Relevant bibliographies by topics / Aif1

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Academic literature on the topic 'Aif1'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Aif1"

1

Wissing, Silke, Paula Ludovico, Eva Herker, et al. "An AIF orthologue regulates apoptosis in yeast." Journal of Cell Biology 166, no. 7 (2004): 969–74. http://dx.doi.org/10.1083/jcb.200404138.

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Apoptosis-inducing factor (AIF), a key regulator of cell death, is essential for normal mammalian development and participates in pathological apoptosis. The proapoptotic nature of AIF and its mode of action are controversial. Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis. Similar to mammalian AIF, Ynr074cp is located in mitochondria and translocates to the nucleus of yeast cells in response to apoptotic stimuli. Purified Ynr074cp degrades yeast nuclei and plasmid DNA. YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis. Conversely, overexpression of Ynr074cp strongly stimulates apoptotic cell death induced by hydrogen peroxide and this effect is attenuated by disruption of cyclophilin A or the yeast caspase YCA1. We conclude that Ynr074cp is a cell death effector in yeast and rename it AIF-1 (Aif1p, gene AIF1).
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Gong, Xiaocheng, Xuepeng Li, Xin You, et al. "AIF1 was identified as an up-regulated gene contributing to CSFV Shimen infection in porcine alveolar macrophage 3D4/21 cells." PeerJ 8 (February 17, 2020): e8543. http://dx.doi.org/10.7717/peerj.8543.

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Classical swine fever (CSF) is a disease that is characterized by diffuse hemorrhaging, high fever, and high mortality rates. The pro-inflammatory characteristics of allograft inflammatory factor 1 (AIF1) have been well documented; however, insufficient attention has been given to porcine AIF1. In the present study, AIF1 was identified as a key player contributing to CSFV Shimen infection in porcine alveolar macrophage (PAM) 3D4/21 cell line. Our evaluation showed that AIF1 mRNA and protein are expressed at a time-dependent high level in CSFV Shimen-infected PAM 3D4/21 cells. The transcription and translation of IL6 were also significantly upregulated in infected PAM 3D4/21 cells. By utilizing overexpression RNAs approach, we showed that the cellular AIF1 induced an increased IL6 in PAM 3D4/21 cells. Furthermore, silencing of AIF1 suppressed CSFV Shimen-induced IL6 production in PAM 3D4/21 cells and also inhibited CSFV replication, whereas overexpression of recombinant AIF1 was beneficial for the replication of CSFV Shimen and promoting IL6 production in CSFV Shimen-infected PAM 3D4/21 cells. It is suggested CSFV Shimen induced IL6 in PAM 3D4/21 cells via AIF1 activation, which help clarify the AIF1-related inflammatory processes that occur on CSFV Shimen infected macrophages.
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Chai, Yi, Wei Liu, Junhua Wang, Libo Hu, and Yuqi Zhang. "IMMU-29. AIF1 IS A PROGNOSTIC BIOMARKER AND CORRELATED WITH IMMUNE INFILTRATES IN GLIOMAS." Neuro-Oncology 22, Supplement_3 (2020): iii365. http://dx.doi.org/10.1093/neuonc/noaa222.383.

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Abstract Gliomas remain highly variable clinical behaviors, leading to emerging studies to identify prognostic factors. AIF1 (Allograft Inflammatory Factor 1) is critical for promoting both macrophage- and dendritic cells (DCs)-mediated inflammatory response and growth of vascular smooth muscle cells and T-lymphocytes. Through comparative analyses of primary LGG patients from The Cancer Genome Atlas (TCGA) dataset and Chinese Glioma Genome Atlas(CGGA) dataset, we reported that the expression level and methylation level of AIF1 gene vary among glioma patients and AIF1 expression or gene body methylation is significantly associated with glioma patient survival. Cox regression results confirmed that AIF1 played an independent predictor of survival in lower-grade glioma(LGG), with a cox coefficient of 0.251 indicating a worse prognosis. Moreover, AIF1 expression was positively correlated with infiltrating levels of CD4+ T and B cells, macrophages, neutrophils, and DCs in LGG and glioblastoma(GBM). AIF1 expression also showed strong correlations with specific immune cell markers in LGG and GBM. In addition, AIF1 expression potentially contributed to the regulation of glioma-associated macrophages and microglia. In conclusion, our findings suggested that AIF1 was correlated with prognosis and immune infiltrating levels, and it can be used as a prognostic factor in gliomas.
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Zheng, Wei, Dejian Zhao, Hui Zhang, Prameladevi Chinnasamy, Nicholas Sibinga, and Jeffrey W. Pollard. "Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases." Wellcome Open Research 6 (March 8, 2021): 52. http://dx.doi.org/10.12688/wellcomeopenres.16569.1.

