Why the European Parliament has a better gender balance than national parliaments

Across Europe there is a wide variation in the percentage of female representatives in national parliaments, with the gender balance typically skewed toward male representatives. But what can the European Parliament tell us about mechanisms for ensuring a better gender balance? Jessica Fortin-Rittberger and Berthold Rittberger write that there is a clear ‘gender gap’ between the European Parliament and national parliaments, with the European Parliament consistently containing a higher percentage of female representatives than national parliaments overall. The exact reasons for this are unclear, however, and may relate to the candidate recruitment procedures employed by political parties

Rho GTPasen der RhoBTB Familie: Charakterisierung und Rolle in der Tumorentstehung

Rho Proteine sind an einer Vielzahl zellulärer Prozesse wie Vesikeltransport, Morphogenese, Mikrotubuli-Organisation, Zytokinese, Genexpression, Zellzyklus-Progression, Apoptose und Tumorigenese beteiligt. Alle Mitglieder agieren als molekulare Schalter, indem sie zwischen einem aktiven GTP-gebundenen und einem inaktiven GDP-gebundenen Status wechseln. Eine Subfamilie der Rho GTPasen, die RhoBTB, wird in Vertebraten durch drei Isoformen repräsentiert. Sie umfassen ca. 600 Aminosäuren und werden durch eine GTPase Domäne, eine prolinreiche Region, einem Tandem von zwei BTB Domänen und einem Carboxylterminus von unbekannter Funktion charakterisiert. In situ-Hybridisierungen zeigten, dass RHOBTB1 und RHOBTB3 spezifisch in Endothelzellen und Spermatiden exprimiert werden, was auf eine Funktion in Entwicklungsprozessen wie der Angiogenese und Spermatogenese hindeutet. Veröffentlichungen zeigten, dass BTB Domänen an der Ausbildung von Cullin3-abhängigen Ubiquitin Ligasen beteiligt sind. Zudem werden RhoBTB2/DBC2 und RhoBTB1 als Kandidaten für Tumorsuppressorgenen diskutiert. Das Ziel dieser Arbeit ist die Rolle der RhoBTB Proteine in der Tumorentstehung zu entschlüsseln und die Signalwege aufzudecken, in die sie involviert sind. Zunächst haben wir die Bindung der RhoBTB Proteine mit Cullinen bewiesen. Hefe Hybrid-Analysen zeigten Interaktionen mit RhoBTB2 sowie dem C-terminalen Bereich (B1B2C) von RhoBTB3 mit Cullin3 und Cullin5 durch das Tandem der BTB Domänen. Die Bindung mit RhoBTB konnte hierbei auf die ersten 41 Aminosäuren von Cullin3 begrenzt werden. Mit Koimmunpräzipitations-experimenten wurde die Bindung bestätigt und weiterhin gezeigt, dass die erste BTB Domäne von RhoBTB3 mit Cullin3 interagiert. Auf die gleiche Weise wurde Homodimerisierung von RhoBTB3 und interessanterweise Heterodimerisierung von RhoBTB3 mit RhoBTB2 durch die BTB Domänen gezeigt. Ein ganz neuer Aspekt war die Interaktion der GTPase Domäne von RhoBTB2 sowie RhoBTB3 mit den BTB Domänen. Wir postulieren, dass diese intramolekulare Interaktion der GTPase Domäne und der BTB Domäne die regulatorische Funktion übernimmt. Die Bindung könnte die Dimerisierung, die möglicherweise für die Formation von Cullin3 Komplexen und Substraten mit RhoBTB Proteinen nötig ist unterbinden. RhoBTB3 zeigte auch eine Interaktion mit Ubiquitin-konjugierenden Enzym E2, welches die Ubiquitinkette auf die Substrate überträgt. Neben den noch unbekannten Substraten wird RhoBTB3 selbst im Proteasom abgebaut. Zur Entschlüsselung der Rolle in der Tumorentstehung wurden Expressionsmuster von RHOBTB und CUL Genen mit Hilfe eines cancer profiling arrays und cancer cell line profiling array analysiert. RHOBTB zeigte in allen Nierenproben und in 80% der Brustproben niedrigere Expression in tumoralen Geweben als in normalen Geweben. Es bestehen hohe Korrelationen in der Änderung der Expressionslevel zwischen RHOBTB3 und CUL3, was auf eine Ko-Regulation der Proteine hindeutet. Untersuchungen der subzellulären Lokalisation zeigten für alle drei Isoformen eine Expression als punktförmige Struktur um den Nukleus. In diesem Bereich kolokalisieren die RhoBTB Proteine mit allen Cullinen und lassen eine große Komplexbildung in Aggregaten vermuten. Wir postulieren ein Modell, in dem RhoBTB Proteine durch Formation von Cullin Komplexen zum Abbau spezifischer Substrate führen und die Suppression der RhoBTB Proteine zur Anreicherung der Substrate und Zellproliferation führt

