Książki: „CRITICAL GENES”

1

Fly, Jones Beau, Scherpelz Martha S i Thelen Judith N, red. Cells and genes and me? Columbus, Ohio: Zaner-Bloser, 1992.

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Yan, Bin. Decoding critical genes of enterprises: The bionic laws for organizational longevity. Paramus, New Jersey: Homa & Sekey Books, 2013.

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Your genes, your health: A critical family guide that could save your life. New York: Oxford University Press, 2011.

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La Genesi: Con discussioni critiche. Firenze: Biblioteca scientifico-religiosa, 1985.

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1950-, Dixon Wheeler W., red. Film genre 2000: New critical essays. Albany: State University of New York Press, 2000.

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1953-, Dunn David, red. Harry Partch: An anthology of critical perspectives. Australia: Harwood Academic Publishers, 2000.

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Émile Bertaux tra storia dell'arte e meridionalismo: La genesi de L'art dans l'Italie méridionale. [Rome, Italy]: École française de Rome, 2007.

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1966-, Weiner Robert G., red. Perspectives on the Grateful Dead: Critical writings. Westport, Conn: Greenwood Press, 1999.

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John, Knowles, i Brainard Paul, red. Critica musica: Essays in honor of Paul Brainard. Australia: Gordon and Breach, 1996.

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Defining the sacred songs: Genre, tradition, and the post-critical interpretation of the Psalms. Sheffield, England: Sheffield Academic Press, 1999.

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B, Scott Derek, red. Critical musicological reflections: Essays in honour of Derek B. Scott. Burlington, VT: Ashgate, 2012.

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Musical meaning: Toward a critical history. Berkeley: University of California Press, 2002.

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13

Riechers, Hans-Christian. Peter Szondi: Eine intellektuelle Biographie. Frankfurt: Campus Verlag, 2020.

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Intorno al testo di "Senilità.": Studio critico e filologico sulla genesi e sull'evoluzione del secondo romanzo sveviano seguito dall'edizione critica della princeps. Genève: Droz, 2011.

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15

Canadell, Roger, Josep-Anton Fernàndez i Iribarren Teresa. Narratives of Violence. Venice: Fondazione Università Ca’ Foscari, 2021. http://dx.doi.org/10.30687/978-88-6969-460-8.

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This book is an invitation to read a selection of narratives of violence with the purpose of fostering global imaginaries based on respect, recognition, and empathy, especially towards those who are most vulnerable. It offers critical readings of nine works of various genres, originally written in different languages, by Caterina Albert (Catalonia), Mrīrīda n’ait ‘Atiq (Morocco), Eva Koch (Denmark), Pius Alibek (Iraq-Catalonia), Janina Hescheles (Poland), Leila Abdelrazaq (Palestine), María Galindo and Sonia Sánchez (Argentina), Arundhati Roy (India), and Juan Pablo Villalobos (Mexico).

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16

Trans-Atlantic passages: Philip Hale on the Boston Symphony Orchestra, 1889-1933. New York, NY: Palgrave Macmillan, 2014.

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Teixeira, António. A critical study and translation of António José da Silva's Cretan labyrinth: A puppet opera. Lewiston, N.Y: E. Mellen Press, 2004.

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1946-, Lyons John D., i McKinley Mary B, red. Critical tales: New studies of the Heptameron and early modern culture. Philadelphia: University of Pennsylvania Press, 1993.

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19

Aubrey, Milunsky Dsc. Your Genes, Your Health: A Critical Family Guide That Could Save Your Life. Oxford University Press, 2011.

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Okasha, Samir. Genes and Groups as Agents. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198815082.003.0003.

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In some applications of agential thinking in evolutionary biology, genes and groups, rather than individuals, are the entities that are treated as agents with goals. The genes-as-agents concept is applicable only in cases of intra-genomic conflict, where it helps to make sense of the phenotypic consequences of such conflict. The groups-as-agents concept is applicable only when groups are adapted units, and where within-group conflict is either absent or suppressed; for otherwise the unity-of-purpose constraint on agency will not be satisfied. The idea of group agency has also arisen in social science, where the discussion closely parallels the biological discussion. In both cases, the critical issue is how individuals’ interests can be aligned with that of their group. One such alignment mechanism is the veil-of-ignorance, which deprives individuals of the information needed to pursue their self-interest at the group’s expense.

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Wade, Tracey D., i Cynthia Bulik. Genetic Influences on Eating Disorders. Redaktorzy W. Stewart Agras i Athena Robinson. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190620998.013.5.

