The Social and Political Dimensions of the Ebola Response: Global Inequality, Climate Change, and Infectious Disease

The 2014 Ebola crisis has highlighted public-health vulnerabilities in Liberia, Sierra Leone, and Guinea – countries ravaged by extreme poverty, deforestation and mining-related disruption of livelihoods and ecosystems, and bloody civil wars in the cases of Liberia and Sierra Leone. Ebola’s emergence and impact are grounded in the legacy of colonialism and its creation of enduring inequalities within African nations and globally, via neoliberalism and the Washington Consensus. Recent experiences with new and emerging diseases such as SARS and various strains of HN influenzas have demonstrated the effectiveness of a coordinated local and global public health and education-oriented response to contain epidemics. To what extent is international assistance to fight Ebola strengthening local public health and medical capacity in a sustainable way, so that other emerging disease threats, which are accelerating with climate change, may be met successfully? This chapter considers the wide-ranging socio-political, medical, legal and environmental factors that have contributed to the rapid spread of Ebola, with particular emphasis on the politics of the global and public health response and the role of gender, social inequality, colonialism and racism as they relate to the mobilization and establishment of the public health infrastructure required to combat Ebola and other emerging diseases in times of climate change

Understanding and using quantitative genetic variation

Quantitative genetics, or the genetics of complex traits, is the study of those characters which are not affected by the action of just a few major genes. Its basis is in statistical models and methodology, albeit based on many strong assumptions. While these are formally unrealistic, methods work. Analyses using dense molecular markers are greatly increasing information about the architecture of these traits, but while some genes of large effect are found, even many dozens of genes do not explain all the variation. Hence, new methods of prediction of merit in breeding programmes are again based on essentially numerical methods, but incorporating genomic information. Long-term selection responses are revealed in laboratory selection experiments, and prospects for continued genetic improvement are high. There is extensive genetic variation in natural populations, but better estimates of covariances among multiple traits and their relation to fitness are needed. Methods based on summary statistics and predictions rather than at the individual gene level seem likely to prevail for some time yet

The State Socialist Mortality Syndrome

Death rates for working-age men in European state socialist countries deviated from general improvements in survival observed in the rest of Europe during the 20th century. The magnitude of structural labor force changes across countries correlates with lagged increases in death rates for men in the working ages. This pattern is consistent with a hypothesis that hyper-development of heavy industry and stagnation (even contraction) of the service sector created anomic conditions leading to unhealthy lifestyles and self-destructive behavior among men moving from primary-sector to secondary-sector occupations. Occupational contrasts within countries similarly show concentration of rising male death rates among blue collar workers. Collapse of state socialist systems produced rapid corrections in labor force structure after 1990, again correlated with a fading of the state socialist mortality syndrome in following decades

New Sites/Sights: Exploring the White Spaces of Organization

Contemporary organization is increasingly understood as contingent and improvisational - and immersed in complex and shadowy realities where customary assumptions about the space and time of organization no longer hold. This Special Issue invites organization studies into an ambivalent space of sites/sights in organization, the double-play of this modest conceptual proposal necessary in order to open up the complex folding of the epistemological and the ontological in organization today. In this introduction we seek to establish and position a distinctive approach to what we claim to be ‘white spaces’ in organization. We show that any adequate treatment of these white spaces compels a significant breaching of the disciplinary norms of organization studies. Our argument derives from a consideration of a range of recently emerging concepts and analyses in the study of organization, all of which are suggestive of crisis and of emerging (anti-)forms of organization. This edition of Organization Studies publishes six papers and three originally commissioned book reviews that help advance this emerging problematic in organization, and which in their various ways extend our understanding of possible organizing futures. </jats:p

Population structure, connectivity, and demographic history of an apex marine predator, the bull shark <i>Carcharhinus leucas</i>

