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1
Institut d'aménagement et d'urbanisme de la région d'Île de France., ed. La mutation du site de Billancourt: Contexte et enjeu d'un projet. Paris: I.A.U.R.I.F., 1990.
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2
McPherson, M.J., (Ed.), ed. Directed Mutagenesis: A Practical Approach. Oxford: I.R.L. P., 1991.
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3
J, McPherson M., ed. Directed mutagenesis: A practical approach. Oxford [England]: IRL Press, 1991.
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4
R, Ballain, ed. Sites urbains en mutation: Territoires et trajectoires. Paris: L'Harmattan, 1990.
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5
Meslé, Jean-Yves. SMN, Société métallurgique de Normandie: Mémoires et mutations d'un site industriel. Bayeux: OREP, 2013.
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6
Khan, Amir R. Mutational and structural analysis of second-site transmembrane region mutants of phage M13 coat protein. Ottawa: National Library of Canada, 1993.
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7
McPherson, M. J. Directed Mutagenesis: A Practical Approach (Practical Approach Series). Oxford University Press, USA, 1991.
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8
McPherson, M. J. Directed Mutagenesis: A Practical Approach (The Practical Approach Series). Oxford University Press, USA, 1991.
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9
Bergmann, Carsten, and Klaus Zerres. Autosomal recessive polycystic kidney disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0313.
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Autosomal recessive polycystic kidney disease (ARPKD) is an important cause of childhood renal- and liver-related morbidity and mortality with variable disease expression. Many patients manifest peri- or neonatally with a mortality rate of 30–50%, whereas others survive to adulthood with only minor clinical features. ARPKD is typically caused by mutations in the PKHD1 gene that encodes a 4074-amino acid type 1 single-pass transmembrane protein called fibrocystin or polyductin. Fibrocystin/polyductin is among other cystoproteins expressed in primary cilia, basal bodies, and centrosomes, but its exact function has still not been fully unravelled. Mutations were found to be scattered throughout the gene with many of them being private to single families. Correlations have been drawn for the type of mutation rather than for the site of the individual mutation. Virtually all patients carrying two truncating mutations display a severe phenotype with peri- or neonatal demise while surviving patients bear at least one hypomorphic missense mutation. However, about 20–30% of all sibships exhibit major intrafamilial phenotypic variability and it becomes increasingly obvious that ARPKD is clinically and genetically much more heterogeneous and complex than previously thought.
10
Walsh, Bruce, and Michael Lynch. The Genetic Effective Size of a Population. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0003.
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The effects of genetic drift usually assume an idealized population of constant size. This chapter shows how the population size for such an idealized population can be replaced with an effective population size for populations with age structure, unequal sex ratios, a history of expansion or contraction, inbreeding, and population subdivision. These demographic features impact the entire genome more or less equally. A relatively recent understanding is that selection at a site can dramatically reduce the local effective population size experienced by nearby linked sites (the Hill-Robertson effect). This can arise from background selection to remove deleterious new mutations or from selective sweeps wherein favorable new mutations are driven toward fixation. The Hill-Robertson effect is a general way to describe the fact that selection at a site makes selection are other linked sites less efficient, and, therefore, more neutral. This chapter discusses the implications of this finding for genome structure.
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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.
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Walsh, Bruce, and Michael Lynch. The Nonadaptive Forces of Evolution. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0004.
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This chapter examines the relative strengths of the nonadaptive evolutionary forces (drift, mutation, recombination) acting on genomes. It reviews estimators for effective population size, mutation rate, and recombination rate, and summarizes the known genomic results over a wide range of taxa. The mutation rate tends to be lower in organisms with larger effective population sizes, consistent with the drift-barrier hypothesis wherein selection is ineffective when it is less than the reciprocal of the effective population size.
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Frankham, Richard, Jonathan D. Ballou, Katherine Ralls, Mark D. B. Eldridge, Michele R. Dudash, Charles B. Fenster, Robert C. Lacy, and Paul Sunnucks. Loss of genetic diversity reduces ability to adapt. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198783398.003.0004.
