344 research outputs found

    With and Without Galton

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    In 1865, British polymath Francis Galton published his initial thoughts about the scientific field that would become ‘eugenics.’ The same year, Russian physician Vasilii Florinskii addressed similar issues in a sizeable treatise, entitled Human Perfection and Degeneration. Initially unheralded, Florinskii’s book would go on to have a remarkable afterlife in twentieth- and twenty-first-century Russia. In this lucid and insightful work, Nikolai Krementsov argues that the concept of eugenics brings together ideas, values, practices, and fears energised by a focus on the future. It has proven so seductive to different groups over time because it provides a way to grapple with fundamental existential questions of human nature and destiny. With and Without Galton develops this argument by tracing the life-story of Florinskii’s monograph from its uncelebrated arrival amid the Russian empire’s Great Reforms, to its reissue after the Bolshevik Revolution, its decline under Stalinism, and its subsequent resurgence: first, as a founding document of medical genetics, and most recently, as a manifesto for nationalists and racial purists. Krementsov’s meticulously researched ‘biography of a book’ sheds light not only on the peculiar fate of eugenics in Russia, but also on its convoluted transnational history, elucidating the field’s protean nature and its continuing and contested appeal to diverse audiences, multiple local trajectories, and global trends. It is required reading for historians of eugenics, science, medicine, education, literature, and Russia, and it will also appeal to the general reader looking for a deeper understanding of this challenging subject

    With and Without Galton

    Get PDF
    In 1865, British polymath Francis Galton published his initial thoughts about the scientific field that would become ‘eugenics.’ The same year, Russian physician Vasilii Florinskii addressed similar issues in a sizeable treatise, entitled Human Perfection and Degeneration. Initially unheralded, Florinskii’s book would go on to have a remarkable afterlife in twentieth- and twenty-first-century Russia. In this lucid and insightful work, Nikolai Krementsov argues that the concept of eugenics brings together ideas, values, practices, and fears energised by a focus on the future. It has proven so seductive to different groups over time because it provides a way to grapple with fundamental existential questions of human nature and destiny. With and Without Galton develops this argument by tracing the life-story of Florinskii’s monograph from its uncelebrated arrival amid the Russian empire’s Great Reforms, to its reissue after the Bolshevik Revolution, its decline under Stalinism, and its subsequent resurgence: first, as a founding document of medical genetics, and most recently, as a manifesto for nationalists and racial purists. Krementsov’s meticulously researched ‘biography of a book’ sheds light not only on the peculiar fate of eugenics in Russia, but also on its convoluted transnational history, elucidating the field’s protean nature and its continuing and contested appeal to diverse audiences, multiple local trajectories, and global trends. It is required reading for historians of eugenics, science, medicine, education, literature, and Russia, and it will also appeal to the general reader looking for a deeper understanding of this challenging subject

    Climate modification and climate change debates amongst Soviet physical geographers, 1940s-1960s

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    This review provides an insight into some of the main themes characterizing the work of Soviet physical geographers concerning climate during the decade following the Second World War. Post-1945, pressure was placed upon geography via the state and the Academy of Sciences to ensure that its activities were of practical use to the development of the socialist economy and this was particularly evident in the case of work related to climate and climate modification. The review is divided into four main sections. First, it provides an understanding of the range of work carried out by physical geographers with respect to climate and related phenomena in the late 1940s and 1950s. Second, it focuses on the work of geographers and climatologists in relation to the heat and water balance at the earth's surface, which attracted considerable attention within geographical circles as well as more broadly within Soviet science during the 1950s. Third, it reflects upon the way in which Soviet geography utilized its understanding of climate systems in order to participate in national schemes concerned with the modification of the climate and the transformation of nature. Finally, the review highlights the maturing of climate modification debates among geographers and cognate scientists during the late 1950s and early 1960s with the emergence of competing discussions over the potential for human activity to result in both positive and negative consequences for the global climate system

    The National Pattern of Lysenkoism in Romania

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    Lysenkoism as a practice, theory and ideology was introduced in Romania in 1949, as part of the structural changes of the scientific institutions, namely the subordination of the Romanian Academy to the communist state. Beyond the similarity with other countries of the Eastern bloc, the original trend in the case of Romania was the interference between Lysenkoism and the neo-Lamarckian context, strongly represented before World War II in biology and agronomy. This explains the fact that Romanian scientists maintained references to Michurin until the early 1970s, long after the official introduction of genetics. The national pattern of Lysenkoism focused on the continuity of the Romanian science

    Mapping of tetraspanin-enriched microdomains that can function as gateways for HIV-1

