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1.
Bioessays ; 43(6): e2100078, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33825205

RESUMO

In this report, we look at the challenges posed by the outbreak of COVID-19 and how the Executive Board of these two congresses succeeded in overcoming those challenges and holding two congresses. The approach for a large festival with different virtual setting components provided a suitable solution that led to exemplary achievements and created an appropriate model for future virtual or combined virtual and face-to-face events. These events proved that pandemic problems could not limit the organizers, pushing them to make better use of the facilities and turning this threat into an opportunity.


Assuntos
Congressos como Assunto/organização & administração , Genética , Gêmeos , Distinções e Prêmios , Pesquisa Biomédica , Humanos , Irã (Geográfico)
2.
Mol Cell ; 81(8): 1617-1630, 2021 04 15.
Artigo em Inglês | MEDLINE | ID: mdl-33689749

RESUMO

Multi-dimensional omics profiling continues to illuminate the complexity of cellular processes. Because of difficult mechanistic interpretation of phenotypes induced by slow perturbation, fast experimental setups are increasingly used to dissect causal interactions directly in cells. Here we review a growing body of studies that leverage rapid pharmacological perturbation to delineate causality in gene control. When coupled with kinetically matched readouts, fast chemical genetic tools allow recording of primary phenotypes before confounding secondary effects manifest. The toolbox encompasses directly acting probes, such as active-site inhibitors and proteolysis-targeting chimeras, as well as strategies using genetic engineering to render target proteins chemically tractable, such as analog-sensitive and degron systems. We anticipate that extrapolation of these concepts to single-cell setups will further transform our mechanistic understanding of transcriptional control in the future. Importantly, the concept of leveraging speed to derive causality should be broadly applicable to many aspects of biological regulation.


Assuntos
Engenharia Genética/métodos , Transcrição Genética/genética , Animais , Regulação da Expressão Gênica/genética , Genética , Humanos , Proteólise
3.
Nat Genet ; 53(1): 1, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33414547
4.
Nat Rev Rheumatol ; 17(2): 109-118, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33361770

RESUMO

The axial spondyloarthritis (axSpA) disease concept has undergone substantial change from when the entity ankylosing spondylitis was defined by the modified New York criteria in 1984. Developments in imaging, therapy and genetics have all contributed to changing the concept of axSpA from one of erosions in the sacroiliac joints to a spectrum of disease with and without changes evident on plain radiographs. Changes to the previously held concept and construct of the disease have also necessitated new classification criteria. The use of MRI, primarily of the sacroiliac joints, has substantially altered the diagnosis and differential diagnosis of axSpA. Many in the axSpA community believe that the current classification criteria lack specificity, and the CLASSIC study is underway to examine this area. Although much about the evolving axSpA disease concept is universally agreed, there remains disagreement about operationalizing aspects of it, such as the requirement for the objective demonstration of axial inflammation for the classification of axSpA. New imaging technologies, biomarkers and genetics data will probably necessitate ongoing revision of axSpA classification criteria. Advances in our knowledge of the biology of axSpA will settle some differences in opinion as to how the disease concept is applied to the classification and diagnosis of patients.


Assuntos
Articulação Sacroilíaca/diagnóstico por imagem , Espondilartrite/classificação , Espondilartrite/diagnóstico , Espondilite Anquilosante/diagnóstico por imagem , Adulto , Biomarcadores/análise , Diagnóstico Diferencial , Feminino , Genética/instrumentação , Humanos , Inflamação/patologia , Imagem por Ressonância Magnética/métodos , Masculino , Radiografia/métodos , Articulação Sacroilíaca/patologia , Espondilartrite/tratamento farmacológico , Espondilartrite/patologia
6.
Rev. Fac. Med. (Bogotá) ; 68(4): 597-602, oct.-dic. 2020.
Artigo em Espanhol | LILACS, COLNAL | ID: biblio-1149561

RESUMO

Resumen Los avances en la investigación clínica, genética y molecular del cáncer colorrectal (CCR) realizados durante los últimos años han permitido su detección temprana, así como su tratamiento oportuno. Sin embargo, uno de los mayores desafíos de esta enfermedad es su naturaleza heterogénea y la participación de diversas vías moleculares en su carcinogénesis. La implementación de las tecnologías ómicas -como la genómica, la proteómica, la transcriptómica y la epigenómica- en la investigación biomédica de pacientes con CCR hereditario ha permitido identificar nuevos genes o polimorfismos de nucléotido único (SNP, por su sigla en inglés) que afectan la expresividad del cáncer. Por otra parte, las herramientas bioinformáticas han contribuido a generar nuevas hipótesis sobre el CCR, orientando el abordaje de estos pacientes hacia una medicina personalizada. Este avance científico y tecnológico tiene un impacto en la salud, tanto a nivel individual como colectivo, por lo que es importante reflexionar sobre la viabilidad de desarrollar estrategias de salud pública para la implementación de un programa integral y genético de prevención y manejo del cáncer en Perú, en especial del CCR hereditario.