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Background: Metastatic breast cancer cells recruit macrophages (metastasis-associated macrophages, or MAMs) to facilitate their seeding, survival and outgrowth. However, a comprehensive understanding of the gene expression program in MAMs and how this program contributes to metastasis remain elusive. Methods: We compared the transcriptomes of MAMs recruited to lung metastases and resident alveolar macrophages (RAMs) and identified a large variety of differentially expressed genes and their associated signaling pathways. Some of the changes were validated using qRT-PCR and immunofluorescence. To probe the functional relevance to metastatic growth, a gene-targeting mouse model of female mice in the C57BL6/J background was used to study allograft inflammatory factor 1 (AIF1, also known as ionized calcium-binding adapter molecule 1 or IBA1). Results: Interferon signaling is one of the most activated pathways in MAMs, with strong upregulation of multiple components of the pathway and a significant enrichment for the gene signatures of interferon-alpha-treated human macrophages. Aif1, an interferon-responsive gene that regulates multiple macrophage activities, was robustly induced in MAMs. Aif1 deficiency in MAMs, however, did not affect development of lung metastases, suggesting that AIF1 indicates MAM activation but is dispensable for regulating metastasis. Conclusions: The drastically different gene expression profile of MAMs as compared to RAMs suggests an important role in promoting metastatic growth. Dissection of the underlying mechanisms and functional validation of potential targets in the profile may provide novel therapeutic strategies for the treatment of metastatic diseases.
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Zheng, Wei, Dejian Zhao, Hui Zhang, Prameladevi Chinnasamy, Nicholas Sibinga, and Jeffrey W. Pollard. "Induction of interferon signaling and allograft inflammatory factor 1 in macrophages in a mouse model of breast cancer metastases." Wellcome Open Research 6 (June 23, 2021): 52. http://dx.doi.org/10.12688/wellcomeopenres.16569.2.

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Background: Metastatic breast cancer cells recruit macrophages (metastasis-associated macrophages, or MAMs) to facilitate their seeding, survival and outgrowth. However, a comprehensive understanding of the gene expression program in MAMs and how this program contributes to metastasis remain elusive. Methods: We compared the transcriptomes of MAMs recruited to lung metastases and resident alveolar macrophages (RAMs) and identified a large variety of differentially expressed genes and their associated signaling pathways. Some of the changes were validated using qRT-PCR and immunofluorescence. To probe the functional relevance to metastatic growth, a gene-targeting mouse model of female mice in the C57BL6/J background was used to study allograft inflammatory factor 1 (AIF1, also known as ionized calcium-binding adapter molecule 1 or IBA1). Results: Interferon signaling is one of the most activated pathways in MAMs, with strong upregulation of multiple components of the pathway and a significant enrichment for the gene signatures of interferon-alpha-treated human macrophages. Aif1, an interferon-responsive gene that regulates multiple macrophage activities, was robustly induced in MAMs. Aif1 deficiency in MAMs, however, did not affect development of lung metastases, suggesting that AIF1 indicates MAM activation but is dispensable for regulating metastasis. Conclusions: The drastically different gene expression profile of MAMs as compared to RAMs suggests an important role in promoting metastatic growth. Dissection of the underlying mechanisms and functional validation of potential targets in the profile may provide novel therapeutic strategies for the treatment of metastatic diseases.
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Han, Binsong, Yaqiong Jian, Xubin Xia, Wei Hu, Lina Zhang, and Peng Zhou. "Studying the effects of sea cucumber ovum powder on nonalcoholic fatty liver disease by proteomics techniques in a rat model." Food & Function 11, no. 7 (2020): 6139–47. http://dx.doi.org/10.1039/d0fo00741b.

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Schmitt, Emmanuelle, Pierre-Damien Coureux, Auriane Monestier, Etienne Dubiez, and Yves Mechulam. "Start Codon Recognition in Eukaryotic and Archaeal Translation Initiation: A Common Structural Core." International Journal of Molecular Sciences 20, no. 4 (2019): 939. http://dx.doi.org/10.3390/ijms20040939.

