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1
Hamamoto, Takeshi, and Takashi Ohsawa. Floating Body Cell: A Novel Capacitor-Less DRAM Cell. Jenny Stanford Publishing, 2011.
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2
Potts, Julie. Pay Less Attention to Your Cell, More Attention to Your Soul. Independently Published, 2022.
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3
Goldstein, Julia L. F. Material Value: More Sustainable, Less Wasteful Manufacturing of Everything from Cell Phones to Cleaning Products. Bebo Press, 2019.
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4
Material Value: More Sustainable, Less Wasteful Manufacturing of Everything from Cell Phones to Cleaning Products. Bebo Press, 2019.
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5
Goldstein, Julia L. F. Material Value: More Sustainable, Less Wasteful Manufacturing of Everything from Cell Phones to Cleaning Products. Bebo Press, 2019.
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6
Ferdek, Pawel, Wei Huang, Monika Jakubowska, and Ole Holger Petersen, eds. Spotlight on the Background Actors - Physiology and Pathophysiology of Supporting, Accessory and Less Common Cell Types in the Gastrointestinal Tract. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-992-2.
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Kahn, S. Lowell. Bland Lipiodol-Assisted Thermal Ablation of Renal Cell Carcinoma. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0073.
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Surgical resection of renal cell carcinoma (RCC) remains the standard of care given the excellent reported outcomes for early stage disease, with 5-year cancer-specific survival (CSS) rates of 97% for pT1a and 87% for pT1b tumors after nephrectomy. Outcomes after partial nephrectomy are equally encouraging, with 5- and 10-year CSS rates of 92% and 80%, respectively, across all stages and 96% and 90%, respectively, for tumors less than 4 cm. Transarterial embolization prior to thermal ablation for RCC is far less frequent, but it is described in the literature. To date, there are no randomized controlled studies that demonstrate a benefit of combined therapy over radiofrequency ablation (RFA) or cryoablation alone. However, lipiodol is profoundly radiopaque, and utilization prior to RFA or cryoablation may aid in the visualization of the tumor.
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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.
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Spinella, Philip C., and Jeffrey J. Bednarski. Hematology and Oncology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0013.
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Coagulopathy, thrombosis, and other hematological abnormalities are common in the pediatric intensive care unit . Current guidelines recommend red blood cell transfusion for a hemoglobin concentration less than 7 g/dL in critically ill, hemodynamically stable patients; platelets for a concentration less than 10,000 in nonbleeding patients; and cryoprecipitate in bleeding patients for fibrinogen values less than 100 to 150 mg/dL. Massive transfusion protocols that push blood products to the bedside are more practical than reactive protocols. Transfusion reactions include transfusion-associated acute lung injury and transfusion-associated circulatory overload. Hematologic crises in the PICU are commonly complications of other primary disorders. Sickle cell disease may lead to acute chest syndrome, sequestration crisis, and stroke, and require aggressive intervention. Oncological diseases produce hyperleukocytosis, tumor lysis syndrome, veno-occlusive disease, graft-versus-host disease, and sepsis in association with leukopenia. A relatively newly recognized disorder, hemophagocytic lymphohistiocytosis, requires early recognition and treatment to avoid adverse outcomes.
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Bunch, Chris. Haemolytic anaemia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0280.
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Haemolytic anaemias occur when the rate of red-cell breakdown is increased and exceeds the marrow’s capacity to generate new cells. Increased red-cell destruction, or haemolysis, may reflect a broad range of disorders. Some involve intrinsic defects in the red cell itself; in others, the red cells are normal but are subjected to external factors which lead to premature destruction. Many of the intrinsic defects are due to inherited disorders affecting the red-cell membrane, its enzymes, or haemoglobin. The marrow can normally compensate for moderate haemolysis by increasing red-cell production up to tenfold. Only when haemolysis is severe and the red-cell lifespan is reduced to less than about 15 days, or the marrow is unable to compensate, will anaemia occur. This chapter addresses the diagnosis, investigation, and management of haemolytic anaemias, including hereditary spherocytosis, paroxysmal nocturnal haemoglobinuria, glucose-6-phosphate dehydrogenase deficiency, haemoglobinopathies, and mechanical and immune haemolytic anaemias.