Abstract Progress in clinical, genetic and molecular research of colorectal cancer (CRC) in recent years has allowed its early detection and timely and targeted treatment. However, one of the greatest challenges is the heterogeneous nature of CRC and the involvement of various molecular pathways in its carcinogenesis. The implementation of technologies known as omics -such as genomics, proteomics, transcriptomics and epigenomics- in biomedical research on patients with hereditary CRC has allowed the identification of new genes or single nucleotide polymorphisms (SNPs) that affect the expressivity of cancer. Bioinformatics tools have also contributed to generate new hypotheses about CRC, guiding the approach to these patients towards personalized medicine. This scientific and technological progress has an impact on health, both at the individual and the collective level, so it is important to reflect on the feasibility of developing public health strategies for the implementation of a comprehensive and genetic program for the prevention and treatment of cancer in Peru, especially hereditary CRC.


Assuntos
Humanos , Neoplasias Colorretais , Saúde Pública , Genética
7.
Rev. Fac. Med. (Bogotá) ; 68(4): 586-596, oct.-dic. 2020. tab, graf
Artigo em Espanhol | LILACS, COLNAL | ID: biblio-1149560

RESUMO

Resumen El delirio en pacientes críticos es una condición médica que afecta tanto a adultos como a niños; en ambas poblaciones implica graves complicaciones como estancia hospitalaria prolongada, alto riesgo de muerte y deterioro cognitivo a largo plazo, así como mayores costos económicos en cuanto a la prestación de servicios de salud. La principal dificultad de esta condición en la población pediátrica es su adecuado reconocimiento, ya que puede presentarse en edades muy tempranas, incluso en niños lactantes, cuando sus signos y síntomas pueden confundirse o superponerse con otras patologías, tales como el síndrome de abstinencia. En consecuencia, en estos casos el uso de herramientas diagnósticas puede ser una labor compleja que implica múltiples dificultades. Antes de 2011 no había muchos estudios que abordaran la evaluación del delirio en niños. Sin embargo, ese mismo año se estableció la primera escala desarrollada específicamente para el monitoreo de pacientes en unidades de cuidado intensivo pediátrico, lo que llevó a un aumento significativo del número de casos de delirio en niños menores de 5 años críticamente enfermos; esta situación hizo que los pediatras se interesaran más en estudiar esta importante patología. La presente reflexión, basada en una revisión de la literatura, busca actualizar el amplio espectro fisiopatológico del delirio en niños críticamente enfermos y, de esta forma, mejorar su tamizaje, diagnóstico e intervenciones terapéuticas tempranas en todas las edades pediátricas, incluso en menores de 5 años.


Abstract Delirium in critically ill patients is a medical condition that affects adults and children alike and has serious consequences for both populations, including prolonged hospital stay, high risk of death, long-term cognitive impairment, as well as increased health care costs. In the pediatric population, the main complication of this condition lies in its difficult recognition given that it can occur at very early ages, even in infants, when its signs and symptoms can be confused or overlapped with other pathologies such as withdrawal syndrome. Consequently, diagnostic tools may be more difficult to implement and use in these cases. Studies on delirium in children were scarce until 2011, when the first scale designed specifically for monitoring patients in pediatric intensive care units was developed. Thanks to this scale, the number of delirium cases in critically ill children under 5 years of age significantly increased, which in turn, made pediatricians to be more interested in studying this important pathology. This reflection paper, based on a literature review, seeks to update the broad physiopathological spectrum of delirium in critically ill children and thus improve their screening, diagnosis and early treatment in all pediatric age groups, even in patients under 5 years of age.