Recruitment procedures shape the gender composition of party lists in European Parliament elections

Different countries select their Members of the European Parliament in different manners, with Britain opting for a party list system based on regional (in the case of England) and national constituencies (in the cases of Scotland, Wales, and Northern Ireland). The European Parliament has better gender representation than most legislatures, however as Jessica Fortin-Rittberger, Berthold Rittberger, and Sarah Dingler argue, the recruitment procedures used by parties shape the gender composition of the lists that prospective MEPs appear on

Investigating frictional contact behavior for soft material robot simulations

The ability to interact safely with the environment is known as one of the major advantages of soft robots (SRs). Due to their low material stiffness, these continuously deformable robots offer inherent flexibility. These advantages make them suitable for application that involve human-robot collaboration in industrial settings as well as medical application such as minimally invasive surgery. To date only few research groups have analyzed the contact and frictional behavior of soft robots. In fact, the contact behavior is often oversimplified or neglected. Motivated by the idea to bridge this gap, this work presents measurements and the resulting coefficient of friction (COF) for silicone rubbers that are widely used in the field of SRs and different contact partners which depend on contact pressure and ambient temperature. From these measurements, a more representative contact model is established and used to more accurately simulate soft material robots’ frictional contact behavior. Moreover the influence of friction and therefore the need to implement frictional behavior is demonstrated for a typical application of a SR

Linagliptin and its effects on hyperglycaemia and albuminuria in patients with type 2 diabetes and renal dysfunction : the randomized MARLINA-T2D trial

Aims: The MARLINA-T2D study (ClinicalTrials. gov, NCT01792518) was designed to investigate the glycaemic and renal effects of linagliptin added to standard-of-care in individuals with type 2 diabetes and albuminuria. Methods: A total of 360 individuals with type 2 diabetes, HbA1c 6.5% to 10.0% (48-86 mmol/ mol), estimated glomerular filtration rate (eGFR) >= 30 mL/min/1.73 m(2) and urinary albumin-tocreatinine ratio (UACR) 30-3000 mg/g despite single agent renin-angiotensin-system blockade were randomized to double-blind linagliptin (n = 182) or placebo (n = 178) for 24 weeks. The primary and key secondary endpoints were change from baseline in HbA1c at week 24 and time-weighted average of percentage change from baseline in UACR over 24 weeks, respectively. Results: Baseline mean HbA1c and geometric mean (gMean) UACR were 7.8% +/- 0.9% (62.2 +/- 9.6 mmol/mol) and 126 mg/g, respectively; 73.7% and 20.3% of participants had microalbuminuria or macroalbuminuria, respectively. After 24 weeks, the placebo-adjusted mean change in HbA1c from baseline was -0.60% (-6.6 mmol/mol) (95% confidence interval [CI], -0.78 to -0.43 [-8.5 to -4.7 mmol/mol]; P Conclusions: In individuals at early stages of diabetic kidney disease, linagliptin significantly improved glycaemic control but did not significantly lower albuminuria. There was no significant change in placebo-adjusted eGFR. Detection of clinically relevant renal effects of linagliptin may require longer treatment, as its main experimental effects in animal studies have been to reduce interstitial fibrosis rather than alter glomerular haemodynamics.Peer reviewe

Suppression of xylan endotransglycosylase PtxtXyn10A affects cellulose microfibril angle in secondary wall in aspen wood.

