Academic literature on the topic 'Niemann Pick Type C'

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Journal articles on the topic "Niemann Pick Type C"

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Patterson, M. C., and P. G. Pentchev. "Niemann-Pick; Type C." Neurology 46, no. 6 (June 1, 1996): 1785–86. http://dx.doi.org/10.1212/wnl.46.6.1785-b.

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Millichap, J. Gordon. "Niemann-Pick Disease Type C." Pediatric Neurology Briefs 3, no. 9 (September 1, 1989): 68. http://dx.doi.org/10.15844/pedneurbriefs-3-9-7.

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Cobcroft, Ralph. "Type C Niemann-Pick disease." British Journal of Haematology 111, no. 3 (December 2000): 718. http://dx.doi.org/10.1046/j.1365-2141.2000.02536.x.

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Tarugi, Patrizia, Giorgia Ballarini, Bruno Bembi, Carla Battisti, Silvia Palmeri, Francesca Panzani, Enza Di Leo, Cristina Martini, Antonio Federico, and Sebastiano Calandra. "Niemann-Pick type C disease." Journal of Lipid Research 43, no. 11 (August 16, 2002): 1908–19. http://dx.doi.org/10.1194/jlr.m200203-jlr200.

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Cobcroft, Ralph. "Type C Niemann-Pick disease." British Journal of Haematology 111, no. 3 (December 2000): 718. http://dx.doi.org/10.1111/j.1365-2141.2000.02536.x.

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Yu, Daozhan, Manju Swaroop, Mengqiao Wang, Ulrich Baxa, Rongze Yang, Yiping Yan, Turhan Coksaygan, et al. "Niemann–Pick Disease Type C." Journal of Biomolecular Screening 19, no. 8 (June 6, 2014): 1164–73. http://dx.doi.org/10.1177/1087057114537378.

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Niemann–Pick disease type C (NPC) is a rare neurodegenerative disorder caused by recessive mutations in the NPC1 or NPC2 gene that result in lysosomal accumulation of unesterified cholesterol in patient cells. Patient fibroblasts have been used for evaluation of compound efficacy, although neuronal degeneration is the hallmark of NPC disease. Here, we report the application of human NPC1 neural stem cells as a cell-based disease model to evaluate nine compounds that have been reported to be efficacious in the NPC1 fibroblasts and mouse models. These cells are differentiated from NPC1 induced pluripotent stem cells and exhibit a phenotype of lysosomal cholesterol accumulation. Treatment of these cells with hydroxypropyl-β-cyclodextrin, methyl-β-cyclodextrin, and δ-tocopherol significantly ameliorated the lysosomal cholesterol accumulation. Combined treatment with cyclodextrin and δ-tocopherol shows an additive or synergistic effect that otherwise requires 10-fold higher concentration of cyclodextrin alone. In addition, we found that hydroxypropyl-β-cyclodextrin is much more potent and efficacious in the NPC1 neural stem cells compared to the NPC1 fibroblasts. Miglustat, suberoylanilide hydroxamic acid, curcumin, lovastatin, pravastatin, and rapamycin did not, however, have significant effects in these cells. The results demonstrate that patient-derived NPC1 neural stem cells can be used as a model system for evaluation of drug efficacy and study of disease pathogenesis.
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Elleder, M., A. Jirásek, F. Šmíd, J. Ledvinová, and G. T. N. Besley. "Niemann-Pick disease type C." Acta Neuropathologica 66, no. 4 (December 1985): 325–36. http://dx.doi.org/10.1007/bf00690966.

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Vanier, MT, and G. Millat. "Niemann-Pick disease type C." Clinical Genetics 64, no. 4 (September 15, 2003): 269–81. http://dx.doi.org/10.1034/j.1399-0004.2003.00147.x.

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Liscum, Laura, and Judeth J. Klansek. "Niemann–Pick disease type C." Current Opinion in Lipidology 9, no. 2 (April 1998): 131–35. http://dx.doi.org/10.1097/00041433-199804000-00009.

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Tohyama, Jun, Mitsuhiro Kato, Tatsuya Koeda, and Kousaku Ohno. "Type C Niemann-Pick disease." Brain and Development 15, no. 4 (July 1993): 316–17. http://dx.doi.org/10.1016/0387-7604(93)90033-5.

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Dissertations / Theses on the topic "Niemann Pick Type C"

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Lloyd-Evans, Emyr. "Cell biology of Niemann-Pick type C disease." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437185.

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Colaço, Alexandria Nicole. "Niemann-Pick Type C disease : pathogenesis and therapy." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:d75bf036-acc9-4c6f-89ad-7708d2996937.