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The current chapter reviews our progress in understanding how genes influence eating disorders by addressing the following areas: (1) how recognition of genetic influences on eating disorders emerged; (2) the complexities of gene environment interplay; (3) what twin studies can tell us about gene environment interplay, and (4) the current state of molecular genetic studies. It is concluded that both genes and nonshared environment play a critical role in the explanatory framework for the etiology of eating disorders. Shared environment is likely to contribute to the development of cognition and attitudes that may initiate disordered eating practices. Researchers are on the cusp of identifying specific genes that are implicated, and explication of the manner in which genes and the environment work together to increase risk for eating disorders hinges on the collection of larger samples.

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22

Burghes, Arthur H. M., i Vicki L. McGovern. Spinal Muscular Atrophy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0034.

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Spinal muscular atrophies affect the lower motor neuron. The most common SMA maps to 5q is an autosomal recessive disorder. SMA is caused by loss or mutation of the SMN1 gene and retention of the SMN2 gene, and these genes lie in a complex area of the genome. Mild missense alleles of SMN1 work to complement SMN2 to give function and therapeutics that restore SMN levels are in clinical testing. Modifiers that lie outside the SMN gene locus and influence severity clearly exist, but what they are remains unknown as do the critical genes affected by SMN deficiency.

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23

Mong H Tan Ph.D. Gods, Genes, Conscience: A Socio-Intellectual Survey of our Dynamic Mind, Life, all Creations in Between and Beyond, on Earth--or, A Critical Readers ... Present, Future; in Continuum, ad Infinitum. iUniverse, Inc., 2006.

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24

Barber, Stephen. Jean Genet (Reaktion Books - Critical Lives). Reaktion Books, 2005.

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Zuccato, Chiara, i Elena Cattaneo. Normal Function of Huntingtin. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0011.

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Huntingtin (HTT) is the 3,144–amino acid protein product of the Huntington’s disease gene (HTT), which can be traced back through 800 million years of evolution. It carries a trinucleotide CAG repeat that encodes polyglutamine (polyQ) at an evolutionarily conserved NH2-terminal position in exon 1. This chapter discusses the discoveries that have mapped the evolutionary history of HTT and the CAG repeat and the critical role of the protein in development as well as its activities in the adult brain. During embryogenesis, HTT is critical for gastrulation, neurulation, and neurogenesis. In the adult brain, HTT acts as an antiapoptotic protein and promotes transcription of neuronal genes and vesicle transport. Subversion or exacerbation of HTT brain function by an abnormally expanded polyQ repeat contributes to neuronal vulnerability in HD and suggests that loss of normal HTT function may be implicated in the disease.

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Walsh, Richard A. Siblings with Instability. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0015.

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Over the past 5 years, there has been a shift in the approach to searching for a genetic diagnosis in familial ataxic syndromes. Whereas in the past, a limited but expensive search through a selection of commercially available genes using Sanger sequencing was performed, there is now widespread availability of gene panels utilizing next-generation sequencing techniques. This is an efficient and powerful approach that may achieve a diagnosis in more than 30% of patients with a familial ataxia that remain undiagnosed. However, accurate phenotyping remains critical to allow interpretation of sequence variants of uncertain significance, to identify biomarkers that may be useful to monitor future therapies, and to assist with the identification of underlying pathophysiology.

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27

Trocello, Jean-Marc, i France Woimant. Disorders of Copper and Iron Metabolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0044.

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Both copper and iron are essential metals that have a critical function in a series of biochemical pathways. This chapter describes the disorders associated with genetic abnormalities in copper and iron metabolic pathways and their manifestations in adult patients. Mutations in the genes of the copper transporting P-type ATPases, ATP7A and ATP7B are associated with Wilson disease, Menkes disease, occipital horn syndrome and ATP7A-related distal motor neuropathy. Neurodegeneration with brain iron accumulation (NBIA) is a group of disorders characterized by excess iron deposition in globus pallidus, substantia nigra pars reticulata, striata and cerebellar dentate nuclei. Several genes associated with NBIA have been identified.

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Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards i Cyrus Cooper. Environment. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0038.

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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.

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Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards i Cyrus Cooper. Environment. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0038_update_001.

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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.

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Kühn, Wolfgang, i Gerd Walz. The molecular basis of ciliopathies and cyst formation. Redaktor Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.

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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.

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Music, Modern Culture and the Critical Ear. Taylor & Francis Group, 2017.

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Winters, Ben, i Nicholas Attfield. Music, Modern Culture, and the Critical Ear. Taylor & Francis Group, 2017.

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33

Gene Therapy for Acute and Acquired Diseases. Springer, 2001.

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Factor, Phillip H. Gene Therapy for Acute and Acquired Diseases. Springer, 2012.