Assuntos
Humanos , Neoplasias Colorretais , Genética , Saúde Pública
8.
Proc Natl Acad Sci U S A ; 117(42): 25963-25965, 2020 10 20.
Artigo em Inglês | MEDLINE | ID: mdl-33046646
9.
Can J Nurs Res ; 52(3): 199-208, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32893692

RESUMO

Precision health is the integration of personal genomic data with biological, environmental, behavioral, and other information relevant to the care of a patient. Genetics and genomics are essential components of precision health. Genetics is the study of the effects of individual genes, and genomics is the study of all the components of the genome and interactions between genes, environmental factors, and other psychosocial and cultural factors. Knowledge about the role of genetics and genomics on health outcomes has increased substantially since the completion of the human genome project in 2003. Insights about genetics and genomics obtained from bench science are now having positive clinical implications on patient health outcomes. Nurses have the potential to make distinct contributions to precision health due to their unique role in the health care system. In this article, we discuss gaps in the development of precision health in nursing and how nursing can expand the definition of precision health to actualize its potential. Precision health plays a role in nursing practice. Understanding this connection positions nurses to incorporate genetic and genomic knowledge into their nursing practice.


Assuntos
Padrões de Prática em Enfermagem/organização & administração , Medicina de Precisão/enfermagem , Genética , Genômica , Humanos
10.
Nat Commun ; 11(1): 4505, 2020 09 09.
Artigo em Inglês | MEDLINE | ID: mdl-32908148

RESUMO

Evidence for transgenerational inheritance of epigenetic information in vertebrates is scarce. Aberrant patterns of DNA methylation in gametes may set the stage for transmission into future generations. Here, we describe a viable hypomorphic allele of dnmt1 in zebrafish that causes widespread demethylation of CpG dinucleotides in sperm and somatic tissues. We find that homozygous mutants are essentially normal, with the exception of drastically impaired lymphopoiesis, affecting both larval and adult phases of T cell development. The phenotype of impaired larval (but not adult) T cell development is transmitted to subsequent generations by genotypically wildtype fish. We further find that about 200 differentially methylated regions in sperm DNA of transmitting and non-transmitting males, including hypermethylated sites associated with runx3 and rptor genes, whose reduced activities are associated with impaired larval T cell development. Our results indicate a particular sensitivity of larval T cell development to transgenerationally inherited epimutations.


Assuntos
Diferenciação Celular/genética , Genes Recessivos , Larva/crescimento & desenvolvimento , Linfopoese/genética , Linfócitos T/fisiologia , Alelos , Animais , Animais Geneticamente Modificados , Subunidade alfa 3 de Fator de Ligação ao Core/genética , DNA (Citosina-5-)-Metiltransferase 1/genética , DNA (Citosina-5-)-Metiltransferase 1/metabolismo , Metilação de DNA , Epigênese Genética , Feminino , Genética , Larva/citologia , Masculino , Mutação , Proteína Regulatória Associada a mTOR/genética , Espermatozoides/metabolismo , Peixe-Zebra/genética , Proteínas de Peixe-Zebra/genética , Proteínas de Peixe-Zebra/metabolismo
12.
13.
Dement. neuropsychol ; 14(3): 223-236, July-Sept. 2020. tab, graf
Artigo em Inglês | LILACS | ID: biblio-1133644

RESUMO

ABSTRACT. Alzheimer's disease (AD) and frontotemporal dementia (FTD) are neurodegenerative disorders that result in a significant burden to both patients and caregivers. By 2050, the number of people with dementia in Latin America will increase 4-fold. A deep understanding of the relevant genetic factors of AD and FTD is fundamental to tackle this reality through prevention. A review of different genetic variants that cause AD or FTD in Latin America was conducted. We searched Medline and PubMed databases using the keywords "Alzheimer's disease," "frontotemporal dementia," "mutation," "America," and "Latin America," besides specific Latin American countries. Forty-five items were chosen and analyzed. PSEN1 mutations are the commonest cause of genetic early-onset Alzheimer's disease (EOAD), followed by PSEN2 and APP mutations. Genetic FTD can be mainly explained by GRN and MAPT mutations, as well as C9orf72 G4C2 repeat expansion. APOE ε4 can modify the prevalence and incidence of late-onset Alzheimer's disease (LOAD), in addition to the cognitive performance in affected carriers.


RESUMO. A doença de Alzheimer (DA) e a demência frontotemporal (DFT) são distúrbios neurodegenerativos que causam uma sobrecarga significativa para pacientes e cuidadores. Em 2050, o número de pessoas com demência na América Latina aumentará 4 vezes. Uma compreensão profunda dos fatores genéticos relevantes da DA e da DFT é fundamental para enfrentar essa realidade por meio da prevenção. Foi realizada uma revisão de diferentes variantes genéticas que causam a DA ou a DFT na América Latina. Pesquisamos os bancos de dados Medline e PubMed usando as palavras-chave "doença de Alzheimer", "demência frontotemporal", "mutação", "América" e "América Latina", além de países latino-americanos específicos. Quarenta e cinco itens foram escolhidos e analisados. As mutações do PSEN1 são a causa mais comum da doença de Alzheimer genética de início precoce (DAIP), seguida pelas mutações do PSEN2 e da APP. A DFT genética pode ser explicada principalmente por mutações no GRN, MAPT e expansões repetidas da C9orf72 G4C2. O APOE ε4 pode modificar a prevalência e a incidência da doença de Alzheimer de início tardio (DAIT), mas também o desempenho cognitivo em portadores afetados.


