Competition between vitrification and crystallization of methanol at high pressure

Competition between vitrification and crystallization of methanol at high pressure Brugmans, M.J.P.; Vos, W.L. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. We have studied methanol at high pressure up to 33 GPa at room temperature with x-ray diffraction, optical ͑polarization͒ microscopy, Raman spectroscopy, and detection of hydrostaticity. A competition between crystallization and vitrification is observed when methanol is superpressed beyond the freezing pressure of 3.5 GPa: between 5.0 and 10.5 GPa crystals can nucleate, but if this region is surpassed quickly enough ͑within a few seconds͒, methanol remains amorphous. For the first time the nucleation rate and the crystal growth velocity have been studied as a function of pressure. These kinetic properties can be described by classical nucleation theory in agreement with, respectively, Turnbull-Fisher and Wilson-Frenkel type behavior using one and the same activated hard-sphere diffusion coefficient. The experimental nucleation rate and the crystal growth velocity are both effectively reduced to zero above 10.5 GPa, because the diffusion is suppressed. At these pressures methanol is compressed into a glass

Competition between vitrification and crystallization of methanol at high pressure

Competition between vitrification and crystallization of methanol at high pressure Brugmans, M.J.P.; Vos, W.L. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. We have studied methanol at high pressure up to 33 GPa at room temperature with x-ray diffraction, optical ͑polarization͒ microscopy, Raman spectroscopy, and detection of hydrostaticity. A competition between crystallization and vitrification is observed when methanol is superpressed beyond the freezing pressure of 3.5 GPa: between 5.0 and 10.5 GPa crystals can nucleate, but if this region is surpassed quickly enough ͑within a few seconds͒, methanol remains amorphous. For the first time the nucleation rate and the crystal growth velocity have been studied as a function of pressure. These kinetic properties can be described by classical nucleation theory in agreement with, respectively, Turnbull-Fisher and Wilson-Frenkel type behavior using one and the same activated hard-sphere diffusion coefficient. The experimental nucleation rate and the crystal growth velocity are both effectively reduced to zero above 10.5 GPa, because the diffusion is suppressed. At these pressures methanol is compressed into a glass

The roots of "Western European societal evolution". A concept of Europe by Jenő Szűcs

Jenő Szűcs wrote his essay entitled Sketch on the three regions of Europe in the early 1980s in Hungary. During these years, a historically well-argued opinion emphasising a substantial difference between Central European and Eastern European societies was warmly received in various circles of the political opposition. In a wider European perspective Szűcs used the old “liberty topos” which claims that the history of Europe is no other than the fulfillment of liberty. In his Sketch, Szűcs does not only concentrate on questions concerning the Middle Ages in Western Europe. Yet it is this stream of thought which brought a new perspective to explaining European history. His picture of the Middle Ages represents well that there is a way to integrate all typical Western motifs of post-war self-definition into a single theory. Mainly, the “liberty motif”, as a sign of “Europeanism” – in the interpretation of Bibó’s concept, Anglo-saxon Marxists and Weber’s social theory –, developed from medieval concepts of state and society and from an analysis of economic and social structures. Szűcs’s historical aspect was a typical intellectual product of the 1980s: this was the time when a few Central European historians started to outline non-Marxist aspects of social theory and categories of modernisation theories, but concealing them with Marxist terminology

Voltage-probe-controlled breakdown of the quantum Hall effect

Wetensch. publicatieFaculteit der Wiskunde en Natuurwetenschappe

Mutations in Known Monogenic High Bone Mass Loci Only Explain a Small Proportion of High Bone Mass Cases.

