Relevant bibliographies by topics / HIGM1

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'HIGM1'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "HIGM1"

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Vavassori, Valentina, Elisabetta Mercuri, Genni Marcovecchio, Maria Carmina Castiello, Daniele Canarutto, Claudia Asperti, Aurelien Jacob, et al. "Towards Clinical Translation of Hematopoietic Cell Gene Editing for Treating Hyper-IgM Type 1." Blood 138, Supplement 1 (November 5, 2021): 3978. http://dx.doi.org/10.1182/blood-2021-148572.

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Abstract Hyper-IgM Type 1 (HIGM1) is caused by mutations of CD40L, whose absence in CD4 T cells impairs signaling for B cell activation and Ig class-switching. Since unregulated CD40L expression leads to lymphoproliferations/lymphomas in the mouse model of the disease, gene correction must preserve the physiological regulation of the gene. Gene editing of either autologous T cells or hematopoietic stem cells (HSC) held promise for treating HIGM1. We developed a "one size fits all" editing strategy to insert a 5'-truncated corrective CD40L cDNA in the first intron of the native human gene, effectively making expression conditional to targeted insertion in the intended locus. By exploiting a protocol that preserves T stem memory cells (TSCM), we reproducibly obtained ~40% of editing efficiency in healthy donor and patients derived T cells, restoring regulated, although partial, CD40L surface expression. The reconstituted level of expression, however, was sufficient to fully restore helper function to B cells. In order to select, track and potentially deplete edited T cells, we coupled the corrective cDNA with a clinically compatible selector gene and confirmed that enriched T cells preserved their engraftment capacity in NSG mice. Unexpectedly, the presence of an IRES-linked downstream coding frame counteracted the shorter half-life of transcript from the edited locus, allowing replenishment of intracellular stores and surface translocation of physiological amounts of CD40L upon activation. We also tailored the CD40L editing strategy to human HSC, reaching up to 15-30% editing in HSC long term engrafting NSG mice, depending on the HSC source. We then modelled the therapeutic potential of both T cell and HSC gene therapy by infusing increasing proportions of WT murine cells, as surrogates of edited cells, in HIGM1 mice. Administration of functional T cells at clinically relevant doses in HIGM1 mice, preconditioned or not with different lymphodepleting regimens, achieved long term stable T cell engraftment and partial rescue of antigen specific IgG response and germinal center formation in splenic follicles after vaccination with a thymus dependent antigen. Remarkably, infusion of T cells from mice pre-exposed to the antigen, mimicking treatment of chronically infected patients, was effective even in absence of conditioning and protected the mice from a disease relevant infection induced by the opportunistic pathogen Pneumocystis murina. Transplantation of functional T cells admixed with an equal number of HIGM1 T cells resulted in lower vaccination response, indicating competition between WT and HIGM1 cells and implying that increasing the fraction of corrected cells in the graft by selection would improve immune reconstitution. Concerning HSC gene therapy, transplanting 25% WT cells along with HIGM1 ones in HIGM1 mice - mirroring the editing efficiencies achieved in human HSC - rescued antigen specific IgG response and established protection from pathogen comparably to T cell therapy. These findings suggest that autologous edited T cells can provide immediate and substantial benefits to HIGM1 patients and position T cell as competitive strategy to HSC gene therapy, because of more straightforward translation, lower safety challenges and potentially comparable clinical benefits. We thus embarked in assessing GMP compliant reagents and protocols for T cell activation, culture and editing and developed a scalable manufacturing process. Optimization of clinical grade culture conditions allowed further increasing editing efficiency, total cellular yield and maintenance of TSCM thus paving the way to the design of a clinical trial. Disclosures Naldini: Genenta Science: Consultancy, Current equity holder in publicly-traded company, Membership on an entity's Board of Directors or advisory committees, Other: Founder.
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Callard, R. E., S. H. Smith, J. Herbert, G. Morgan, M. Padayachee, S. Lederman, L. Chess, R. A. Kroczek, W. C. Fanslow, and R. J. Armitage. "CD40 ligand (CD40L) expression and B cell function in agammaglobulinemia with normal or elevated levels of IgM (HIM). Comparison of X-linked, autosomal recessive, and non-X-linked forms of the disease, and obligate carriers." Journal of Immunology 153, no. 7 (October 1, 1994): 3295–306. http://dx.doi.org/10.4049/jimmunol.153.7.3295.