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    Specific spatial arrangements of proteins and lipids are central to the coordination of many biological processes. Tetraspanins have been proposed to laterally organize cellular membranes via specific associations with each other and with distinct integrins. Here, we reveal the presence of tetraspanin-enriched microdomains (TEMs) containing the tetraspanins CD9, CD63, CD81, and CD82 at the plasma membrane. Fluorescence and immunoelectron microscopic analyses document that the surface of HeLa cells is covered by several hundred TEMs, each extending over a few hundred nanometers and containing predominantly two or more tetraspanins. Further, we reveal that the human immunodeficiency virus type 1 (HIV-1) Gag protein, which directs viral assembly and release, accumulates at surface TEMs together with the HIV-1 envelope glycoprotein. TSG101 and VPS28, components of the mammalian ESCRT1 (endosomal sorting complex required for transport), which is part of the cellular extravesiculation machinery critical for HIV-1 budding, are also recruited to cell surface TEMs upon virus expression, suggesting that HIV-1 egress can be gated through these newly mapped microdomains

    Myosin V: regulation by calcium, calmodulin, and the tail domain

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    Calcium activates the ATPase activity of tissue-purified myosin V, but not that of shorter expressed constructs. Here, we resolve this discrepancy by comparing an expressed full-length myosin V (dFull) to three shorter constructs. Only dFull has low ATPase activity in EGTA, and significantly higher activity in calcium. Based on hydrodynamic data and electron microscopic images, the inhibited state is due to a compact conformation that is possible only with the whole molecule. The paradoxical finding that dFull moved actin in EGTA suggests that binding of the molecule to the substratum turns it on, perhaps mimicking cargo activation. Calcium slows, but does not stop the rate of actin movement if excess calmodulin (CaM) is present. Without excess CaM, calcium binding to the high affinity sites dissociates CaM and stops motility. We propose that a folded-to-extended conformational change that is controlled by calcium and CaM, and probably by cargo binding itself, regulates myosin V's ability to transport cargo in the cell

    Tetraspanins regulate cell-to-cell transmission of HIV-1

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    <p>Abstract</p> <p>Background</p> <p>The presence of the tetraspanins CD9, CD63, CD81 and CD82 at HIV-1 budding sites, at the virological synapse (VS), and their enrichment in HIV-1 virions has been well-documented, but it remained unclear if these proteins play a role in the late phase of the viral replication cycle. Here we used overexpression and knockdown approaches to address this question.</p> <p>Results</p> <p>Neither ablation of CD9, CD63 and/or CD81, nor overexpression of these tetraspanins was found to affect the efficiency of virus release. However, confirming recently reported data, tetraspanin overexpression in virus-producing cells resulted in the release of virions with substantially reduced infectivity. We also investigated the roles of these tetraspanins in cell-to-cell transmission of HIV-1. Overexpression of CD9 and CD63 led to reduced cell-to-cell transmission of this virus. Interestingly, in knockdown experiments we found that ablation of CD63, CD9 and/or CD81 had no effect on cell-free infectivity. However, knockdown of CD81, but not CD9 and CD63, enhanced productive particle transmission to target cells, suggesting additional roles for tetraspanins in the transmission process. Finally, tetraspanins were found to be downregulated in HIV-1-infected T lymphocytes, suggesting that HIV-1 modulates the levels of these proteins in order to maximize the efficiency of its transmission within the host.</p> <p>Conclusion</p> <p>Altogether, these results establish an active role of tetraspanins in HIV-1 producer cells.</p

    Rab27a controls HIV-1 assembly by regulating plasma membrane levels of phosphatidylinositol 4,5-bisphosphate

