Relevant bibliographies by topics / GM1

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Academic literature on the topic 'GM1'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "GM1"

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Langman, L. J., A. B. Leichtman, W. F. Weitzel, and R. W. Yatscoff. "Steady-state concentration of cyclosporin G (OG37-325) and its metabolites in renal transplant recipients." Clinical Chemistry 40, no. 4 (April 1, 1994): 613–16. http://dx.doi.org/10.1093/clinchem/40.4.613.

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Abstract The steady-state concentrations of cyclosporin G (OG37-325) (CsG) and six of its metabolites (GM1, GM9, GM4N, GM1c, GM1c9, GM19) were measured throughout the 12-h dosing interval in six renal transplant recipients receiving CsG as prophylaxis against acute cellular rejection. The mean 12-h whole-blood trough concentrations (micrograms/L) were CsG, 131 +/- 26; GM1, 79 +/- 55; GM9, 110 +/- 114; GM4N, 28 +/- 18; GM1c, 31 +/- 18; GM1c9, 216 +/- 145; and GM19, 303 +/- 217. The relative concentration of the primary metabolites (GM1, GM9, GM4N) remained stable with respect to CsG throughout the dosing interval, whereas that of the secondary metabolites increased. The secondary metabolites GM19 and GM1c9 exhibited extensive between-patient variation. We investigated the effect of these metabolites on commercially available monoclonal antibody-based fluorescence polarization immunoassays (FPIA) and RIAs adapted for measurement of CsG. The 12-h whole-blood trough concentrations measured by FPIA and RIA exceed those measured by HPLC by 19% and 36%, respectively. These measured biases corresponded closely with the calculated biases (FPIA 19%, RIA 28%) based on the known cross-reactivities of CsG metabolites and their concentrations. These results suggest that cross-reactivity with metabolites account for a large part of the bias observed in immunoassays of CsG.
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Yamazaki, Yasuhiro, Yasuhiro Horibata, Yasuko Nagatsuka, Yoshio Hirabayashi, and Tsutomu Hashikawa. "Fucoganglioside α-fucosyl(α-galactosyl)-GM1: a novel member of lipid membrane microdomain components involved in PC12 cell neuritogenesis." Biochemical Journal 407, no. 1 (September 12, 2007): 31–40. http://dx.doi.org/10.1042/bj20070090.

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In order to search for novel components of lipid membrane microdomains involved in neural signalling pathways, mAbs (monoclonal antibodies) were raised against the detergent-insoluble membrane fraction of PC12 (pheochromocytoma) cells. Among the 22 hybrid clones, mAb PR#1 specifically detected a fucoganglioside Fuc(Gal)-GM1 [α-fucosyl(α-galactosyl)-GM1], a ganglioside homologous with GM1a (II3NeuAc,GgOse4Cer), as a novel member of microdomain components with biological functions. In the presence of mAb PR#1 in the culture medium, the outgrowth of neurites was induced in PC12 cells in a dose-dependent manner, with no effects on cell proliferation, suggesting that Fuc(Gal)-GM1 is preferentially involved in PC12 cell neuritogenesis. Effects through Fuc(Gal)-GM1 were different from those through GM1a during differentiation, e.g. under PR#1 treatment on Fuc(Gal)-GM1, round cell bodies with thinner cell processes were induced, whereas treatment with CTB (cholera toxin B subunit), a specific probe for GM1a, produced flattened cell bodies with thicker pro-cesses. Molecular analysis demonstrated that the PR#1–Fuc(Gal)-GM1 pathway was associated with Fyn and Yes of the Src family of kinases, although Src itself was not involved. No association was found with TrkA (tropomyosin receptor kinase A) and ERKs (extracellular-signal-regulated kinases), which are responsible for GM1a-induced differentiation. From these findings, it is suggested that a fucoganglioside Fuc(Gal)-GM1 provides a functional platform distinct from that of GM1a for signal transduction in PC12 cell differentiation.
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Alrebdi, Haifa I., and Thabit Barakat. "The Radiative Δ(1600) → γN Decay in the Light-Cone QCD Sum Rules." Universe 7, no. 8 (July 21, 2021): 255. http://dx.doi.org/10.3390/universe7080255.

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Within the framework of the light-cone QCD sum rules method (LCSR’s), the radiative Δ(1600)→γN decay is studied. In particular, the magnetic dipole moment GM1(0) and the electric quadrupole moment GE1(0) are estimated. We also calculate the ratio REM=−GE1(0)GM1(0) and the decay rate. The predicted multipole moments and the decay rate strongly agree with the existing experimental results as well as with the other available phenomenological approaches.
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IWAMORI, Masao, and Steven E. DOMINO. "Tissue-specific loss of fucosylated glycolipids in mice with targeted deletion of alpha(1,2)fucosyltransferase genes." Biochemical Journal 380, no. 1 (May 15, 2004): 75–81. http://dx.doi.org/10.1042/bj20031668.

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Glycolipids in epithelial tissues of the gastrointestinal tract act as receptors for enteric bacteria and are implicated in the activation of the intestinal immune system. To clarify the genes involved in the fucosylation of the major glycolipids, substrate glycolipids and fucosylated products were measured in tissues of wild-type and mutant mice lacking α(1,2)fucosyltransferase genes FUT1 or FUT2. Quantitative determination was performed by TLC-immunostaining for GA1 (Gg4Cer), FGA1 (fucosyl GA1), GM1 (II3NeuAc-Gg4Cer), FGM1 (fucosyl GM1), and Forssman glycolipids. Both FGM1 and FGA1 completely disappeared from the antrum, cecum, and colon of FUT2-null mice, but not those of FUT1-null and wild-type mice. Precursor glycolipids, GM1 and GA1, accumulated in tissues of FUT2-null mice, indicating that the FUT2-encoded enzyme preferentially participates in the fucosylation of GA1 and GM1 in these tissues. Female reproductive organs were similarly found to utilize FUT2 for the fucosylation of glycolipids FGA1 (uterus and cervix), and FGM1 (ovary), due to their absence in FUT2-null mice. In FUT1-null mice FGA1 was lost from the pancreas, but was present in wild-type and FUT2-null mice, indicating that FUT1 is essential for fucosylation of GA1 in the pancreas. Ulex europaeus agglutinin-I lectin histochemistry for α(1,2)fucose residues confirmed the absence of α(1,2)fucose residues from the apical surface of pancreatic acinar glands of FUT1-null mice. Ileum, epididymis, and testis retained specific fucosylated glycolipids, irrespective of targeted deletion of either gene, indicating either compensation for or redundancy of the α(1,2)fucosyltransferase genes in these tissues.
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Bisel, Blaine, Francesco S. Pavone, and Martino Calamai. "GM1 and GM2 gangliosides: recent developments." BioMolecular Concepts 5, no. 1 (March 1, 2014): 87–93. http://dx.doi.org/10.1515/bmc-2013-0039.