11
Elham, Bayat. Neurologic Manifestations of Hematological Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0193.
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A wide sprectum of hematologic disorders affect the central and peripheral nervous system. These disorders include porphyria, thrombotic thrombocytopenic purpura-hemolytic uremic syndromes, sickle cell disease, plasma cell dyscrasias, monoclonal gammopathy, primary systemic amyloidosis, primary systemic amyloidosis, Waldonstrom’s macroglobulinemia, myeloproliferative syndromes, cryoglobulinemia, and polycythemia vera. Some, like porphyria, cause both central and peripheral nervous system manifestations including sensory/motor peripheral neuropathy, dysautonomia, pain, seizures, and abdominal pain. Others such as sickle cell disease primarily affect the brain and cause both clinically apparent strokes associated with a vasculopathy of large intracranial blood vessels, as well as less obvious microstrokes that cause progressive cognitive decline if not treated.
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Matin, Rubeta, Jane McGregor, and Catherine Harwood. Skin cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0259.
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Skin cancer is very common in the UK, and its incidence is rising rapidly. There are two broad classes of primary skin cancer: non-melanoma and melanoma. Non-melanoma skin cancer is the commonest form (100 000 cases diagnosed annually in the UK), accounting for nine out of ten skin cancers and includes basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Cutaneous melanoma is less common (10 000 cases diagnosed in the UK annually) but confers a significantly worse prognosis and accounts for 75% of skin cancer related deaths. There are also a number of other, rarer, non-melanoma skin cancers (e.g. appendageal carcinomas, Merkel cell carcinoma, sarcomas, vascular malignancies, and cutaneous lymphomas); however, these account for less than 1% of all skin cancers in the UK and so will not be specifically discussed in this chapter. Cutaneous metastases can occur secondary to any internal cancer or, indeed, to skin cancer (e.g. melanoma). In most cases, cutaneous metastasis occurs after the diagnosis of a primary cancer and usually in late stages of the disease but, in some cases, it may be the first presentation, in which case it should prompt a thorough investigation for the primary malignancy.
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Wingard, John R. Introduction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199938568.003.0300.
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This chapter starts by explaining that the goal of allogeneic stem cell transplantation is the establishment of donor hematopoiesis and immunity in the recipient to treat an antecedent marrow failure disorder or to achieve a graft-versus-cancer effect to treat a neoplastic disease. The goal of autologous hematopoietic stem cell transplant (HSCT) is very different from allogeneic HSCT. In autologous HSCT, the goal of the graft is simpler: it is to rescue the myelotoxic effects of high-dose chemotherapy. Neutropenia is shorter, cellular immunodeficiency is less profound, and immune reconstitution is quicker. Infectious exposures before transplant play an important role after transplant. Although an infection may be effectively treated and under good control before transplant, reactivation may occur after transplant. The search for risk factors that can identify individuals at greatest risk for various types of infection has led to the identification of neutropenia, lymphopenia (or low CD4+ cell counts), low levels of immunoglobulin, and GVHD, prior infection by organisms that may persist in the recipient or donor, and a number of other factors in certain situations. The chapter concludes that one of the biggest challenges is distinguishing infection from some other noninfectious etiology of a syndrome.
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Hjalgrim, Henrik, Ellen T. Chang, and Sally L. Glaser. Hodgkin Lymphoma. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0039.
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Hodgkin lymphoma (HL) is a malignant neoplasm of the lymphatic system. The malignant cell clone derives from germinal center B lymphocytes in ~98% of cases, the rest being of T-lymphocyte origin. Each year, HL is diagnosed in roughly 66,000 individuals worldwide. HL is curable with modern therapy in the vast majority of patients, with five-year survival rates exceeding 90% for early-stage disease. However, so far this excellent prognosis has been achieved at the expense of a high incidence of severe long-term treatment complications such as secondary malignancies, and endocrine and cardiovascular diseases. In affluent Western countries, HL occurrence follows a distinctive and unusual bimodal age distribution, with one incidence peak among adolescents and younger adults and another in older adults. In socioeconomically less affluent populations, in contrast, the adolescent and younger-adult incidence peak is less pronounced, whereas incidence of HL in young boys may be higher than in affluent populations.
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Rush, David N., and Peter W. Nickerson. Rejection. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0283_update_001.
