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1
Abdul-Karim, Ahmad Bashur. A study of some of the aspects of epithelial and endothelial cels in relation to human renal transplantation. Birmingham: University of Birmingham, 1995.
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2
Tari, Shahryar Rafi. Characterization of AZT transport properties in a continuous renal epithelial cell line. Ottawa: National Library of Canada, 1995.
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3
Li, Qingxue. Epstein-Barr virus infection and replication in a human epithelial cell system. Birmingham: University of Birmingham, 1992.
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4
Beaulieu, Jean-François. Extracellular matrix components and integrins in relationship to human intestinal epithelial cell differentiation. Stuttgart: G. Fischer, 1997.
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5
Holcroft, Cynthia Jean. ATP threshold for loss of epithelial cell polarity and elaboration of fodrin cleavage products following in vivo ischemic renal injury. [New Haven, Conn: s.n.], 1996.
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6
Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.
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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.
7
E, Milo George, Casto Bruce C, and Shuler Charles Fredric 1953-, eds. Transformation of human epithelial cells: Molecular and oncogenetic mechanisms. Boca Raton: CRC Press, 1992.
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8
Transformation of Human Epithelial Cells: Molecular and Oncogenetic Mechanisms. Taylor & Francis Group, 2017.
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9
Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.
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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.
10
Lechner, Mark Stewart. Mechanisms of epithelial cell transformation by human papillomavirus and simian virus 40. 1993.
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11
Tang, Peter Shih-Yi. Lipopolysaccharide-induced caspase-independent programmed cell death of human alveolar epithelial cells. 2006.
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12
Farghaly, Samir A. Adoptive Cell Immunotherapy for Epithelial Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0005.
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The standard management for epithelial ovarian cancer (EOC) is a combination of aggressive debulking surgery with residual tumor of less than 1 cm and platinum-based chemotherapy. However, a high percentage of patients experience disease recurrence. Extensive efforts to find new therapeutic options have been made, albeit cancer cells develop drug resistance and malignant progression occurs. Novel therapeutic strategies are needed to enhance progression-free survival and overall survival of patients with advanced EOC. Several preclinical and clinical studies investigated feasibility and efficacy of adoptive cell therapy (ACT) in EOC. The aim of this chapter is to present an overview of ACT in EOC, focusing on Human Leukocyte Antigen (HLA)-restricted tumor infiltrating lymphocytes and MHC-independent immune effectors such as natural killer and cytokine-induced killer. The available data suggest that ACT may provide the best outcome in patients with low tumor burden, minimal residual disease, or maintenance therapy. Further preclinical studies and clinical trials are needed.
13
Srisawat, Nattachai, and John A. Kellum. Promoting renal recovery in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0379.
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Better understanding the process of renal recovery following acute kidney injury (AKI) is one of the key steps in improving AKI outcome. We are still lacking the standard definition of renal recovery. Recent progress on the pathophysiology of renal injury and recovery is encouraging. Repopulation of surviving renal tubular epithelial cells with the assistance of certain renal epithelial cell and specific growth factors, play a major role in the recovery process. Moreover, accurate prediction would help physicians distinguish patients with poor renal prognosis in whom further therapy is likely to be futile from those who are likely to have good renal prognosis. Unfortunately, current general clinical severity scores (APACHE, SOFA, etc.) and AKI-specific severity scores are not good predictors of renal recovery. This review describes the current definition, pathobiology of renal recovery, epidemiology of renal recovery, the role of clinical severity scores, and novel biomarkers in predicting renal recovery, and strategies for facilitating renal recovery.
14
Characterization of the interaction of Escherichia coli O157:H7 intimin with a human colonic epithelial cell line (HCT-8). Ottawa: National Library of Canada, 1995.
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15
L, Noah Terry, and United States. Environmental Protection Agency., eds. The Response of a human bronchial epithelial cell line to histamine: Intracellular calcium changes and extracellular release of inflammatory mediators. [Washington, D.C: U.S. Environmental Protection Agency, 1992.