Assuntos
Humanos , Doença de Alzheimer , Demência Frontotemporal , Genética , América Latina
14.
Hist Philos Life Sci ; 42(3): 36, 2020 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-32779040

RESUMO

It has become customary in multilevel selection theory to use the same terms (namely "multilevel selection 1" and "multilevel selection 2") to denote both two explanatory goals (explaining why certain individual- and, respectively, group-level traits spread) and two explanatory means (namely, two kinds of group selection we may appeal to in such explanations). This paper spells out some of the benefits that derive from avoiding this terminological conflation. I argue that keeping explanatory means and goals well apart allows us to see that, contrary to a popular recent idea, Price's equation and contextual analysis-the statistical methods most extensively used for measuring the effects of certain evolutionary factors (like individual selection, group selection etc.) on the change in the focal individual trait in multilevel selection scenarios-do not come with built-in notions of group selection and, therefore, the efficacy of these methods at analyzing various kinds of cases does not constitute a basis for deciding how group selection should best be defined. Moreover, contrary to another widely accepted idea, I argue that more than one type of group selection may serve as explanatory means when one's goal is that of explaining the evolution of individual traits in multilevel selection scenarios and I spell out how this explanatory role should be understood.


Assuntos
Genética , Seleção Genética , Terminologia como Assunto , Evolução Biológica , Traços de História de Vida , Modelos Genéticos , Fenótipo
15.
Rev. bras. ortop ; 55(4): 470-475, Jul.-Aug. 2020. tab, graf
Artigo em Inglês | LILACS | ID: biblio-1138040

RESUMO

Abstract Objective To evaluate the prevalence of family history of rotator cuff tear and the presence of tendinopathy in other joints in patients with rotator cuff tears and to compare them with paired controls. To estimate the odds ratio for rotator cuff tear for these two risk factors. Methods We performed a case-control study comparing patients submitted to treatment for rotator cuff tear with asymptomatic controls. All cases and controls were evaluated by imaging exams and matched by age (±2 years) and gender. We conducted an interview using a standardized questionnaire, and collected data on various risk factors. Results We evaluated 144 patients, 72 per group. Patients with rotator cuff tears reported a higher number of consanguineous relatives who underwent treatment for the same disease and tendon injuries in other joints compared to the controls (p= 0.005 and p= 0.045 respectively). Individuals with a family history of treatment for rotator cuff tear or with tendinopathies in other joints were more likely to present a rotator cuff tear, with odds ratios of 3.3 (95% confidence interval [95%CI] = 1.4-7.7) and 2.7 (95%CI = 1.1-6.9) respectively. Conclusions Patients with rotator cuff tear have a higher prevalence of family members with the same disease and tendinopathies or tendon injuries in other joints. The presence of consanguineous relatives with treatment for rotator cuff and tendinopathies in other joints are risk factors for the presence of rotator cuff tears.


Resumo Objetivo Avaliar as prevalências de antecedente familiar de rotura do manguito e de tendinopatia em outras articulações em pacientes com rotura do manguito rotador e compará-las com controles pareados. Estimar a razão de chances de uma rotura do manguito rotador para estes dois fatores de risco. Métodos Realizamos um estudo de caso-controle comparando pacientes submetidos ao tratamento para rotura do manguito rotador com controles assintomáticos. Todos os casos e controles foram avaliados por exames de imagem e pareados por idade (±2 anos) e sexo. Realizamos uma entrevista utilizando um questionário padronizado, e coletamos dados referentes a vários fatores de risco. Resultados Avaliamos 144 pacientes, 72 por grupo. Os pacientes com rotura do manguito rotador relataram, em maior número, a presença de familiares consanguíneos que realizaram tratamento para a mesma doença e de lesões tendíneas em outras articulações em relação aos indivíduos controles (p= 0,005 e p= 0,045, respectivamente). Indivíduos com antecedente familiar de tratamento para rotura do manguito rotador ou com tendinopatias em outras articulações tiveram maior probabilidade de apresentar rotura do manguito rotador, com razões de chances de 3,3 (intervalo de confiança de 95% [IC95%] = 1,4-7,7) e 2,7 (IC95% = 1,1-6,9), respectivamente. Conclusões Os pacientes com rotura do manguito rotador têm maior prevalência de familiares com a mesma doença e de tendinopatias ou lesões tendíneas em outras articulações. A presença de familiares consanguíneos com tratamento para rotura do manguito rotador e tendinopatias em outras articulações são fatores de risco para presença de roturas do manguito rotador.


Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Traumatismos dos Tendões , Estudos de Casos e Controles , Probabilidade , Inquéritos e Questionários , Fatores de Risco , Manguito Rotador , Confiança , Tendinopatia , Controle , Identidade de Gênero , Genética , Anamnese
16.
Nat Commun ; 11(1): 3442, 2020 07 10.
Artigo em Inglês | MEDLINE | ID: mdl-32651390

RESUMO

Genomic evolution, transmission and pathogenesis of Streptococcus pneumoniae, an opportunistic human-adapted pathogen, is driven principally by nasopharyngeal carriage. However, little is known about genomic changes during natural colonisation. Here, we use whole-genome sequencing to investigate within-host microevolution of naturally carried pneumococci in ninety-eight infants intensively sampled sequentially from birth until twelve months in a high-carriage African setting. We show that neutral evolution and nucleotide substitution rates up to forty-fold faster than observed over longer timescales in S. pneumoniae and other bacteria drives high within-host pneumococcal genetic diversity. Highly divergent co-existing strain variants emerge during colonisation episodes through real-time intra-host homologous recombination while the rest are co-transmitted or acquired independently during multiple colonisation episodes. Genic and intergenic parallel evolution occur particularly in antibiotic resistance, immune evasion and epithelial adhesion genes. Our findings suggest that within-host microevolution is rapid and adaptive during natural colonisation.


Assuntos
Infecções Pneumocócicas/genética , Streptococcus pneumoniae/genética , Evolução Molecular , Genética , Genoma Bacteriano/genética , Humanos , Sequenciamento Completo do Genoma
17.
PLoS One ; 15(7): e0233398, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32609717

RESUMO

The objective is to improve the prediction accuracy of foundation pit deformation in geotechnical engineering, thereby provide early warning for engineering practice. The digital close-range photogrammetry is used to obtain monitoring data. The error compensation method is used to optimize the center of the monitoring point. Aiming at the limitations of back propagation neural network (BPNN), a genetic algorithm (GA)-optimized BPNN algorithm is proposed. Then, the optimized algorithm is applied to predict the deformation and displacement of foundation pits from three aspects, i.e., simple horizontal displacement, simple longitudinal displacement, and the combination of horizontal and longitudinal displacements. Meanwhile, the time domain, space domain, and time-space domain are used as input features to compare the prediction results of the BPNN model and the GA-optimized BPNN model. Finally, the GA-improved BPNN is compared with the Support Vector Regression (SVR) model and Random Forest (RF) model. The results show that the prediction result, obtained by simultaneously using horizontal displacement and longitudinal displacement as input features, has smaller errors; also, the actual output is closer to the expected output. Compared with the prediction result with time domain and space domain as input features, the prediction result with time-space domain as input features is closer to the expected output. Taking the combination of time and space domains as input features, compared with the BPNN model, the GA-optimized BPNN model has a lower Root Mean Squared Error (RMSE) value (0.0163), a larger Index of Agreement (IA) value (0.9800), and a shorter training time (7.08 s). Compared with the SVR model and RF model, the GA-improved BPNN model has a lower Root Mean Squared Error (RMSE) value (0.0211), a larger Index of Agreement (IA) value (0.9706), and shorter training time (7.61 s). Therefore, the foundation pit deformation prediction model based on BPNN and GA has strong prediction ability, which can be popularized and applied in similar geotechnical engineering.