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    During the late stages of the HIV-1 replication cycle, the viral polyprotein Pr55Gag is recruited to the plasma membrane (PM), where it binds phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and directs HIV-1 assembly. We show that Rab27a controls the trafficking of late endosomes carrying phosphatidylinositol 4-kinase type 2 α (PI4KIIα) toward the PM of CD4+ T cells. Hence, Rab27a promotes high levels of PM phosphatidylinositol 4-phosphate and the localized production of PI(4,5)P2, therefore controlling Pr55Gag membrane association. Rab27a also controls PI(4,5)P2 levels at the virus-containing compartments of macrophages. By screening Rab27a effectors, we identified that Slp2a, Slp3, and Slac2b are required for the association of Pr55Gag with the PM and that Slp2a cooperates with Rab27a in the recruitment of PI4KIIα to the PM. We conclude that by directing the trafficking of PI4KIIα-positive endosomes toward the PM, Rab27a controls PI(4,5)P2 production and, consequently, HIV-1 replication.Fil: Pereyra Gerber, Federico Pehuén. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Cabrini, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Jancic, Carolina Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Paoletti, Luciana Elisa. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Banchio, Claudia Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Von Bilderling, Catalina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; ArgentinaFil: Sigaut, Lorena. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Centro de Microscopías Avanzadas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Pietrasanta, Lia. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Centro de Microscopías Avanzadas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Duette, Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Freed, Eric O.. National Cancer Institute at Frederick; Estados UnidosFil: Basile, Genevieve de Saint. Institut National de la Santé et de la Recherche Médicale; FranciaFil: Moita, Catarina Ferreira. Instituto Gulbenkian de Ciencia; PortugalFil: Moita, Luis Ferreira. Instituto Gulbenkian de Ciencia; PortugalFil: Amigorena, Sebastian. Institute Curie; FranciaFil: Benaroch, Philippe. Institute Curie; FranciaFil: Geffner, Jorge Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Ostrowski, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentin

    Totalitarianism and geography: L.S. Berg and the defence of an academic discipline in the age of Stalin

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    In considering the complex relationship between science and politics, the article focuses upon the career of the eminent Russian scholar, Lev Semenovich Berg (1876–1950), one of the leading geographers of the Stalin period. Already before the Russian Revolution, Berg had developed a naturalistic notion of landscape geography which later appeared to contradict some aspects of Marxist–Leninist ideology. Based partly upon Berg's personal archive, the article discusses the effects of the 1917 revolution, the radical changes which Stalin's cultural revolution (from the late 1920s) brought upon Soviet science, and the attacks made upon Berg and his concept of landscape geography thereafter. The ways in which Berg managed to defend his notion of geography (sometimes in surprisingly bold ways) are considered. It is argued that geography's position under Stalin was different from that of certain other disciplines in that its ideological disputes may have been regarded as of little significance by the party leaders, certainly by comparison with its practical importance, thus providing a degree of ‘freedom’ for some geographers at least analogous to that which has been described by Weiner (1999. A little corner of freedom: Russian nature protection from Stalin to Gorbachev. Berkeley: University of California Press) for conservationists. It is concluded that Berg and others successfully upheld a concept of scientific integrity and limited autonomy even under Stalinism, and that, in an era of ‘Big Science’, no modernizing state could or can afford to emasculate these things entirely

    Sex-Specific Gene-by-Vitamin D Interactions Regulate Susceptibility to Central Nervous System Autoimmunity

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    Vitamin D3 (VitD) insufficiency is postulated to represent a major modifiable risk factor for multiple sclerosis (MS). While low VitD levels strongly correlate with higher MS risk in white populations, this is not the case for other ethnic groups, suggesting the existence of a genetic component. Moreover, VitD supplementation studies in MS so far have not shown a consistent benefit. We sought to determine whether direct manipulation of VitD levels modulates central nervous system autoimmune disease in a sex-by-genotype-dependent manner. To this end, we used a dietary model of VitD modulation, together with the autoimmune animal model of MS, experimental autoimmune encephalomyelitis (EAE). To assess the impact of genotype-by-VitD interactions on EAE susceptibility, we utilized a chromosome substitution (consomic) mouse model that incorporates the genetic diversity of wild-derived PWD/PhJ mice. High VitD was protective in EAE in female, but not male C57BL/6J (B6) mice, and had no effect in EAE-resistant PWD/PhJ (PWD) mice. EAE protection was accompanied by sex- and genotype-specific suppression of proinflammatory transcriptional programs in CD4 T effector cells, but not CD4 regulatory T cells. Decreased expression of proinflammatory genes was observed with high VitD in female CD4 T effector cells, specifically implicating a key role of MHC class II genes, interferon gamma, and Th1 cell-mediated neuroinflammation. In consomic strains, effects of VitD on EAE were also sex- and genotype dependent, whereby high VitD: (1) was protective, (2) had no effect, and (3) unexpectedly had disease-exacerbating effects. Systemic levels of 25(OH)D differed across consomic strains, with higher levels associated with EAE protection only in females. Analysis of expression of key known VitD metabolism genes between B6 and PWD mice revealed that their expression is genetically determined and sex specific and implicated Cyp27b1 and Vdr as candidate genes responsible for differential EAE responses to VitD modulation. Taken together, our results support the observation that the association between VitD status and MS susceptibility is genotype dependent and suggest that the outcome of VitD status in MS is determined by gene-by-sex interactions
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