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Niemann-Pick disease Type C is a rare, lysosomal storage disorder caused by defects in either NPC1 (95% of cases) or NPC2, and characterized by progressive neurodegeneration that ultimately results in premature death. The function of the NPC1 protein still remains poorly understood and how the NPC1 or NPC2 proteins interact, or the functions of the pathways they regulate still remains unknown. We have found unexpected links between NPC and other human diseases - particularly Tangier disease, suggesting that the NPC cellular pathway is more broadly involved in human disease than previously suggested. To gain further insight into the function of NPC1 and proteins it interacts with we used the yeast orthologue, Ncr1p. I recreated the ?ncr1 mutant and characterized the mutant using an array of systematic screens to identify different processes and pathways that may play a role in NPC pathogenesis. The screen implicated mitochondrial dysfunction, defects in metal ion homeostasis and lipid trafficking, cytoskeleton dysfunction and nutrient sensing deficiencies. These screens were validated in the Npc1-/- mouse model, where the effects of modulating kinases also emerged as a potential therapeutic option. In addition to kinases, we examined the therapeutic potential of the FDA-approved hypertension drug, losartan. Losartan ameliorated the acidic store Ca2+ defect, which characterizes NPC, and all downstream pathologies as well as in combination with miglustat reduced levels of neuroinflammation in the mouse model. Furthermore, the cyclodextrin analogue Crysmeb was also examined as a novel therapy for NPC, and was found to have significant survival benefits as compared to HPβCD, the cyclodextrin compound currently in clinical trials. Taken together, in this thesis I have identified novel aspects of NPC pathogenesis, as well as mechanistic links between NPC and Tangier disease - which has led to miglustat treatment options for two patients at Addenbrooke's Hostpital, Cambridge. Additionally, taking advantage of the convergent disease mechanisms I have examined treatments (losartan/Crysmeb) that take advantage of the similarities and differences between these two disorders paving the way for potential clinical studies in the future.
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Al, Eisa Nada. "Evaluation of new therapies in Niemann-Pick type C disease." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:1538a0d6-b08e-444c-900d-de3ea3834ca5.

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Blom, Titta S. "Characterisation of cellular defects in Niemann-Pick type C disease." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/blom/.

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RAQUIN, JANICK. "Maladie de niemann-pick type c forme juvenile : a propos d'un cas." Reims, 1994. http://www.theses.fr/1994REIMM032.

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Aubonnet, Patrick. "Nouvelles approches dans le diagnostic du type C de la maladie de Niemann-Pick : à propos d'un cas clinique." Nice, 1990. http://www.theses.fr/1990NICE6524.

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Fluegel, Megan L. "Establishment of a Drosophila model of Niemann-Pick type C disease /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5065.

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Hughes, Michael. "The development of gene therapy for Niemann-Pick Type C disease." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10040556/.

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Niemann-Pick Type C (NP-C) is a lysosomal storage disorder with neurological and visceral pathology, for which there is currently no major disease modifying treatment. Loss of NPC1 function, a late endosomal transmembrane protein, leads to systemic intracellular lipid accumulation. The subsequent premature death is usually associated with neurological manifestations, such as neurodegeneration and neuroinflammation. This project focuses on the development and preclinical evaluation of gene therapy for NP-C in a mouse model using an adeno-associated viral (AAV) vector. The vector would be capable of delivering and expressing human NPC1 in the mouse brain and providing therapeutic benefit. AAV vectors exhibit efficient and widespread gene delivery throughout the brain, however their limited packaging capacity can be a constraint for larger genes. In this project extensive construct modifications were carried out to incorporate the relatively large NPC1 cDNA into a functional AAV serotype 9 vector, where NPC1 is controlled by a constitutively active neuronal promoter. Initial in vivo testing demonstrated successful NPC1 over-expression in administered mouse brains, compared to endogenous NPC1 levels in unadministered controls. No indications of toxicity were observed as a result of exogenous NPC1 overexpression in vivo. A series of preclinical proof of concept survival studies were subsequently carried out on the Npc1-/- model, where newborn Npc1-/- mice were administered with 4.6 x 109 vector genomes of AAV9-NPC1 via intracerebroventricular injections. Treated Npc1-/- mice exhibited an increased lifespan (median survival - 116.5 days) compared to untreated Npc1-/- mice (median survival - 75.5 days). Low dose treated mice exhibited permanent normalisation of locomotor function and significant neuronal rescue in all brain regions analysed. A subsequent study with a 65-fold dose increase resulted in an additional significant extension of lifespan, along with improved weight maintenance. Combined, these results demonstrate the potential beneficial use of gene therapy for NP-C and support the further development of this approach.
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Brown, Gemma Louise. "Analysis of the Caenorhabditis elegans model of Niemann-Pick Type C Disease." Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412394.

