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Yang, Z.H.; Zhang, J.B.; Gay, R.; Zhuang, L.Q.; Lee, H.M. |
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Building a semantic-rich service-oriented manufacturing environment |
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2005 |
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Web Information Systems Engineering – Wise 2005 |
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3806 |
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623-632 |
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ISI:000233809200069 |
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450 |
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Thomas, E.R.; van Wessem, J.M.; Roberts, J.; Isaksson, E.; Schlosser, E.; Fudge, T.; Vallelonga, P.; Medley, B.; Lenaerts, J.; Bertler, N.; van den Broeke, M.R.; Dixon, D.A.; Frezzotti, M.; Stenni, B.; Curran, M.; Ekaykin, A.A. |
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Title |
Review of regional Antarctic snow accumulation over the past 1000 years |
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Journal Article |
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2017 |
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Clim. Past Discuss. |
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2017 |
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1-42 |
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Here we review Antarctic snow accumulation variability, at the regional scale, over the past 1000 years. A total of 80 ice core snow accumulation records were gathered, as part of a community led project coordinated by the PAGES Antarctica 2k working group. The ice cores were assigned to seven geographical regions, separating the high accumulation coastal zones below 2000 m elevation from the dry central Antarctic Plateau. The regional composites of annual snow accumulation were evaluated against modelled surface mass balance (SMB) from RACMO2.4 and precipitation from ERA-interim reanalysis. With the exception of the Weddell Sea coast, the low-elevation composites capture the regional precipitation and SMB variability. The central Antarctic sites lack coherency and are either not representing regional precipitation or indicate the models inability to capture relevant precipitation processes in the cold, dry central plateau. The drivers of precipitation are reviewed for each region and the temporal variability and trends evaluated over the past 100, 200 and 1000 years. Our study suggests an overall increase in SMB across the grounded Antarctic ice sheet of ~ 44 GT since 1800 AD, with the largest (area-weighted) contribution from the Antarctic Peninsula (AP). Only four ice core records cover the full 1000 years and suggest a decrease in snow accumulation during this period. However, our study emphasizes the importance of low elevation coastal zones (especially AP and DML), which have been underrepresented in previous investigations of temporal snow accumulation. |
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1814-9359 |
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refbase @ user @ thomas_review_2017 |
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17462 |
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Weick, J.P. |
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Title |
Functional Properties of Human Stem Cell-Derived Neurons in Health and Disease |
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Journal Article |
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2016 |
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Stem Cells International |
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Stem Cells Int |
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2016 |
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4190438 |
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Stem cell-derived neurons from various source materials present unique model systems to examine the fundamental properties of central nervous system (CNS) development as well as the molecular underpinnings of disease phenotypes. In order to more accurately assess potential therapies for neurological disorders, multiple strategies have been employed in recent years to produce neuronal populations that accurately represent in vivo regional and transmitter phenotypes. These include new technologies such as direct conversion of somatic cell types into neurons and glia which may accelerate maturation and retain genetic hallmarks of aging. In addition, novel forms of genetic manipulations have brought human stem cells nearly on par with those of rodent with respect to gene targeting. For neurons of the CNS, the ultimate phenotypic characterization lies with their ability to recapitulate functional properties such as passive and active membrane characteristics, synaptic activity, and plasticity. These features critically depend on the coordinated expression and localization of hundreds of ion channels and receptors, as well as scaffolding and signaling molecules. In this review I will highlight the current state of knowledge regarding functional properties of human stem cell-derived neurons, with a primary focus on pluripotent stem cells. While significant advances have been made, critical hurdles must be overcome in order for this technology to support progression toward clinical applications. |
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Department of Neurosciences, University of New Mexico Health Science Center, Fitz Hall Room 145, 915 Camino de Salud NE, Albuquerque, NM 87131, USA |
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1687-966X |
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PMID:27274733; PMCID:PMC4870377 |