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AbstractGM1 and GM2 gangliosides are important components of the cell membrane and play an integral role in cell signaling and metabolism. In this conceptual overview, we discuss recent developments in our understanding of the basic biological functions of GM1 and GM2 and their involvement in several diseases. In addition to a well-established spectrum of disorders known as gangliosidoses, such as Tay-Sachs disease, more and more evidence points at an involvement of GM1 in Alzheimer’s and Parkinson’s diseases. New emerging methodologies spanning from single-molecule imaging in vivo to simulations in silico have complemented standard studies based on ganglioside extraction.
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&NA;. "GM1." Inpharma Weekly &NA;, no. 839 (May 1992): 11. http://dx.doi.org/10.2165/00128413-199208390-00017.

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Sugimoto, Mamoru, Masaaki Numata, Katsuya Koike, Yoshiaki Nakahara, and Tomoya Ogawa. "Total synthesis of gangliosides GM1 and GM2." Carbohydrate Research 156 (November 1986): C1—C5. http://dx.doi.org/10.1016/s0008-6215(00)90125-3.

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Park, Hyun Jung, Gil-Ja Jhon, Seong Jun Han, and Young Kee Kang. "Conformational study of asialo-GM1 (GA1) ganglioside." Biopolymers 42, no. 1 (July 1997): 19–35. http://dx.doi.org/10.1002/(sici)1097-0282(199707)42:1<19::aid-bip3>3.0.co;2-4.

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LI, Su-Chen, Yu-Teh LI, Setsuko MORIYA, and Taeko MIYAGI. "Degradation of GM1 and GM2 by mammalian sialidases." Biochemical Journal 360, no. 1 (November 8, 2001): 233–37. http://dx.doi.org/10.1042/bj3600233.

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In mammalian tissues, the pathway known for the catabolism ofGM1[Galβ3GalNAcβ4(Neu5Acα3)Galβ4GlcCer;where Cer is ceramide] is the conversion of this ganglioside into GM2 [GalNAcβ4(Neu5Acα3)Galβ4GlcβCer] by β-galactosidase followed by the conversion of GM2 into GM3 (Neu5Acα3Galβ4GlcβCer) by β-N-acetylhexosaminidase A (Hex A). However, the question of whether or not GM1 and GM2 can also be respectively converted into asialo-GM1 (Galβ3GalNAcβ4Galβ4GlcCer; GA1) and asialo-GM2 (GalNAcβ4Galβ4GlcβCer, GA2) by mammalian sialidases has not been resolved. This is due to the fact that sialidases purified from mammalian tissues always contained detergents that interfered with the in vitro hydrolysis of GM1 and GM2 in the presence of an activator protein. The mouse model of human type B Tay–Sachs disease created by the disruption of the Hexa gene showed no neurological abnormalities, with milder clinical symptoms than the human counterpart, and the accumulation of GM2 in the brains of affected mice was only limited to certain regions [Sango, Yamanaka, Hoffmann, Okuda, Grinberg, Westphal, McDonald, Crawley, Sandhoff, Suzuki and Proia (1995) Nat. Genet. 11, 170–176]. These results suggest the possible presence of an alternative catabolic pathway (the GA2 pathway) in mouse to convert GM2 into GA2 by sialidase. To show the existence of this pathway, we have used recombinant mammalian cytosolic sialidase and membrane-associated sialidase to study the desialylation of GM1 and GM2. We found that the mouse membrane-bound sialidase was able to convert GM1 and GM2 into their respective asialo-derivatives in the presence of human or mouse GM2 activator protein. The cytosolic sialidase did not exhibit this activity. Our results suggest that, in vivo, the stable NeuAc of GM1 and GM2 may be removed by the mammalian membrane-associated sialidase in the presence of GM2 activator protein. They also support the presence of the GA2 pathway for the catabolism of GM2 in mouse.
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Santi, P. A., P. Mancini, and C. Barnes. "Identification and localization of the GM1 ganglioside in the cochlea using thin-layer chromatography and cholera toxin." Journal of Histochemistry & Cytochemistry 42, no. 6 (June 1994): 705–16. http://dx.doi.org/10.1177/42.6.8189033.

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Using high-performance thin-layer chromatography, we identified GM1, GM3, GD3, GD1a, GT1b, GQ1b, and other gangliosides in chinchilla cochlea and cerebellum. GM1 was also identified on chromatograms with the B-subunit of cholera toxin (BCT). BCT was also used to determine the distribution of GM1 in fixed and unfixed tissues from cochlea, cerebellum, and sciatic nerve. Positive control tissues showed expected labeling of GM1 by BCT. Negative controls showed expected suppression of BCT binding to GM1 after GM1 extraction and GM1 absorption. In the cochlea, GM1 appeared abundant in plasma membranes of most epithelial cells lining the endolymphatic surface of the scala media, including the interdental, inner supporting, pillar, Deiters, Hensen, Claudius, Boettcher, spiral prominence, and external sulcus. GM1 appeared less abundant in cells of the stria vascularis, Reissner's membrane, and in nerve fibers. In hair cells, the stereocilia appeared to contain GM1; however, the endolymphatic surface of the cuticular plate and the body of the outer hair cells appeared to contain little GM1. In addition, the tectorial membrane, connective tissue of the spiral limbus, and amorphous layer of the basilar membrane also appeared to contain little GM1. Enzymatic degradation of glycoproteins and transformation of polysialogangliosides to GM1 increased the reactivity of BCT to cochlear GM1. This further supported the presence of GM1 and other gangliosides in the cochlea. Although the functional significance of GM1 and other gangliosides in the cochlea is not yet known, they are likely to play important roles in membrane function.
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Dissertations / Theses on the topic "GM1"

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Arthur, Julian. "Novel Therapies and Biochemical Insights for the GM1 and GM2 Gangliosidoses." Thesis, Boston College, 2011. http://hdl.handle.net/2345/3855.

