Winning Organizational Campaigns, Communicating Adverse Consequences of Unionism: The Board’s View, circa 1980

Article about union-free work environments

A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci.

We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies. In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q13.1, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q37.1. We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p16.3, 8q24.21 and 8q24.3, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions. Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis

A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci.

We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies. In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q13.1, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q37.1. We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p16.3, 8q24.21 and 8q24.3, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions. Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis

Connexin Mediated Cataract Prevention in Mice

Cataracts, named for any opacity in the ocular lens, remain the leading cause of vision loss in the world. Non-surgical methods for cataract prevention are still elusive. We have genetically tested whether enhanced lens gap junction communication, provided by increased α3 connexin (Cx46) proteins expressed from α8(Kiα3) knock-in alleles in Gja8tm1(Gja3)Tww mice, could prevent nuclear cataracts caused by the γB-crystallin S11R mutation in CrygbS11R/S11R mice. Remarkably, homozygous knock-in α8(Kiα3/Kiα3) mice fully prevented nuclear cataracts, while single knock-in α8(Kiα3/−) allele mice showed variable suppression of nuclear opacities in CrygbS11R/S11R mutant mice. Cataract prevention was correlated with the suppression of many pathological processes, including crystallin degradation and fiber cell degeneration, as well as preservation of normal calcium levels and stable actin filaments in the lens. This work demonstrates that enhanced intercellular gap junction communication can effectively prevent or delay nuclear cataract formation and suggests that small metabolites transported through gap junction channels protect the stability of crystallin proteins and the cytoskeletal structures in the lens core. Thus, the use of an array of small molecules to promote lens homeostasis may become a feasible non-surgical approach for nuclear cataract prevention in the future

Storm impacts on phytoplankton community dynamics in lakes

In many regions across the globe, extreme weather events, such as storms, have increased in frequency, intensity and duration. Ecological theory predicts that such extreme events should have large impacts on ecosystem structure and function. For lake ecosystems, high winds and rainfall associated with storms are linked by short term runoff events from catchments and physical mixing of the water column. Although we have a well-developed understanding of how such wind and precipitation events alter lake physical processes, our mechanistic understanding of how these short-term disturbances 48 translate from physical forcing to changes in phytoplankton communities is poor. Here, we provide a conceptual model that identifies how key storm features (i.e., the frequency, intensity, and duration of wind and precipitation) interact with attributes of lakes and their watersheds to generate changes in a lake’s physical and chemical environment and subsequently phytoplankton community structure and dynamics. We summarize the current understanding of storm-phytoplankton dynamics, identify knowledge gaps with a systematic review of the literature, and suggest future research directions by generating testable hypotheses across a global gradient of lake types and environmental conditions.Fil: Stockwell, Jason D.. University of Vermont; Estados UnidosFil: Adrian, Rita. Leibniz Institute of Freshwater Ecology and Inland Fisheries; AlemaniaFil: Andersen, Mikkel. Dundalk Institute of Technology; IrlandaFil: Anneville, Orlane. Institut National de la Recherche Agronomique; FranciaFil: Bhattacharya, Ruchi. University of Missouri; Estados UnidosFil: Burns, Wilton G.. University of Vermont; Estados UnidosFil: Carey, Cayelan C.. Virginia Tech University; Estados UnidosFil: Carvalho, Laurence. Freshwater Restoration & Sustainability Group; Reino UnidoFil: Chang, ChunWei. National Taiwan University; República de ChinaFil: De Senerpont Domis, Lisette N.. Netherlands Institute of Ecology; Países BajosFil: Doubek, Jonathan P.. University of Vermont; Estados UnidosFil: Dur, Gaël. Shizuoka University; JapónFil: Frassl, Marieke A.. Griffith University; AustraliaFil: Gessner, Mark O.. Leibniz Institute of Freshwater Ecology and Inland Fisheries; AlemaniaFil: Hejzlar, Josef. Biology Centre of the Czech Academy of Sciences; República ChecaFil: Ibelings, Bas W.. University of Geneva; SuizaFil: Janatian, Nasim. Estonian University of Life Sciences; EstoniaFil: Kpodonu, Alfred T. N. K.. City University of New York; Estados UnidosFil: Lajeunesse, Marc J.. University of South Florida; Estados UnidosFil: Lewandowska, Aleksandra M.. Tvarminne Zoological Station; FinlandiaFil: Llames, Maria Eugenia del Rosario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Investigaciones Biotecnológicas. Universidad Nacional de San Martín. Instituto de Investigaciones Biotecnológicas; ArgentinaFil: Matsuzaki, Shin-ichiro S.. National Institute for Environmental Studies; JapónFil: Nodine, Emily R.. Rollins College; Estados UnidosFil: Nõges, Peeter. Estonian University of Life Sciences; EstoniaFil: Park, Ho-Dong. Shinshu University; JapónFil: Patil, Vijay P.. US Geological Survey; Estados UnidosFil: Pomati, Francesco. Swiss Federal Institute of Water Science and Technology; SuizaFil: Rimmer, Alon. Kinneret Limnological Laboratory; IsraelFil: Rinke, Karsten. Helmholtz-Centre for Environmental Research; AlemaniaFil: Rudstam, Lars G.. Cornell University; Estados UnidosFil: Rusak, James A.. Ontario Ministry of the Environment and Climate Change; CanadáFil: Salmaso, Nico. Research and Innovation Centre - Fondazione Mach; ItaliaFil: Schmitt, François. Laboratoire d’Océanologie et de Géosciences; FranciaFil: Seltmann, Christian T.. Dundalk Institute of Technology; IrlandaFil: Souissi, Sami. Universite Lille; FranciaFil: Straile, Dietmar. University of Konstanz; AlemaniaFil: Thackeray, Stephen J.. Lancaster Environment Centre; Reino UnidoFil: Thiery, Wim. Vrije Unviversiteit Brussel; Bélgica. Institute for Atmospheric and Climate Science; SuizaFil: Urrutia Cordero, Pablo. Uppsala University; SueciaFil: Venail, Patrick. Universidad de Ginebra; SuizaFil: Verburg, Piet. 8National Institute of Water and Atmospheric Research; Nueva ZelandaFil: Williamson, Tanner J.. Miami University; Estados UnidosFil: Wilson, Harriet L.. Dundalk Institute of Technology; IrlandaFil: Zohary, Tamar. Israel Oceanographic & Limnological Research; IsraelGLEON 20: All Hands' MeetingRottnest IslandAustraliaUniversity of Western AustraliaUniversity of AdelaideGlobal Lake Ecological Observatory Networ