High bone mass (HBM) can be an incidental clinical finding; however, monogenic HBM disorders (eg, LRP5 or SOST mutations) are rare. We aimed to determine to what extent HBM is explained by mutations in known HBM genes. A total of 258 unrelated HBM cases were identified from a review of 335,115 DXA scans from 13 UK centers. Cases were assessed clinically and underwent sequencing of known anabolic HBM loci: LRP5 (exons 2, 3, 4), LRP4 (exons 25, 26), SOST (exons 1, 2, and the van Buchem's disease [VBD] 52-kb intronic deletion 3'). Family members were assessed for HBM segregation with identified variants. Three-dimensional protein models were constructed for identified variants. Two novel missense LRP5 HBM mutations ([c.518C>T; p.Thr173Met], [c.796C>T; p.Arg266Cys]) were identified, plus three previously reported missense LRP5 mutations ([c.593A>G; p.Asn198Ser], [c.724G>A; p.Ala242Thr], [c.266A>G; p.Gln89Arg]), associated with HBM in 11 adults from seven families. Individuals with LRP5 HBM (∼prevalence 5/100,000) displayed a variable phenotype of skeletal dysplasia with increased trabecular BMD and cortical thickness on HRpQCT, and gynoid fat mass accumulation on DXA, compared with both non-LRP5 HBM and controls. One mostly asymptomatic woman carried a novel heterozygous nonsense SOST mutation (c.530C>A; p.Ser177X) predicted to prematurely truncate sclerostin. Protein modeling suggests the severity of the LRP5-HBM phenotype corresponds to the degree of protein disruption and the consequent effect on SOST-LRP5 binding. We predict p.Asn198Ser and p.Ala242Thr directly disrupt SOST binding; both correspond to severe HBM phenotypes (BMD Z-scores +3.1 to +12.2, inability to float). Less disruptive structural alterations predicted from p.Arg266Cys, p.Thr173Met, and p.Gln89Arg were associated with less severe phenotypes (Z-scores +2.4 to +6.2, ability to float). In conclusion, although mutations in known HBM loci may be asymptomatic, they only account for a very small proportion (∼3%) of HBM individuals, suggesting the great majority are explained by either unknown monogenic causes or polygenic inheritance.This study was supported by The Wellcome Trust and NIHR CRN (portfolio number 5163). CLG was funded by a Wellcome Trust Clinical Research Training Fellowship (080280/Z/06/Z), the EU 7th Framework Programme under grant agreement number 247642 (GEoCoDE), a British Geriatric Society travel grant, and is now funded by Arthritis Research UK (grant ref 20000). SH acknowledges Arthritis Research UK support (grant ref 19580). KESP acknowledges the support of Cambridge NIHR Biomedical Research Centre. KAW is supported by the core programme of the MRC Nutrition and Bone Health group at MRC Human Nutrition Research, funded by the UK Medical Research Council (Grant code U10590371). EM acknowledges support of the Sheffield Teaching Hospitals Foundation Trust Clinical Research Facility. The SGC is a registered charity (no. 1097737) that receives funds from AbbVie, Bayer, Boehringer Ingelheim, Genome Canada (Ontario Genomics Institute OGI- 055), GlaxoSmithKline, Janssen, Lilly Canada, Novartis Research Foundation, Ontario Ministry of Economic Development & Innovation, Pfizer, Takeda, and Wellcome Trust (092809/Z/10/Z).This is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1002/jbmr.270

The Mitotic Arrest Deficient Protein MAD2B Interacts with the Small GTPase RAN throughout the Cell Cycle

Contains fulltext : 81260.pdf (publisher's version ) (Open Access)BACKGROUND: Previously, we identified the mitotic arrest deficient protein MAD2B (MAD2L2) as a bona fide interactor of the renal cell carcinoma (RCC)-associated protein PRCC. In addition, we found that fusion of PRCC with the transcription factor TFE3 in t(X;1)(p11;q21)-positive RCCs results in an impairment of this interaction and, concomitantly, an abrogation of cell cycle progression. Although MAD2B is thought to inhibit the anaphase promoting complex (APC) by binding to CDC20 and/or CDH1(FZR1), its exact role in cell cycle control still remains to be established. METHODOLOGY/PRINCIPAL FINDINGS: Using a yeast two-hybrid interaction trap we identified the small GTPase RAN, a well-known cell cycle regulator, as a novel MAD2B binding protein. Endogenous interaction was established in mammalian cells via co-localization and co-immunoprecipitation of the respective proteins. The interaction domain of RAN could be assigned to a C-terminal moiety of 60 amino acids, whereas MAD2B had to be present in its full-length conformation. The MAD2B-RAN interaction was found to persist throughout the cell cycle. During mitosis, co-localization at the spindle was observed. CONCLUSIONS/SIGNIFICANCE: The small GTPase RAN is a novel MAD2B binding protein. This novel protein-protein interaction may play a role in (i) the control over the spindle checkpoint during mitosis and (ii) the regulation of nucleocytoplasmic trafficking during interphase

Diversity and linkage disequilibrium analysis within a selected set of cultivated tomatoes

Within the Dutch genomics initiative the “Centre for Biosystems Genomics” (CBSG) a major research effort is directed at the identification and unraveling of processes and mechanisms affecting fruit quality in tomato. The basis of this fruit quality program was a diverse set of 94 cultivated tomato cultivars, representing a wide spectrum of phenotypes for quality related traits. This paper describes a diversity study performed on these cultivars, using information of 882 AFLP markers, of which 304 markers had a known map position. The AFLP markers were scored as much as possible in a co-dominant fashion. We investigated genome distribution and coverage for the mapped markers and conclude that it proved difficult to arrive at a dense and uniformly distributed coverage of the genome with markers. Mapped markers and unmapped markers were used to investigate population structure. A clear substructure was observed which seemed to coincide with a grouping based on fruit size. Finally, we studied amount and decay of linkage disequilibrium (LD) along the chromosomes. LD was observed over considerable (genetic) distances. We discuss the feasibility of marker-trait association studies and conclude that the amount of genetic variation in our set of cultivars is limited, but that there exists scope for association studies

