1,535 research outputs found
FIGURE 7 in Taxonomic revision of the genus Hemigyrus Brunner von Wattenwyl, 1893 (Orthoptera: Tettigoniidae: Pseudophyllinae)
No full textFIGURE 7. Morphological features of H. (H.) amplus. A. frons in fronto-ventral view; B. head and pronotum in dorsal view; C. pronotum in lateral view; D. sterna in ventral view; E. abdominal terminal in dorsal view; F. abdominal terminal in ventral view; G. subgenital plate in ventral view; H. ovipositor in lateral view. A–F. male; G, H. female. Scale bar= 2mm.Published as part of Xie, Hui-Cong, Wang, Han-Qiang, Zong, Jing-Song, Li, Kai & He, Zhu-Qing, 2022, Taxonomic revision of the genus Hemigyrus Brunner von Wattenwyl, 1893 (Orthoptera: Tettigoniidae: Pseudophyllinae), pp. 97-115 in Zootaxa 5092 (1) on page 106, DOI: 10.11646/zootaxa.5092.1.5, http://zenodo.org/record/586967
FIGURE 6 in Taxonomic revision of the genus Hemigyrus Brunner von Wattenwyl, 1893 (Orthoptera: Tettigoniidae: Pseudophyllinae)
No full textFIGURE 6. Morphological features of H. (H.) tonkinensis. A. frons in fronto-ventral view; B. head and pronotum in dorsal view; C. pronotum in lateral view; D. sterna in ventral view; E. abdominal terminal in dorsal view; F. abdominal terminal in ventral view; G. subgenital plate in ventral view; H. ovipositor in lateral view. A–F. male; G, H. female. Scale bar= 2mm.Published as part of Xie, Hui-Cong, Wang, Han-Qiang, Zong, Jing-Song, Li, Kai & He, Zhu-Qing, 2022, Taxonomic revision of the genus Hemigyrus Brunner von Wattenwyl, 1893 (Orthoptera: Tettigoniidae: Pseudophyllinae), pp. 97-115 in Zootaxa 5092 (1) on page 105, DOI: 10.11646/zootaxa.5092.1.5, http://zenodo.org/record/586967
Check-list of European Orthoptera
No full textList of all 974 recognized species of Ensifera (Tettigonioidea: 458, Rhaphidophoroidea: 44, Grylloidea: 91) and Caelifera (Tetrigoidea: 12, Tridactyloidea: 6, Acridoidea: 363) in Europe including information about their distribution.Aufstellung aller 974 derzeitig anerkannten Arten der Ensifera (Tettigonioidea: 458, Rhaphidophoroidea: 44, Grylloidea: 91) and Caelifera (Tetrigoidea: 12, Tridactyloidea: 6, Acridoidea: 363) in Europa mit Angabe der Verbreitungsgebiete
EUCP Atlas of constrained climate projections
No full textWhat's Changed Change author order in citation.cff by @Peter9192 in https://github.com/eucp-project/atlas/pull/61 Full Changelog: https://github.com/eucp-project/atlas/compare/0.1.0...0.1.1Kalverla, P., Alidoost, F., Liu, Y., Verhoeven, S., Vreede, B., Booth, B., Coppola, E., Nogherotto, R., Brunner, L., Harris, G., Qasmi, S., Ballinger, A., Hegerl, G., McSweeney, C., O'Reilly, C., Palmer, T., Ribes, A., & de Vries, H. (2021). EUCP Atlas of constrained climate projections (0.1.1). Zenodo. https://doi.org/10.5281/zenodo.565474
From oncogenic replication stress to drug resistance : F-box proteins as signalling hubs in cancer
No full textCancer arises from cells that acquire genetic and epigenetic changes during the course of a, sometimes decades-long, somatic evolutionary process. These changes result in deregulation of a multitude of cellular processes leading to novel capabilities, often referred to as hallmarks of cancer, and a strong selective advantage for these cells albeit at a dramatic cost to the organism as a whole. Both, gene expression but also turn-over of gene products can become deregulated. The ubiquitin-proteasome system is responsible for the targeted degradation of proteins, and components of this system are altered during cancer development. Target specificity of this system is largely attained through E3 ubiquitin ligases that mediate the covalent attachment of ubiquitin to their substrates. The largest group of E3s are cullin-RING domain ligases (CRLs) with SKP1-cullin1-F-box protein (SCF) E3 ligases, or CRL1, representing one of the best-characterised subgroups of CRLs. These SCF ligases are multiprotein complexes containing one of, in human cells, 69 F-box proteins which function as substrate-adaptor subunits. Collectively, the family of F-box proteins has been found to be critically involved in virtually all the cancer hallmarks. However, despite their important role in cancer development, only a handful of SCFs has been molecularly and functionally well- characterised and detailed knowledge of how deregulation of specific SCF ligases and downstream substrate effectors impinges on cancer traits is lacking.One of the main aims of the work presented in this thesis is to find cellular vulnerabilities resulting from deregulation of F-box proteins in cancer. FBXW7 is the most commonly mutated F-box protein in human cancers. Its inactivation leads to upregulation of its substrates including cyclin E, MYC or SOX9 (paper IV) resulting in deregulated proliferation, increased metastasis and drug resistance but also replication stress. Cancer cells undergoing replication stress become more dependent on signalling pathways detecting and repairing