25 results on '"Winden K"'
Search Results
2. Rechtsfragen der täglichen Bankpraxis
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Winden, K., Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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3. Bankrecht
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Felkau, Werner, primary, Nielsen, Jens, additional, Kohler, Klaus, additional, Heinsius, Theodor, additional, Delorme, H., additional, Lehmann, K. H., additional, Schmid, Erich K., additional, Winden, K., additional, Bohn, H., additional, and Weimar, Wilhelm, additional
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- 1975
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4. To localise or to be localised with Wifi in the Hubei museum?
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Verbree, E. (author), Zlatanova, S. (author), Van Winden, K. (author), Van der Laan, E.B. (author), Makri, A. (author), Taizhou, L. (author), Haojun, A. (author), Verbree, E. (author), Zlatanova, S. (author), Van Winden, K. (author), Van der Laan, E.B. (author), Makri, A. (author), Taizhou, L. (author), and Haojun, A. (author)
- Abstract
Indoor localisation is in demand for a variety of applications within the built environment. An overall solution based on a single technology has not yet been determined. The aim of this paper is to gain insight on Signal Strength monitoring by a special kind of WiFi Monitors in comparison to the commonly known fingerprinting method for the purpose of a 3D indoor navigation system. Ttwo different WiFi based localisation techniques are tested during the MSc Geomatics DaRen Syntheses Project in the Hubei Provincial Museum, China. The first method detects the beacon frames send by smartphones, laptops and other WiFi enabled devices in range using Libelium Meshlium Xtreme monitors. Their MAC addresses and the signal strength is measured by the Meshlium Xtreme and stored on an external database. We call this method WiFi monitoring. The second method a Wifi enabled device, like a smartphone, measures the signal strength of multiple Wifi Access Points in range to localise itself based on a previously created radio map. This method is known as WiFi fingerprinting. Both methods have some advantages and disadvantages. Advantages of the common way of WiFi fingerprinting are that the implementation costs are relatively low, because it is usually possible to use (a part of) the existing WiFi AP infrastructure. WiFi fingerprinting can reach a relatively high accuracy in the order of magnitude of meters. Finally, the location granularity can be adjusted to what is necessary for the purpose of the indoor localisation. This makes it employable for a wide range of purposes. The question remains how suitable these methods are for a 3D indoor navigation system for the Hubei provincial museum. One important aspect is the localisation-granularity necessary for the application. In a museum it is not necessary to know the exact X,Y position of a user (such high accuracy is unnecessary), more important is to know in which room the user is located so the information on exhibitions can be pre, OTB Research, OTB Research Institute for the Built Environment
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- 2013
5. Automatically Constructing the Third Dimension of IMGeo
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Winden, K. van, Kreveld, M.J. van (Thesis Advisor), Winden, K. van, and Kreveld, M.J. van (Thesis Advisor)
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The past year a new Dutch standard for the registration of large scale topography was released, called IMGeo 2.0. This standard includes descriptions and attributes for the majority of objects seen in public spaces. A possible extension to IMGeo 2.0 allows all objects to be modelled in 3D, based on object descriptions and techniques from the CityGML standard. This thesis explores the feasibility of automatically constructing such 3D models by combining 2D geometries and 3D height information. Numerous methods for this type of construction already exist, differing in objects reconstructed, amount of detail, restrictions on construction approach, assumptions on input data and requirements on output data. The approaches created in this thesis aim to construct 3D models in a robust way, accepting sub-optimal results as long as they are a decent and valid representation of reality. Four different construction methods were designed. The first builds large 2.5D terrain models based on point triangulation. These 2.5D surface models form the basis of the actual 3D models. The second and third method construct horizontal roof 3D block models of buildings, with one approach dividing the roof based on point clusters and the other using repeated square subdivisions. The last and most complex method tries to construct 3D building models with full roof shapes using plane and line detection techniques. Degrees of success vary across these methods, with lower success rates the more complex the models become. The constructed terrain model has a number of improvements over a standard triangulation, but terrain generalization is really a field of its own and a lot more improvement can be accomplished. The methods for block models proved to be robust and performed quite well, but can be improved with respect to roof border accuracy. The method that constructs full roof shapes is not robust enough yet, but shows promising possibilities. Overall some creative ways to automatically constru