Comparison of anonymous and targeted molecular markers for the estimation of genetic diversity in ex situ conserved Lactuca

The anonymous marker systems microsatellites (simple sequence repeats), amplified fragment length polymorphisms and sequence-specific amplified polymorphisms were compared with the targeted marker systems sequence-related amplified polymorphisms, target region amplification polymorphisms and nucleotide binding site profiling for their ability to describe the genetic diversity in a selected set of 80 Lactuca accessions. The accessions were also described morphologically, and all characterisation methods were evaluated against the genetic diversity assessed by a panel of three crop experts. The morphological data showed a low level of association with the molecular data, and did not display a consistently better relationship with the experts’ assessments in comparison with the molecular data. In general, the diversity described by the targeted molecular markers did not differ markedly from that of the anonymous markers, resulting in only slight differences in performance when related to the expert-based assessments. It was argued that markers targeted to specific gene sequences may still behave as anonymous markers and that the type of marker system used is irrelevant when at low taxonomic levels a clear genetic structure is absent due to intensive breeding activities

The Mitotic Arrest Deficient Protein MAD2B Interacts with the Clathrin Light Chain A during Mitosis

Contains fulltext : 87811.pdf (publisher's version ) (Open Access)BACKGROUND: Although the mitotic arrest deficient protein MAD2B (MAD2L2) is thought to inhibit the anaphase promoting complex (APC) by binding to CDC20 and/or CDH1 (FZR1), its exact role in cell cycle control still remains to be established. METHODOLOGY/PRINCIPAL FINDINGS: Using a yeast two-hybrid interaction trap we identified the human clathrin light chain A (CLTA) as a novel MAD2B binding protein. A direct interaction was established in mammalian cells via GST pull-down and endogenous co-immunoprecipitation during the G2/M phase of the cell cycle. Through subsequent confocal laser scanning microscopy we found that MAD2B and CLTA co-localize at the mitotic spindle. Clathrin forms a trimeric structure, i.e., the clathrin triskelion, consisting of three heavy chains (CLTC), each with an associated light chain. This clathrin structure has previously been shown to be required for the function of the mitotic spindle through stabilization of kinetochore fibers. Upon siRNA-mediated MAD2B depletion, we found that CLTA was no longer concentrated at the mitotic spindle but, instead, diffusely distributed throughout the cell. In addition, we found a marked increase in the percentage of misaligned chromosomes. CONCLUSIONS/SIGNIFICANCE: Previously, we identified MAD2B as an interactor of the renal cell carcinoma (RCC)-associated protein PRCC. In addition, we found that fusion of PRCC with the transcription factor TFE3 in t(X;1)(p11;q21)-positive RCCs results in an impairment of this interaction and a concomitant failure to shuttle MAD2B to the nucleus. Our current data show that MAD2B interacts with CLTA during the G2/M phase of the cell cycle and that depletion of MAD2B leads to a marked increase in the percentage of misaligned chromosomes and a redistribution of CLTA during mitosis

A novel approach to locate Phytophthora infestans resistance genes on the potato genetic map

Mapping resistance genes is usually accomplished by phenotyping a segregating population for the resistance trait and genotyping it using a large number of markers. Most resistance genes are of the NBS-LRR type, of which an increasing number is sequenced. These genes and their analogs (RGAs) are often organized in clusters. Clusters tend to be rather homogenous, viz. containing genes that show high sequence similarity with each other. From many of these clusters the map position is known. In this study we present and test a novel method to quickly identify to which cluster a new resistance gene belongs and to produce markers that can be used for introgression breeding. We used NBS profiling to identify markers in bulked DNA samples prepared from resistant and susceptible genotypes of small segregating populations. Markers co-segregating with resistance can be tested on individual plants and directly used for breeding. To identify the resistance gene cluster a gene belongs to, the fragments were sequenced and the sequences analyzed using bioinformatics tools. Putative map positions arising from this analysis were validated using markers mapped in the segregating population. The versatility of the approach is demonstrated with a number of populations derived from wild Solanum species segregating for P. infestans resistance. Newly identified P. infestans resistance genes originating from S. verrucosum, S. schenckii, and S. capsicibaccatum could be mapped to potato chromosomes 6, 4, and 11, respectively