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Berlin Brandenburg

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  • 1
    Language: English
    In: Zeitschrift für anorganische und allgemeine Chemie, August 2011, Vol.637(10), pp.1314-1321
    Description: A series of 9 new Reineckate salts, [Cr(NCS)(NH)] with various large organic cations = tetraalkylammonium, [N], = ‐butyl, ‐dodecyl; 1‐alkyl‐3‐methylimidazolium, (MIm): = methyl, ethyl, propyl, ‐butyl, and ‐hexyl; = 1,3‐dimethyl‐2,4,5‐triphenylimidazolium and = 1,2,3,4,5‐pentamethylimidazolium was synthesized. The melting point of each compound was measured to see if any belongs to the group of metal‐containing Ionic Liquids with low melting points. Each compound was further characterized by elemental analysis, NMR, IR, and UV/Vis spectroscopy. From NMR investigations information about the magnetic behavior was derivedusing the method. It has been found that every compound is paramagnetic with effective magnetic moments of spin‐only Cr. The structures of the Reineckates with = tetra‐‐butyl‐ammonium, tetra‐‐dodecyl‐ammonium, 1‐ethyl‐3‐methylimidazolium, and 1,2,3,4,5‐pentamethylimidazolium were determined by single‐crystal X‐ray diffraction measurements: (BuN)[Cr(NCS)(NH)]: monoclinic, 2/ (no. 15), = 12.0818(8), = 10.2425(8), = 24.222(2) Å, = 98.324(3)°, = 4, 1()/2() = 0.0332/0.0871; {(CH)N}[Cr(NCS)(NH)]·0.85HO: triclinic, (no. 2), = 8.4049(1), = 20.1525(4), = 20.7908(4) Å, = 67.487(1)°, = 81.328(1)°, = 78.040(1)°, = 2, 1()/2() = 0.0533/0.1343; (EMIm)[Cr(NCS)(NH)]: orthorhombic, (no. 57), = 8.765(2), = 15.888(3), = 14.191(3) Å, = 4, 1()/2() = 0.0466/0.1271; (PeMIm)[Cr(NCS)(NH)]: monoclinic, 2/ (no. 14), = 6.0817(2), =13.9811(5), = 25.2902(9) Å, = 90.075(2)°, = 4, 1()/2() = 0.0405/0.1111.
    Keywords: Chromium ; Crystal Structure ; Reinecke’s Salt ; Imidazolium
    ISSN: 0044-2313
    E-ISSN: 1521-3749
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  • 2
    Language: English
    In: Cancer Research, 07/01/2018, Vol.78(13 Supplement), pp.3172-3172
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 3
    In: Physical Chemistry Chemical Physics, 2014, Vol.16(7), pp.2971-2980
    Description: The determination of vaporization enthalpies of extremely low volatility ionic liquids is challenging and time consuming due to the low values of vapor pressure. In addition, these liquids tend to decompose even at temperatures where the vapor pressure is still low. Conventional methods for determination of vaporization enthalpies are thus limited to temperatures below the decomposition temperature. Here we present a new method for the determination of vaporization enthalpies of such liquids using differential fast scanning calorimetry. We have developed and proven this method using [EMIm][NTf 2 ] at temperatures of up to 750 K and in different atmospheres. It was demonstrated that evaporation is still the dominating process of mass loss even at such highly elevated temperatures. In addition, since the method allows very high heating rates (up to 10 5 K s 1 ), much higher temperatures can be reached in the measurement of the mass loss rate as compared to common devices without significant decomposition of the ionic liquid. We discuss the advantages and limits of this new method of vaporization enthalpy determination and compare the results with data obtained from established methods.