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Abstract Hyper-IgM syndrome is a rare immunodeficiency characterized by low or absent IgG, IgA, and IgE with normal or elevated levels of IgM. It can occur as an acquired or familial disorder with either X-linked or autosomal modes of inheritance. The X-linked form (HIGM1) is a result of mutations in the CD40 ligand (CD40L) gene, but the defect in non-X-linked forms of the disease (HIM) has not been determined. We show here that CD40L expression on activated T cells from non-X-linked patients can be detected by CD40Fc, 5c8 Mab, and anti-TRAP, whereas activated T cells from HIGM1 patients either had no detectable CD40L (Type I), or stained with anti-TRAP but not CD40Fc or 5c8 (Type II). Activated T cells from obligate carriers varied from low to normal expression of CD40L. B cells from HIGM1 and non-X-linked HIM patients proliferated in response to CD40L. Costimulation of B cells from HIGM1, from sporadic HIM, or from non-X-linked HIM patients with CD40L plus IL-2 resulted in some IgM production, but no significant IgG or IgA. Costimulation with CD40L plus IL-10 resulted in significant IgG and/or IgA secretion by B cells from some HIGM1 patients, but consistently failed to stimulate IgG or IgA secretion by B cells from non-X-linked patients. In addition, costimulation with CD40L and IL-4 failed to induce IgE secretion by B cells from one non-X-linked HIM patient, and induced a weak response in another. These results suggest that patients with non-X-linked forms of HIM may have an intrinsic B cell defect preventing heavy chain switching, which is not related to expression of CD40L.
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Shimoda, Michiko, Yoko Takada, Emanual Maverakis, Brunhilde Felding, and Yoshikazu Takada. "CD40L acts as an allosteric activator of integrins for signal transduction independent of inside-out signaling." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 24.04. http://dx.doi.org/10.4049/jimmunol.206.supp.24.04.

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Abstract CD40L plays a major role in immune response and is a target for inflammatory disease therapy. Besides CD40, CD40L binds to several integrins but their role in signaling is unclear. We showed that integrins αvβ3 and α5β1 bind to the CD40L trimeric interface through classical ligand binding site of integrins (site 1). Several CD40L mutants from HIGM1 (hyper-IgM syndrome type 1) patients were clustered in trimeric interface and defective in integrin binding, and in NF-κB and B cell activation, but still bound CD40 and acted as antagonists of CD40L signaling. Thus, integrins play a critical role in CD40L signaling. Previous studies showed that CX3CL1 and sPLA2-IIA can activate integrins by binding to a recently identified allosteric site (site 2) of integrins. Using cell-free assays, we found that soluble (s)-CD40L activated soluble integrins, α4β1, αvβ3 and α5β1, and induced their binding to known specific ligands independent of inside-out signaling. Also, sCD40L activated cell-surface integrins in CHO cells lacking CD40. Finally, sCD40L bound to a cyclic peptide derived from site 2. These findings indicate that CD40L acts as an allosteric activator of integrins by binding to site 2. Docking simulation predicted that the integrin site 2-binding site of CD40L is located outside of CD40L trimer. Importantly, four HIGM1 mutations are clustered in the predicted site 2-binding site of CD40L. The K143T and G144E mutants were the most defective in integrin activation, indicating that integrin binding occurs around these residues of the predicted site 2-binding site. We propose that allosteric integrin activation by CD40L plays a role in CD40L signaling and that defective integrin site 2-binding may be causal for defective CD40L signaling in HIGM1.
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Life, P., J. F. Gauchat, V. Schnuriger, S. Estoppey, G. Mazzei, A. Durandy, A. Fischer, and J. Y. Bonnefoy. "T cell clones from an X-linked hyper-immunoglobulin (IgM) patient induce IgE synthesis in vitro despite expression of nonfunctional CD40 ligand." Journal of Experimental Medicine 180, no. 5 (November 1, 1994): 1775–84. http://dx.doi.org/10.1084/jem.180.5.1775.