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- 2012
6. To localise or to be localised with WiFi in the Hubei museum?
- Author
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Verbree, E., primary, Zlatanova, S., additional, van Winden, K. B. A., additional, van der Laan, E. B., additional, Makri, A., additional, Taizhou, L., additional, and Haojun, A., additional
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- 2013
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7. CCDC22: a novel candidate gene for syndromic X-linked intellectual disability
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Voineagu, I, primary, Huang, L, additional, Winden, K, additional, Lazaro, M, additional, Haan, E, additional, Nelson, J, additional, McGaughran, J, additional, Nguyen, L S, additional, Friend, K, additional, Hackett, A, additional, Field, M, additional, Gecz, J, additional, and Geschwind, D, additional
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- 2011
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8. Arbeitsrecht
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Bohn, H., Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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9. Börsenrecht
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Lehmann, K. H., Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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10. Verfahrens- und Insolvenzrecht
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Schmid, Erich K., Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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11. Recht der Wertpapiere
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Delorme, H., Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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12. Grundzüge des Handelsrechts
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Nielsen, Jens, Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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13. Kreditsicherungsrecht
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Heinsius, Theodor, Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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14. Der Bankvertrag
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Kohler, Klaus, Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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15. Praktische Rechtsfälle
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Weimar, Wilhelm, Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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16. Grundzüge des bürgerlichen Rechts
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Felkau, Werner, Felkau, Werner, Nielsen, Jens, Kohler, Klaus, Heinsius, Theodor, Delorme, H., Lehmann, K. H., Schmid, Erich K., Winden, K., Bohn, H., and Weimar, Wilhelm
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- 1975
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17. High-content screening identifies a small molecule that restores AP-4-dependent protein trafficking in neuronal models of AP-4-associated hereditary spastic paraplegia.
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Saffari A, Brechmann B, Böger C, Saber WA, Jumo H, Whye D, Wood D, Wahlster L, Alecu JE, Ziegler M, Scheffold M, Winden K, Hubbs J, Buttermore ED, Barrett L, Borner GHH, Davies AK, Ebrahimi-Fakhari D, and Sahin M
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- Humans, Proteomics, Neurons metabolism, Protein Transport, Proteins metabolism, Mutation, Spastic Paraplegia, Hereditary drug therapy, Spastic Paraplegia, Hereditary genetics, Spastic Paraplegia, Hereditary metabolism
- Abstract
Unbiased phenotypic screens in patient-relevant disease models offer the potential to detect therapeutic targets for rare diseases. In this study, we developed a high-throughput screening assay to identify molecules that correct aberrant protein trafficking in adapter protein complex 4 (AP-4) deficiency, a rare but prototypical form of childhood-onset hereditary spastic paraplegia characterized by mislocalization of the autophagy protein ATG9A. Using high-content microscopy and an automated image analysis pipeline, we screened a diversity library of 28,864 small molecules and identified a lead compound, BCH-HSP-C01, that restored ATG9A pathology in multiple disease models, including patient-derived fibroblasts and induced pluripotent stem cell-derived neurons. We used multiparametric orthogonal strategies and integrated transcriptomic and proteomic approaches to delineate potential mechanisms of action of BCH-HSP-C01. Our results define molecular regulators of intracellular ATG9A trafficking and characterize a lead compound for the treatment of AP-4 deficiency, providing important proof-of-concept data for future studies., (© 2024. The Author(s).)
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- 2024
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18. High-Content Small Molecule Screen Identifies a Novel Compound That Restores AP-4-Dependent Protein Trafficking in Neuronal Models of AP-4-Associated Hereditary Spastic Paraplegia.
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Saffari A, Brechmann B, Boeger C, Saber WA, Jumo H, Whye D, Wood D, Wahlster L, Alecu J, Ziegler M, Scheffold M, Winden K, Hubbs J, Buttermore E, Barrett L, Borner G, Davies A, Sahin M, and Ebrahimi-Fakhari D
- Abstract
Unbiased phenotypic screens in patient-relevant disease models offer the potential to detect novel therapeutic targets for rare diseases. In this study, we developed a high-throughput screening assay to identify molecules that correct aberrant protein trafficking in adaptor protein complex 4 (AP-4) deficiency, a rare but prototypical form of childhood-onset hereditary spastic paraplegia, characterized by mislocalization of the autophagy protein ATG9A. Using high-content microscopy and an automated image analysis pipeline, we screened a diversity library of 28,864 small molecules and identified a lead compound, C - 01 , that restored ATG9A pathology in multiple disease models, including patient-derived fibroblasts and induced pluripotent stem cell-derived neurons. We used multiparametric orthogonal strategies and integrated transcriptomic and proteomic approaches to delineate putative molecular targets of C - 01 and potential mechanisms of action. Our results define molecular regulators of intracellular ATG9A trafficking and characterize a lead compound for the treatment of AP-4 deficiency, providing important proof-of-concept data for future Investigational New Drug (IND)-enabling studies., Competing Interests: COMPETING INTERESTS This work was supported by a joint research agreement between Boston Children’s Hospital and Mitobridge Inc., now owned by Astellas Pharmaceuticals Inc.. D.E.F. has served as a consultant to Health Advances LLC, has received speaker honoraria from the Movement Disorders Society, and publishing royalties from Cambridge University Press. M.S. reports grant support from Novartis, Biogen, Astellas, Aeovian, Bridgebio, and Aucta unrelated to this project. He has served on Scientific Advisory Boards for Novartis, Roche, Regenxbio, SpringWorks Therapeutics, Jaguar Therapeutics and Alkermes.