Knowledge of population structure, connectivity, and effective population size remains limited for many marine apex predators, including the bull shark Carcharhinus leucas. This large‐bodied coastal shark is distributed worldwide in warm temperate and tropical waters, and uses estuaries and rivers as nurseries. As an apex predator, the bull shark likely plays a vital ecological role within marine food webs, but is at risk due to inshore habitat degradation and various fishing pressures. We investigated the bull shark\u27s global population structure and demographic history by analyzing the genetic diversity of 370 individuals from 11 different locations using 25 microsatellite loci and three mitochondrial genes (CR, nd4, and cytb). Both types of markers revealed clustering between sharks from the Western Atlantic and those from the Western Pacific and the Western Indian Ocean, with no contemporary gene flow. Microsatellite data suggested low differentiation between the Western Indian Ocean and the Western Pacific, but substantial differentiation was found using mitochondrial DNA. Integrating information from both types of markers and using Bayesian computation with a random forest procedure (ABC‐RF), this discordance was found to be due to a complete lack of contemporary gene flow. High genetic connectivity was found both within the Western Indian Ocean and within the Western Pacific. In conclusion, these results suggest important structuring of bull shark populations globally with important gene flow occurring along coastlines, highlighting the need for management and conservation plans on regional scales rather than oceanic basin scale

Seismicity along the Pacific-North American plate boundary in California and western Nevada, 1980-81

Beginning in 1980, the number and distribution of telemetered, high-gain seismic stations operated in California and western Nevada provided the capability for locating earthquakes of M ≥ 2.0 occurring throughout the broadly-deforming Pacific-North American plate boundary from the Salton Trough to the Mendocino triple junction and as far inland as the western Great Basin. Four networks combine to provide this capability: (1) the 300-station Central California Network operated by the U.S. Geological Survey from Menlo Park, CA; (2) the 200-station Southern California Network operated jointly by the California Institute of Technology (CIT) and the U. S. Geological Survey from Pasadena, CA; (3) the 40-station Western Nevada-Eastern California Network operated by the University of Nevada from Reno, NV; and (4) the 55-station Southern Nevada Network operated by the U.S. Geological Survey from Golden, CO. The distribution of earthquake hypocenters located by this combination of networks for 1980 and 1981 brings into focus detailed seismicity patterns within the broad bands of earthquake activity that have persisted for SO years or more based on locations of M ≥ 3 earthquakes from the regional networks operated by CIT and the University of California, Berkeley, since the early 1930's. The precise focal parameters of M ≥ 2.0 earthquakes afforded by these four telemetered networks provide critical constraints on the kinematics of seismogenic deformation of the western margin of the North American plate adjacent to the San Andreas transform-fault system

Interspecific comparisons of C\u3csub\u3e3\u3c/sub\u3e turfgrass for tennis use: I. Wear tolerance and carrying capacity under actual match play

Previous studies in the evaluation of wear tolerance have been conducted using wear simulators. Research to investigate wear tolerance of C3 turfgrasses under actual playing conditions and their carrying capacity is limited. Three grass tennis courts (replicates) maintained as official size (single) courts were constructed. Eight species and cultivars were randomized within the three courts (blocks): (1) ‘Keeneland’ Kentucky bluegrass (KB, Poa pratensis L.), (2) ‘Rubix’ KB, (3) ‘Villa’ velvet bentgrass (VBG, Agrostis canina L.), (4) ‘Puritan’ colonial bentgrass (CL, Agrostis capillaris L.), (5) ‘007’ creeping bentgrass (CB, Agrostis stolonifera L.), (6) fine fescue (FF, Festuca spp.) mixture, (7) ‘Karma’ perennial ryegrass (PR, Lolium perenne L.), and (8) ‘Wicked’ PR. Injury at the baseline was measured by counting healthy grass on four dates in 2017 and 2019 using an intersect grid. Carrying capacity at the baseline was derived as hours of play to sustain 90, 80, 70, and 60% grass cover. After 6 wk of actual tennis play involving \u3e120 participating players in 2017 and 2019, KB and PR were superior to other C3 turfgrass for wear tolerance and carrying capacity. These two species exhibited four times the carrying capacity of FF species and nearly 60% more carrying capacity than bentgrass (BG) species. Species of BG afforded higher shoot density and better traction than KB and PR, with VBG exhibiting the best traction, and FF and PR exhibiting the poorest traction. In 2017, greater cell wall content increased wear tolerance and carrying capacity. Velvet bentgrass was as good as KB and PR in overall wear tolerance and carrying capacity under actual match play