Assuntos
Engenharia , Geologia , Redes Neurais de Computação , Genética
18.
Hist Philos Life Sci ; 42(3): 32, 2020 Jul 20.
Artigo em Inglês | MEDLINE | ID: mdl-32691291

RESUMO

The Central Dogma of molecular biology, which holds that DNA makes protein and not the other way around, is as influential as it is controversial. Some believe the Dogma has outlived its usefulness, either because it fails to fully capture the ins-and-outs of protein synthesis (Griffiths and Stotz in Genetics and philosophy Cambridge introductions to philosophy and biology, Cambridge University Press, Cambridge, 2013; Stotz in Hist Philos Life Sci 28(4):533-548, 2006), because it turns on a confused notion of information (Sarkar in Molecular models of life, MIT Press, Cambridge, 2004), or because it problematically assumes the unidirectional flow of information from DNA to protein (Gottlieb, in: Oyama, Griffiths, Gray (eds), Cycles of contingency: developmental systems and evolution, MIT Press, Cambridge, 2001). This paper evaluates an underexplored defense of the Dogma, which relies on the assumption that the Dogma and the Inheritance of Acquired Traits, a principle which dates as far back as Jean Baptiste-Lamarck, are incompatible principles (Smith in The theory of evolution, Cambridge University Press, Cambridge, 1993; Judson in The eighth day of creation, Jonathan Cape, London, 1979; Dawkins in The extended phenotype, Oxford University Press, Oxford, 1970; Cobb in PLoS Biol 15(9):e2003243, 2017. https://doi.org/10.1371/journal.pbio.2003243 ; Wilkins in BioEssays 24(10):960-973, 2002. https://doi.org/10.1002/bies.10167 ; Graur The fallacious commingling of two unrelated hypotheses: 'the central dogma' and 'dna makes rna makes protein'. Judge Starling., 2018. http://judgestarling.tumblr.com/post/177554581856/the-fallacious-commingling-of-two-unrelated ). By appealing to empirical evidence in molecular science, I argue that this apparent incompatibility is indeed merely apparent. I conclude by briefly demonstrating how these considerations bear on the topic of conceptual pluralism in the philosophy of science (Stencel and Proszewska in Found Sci 23(4):603-620, 2018. https://doi.org/10.1007/s10699-017-9543-x ; Lu and Bourrat in Br J Philos Sci 69(3):775-800, 2018. https://doi.org/10.1093/bjps/axx019 ).


Assuntos
Genética , Hereditariedade , Filosofia
19.
J Hist Biol ; 53(3): 451-484, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32524311

RESUMO

In 1869, Johann Friedrich Miescher discovered a new substance in the nucleus of living cells. The substance, which he called nuclein, is now known as DNA, yet both Miescher's name and his theoretical ideas about nuclein are all but forgotten. This paper traces the trajectory of Miescher's reception in the historiography of genetics. To his critics, Miescher was a "contaminator," whose preparations were impure. Modern historians portrayed him as a "confuser," whose misunderstandings delayed the development of molecular biology. Each of these portrayals reflects the disciplinary context in which Miescher's work was evaluated. Using archival sources to unearth Miescher's unpublished speculations-including an analogy between the hereditary material and language, and a speculation that a series of asymmetric carbon atoms could account for hereditary variation-this paper clarifies the ways in which the past was judged through the lens of contemporary concerns. It also shows how organization, structure, function, and information were already being considered when nuclein was first discovered nearly 150 years ago.


Assuntos
DNA/história , Genética/história , Historiografia , Biologia Molecular/história , Química/história , Cromatina/isolamento & purificação , DNA/isolamento & purificação , História do Século XIX , Humanos , Relações Interprofissionais , Supuração/história , Suíça
20.
Hist Philos Life Sci ; 42(2): 27, 2020 Jun 16.
Artigo em Inglês | MEDLINE | ID: mdl-32548727

RESUMO

The history of genetics and the evolutionary theory in the USSR is multidimensional. Only in the 1920s after the October Revolution, and due in large part to that Revolution, the science of genetics arose in Soviet Russia. Genetics was limited, but not obliterated in the second half of the 1950s, and was restored in the late 1960s, after the resignation of Nikita S. Khrushchev. In the subsequent period, Soviet genetics experienced a resurgence, though one not as successful as geneticists would have liked. The Communist party bodies interfered constantly, but with different consequences for the development of genetics than when the earlier periods. The main troubles for Soviet genetics occurred during the unique, well-known, most contradictory, and tragic Stalinist period. The start date for the defeat of genetics is also known-August, 1948. In the social history of science and especially in the history of evolutionary biology (including genetics) it is natural, necessary, and even expected to adopt an evolutionary approach. In particular, historians of science need to consider and explain the evolution and dependence of Soviet science in regards to the evolution of Soviet society, the Soviet state, and the Communist party. This evolutionary perspective reflects the standards of evolutionary biology, evolutionary macrosociology, and also the history of science.


Assuntos
Comunismo/história , Genética/história , História do Século XX , U.R.S.S.
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