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- 2023
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19. Low maternal vitamin D is associated with increased risk of congenital and peri/postnatal transmission of Cytomegalovirus in women with HIV.
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Bearden A, Van Winden K, Frederick T, Kono N, Operskalski E, Pandian R, Barton L, Stek A, and Kovacs A
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- Adult, Antiviral Agents therapeutic use, CD4 Lymphocyte Count, Cohort Studies, Cytomegalovirus genetics, Cytomegalovirus pathogenicity, Cytomegalovirus Infections immunology, DNA, Viral blood, Female, HIV Infections complications, Humans, Infant, Infant, Newborn, Plasma virology, Pregnancy, Pregnancy Complications, Infectious drug therapy, Retrospective Studies, Viral Load, Vitamin D metabolism, Vitamin D Deficiency physiopathology, Cytomegalovirus Infections transmission, Infectious Disease Transmission, Vertical prevention & control, Vitamin D Deficiency metabolism
- Abstract
Background: CMV infection of the fetus or neonate can lead to devastating disease, and there are no effective prevention strategies to date. Vitamin D is a potent immunomodulator, supports antiviral immune responses, and plays an important role in placental immunity., Methods: Retrospective cohort study to evaluate the impact of low maternal vitamin D on congenital and early postnatal transmission of CMV among HIV-infected, non-breastfeeding women and their HIV exposed but negative infants from an urban HIV clinic. Vitamin D panel was performed on stored maternal plasma obtained near time of delivery. Infant CMV testing at 0-6 months included urine and oral cultures, and/or serum polymerase chain reaction testing., Results: Cohort included 340 mother-infant pairs (births 1991-2014). Among 38 infants (11%) with a CMV+ test between 0-6 months, 4.7% (14/300) had congenital CMV transmission (CMV+ test 0-3 weeks), and 7.6% (24/315) had peri/postnatal CMV (CMV+ test >3 weeks-6 months). Women with lower calcitriol (1,25-dihydroxyvitamin D), the active form of vitamin D, were more likely to have an infant with congenital (OR 12.2 [95% CI 1.61-92.2] P = 0.02) and peri/postnatal (OR 9.84 [95% CI 2.63-36.8] P = 0.0007) infections in multivariate analyses, independent of maternal HIV viral load and CD4 count., Conclusion: This study demonstrates an association between inadequate maternal calcitriol during pregnancy and increased congenital and early postnatal acquisition of CMV among non-breastfeeding women with HIV and their HIV negative infants., Competing Interests: RP is the salaried Director of Pan Laboratories, Irvine, CA. There are no patents, products in development or marketed products to declare. This does not alter our adherence to PLOS ONE policies on sharing data and materials.
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- 2020
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20. Purkinje cells derived from TSC patients display hypoexcitability and synaptic deficits associated with reduced FMRP levels and reversed by rapamycin.