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Thesis advisor: Thomas N. Seyfried
Gangliosides are glycosphingolipids (GSLs) containing sialic acids that play numerous roles in neuronal maturation, apoptotic signaling, angiogenesis, and cell surface receptor activity. The GM1 and GM2 gangliosidoses are a series of autosomal recessive lysosomal storage disorders (LSDs) characterized by an inability to degrade these lipid molecules. GM1 gangliosidosis is caused by a mutation in the lysosomal hydrolase β-galactosidase, resulting in neuronal storage of ganglioside GM1 and asialo GA1. Tay-Sachs (TS) and Sandhoff Disease (SD) are GM2 gangliosidoses caused by mutations in either the α or β subunits, respectively, of the heterodimeric protein β- hexosaminidase A, resulting in the storage of ganglioside GM2 and asialo GA2. The accumulation of excess ganglioside in the central nervous system leads to abnormal intracellular vacuoles, neuronal loss, demyelination, ataxia, dementia, and premature death. In my studies, I have shown that accumulation of GM1 ganglioside may not coincide with secondary storage of cholesterol, by providing evidence that cholesterol-binding fluorescent molecule filipin reacted to GM1 ganglioside in the absence of cholesterol. In an effort to combat the early-onset gangliosidoses, I have explored the effects of combining Neural Stem Cells (NSCs) with Substrate Reduction Therapy (SRT) in juvenile Sandhoff mice. The analysis showed that SRT was more effective than NSCs in reducing stored GM2 and GA2 in young mice, and no synergy was observed. In adult GM1 gangliosidosis, Tay- Sachs, and Sandhoff mice, Adeno-Associated Viral (AAV) vector gene therapy was used to restore therapeutic levels of wild-type enzyme to the CNS. AAV therapy corrected ganglioside storage and ameliorated myelin-associated lipid loss in all tissues assayed, increasing motor performance and life in effected animals. Lastly, AAV therapy was also successful in a feline model of Sandhoff disease. These results in juvenile and adult model systems point the way towards multiple effective clinical therapies in the near future
Thesis (PhD) — Boston College, 2011
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Elliot-Smith, Elena. "GM1 gangliosidosis : therapy and pathogenesis." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425028.

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DI, BIASE ERIKA. "GM1 OLIGOSACCHARIDE ACCOUNTS FOR GM1 ROLE IN ENHANCING NEURONAL DEVELOPMENT ACTING ON TRKA-MAPK PATHWAY." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/692335.

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Il ganglioside GM1 è un glicosfingolipide mono-sialilato presente nello strato esterno della membrana plasmatica cellulare ed è particolarmente abbondante nei neuroni. Numerosi studi in vitro e in vivo evidenziano il ruolo del GM1 non solo come componente strutturale ma anche come regolatore di diversi processi cellulari. Infatti, l'arricchimento di GM1 nei microdomini di membrana promuove il differenziamento e la protezione neuronale. Inoltre il contenuto di GM1 è essenziale per la sopravvivenza e il mantenimento dei neuroni. Nonostante vi siano numerose evidenze sugli effetti neuronotrofici mediati dal GM1, la conoscenza del meccanismo d'azione sottostante è scarsa. Recentemente, la catena oligosaccaridica del GM1 (oligoGM1) è stata identificata come responsabile delle proprietà neuritogeniche del ganglioside GM1 nelle cellule di neuroblastoma. Gli effetti mediati dall’oligoGM1 dipendono dal suo legame con il recettore specifico dell’ NGF, il TrkA, determinando così l'attivazione della via TrkA-MAPK. In questo contesto, il mio lavoro di dottorato mirava a confermare il ruolo dell’oligoGM1, come componente bioattiva dell’intero ganglioside GM1, capace di stimolare i processi di differenziaziamento e maturazione dei neuroni granulari cerebellari di topo. Come prima cosa, abbiamo eseguito analisi morfologiche in time -course sui neuroni primari coltivati in presenza o in assenza dei gangliosidi GM1 o GD1a (il quale rappresenta il diretto precursore catabolico del GM1), somministrati esogenamente. Abbiamo osservato che entrambi i gangliosidi aumentavano l’aggregazione e l'arborizzazione dei neuroni. Dopo successiva somministrazione dei rispettivi oligosaccaridi, abbiamo osservato che solo l’oligoGM1 favoriva la migrazione dei neuroni, mentre l’oligoGD1a non induceva nessun effetto discriminante rispetto alle cellule controllo. Questo risultato suggerisce l'importanza della specifica struttura saccaridica del GM1 nella mediazione degli effetti neuronotrofici del ganglioside. Quindi abbiamo caratterizzato biochimicamente l'effetto mediato dall’oligoGM1 nei neuroni e abbiamo osservato un più elevato tasso di fosforilazione delle proteine FAK e Src, le quali rappresentano i regolatori intracellulari chiave della motilità neuronale. Inoltre, in presenza dell’ oligoGM1 i neuroni granulari cerebellari mostravano un aumento del livello di marcatori neuronali specifici (ad es. β3-Tubulina, Tau, Neuroglicano C, Sinapsina), suggerendo uno stadio di maturazione più avanzato rispetto ai controlli. Inoltre, abbiamo scoperto che l'oligoGM1 accelera l'espressione del pattern di gangliosidi tipico dei neuroni maturi che è caratterizzato da alti livelli di gangliosidi complessi (cioè GM1, GD1a, GD1b e GT1b) e basso livello del ganglioside più semplice GM3. Per studiare il meccanismo d'azione dell'oligoGM1, abbiamo usato il suo derivato marcato con il trizio e abbiamo scoperto che l'oligoGM1 interagisce con la superficie cellulare senza entrare nelle cellule. Questa scoperta suggerisce la presenza di un bersaglio biologico sulla membrana plasmatica neuronale. È interessante notare che abbiamo riscontrato una precoce attivazione della via di segnalazione del TrkA associata alle MAP chinasi in seguito alla somministrazione dell’oligoGM1 nelle culture neuronali. Questo risultato suggerisce che questo evento rappresenti un punto di partenza degli effetti dell’ oligoGM1 nei neuroni. I nostri dati rivelano che gli effetti del ganglioside GM1 sul differenziamento e la maturazione neuronale sono mediati dalla sua porzione di oligosaccaride. Infatti, l’oligoGM1 interagisce con la superficie cellulare, innescando così l'attivazione di processi biochimici intracellulari che sono responsabili della migrazione neuronale, dell'emissione dei dendriti e della crescita degli assoni. Nel complesso, i nostri risultati sottolineano l'importanza dell’ oligoGM1 come un nuovo e promettente fattore neurotrofico.
The GM1 ganglioside is a mono-sialylated glycosphingolipid present in the outer layer of the cell plasma membrane and abundant in neurons. Numerous in vitro and in vivo studies highlight the role of GM1 not only as a structural component but also as a functional regulator. Indeed, GM1 enrichment in membrane microdomains promotes neuronal differentiation and protection, and the GM1 content is essential for neuronal survival and maintenance. Despite many lines of evidence on the GM1-mediated neuronotrophic effects, our knowledge on the underlying mechanism of action is scant. Recently, the oligosaccharide chain of GM1 (oligoGM1) has been identified as responsible for the neuritogenic properties of the GM1 ganglioside in neuroblastoma cells. The oligoGM1-mediated effects depend on its binding to the NGF specific receptor TrkA, thus resulting in the TrkA-MAPK pathway activation. In this context, my PhD work aimed to confirm the role of the oligoGM1, as the bioactive portion of the entire GM1 ganglioside, capable of enhancing the differentiation and maturation processes of mouse cerebellar granule neurons. First, we performed time course morphological analyses on mouse primary neurons plated in the presence or absence of exogenously administered gangliosides GM1 or GD1a (direct GM1 catabolic precursor). We found that both gangliosides increased neuron clustering and arborization, however only oligoGM1 and not oligoGD1a induced the same effects in prompting neuron migration. This result suggests the importance of the specific GM1 saccharide structure in mediating neuronotrophic effects. Then we characterized biochemically the oligoGM1-mediated effect in mouse primary neurons, and we observed a higher phosphorylation rate of FAK and Src proteins which are the intracellular key regulators of neuronal motility. Moreover, in the presence of oligoGM1 cerebellar granule neurons showed increased level of specific neuronal markers (e.g., β3-Tubulin, Tau, Neuroglycan C, Synapsin), suggesting an advanced stage of maturation compared to controls. In addition, we found that the oligoGM1 accelerates the expression of the typical ganglioside pattern of mature neurons which is characterized by high levels of complex gangliosides (i.e., GM1, GD1a, GD1b, and GT1b) and low level of the simplest one, the GM3 ganglioside. To study the mechanism of action of the oligoGM1, we used its tritium labeled derivative and we found that the oligoGM1 interacts with the cell surface without entering the cells. This finding suggests the presence of a biological target at the neuronal plasma membrane. Interestingly, we observed the TrkA-MAP kinase pathway activation as an early event underlying oligoGM1 effects in neurons. Our data reveal that the effects of GM1 ganglioside on neuronal differentiation and maturation are mediated by its oligosaccharide portion. Indeed, oligoGM1 interacts with the cell surface, thus triggering the activation of intracellular biochemical pathways that are responsible for neuronal migration, dendrites emission and axon growth. Overall, our results point out the importance of oligoGM1 as a new promising neurotrophic player.
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Kannebley, João Stein 1971. "Aspectos clínicos, radiológicos e neuroimagem em 12 pacientes com Gangliosidose GM1, formas juvenil e crônica." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312528.