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The induction of immunoglobulin E (IgE) switching in B cells requires at least two signals. The first is given by either of the soluble lymphokines interleukin 4 (IL-4) or IL-13, whereas the second is contact dependent. It has been widely reported that a second signal can be provided by the CD40 ligand (CD40L) expressed on the surface of T cells, mast cells, and basophils. A defect in the CD40L has been shown recently to be responsible for the lack of IgE, IgA, and IgG, characteristic of the childhood X-linked immunodeficiency, hyper IgM syndrome (HIGM1). IgE can however be detected in the serum of some HIGM1 patients. In this study, we isolated T cell clones and lines using phytohemagglutinin (PHA) and allergen, respectively, from the peripheral blood of one such patient who expressed a truncated form of CD40L, and investigated their ability to induce IgE switching in highly purified, normal tonsillar B cells in vitro. Unexpectedly, 4 of 12 PHA clones tested induced contact-dependent IgE synthesis in the presence of exogenous IL-4. These clones were also shown to strongly upregulated IL-4-induced germline epsilon RNA and formed dense aggregates with B cells. Of the four helper clones, three were CD8+, of which two were characteristic of the T helper cell 2 (Th2) subtype. Two allergen-specific HIGM1 T cell lines, both of the Th0 subtype, could also drive IgE synthesis when prestimulated using specific allergen. All clones and lines were negative for surface expression of CD40L, and the mutated form of CD40L was confirmed for a representative clone by RNase protection assay and sequencing. The IgE helper activity could not be attributed to membrane tumor necrosis factor alpha (TNF-alpha) although it was strongly expressed on activated clones, and the addition of neutralizing anti-TNF-alpha antibody did not abrogate IgE synthesis. These results therefore suggest the involvement of T cell surface molecules other than CD40L in the induction of IgE synthesis, and that these molecules may also be implicated in other aspects of T-B cell interactions.
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Padayachee, M., R. J. Levinsky, C. Kinnon, A. Finn, C. McKeown, C. Feighery, L. D. Notarangelo, R. W. Hendriks, A. P. Read, and S. Malcolm. "Mapping of the X linked form of hyper IgM syndrome (HIGM1)." Journal of Medical Genetics 30, no. 3 (March 1, 1993): 202–5. http://dx.doi.org/10.1136/jmg.30.3.202.

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Kroczek, Richard A., Daniel Graf, Duilio Brugnoni, Silvia Giliani, Ulf Korthauer, Alberto Ugazio, Gabriele Senger, Hans W. Mages, Anna Villa, and Luigi D. Notarangelo. "Defective Expression of CD40 Ligand on T Cells Causes "X-Linked Immunodeficiency with Hyper-IgM (HIGM1)"." Immunological Reviews 138, no. 1 (April 1994): 39–59. http://dx.doi.org/10.1111/j.1600-065x.1994.tb00846.x.

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Padayachee, M., C. Feighery, A. Finn, C. McKeown, R. J. Levinsky, C. Kinnon, and S. Malcolm. "Mapping of the x-linked form of hyper-IgM syndrome (HIGM1) to Xq26 by close linkage to HPRT." Genomics 14, no. 2 (October 1992): 551–53. http://dx.doi.org/10.1016/s0888-7543(05)80270-8.

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Fontana, Stefania, Daniele Moratto, Surinder Mangal, Maria De Francesco, William Vermi, Simona Ferrari, Fabio Facchetti, et al. "Functional defects of dendritic cells in patients with CD40 deficiency." Blood 102, no. 12 (December 1, 2003): 4099–106. http://dx.doi.org/10.1182/blood-2003-04-1244.

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Abstract We have recently identified 2 patients with a rare autosomal recessive form of hyper IgM disease, known as HIGM3, caused by mutations in the CD40 gene. These patients had opportunistic infections observed on X-linked hyper IgM syndrome (HIGM), suggesting that the CD40-CD40 ligand interaction is important for promoting T-cell-mediated immunity. To evaluate whether innate immunity signals may substitute CD154 for inducing the maturation of dendritic cells (DCs), we analyzed monocyte-derived DCs in these patients. Monocyte-derived DCs of HIGM3 subjects on ex vivo stimulation with tumor necrosis factor-α (TNF-α) or lipopolysaccharide (LPS) combined with interferon-γ (IFN-γ) normally express all the markers of mature DCs, such as CD83 and DC-LAMP. However, cell surface levels of HLA-DR in mature DCs are reduced, as is costimulatory activity of these cells for allogeneic naive T cells. In addition, CD40-deficient DCs secrete lower amounts of interleukin-12 (IL-12) but larger quantities of IL-10 than control subjects. Finally, analysis of circulating plasmacytoid DCs demonstrates a normal percentage of this subset in CD40-deficient cells, but IFN-α secretion in response to herpes simplex virus 1 (HSV-1) infection is severely reduced in patients. These observations suggest that the severe impairment of DC maturation may contribute to the defect of T-cell-mediated immunity observed in HIGM3 patients. (Blood. 2003;102:
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Hollenbaugh, D., L. H. Wu, H. D. Ochs, S. Nonoyama, L. S. Grosmaire, J. A. Ledbetter, R. J. Noelle, H. Hill, and A. Aruffo. "The random inactivation of the X chromosome carrying the defective gene responsible for X-linked hyper IgM syndrome (X-HIM) in female carriers of HIGM1." Journal of Clinical Investigation 94, no. 2 (August 1, 1994): 616–22. http://dx.doi.org/10.1172/jci117377.

