57 research outputs found

    Katalog pameran warisan budaya bersama

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    WaIaupun Bataviasche Genootschap Van Kunsten en Wetenschappen jauh lebih tua dari pada Rijksmuseum voor volkenkude, kedua lembaga itu mempunyai banyak persamaan. ilmu pengetahuan oleh kedua lembaga senan tiasa dianggap yang terpenting dan sepanjang abad ke-19 berkembang hal yang sama daIam kebijaksanaan pengumpulan koleksi. Sejak 1862 secara resmi telah disepakati pembagian koleksi untuk Batavia maupun Leiden, tetapi sebelum itupun secara teratur telah terjadi pembagian antara kedua museum. Titik tolak dari proyek kerjasama Warisan Budaya Bersama indonesia-Belanda antara Museum Nasional di Jakarta dan Rijksmuseum voor volkenkunde di Leiden, adalah ungkapan dalam Notu lenrapat dari Bataviaasche Genootschap dari tahun 1863

    A minimalistic cyclic ice-binding peptide from phage display

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    Developing molecules that emulate the properties of naturally occurring ice-binding proteins (IBPs) is a daunting challenge. Rather than relying on the (limited) existing structure–property relationships that have been established for IBPs, here we report the use of phage display for the identification of short peptide mimics of IBPs. To this end, an ice-affinity selection protocol is developed, which enables the selection of a cyclic ice-binding peptide containing just 14 amino acids. Mutational analysis identifies three residues, Asp8, Thr10 and Thr14, which are found to be essential for ice binding. Molecular dynamics simulations reveal that the side chain of Thr10 hydrophobically binds to ice revealing a potential mechanism. To demonstrate the biotechnological potential of this peptide, it is expressed as a fusion (‘Ice-Tag’) with mCherry and used to purify proteins directly from cell lysate

    High-density genetic mapping identifies new susceptibility loci for rheumatoid arthritis.

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    Using the Immunochip custom SNP array, which was designed for dense genotyping of 186 loci identified through genome-wide association studies (GWAS), we analyzed 11,475 individuals with rheumatoid arthritis (cases) of European ancestry and 15,870 controls for 129,464 markers. We combined these data in a meta-analysis with GWAS data from additional independent cases (n = 2,363) and controls (n = 17,872). We identified 14 new susceptibility loci, 9 of which were associated with rheumatoid arthritis overall and five of which were specifically associated with disease that was positive for anticitrullinated peptide antibodies, bringing the number of confirmed rheumatoid arthritis risk loci in individuals of European ancestry to 46. We refined the peak of association to a single gene for 19 loci, identified secondary independent effects at 6 loci and identified association to low-frequency variants at 4 loci. Bioinformatic analyses generated strong hypotheses for the causal SNP at seven loci. This study illustrates the advantages of dense SNP mapping analysis to inform subsequent functional investigations

    Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

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    The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

    Kolders

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    Quantitative retrieval of Soil Organic Carbon using laboratory spectroscopy and spectral indices

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    Soil Organic Carbon (SOC) has been identified as one of the major C sinks in the global carbon cycle, of which the exact size and spatial distribution are still difficult to determine quantitatively. Estimation of the amount of SOC present using remote sensing is mostly based on the overall decrease in reflectance in the solar reflective part of the electromagnetic spectrum. However, moisture content and soil roughness result in a comparable decrease, resulting in ambiguous identification of a specific soil type. Depending on the decomposition stage, SOC contains biochemical constituents like lignin and cellulose. Absorption features related to these constituents can be used to determine the SOC content of the soil. We investigated nine different soil types (n=40), originating from a wide range of climatic zones and a large variety in SOC content (0.06 – 45.1%). Spectral measurements of all soil samples were performed in a controlled laboratory environment. The ability of several spectral indices related to biochemical constituents’ detection towards the quantification of SOC were tested. Good relations were found for indices based on the visible part of the spectrum and for the absorption features related to cellulose. Cross validation was used to evaluate the predictive capacity of the spectral indices. The results demonstrate that it is feasible to use spectral indices derived from laboratory measurements to predict SOC in various soil types. The results allow establishing a perspective towards spatial distributed mapping of SOC using imaging spectroscopy

    Acquisitions: History and Print Room

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