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Orientador: Carlos Eduardo Steiner
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: A gangliosidose GM1 é uma doença rara causada pela deficiência da enzima ?-galactosidase, decorrente de mutações no gene GLB1, acarretando o acúmulo de gangliosídeos, principalmente o GM1. É classificada em três formas dependendo da idade de início dos sintomas. Em todas ocorrem alterações esqueléticas e deterioração neurológica, sendo que na forma adulta predominam sinais extrapiramidais como distonia. No presente estudo descrevemos as características de 12 pacientes com gangliosidose GM1 nas formas juvenil e crônica de 10 famílias não aparentadas provenientes da região de Campinas, SP, e do sul do estado de Minas Gerais. Foram detalhados a história clínica e o exame físico, em especial o neurológico, bem como de aspectos radiológicos, ultrassonográficos, ecocardiográficos e de neuroimagem. Metade dos casos iniciou com queixas ósteo-articulares e outra metade com sintomas neurológicos, porém com a evolução todos apresentaram uma combinação de disostose múltipla e neurodegeneração. Opacificação de córnea e angioqueratomas foram vistos em um caso, cada. Outros sinais comumente associados às doenças de depósito lisossômico não foram vistos nesta casuística. Todos apresentaram baixa estatura, disostose múltipla, disartria e prejuízo nas atividades de vida diária, 10 tinham distonia e disfagia, nove atrofia muscular e oito sinais piramidais e alterações da movimentação ocular. Barra óssea e os odontoideum foram vistos em dois casos, sendo alterações previamente não descritas nessa condição. Exames de neuroimagem mostraram aumento do sistema ventricular e hipointensidade de sinal em globos pálidos em todos, além de deformidades vertebrais, hiperintensidade de sinal de putâmen e atrofia cortical na maioria. Alterações em tálamo, substância branca ou atrofia cerebelar não foram identificadas nessa série
Abstract: GM1 gangliosidosis is a rare disorder caused by deficiency in ?-galactosidase activity due to mutations in the GLB1 gene, leading to acumulation of gangliosides in multiple organs. Three main clinical forms have been described according to the age of onset. All present with skeletal deformities and neurologic deterioration, and in the adult form extrapyramidal signs including dystonia are frequent. In the present study we describe 12 subjects of 10 unrelated families from the region of Campinas and the southern state of Minas Gerais. Clinical information included detailed history, full neurologic examination, radiologic, ultrasonographic, echocardiographic, and neuroimaging description. Half of subjects presented initially with skeletal deformities, while the remaining opened clinical presentation with neurologic features. However, over time all presented dysostosis multiplex and neurodegeneration. Corneal clouding and angiokeratomas were seen in one individual each. Other features commonly described in lysosomal storage disorders were not found in this series. All subjects presented with short stature, dysostosis multiplex, dysarthria, and impairment of activities of daily living, 10 had extrapyramidal signs, nine had muscular atrophy, and eight had pyramidal signs and mild oculomotor abnormalities. A vertebral bone bar and os odontoideum were found in two patients, being previously undescribed in this condition. Neuroimaging revealed enlargement of the ventricular system and hypointensity of globus pallidus in all, besides vertebral deformities, putaminal hyperintensity, and cortical atrophy in most patients. Thalamic changes, abnormal white matter or cerebellar atrophy were not seen in this series
Mestrado
Genetica Medica
Mestre em Ciências Médicas
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Fink, Erin Nicole. "GM1 signaling through the GDNF receptor complex." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1198013799.

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Baptista, Marcella Bergamini de 1988. "Análise de mutações no gene GLB1 em pacientes com gangliosidose GM1 formas juvenil e crônica." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308543.