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Rejection of the transplanted kidney is an important cause of graft loss despite modern cross-matching techniques and immunosuppressive agents. The incidence of acute rejection episodes in the first post-transplant year is down to less than 15% in low-risk recipients, but as many as one-third of allograft losses over 10 years result from alloimmunity. Rejection may occur at any time following transplantation, from minutes—hyperacute, to days—acute, or in the longer term—chronic. Rejection can be predominantly through either T-cell-mediated or antibody-mediated mechanisms. It may present clinically as either abrupt or insidious dysfunction of the graft, or it may be subclinical and thus silent, detected only by protocol biopsy or other technology. The prevention and treatment of T-cell-mediated rejection is usually successful with current immunosuppressive agents. Antibody-mediated rejection, on the other hand, is not easily treated and is the principal cause of late renal allograft loss. This chapter presents the concepts and details of this central issue in clinical transplantation.
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Wolf, Farrah J., and Jason Iannuccilli. Percutaneous Thermal Ablation: Hydrodissection and Balloon Displacement to Protect Adjacent Non-Target Critical Structures. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0071.
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This chapter describes techniques that may be utilized to protect soft tissue structures and vessels that lie less than 1 cm from the planned ablation zone from thermal injury. Hydrodissection with dextrose 5% in water combined with non-ionic contrast material may be used as a means of providing mechanical displacement. Alternatively, an angioplasty balloon inflated with air may be used to provide both physical displacement and thermal insulation. This chapter provides an overview of the percutaneous image-guided thermal ablation technique as well as clinical examples, including microwave ablation of a renal cell carcinoma and radiofrequency ablation of a hepatocellular carcinoma, utilizing hydrodissection and balloon displacement techniques.
17
Rees, David. Haemoglobinopathies. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0172.
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Inherited abnormalities of the globin genes are the commonest single-gene disorders in the world and fall into two main groups: thalassaemias and sickle cell disease. Thalassaemias are due to quantitative defects in globin chain synthesis which cause variable anaemia and ineffective erythropoiesis. Thalassaemia was initially thought to be a disease of the bones due to uncontrolled bone marrow expansion causing bony distortion, although this is now unusual with appropriate blood transfusions. Osteopenia, often severe, is a feature of most patients with thalassaemia major and intermedia, caused by bone marrow expansion, iron overload, endocrinopathy, and iron chelation. Treatment with bisphosphonates is generally recommended. Other rheumatological manifestations include arthropathy associated with the use of the iron chelator deferiprone. Sickle cell disease involves a group of conditions caused by polymerization of the abnormal -globin chain, resulting in abnormal erythrocytes which cause vaso-occlusion, vasculopathy, and ischaemic tissue damage. The characteristic symptom is acute bone pain caused by vaso-occlusion; typical episodes require treatment with opiate analgesia and resolve spontaneously by 5 days with no lasting bone damage. The frequency of acute episodes varies widely between patients. The incidence of osteomyelitis is increased, particularly with salmonella, although it is much rarer than acute vaso-occlusion. Avascular necrosis can affect the hips, and less commonly the shoulders and knees. Coincidental rheumatological disease sometimes complicates the condition, particularly systemic lupus erythematosus (SLE) which is more prevalent in populations at increased risk of sickle cell disease.
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Rees, David. Haemoglobinopathies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0172_update_001.
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Inherited abnormalities of the globin genes are the commonest single-gene disorders in the world and fall into two main groups: thalassaemias and sickle cell disease. Thalassaemias are due to quantitative defects in globin chain synthesis which cause variable anaemia and ineffective erythropoiesis. Thalassaemia was initially thought to be a disease of the bones due to uncontrolled bone marrow expansion causing bony distortion, although this is now unusual with appropriate blood transfusions. Osteopenia, often severe, is a feature of most patients with thalassaemia major and intermedia, caused by bone marrow expansion, iron overload, endocrinopathy, and iron chelation. Treatment with bisphosphonates is generally recommended. Other rheumatological manifestations include arthropathy associated with the use of the iron chelator deferiprone. Sickle cell disease involves a group of conditions caused by polymerization of the abnormal -globin chain, resulting in abnormal erythrocytes which cause vaso-occlusion, vasculopathy, and ischaemic tissue damage. The characteristic symptom is acute bone pain caused by vaso-occlusion; typical episodes require treatment with opiate analgesia and resolve spontaneously by 5 days with no lasting bone damage. The frequency of acute episodes varies widely between patients. The incidence of osteomyelitis is increased, particularly with salmonella, although it is much rarer than acute vaso-occlusion. Avascular necrosis can affect the hips, and less commonly the shoulders and knees. Coincidental rheumatological disease sometimes complicates the condition, particularly systemic lupus erythematosus (SLE) which is more prevalent in populations at increased risk of sickle cell disease.