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Buard, Isabelle. "Relevance of glial cells in cellular mechanisms underlying the Niemann-Pick type C disease." Université Louis Pasteur (Strasbourg) (1971-2008), 2006. https://publication-theses.unistra.fr/public/theses_doctorat/2006/BUARD_Isabelle_2006.pdf.

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La maladie de Niemann-Pick type C (NPC) est une pathologie rare caractérisée par une hépatosplénomégalie progressive et une dégénérescence du système nerveux central due à des mutations dans le gène npc1. Chez les malades, les tissus montrent une accumulation intracellulaire anormale de cholestérol et de glycosphingolipides. Dans le cervelet, les cellules de Purkinje sont spécifiquement affectées, présentant une dégénérescence massive et une morphologie dendritique anormale. Il reste encore à déterminer la raison pour laquelle une déficience en NPC1, protéine qui interviendrait dans le transport intracellulaire de cholestérol, induit la neurodégénérescence. Une question importante est si les neurones meurent de façon autonome ou dû à des interactions neurone-glie défectueuses. Nous avons postulé que le cholestérol issu de la glie serait nécessaire pour la formation et le maintien des synapses et qu'une privation de NPC1 induirait une perte des synapses et ainsi, la mort neuronale. Pour tester cette hypothèse, nous avons établi des nouvelles cultures primaires de neurones cerebelleux isolés de la glie à partir de souris postnatales. Grâce à l'utilisation d'un modèle murin pour NPC, ces cultures nous ont permis de déterminer l'importance de NPC1 sous forme fonctionnelle dans les neurones et les cellules gliales pour le développement et la fonction des synapses. Afin d'étudier les synapses, nous avons enregistré l'activité synaptique dans les cellules granulaires (GCs) et de Purkinje (PCs) par la méthode du voltage imposé en configuration cellule-entière. En absence de glie, seules les GCs ont établi des connections synaptiques. Les cellules gliales ont favorisé le développement des synapses entre GCs et PCs indépendamment de la présence de NPC1 fonctionnelle dans les neurones ou dans la glie. En revanche, l'absence de NPC1 dans les GCs et/ou dans la glie a altéré dramatiquement la synaptogenèse entre les GCs. Basée sur ces résultats, nous proposons l'hypothèse suivante: l'altération, suivie par la dégénérescence, des PCs dans la maladie de NPC serait causée par un développement ou une fonction déficiente des synapses au niveau des GCs
Niemann-Pick type C disease (NPC) is a rare autosomal recessive lysosomal storage disease due to mutations in the npc1 gene. NPC patients show progressive hepatosplenomegaly and central nervous system degeneration and abnormal intracellular accumulation of cholesterol and glycosphingolipids in different tissues. In the cerebellum, Purkinje cells are specifically affected showing abnormal dendritic morphology and a high rate of cell death. So far, it is unclear how a defect in NPC1, which is thought to mediate the intracellular transport of cholesterol, causes neurodegeneration. An important question is whether neurons die in a cell-autonomous manner or due to a breakdown of neuron-glia interactions. We have postulated that glia-derived cholesterol is necessary for the synapse formation and maintenance and that a defect in NPC1 causes loss of synapses and subsequently neuronal cell death. To test this hypothesis, we established new glia-free primary cultures of immunoisolated cerebellar neurons from postnatal mice. These cultures together with a mouse model of NPC allowed to determine the relevance of functional NPC1 in neurons and glial cells for synapse development and function. To study synapses, we recorded synaptic activity in granule cells (GCs) and Purkinje cells (PCs) by whole-cell patch-clamp. In the absence of glia, only GCs but not PCs formed synaptic connections. Glial cells promoted development of synapses between GCs and PCs independently from the presence of functional NPC1 in neurons or in glia. In contrast, absence of NPC1 in GCs and/or in glia impaired dramatically synaptogenesis between GCs. Based on our results, we hypothesize that the impairment and ultimately degeneration of PCs in NPC is caused by deficient synapse development or function in GCs
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Books on the topic "Niemann Pick Type C"

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Bowler, Lynne Marie. Abnormal cholesterol metabolism in Niemann-Pick disease type C. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1992.

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Sedel, Frédéric. Niemann-Pick Disease Type C. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0053.