damaged DNA (papers I and III) and are consequently more sensitive to therapies targeting checkpoint and repair proteins such as WEE1, ATR or DNA-PK kinases (paper II).In paper I we describe a novel function for the largely uncharacterised F-box protein FBXL12 in regulating the response to oncogene-induced replication stress. FBXL12 complements the Fanconi anaemia (FA) DNA repair pathway by targeting its central component FANCD2 for proteasomal degradation. The FA pathway not only plays a crucial role in resilience to endogenous sources of replication stress but also to drug-induced stress. FBXL12 and cyclin E are upregulated and correlated in human cancers and depletion of FBXL12 results in increased sensitivity to replication stress which posits FBXL12 as a potential cancer drug target. Ablation or pharmacological inhibition of FBXL12 prevents degradation of FANCD2 and breast cancer cells are sensitised to the adverse effects of drug- as well as oncogenic cyclin E-induced replication stress.In paper II we focus on exploring further ways of sensitising cancer cells to replication stress. We performed a screen to identify potential viability markers in response to replication stress induced by WEE1 inhibitor AZD1775 and discover novel synergistic combinations. Additionally, we determine a subset of basal-like breast cancer cells that responds to treatment initially but recovers after treatment cessation and identify PTEN as a novel predictive marker for such responses, with cells expressing low levels of PTEN being highly sensitive acutely and failing to recover. Furthermore, inactivation or genomic deletion of DNA-PK, an apical DNA damage kinase, attenuates recovery and sensitises basal-like breast cancer cells to AZD1775. Mechanistically, loss of PTEN or DNA-PK impair CHK1 activation and S-phase arrest in response to AZD1775 treatment, which finally ensues lethal replication stress and loss of survival.In paper III we concentrate on FBXO28, another poorly-studied member of the F-box family, which we find to degrade ARHGEF6 and ARHGEF7 activators of the Rho-type GTPase RAC1, involved in cell motility. Surprisingly, we identify a novel function for FBXO28 and ARHGEF6/7 in promoting the repair of breaks in heterochromatin DNA. Following DNA damage, tightly chromatin-bound FBXO28 is released and promotes degradation of nucleoplasmic ARHGEF6/7 to modulate activation and inactivation cycles of nuclear RAC1 and allow for efficient resolution of H3K9me2/3-positive damaged sites.In paper IV we add a key oncogenic transcription factor to the growing list of FBXW7 substrates; SOX9. FBXW7 ubiquitylates and degrades SOX9 upon phosphorylation by GSK3β. Mutation and inactivation of FBXW7 in medulloblastoma concurs with elevated SOX9 protein expression and poor patient outcome. In medulloblastoma cell line models we demonstrate increased cell motility, metastasis and increased resistance to cytostatic treatment after expression of a non-degradable SOX9 mutant. Conversely, inhibition of the PI3K/AKT/mTOR pathway promoted GSK3β-dependent SOX9 degradation and sensitised FBXW7-proficient medulloblastoma cells to cisplatin.List of scientific papersI. Brunner, A.§, Johansson, H., Kourtesakis, A., Viiliäinen, J., Widschwendtner, M., Wohlschlegel, J., Lehtiö, J., Spruck, C., Orre, L.M., Rantala, J. K. and Sangfelt, O.§. Degradation of FANCD2 by SCF-FBXL12 alleviates cyclin E-driven replication stress and maintains genomic integrity. §Corresponding author. [Manuscript]II. Brunner, A.*, Suryo Rahmanto, A.*, Johansson, H.±, Franco, M.±, Viiliäinen, J., Gazi, M., Frings, O., Fredlund, E., Lehtiö, J., Rantala, J. K., Larsson, L.-G. and Sangfelt, O§. PTEN and DNA-PK as determinants of sensitivity and recovery in response to WEE1 inhibitor AZD1775 in human breast cancer. eLife. 2020;9:e57894. *Equal contribution, ±Equal contribution, §Corresponding author. https://doi.org/10.7554/eLife.57894 III. Čermák, L.*§, Brunner, A.*, Baloghová, N., Ueberheide, B., Ng, H.-F., Wohlschlegel, J., Manser, E., Sangfelt, O.±§ and Pagano, M±§. FBXO28 controls nuclear RAC1 activity and safeguards efficient heterochromatin DNA repair by targeting ARHGEF6/7 for degradation. *Equal contribution, ±Equal contribution, §Corresponding author. [Manuscript]IV. Suryo Rahmanto, A.*, Savov, V.*, Brunner, A.±, Sara Bolin, S.±, Weishaupt, H.±, Malyukova, A., Rosén, G., Čančer, M., Hutter, S., Sundström, A., Kawauchi, D., Jones, D. T. W., Spruck, C., Taylor, M. D., Cho, Y.-J., Pfister, S.M., Kool, M., Korshunov, A., Swartling, F. J.§ and Sangfelt, O§. FBW7 suppression leads to SOX9 stabilization and increased malignancy in medulloblastoma. EMBO J. 35(20): 2192–2212. *Equal contribution, ±Equal contribution, §Corresponding author. https://doi.org/10.15252/embj.201693889 </p
Large scale wavefront reconstruction for the next generation of Extreme Large Scale Telescopes (E-ELT)