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Hoang, Ngoc H., Vera Strogolova, Jaramys J. Mosley, Rosemary A. Stuart, and Jonathan Hosler. "Hypoxia-inducible gene domain 1 proteins in yeast mitochondria protect against proton leak through complex IV." Journal of Biological Chemistry 294, no. 46 (October 7, 2019): 17669–77. http://dx.doi.org/10.1074/jbc.ra119.010317.

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Hypoxia-inducible gene domain 1 (HIGD1) proteins are small integral membrane proteins, conserved from bacteria to humans, that associate with oxidative phosphorylation supercomplexes. Using yeast as a model organism, we have shown previously that its two HIGD1 proteins, Rcf1 and Rcf2, are required for the generation and maintenance of a normal membrane potential (ΔΨ) across the inner mitochondrial membrane (IMM). We postulated that the lower ΔΨ observed in the absence of the HIGD1 proteins may be due to decreased proton pumping by complex IV (CIV) or enhanced leak of protons across the IMM. Here we measured the ΔΨ generated by complex III (CIII) to discriminate between these possibilities. First, we found that the decreased ΔΨ observed in the absence of the HIGD1 proteins cannot be due to decreased proton pumping by CIV because CIII, operating alone, also exhibited a decreased ΔΨ when HIGD1 proteins were absent. Because CIII can neither lower its pumping stoichiometry nor transfer protons completely across the IMM, this result indicates that HIGD1 protein ablation enhances proton leak across the IMM. Second, we demonstrate that this proton leak occurs through CIV because ΔΨ generation by CIII is restored when CIV is removed from the cell. Third, the proton leak appeared to take place through an inactive population of CIV that accumulates when HIGD1 proteins are absent. We conclude that HIGD1 proteins in yeast prevent CIV inactivation, likely by preventing the loss of lipids bound within the Cox3 protein of CIV.
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Dissertations / Theses on the topic "HIGM1"

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MERCURI, ELISABETTA. "PRECLINICAL MODELING HIGHLIGHTS THE THERAPEUTIC POTENTIAL OF THE ADOPTIVE TRANSPLANT OF GENE CORRECTED T CELLS IN X-LINKED HYPER-IGM IMMUNODEFICIENCY." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263922.