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Environmental change is a ubiquitous feature of the conditions faced by species, so they must either evolve, move to avoid threats, or perish. Species require genetic diversity to evolve to cope with environmental change through natural selection (adaptive evolution). The ability of populations to undergo adaptive evolution depends upon the strength of selection, genetic diversity, effective population size, mutation rates and number of generations. Loss of genetic diversity in small populations reduces their ability to evolve to cope with environmental change, thus increasing their extinction risk. Adaptive evolution in the short to medium term predominantly utilizes pre-existing genetic diversity, but new mutations make increasing contributions in later generations. Evolutionary potential can be estimated from the heritability of fitness in the environment of interest, or by extrapolation from genomic diversity.
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Walsh, Bruce, and Michael Lynch. Long-term Response: 2. Finite Population Size and Mutation. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0026.
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In a finite population, drift is often more important than selection in removing any initial additive variance. This chapter examines the joint impact of selection, drift, and mutation on the long-term response in a quantitative trait. One key result is the remarkable finding of Robertson that the expected long-term response from any initial additive variance is bounded above by the product of twice the effective population size times the initial response. This result implies that the optimal selection intensity for long-term response it to save half of the population in each generation.
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Schmeink, Lars. The Utopian, the Dystopian, and the Heroic Deeds of One. Liverpool University Press, 2017. http://dx.doi.org/10.5949/liverpool/9781781383766.003.0006.
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Chapter 6 discusses the TV series Heroes as more optimistic in its depiction of the social consequences of posthuman evolution than the other texts analyzed. The show's premise of posthumanity as a result of evolutionary mutation reflects radical changes in subjectivity not onto an elite few, as in classic superhero narratives, but onto the everyday man. The series consequently emphasizes the potential of the posthuman condition as a catalyst for global social and political change – a solution to the 'big issues' that elude the current institutions of power. The posthuman becomes the site of struggle over the potential changes to the future, in effect over the concept of utopia. In contrasting dystopian futures with the present possibility of change through posthumanity, the show allows a utopian space to emerge, in which global issues such as the war on terror can be solved and attacks such as those on 9/11 could be prevented. In this, Heroes returns to humanist notions and concepts of history as events shaped by exceptional individuals, while at the same time complicating them with communal images of a cooperative and interconnected posthuman subjectivity.
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Walsh, Bruce, and Michael Lynch. Hitchhiking and Selective Sweeps. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198830870.003.0008.
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When a favorable allele increases in frequency, it alters the coalescent structure (the pattern of times back to a common ancestor) at linked sites relative to that under drift. This creates patterns of sequence polymorphism than can be used to potentially detect ongoing, or very recent, selection. This idea of a neutral allele hitchhiking up to high frequency when coupled to a favorable allele is the notion of a selective sweep, and this chapter reviews the considerable body of associated population-genetics theory on sweeps. Different types of sweeps leave different signatures, resulting in the very diverse collection of tests of selection discussed in Chapter 9. Either a history of recurrent sweeps, or of background selection, results in linked genomic regions of reduced effective population size. This implies that more mutations in sich regions are efficiently neutral, which can result in increased substitution rates and lower codon bias. Finally, the chapter examines the theory for when response is expected to start from existing variation, as opposed to waiting for the appearance of new mutations.
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Frankham, Richard, Jonathan D. Ballou, Katherine Ralls, Mark D. B. Eldridge, Michele R. Dudash, Charles B. Fenster, Robert C. Lacy, and Paul Sunnucks. Evolutionary genetics of small populations. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198783398.003.0002.
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Genetic management of fragmented populations involves the application of evolutionary genetic theory and knowledge to alleviate problems due to inbreeding and loss of genetic diversity in small population fragments. Populations evolve through the effects of mutation, natural selection, chance (genetic drift) and gene flow (migration). Large outbreeding, sexually reproducing populations typically contain substantial genetic diversity, while small populations typically contain reduced levels. Genetic impacts of small population size on inbreeding, loss of genetic diversity and population differentiation are determined by the genetically effective population size, which is usually much smaller than the number of individuals.
18
Psylicon Beach. Scholastic Press, 1998.
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19
Saleem, Moin A., and Corinne Antignac. Molecular basis of nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0327_update_001.
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Nephrotic syndrome is broadly a disorder of the glomerular filtration barrier, but in practice the site of dysfunction in the great majority of pathologies is in the podocyte. Genetic causes of nephrotic syndrome provide the strongest proof of this. Almost all the genetic associations with nephrotic syndrome are podocyte proteins. Some basement membrane protein mutations associated with nephrotic syndrome may act through signalling to podocytes, or by causing severe disruption to their environment.