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Sundberg M, Tochitsky I, Buchholz DE, Winden K, Kujala V, Kapur K, Cataltepe D, Turner D, Han MJ, Woolf CJ, Hatten ME, and Sahin M
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- Adult, Autism Spectrum Disorder complications, Autism Spectrum Disorder metabolism, Cerebellar Diseases metabolism, Cerebellum metabolism, Child, Child, Preschool, Female, Fragile X Mental Retardation Protein drug effects, Fragile X Mental Retardation Protein metabolism, Humans, Induced Pluripotent Stem Cells metabolism, Mechanistic Target of Rapamycin Complex 1 genetics, Models, Biological, Purkinje Cells pathology, Sirolimus pharmacology, Synapses metabolism, Synapses physiology, TOR Serine-Threonine Kinases metabolism, Tuberous Sclerosis physiopathology, Tuberous Sclerosis Complex 1 Protein, Tuberous Sclerosis Complex 2 Protein, Tumor Suppressor Proteins genetics, Purkinje Cells metabolism, Tuberous Sclerosis metabolism
- Abstract
Accumulating evidence suggests that cerebellar dysfunction early in life is associated with autism spectrum disorder (ASD), but the molecular mechanisms underlying the cerebellar deficits at the cellular level are unclear. Tuberous sclerosis complex (TSC) is a neurocutaneous disorder that often presents with ASD. Here, we developed a cerebellar Purkinje cell (PC) model of TSC with patient-derived human induced pluripotent stem cells (hiPSCs) to characterize the molecular mechanisms underlying cerebellar abnormalities in ASD and TSC. Our results show that hiPSC-derived PCs from patients with pathogenic TSC2 mutations displayed mTORC1 pathway hyperactivation, defects in neuronal differentiation and RNA regulation, hypoexcitability and reduced synaptic activity when compared with those derived from controls. Our gene expression analyses revealed downregulation of several components of fragile X mental retardation protein (FMRP) targets in TSC2-deficient hiPSC-PCs. We detected decreased expression of FMRP, glutamate receptor δ2 (GRID2), and pre- and post-synaptic markers such as synaptophysin and PSD95 in the TSC2-deficient hiPSC-PCs. The mTOR inhibitor rapamycin rescued the deficits in differentiation, synaptic dysfunction, and hypoexcitability of TSC2 mutant hiPSC-PCs in vitro. Our findings suggest that these gene expression changes and cellular abnormalities contribute to aberrant PC function during development in TSC affected individuals.
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- 2018
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21. Neuronal CTGF/CCN2 negatively regulates myelination in a mouse model of tuberous sclerosis complex.
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Ercan E, Han JM, Di Nardo A, Winden K, Han MJ, Hoyo L, Saffari A, Leask A, Geschwind DH, and Sahin M
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- Animals, Disease Models, Animal, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Oligodendroglia physiology, Rats, TOR Serine-Threonine Kinases physiology, Tuberous Sclerosis Complex 1 Protein, Tuberous Sclerosis Complex 2 Protein, Tumor Suppressor Proteins physiology, Connective Tissue Growth Factor physiology, Myelin Sheath physiology, Neurons physiology, Tuberous Sclerosis physiopathology
- Abstract
Disruption of myelination during development has been implicated in a range of neurodevelopmental disorders including tuberous sclerosis complex (TSC). TSC patients with autism display impairments in white matter integrity. Similarly, mice lacking neuronal Tsc1 have a hypomyelination phenotype. However, the mechanisms that underlie these phenotypes remain unknown. In this study, we demonstrate that neuronal TSC1/2 orchestrates a program of oligodendrocyte maturation through the regulated secretion of connective tissue growth factor (CTGF). We characterize oligodendrocyte maturation both in vitro and in vivo. We find that neuron-specific Tsc1 deletion results in an increase in CTGF secretion that non-cell autonomously stunts oligodendrocyte development and decreases the total number of oligodendrocytes. Genetic deletion of CTGF from neurons, in turn, mitigates the TSC-dependent hypomyelination phenotype. These results show that the mechanistic target of rapamycin (mTOR) pathway in neurons regulates CTGF production and secretion, revealing a paracrine mechanism by which neuronal signaling regulates oligodendrocyte maturation and myelination in TSC. This study highlights the role of mTOR-dependent signaling between neuronal and nonneuronal cells in the regulation of myelin and identifies an additional therapeutic avenue for this disease., (© 2017 Ercan et al.)
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- 2017
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22. Cell-type-specific miR-431 dysregulation in a motor neuron model of spinal muscular atrophy.
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Wertz MH, Winden K, Neveu P, Ng SY, Ercan E, and Sahin M
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- Animals, Disease Models, Animal, Gene Expression Regulation, High-Throughput Nucleotide Sequencing, Humans, Mice, Mice, Knockout, MicroRNAs biosynthesis, Microarray Analysis, Motor Neurons metabolism, Motor Neurons pathology, Muscular Atrophy, Spinal physiopathology, Neurites metabolism, Neurites pathology, MicroRNAs genetics, Muscular Atrophy, Spinal genetics, Survival of Motor Neuron 1 Protein genetics
- Abstract
Spinal muscular atrophy (SMA) is an autosomal-recessive pediatric neurodegenerative disease characterized by selective loss of spinal motor neurons. It is caused by mutation in the survival of motor neuron 1, SMN1, gene and leads to loss of function of the full-length SMN protein. microRNAs (miRNAs) are small RNAs that are involved in post-transcriptional regulation of gene expression. Prior studies have implicated miRNAs in the pathogenesis of motor neuron disease. We hypothesized that motor neuron-specific miRNA expression changes are involved in their selective vulnerability in SMA. Therefore, we sought to determine the effect of SMN loss on miRNAs and their target mRNAs in spinal motor neurons. We used microarray and RNAseq to profile both miRNA and mRNA expression in primary spinal motor neuron cultures after acute SMN knockdown. By integrating the miRNA:mRNA profiles, a number of dysregulated miRNAs were identified with enrichment in differentially expressed putative mRNA targets. miR-431 expression was highly increased, and a number of its putative mRNA targets were significantly downregulated in motor neurons after SMN loss. Further, we found that miR-431 regulates motor neuron neurite length by targeting several molecules previously identified to play a role in motor neuron axon outgrowth, including chondrolectin. Together, our findings indicate that cell-type-specific dysregulation of miR-431 plays a role in the SMA motor neuron phenotype., (© The Author 2016. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
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- 2016
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23. Human-specific transcriptional networks in the brain.