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La terapia genica di cellule staminali ematopoietiche (HSC) ha prodotto benefici clinici in diversi pazienti affetti da una varietà di malattie genetiche. Tuttavia, l’uso di vettori che si integrano nel genoma in modo semi-casuale pone il rischio di mutagenesi inserzionale e di una espressione del transgene ectopica/non regolata. Quest’ultimo problema è particolarmente rilevante quando si trattano geni strettamente regolati attivi sulla proliferazione cellulare, come il gene CD40LG, la cui espressione sulle cellule T attivate porta all’attivazione contatto-dipendente delle cellule B, alla loro proliferazione ed allo scambio di classe delle immunoglobuline. Poichè le sue mutazioni causano l’immunodeficienza legata all’X con iper-IgM (HIGM1), il trasferimento genico in HSC è stato proposto come potenziale trattamento per questa sindrome. Anche se piccole quantità di cellule trasdotte hanno ripristinato la funzione immunitaria umorale e cellulare in un modello murino di HIGM1, l’espressione costitutiva di CD40LG in timociti o in cellule T periferiche ha portato a linfoproliferazioni, molte delle quali sono progredite a linfom. Le strategie di riparazione genica che preservano il controllo fisiologico dell’espressione del gene corretto potrebbero quindi rappresentare un approccio più promettente per il trattamento di HIGM1. In questo studio sfruttiamo il meccanismo Homology Directed Repair (HDR) per la correzione in situ della maggior parte delle mutazioni responsabili della sindrome HIGM1 presenti nel gene CD40L, con l’obiettivo di ristabilirne la funzione e il controllo dell’espressione. In particolare sfruttiamo il sistema CRISPR/Cas9 per promuovere l’integrazione sito-specifica di una copia funzionale di parte del gene CD40L a valle del suo promotore endogeno, correggendo così la maggior parte delle mutazioni responsabili della malattia. Dato che il difetto genetico non è deleterio per le cellule T, questo tipo di malattia ci offre l’opportunità unica di sviluppare una terapia genica basata sulla correzione di cellule T autologhe. Al fine di stabilire quali sono le dosi terapeutiche e le condizioni di trapianto necessarie per ottenere la ricostituzione immunitaria e il ripristino delle funzioni immunologiche con cellule corrette, abbiamo infuso diverse dosi di cellule T WT in topi HIGM1 pre-condizionati o meno con diversi regimi linfodepletanti ed eseguito trapianti competitivi di cellule staminali ematopoietiche WT e Cd40lg - / - nel modello animale. Mentre l’ analisi del sangue periferico ha dimostrato la persistenza a lungo termine di cellule T in tutte le condizioni, sono stati ottenuti livelli di attecchimento più elevati nei topi trapiantati dopo il trattamento chemioterapico con ciclofosfamide (CPA). Tutti i topi trapiantati hanno mostrato un parziale ripristino della risposta IgG specifica dopo immunizzazione con TNP-KLH, ma è stato osservato un ripristino più elevato nei topi pre-condizionati con CPA. Questi topi hanno anche mostrato la presenza di centri germinativi nella milza. Topi HIGM1 ricostituiti con dosi crescenti di HSPC WT hanno mostrato un ripristino dose-dipendente della risposta immunitaria T dipendente. In particolare, abbiamo dimostrato che il 10% di HSPC funzionali è sufficiente a ripristinare parzialmente la capacità di produrre anticorpi specifici contro diversi antigeni oltre che ad attenuare l'infezione in topi HIGM1 inoculati con il patogeno Pneumocystis murina. Il nostro obiettivo futuro è quello di dimostrare il ripristino della risposta immunitaria contro l'infezione da pneumocystis murina in topi HIGM1 trapiantati con cellule T CD4 + WT. In caso di successo, i nostri risultati saranno strumentali per stabilire il potenziale terapeutico di un approccio di correzione genica basato sulle cellule T per il trattamento della sindrome HIGM1 che potrebbe fungere da terapia ponte per una terapia definitiva basata sul trapianto di HSPC corrette.
Background The X-linked hyper-IgM syndrome type I (HIGM1) is caused by inactivating mutations in the CD40 ligand gene (CD40LG) that disrupt the T cell helper function on B cells and macrophages. This disease represents an ideal candidate for a gene correction strategy because preclinical studies of Hematopoietic Stem Cell (HSC) gene therapy have already shown i) evidence of potential efficacy even with few amounts of transduced cells; ii) critical safety issues due to unregulated transgene expression. Since in HIGM1 the genetic defect is not lethal to T cells, we aim to apply our gene editing strategy on autologous T cells that could be used to provide immediate therapeutic benefit to the patients by resolving pre-existing infections prior to a definitive HSPC transplant. Methods To establish which are the therapeutic threshold levels and transplant conditions required to achieve immune reconstitution and functional immunologic restoration with corrected cells, we infused different doses of WT T cells into HIGM1 mice pre-conditioned or not with different lymphodepleting regimens and performed competitive transplants of WT and Cd40lg-/- HSPC in the mouse model. Results While longitudinal blood analyses showed a long-term, stable T cell engraftment in all the conditions, highest engraftment rates were obtained in mice transplanted after chemotherapy treatment with cyclophosphamide (CPA). All the transplanted mice showed a partial rescue of the antigen-specific IgG response after immunization with Keyhole Limpet Hemocyanin (TNP-KLH) but a higher rescue was observed in mice pre-conditioned with CPA. These mice also showed the presence of TNP-KLH specific IgG producing B cells and germinal centers within splenic lymphoid follicles. HIGM1 mice reconstituted with increasing proportions of WT HSPC displayed a dose-dependent rescue of the T cell mediated immune response. In particular we found that 10% of WT HSPC is sufficient to partially restore serologic immunity against different antigens as well as to attenuate infection in HIGM1 mice challenged with Pneumocystis murina. Conclusions Our current efforts are aimed to demonstrate functional restoration of the immune response against Pneumocystis murina infection in HIGM1 mice that received adoptive transfer of WT CD4+ T cells. If successful, our findings will be instrumental to establish the therapeutic potential of a T cell gene correction approach for the treatment of the HIGM1 disease that could act as a bridge therapy to the HSPC-based strategy.
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Pereira, Renato de Pontes. "HIGMN : an IGMN-based hierarchical architecture and its applications for robotic tasks." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/80752.