20
Krupkin, Alexander Bennett. Chloroplast DNA phylogeny of hard pines (subgenus Pinus): Inference from site mutations and multiple small (1-10 Kb) inversions. 1992.
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21
Wagner, Carsten A., and Olivier Devuyst. Renal acid–base homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0024.
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The kidney is central to acid–base homeostasis. Major processes are reabsorption of filtered bicarbonate, de novo synthesis of bicarbonate from ammoniagenesis, and net excretion of protons. The latter requires buffers such as ammonium, phosphate, citrate and other bases binding protons (so-called titratable acids). The proximal tubule is the major site of bicarbonate reabsorption and only site of ammoniagenesis. The thick ascending limb and the distal convoluted tubule handle ammonia/ammonium and complete bicarbonate reabsorption. The collecting duct system excretes protons and ammonium, but may switch to net bicarbonate secretion. The kidney displays a great plasticity to adapt acid or bicarbonate excretion. Angiotensin II, aldosterone and endothelin are involved in regulating these processes, and they induce morphological changes along the nephron. Inborn and acquired disorders of renal acid–base handling are caused by mutations in acid–base transport proteins or by dysregulation of adaptive mechanisms.
22
Sage, Evelyne, Regen Drouin, Donat P. Hader, Mahmoud Rouabhia, and Giulio Jori. From DNA Photolesions to Mutations, Skin Cancer and Cell Death. Royal Society of Chemistry, The, 2007.
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23
Schreuder, Michiel F. Renal tubular dysgenesis. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0350.
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Renal tubular dysgenesis involves the absence or incomplete differentiation of proximal tubular nephron segments. Due to the lack of a patent nephron, it is characterized by (fetal) anuria and subsequent oligohydramnios, pulmonary hypoplasia, premature birth with severe and refractory arterial hypotension, and fetal or neonatal death. The main cause for renal tubular dysgenesis is a genetic mutation in the renin–angiotensin system, which has shown an autosomal recessive trait. Maternal use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers during pregnancy can have similar blocking effects on the fetal renin–angiotensin system, which may lead to renal tubular dysgenesis. Even though there is no actual renal function, ultrasound usually shows kidneys of normal size and architecture with an intact corticomedullary differentiation. Most patients with renal tubular dysgenesis do not survive beyond the neonatal period. A few patients have been described to survive with respiratory support, vasopressor treatment, and dialysis.
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Sayer, John A., and Roslyn J. Simms. Nephronophthisis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0317_update_001.
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Nephronophthisis (NPHP) is a clinically heterogeneous autosomal recessive cystic kidney disease and the leading genetic cause of end-stage renal failure in children and young adults. Whilst enlarged dysplastic cystic kidneys are associated with infantile NPHP, more typically renal ultrasound reveals normal kidney size and corticomedullary cysts in a child with polyuria and secondary enuresis. Extrarenal manifestations occur in 10–15% including retinal degeneration, cerebellar vermis hypoplasia and liver fibrosis, requiring referral to other specialists. Mutations in 18 genes have been identified to cause NPHP, but a genetic diagnosis still cannot be found in many patients. NPHP is classified as a ciliopathy because of the localization of the protein products of the associated genes. Currently there is no specific therapy for NPHP.
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Joyner, Alexandra, ed. Gene Targeting. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780199637928.001.0001.
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Since the publication of the first edition of Gene Targeting: A Practical Approach in 1993 there have been many advances in gene targeting and this new edition has been thoroughly updated and rewritten to include all the major new techniques. It provides not only tried-and-tested practical protocols but detailed guidance on their use and applications. As with the previous edition Gene Targeting: A Practical Approach 2e concentrates on gene targeting in mouse ES cells, but the techniques described can be easily adapted to applications in tissue culture including those for human cells. The first chapter covers the design of gene targeting vectors for mammalian cells and describes how to distinguish random integrations from homologous recombination. It is followed by a chapter on extending conventional gene targeting manipulations by using site-specific recombination using the Cre-loxP and Flp-FRT systems to produce 'clean' germline mutations and conditionally (in)activating genes. Chapter 3 describes methods for introducing DNA into ES cells for homologous recombination, selection and screening procedures for identifying and recovering targeted cell clones, and a simple method for establishing new ES cell lines. Chapter 4 discusses the pros and cons or aggregation versus blastocyst injection to create chimeras, focusing on the technical aspects of generating aggregation chimeras and then describes some of the uses of chimeras. The next topic covered is gene trap strategies; the structure, components, design, and modification of GT vectors, the various types of GT screens, and the molecular analysis of GT integrations. The final chapter explains the use of classical genetics in gene targeting and phenotype interpretation to create mutations and elucidate gene functions. Gene Targeting: A Practical Approach 2e will therefore be of great value to all researchers studying gene function.