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Orientador: Carlos Eduardo Steiner
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: Gangliosidose GM1 é uma doença autossômica recessiva rara, classificada em três formas clínicas de acordo com a idade de apresentação dos sintomas e a gravidade, provocada pela deficiência da enzima lisossômica ?-galactosidase que leva ao acúmulo, principalmente, do gangliosídeo GM1. A forma juvenil geralmente apresenta início entre sete meses e três anos de idade, com progressão lenta dos sinais neurológicos, dimorfismos menos graves que na forma infantil e deformidades ósseas. A forma crônica é caracterizada por apresentações clínicas mais leves e sintomas extrapiramidais. O gene codificador da enzima é o GLB1, no qual mais de 130 mutações foram descritas. No presente estudo foi realizada a caracterização molecular de 10 indivíduos de nove famílias não relacionadas diagnosticados com gangliosidose GM1, nas formas juvenil e crônica. Todas as famílias são originárias do interior do estado de São Paulo ou do sul do estado de Minas Gerais. Para a análise realizada foi possível identificar a mutação anteriormente descrita p.T500A, em sete das nove famílias estudadas, a inserção c.1717- 1722insG e a mutação p.R59H foram encontradas em duas famílias (a última segregou juntamente com o polimorfismo descrito IVS12+8T>C). As demais mutações descritas (p.F107L, p.L173P, p.R201H, p.G311R) foram encontradas em uma família cada. Uma alteração neutra (p.P152P) e duas mutações (p.I354S e p.T384S) são inéditas. Foi possível identificar a ocorrência de uma mutação de novo em uma família. Todas as mutações foram encontradas em heterozigose
Abstract: GM1 gangliosidosis is a rare autosomal recessive, classified in three clinical types according to age of onset and severity. The disease is caused by the deficiency of lysosomal enzyme ?-galactosidase that leads to the accumulation of GM1 ganglioside. The juvenile form usually shows an onset between seven months and three years of age, with slowly progressive neurological signs, less severe dysmorphisms than the infantile form and skeletal changes. The adult form is specified by a milder clinical manifestations and extrapyramidal signs. The lysossomal enzyme is coded by the GLB1 gene which more than 130 mutations have been decribed. In the present study it was genotyped 10 individuals of nine unrelated families originated from the States of São Paulo and Minas Gerais diagnosed with the juvenile and chronic forms of the disease. It was possible to find the previously described mutations p.T500A in seven of the nine families, c.1717-1722insG and p.R59H in two alleles (the latter also segregating with IVS12+8T>C), and p.F107L, p.L173P, p.R201H, and p.G311R in one familie each. One neutral alteration (p.P152P) and two mutations (p.I354S and p.T384S) are described for the first time. The occurrence of a de novo mutation was seen in one family. All patients presented as heterozygous compound
Mestrado
Ciencias Biomedicas
Mestra em Ciências Médicas
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Maggioni, M. "GM1-MEDIATED NEURODIFFERENTIATION IS PROMOTED BY OLIGOGM1-TRKA INTERACTION." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/543684.

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The present study proposes a clarification on the molecular mechanism by which ganglioside GM1 promotes neurodifferentiation, demonstrating in vitro that neurotrophic functions are exerted by an interaction between the oligosaccharide portion (OligoGM1) and an extracellular domain of TrkA receptor. Similarly to the entire molecule, the oligosaccharide portion of ganglioside GM1, rather than ceramide, is responsible for neurodifferentiation by augmenting neurite elongation and by increasing the expression of neurofilament proteins in mouse neuroblastoma cell line Neuro2a (N2a). Conversely, the single components of OligoGM1 (asialo-OligoGM1, OligoGM2, OligoGM3, sialic acid or galactose) are not able to induce a neuro-like morphology. The neurodifferentiative effect is exerted instead by fucosyl-OligoGM1. Contrarily to GM1, exogenous OligoGM1 never integrates in the plasma membrane composition and does not belong to the intracellular metabolism: the unique interaction with N2a is characterized by a weak non-covalent association to the plasma membrane that suggests the existence of an OligoGM1-stimulated target on the cell surface. In fact, the neurotrophic properties of GM1 oligosaccharide are exerted by activating TrkA receptor and the following cascade leading to neurodifferentiation event. The second part of this study elucidates the interaction between GM1 and TrkA, revealing a direct association of OligoGM1 to an extracellular domain of the receptor. Photolabeling experiments, performed employing nitrogen azide radiolabeled GM1 derivatives, show a direct association of the oligosaccharide chain to TrkA. Moreover, a bioinformatics study reveals that OligoGM1 fits perfectly in a pocket of the TrkA-NGF complex, stabilizing and favoring their intermolecular interactions as revealed by the increase in energy associated to the new complex TrkA-NGF-OligoGM1. A precise molecular recognition process between OligoGM1 and a specific extracellular domain of the TrkA receptor is supposed. According to the weak association of OligoGM1 to the cell surface, no covalent bounds between OligoGM1 and TrkA-NGF complex were found. For the first time the molecular mechanism by which GM1 exerts its neurodifferentiative potential was identified, finding out a direct interaction between the oligosaccharide portion and an extracellular domain of TrkA receptor responsible for enhancing the signal transduction related to the neurodifferentiation pathway.
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FATO, PAMELA. "EVALUATION OF THE GM1 OLIGOSACCHARIDE ROLE IN NEURONAL DIFFERENTIATION." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/796885.

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GM1 is a mono-sialo ganglioside with amphiphilic character due to the presence of a hydrophobic group, ceramide, and a hydrophilic head (oligosaccharide chain). GM1 represents one of the most important modulator in the nervous system where it is involve in maturations of neurons, differentiation, increase responses to neurotrophic factors, protection against neuronal death and reduction brain damage. The effects of GM1 are known in vitro and in vivo, but the molecular mechanism of action underlying the GM1 properties is unknown. The present work aims to analyze the mechanism of action of GM1, and in particular to demonstrate that the effects of this ganglioside are attributable to the action of its oligosaccharide portion (OligoGM1) and not to the entire molecule. To reach our purpose we used mouse neuroblastoma cell line Neuro2a (N2a). Like GM1, OligoGM1 promotes neurodifferentiation by increasing both neurite elongation and the expression of neurofilament proteins in N2a cell. A similar effect was obtained with the use of fucosyl-OligoGM1 but not with the administration of asialo-OligoGM1, OligoGM2, OligoGM3, sialic acid or galactose (single components of Oligo GM1). OligoGM1, in N2a cells, activates ERK1/2 pathway binding to the NGF specific receptor TrkA present on the cell surface. To study this mechanism of action we used tritium labeled derivative of OligoGM1. The activator for GM1 mediated functions (differentiation and protection) is the interaction between OligoGM1 and TrkA. This was established with the use of a TrkA inhibition. With a bioinformatics study it was established that OligoGM1 inserts in a pocket of the TrkA-NGF complex. An increase in energy associated to the complex TrkA-NGF-OligoGM1 indicates greater stability of intermolecular interactions. All the results lead to the conclusion that the bioactive portion of GM1, in neuronal differentiation and protection, is represented by its hydrophilic chain (OligoGM1). These conclusions open up new perspectives on the therapeutic use of gangliosides.
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LUNGHI, GIULIA. "GM1 OLIGOSACCHARIDE MODULATION OF CALCIUM SIGNALLING IN NEURONAL FUNCTIONS." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/792078.