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Turner, Neil. Exercise-related pseudonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0049.
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Vigorous and prolonged physical exercise can produce a range of urinary abnormalities which would normally be considered alarming. They include haematuria, haemoglobinuria, the appearance in urine of red cells in urine, some fragmented in a ‘glomerular’ manner, red cell cast formation, and proteinuria. A variety of names have been given to these syndromes, including march haematuria and march haemoglobinuria. Mostly these changes seem benign and self-limiting. Rarely they are associated with acute kidney injury but this is often in the context of other renal insults, extreme dehydration, or hyperpyrexic conditions. Vigorous exercise is also commonly associated with various electrolyte changes related to both over- and under-hydration. These can complicate assessment. Transient proteinuria in the absence of haematuria appears to be a physiological response to even short-term exercise, its degree related to the intensity of the exercise. Causation of these syndromes is mixed and not fully explained. There is good evidence for physical trauma to red cells being a significant part, but this cannot explain the appearance of glomerular red cells and red cell casts. Exercise-related changes mostly resolve within less than a day, and almost all by 72 hours.
20
Vervaet, Benjamin A., and Marc E. De Broe. Cell biology of nephrocalcinosis/nephrolithiasis. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0204.
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A dozen conditions are regularly associated with nephrocalcinosis, and two dozen more less frequently. Mechanisms of intratubular and interstitial crystal formation, and propagation or removal, as well as inhibitors of crystal formation, are described.
21
Southwood, Russell. Less Walk More Talk: How Celtel and the Mobile Phone Changed Africa. Wiley & Sons, Limited, John, 2020.
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22
Poretti, Andrea, and Michael V. Johnston. Genetic Disorders and Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0110.
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A variety of monogenic and polygenic genetic disorders have been linked to stroke, making it important for the clinician to keep up with the new discoveries and the potential to provide new gene-based therapies. Hematologic disorders such as sickle cell disease and thrombophilia due to mutations in prothrombin, factor V Leiden, and homocysteine metabolism are fairly well known, but mutations in mitochondrial metabolism and matrix metalloproteinases are less recognized. In addition, results of genome-wide association studies (GWAS) in stroke populations are revealing mutations that could predispose to stroke in specific ethnic populations. These studies are also revealing some crossover in mutations between stroke and familial hemiplegic migraine as well as mutations in growth factors such as brain derived neurotrophic factor (BDNF) that appear to influence the recovery from stroke by altering cortical plasticity.
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Johnson, Elizabeth M. Hyaline moulds. 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/9780198755388.003.0017.
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Hyaline moulds are fungi that grow predominantly in a filamentous form with colourless hyphae. This is not a taxonomic grouping and encompasses many thousands of different fungal genera. However, there is a small subset of environmental saprobes or plant pathogenic moulds, currently comprising at least 75 species from 30 different genera, that are opportunistic human pathogens and have been implicated in invasive infections referred to as hyalohyphomycosis. In addition they may cause less invasive cutaneous, subcutaneous, mucous membrane, and corneal infections. This group of organisms includes Fusarium, Sarocladium, Paecilomyces, Purpureocillium, Scedosporium, Rasamsonia, and Scopulariopsis spp., and it is these that form the focus of this chapter. Aspects of taxonomy, cell biology, pathogenesis, epidemiology, incidence, risk factors, presentation, diagnosis, and treatment are discussed with particular reference to those features that are specific to hyaline moulds.
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Brinton, Louise A., Mia M. Gaudet, and Gretchen L. Gierach. Breast Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0045.