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Niemann-Pick disease type C (NPC) is a fatal neurovisceral lipid storage disease of autosomal inheritance resulting from mutations in either the NPC1 (95% of families) or NPC2 gene. The encoded proteins appear to be involved in lysosomal/late endosomal transport of cholesterol, glycolipids, and other molecules, but their exact function is still unknown. The clinical spectrum of the disease ranges from a neonatal rapidly fatal disorder to an adult-onset chronic neurodegenerative disease characterized prominently by psychiatric disorders, cerebellar ataxia, cognitive decline, and vertical supranuclear gaze palsy. Miglustat is the only treatment approved to date which has been demonstrated to slow or halt disease progression.
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Wraith. Understanding Niemann Pick Disease Type C and Its Potential Treatment. Wiley & Sons, Incorporated, John, 2008.

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Geberhiwot, Tarekegn, and Carla E. M. Hollak. Niemann-Pick Disease Type B. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0048.

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Niemann-Pick disease type B (NPDB) is caused by deficient activity of sphingomyelin phosphodiesterase leading to the accumulation of sphingomyelin and other lipids, primarily within macrophages. The disease is characterised by hepatosplenomegaly, a bleeding tendency, interstitial lung disease and an atherogenic lipid profile. The diagnosis of NPDB is usually made in childhood after organomegaly is noted, and patients often survive into adulthood. The diagnostic work up includes enzymatic determination of sphingomyelinase activity, mutational analysis and screening and/or quantification for target organ involvement. NPDB has a variable clinical expression and may be a life-limiting disorder with significant morbidity and mortality. There is no disease specific therapy yet and hence management is symptomatic with particular attention to treating the long term complications of the disease.
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Book chapters on the topic "Niemann Pick Type C"

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Nadjar, Yann, and Marie T. Vanier. "Niemann-Pick Disease Type C." In Neurometabolic Hereditary Diseases of Adults, 121–46. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-76148-0_6.

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Vanier, Marie T., and Marc C. Patterson. "Niemann-Pick Disease Type C." In Lysosomal Storage Disorders, 87–93. Oxford: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118514672.ch11.

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Ballout, Rami A. "Niemann-Pick Disease Type C (NPC)." In Genetic Syndromes, 1–10. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-66816-1_1339-1.

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Bi, Xiaoning, and Guanghong Liao. "Cholesterol in Niemann–Pick Type C disease." In Cholesterol Binding and Cholesterol Transport Proteins:, 319–35. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-8622-8_11.

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Vanier, M. T., P. Pentchev, C. Rodriguez-Lafrasse, and R. Rousson. "Niemann-Pick Disease Type C: An Update." In Journal of Inherited Metabolic Disease, 580–95. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-9749-6_15.

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Mavridou, Irene, Evangelia Dimitriou, Marie T. Vanier, Lluisa Vilageliu, Daniel Grinberg, Philippe Latour, Athina Xaidara, et al. "The Spectrum of Niemann-Pick Type C Disease in Greece." In JIMD Reports, 41–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/8904_2016_41.

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Federico, A., S. Palmeri, O. Van Diggelen, E. Ferrari, and G. C. Guazzi. "Juvenile Dystonia without Vertical Gaze Paralysis: Niemann—Pick Type C Disease." In Practical Developments in Inherited Metabolic Disease: DNA Analysis, Phenylketonuria and Screening for Congenital Adrenal Hyperplasia, 314–16. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4131-1_58.

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Sokol, J., M. Vanier, and P. Pentchev. "Niemann-Pick Disease Type C: A Lesion in Intracellular Cholesterol Transport." In Lipid Storage Disorders, 169–73. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1029-7_20.

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Siemes, H., M. T. Vanier, and K. Harzer. "Morbus Niemann-Pick Typ C — Auf Umwegen zur Diagnose." In Aktuelle Neuropädiatrie 1989, 109–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93411-7_18.

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Traschütz, Andreas, and Michael Thomas Heneka. "Screening for Niemann-Pick Type C Disease in a Memory Clinic Cohort." In JIMD Reports, 109–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/8904_2018_133.

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Conference papers on the topic "Niemann Pick Type C"

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Leppmeier, L. "“Weak with Laughter”: Cataplexy as a Hint for Early Diagnosis of Niemann-Pick Type C (NPC)?" In Abstracts of the 46th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1739713.

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Veress, Alexander I., Jeffrey A. Weiss, Robert J. Gillies, Anton E. Bowden, Jean-Philippe Galons, and Richard D. Rabbitt. "Deformable Image Registration of Mouse Brain MRI Data Using Hyperelastic Warping." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32375.