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Understanding molecular mechanisms of ribosomal translation sheds light on the emergence and evolution of protein synthesis in the three domains of life. Universally, ribosomal translation is described in three steps: initiation, elongation and termination. During initiation, a macromolecular complex assembled around the small ribosomal subunit selects the start codon on the mRNA and defines the open reading frame. In this review, we focus on the comparison of start codon selection mechanisms in eukaryotes and archaea. Eukaryotic translation initiation is a very complicated process, involving many initiation factors. The most widespread mechanism for the discovery of the start codon is the scanning of the mRNA by a pre-initiation complex until the first AUG codon in a correct context is found. In archaea, long-range scanning does not occur because of the presence of Shine-Dalgarno (SD) sequences or of short 5′ untranslated regions. However, archaeal and eukaryotic translation initiations have three initiation factors in common: e/aIF1, e/aIF1A and e/aIF2 are directly involved in the selection of the start codon. Therefore, the idea that these archaeal and eukaryotic factors fulfill similar functions within a common structural ribosomal core complex has emerged. A divergence between eukaryotic and archaeal factors allowed for the adaptation to the long-range scanning process versus the SD mediated prepositioning of the ribosome.
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Zhou, Jing, Jun Wu, Bo Li, et al. "PU.1 Is Essential For MLL Leukemia Via Activation Of The Meis/HOX Pathway and A Monocytic Cytokine Mediated Anti-Apoptotic Inflammatory Program." Blood 122, no. 21 (2013): 1276. http://dx.doi.org/10.1182/blood.v122.21.1276.1276.

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Abstract Aberrant transcriptional programs play a critical role in the development of acute myeloid leukemias (AMLs). Although persistent over-expression of MEIS1 and HOXA9 has been shown to be essential for the initiation and maintenance of MLL-associated leukemia, it is still poorly understood what additional transcriptional regulators, independent of the MLL fusion-driven MEIS/HOX pathway, dictate the development of MLL leukemia. Considering that AMLs with MLL translocation are typically associated with the monocytic lineage (FAB M4 and M5), we explored the potential role of the monocytic lineage-specific transcriptional program in MLL leukemia. Using 97 genome-wide expression profiles of human MLL leukemias, we constructed an MLL distinctive transcriptional regulatory network. In addition to well-known transcriptional factors in leukemia development such as MEIS1 and HOXA family genes, we identified a highly active monocyte-specific gene signature that includes transcription factor PU.1. In our effort to determine the functional role of PU.1 in MLL leukemia, we found that lower PU.1 expression significantly delayed the onset of MLL- AF9 induced leukemia in primary bone marrow transplantation assay. MLL leukemia failed to maintain in vivo upon induced deletion of the PU.1 gene. To examine the clinical relevance of the PU.1 in AML patients, we further performed multivariate Cox proportional-hazards regression analysis in four published datasets of patients with AML, for whom gene expression and time-to-event data were available. We found that a PU.1-regulated 40-gene signature showed profound concordance with prognosis in segregating high-risk and low-risk AML patients. When specific subgroups of AMLs were examined, the PU.1 expression signature could predict patient outcome for MLL patients, but not in other major AMLs, such as t(8;21), t(15;17) and inv(16). We further explored the molecular mechanisms underlying the critical role of the PU.1 program in MLL leukemia. Functional annotation of this PU.1 expression signature identified the MEIS/HOX pathway (MEIS1, FLT3, KIT), as well as key genes in the inflammatory response (AIF1, NF-KB1 and CD180). We showed that PU.1 is required to maintain high expression of Meis1 and Pbx3 and also important downstream genes in the MEIS/HOX pathway that includes known MEIS/HOX targets c-Kit and Flt3. Using ChIP-sequencing, we demonstrated that PU.1 interacts with the MEIS/HOX regulatory program through co-binding with MEIS1 at the target genomic regions in a MLL-ENL cell line. In our effort to determine the role of PU.1-controlled inflammatory response genes, we found that the growth inhibition in PU.1 knockdown MLL leukemic cells was partially rescued by addition of the monocytic inflammatory cytokine AIF1. AIF1 provides an anti-apoptotic effect through activation of the NF-ƒÛB pathway and additional known apoptosis regulators. Interestingly, AML patients with higher expression of both AIF1 and MEIS1 had a significantly shorter overall survival time than those with lower expression of both genes. Patients with high expression of either MEIS1 or AIF1 had medium survival possibilities. Notably, the prognostic value of AIF1 and MEIS1 remained in those with monocytic AMLs (P=0.00079), but not in the non- monocytic group of patients (p=0.105). Collectively, these results strongly suggest that the monocyte-specific inflammatory cytokine AIF1 is an MEIS/HOX independent essential regulator in monocytic AMLs such as MLL leukemia. Loss of function PU.1 is leukemogenic in mouse models. Suppression of PU.1 activity is also required for the development of human myelocytic M2/M3 leukemia. Here we reveal a converse role for PU.1 as an essential positive regulator in the development of MLL myeloid leukemia, mostly M4/M5 monocytic AMLs. Our study demonstrats that the monocyte-specific PU.1-driven transcriptional program independently contributes to the development of myeloid MLL leukemia, in parallel with the MLL fusion pathway. PU.1 and downstream macrophage specific inflammatory cytokine AIF1 have important prognostic value and may serve as novel therapeutic targets for MLL leukemias. Disclosures: No relevant conflicts of interest to declare.
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Cai, Linzhi, Sabrina V. Kirchleitner, Dongxu Zhao, et al. "Glioblastoma Exhibits Inter-Individual Heterogeneity of TSPO and LAT1 Expression in Neoplastic and Parenchymal Cells." International Journal of Molecular Sciences 21, no. 2 (2020): 612. http://dx.doi.org/10.3390/ijms21020612.