Pratos e mais pratos: louças domésticas, divisões culturais e limites sociais no Rio de Janeiro, século XIX

Reply to ten comments on a paper published in the last issue of this journal. The discussion follows along six main lines: History museums, identity, ideology and the category of nation; the need of material collections and their modalities: patrimonial, operational, virtual; theater versus laboratory; visitors and their ambiguities; Public History: the museum and the academy.Resposta aos comentários de dez especialistas que contribuíram no debate de texto publicado no último número desta revista. A discussão orientou-se segundo seis tópicos principais: museus históricos, identidade, ideologia e a categoria de nação; a necessidade de acervos materiais e suas modalidades: acervo patrimonial, operacional, virtual; teatro versus laboratório; o público e suas ambigüidades; História Pública: o museu e a Academia

A sequence variant at 4p16.3 confers susceptibility to urinary bladder cancer

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldPreviously, we reported germline DNA variants associated with risk of urinary bladder cancer (UBC) in Dutch and Icelandic subjects. Here we expanded the Icelandic sample set and tested the top 20 markers from the combined analysis in several European case-control sample sets, with a total of 4,739 cases and 45,549 controls. The T allele of rs798766 on 4p16.3 was found to associate with UBC (odds ratio = 1.24, P = 9.9 x 10(-12)). rs798766 is located in an intron of TACC3, 70 kb from FGFR3, which often harbors activating somatic mutations in low-grade, noninvasive UBC. Notably, rs798766[T] shows stronger association with low-grade and low-stage UBC than with more aggressive forms of the disease and is associated with higher risk of recurrence in low-grade stage Ta tumors. The frequency of rs798766[T] is higher in Ta tumors that carry an activating mutation in FGFR3 than in Ta tumors with wild-type FGFR3. Our results show a link between germline variants, somatic mutations of FGFR3 and risk of UBC.info:eu-repo/grantAgreement/EC/FP7/21807

HMOX1 Gene Promoter Alleles and High HO-1 Levels Are Associated with Severe Malaria in Gambian Children

Heme oxygenase 1 (HO-1) is an essential enzyme induced by heme and multiple stimuli associated with critical illness. In humans, polymorphisms in the HMOX1 gene promoter may influence the magnitude of HO-1 expression. In many diseases including murine malaria, HO-1 induction produces protective anti-inflammatory effects, but observations from patients suggest these may be limited to a narrow range of HO-1 induction, prompting us to investigate the role of HO-1 in malaria infection. In 307 Gambian children with either severe or uncomplicated P. falciparum malaria, we characterized the associations of HMOX1 promoter polymorphisms, HMOX1 mRNA inducibility, HO-1 protein levels in leucocytes (flow cytometry), and plasma (ELISA) with disease severity. The (GT)n repeat polymorphism in the HMOX1 promoter was associated with HMOX1 mRNA expression in white blood cells in vitro, and with severe disease and death, while high HO-1 levels were associated with severe disease. Neutrophils were the main HO-1-expressing cells in peripheral blood, and HMOX1 mRNA expression was upregulated by heme-moieties of lysed erythrocytes. We provide mechanistic evidence that induction of HMOX1 expression in neutrophils potentiates the respiratory burst, and propose this may be part of the causal pathway explaining the association between short (GT)n repeats and increased disease severity in malaria and other critical illnesses. Our findings suggest a genetic predisposition to higher levels of HO-1 is associated with severe illness, and enhances the neutrophil burst leading to oxidative damage of endothelial cells. These add important information to the discussion about possible therapeutic manipulation of HO-1 in critically ill patients

Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences

The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & Nemésio 2007; Donegan 2008, 2009; Nemésio 2009a–b; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on 18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based researchers who signed it in the short time span from 20 September to 6 October 2016