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refbase @ user @ |
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16675 |
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Pfaender, S.; Fohr, K.; Lutz, A.-K.; Putz, S.; Achberger, K.; Linta, L.; Liebau, S.; Boeckers, T.M.; Grabrucker, A.M. |
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Title |
Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells |
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2016 |
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Neural Plasticity |
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Neural Plast |
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2016 |
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3760702 |
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Apoptosis/physiology; Cell Survival/physiology; Homeostasis/*physiology; Humans; Induced Pluripotent Stem Cells/cytology/*metabolism; Neurogenesis/*physiology; Neurons/cytology/*metabolism; Signal Transduction/physiology; Zinc/*metabolism |
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Disturbances in neuronal differentiation and function are an underlying factor of many brain disorders. Zinc homeostasis and signaling are important mediators for a normal brain development and function, given that zinc deficiency was shown to result in cognitive and emotional deficits in animal models that might be associated with neurodevelopmental disorders. One underlying mechanism of the observed detrimental effects of zinc deficiency on the brain might be impaired proliferation and differentiation of stem cells participating in neurogenesis. Thus, to examine the molecular mechanisms regulating zinc metabolism and signaling in differentiating neurons, using a protocol for motor neuron differentiation, we characterized the expression of zinc homeostasis genes during neurogenesis using human induced pluripotent stem cells (hiPSCs) and evaluated the influence of altered zinc levels on the expression of zinc homeostasis genes, cell survival, cell fate, and neuronal function. Our results show that zinc transporters are highly regulated genes during neuronal differentiation and that low zinc levels are associated with decreased cell survival, altered neuronal differentiation, and, in particular, synaptic function. We conclude that zinc deficiency in a critical time window during brain development might influence brain function by modulating neuronal differentiation. |
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Institute for Anatomy and Cell Biology, Ulm University, 89081 Ulm, Germany; WG Molecular Analysis of Synaptopathies, Neurology Department, Neurocenter of Ulm University, 89081 Ulm, Germany |
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1687-5443 |
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PMID:27247802; PMCID:PMC4876239 |
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refbase @ user @ |
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16677 |
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Author |
Mohan, K.N. |
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Title |
Stem Cell Models to Investigate the Role of DNA Methylation Machinery in Development of Neuropsychiatric Disorders |
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Journal Article |
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2016 |
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Stem Cells International |
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Stem Cells Int |
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2016 |
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4379425 |
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Epigenetic mechanisms underlie differentiation of pluripotent stem cells into different lineages that contain identical genomes but express different sets of cell type-specific genes. Because of high discordance rates in monozygotic twins, epigenetic mechanisms are also implicated in development of neuropsychiatric disorders such as schizophrenia and autism. In support of this notion, increased levels of DNA methyltransferases (DNMTs), DNMT polymorphisms, and dysregulation of DNA methylation network were reported among schizophrenia patients. These results point to the importance of development of DNA methylation machinery-based models for studying the mechanism of abnormal neurogenesis due to certain DNMT alleles or dysregulated DNMTs. Achieving this goal is strongly confronted by embryonic lethality associated with altered levels of epigenetic machinery such as DNMT1 and expensive approaches in developing in vivo models. In light of literature evidence that embryonic stem cells (ESCs) are tolerant of DNMT mutations and advancement in the technology of gene targeting, it is now possible to introduce desired mutations in DNMT loci to generate suitable ESC lines that can help understand the underlying mechanisms by which abnormal levels of DNMTs or their specific mutations/alleles result in abnormal neurogenesis. In the future, these models can facilitate development of suitable drugs for treatment of neuropsychiatric disorders. |
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Department of Biological Sciences, Birla Institute of Technology and Science, Pilani, Hyderabad Campus, Jawaharnagar, Hyderabad 500 078, India |
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1687-966X |
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PMID:26798355; PMCID:PMC4699075 |
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refbase @ user @ |
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16707 |
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