    Keywords: Calorimetry ; Miscellaneous Sciences (So);
    ISSN: 1463-9076
    E-ISSN: 1463-9084
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  • 4
    Language: English
    In: Child's Nervous System, 2012, Vol.28(4), pp.521-532
    Description: Byline: Jasmine Lau (1,2,3,4), Christin Schmidt (1,2,3,4), Shirley L. Markant (5,6), Michael D. Taylor (7,8), Robert J. Wechsler-Reya (5,6), William A. Weiss (1,2,3,4) Keywords: Medulloblastoma; Mouse models; Molecular subgroups; Targeted therapies; Preclinical testing Abstract: Introduction Medulloblastoma, the largest group of embryonal brain tumors, has historically been classified into five variants based on histopathology. More recently, epigenetic and transcriptional analyses of primary tumors have subclassified medulloblastoma into four to six subgroups, most of which are incongruous with histopathological classification. Discussion Improved stratification is required for prognosis and development of targeted treatment strategies, to maximize cure and minimize adverse effects. Several mouse models of medulloblastoma have contributed both to an improved understanding of progression and to developmental therapeutics. In this review, we summarize the classification of human medulloblastoma subtypes based on histopathology and molecular features. We describe existing genetically engineered mouse models, compare these to human disease, and discuss the utility of mouse models for developmental therapeutics. Just as accurate knowledge of the correct molecular subtype of medulloblastoma is critical to the development of targeted therapy in patients, we propose that accurate modeling of each subtype of medulloblastoma in mice will be necessary for preclinical evaluation and optimization of those targeted therapies. Author Affiliation: (1) Department of Neurology, University of California, San Francisco, CA, USA (2) Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA (3) Department of Neurological Surgery and Brain Tumor Research Center, University of California, San Francisco, CA, USA (4) Department of Pediatrics, University of California, San Francisco, CA, USA (5) Tumor Development Program, Sanford-Burnham Medical Research Institute, La Jolla, CA, USA (6) Department of Pharmacology & Cancer Biology, Duke University Medical Center, Durham, NC, USA (7) Division of Neurosurgery, Hospital for Sick Children, University of Toronto, Toronto, ON, Canada (8) Arthur and Sonia Labatt Brain Tumour Research Centre, Program in Developmental and Stem Cell Biology, Hospital for Sick Children, University of Toronto, Toronto, ON, Canada Article History: Registration Date: 18/01/2012 Received Date: 28/12/2011 Accepted Date: 17/01/2012 Online Date: 08/02/2012
    Keywords: Medulloblastoma ; Mouse models ; Molecular subgroups ; Targeted therapies ; Preclinical testing
    ISSN: 0256-7040
    E-ISSN: 1433-0350
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  • 5
  • 6
    In: Neuro-Oncology, 2016, Vol. 18(suppl3), pp.iii143-iii143
    Keywords: Medicine;
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 7
    Language: English
    In: The Journal of neuroscience : the official journal of the Society for Neuroscience, 01 October 2014, Vol.34(40), pp.13486-91
    Description: SMARCA4 (BRG1) and SMARCB1 (INI1) are tumor suppressor genes that are crucially involved in the formation of malignant rhabdoid tumors, such as atypical teratoid/rhabdoid tumor (AT/RT). AT/RTs typically affect infants and occur at various sites of the CNS with a particular frequency in the cerebellum. Here, granule neurons and their progenitors represent the most abundant cell type and are known to give rise to a subset of medulloblastoma, a histologically similar embryonal brain tumor. To test how Smarc proteins influence the development of granule neurons and whether this population may serve as cellular origin for AT/RTs, we specifically deleted Smarca4 and Smarcb1 in cerebellar granule cell precursors. Respective mutant mice displayed severe ataxia and motor coordination deficits, but did not develop any tumors. In fact, they suffered from a severely hypoplastic cerebellum due to a significant inhibition of granule neuron precursor proliferation. Molecularly, this was accompanied by an enhanced activity of Wnt/β-catenin signaling that, by itself, is known to cause a nearly identical phenotype. We further used an hGFAP-cre allele, which deleted Smarcb1 much earlier and in a wider neural precursor population, but we still did not detect any tumor formation in the CNS. In summary, our results emphasize cell-type-dependent roles of Smarc proteins and argue against cerebellar granule cells and other progeny of hGFAP-positive neural precursors as the cellular origin for AT/RTs.