Certain xylanases from family GH10 are highly expressed during secondary wall deposition, but their function is unknown. We carried out functional analyses of the secondary-wall specific PtxtXyn10A in hybrid aspen (Populus tremula × tremuloides). PtxtXyn10A function was analysed by expression studies, overexpression in Arabidopsis protoplasts and by downregulation in aspen. PtxtXyn10A overexpression in Arabidopsis protoplasts resulted in increased xylan endotransglycosylation rather than hydrolysis. In aspen, the enzyme was found to be proteolytically processed to a 68 kDa peptide and residing in cell walls. Its downregulation resulted in a corresponding decrease in xylan endotransglycosylase activity and no change in xylanase activity. This did not alter xylan molecular weight or its branching pattern but affected the cellulose-microfibril angle in wood fibres, increased primary growth (stem elongation, leaf formation and enlargement) and reduced the tendency to form tension wood. Transcriptomes of transgenic plants showed downregulation of tension wood related genes and changes in stress-responsive genes. The data indicate that PtxtXyn10A acts as a xylan endotransglycosylase and its main function is to release tensional stresses arising during secondary wall deposition. Furthermore, they suggest that regulation of stresses in secondary walls plays a vital role in plant development.Formas (including HemiPop and FuncFiber), Swedish Research Council (VR), Swedish Governmental Agency for Innovation Systems (VINNOVA), Swedish Center for Biomimetic Fiber Engineering (funded by the Knut & Alice Wallenberg Foundation and the Foundation for Strategic Research), European projects EDEN (QLK5-CT-2001-00443) and RENEWALL, FORE, Bio4Energy, Wood Ultrastructure Research Centre, SamNordisk Skogsforskning (project no. 107), Japan Society for the Promotion of Science (JSPS KAKENHI Grant Number 24580243) and the Academy of Finland (1127759).This is the accepted manuscript. The final version is available at http://onlinelibrary.wiley.com/doi/10.1111/nph.13099/abstract

Causal Agents of Hop Dying

Stockfaule Hopfenpflanzen im Hopfenanbaugebiet Spalt bei Nürnberg weisen Befall mit dem Gefäßparasiten Ceratocystis paradoxa auf. Aus Bodenproben von über 100-jährigen Hopfengärten konnten die Pilze Fusarium oxysporum und F. equiseti isoliert werden. Bei der mikroskopischen Untersuchung von Hopfenwurzeln wurden Pilze der Gattungen Rhizoctonia und Pythium gefunden, die als Wurzelfäule-Erreger bekannt sind. An Faserwurzeln war starker Befall mit Hopfen-Zystennematoden (Heterodera humili), sowie an Haarwurzeln Befall mit Strahlenpilzen (Actinomycetes) zu erkennen, die für Bodenmüdigkeitserscheinungen verantwortlich sind.Rotten hop-stocks in the hop growing area of Spalt near Nuremberg were attacked by the vessels-invading fungus Ceratocystis paradoxa. The fungi Fusarium oxysporum and F. equiseti could be isolated from soil of a 100 years old hop garden. By microscopic examination, fungi of the genera Rhizoctonia and Pythium were found, which are known as root rot pathogens. The filamentous roots were severely attacked by hop cyst nematodes (Heterodera humili), and the hairy roots were infested with Actinomycetes, both responsible for the soil exhaustion syndrom

The Mother Centriole Plays an Instructive Role in Defining Cell Geometry

Centriole positioning is a key step in establishment and propagation of cell geometry, but the mechanism of this positioning is unknown. The ability of pre-existing centrioles to induce formation of new centrioles at a defined angle relative to themselves suggests they may have the capacity to transmit spatial information to their daughters. Using three-dimensional computer-aided analysis of cell morphology in Chlamydomonas, we identify six genes required for centriole positioning relative to overall cell polarity, four of which have known sequences. We show that the distal portion of the centriole is critical for positioning, and that the centriole positions the nucleus rather than vice versa. We obtain evidence that the daughter centriole is unable to respond to normal positioning cues and relies on the mother for positional information. Our results represent a clear example of “cytotaxis” as defined by Sonneborn, and suggest that centrioles can play a key function in propagation of cellular geometry from one generation to the next. The genes documented here that are required for proper centriole positioning may represent a new class of ciliary disease genes, defects in which would be expected to cause disorganized ciliary position and impaired function