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16
R, Reddel Roger, and United States. Environmental Protection Agency., eds. A Human bronchial epithelial cell strain with unusual in vitro growth potential which undergoes neoplastic transformation after SV40 T antigen gene transfection. [Washington, D.C: U.S. Environmental Protection Agency, 1992.
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17
Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.
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Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.
18
Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.
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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.
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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.
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Lameire, Norbert, Raymond Vanholder, and Wim Van Biesen. Clinical approach to the patient with acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0222_update_001.
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The prognosis of acute kidney injury (AKI) depends on early diagnosis and therapy. A multitude of causes are classified according to their origin as prerenal, intrinsic (intrarenal), and post-renal.Prerenal AKI means a loss of renal function despite intact nephrons, for example, because of volume depletion and/or hypotension.There is a broad spectrum of intrinsic causes of AKI including acute tubular necrosis (ATN), interstitial nephritis, glomerulonephritis, and vasculitis. Evaluation includes careful review of the patient’s history, physical examination, urinalysis, selected urine chemistries, imaging of the urinary tree, and eventual kidney biopsy. The history should focus on the tempo of loss of function (if known), associated systemic diseases, and symptoms related to the urinary tract (especially those that suggest obstruction). In addition, a review of the medications looking for potentially nephrotoxic drugs is essential. The physical examination is directed towards the identification of findings of a systemic disease and a detailed assessment of the patient’s haemodynamic status. This latter goal may require invasive monitoring, especially in the oliguric patient with conflicting clinical findings, where the physical examination has limited accuracy.Excluding urinary tract obstruction is necessary in all cases and may be established easily by renal ultrasound.Distinction between the two most common causes of AKI (prerenal AKI and ATN) is sometimes difficult, especially because the clinical examination is often misleading in the setting of mild volume depletion or overload. Urinary chemistries, like calculation of the fractional excretion of sodium (FENa), may be used to help in this distinction. In contrast to FENa, the fractional excretion of urea has the advantage of being rather independent of diuretic therapy. Response to fluid repletion is still regarded as the gold standard in the differentiation between prerenal and intrinsic AKI. Return of renal function to baseline or resuming of diuresis within 24 to 72 hours is considered to indicate ‘transient, mostly prerenal AKI’, whereas persistent renal failure usually indicates intrinsic disease. Transient AKI may, however, also occur in short-lived ATN. Furthermore, rapid fluid application is contraindicated in a substantial number of patients, such as those with congestive heart failure.‘Muddy brown’ casts and/or tubular epithelial cell casts in the urine sediment are typically seen in patients with ATN. Their presence is an important tool in the distinction between ATN and prerenal AKI, which is characterized by a normal sediment, or by occasional hyaline casts. There is a possible role for new serum and/or urinary biomarkers in the diagnosis and prognosis of the patient with AKI, including the differential diagnosis between pre-renal AKI and ATN. Further studies are needed before their routine determination can be recommended.When a diagnosis cannot be made with reasonable certainty through this evaluation, renal biopsy should be considered; when intrarenal causes such as crescentic glomerulonephritis or vasculitis are suspected, immediate biopsy to avoid delay in the initiation of therapy is mandatory.
21
Frisch, Morten. Penile Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0055.
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Penile cancers are rare primary malignancies located on the glans, foreskin, or shaft of the penis, excluding the urethra. The vast majority of penile cancers are epithelial tumors representing histological subtypes of squamous cell carcinoma (SCC). Most penile SCCs are believed to develop through pre-invasive lesions known as penile intraepithelial neoplasia and penile carcinoma in situ. They account for 0.1%–0.3% of all incident cancers (excluding non-melanoma skin cancers) in the United States and other developed countries and up to 1% of all cancers in some countries in sub-Saharan Africa. Penile cancers are rare in men younger than 40 years, and are typically diagnosed among men above age 60. The two most important risk factors are pathological phimosis and infection with high-risk types of human papillomaviruses (HPV), both of which are preventable conditions.