Attempting to distinguish between endogenous and contaminating cytokeratins in a corneal proteomic study

<p>Abstract</p> <p>Background</p> <p>The observation of cytokeratins (CK's) in mass spectrometry based studies raises the question of whether the identified CK is a true endogenous protein from the sample or simply represents a contaminant. This issue is especially important in proteomic studies of the corneal epithelium where several CK's have previously been reported to mark the stages of differentiation from corneal epithelial stem cell to the differentiated cell.</p> <p>Methods</p> <p>Here we describe a method to distinguish very likely endogenous from uncertain endogenous CK's in a mass spectrometry based proteomic study. In this study the CK identifications from 102 human corneal samples were compared with the number of human CK identifications found in 102 murine thymic lymphoma samples.</p> <p>Results</p> <p>It was anticipated that the CK's that were identified with a frequency of <5%, <it>i.e. </it>in less than one spot for every 20 spots analysed, are very likely to be endogenous and thereby represent a 'biologically significant' identification. CK's observed with a frequency >5% are uncertain endogenous since they may represent true endogenous CK's but the probability of contamination is high and therefore needs careful consideration. This was confirmed by comparison with a study of mouse samples where all identified human CK's are contaminants.</p> <p>Conclusions</p> <p>CK's 3, 4, 7, 8, 11, 12, 13, 15, 17, 18, 19, 20 and 23 are very likely to be endogenous proteins if identified in a corneal study, whilst CK's 1, 2e, 5, 6A, 9, 10, 14 and 16 may be endogenous although some are likely to be contaminants in a proteomic study. Further immunohistochemical analysis and a search of the current literature largely supported the distinction.</p

The PPCD1 Mouse: Characterization of a Mouse Model for Posterior Polymorphous Corneal Dystrophy and Identification of a Candidate Gene

The PPCD1 mouse, a spontaneous mutant that arose in our mouse colony, is characterized by an enlarged anterior chamber resulting from metaplasia of the corneal endothelium and blockage of the iridocorneal angle by epithelialized corneal endothelial cells. The presence of stratified multilayered corneal endothelial cells with abnormal patterns of cytokeratin expression are remarkably similar to those observed in human posterior polymorphous corneal dystrophy (PPCD) and the sporadic condition, iridocorneal endothelial syndrome. Affected eyes exhibit epithelialized corneal endothelial cells, with inappropriate cytokeratin expression and proliferation over the iridocorneal angle and posterior cornea. We have termed this the “mouse PPCD1” phenotype and mapped the mouse locus for this phenotype, designated “Ppcd1”, to a 6.1 Mbp interval on Chromosome 2, which is syntenic to the human Chromosome 20 PPCD1 interval. Inheritance of the mouse PPCD1 phenotype is autosomal dominant, with complete penetrance on the sensitive DBA/2J background and decreased penetrance on the C57BL/6J background. Comparative genome hybridization has identified a hemizygous 78 Kbp duplication in the mapped interval. The endpoints of the duplication are located in positions that disrupt the genes Csrp2bp and 6330439K17Rik and lead to duplication of the pseudogene LOC100043552. Quantitative reverse transcriptase-PCR indicates that expression levels of Csrp2bp and 6330439K17Rik are decreased in eyes of PPCD1 mice. Based on the observations of decreased gene expression levels, association with ZEB1-related pathways, and the report of corneal opacities in Csrp2bptm1a(KOMP)Wtsi heterozygotes and embryonic lethality in nulls, we postulate that duplication of the 78 Kbp segment leading to haploinsufficiency of Csrp2bp is responsible for the mouse PPCD1 phenotype. Similarly, CSRP2BP haploinsufficiency may lead to human PPCD