Multiple mechanisms disrupt the let-7 microRNA family in neuroblastoma

Poor prognosis in neuroblastoma is associated with genetic amplification of MYCN. MYCN is itself a target of let-7, a tumour suppressor family of microRNAs implicated in numerous cancers. LIN28B, an inhibitor of let-7 biogenesis, is overexpressed in neuroblastoma and has been reported to regulate MYCN. Here we show, however, that LIN28B is dispensable in MYCN-amplified neuroblastoma cell lines, despite de-repression of let-7. We further demonstrate that MYCN messenger RNA levels in amplified disease are exceptionally high and sufficient to sponge let-7, which reconciles the dispensability of LIN28B. We found that genetic loss of let-7 is common in neuroblastoma, inversely associated with MYCN amplification, and independently associated with poor outcomes, providing a rationale for chromosomal loss patterns in neuroblastoma. We propose that let-7 disruption by LIN28B, MYCN sponging, or genetic loss is a unifying mechanism of neuroblastoma development with broad implications for cancer pathogenesis.United States. National Institutes of Health (R01GM107536)Alex's Lemonade Stand FoundationHoward Hughes Medical InstituteBoston Children's Hospital. Manton Center for Orphan Disease ResearchNational Institute of General Medical Sciences (U.S.) (T32GM007753

Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics

Funding Information: Researchers were funded by investment from the European Regional Development Fund (ERDF) and the European Social Fund (ESF) Convergence Programme for Cornwall and the Isles of Scilly [J.T.]; European Research Council (ERC) [grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC to T.M.F., A.R.W.], [ERC Consolidator Grant, ERC-2014-CoG-648916 to V.W.V.J.], [P.R.N.]; University of Bergen, KG Jebsen and Helse Vest [P.R.N.]; Wellcome Trust Senior Investigator Awards [A.T.H. (WT098395), M.I.M. (WT098381)]; National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0611–10219); Sir Henry Dale Fellowship (Wellcome Trust and Royal Society grant: WT104150) [R.M.F., R.N.B.]; 4-year studentship (Grant Code: WT083431MF) [R.C.R]; the European Research Council under the European Union’s Seventh Framework Programme (FP/2007– 2013)/ERC Grant Agreement (grant number 669545; Develop Obese) [D.A.L.]; US National Institute of Health (grant: R01 DK10324) [D.A.L, C.L.R]; Wellcome Trust GWAS grant (WT088806) [D.A.L] and NIHR Senior Investigator Award (NF-SI-0611–10196) [D.A.L]; Wellcome Trust Institutional Strategic Support Award (WT097835MF) [M.A.T.]; The Diabetes Research and Wellness Foundation Non-Clinical Fellowship [J.T.]; Australian National Health and Medical Research Council Early Career Fellowship (APP1104818) [N.M.W.]; Daniel B. Burke Endowed Chair for Diabetes Research [S.F.A.G.]; UK Medical Research Council Unit grants MC_UU_12013_5 [R.C.R, L.P, S.R, C.L.R, D.M.E., D.A.L.] and MC_UU_12013_4 [D.M.E.]; Medical Research Council (grant: MR/M005070/1) [M.N.W., S.E.J.]; Australian Research Council Future Fellowship (FT130101709) [D.M.E] and (FT110100548) [S.E.M.]; NIHR Oxford Biomedical Research Centre (BRC); Oak Foundation Fellowship and Novo Nordisk Foundation (12955) [B.F.]; FRQS research scholar and Clinical Scientist Award by the Canadian Diabetes Association and the Maud Menten Award from the Institute of Genetics– Canadian Institute of Health Research (CIHR) [MFH]; CIHR— Frederick Banting and Charles Best Canada Graduate Scholarships [C.A.]; FRQS [L.B.]; Netherlands Organization for Health Research and Development (ZonMw–VIDI 016.136.361) [V.W.V.J.]; National Institute on Aging (R01AG29451) [J.M.M.]; 2010–2011 PRIN funds of the University of Ferrara—Holder: Prof. Guido Barbujani, Supervisor: Prof. Chiara Scapoli—and in part sponsored by the European Foundation for the Study of Diabetes (EFSD) Albert Renold Travel Fellowships for Young Scientists, ‘5 per mille’ contribution assigned to the University of Ferrara, income tax return year 2009 and the ENGAGE Exchange and Mobility Program for ENGAGE training funds, ENGAGE project, grant agreement HEALTH-F4–2007-201413 [L.M.]; ESRC (RES-060–23-0011) [C.L.R.]; National Institute of Health Research ([S.D., M.I.M.], Senior Investigator Award (NF-SI-0611–10196) [D.A.L]); Australian NHMRC Fellowships Scheme (619667) [G.W.M]. For study-specific funding, please see Supplementary Material. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Funding to pay the Open Access publication charges for this article was provided by the Charity Open Access Fund (COAF). Funding Information: We are extremely grateful to the participants and families who contributed to all of the studies and the teams of investigators involved in each one. These include interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. This research has been conducted using the UK Biobank Resource (Application numbers 7036 and 12703). For additional study-specific acknowledgements, please see Supplementary Material. Conflict of Interest statement. D.A.L. has received support from Roche Diagnostics and Medtronic for biomarker research unrelated to the work presented here. Funding Researchers were funded by investment from the European Regional Development Fund (ERDF) and the European Social Fund (ESF) Convergence Programme for Cornwall and the Isles of Scilly [J.T.]; European Research Council (ERC) [grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC to T.M.F., A.R.W.], [ERC Consolidator Grant, ERC-2014-CoG-648916 to V.W.V.J.], [P.R.N.]; University of Bergen, KG Jebsen and Helse Vest [P.R.N.]; Wellcome Trust Senior Investigator Awards [A.T.H. (WT098395), M.I.M. (WT098381)]; National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0611-10219); Sir Henry Dale Fellowship (Wellcome Trust and Royal Society grant: WT104150) [R.M.F., R.N.B.]; 4-year studentship (Grant Code: WT083431MF) [R.C.R]; the European Research Council under the European Union's Seventh Framework Programme (FP/2007-2013)/ERC Grant Agreement (grant number 669545; Develop Obese) [D.A.L.]; US National Institute of Health (grant: R01 DK10324) [D.A.L, C.L.R]; Wellcome Trust GWAS grant (WT088806) [D.A.L] and NIHR Senior Investigator Award (NF-SI-0611-10196) [D.A.L]; Wellcome Trust Institutional Strategic Support Award (WT097835MF) [M.A.T.]; The Diabetes Research and Wellness Foundation Non-Clinical Fellowship [J.T.]; Australian National Health and Medical Research Council Early Career Fellowship (APP1104818) [N.M.W.]; Daniel B. Burke Endowed Chair for Diabetes Research [S.F.A.G.]; UK Medical Research Council Unit grants MC_UU_12013_5 [R.C.R, L.P, S.R, C.L.R, D.M.E., D.A.L.] and MC_UU_12013_4 [D.M.E.]; Medical Research Council (grant: MR/M005070/1) [M.N.W., S.E.J.]; Australian Research Council Future Fellowship (FT130101709) [D.M.E] and (FT110100548) [S.E.M.]; NIHR Oxford Biomedical Research Centre (BRC); Oak Foundation Fellowship and Novo Nordisk Foundation (12955) [B.F.]; FRQS research scholar and Clinical Scientist Award by the Canadian Diabetes Association and the Maud Menten Award from the Institute of Genetics-Canadian Institute of Health Research (CIHR) [MFH]; CIHR-Frederick Banting and Charles Best Canada Graduate Scholarships [C.A.]; FRQS [L.B.]; Netherlands Organization for Health Research and Development (ZonMw-VIDI 016.136.361) [V.W.V.J.]; National Institute on Aging (R01AG29451) [J.M.M.]; 2010-2011 PRIN funds of the University of Ferrara-Holder: Prof. Guido Barbujani, Supervisor: Prof. Chiara Scapoli-and in part sponsored by the European Foundation for the Study of Diabetes (EFSD) Albert Renold Travel Fellowships for Young Scientists, '5 per mille' contribution assigned to the University of Ferrara, income tax return year 2009 and the ENGAGE Exchange and Mobility Program for ENGAGE training funds, ENGAGE project, grant agreement HEALTH-F4-2007-201413 [L.M.]; ESRC (RES-060-23-0011) [C.L.R.]; National Institute of Health Research ([S.D., M.I.M.], Senior Investigator Award (NFSI-0611-10196) [D.A.L]); Australian NHMRC Fellowships Scheme (619667) [G.W.M]. For study-specific funding, please see Supplementary Material. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Funding to pay the Open Access publication charges for this article was provided by the Charity Open Access Fund (COAF). Publisher Copyright: © The Author(s) 2018.Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P<5 x 10(-8). In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.Peer reviewe