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(Editor), E. Sage, R. Drouin (Editor), and M. Rouabhia (Editor), eds. From DNA Photolesions to Mutations, Skin Cancer and Cell Death (Comprehensive Series in Photochemical & Photobiological Sciences). Royal Society of Chemistry, 2006.
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27
Arnodlz, Justin. Python for Hackers and Pentesters Full Guides: You'll Explore the Darker Side of Python's Capabilities--Writing Network Sniffers, Stealing Email Credentials, Brute Forcing Directories, Crafting Mutation Fuzzers, Infecting Virtual Machines... . Independently Published, 2021.
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28
Matthew Kynes, J. Hemophilia (Presentation in Emergency Surgery). Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0085.
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Hemophilia is a complex disease of variable severity that affects clotting function and has significant implications in perioperative and emergency care. Hereditary or de novo mutations cause deficiencies in factor VIII or IX production, which may manifest as spontaneous bleeding into joint spaces, muscles, or other sites in severe forms of the disease. Intracranial bleeding is one of the most serious and often fatal complications. In a patient with abnormal bleeding, laboratory results indicative of hemophilia include an increased partial prothromboplastin time (PT), with normal prothrombin time/international normalized ratio (PTT/INR) and normal platelet count. The diagnosis is confirmed with specific factor assays. Advances in prophylaxis with factor replacement have improved outcomes and reduced bleeding episodes in hemophilia. However, patients with hemophilia may present emergently for operation and require factor replacement. In patients that have developed antibodies to factor replacement, clotting factor bypass agents may be required to control bleeding.
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Mordden, Ethan. Fosse & Verdon and Kander & Ebb. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190651794.003.0008.
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This chapter chronicles the rise of Gwen Verdon and Bob Fosse as well as John Kander and Fred Ebb in the theatre industry. Their careers reveal how much the musical was transforming itself by the late 1940s, and how comfortably it moved between musical comedy and the musical play, uncovering ways of aligning them in innovative mutations. Moreover, the musical had come to amalgamate the responsibilities of director and choreographer and make the rise of the naturalistic actor not only possible but necessary. In a way, one could say that a Chicago musical was unthinkable until the liberation of Fosse and Verdon and the evolution of Kander and Ebb, out of musical comedy into the commentative show. Like Show Boat, Oklahoma!, and West Side Story, Chicago is an exhibition piece in the development of the elite yet populist and idealistic yet subversive national art form, the musical.
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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Breast cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0014_update_001.
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Thoracic cancer examines the epidemiology, aetiology, and role of screening and prevention in the reduction of deaths from lung cancer, the majority caused by cigarette smoking. The pathology and genetics of lung cancer, with particular note of the driver mutations, are followed by the symptoms and signs of the disease. Appropriate investigations are described to stage the tumour. The optimum treatment for localised non-small cell lung cancer (NSCLC) is surgical resection, followed in some cases by adjuvant chemotherapy. However, most cases present with disease too advanced for surgery, and for these chemotherapy and radiotherapy are appropriate. Metastatic NSCLC can be treated with platinum based doublet chemotherapy with modest palliative benefits. Metastatic NSCLC with specific driver mutations are amenable to control by targeted therapy. Locally advanced NSCLC is often treated with similar chemotherapy and radiotherapy, ideally administered concurrently, to achieve symptom relief but also improved survival rates. Short course simple radiotherapy offers symptom relief in patients not fit for chemotherapy. Patients with localised NSCLC who are not fit for surgery, may benefit from radical radiotherapy, particularly stereotactic radiotherapy. Small cell lung cancer (SCLC) is characterised by almost universal systemic spread, so that surgery is rarely appropriate. Staging is similar to NSCLC, and chemotherapy is the mainstay of treatment, usually cisplatin or carboplatin combined with etoposide. When possible, this is combined with concurrent thoracic irradiation covering all radiological sites of disease. Prophylactic cranial irradiation reduces the risk of CNS disease. Malignant pleural mesothelioma is caused by occupational asbestos exposure. Symptoms and signs, investigation and staging, and management are discussed. Thymic tumours, their pathology, presenting symptoms including paraneoplastic syndromes, investigation, staging and treatment are reviewed.