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Breast cancer is the most frequently diagnosed cancer in women worldwide, with annual estimates of 1.7 million newly diagnosed cases and 522,000 deaths. Although more breast cancers are diagnosed in economically developed than in developing countries, the reverse is true for mortality, reflecting limited screening and less effective treatments in the latter. Breast cancer incidence has been on the rise in the United States for many years, but in recent years this is restricted to certain subgroups, while internationally there have been continued generalized increases, likely reflecting adoption of more Westernized lifestyles. Breast cancer is widely recognized as being hormonally influenced, with most of the established risk factors believed to reflect the influence of cumulative exposure of the breast to stimulatory effects of ovarian hormones—leading to increased cellular proliferation, which in turn can result in genetic errors during cell division.
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McDougal, Topher L. Trade Networks and the Management of the Combat Frontier. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198792598.003.0007.
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This chapter fleshes out the causal mechanisms motivating the results of Chapter 5 with interviews of traders who cross the Maoist territorial border. It contends the hierarchical form of the caste-based Indian society gives rise to trade networks in which a caste-based division of labor arises: lower-castes engage in local trade, higher-castes in long-distance trade. By enforcing the caste bar on tribal people in long-distance trade, long-distance traders ensure that trade taking place between Maoist-held hinterlands and government-controlled cities remains in the hands of an elite few. Those elite long-distance traders can then strike deals with Maoist cells for trade access, thereby incentivizing Maoists to firmly hold onto their own territory, while discouraging them from taking over such profitable towns. Moreover, this mechanism helps explain why well-connected towns are less violently targeted by rebels: they tend to have more upper-caste traders, limiting their bargaining power vis-à-vis Maoist cell leaders.
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Jacobs, Samantha E., Catherine B. Small, and Thomas J. Walsh. Fungal diseases of the respiratory tract. 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/9780198755388.003.0030.
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Fungal respiratory infections are important causes of morbidity and mortality in immunocompromised patients. Invasive aspergillosis remains the most common invasive fungal infection whereas other filamentous fungi, such as Fusarium spp., Mucorales, and Scedosporium spp., are increasing in frequency, particularly in neutropenic hosts. Endemic mycoses, including those due to Histoplasma capsulatum, Coccidioides spp., and Talaromyces marneffei, are increasingly prevalent in patients with cell-mediated immunodeficiencies in respective geographic regions. Culture remains the gold standard of diagnosis but has limited sensitivity and often requires invasive procedures. Non-invasive diagnostic tests, including the serum sandwich enzyme immunoassay for the detection of galactomannan, the (1→3)-β-D-glucan assay, and molecular amplification methods have been developed to facilitate early and accurate diagnosis. Successful therapy depends upon early initiation of antifungal agents and reversal of immunosuppression. Lipid formulations of amphotericin B and newer generation triazoles including voriconazole, posaconazole, and isavuconazole have expanded the ability to treat multi-drug resistant pathogens more effectively and with less toxicity.
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Hjalgrim, Henrik, Mads Melbye, and Pagona Lagiou. Hodgkin Lymphoma. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0026.
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The descriptive epidemiology of Hodgkin lymphoma (HL) has demonstrated marked variation by age, sex, social class, and time, strongly suggesting both a role of environmental factors and the existence of etiologically diverse HL subtypes. There is increasing evidence that Epstein Barr virus (EBV)–positive and EBV-negative classical HLs define two variants with separate etiologies. The risk for both increases with family history, whereas immune dysfunction and infectious mononucleosis have been implicated in EBV-positive HL risk only. Despite being the less common of the two, the natural history of EBV-positive HL is currently the best understood, both with respect to how EBV may contribute to malignant cell transformation and in relation to constitutional and environmental risk factors. Meanwhile, the understanding of the natural history of EBV-negative HL is meager. Future research for EBV-negative HL is expected to focus on its presumed infectious etiology, for which there are currently no strong candidates.
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Robinson, Peter. Shakespeare’s Loose Ends and the Contemporary Poet. Edited by Jonathan Post. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199607747.013.0026.