22
Murphy, Barbara A., Lauren A. Zatarain, Anthony J. Cmelak, Steven Bayles, Ellie Dowling, Cheryl R. Billante, Sheila Ridner, et al. Palliative issues in the care of patients with cancer of the head and neck. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0145.
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Head and neck cancer (HNC) refers to tumours arising from the epithelial lining of the upper aerodigestive track, including the oral cavity, larynx, pharynx, paranasal sinuses, and salivary glands. There are 50,000 cases of HNC diagnosed annually within the United States. The majority of tumours (> 90%) are squamous cell carcinomas. Risk factors include tobacco, alcohol, and areca nuts; human papilloma virus (HPV) or Epstein-Barr virus; and mucosal irritation. Previously considered to be a disease of older adults, the epidemic of HPV-associated oropharyngeal cancers has led to a striking increase in HNC among middle-aged adults. Symptoms are usually present at the time of diagnosis and remain problematic through the terminal phase. For those patients who are cured, long-term biopsychosocial sequelae may persist for years. Thus, assessment and treatment of palliative issues is an intrinsic and vital component of care for the HNC patient.
23
DeAngelis, Lisa M. Primary Central Nervous System Lymphoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0133.
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The lymphoid nature of PCNSL was established unequivocally by modern immunohistochemical techniques. PCNSL has been associated with a variety of congenital (Wiskott-Aldrich syndrome, ataxia-telangiectasia) and acquired (human immunodeficiency virus [HIV], renal transplant recipients) immunodeficiency states. PCNSL tends to be supratentorial, periventricular, and involve the deep structures such as the basal ganglia. The Epstein-Barr virus (EBV) plays an important role in initiating the development of PCNSL in immunocompromised patients includinig those with HIV infection. Leukoencephalopathy is a serious complication of effective PCNSL treatment, but apparent only when the patient is in a durable remission. Treatment utilizes chemotherapy with or without radiation, which can cause more cognitive disability than chemotherapy, and autologous stem cell therapy is under investigation in selected patients.
24
Morris, Peter J., and Jeremy R. Chapman. The evolution of kidney transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0275.
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The history of kidney transplantation starts in 1902 with Ullman transplanting kidneys between dogs, and Carrel’s development of vascular anastomotic techniques. The developments in the 1950s in Boston, Paris, and the laboratories of Medawar and others demonstrated both proof of the principle and some of the barriers to clinical kidney transplantation. The 1960s laid the groundwork for organ preservation, immunosuppression, and histocompatibility leading to the creation of transplant units in many countries. In the 1970s, there was steady progress in understanding the immunology of allograft rejection and its suppression. The advent of azathioprine used with steroids in the early 1960s resulted in 1-year graft survival rates of around 60% and patient survival of 90% in good units. However, with the introduction of ciclosporin in the early 1980s, renal transplantation became an even more reliable renal replacement option as there was a dramatic reduction in the incidence of irreversible acute rejection. The 1990s saw the introduction of both better immunosuppression and better infection prophylaxis, which further improved patient outcomes. The first decade of the twenty-first century has been characterized by the promise of new technologies in many areas, only some of which have delivered clinical benefit. Molecular human leucocyte antigen (HLA) typing and detection of antibodies to HLA antigens, standardized immunosuppression and anti-infective prophylaxis, surveillance biopsy, and developing systems for increasing donation rates are delivering major benefits. Gene biomarkers, stem cell therapy, and tolerance protocols have yet to make an impact. This chapter describes the historical development of transplantation and how it has yielded the results delivered in clinical practice today.
25
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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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Gynaecological cancers. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0020_update_001.