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Monani, Umrao R., and Darryl C. De Vivo. Spinal Muscular Atrophy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0033.
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Spinal muscular atrophy (SMA) is a common, inherited, pediatric motor neuron disorder caused by insufficient SMN protein. As of yet, there is no good treatment for the disease. SMA has an incidence of ~1 in 10,000 newborns carrier frequency of 1 in 50, making it the most common inherited cause of infant mortality. Patients with severe SMA, or Werdnig-Hoffman disease, typically manifest weakness during the first 6 months of life. Such patients are so debilitated that they never sit independently, frequently succumbing to the disease before age 2 years. A much milder form of SMA, Kugelberg-Welander disease, with onset after 18 months of age, often during childhood and characterized by prolonged ambulation and a normal life expectancy, was described in 1956. In 1995 mutations in a novel gene, Survival of Motor Neuron 1 (SMN1), were determined to be the specific cause of SMA.
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Budimirovic, Dejan B., and Megha Subramanian. Neurobiology of Autism and Intellectual Disability. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0052.
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Fragile X syndrome (FXS) is a neurodevelopmental disorder that manifests with a range of cognitive, behavioral, and social impairments. It is a monogenetic disease caused by silencing of the FMR1 gene, in contrast to autism spectrum disorder (ASD) that is a behaviorally-defined set of complex disorders. Because ASD is a major and growing public health concern, current research is focused on identifying common therapeutic targets among patients with different molecular etiologies. Due to the prevalence of ASD in FXS and its shared neurophysiology with ASD, FXS has been extensively studied as a model for ASD. Studies in the animal models have provided breakthrough insights into the pathophysiology of FXS that have led to novel therapeutic targets for its core deficits (e.g., mGluR theory of fragile X). Yet recent clinical trials of both GABA-B agonist and mGluR5 antagonist revealed a lack of specific and sensitive outcome measures capturing the full range of improvements of patients with FXS. Recent research shows promise for the mapping of the multitude of genetic variants in ASD onto shared pathways with FXS. Nonetheless, in light of the huge level of locus heterogeneity in ASD, further effort in finding convergence in specific molecular pathways and reliable biomarkers is required in order to perform targeted treatment trials with sufficient sample size. This chapter focuses on the neurobehavioral phenotype caused by a full-mutation of the FMR1 gene, namely FXS, and the neurobiology of this disorder of relevance to the targeted molecular treatments of its core symptoms.
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Clarke, Andrew. Temperature and diversity. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780199551668.003.0015.
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The diversity (species richness) of plants and animals is typically highest in the tropics and the strongest environmental correlate of species richness is often climate. The energy for plant production is sunlight, but the rate is governed jointly by temperature and the availability of water (as captured by actual evapotranspiration, AET). Greater production is then linked to higher diversity because larger population size protects against stochastic extinction (the more individuals mechanism). A greater biomass and diversity of plants allows for a greater diversity of herbivores and so on through the food web, though the correlation with climate (AET) gets progressively weaker at higher trophic levels. This is the basis of the species-energy theory of diversity. The Metabolic Theory of Biodiversity posits a mechanistic explanation for higher diversity in warmer places mediated through an enhanced generation of mutations as a by-product of the faster metabolic rate associated with a higher body temperature. Evidence for this is equivocal, and this mechanism cannot explain the strong association between endotherm species richness and climate. The striking differences between the northern and southern hemispheres point to an important role for history, particularly recent glacial history, in influencing current patterns of diversity. We still lack a comprehensive theory of biological diversity, but evidence points to a complex series of factors being important, with the dominant ones being energy and time (history).
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Matiazzi, Estevam. O Desvelar da Poesia. Brazil Publishing, 2021. http://dx.doi.org/10.31012/978-65-5861-754-9.