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O recente campo de Deep Learning introduziu a área de Aprendizagem de Máquina novos métodos baseados em representações distribuídas e abstratas dos dados de treinamento ao longo de estruturas hierárquicas. A organização hierárquica de camadas permite que esses métodos guardem informações distribuídas sobre os sinais sensoriais e criem conceitos com diferentes níveis de abstração para representar os dados de entrada. Este trabalho investiga o impacto de uma estrutura hierárquica inspirada pelas ideias apresentadas em Deep Learning, e com base na Incremental Gaussian Mixture Network (IGMN), uma rede neural probabilística com aprendizagem online e incremental, especialmente adequada para as tarefas de robótica. Como resultado, foi desenvolvida uma arquitetura hierárquica, denominada Hierarchical Incremental Gaussian Mixture Network (HIGMN), que combina dois níveis de IGMNs. As camadas de primeiro nível da HIGMN são capazes de aprender conceitos a partir de dados de diferentes domínios que são então relacionados na camada de segundo nível. O modelo proposto foi comparado com a IGMN em tarefas de robótica, em especial, na tarefa de aprender e reproduzir um comportamento de seguir paredes, com base em uma abordagem de Aprendizado por Demonstração. Os experimentos mostraram como a HIGMN pode executar três diferentes tarefas em paralelo (aprendizagem de conceitos, segmentação de comportamento, e aprendizagem e reprodução de comportamentos) e sua capacidade de aprender um comportamento de seguir paredes e reproduzi-lo em ambientes desconhecidos com novas informações sensoriais. A HIGMN conseguiu reproduzir o comportamento de seguir paredes depois de uma única, simples e curta demonstração do comportamento. Além disso, ela adquiriu conhecimento de diferentes tipos: informações sobre o ambiente, a cinemática do robô, e o comportamento alvo.
The recent field of Deep Learning has introduced to Machine Learning new meth- ods based on distributed abstract representations of the training data throughout hierarchical structures. The hierarchical organization of layers allows these meth- ods to store distributed information on sensory signals and to create concepts with different abstraction levels to represent the input data. This work investigates the impact of a hierarchical structure inspired by ideas on Deep Learning and based on the Incremental Gaussian Mixture Network (IGMN), a probabilistic neural network with an on-line and incremental learning, specially suitable for robotic tasks. As a result, a hierarchical architecture, called Hierarchical Incremental Gaussian Mixture Network (HIGMN), was developed, which combines two levels of IGMNs. The HIGMN first-level layers are able to learn concepts from data of different domains that are then related in the second-level layer. The proposed model was compared with the IGMN regarding robotic tasks, in special, the task of learning and repro- ducing a wall-following behavior, based on a Learning from Demonstration (LfD) approach. The experiments showed how the HIGMN can perform parallely three different tasks concept learning, behavior segmentation, and learning and repro- ducing behaviors and its ability to learn a wall-following behavior and to perform it in unknown environments with new sensory information. HIGMN could reproduce the wall-following behavior after a single, simple, and short demonstration of the behavior. Moreover, it acquired different types of knowledge: information on the environment, the robot kinematics, and the target behavior.
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Parmar, Gaganvir. "Protein Factors Regulating Mitochondrial Respiratory Supercomplexes." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42350.

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Berger, Bettina [Verfasser]. "The role of HIG1/MYB51 in the regulation of indolic glucosinolate biosynthesis / vorgelegt von Bettina Berger." 2007. http://d-nb.info/985441240/34.