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It has been already demonstrated that the oligosaccharide chain (OligoGM1) of the ganglioside GM1, β-Gal-(1-3)-β-GalNAc-(1-4)-[α-Neu5Ac-(2-3)]-β-Gal-(1-4)-β-Glc-(1-1)-Ceramide, promotes neurodifferentiation in the Neuro2a murine neuroblastoma cells, used as a model, by directly interacting with the NGF specific receptor TrkA, leading to the activation of ERK1/2 downstream pathway. In this context, my PhD work aimed to investigate which other biochemical pathways, in addition to TrkA-MAPK cascade activation, are prompted by OligoGM1, with an emphasis on Ca2+ modulating factors. A proteomic analysis (nLC-ESi-MS-MS) performed on Neuro2a cells treated with 50 µM OligoGM1 for 24 hours led to the identification and quantification of 324 proteins exclusively expressed by OligoGM1-treated cells. Interestingly, some of these proteins are involved in the regulation of Ca2+ homeostasis and in Ca2+-dependent differentiative pathways. In order to evaluate if OligoGM1 administration was able to modulate Ca2+ flow, we performed calcium-imaging experiments on Neuro2a cells using the Ca2+-sensitive Fluo-4 probe. Starting from 5 minutes upon OligoGM1 administration to undifferentiated Neuro2a, a significant increase in Ca2+ influx occurs. At the same time an increased activation of TrkA membrane receptor was observed and, importantly, the addition of a specific TrkA inhibitor abolished the OligoGM1 mediated increase of the cytosolic Ca2+, suggesting that the opening of the cell Ca2+ channels following OligoGM1 administration depends on the activation of TrkA receptor. To unveil which cellular pathway activated by OligoGM1 could lead to the increase of intracellular Ca2+, time-course immunoblotting analyses were performed. The data revealed that following TrkA activation, OligoGM1 induced the activation of phospholipase PLCγ1 which converts phosphatidylinositol 4,5-bisphosphate (PIP2) to diacyglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3), the second messengers that propagate cellular signalling via Ca2+ mobilization. Moreover, we observed a hyperphosphorylation of the DAG substrate, protein kinase C (PKC), which is a priming event that enables its catalytic activation in response to lipid second messengers, and we found its enrichment in lipid rafts, events that consolidate its activation. When calcium-imaging experiments where performed in the presence of xestospongin C, a potent inhibitor of IP3 receptors on endoplasmic reticulum, a reduction of about 50% of Ca2+ influx was observed, suggesting that the Ca2+ flows moved by the OligoGM1 come not only from intracellular storages, but probably also from the extracellular environment. Accordingly, in the presence of both extracellular (EGTA) and intracellular (BAPTA-AM) Ca2+ chelators the neuritogenic effect induced by OligoGM1 was abolished. The work described in this thesis confirms that the effects of GM1 ganglioside on neuronal differentiation are mediated by its oligosaccharide portion. In particular, here I highlight that the oligosaccharide, initiating a signalling cascade on the cell surface, is responsible alone for the balancing of the intracellular Ca2+ levels that underlie neurite sprouting, which have historically been attributed to the whole GM1 ganglioside and its role as lipid inserted into the plasma membrane. In this way, these data give additional information on the molecular characterization of the mechanisms by which GM1 exerts its neuronal functions.
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Kreutzer, Robert. "Charakterisierung des genetischen Defektes der GM1-Gangliosidose beim Alaskan Husky." Wettenberg : VVB Laufersweiler, 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976072424.

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Books on the topic "GM1"

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Vogel, Patric U. B. GMP-Risikoanalysen. Wiesbaden: Springer Fachmedien Wiesbaden, 2021. http://dx.doi.org/10.1007/978-3-658-35208-0.

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Kim, Cheorl-Ho. GM3 Signaling. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5652-4.

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Fahmi, Ali. Bahaya GMO. Jakarta: Federasi Serikat Petani Indonesia, 2005.

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United States. Navy Dept. Bureau of Medicine and Surgery., ed. GMO manual. Washington, DC: Bureau of Medicine and Surgery, 1995.

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Mahel, Stephane. John Nunn GMI. s.l: Damier de L'Opera, 1990.

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Parekh, Sarad R., ed. The GMO Handbook. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-801-4.

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Priewe, Jesko, and Daniel Tümmers, eds. Kompendium Vorklinik - GK1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-32878-0.

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Guncheon, Michael A. Canon PowerShot G11. New York: Lark Books, 2010.

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Reig, Candid, Susana Cardoso, and Subhas Chandra Mukhopadhyay. Giant Magnetoresistance (GMR) Sensors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37172-1.

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Sauer, Karin, ed. c-di-GMP Signaling. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7240-1.

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Book chapters on the topic "GM1"

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Valk, Jacob, and Marjo S. van der Knaap. "GM1 Gangliosidosis." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 88–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_11.

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van der Knaap, Marjo S., and Jacob Valk. "GM1 Gangliosidosis." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 76–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03078-3_9.

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Senarathne, Udara D., Neluwa-Liyanage R. Indika, Eresha Jasinge, and Karolina M. Stepien. "GM1 Gangliosidosis." In Genetic Syndromes, 1–7. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-319-66816-1_1752-1.

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Charria-Ortiz, Gustavo. "The GM1 Gangliosidoses." In Lysosomal Storage Disorders, 217–28. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-70909-3_15.

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Furukawa, Koichi. "β3-Galactosyltransferase-IV (GM1 Synthase)." In Handbook of Glycosyltransferases and Related Genes, 33–36. Tokyo: Springer Japan, 2002. http://dx.doi.org/10.1007/978-4-431-67877-9_5.

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Issakainen, J., R. Gitzelmann, A. Giedion, and E. Boltshauser. "GM1-Gangliosidose Typ II (juvenile Form)." In Aktuelle Neuropädiatrie 1989, 105–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-93411-7_17.

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Scarpino, O., C. Martinazzo, M. Magi, and R. Bruno. "GM1 Ganglioside Therapy in Acute Ischemic Stroke." In Cerebral Ischemia and Dementia, 435–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76208-6_54.

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Seren, M. S., A. Lazzaro, M. C. Comelli, R. Canella, R. Zanoni, D. Guidolin, and H. Manev. "Monosialoganglioside GM1 in Experimental Models of Stroke." In Cerebral Ischemia and Basic Mechanisms, 125–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78151-3_13.

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Bassi, S., M. G. Albizzati, M. Sbacchi, L. Frattola, and M. Massarotti. "Subacute Phase of Stroke Treated with Ganglioside GM1." In Gangliosides and Neuronal Plasticity, 461–63. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4757-5309-7_38.

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Toffano, G., L. Cavicchioli, S. Calzolari, A. Zanotti, K. Fuxe, and L. F. Agnati. "GM1 Ganglioside Treatment Affects the Plasticity of Striatal Dopamine Receptors." In Dopaminergic Systems and their Regulation, 423–24. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_50.