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Genitourinary cancers examines the malignancies arising in the kidney, ureter, bladder, prostate, testis, and penis. Renal cancer has high propensity for systemic spread, largely mediated by overexpression of vascular endothelial growth factor (VEGF). Treatments include surgery, immunotherapy, and targeted therapy. Wilms tumour, a childhood malignancy of the kidney, warrants specialist paediatric oncology management to provide expertise in its unique pathology, staging, and treatment, often with surgery and chemotherapy. Cancer of the bladder and ureters, another tobacco related cancer, may present as either superficial or invasive disease. The former is managed by transurethral resection and intravesical therapy. The latter may require radical surgery, preoperative chemotherapy, or radiotherapy. Prostate cancer, the commonest male cancer, is an androgen dependent malignancy. It has attracted controversy with regards to PSA screening, and potential over treatment with radical prostatectomy. Division into low, intermediate, and high risk disease according to tumour grade, stage, and PSA helps in deciding best treatment, antiandrogen therapy for metastatic disease, radiotherapy and adjuvant hormone therapy for locally advanced disease, either surgery or radiotherapy for early intermediate risk disease, and active monitoring for low risk cases. Testicular cancer divides according to pathology into seminoma, nonseminomatous germ cell tumours (NSGCT), and mixed tumours, the latter two frequently producing tumour markers, alpha-fetoprotein (AFP) and/or human chorionic gonadotrophin (HCG). Stage I disease is managed by inguinal orchidectomy and surveillance or adjuvant chemotherapy. More advanced disease is managed by chemotherapy, with high probability of cure in the majority. Penile cancer, often HPV related, can be excised when it presents early, but delay in presentation may lead to regional and systemic spread with poor prognosis.
27
Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.
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The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
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Howard, Colin R. Arenaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0032.
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There are few groups of viral zoonoses that have attracted such widespread publicity as the arenaviruses, particularly during the 1960’s and 1970’s when Lassa emerged as a major cause of haemorrhagic disease in West Africa. More than any other zoonoses, members of the family are used extensively for the study of virus-host relationships. Thus the study of this unique group of enveloped, single-stranded RNA viruses has been pursued for two quite separate reasons. First, lymphocytic choriomeningitis virus (LCM) has been used as a model of persistent virus infections for over half a century; its study has contributed, and continues to contribute, a number of cardinal concepts to our present understanding of immunology. LCM virus remains the prototype of the Arenaviridae and is a common infection of laboratory mice, rats and hamsters. Once thought rare in humans there is now increasing evidence of LCM virus being implicated in renal disease and as a complication in organ transplantation. Second, certain arenaviruses cause severe haemorrhagic diseases in man, notably Lassa fever in Africa, Argentine and Bolivian haemorrhagic fevers in South America, Guaranito infection in Venezuela and Chaparé virus in Bolivia. The latter is a prime example for the need of ever-continuing vigilance for the emergence of new viral diseases; over the past few years several new arenaviruses have been reported as implicated with severe human disease and indeed the number of new arenaviruses discovered since the last edition of this book have increased the size of this virus family significantly.In common with LCM, the natural reservoir of these infections is a limited number of rodent species (Howard, 1986). Although the initial isolates from South America were at first erroneously designated as newly defined arboviruses, there is no evidence to implicate arthropod transmission for any arenavirus. However, similar methods of isolation and the necessity of trapping small animals have meant that the majority of arenaviruses have been isolated by workers in the arbovirus field. A good example of this is Guaranito virus that emerged during investigation of a dengue virus outbreak in Venezuela (Salas et al. 1991).There is an interesting spectrum of pathological processes among these viruses. All the evidence so far available suggests that the morbidity of Lassa fever and South American haemorrhagic fevers due to arenavirus infection results from the direct cytopathic action of these agents. This is in sharp contrast to the immunopathological basis of ‘classic’ lymphocytic choriomeningitis disease seen in adult mice infected with LCM virus and the use of this system for elucidating the phenomenon of H2-restriction of the host cytotoxic T cell response (Zinkernagel and Doherty 1979). Despite the utility of this experimental model for dissecting the nature of the immune response to virus infection and the growing interest in arenaviruses of rodents, there remains much to be done to elucidate the pathogenesis of these infections in humans.