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‘Shakespeare’s Loose Ends and the Contemporary Poet’ contains detailed readings of individual poems with a Shakespearean theme by John Ashbery (‘Friar Laurence’s Cell’), Elizabeth Bishop (‘Twelfth Morning; or What You Will’), Roy Fisher (‘Barnardine’s Reply’), alongside passages from Geoffrey Hill’s ‘Funeral Music’ and The Triumph of Love, as well as observations about a number of other Shakespeare-inspired poems. It deploys them to sustain and illustrate an argument that contrasts with the noted attempts by earlier modernist poets such as Yeats, Eliot, Auden, and Ted Hughes to incorporate theories of Shakespeare’s organic creative unity into their oeuvres. Rather, this chapter proposes that it is the heterogeneity, the loose ends and frayed edges of the Shakespearean corpus that have inspired contemporary poets, prompting them to come at their own materials by means of the oblique angles provided by minor characters, such as Barnardine in Measure for Measure or the poet Cinna in Julius Ceasar, and less highly regarded plays, such as the early Henry VI cycle, finding thematic suggestions in implications that remain to be spelt-out in Shakespearean scenes, dialogues, and plot trajectories.
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Clarke, Andrew. Global temperature and life. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0014.
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The extreme meteorological surface air temperatures recorded to date are –89.2 oC in Antarctica, and 56.7 oC in Death Valley, California. Ground temperatures can be higher or lower than these air temperatures. The bulk of oceanic water is cold (< 4 oC) and thermally stable. Whilst data on limits to survival attract considerable attention, the thermal limits to completion of the life cycle (which define the limits to life) are much less well known. Currently identified upper thermal limits for growth are 122 oC for archaeans, 100 oC for bacteria and ~60 oC for unicellular eukaryotes. No unicells appear to grow below –20 oC, a limit that is probably set by dehydration-linked vitrification of the cell interior. The lower thermal limits for survival in multicellular organisms in the natural world extend to at least –70 oC. However in all cases known to date, completion of the life cycle requires summer warmth and the lowest temperature for completion of a multicellular eukaryote life cycle appears to be ~0 oC for invertebrates in glacial meltwater and ~–2 oC for marine invertebrates and fish living on the continental shelves around Antarctica.
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Reber, Arthur S. The First Minds. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190854157.001.0001.
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The book presents a novel theory of the origins of mind and consciousness dubbed the Cellular Basis of Consciousness (CBC). It argues that sentience emerged with life itself. The most primitive unicellular species of bacteria are conscious, though it is a sentience of a primitive kind. They have minds, though they are tiny and limited in scope. There is nothing even close to this thesis in the current literature on consciousness. Hints that cells might be conscious can be found in the writings of a few cell biologists, but a fully developed theory has never been put forward before. Other approaches to the origins of consciousness are examined and shown to be seriously or fatally flawed, specifically ones based on: (a) the assumption that minds are computational and can be captured by an artificial intelligence (AI), (b) efforts to discover the neurocorrelates of mental experiences, the so-called Hard Problem, and (c) looking for consciousness in less complex species by identifying those that possess precursors of those neurocorrelates. Each of these approaches is shown to be either essentially impossible (the AI models) or so burdened by philosophical and empirical difficulties that they are effectively unworkable. The CBC approach is developed using standard models of evolutionary biology. The remarkable repertoire of single-celled species that micro- and cell-biologists have discovered is reviewed. Bacteria, for example, have sophisticated sensory and perceptual systems, learn, form memories, make decisions based on information about their environment relative to internal metabolic states, communicate with one another, and even show a primitive form of altruism. All such functions are indicators of sentience. Conversations with a caterpillar function as a literary vehicle Finally, the implications of the CBC model are discussed along with a number of related issues in evolutionary biology, philosophy of mind, the possibility of sentient plants, the ethical repercussions of universal animal sentience, and the long-range impact of adopting the CBC stance.
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Niaudet, Patrick, and Alain Meyrier. Minimal change disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0056_update_001.
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Minimal change disease is characteristically responsive to high-dose corticosteroids. As this is the most common cause of nephrotic syndrome in children, and responses are usually prompt, response to 60 mg/m2/day of oral prednisolone (max. 80 mg) is often used as a diagnostic test. Adults respond more slowly and have a wider differential diagnosis, and often a high risk of side effects, so therapy is not recommended without confirmation by renal biopsy. Then first-line treatment is again prednisolone or prednisone, at 1 mg/kg/day (max. 60 mg). KDIGO and other treatment protocols recommend 6 weeks treatment at full dose then 6 weeks at half dose. Shorter protocols seem to increase the risk of relapse. Children frequently have a relapsing pattern of disease which may be managed by less extreme steroid exposure, but for which second-line therapies may be needed to avoid severe steroid side effects. This can arise in adults too. Some children and adults have steroid-dependent or steroid-resistant disease, leading to earlier initiation of treatment with second-line agents. These include levamisole, calcineurin inhibitors, mycophenolate mofetil, and anti-B cell antibodies. The evidence for these and recommendations for relapsing/resistant disease are given in this chapter.