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Quantification of time-dependent changes in three-dimensional morphology of brain structures and neural pathways is a fundamental requirement in studies of neurodevelopment, remodeling and progression of neurological diseases [1]. However, local measures of this kind are extremely difficult due to a lack of clear fiducials. Our motivation to develop a reliable technique to quantify time-dependent changes in neuroanatomy originated with the problem of tracking progression of Niemann-Pick disease type C (NP-C), a heritable disease that causes alterations in brain development [2].
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Patterson, Marc C., Eugen Mengel, Rosalia M. Da Riol, Mireia Del Toro, Federica Deodato, Matthias Gautschi, Stephanie Grunewald, et al. "Persistent Effect of Arimoclomol in Patients with Niemann-Pick Disease Type C: 24-Month Results from an Open-Label Extension of a Pivotal Phase 2/3 Study." In Abstracts of the 46th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1739640.

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SURINLERT, PIYAPORN. "IDENTIFICATION AND EXPRESSION OF NIEMANN PICK TYPE C2 LIKE GENE IN MALE REPRODUCTIVE TRACTS OF MACROBRACHIUM ROSENBERGII." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.68.

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Griese, M., VR Aldana, F. Brasch, MM Cabrera, BJ Karam, G. Liebisch, P. Lohse, et al. "Presenting Respiratory Disease in Niemann-Pick Type-C2 Is Caused by Pulmonary Alveolar Proteinosis (PAP) with Defective Surfactant." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5964.

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Frank, Nathalie, and Jochen Baumkötter. "P 1111. Case Report of a Juvenile Patient with Niemann–Pick’s Disease Type C." In Abstracts of the 44th Annual Meeting of the Society for Neuropediatrics. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1675979.

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Eberlein, C., M. Deest, A. Das, S. Bleich, and H. Frieling. "Cariprazine in the treatment of a long lasting psychosis in a female patient with Morbus Niemann-Pick Type B." In Abstracts of the 2nd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3403038.

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Schöler, David, JanPhilipp Köhler, Petra May, Eva Thimm, Ertan Mayatepek, Tom Luedde, and Stephan vom Dahl. "Niemann-Pick type B as ultra-rare differential diagnosis in hepatomegaly, steatohepatitis, low HDL and increased plasma chitotriosidase activity: three case reports." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740750.

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Lee, Po-Chih. "One Novel Isoconstrained Parallel Robot With Schoenflies-Motion." In ASME 2013 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/detc2013-12502.

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The coupling between two opposite bars of the hinged parallelogram produces relative 1-DoF circular translation and the opposite bars can move but remain parallel. From the point of view of kinematics, a hinged parallelogram is equivalent to a prismatic pair for a small motion. On the basis of a special parallel mechanism with the limb architecture of type CPUh (C and P denote cylindrical and prismatic pairs; Uh indicates the pseudo-universal-joint having one revolute and one screw pairs with the intersecting axes), we provide one novel Schoenflies-motion isoconstrained CPaUh//CPaUh robot with only two limbs having the hinged parallelograms for the fast pick-and-place operation of the assembly and packaging applications. This type of robot is compact for not only its structure but also its actuation. The robot architecture and kinematics including inverse and forward solutions are studied. In addition, Jacobian matrix, singularity analysis and workspace are further discussed. It is hoped that the evaluations of such two-limb parallel mechanism can be useful for possible application in industry where pick-and-place motion and higher accuracy are required.
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Kang, Sukhvinder, David Miller, and John Cennamo. "Closed Loop Liquid Cooling for High Performance Computer Systems." In ASME 2007 InterPACK Conference collocated with the ASME/JSME 2007 Thermal Engineering Heat Transfer Summer Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/ipack2007-33870.

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The power dissipation levels in high performance personal computers continue to increase rapidly while the silicon die temperature requirements remain unchanged or have been lowered. Advanced air cooling solutions for the major heat sources such as CPU and GPU modules use heat pipes and high flow rate fans to manage the heat load at the expense of significant increases in the sound power emitted by the computer system. Closed loop liquid cooling systems offer an excellent means to efficiently meet the combined challenges of high heat loads, low thermal resistance, and low noise while easily managing die level heat fluxes in excess of 500 W/cm2. This paper describes the design and attributes of an advanced liquid cooling system that can cool single or multiple heat sources within the computer system. The cooling system described use copper cold plates with meso scale channels to pick up heat from CPU and GPU type heat sources and highly efficient liquid-to-air heat exchangers with flat copper tubes and plain fins to transfer the heat to air by forced convection. A water based coolant is used for high thermal performance and additives are used to provide burst protection to the cooling system at temperatures down to −40 °C and corrosion protection to critical components. A highly reliable compact pump is used to circulate the fluid in a closed loop. The overall system is integrated using assembly methods and materials that enable very low fluid permeation for long life.
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