    Keywords: At/Rt ; Smarc ; Brain ; Cerebellum ; Development ; Tumor ; Cerebellum -- Growth & Development ; Chromosomal Proteins, Non-Histone -- Deficiency ; DNA Helicases -- Deficiency ; Gene Expression Regulation, Developmental -- Genetics ; Nuclear Proteins -- Deficiency ; Transcription Factors -- Deficiency
    ISSN: 02706474
    E-ISSN: 1529-2401
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  • 8
    In: Neuro-Oncology, 2018, Vol. 20(suppl2), pp.i70-i70
    Description: Embryonal Tumors with Multilayered Rosettes (ETMRs) are aggressive pediatric brain tumors mainly occurring in infants. In order to develop alternative treatment strategies for this deadly disease there is an urgent need for better understanding the mechanisms driving these tumors. We therefore analyzed a cohort of 60 ETMRs using whole genome and panel sequencing, DNA methylation, mRNA expression profiling, and miRNA sequencing. The genetic hallmark of ETMRs is amplification of miRNA cluster C19MC fused to TTYH1 present in ~90% of all ETMRs. ETMRs lacking the C19MC amplification are biologically highly similar to tumors with C19MC amplification, indicating that they do not represent a distinct subgroup. DNA sequencing revealed germline mutations affecting DNA repair genes or miRNA processing genes in a subset of cases, while tumor specific mutations included genes involved in the TP53-, SHH- WNT-, or miRNA processing pathways. Prevalence of mutations in miRNA processing pathways are specifically high in tumors without C19MC amplification, however overall recurrence of mutations is low within our cohort. We also detect high recurrence of genomic instability shown by pluriploidy, large abundance of CNVs, highly upregulated DNA repair pathways and chromothripsis primarily centered around the C19MC amplicon. Structural variations throughout the genome, including the C19MC amplicon, are highly conserved from primary tumor to relapse while other mutations show low conservation. These results suggest ETMR is an entity driven by structural variations rather than single nucleotide variants and could lead to new treatment options, specifically targeting genomic instability, to be tested in preclinical model systems of ETMR.
    Keywords: Medicine;
    ISSN: 1522-8517
    E-ISSN: 1523-5866
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  • 9
    Language: English
    In: Psychopharmacology, 2014, Vol.231(19), pp.3879-3888
    Description: Rationale It has been proposed that green tea extract may have a beneficial impact on cognitive functioning, suggesting promising clinical implications. However, the neural mechanisms underlying this putative cognitive enhancing effect of green tea extract still remain unknown. Objectives This study investigates whether the intake of green tea extract modulates effective brain connectivity during working memory processing and whether connectivity parameters are related to task performance. Material and methods Using a double-blind, counterbalanced, within-subject design, 12 healthy volunteers received a milk whey-based soft drink containing 27.5 g of green tea extract or a milk whey-based soft drink without green tea as control substance while undergoing functional magnetic resonance imaging. Working memory effect on effective connectivity between frontal and parietal brain regions was evaluated using dynamic causal modeling. Results Green tea extract increased the working memory induced modulation of connectivity from the right superior parietal lobule to the middle frontal gyrus. Notably, the magnitude of green tea induced increase in parieto-frontal connectivity positively correlated with improvement in task performance. Conclusions Our findings provide first evidence for the putative beneficial effect of green tea on cognitive functioning, in particular, on working memory processing at the neural system level by suggesting changes in short-term plasticity of parieto-frontal brain connections. Modeling effective connectivity among frontal and parietal brain regions during working memory processing might help to assess the efficacy of green tea for the treatment of cognitive impairments in psychiatric disorders such as dementia. Keywords Cognition * Working memory * Green tea extract * Brain activity * Effective connectivity * Dynamic causal modeling
    Keywords: Cognition ; Working memory ; Green tea extract ; Brain activity ; Effective connectivity ; Dynamic causal modeling
    ISSN: 0033-3158
    E-ISSN: 1432-2072
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  • 10
    Language: English
    In: Psychopharmacology, 2014, Vol.231(19), pp.3939-3939
    Keywords: Biomedicine ; Neurosciences ; Pharmacology/Toxicology ; Psychiatry ; Medicine ; Pharmacy, Therapeutics, & Pharmacology;
    ISSN: 0033-3158
    E-ISSN: 1432-2072
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