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Conference papers on the topic "GM1"

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Bernardi, Anna, and Laura Raimondi. "Conformational analysis of GM1 oligosaccharide in water solution." In The first European conference on computational chemistry (E.C.C.C.1). AIP, 1995. http://dx.doi.org/10.1063/1.47679.

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Turnbull, W. Bruce, Bernie L. Precious, Rick E. Randall, and Steve W. Homans. "DISSECTING THE E. COLI HEAT-LABILE TOXIN-GM1 INTERACTION." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.567.

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Danolic, D., M. Heffer, J. Wagner, I. Skrlec, I. Alvir, I. Mamic, L. Susnjar, L. Marcelic, T. Becejac, and M. Puljiz. "EP280 Role of ganglioside GM1 expression in T lymphocytes membranes in cervical cancer development." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.341.

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Zdora, I., B. Huang, N. de Buhr, D. Eikelberg, W. Baumgärtner, and E. Leitzen. "Satellitengliazellen in einem Mausmodell der GM1-Gangliosidose: Aktivierung von Gliazellen und Expression eines Progenitorzellmarkers." In 65. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1750007.

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Eikelberg, D., A. Lehmbecker, G. Brogden, W. Tongtako, K. Hahn, A. Habierski, J. B. Hennermann, et al. "Axonopathie und Reduktion des Membran-widerstands: Hauptmerkmale in einem neuen Mausmodell für die humane GM1 Gangliosidose." In 63. Jahrestagung der Fachgruppe Pathologie der Deutschen Veterinärmedizinischen Gesellschaft. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1712562.

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Nguyen, Khoa, Yuanqing Yan, Chandra Bartholomeusz, Naoto Ueno, Kim-Anh Do, Michael Andreeff, and V. Lokesh Battula. "Abstract 2875: Knockout of ST8SIA1 inhibits tumorigenesis in triple negative breast cancer by inducing PTEN and ganglioside GM1 mediated tumor growth arrest." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2875.

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Fuentes, Daniela E., and Peter J. Butler. "Dynamics of Membrane Rafts, Talin, and Actin at Nascent and Mechanically Perturbed Focal Adhesions." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-54027.

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A single endothelial cell was deformed at the apical surface by binding a functionalized nanoelectrode probe to a predetermined location on the surface of the cell. After identifying the point of contact, as recognized by the electronic signature of the nanoelectrode, and allowing binding to the cell of the fibronectin-functionalized tip, a focal adhesion site was induced at the probe site. The probe was displaced thereby applying a prescribed shear deformation to the surface of the cell. Locations of membrane rafts were identified by cholera toxin, and focal adhesion proteins were assessed using RFP-talin, and GFP-actin. Mechanical coupling and kinetics of assembly of these labeled proteins were measured using time-lapse fluorescent images taken under 60X with a multi-point confocal scanner. Raft marker GM1, Actin, and Talin were observed to sequentially accumulate at probe site with different kinetics not only upon probe contact but also upon deformation. Following deformation, later transient motion of rafts in the opposite direction of initial deformation was observed suggesting that rafts recoil. In conclusion, we report a novel nanoelectrode-based method for controlled manipulation of the cell surface and observed mechanical coupling of focal adhesions and cross-linked lipid rafts.
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Zhu, Yuchuan, and Xulei Yang. "Dynamical Model Research on Energy-Conversion Process of Giant Magnetstrictive Materials-Based Electrohydrostatic Actuator." In ASME/BATH 2015 Symposium on Fluid Power and Motion Control. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/fpmc2015-9559.

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A giant Magnetstrictive materials-based Electro-hydrostatic Actuator (MEHA) is shown by presenting its structure configuration and working principle, which include a Giant Material Actuator (GMA), pump, two one-way check valves, a cylinder and utilize fluid rectification via one-way check valves to amplify the small, high-frequency vibrations of GMA into large motions of a hydraulic cylinder. The established dynamic model of a MEHA involves five submodels from the viewpoint of energy conversion: the dynamic model of the power amplifier; the dynamic magnetization model that describes the relationship between the exciting current and the magnetization of the Giant Magnetostrictive Material (GMM) rod; the magnetoelastic model describing the relationship between the magnetostrictive strain and the magnetization of GMM rod; the kinetic model of the GMA describing the relationship between the GMA displacement (piston displacement of pump) and the magnetostrictive strain; the cylinder motion model. By the simulation to the above model, dynamic characteristics of MEHA are clearly exhibited by the dynamic response curves, which show a good agreement with the experimental data and gives a scientific explanation about the test results.
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Folly, Julia Carvalho, Lara Emanuelle Silva Reis, and Stella Maris Lins Terrena. "Guillain-Barré Syndrome due to Covid-19: A Review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.553.

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Background: With the pandemic of SARS-CoV-2 virus spreading, there has been an increase in the dissemination of information relating the infection to neuromuscular involvement. Articles indicate an increase in cases of GuillainBarré Syndrome immediately or a few weeks after infection by the virus. Objectives: The present study aimed to gather the current knowledge disclosed in the literature about the onset of Guillain-Barré Syndrome (GBS) related to SARS-CoV-2 infection. Methods: The study design was based on PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses), using the Pubmed database, including articles in Portuguese and English language. Results: Articles that indicated an increase in cases of Guillain-Barré Syndrome dated to publications in April 2020 of cases analyzed since February of the same year. Histopathological analyses that identified the virus in the central nervous system of patients, associated with the detection of anti-anglioside antibodies of the anti-GM1, anti-GD1a and anti-GD1b types in the patients analyzed, represent important findings about GBS associated with Covid-19. Pro-inflammatory cytokines present in the immune response as a result of SARS-COV-2 have been associated with the triggering of neuronal injury. In patients analyzed we observed the manifestation of symptoms between 5 and 21 days after Covid-19 infection, similar to the reported GBS interval after other viral infections. Conclusion: The clinical pictures of patients affected by Covid-19 suggest an intense possible relating between infection by the new coronavirus and autoimmune neuromuscular conditions. Further studies are needed on this association, which has not yet been clarified.
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Chen, Bing, Chin Pan, Paul Ponath, Miho Oyasu, Daniel Menezes, and Pina Cardarelli. "Abstract LB-237: BMS-986012, a fully human anti-fucosyl-GM1 antibody has potent in vitro and in vivo antitumor activity in preclinical models of small cell lung cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-237.

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Reports on the topic "GM1"

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Kolyovska, Vera, and Sonya Ivanova. Neurodegenerative Changes and Demyelination in Serum IgG Antibodies to GM1, GD1a and GM3 Gangliosides in Patients with Secondary Progressive Multiple Sclerosis – Preliminary Results. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2019. http://dx.doi.org/10.7546/crabs.2019.01.15.