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Plutynski, Anya. Explaining Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199967452.001.0001.
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Cancer is the second leading cause of death in the world. Almost everyone’s life is in some way or other affected by cancer. Yet, when faced with a cancer diagnosis, many of us will confront questions we had never before considered: Is cancer one disease, or many? If many, how many exactly? How is cancer classified? What does it mean, exactly, to say that cancer is “genetic,” or “familial”? What exactly are the causes of cancer, and how do scientists come to know about them? When do we have good reason to believe that this or that is a risk factor for cancer? These questions are (in part) empirical ones; however, they are also (in part) philosophical. That is, they are questions about what and how we come to know. They are about how we define and classify disease, what counts as a “natural” classification, what it means to have good evidence, and how we pick out causes as more or less significant. This book takes a close look at these philosophical questions, by examining the conceptual and methodological challenges that arise in cancer research, in disciplines as diverse as cell and molecular biology, epidemiology, clinical medicine, and evolutionary biology.
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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.
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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.
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Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.
Full textAbstract:
The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
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Grant, Robert. Neurocutaneous syndromes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0235.
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This chapter describes several neurocutaneous syndromes, including tuberous sclerosis, neurofibromatosis, Sturge–Weber syndrome, Von-Hippel–Lindau disease and ataxia telangiectasia amongst others.Tuberous sclerosis, also known as Epiloia or Bournville’s Disease, is an autosomal dominant multisystem disease it usually presents in childhood with a characteristic facial rash, adenoma sebaceum, seizures, and sometimes learning difficulties. Central nervous system lesions in tuberous sclerosis are due to a developmental disorder of neurogenesis and neuronal migration. Other organs such as the heart and kidney are less commonly involved. The condition has very variable clinical expression and two-thirds of cases are thought to be new mutations, therefore it is important to examine and screen relatives. Management may involve many specialists and close co-operation between specialists is essential.The neurofibromatoses are autosomal-dominant neurocutaneous disorders that can be divided into ‘peripheral’ and ‘central’ types, although there is significant overlap. The characteristic features of neurofibromatosis type 1 are café au lait spots, neurofibromas, Lisch nodules, osseous lesions, macrocephaly, short stature and mental retardation, axillary freckling, and associations with several different types of tumours.Sturge–Weber syndrome involves a characteristic ‘port-wine’ facial naevus or angioma associated with an underlying leptomeningeal angioma or other vascular anomaly. It affects approximately 1/20 000 people. There can be seizures, low IQ, and underlying cerebral hemisphere atrophy as a result of chronic state of reduced perfusion and increased oxygen extraction. Patients may present with focal seizures which are generally resistant to anticonvulsant medication and can develop glaucoma.Von-Hippel– Lindau disease is one of the most common autosomal-dominant inherited genetic diseases that are associated with familial cancers. Von-Hippel–Lindau disease is characterized by certain types of central nervous system tumours, cerebellar and spinal haemangioblastomas, and retinal angiomas, in conjunction with bilateral renal cysts carcinomas or phaechromocytoma, or pancreatic cysts/islet cell tumours (Neumann and Wiestler 1991).Other neurocutaneous syndromes discussed include Hypomelanosis of Ito, Gorlin syndrome, Sjogren–Larsson syndrome, Proteus syndrome, Hemiatrophy and hemihypertrophy, Menke’s syndrome, Xeroderma pigmentosum and Cockayne’s syndrome.
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Kuypers, Dirk R. J., and Maarten Naesens. Immunosuppression. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.