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Book chapters on the topic "HIGM1"

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Lukas, Thomas J., Daniela V. Rosa, Luiz Alexandre V. Magno, Bruno R. Souza, Marco A. Romano-Silva, Hisao Masai, Kazuhisa Kohda, et al. "Dfp1/Him1/Rad35 (Schizosaccharomyces pombe), Spo6 (a Second Dbf4 Homologue in S. pombe)." In Encyclopedia of Signaling Molecules, 518. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100350.

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"Dfp1/Him1/Rad35 (Schizosaccharomyces pombe)." In Encyclopedia of Signaling Molecules, 1367. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_100987.

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Russo, Barbara, Marco Scotto, Alberto Sillitti, and Giancarlo Succi. "Coordination in Agile and Open Source." In Agile Technologies in Open Source Development, 51–74. IGI Global, 2010. http://dx.doi.org/10.4018/978-1-59904-681-5.ch005.

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Although the situation in the software industry is improved in the last years, the percentage of software project cancelled 18%, or challenged (late, over budget, and with less than the required features) 53% is still high1. Researchers and practitioners are looking for the magic solution or the silver bullet that will allow software companies to overcome the software crisis (Brooks, 1987). New development approaches like AMs and OSD models are some of the solutions identified (Feller & Fitzgerald, 2002; Abrahamsson et al., 2003). One critical problem in software development consist of coordinating interdependent processes involving many interacting stakeholders with different interests, points of view, and expectations (Toffolon & Dakhli, 2000).
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"Hyper-IgM Syndrome (HIGM, HIM, X-linked immunodeficiency with hyper IgM)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 940. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8050.

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"This Group of Primary Antibody Deficiencies Are also Known as Hyper IgM Syndromes (HIGMs)." In Encyclopedia of Medical Immunology, 638. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_300350.

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Conference papers on the topic "HIGM1"

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Eyres, L. A., C. B. Ebert, J. S. Harris, M. M. Fejer, and H. C. Chui. "Fabrication of GaAs Orientation Template Substrates for Quasi-Phasematched Guided-Wave Nonlinear Optics." In Nonlinear Guided Waves and Their Applications. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/nlgw.1995.nfc3.

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Quasi-phasematched nonlinear optical frequency conversion in waveguides is a flexible and efficient technique for generating visible and infrared radiation from low-power near infrared diode lasers. While demonstrated conversion efficiencies have been high1-3, a formidable difficulty remains in the path of widespread implementation of waveguide frequency conversion techniques. The separately fabricated diode lasers and nonlinear waveguides must be aligned together to sub-micron tolerances with high yield and excellent long-term reliability. Monolithic integration of diode lasers and nonlinear devices onto the same substrate is an attractive solution to this problem, particularly if the nonlinear devices are fabricated in semiconductor materials.
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Blumencranz, LE, SC Shivers, S. Untch, TD Treece, E. Yoder, PW Blumencranz, and CE Cox. "Abstract P5-16-05: MINT trial yields MammaPrint High1/High2 risk classes associated with significant differences in pCR and receptor subtype." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p5-16-05.

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Wolf, Denise M., Christina Yau, Lamorna Brown-Swigart, Gillian Hirst, Meredith Buxton, Melissa Paoloni, Olufunmilayo Olopade, et al. "Abstract 859: Gene and pathway differences between MammaPrint High1/High2 risk classes: results from the I-SPY 2 TRIAL in breast 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.am2016-859.

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Yau, Christina, Denise M. Wolf, Ashish Sanil, Jo Chien, Anne Wallace, Judy Boughey, Doug Yee, et al. "Abstract P3-06-29: MammaPrint High1/High2 risk class as a biomarker of response to neratinib plus standard neoadjuvant therapy for breast cancer in the I-SPY 2 TRIAL." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p3-06-29.

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Wolf, Denise M., Christina Yau, Ashish Sanil, Jo Chien, Anne Wallace, Angela DeMichele, Hank Kaplan, et al. "Abstract P3-06-25: MammaPrint High1/High2 risk class as a biomarker of response to veliparib/carboplatin plus standard neoadjuvant therapy for breast cancer in the I-SPY 2 TRIAL." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p3-06-25.

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Wolf, DM, C. Yau, A. Sanil, A. Glas, C. Petricoin, J. Wulfkuhle, L. Brown-Swigart, et al. "Abstract S2-06: DNA repair deficiency biomarkers and MammaPrint high1/(ultra)high2 risk as predictors of veliparib/carboplatin response: Results from the neoadjuvant I-SPY 2 trial for high risk breast cancer." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-s2-06.

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