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Konopka G, Friedrich T, Davis-Turak J, Winden K, Oldham MC, Gao F, Chen L, Wang GZ, Luo R, Preuss TM, and Geschwind DH
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- Animals, CLOCK Proteins genetics, CLOCK Proteins metabolism, Evolution, Molecular, Forkhead Transcription Factors genetics, Forkhead Transcription Factors metabolism, Gene Expression Profiling, Gene Regulatory Networks genetics, Humans, Macaca, Mental Disorders genetics, Oligonucleotide Array Sequence Analysis, Pan troglodytes, Transcription Factors genetics, Brain anatomy & histology, Brain metabolism, Gene Expression physiology, Transcription Factors metabolism
- Abstract
Understanding human-specific patterns of brain gene expression and regulation can provide key insights into human brain evolution and speciation. Here, we use next-generation sequencing, and Illumina and Affymetrix microarray platforms, to compare the transcriptome of human, chimpanzee, and macaque telencephalon. Our analysis reveals a predominance of genes differentially expressed within human frontal lobe and a striking increase in transcriptional complexity specific to the human lineage in the frontal lobe. In contrast, caudate nucleus gene expression is highly conserved. We also identify gene coexpression signatures related to either neuronal processes or neuropsychiatric diseases, including a human-specific module with CLOCK as its hub gene and another module enriched for neuronal morphological processes and genes coexpressed with FOXP2, a gene important for language evolution. These data demonstrate that transcriptional networks have undergone evolutionary remodeling even within a given brain region, providing a window through which to view the foundation of uniquely human cognitive capacities., (Copyright © 2012 Elsevier Inc. All rights reserved.)
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- 2012
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24. Human-specific transcriptional regulation of CNS development genes by FOXP2.
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Konopka G, Bomar JM, Winden K, Coppola G, Jonsson ZO, Gao F, Peng S, Preuss TM, Wohlschlegel JA, and Geschwind DH
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- Animals, Brain cytology, Cell Line, Evolution, Molecular, Forkhead Transcription Factors chemistry, Forkhead Transcription Factors genetics, Humans, Language, Pan troglodytes embryology, Pan troglodytes genetics, Pan troglodytes metabolism, Promoter Regions, Genetic genetics, Species Specificity, Speech physiology, Transcriptional Activation, Brain embryology, Brain metabolism, Forkhead Transcription Factors metabolism, Gene Expression Regulation, Developmental, Transcription, Genetic
- Abstract
The signalling pathways controlling both the evolution and development of language in the human brain remain unknown. So far, the transcription factor FOXP2 (forkhead box P2) is the only gene implicated in Mendelian forms of human speech and language dysfunction. It has been proposed that the amino acid composition in the human variant of FOXP2 has undergone accelerated evolution, and this two-amino-acid change occurred around the time of language emergence in humans. However, this remains controversial, and whether the acquisition of these amino acids in human FOXP2 has any functional consequence in human neurons remains untested. Here we demonstrate that these two human-specific amino acids alter FOXP2 function by conferring differential transcriptional regulation in vitro. We extend these observations in vivo to human and chimpanzee brain, and use network analysis to identify novel relationships among the differentially expressed genes. These data provide experimental support for the functional relevance of changes in FOXP2 that occur on the human lineage, highlighting specific pathways with direct consequences for human brain development and disease in the central nervous system (CNS). Because FOXP2 has an important role in speech and language in humans, the identified targets may have a critical function in the development and evolution of language circuitry in humans.
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- 2009
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25. A step-by-step approach to choosing an information system.
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Winden K
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- Decision Making, United States, Catalogs, Commercial as Topic, Management Information Systems, Nursing Homes organization & administration, Software
- Published
- 1990
Catalog
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