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Gunay, Selim, Fan Hu, Khalid Mosalam, Arpit Nema, Jose Restrepo, Adam Zsarnoczay, and Jack Baker. Blind Prediction of Shaking Table Tests of a New Bridge Bent Design. Pacific Earthquake Engineering Research Center, University of California, Berkeley, CA, November 2020. http://dx.doi.org/10.55461/svks9397.

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Considering the importance of the transportation network and bridge structures, the associated seismic design philosophy is shifting from the basic collapse prevention objective to maintaining functionality on the community scale in the aftermath of moderate to strong earthquakes (i.e., resiliency). In addition to performance, the associated construction philosophy is also being modernized, with the utilization of accelerated bridge construction (ABC) techniques to reduce impacts of construction work on traffic, society, economy, and on-site safety during construction. Recent years have seen several developments towards the design of low-damage bridges and ABC. According to the results of conducted tests, these systems have significant potential to achieve the intended community resiliency objectives. Taking advantage of such potential in the standard design and analysis processes requires proper modeling that adequately characterizes the behavior and response of these bridge systems. To evaluate the current practices and abilities of the structural engineering community to model this type of resiliency-oriented bridges, the Pacific Earthquake Engineering Research Center (PEER) organized a blind prediction contest of a two-column bridge bent consisting of columns with enhanced response characteristics achieved by a well-balanced contribution of self-centering, rocking, and energy dissipation. The parameters of this blind prediction competition are described in this report, and the predictions submitted by different teams are analyzed. In general, forces are predicted better than displacements. The post-tension bar forces and residual displacements are predicted with the best and least accuracy, respectively. Some of the predicted quantities are observed to have coefficient of variation (COV) values larger than 50%; however, in general, the scatter in the predictions amongst different teams is not significantly large. Applied ground motions (GM) in shaking table tests consisted of a series of naturally recorded earthquake acceleration signals, where GM1 is found to be the largest contributor to the displacement error for most of the teams, and GM7 is the largest contributor to the force (hence, the acceleration) error. The large contribution of GM1 to the displacement error is due to the elastic response in GM1 and the errors stemming from the incorrect estimation of the period and damping ratio. The contribution of GM7 to the force error is due to the errors in the estimation of the base-shear capacity. Several teams were able to predict forces and accelerations with only moderate bias. Displacements, however, were systematically underestimated by almost every team. This suggests that there is a general problem either in the assumptions made or the models used to simulate the response of this type of bridge bent with enhanced response characteristics. Predictions of the best-performing teams were consistently and substantially better than average in all response quantities. The engineering community would benefit from learning details of the approach of the best teams and the factors that caused the models of other teams to fail to produce similarly good results. Blind prediction contests provide: (1) very useful information regarding areas where current numerical models might be improved; and (2) quantitative data regarding the uncertainty of analytical models for use in performance-based earthquake engineering evaluations. Such blind prediction contests should be encouraged for other experimental research activities and are planned to be conducted annually by PEER.
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3

Harris, James, Kelly Lechtenberg, and Nikin Patel. GMS Configuration Guide. Office of Scientific and Technical Information (OSTI), December 2021. http://dx.doi.org/10.2172/1835245.

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4

Mate, Adam. The Carrington GMD project. Office of Scientific and Technical Information (OSTI), October 2019. http://dx.doi.org/10.2172/1571580.

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5

Clement, T. P., and N. L. Jones. RT3D tutorials for GMS users. Office of Scientific and Technical Information (OSTI), February 1998. http://dx.doi.org/10.2172/585058.

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6

Brown, Judith Alice, and Kevin Nicholas Long. Modeling the Effect of Glass Microballoon (GMB) Volume Fraction on Behavior of Sylgard/GMB Composites. Office of Scientific and Technical Information (OSTI), May 2017. http://dx.doi.org/10.2172/1367414.

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7

Shiihi, Solomon, U. G. Okafor, Zita Ekeocha, Stephen Robert Byrn, and Kari L. Clase. Improving the Outcome of GMP Inspections by Improving Proficiency of Inspectors through Consistent GMP Trainings. Purdue University, November 2021. http://dx.doi.org/10.5703/1288284317433.

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Abstract:
Approximately 90% of the pharmaceutical inspectors in a pharmacy practice regulatory agency in West Africa have not updated their training on Good Manufacturing Practice (GMP) inspection in at least eight years. However, in the last two years the inspectors relied on learning-on-the job skills. During this time, the agency introduced about 17% of its inspectors to hands-on GMP trainings. GMP is the part of quality assurance that ensures the production or manufacture of medicinal products is consistent in order to control the quality standards appropriate for their intended use as required by the specification of the product. Inspection reports on the Agency’s GMP inspection format in-between 2013 to 2019 across the six geopolitical zones in the country were reviewed retrospectively for gap analysis. Sampling was done in two phases. During the first phase sampling of reports was done by random selection, using a stratified sampling method. In the second phase, inspectors from the Regulatory Agency from different regions were contacted on phone to send in four reports each by email. For those that forwarded four reports, two, were selected. However for those who forwarded one or two, all were considered. Also, the Agency’s inspection format/checklist was compared with the World Health Organization (WHO) GMP checklist and the GMP practice observed. The purpose of this study was to evaluate the reporting skills and the ability of inspectors to interpret findings vis-à-vis their proficiency in inspection activities hence the efficiency of the system. Secondly, the study seeks to establish shortfalls or adequacies of the Agency’s checklist with the aim of reviewing and improving in-line with best global practices. It was observed that different inspectors have different styles and methods of writing reports from the same check-list/inspection format, leading to non-conformances. Interpretations of findings were found to be subjective. However, it was also observed that inspection reports from the few inspectors with the hands-on training in the last two year were more coherent. This indicates that pharmaceutical inspectors need to be trained regularly to increase their knowledge and skills in order to be kept on the same pace. It was also observed that there is a slight deviation in placing sub indicators under the GMP components in the Agency’s GMP inspection format, as compared to the WHO checklist.
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8

Woodroffe, Jesse R., and Lisa Marie Winter. Update on LANL GMD Research Tasks. Office of Scientific and Technical Information (OSTI), September 2018. http://dx.doi.org/10.2172/1469512.

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9

Zuehlke, A. C. GMS/DACS interface acceptance test report. Office of Scientific and Technical Information (OSTI), October 1994. http://dx.doi.org/10.2172/10192320.

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10

Zuehlke, A. C. GMS/DACS interface acceptance test procedure. Office of Scientific and Technical Information (OSTI), September 1994. http://dx.doi.org/10.2172/10185766.

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