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Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids and corticosteroids has been fine-tuned over the last decade, based on empirically derived observations as well as on the results of large multicentre randomized clinical studies. Corticosteroid withdrawal and avoidance are feasible, at least in patients with a low immunological risk, but CNI-free protocols have had few long-term successes. Some minimization strategies have increased risk of developing acute rejection or (donor-specific) anti-HLA antibodies, with deleterious effects on the graft. Mammalian target of rapamycin inhibitors (mTORi) have shown limited benefit in early CNI replacement regimens and their long-term use as primary drug is hampered by intolerance. In the setting of particular malignant disease occurring after transplantation, such as squamous cell carcinoma of the skin and Kaposi’s sarcoma, mTORi seem promising. Induction agents (anti-interleukin 2 receptor monoclonal antibodies, antithymocyte globulins) effectively diminish the risk of early immunological graft loss in recipients with moderate to high immunological risk but at the price of more infectious or malignant complications. While personalized transplantation medicine is only in its early stages of development, attempts are made to quantitatively measure the clinical degree of immunosuppression, to tailor immunosuppressive therapy more specifically to the patient’s individual profile, and to monitor graft status by use of invasive (e.g. surveillance renal biopsies) and non-invasive biomarkers. These scientific endeavours are a necessity to further optimize the current immunosuppressive therapy which will remain for some time to come.
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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/9780199592548.003.0073_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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Grant, Warren, and Martin Scott-Brown. Prevention of cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0350.
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In the UK, the four commonest cancers—lung cancer, breast cancer, colon cancer, and prostate cancer—result in around 62 000 deaths every year. Although deaths from cancer have fallen in the UK over the last 20 years, the UK still suffers from higher cancer death rates than many other countries in Western Europe. In 1999, the UK government produced a White Paper called Saving Lives: Our Healthier Nation that outlined a national target to reduce the death rate from cancer by at least 20% in people under 75 by 2010. The subsequent NHS Cancer Plan of 2000 designed a framework by which to achieve this target through effective prevention, screening, and treatment programmes as well as restructuring and developing new diagnostic and treatment facilities. But do we know enough about the biology of the development of cancer for government health policies alone to force dramatic changes in survival? The science behind the causes of cancer tells us that its origin lies in acquired or inherited genetic abnormalities. Inherited gene mutation syndromes and exposure to environmental mutagens cause cancer, largely through abnormalities in DNA repair mechanisms, leading to uncontrolled cell proliferation. Although screening those thought to be at highest risk, and regulating exposure to environmental carcinogens such as tobacco or ionizing radiation, have reduced, and will continue to reduce, cancer deaths, there are many other environmental factors that have been shown to increase the population risk of cancer. These will be outlined in this chapter. However, the available evidence is largely from retrospective and cross-sectional population-based studies and therefore limits the ability to apply this knowledge to the risk of the individual patient who may been seen in clinic. Although we may be able to put him or her into a high-, intermediate-, or low-risk category, the question ‘will I get cancer, doc?’ is one that we cannot answer with certainty. The NHS Cancer Plan of 2000, designed to reduce cancer deaths in this country and to bring UK treatment results in line with those other countries in Europe, focuses on preventing malignancy as part of its comprehensive cancer management strategy. It highlights that the rich are less likely to develop cancer, and will survive longer if they are diagnosed than those who live in poverty. This may reflect available treatment options, but is more likely to be related to the lifestyle of those with regular work, as they may be more health aware. The Cancer Plan, however, suggests that relieving poverty may be more labour intensive and less rewarding than encouraging positive risk-reducing behaviour in all members of the population. Eating well can reduce the risk of developing many cancers, particularly of the stomach and bowel. The Cancer Plan outlines the ‘Five-a-Day’ programme which was rolled out in 2002 and encouraged people to eat at least five portions of fruit and vegetables per day. Obese people are also at higher risk of cancers, in particular endometrial cancer. A good diet and regular exercise not only reduce obesity but are also independent risk-reducing factors. Alcohol misuse is thought to be a major risk factor in around 3% of all cancers, with the highest risk for cancers of the mouth and throat. As part of the Cancer Plan, the Department of Health promotes physical activity and general health programmes, as well as alcohol and smoking programmes, particularly in deprived areas. Focusing on these healthy lifestyle points can potentially reduce an individual lifetime risk of all cancers. However, our knowledge of the biology of four cancers in particular has led to the development of specific life-saving interventions. Outlined in this chapter are details regarding ongoing prevention strategies for carcinomas of the lung, the breast, the bowel, and the cervix.