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Fitzgerald, Hiram E., i Leon I. Puttler, red. Alcohol Use Disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676001.001.0001.

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Chapters in this volume reflect, to one degree or another, eight critical aspects of contemporary research attempting to understand the etiologic processes that heighten risk or resilience factors for substance use disorders: (1) a focus on systemic frameworks for understanding developmental process, (2) the heterogeneity of developmental pathways, (3) the role of genes and epigenetic–experience transactions, (4) risk cumulative/cascade models of the effects of exposure to adverse childhood experiences, (5) negotiating developmental transitional periods, (6) neurobiological embodiment of adverse childhood experiences, (7) links between alcohol use disorder and tobacco addictive behaviors, and (8) longitudinal studies and data analysis within and between studies.

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36

Critical Perspectives In Canadian Music Education. Wilfrid Laurier University Press, 2012.

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Perkins, Elizabeth C., Shaun P. Brothers i Charles B. Nemeroff. Animal Models for Post-Traumatic Stress Disorder. Redaktorzy Charles B. Nemeroff i Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0024.

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Animal models of post-traumatic stress disorder (PTSD) provide a wellspring of biological information about this complex condition by providing the opportunity to manipulate trauma exposure and measure biological outcomes in a systematic manner that is not possible in clinical studies. Symptoms of PTSD may be induced in animals by physical (immobilization, foot shock, underwater stress) and psychological stressors (exposure to predator, social defeat, early life trauma) or a combination of both. In addition, genetic, epigenetic and transgenic models have been created by breeding animals with a behavioral propensity for maladaptive stress response or by directly manipulating genes that have been implicated in PTSD. The effect of stressors in animals is measured by a variety of means, including observation of behavior, measurement of structural alterations in the brain and of physiological markers such as HPA axis activity and altered gene expression of central nervous system neurotransmitter system components including receptors. By comparing changes observed in stress exposed animals to humans with PTSD and by comparing animal response to treatments that are effective in humans, we can determine the validity of PTSD animal models. The identification of a reliable physiological marker of maladaptive stress response in animals as well as standard use of behavioral cutoff criteria are critical to the development of a valid animal model of PTSD.

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Kaplan, E. Ann. Troubling Genre/Reconstructing Gender. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252036613.003.0005.

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This chapter explores the cultural work that feminist critics performed in “inventing” the genre of the woman's film, and how genre impacts on feminist cinema practices in the current postmodern moment. It argues first that historically, genre was important in providing a useful pathway through which feminist film theorists could assert a critical position vis-à-vis dominant cinematic and critical strategies. That is, feminist critics used genre as a concept to invent a new genre—the women's picture or woman's film—thereby drawing attention to aspects of Hollywood melodrama that had been neglected by (largely male) critics. Secondly, through the examples Sister My Sister (Nancy Meckler, 1994) and Memsahib Rita (Pratibha Parmar, 1994), the chapter shows how some female directors have drawn on traditional Hollywood genres for feminist ends.

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39

Factor, Phillip H. Gene Therapy for Acute and Acquired Diseases. Springer London, Limited, 2012.

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40

New Witches: Critical Essays on 21st Century Television Portrayals. McFarland & Company, Incorporated Publishers, 2021.

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41

Bittner, Edward A., i Shawn P. Fagan. The host response to trauma and burns in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0304.

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Following severe traumatic injury, patients enter a state of immune dysregulation consisting of both exaggerated inflammation and immune suppression. Traditionally, the host response has been viewed as an early systemic inflammatory response syndrome (SIRS) followed temporally by a compensatory anti-inflammatory or immune-suppressive response syndrome (CARS). While this paradigm has been widely accepted across both medical and scientific fields, recent advances have challenged this concept. The Glue grant investigators recently characterized both the initial inflammatory response to injury and the dynamic evolving recovery process. They found: (1) severe injury produces a rapid (< 12 hours) genomic reprioritization in which 80% of the leukocyte transcriptome is altered; (2) similarities in gene expression patterns between different injuries reveal an apparently fundamental response to severe inflammatory stress, which is far more common than different; (3) alterations in the expression of classical inflammatory and anti-inflammatory as well as adaptive immunity genes occur simultaneously, not sequentially after severe injury; (4) the temporal nature of the current SIRS/CARS paradigm is not supported at the level of the leukocyte transcriptome. Complications are not associated with genomic evidence of a ‘second hit’ and differ only in the magnitude and duration of this genomic reprioritization. Furthermore, the delayed clinical recovery with organ injury is not associated with dramatic qualitative differences in the leukocyte transcriptome. Finally, poor correlation between human and rodent inflammatory genomic responses will alter how the host response is studied in the future.