No full textThe spatial resolution of an astronomical telescope is limited by either by the diffraction of light and the amount of aberrations caused in the atmosphere. To increase the diffraction limited resolution, the size of telescopes increases such as the to be build European Extremely Large Telescope (E-ELT). To fully benefit from the increased diffraction limited resolution, also the ability of adaptive optics to compensate for the wavefront aberrations should increase. This is for example done by increase the number of spatial wavefront measurements. This demands algorithms that are computationally efficient and highly parallelizable. In this thesis it is discussed whether the recently introduced Spline based ABeration REconstruction (SABRE) method can be parallelized. It is discussed that SABRE can be solved with the null-space method, resulting in a system of equations similar to the Poisson equation. The Conjugate Gradient (CG) method with different preconditioners, namely the Approximate INVerse (AINV), Algebraic Multigrid (AMG) and Incomplete Cholesky factorization (ICHOL), are used that make use of the sparsity of SABRE are discussed, their scalability and parallelism seem to be promising but the high amount of communication lowers the expectations. Experiments on the Graphics Processing Unit (GPU) give results, that matches with these expectations. Although there is plenty of parallelism, the sparse solvers are limited by the communication and therefore, for the grid sizes discussed in this thesis, slower than their counter ones on the Central Processing Unit (CPU). But there is lot of optimization possible and especially the CG with the AINV has a lot of potential. Further research is required.Systems and ControlDelft Center for Systems and ControlMechanical, Maritime and Materials Engineerin
2017 Curt Stern Award Introduction: Nico Katsanis
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190677.pdf (Publisher’s version ) (Open Access
Understanding Urban Demand for Wild Meat in Vietnam: Implications for Conservation Actions
No full textVietnam is a significant consumer of wildlife, particularly wild meat, in urban restaurant settings. To meet this demand, poaching of wildlife is widespread, threatening regional and international biodiversity. Previous interventions to tackle illegal and potentially unsustainable consumption of wild meat in Vietnam have generally focused on limiting supply. While critical, they have been impeded by a lack of resources, the presence of increasingly organised criminal networks and corruption. Attention is, therefore, turning to the consumer, but a paucity of research investigating consumer demand for wild meat will impede the creation of effective consumer-centred interventions. Here we used a mixed-methods research approach comprising a hypothetical choice modelling survey and qualitative interviews to explore the drivers of wild meat consumption and consumer preferences among residents of Ho Chi Minh City, Vietnam. Our findings indicate that demand for wild meat is heterogeneous and highly context specific. Wild-sourced, rare, and expensive wild meat-types are eaten by those situated towards the top of the societal hierarchy to convey wealth and status and are commonly consumed in lucrative business contexts. Cheaper, legal and farmed substitutes for wild-sourced meats are also consumed, but typically in more casual consumption or social drinking settings. We explore the implications of our results for current conservation interventions in Vietnam that attempt to tackle illegal and potentially unsustainable trade in and consumption of wild meat and detail how our research informs future consumer-centric conservation actions
A novel D458V mutation in the SANS PDZ binding motif causes atypical Usher syndrome
No full textHomozygosity mapping and linkage analysis in a Turkish family with autosomal recessive prelingual sensorineural hearing loss revealed a 15-cM critical region at 17q25.1-25.3 flanked by the polymorphic markers D17S1807 and D17S1806. The maximum two-point lod score was 4.07 at theta=0.0 for the marker D17S801. The linkage interval contains the Usher syndrome 1G gene (USH1G) that is mutated in patients with Usher syndrome (USH) type 1g and encodes the SANS protein. Mutation analysis of USH1G led to the identification of a homozygous missense mutation D458V at the -3 position of the PDZ binding motif of SANS. This mutation was also present homozygously in one out of 64 additional families from Turkey with autosomal recessive nonsyndromic hearing loss and heterozygously in one out of 498 control chromosomes. By molecular modeling, we provide evidence that this mutation impairs the interaction of SANS with harmonin. Ophthalmologic examination and vestibular evaluation of patients from both families revealed mild retinitis pigmentosa and normal vestibular function. These results suggest that these patients suffer from atypical USH
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