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Estevam Matiazzi’s poetics are memorably reflected in the title of his colorful poem collection, most of which are written in poetic prose, with singular didacticism. “Life Seen Through Windows: before and beyond them” is a work marked by movements and approaches in a mutating world view, that established relations with its time. ‘Drunken times’, actually, pandemic times, Covid-19 times. In a cathartic process, the poetic persona gazes outside his window, a narrow spaces’ view that creates an egregore of love. Engaged in the notion of roughness within the historical moment, he creates poems, comforting hearts in distress and full of uncertainties. The title has a direct connection with the works’ poetry; it brings relations in constant change, a shape still undetermined, a state beyond any mold, any casted matter. Beyond anything pre-fixed, anything pre-established. Thus, in a language of light and shadows, “Life Seen Through Windows: before and beyond them” is a beacon in the darkness of these pandemic times (Márcia Lembrança). Life Seen Through Windows – behind and in front of them are 40 poems from quarantine, written in 2020, in the context of Covid-19 pandemic. The view from the windows in the apartment where I live in Belo Horizonte, side by side with the song “Window’s Scenery” – written by Lô Borges and Fernando Brant for the album Corner Club, released in 1972, year in which I was born –, are the inspiration for these poems. Nearly 50 years after this masterpiece, between the slot that remains between buildings, I watch, beyond the windows, the mountain ranges that still encircle the capitol of Minas Gerais, either under blue, open skies or under thick grey clouds… From behind windows, I listen to radios, watch screens and see continued ailments; deforested, burned Amazon, slighted traditional cultures; inflation on the rise, democracy under threat; drama and mire, plots and fire…
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Zhang, Marina, Mark Dodgson, and David Gann. Demystifying China's Innovation Machine. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198861171.001.0001.
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China’s extraordinary economic development is explained in large part by the way it innovates. This book explains how it innovates, which has important implications not only for China but also for the rest of the world. Contrary to widely held views, China’s innovation machine is not created and controlled by an all-powerful government. Instead, it is a complex, interdependent system composed of hundreds of millions of elements, involving bottom-up innovation driven by innovators and entrepreneurs and highly pragmatic and adaptive top-down policy. Using case studies of leading firms and industries, statistics, and policy analysis, the book argues that China’s innovation machine is similar to a natural ecosystem. Innovations in technology, organization, and business model resemble genetic mutations which are random, self-serving and isolated initially, but the best fitting are selected by the market and their impacts are amplified by the innovation machine. This machine draws on China’s massive number of manufacturers, supply chains, innovation clusters, and digitally literate population, connected through supersized digital platforms. China’s innovation suffers from a lack of basic research and reliance upon certain critical technologies from overseas; its scale (size) and scope (diversity) possess attributes that make it self-correcting and stronger in the face of challenges. China’s innovation machine is most effective in a policy environment where the market prevails; policy intervention plays a significant role when market mechanisms are premature or fail. The book concludes that the future success of China’s innovation will depend on continuing policy pragmatism, mass entrepreneurship and innovation, and the development of the ‘new infrastructures’.
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Lamb, Jonathan, ed. A Cultural History of the Sea in the Age of Enlightenment. Bloomsbury Publishing Plc, 2021. http://dx.doi.org/10.5040/9781474207225.
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This volume covers a period when Europeans were making great advances in the production and application of pure knowledge, especially in the fields of navigation and discovery. Thus European powers gained empires around the globe and the benefits that came with them, while the rest of the world had to be content with supplying the raw material (i.e labour, bullion, wood, plants, ore) of these good things. This would not have been possible without navies and trading monopolies, enterprises in which the freedom of the seas was disputed, then gained or lost. The essays in this volume range between three eras in the age of discovery: first, the excitement of seeing something for the first time; second, the experience of understanding the importance of the new thing; and third, the disillusion incident to reframing the prehistory of humanity and its destiny without the usual signposts of an anthropocentric journey from innocence to salvation via sin, atonement and judgment. The maritime contribution to all three eras was enormous not simply because it provided a mobile platform for the inspection of the new but because it proved experimentally that there were no extremes of heroic virtue or of brutal depravity to which humans might not tend when necessity or wantonness called for them. Usually the evil side of humanity was assigned to `savages’ but in the curiously singular person of the pirate, a mirror-image can be found of everyone – really, all people who lived on or by the sea were pirates of a sort. Commencing as an age of rational certainties, the Enlightenment gave way to the opposite. The symmetries of the Linnaean system yielded to the endless process of mutation Buffon called speciation. Rational government of the passions was succeeded by the cult of sensibility and spontaneous emotion. The mathematical exactness of Cartesian knowledge was supplanted by imagination. Sailors returned with pictures of mirages never seen before, the products of Nature’s own imagination that posed a question posed again here: `No doubt they are real, but are they true?’
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Eisen, Tim. The patient with renal cell cancer. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.
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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.
Full textAbstract:
It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.