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42

Pace, Ian, i Nigel McBride. Critical Perspectives on Michael Finnissy: Bright Futures, Dark Pasts. Taylor & Francis Group, 2019.

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Pace, Ian, i Nigel McBride. Critical Perspectives on Michael Finnissy: Bright Futures, Dark Pasts. Taylor & Francis Group, 2019.

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Critical Perspectives on Michael Finnissy: Bright Futures, Dark Pasts. Taylor & Francis Group, 2019.

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45

Pace, Ian, i Nigel McBride. Critical Perspectives on Michael Finnissy: Bright Futures, Dark Pasts. Taylor & Francis Group, 2019.

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46

Pace, Ian, i Nigel McBride. Critical Perspectives on Michael Finnissy: Bright Futures, Dark Pasts. Taylor & Francis Group, 2019.

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47

Critical Essays in Music Education. Taylor & Francis Group, 2012.

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Kirchman, David L. Predation and protists. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0009.

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Protists are involved in many ecological roles in natural environments, including primary production, herbivory and carnivory, and parasitism. Microbial ecologists have been interested in these single-cell eukaryotes since Antonie van Leeuwenhoek saw them in his stool and scum from his teeth. This chapter focuses on the role of protozoa (purely heterotrophic protists) and other protists in grazing on other microbes. Heterotrophic nanoflagellates, 3–5 microns long, are the most important grazers of bacteria and small phytoplankton in aquatic environments. In soils, flagellates are also important, followed by naked amoebae, testate amoebae, and ciliates. Many of these protists feed on their prey by phagocytosis, in which the prey particle is engulfed into a food vacuole into which digestive enzymes are released. This mechanism of grazing explains many factors affecting grazing rates, such as prey numbers, size, and composition. Ingestion rates increase with prey numbers before reaching a maximum, similar to the Michaelis–Menten equation describing uptake as a function of substrate concentration. Protists generally eat prey that are about ten-fold smaller than they are. In addition to flagellates, ciliates and dinoflagellates are often important predators in the microbial world and are critical links between microbial food chains and larger organisms Many protists are capable of photosynthesis. In some cases, the predator benefits from photosynthesis carried out by engulfed, but undigested photosynthetic prey or its chloroplasts. Although much can be learnt from the morphology of large protists, small protists (<10 μ‎m) often cannot be distinguished by morphology, and as seen several times in this book, many of the most abundant and presumably important protists are difficult to cultivate, necessitating the use of cultivation-independent methods analogous to those developed for prokaryotes. Instead of the 16S rRNA gene used for bacteria and archaea, the 18S rRNA gene is key for protists. Studies of this gene have uncovered high diversity in natural protist communities and, along with sequences of other genes, have upended models of eukaryote evolution. These studies indicate that the eukaryotic Tree of Life consists almost entirely of protists, with higher plants, fungi, and animals as mere branches.

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Kagan, Jerome. Temperamental Contributions to Inhibited and Uninhibited Profiles. Redaktor Philip David Zelazo. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199958474.013.0007.

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A temperamental bias is currently defined as a behavioral profile with a partial origin in the child’s biology that varies among individuals. These biases, which appear early in development, are sculpted by experience into a variety of personality profiles. This chapter first describes possible genetic and nongenetic bases for temperamental categories, followed by a detailed presentation of the research on high- and low-reactive infants who are biased to become inhibited or uninhibited children. The chapter concludes with a discussion of the implications of these two temperaments to psychopathology and speculations on the temperamental variation among reproductively isolated human groups. A large number of questions remain unanswered. Perhaps the most critical is discovering the genes and resulting neurochemical or neuroanatomical features that contribute to the high- and low-reactive profiles.

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Kagan, Jerome. Temperamental Contributions to Inhibited and Uninhibited Profiles. Redaktor Philip David Zelazo. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199958474.013.0007_update_001.

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A temperamental bias is currently defined as a behavioral profile with a partial origin in the child’s biology that varies among individuals. These biases, which appear early in development, are sculpted by experience into a variety of personality profiles. This chapter first describes possible genetic and nongenetic bases for temperamental categories, followed by a detailed presentation of the research on high- and low-reactive infants who are biased to become inhibited or uninhibited children. The chapter concludes with a discussion of the implications of these two temperaments to psychopathology and speculations on the temperamental variation among reproductively isolated human groups. A large number of questions remain unanswered. Perhaps the most critical is discovering the genes and resulting neurochemical or neuroanatomical features that contribute to the high- and low-reactive profiles.

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