthcare, and occupational settings are discussed. Case definitions, and a detailed risk assessment, with clear description of close contacts, priority groups, and the required public health actions, are described. ‘Top tips’ are given, to provide practical tips for the reader to think through the public health management of TB, and ‘tools of the trade’ list the laboratory and epidemiological components of the investigation.
23

Hartigan-O’Connor, Dennis J., and Christian Brander. Immunology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0005.

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The key factor in HIV pathogenesis is the decline in CD4+ T cells with resultant immunodeficiency and chronic inflammation. Depletion of CD4+ T cells from the gastrointestinal mucosa followed by microbial translocation and subsequent immune activation are components of disease progression in untreated patients. Symptomatic and occult opportunistic infections including cytomegalovirus contribute to chronic inflammation in persons infected with HIV. Antiretroviral therapy (ART) results in immune reconstitution, with increases in peripheral CD4+ T cell lymphocytes in most persons infected with HIV, although immune recovery is quite variable. A subset of patients with AIDS will develop immune reconstitution inflammatory syndromes after initiation of ART. Approximately 1% of persons with HIV are able to control infection without the need for ART (“elite” controllers). A variety of immune-based therapies, including hydroxyurea, growth hormone, and statins, are being studied in clinical trials and may ultimately play a role in treating persons with HIV infection.
24

Wolf, James, and Carlos A. Pino. Malignant Visceral Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0027.

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Healthcare providers are familiar with the diffuse and poorly localized quality of visceral pain, as well as its somatic referral patterns from internal organs to dermatomal distributions. Visceral pain also involves significant autonomic and emotional components. When primary or metastatic malignancy is responsible for visceral pain, treating the patient’s pathology and symptomatology becomes more complex. Visceral pain can be initiated by distension of hollow organs, mesenteric traction, ischemia, and inflammatory factors, all of which are associated with solid tumors in the abdomen. Furthermore, common analgesics, such as opioids, can negatively affect visceral function, leading to nausea, vomiting, or constipation, which may negate the drugs’ beneficial effects or even worsen pathology and pain. While clinicians have tools to alleviate visceral pain, none has a perfect efficacy or side effect profile. In metastatic disease, the focus of care should be on improvement of a patient’s quality of life based on his or her personal goals and expectations.
25

Pollock, Rob. Total hip replacement: modes of failure. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.007010.

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♦ Total hip replacements (THRs) may fail in various ways. They may become infected, they may be subject to aseptic loosening, they may dislocate, or a periprosthetic fracture may occur. The patient with a failed THR must be thoroughly assessed before treatment is contemplated♦ Infection may be acute or chronic. Assessment involves clinical assessment, plain radiographs, blood tests (C-reactive protein and erythrocyte sedimentation rate), hip aspiration, and, sometimes, nuclear medicine. The acutely infected hip may be treated with one-stage revision. This involves thorough lavage, debridement, and exchange of all modular components as well as long-term antibiotic therapy. The gold standard of treatment for a chronically infected THR is a two-stage revision. Success rates of 80–90% can be expected♦ Aseptic loosening typically occurs at the cement bone interface in hips where a metal-on-polyethylene bearing couple has been used. Bone resorption takes place as a result of an inflammatory response to small wear particles. After infection has been excluded the treatment of choice is a single-stage revision♦ Dislocation may be the result of patient factors, implant factors, or poor surgical technique. It is imperative for the clinician to minimize the risk by selecting patients carefully, using the correct combination of implants and performing surgery accurately♦ The management of periprosthetic fractures depends on how well the implants are fixed and quality of bone stock. Treatment ranges from simple fixation of the fracture through to revision augmented with strut allograft.
26

Compston, Alastair. Multiple sclerosis and other demyelinating diseases. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0871.

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The oligodendrocyte–myelin unit subserves saltatory conduction of the nerve impulse in the healthy central nervous system. At one time, many disease processes were thought exclusively to target the structure and function of myelin. Therefore, they were designated ‘demyelinating diseases’. But recent analyses, based mainly on pathological and imaging studies, (re)emphasize that axons are also directly involved in these disorders during both the acute and chronic phases. Another ambiguity is the extent to which these are inflammatory conditions. Here, distinctions should be made between inflammation, as a generic process, and autoimmunity in which rather a specific set of aetiological and mechanistic conditions pertain. And there are differences between disorders that are driven primarily by immune processes and those in which inflammation occurs in response to pre-existing tissue damage.With these provisos, the pathological processes of demyelination and associated axonal dysfunction often account for episodic neurological symptoms and signs referable to white matter tracts of the brain, optic nerves, or spinal cord when these occur in young people. This is the clinical context in which the possibility of ‘demyelinating disease’ is usually considered by physicians and, increasingly, the informed patient. Neurologists will, with appropriate cautions, also be prepared to diagnose demyelinating disease in older patients presenting with progressive symptoms implicating these same pathways even when there is no suggestive past history. Both in its typical and atypical forms multiple sclerosis remains by far the commonest demyelinating disease. But acute disseminated encephalomyelitis, the leucodystrophies, and central pontine myelinolysis also need to be considered in particular circumstances; and multiple sclerosis itself has a differential diagnosis in which the relapsing-remitting course is mimicked by conditions not associated with direct injury to the axon–glial unit. Since our understanding of the cause, pathogenesis and features of demyelinating disease remains incomplete, classification combines aspects of the aetiology, clinical features, pathology, and laboratory components. Whether the designation ‘multiple sclerosis’ encapsulates one or more conditions is now much debated. We anticipate that a major part of future studies in demyelinating disease will be further to resolve this question of disease heterogeneity leading to a new taxonomy based on mechanisms rather than clinical empiricism. But, for now, the variable ages of onset, unpredictable clinical course, protean clinical manifestations, and non-specific laboratory investigations continue to make demyelinating disease one of the more challenging diagnostic areas in clinical neurology.

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