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Molecular imaging is essential for diagnosis and treatment planning for glioblastoma patients. Positron emission tomography (PET) with tracers for the detection of the solute carrier family 7 member 5 (SLC7A5; also known as the amino acid transporter light chain L system, LAT1) and for the mitochondrial translocator protein (TSPO) is successfully used to provide additional information on tumor volume and prognosis. The current approaches for TSPO-PET and the visualization of tracer ([18F] Fluoroethyltyrosine, FET) uptake by LAT1 (FET-PET) do not yet exploit the full diagnostic potential of these molecular imaging techniques. Therefore, we investigated the expression of TSPO and LAT1 in patient glioblastoma (GBM) samples, as well as in various GBM mouse models representing patient GBMs of different genetic subtypes. By immunohistochemistry, we found that TSPO and LAT1 are upregulated in human GBM samples compared to normal brain tissue. Next, we orthotopically implanted patient-derived GBM cells, as well as genetically engineered murine GBM cells, representing different genetic subtypes of the disease. To determine TSPO and LAT1 expression, we performed immunofluorescence staining. We found that both TSPO and LAT1 expression was increased in tumor regions of the implanted human or murine GBM cells when compared to the neighboring mouse brain tissue. While LAT1 was largely restricted to tumor cells, we found that TSPO was also expressed by microglia, tumor-associated macrophages, endothelial cells, and pericytes. The Cancer Genome Atlas (TCGA)-data analysis corroborates the upregulation of TSPO in a bigger cohort of GBM patient samples compared to tumor-free brain tissue. In addition, AIF1 (the gene encoding for the myeloid cell marker Iba1) was also upregulated in GBM compared to the control. Interestingly, TSPO, as well as AIF1, showed significantly different expression levels depending on the GBM genetic subtype, with the highest expression being exhibited in the mesenchymal subtype. High TSPO and AIF1 expression also correlated with a significant decrease in patient survival compared to low expression. In line with this finding, the expression levels for TSPO and AIF1 were also significantly higher in (isocitrate-dehydrogenase wild-type) IDHWT compared to IDH mutant (IDHMUT) GBM. LAT1 expression, on the other hand, was not different among the individual GBM subtypes. Therefore, we could conclude that FET- and TSPO-PET confer different information on pathological features based on different genetic GBM subtypes and may thus help in planning individualized strategies for brain tumor therapy in the future. A combination of TSPO-PET and FET-PET could be a promising way to visualize tumor-associated myeloid cells and select patients for treatment strategies targeting the myeloid compartment.
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Romanowski, Maciej, Karolina Kłoda, Sławomir Milczarek, et al. "Influence of AIF1 Gene Polymorphisms on Long-Term Kidney Allograft Function." Annals of Transplantation 20 (2015): 506–11. http://dx.doi.org/10.12659/aot.893885.

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Dissertations / Theses on the topic "Aif1"

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Slim, Ferial Amira. "Une isoforme de Allograft Inflammatory Factor-1 (AIF1) impliquée dans le cancer du sein." Master's thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/34495.

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Le cancer du sein (BC) représente l’un des cancers les plus communs et les plus dangereux sur le plan de la mortalité et de l’incidence chez les femmes dans le monde. Celui-ci est d’autant plus récurrent dans les pays développés, notamment le Canada [2]. Il s’agit d’une maladie complexe et multifactorielle dont la sévérité et la réponse au traitement varient selon les cas et dont le diagnostic peut parfois s’avérer délicat dû à l’hétérogénéité de la pathologie. Ce projet a ainsi pour objectif d’étudier un facteur de risque potentiel du BC pouvant servir au diagnostic et au traitement des patientes atteintes. Allograft Inflammatory Factor-1 (AIF1) est une protéine impliquée dans de nombreuses maladies inflammatoires et a été également associée au cancer, cependant, dans la majorité des études, une seule des isoformes a été analysée. Nos analyses de la signature transcriptionnelle d’individus provenant de familles à risque élevé de BC (BRCA1/BRCA2 ou non-BRCA1/2 (BRCAX)) ont permis d’identifier des transcrits significativement et différentiellement exprimés entre ces différents groupes. Parmi ceux-ci, deux variants d’épissage du gène AIF1, appelés AIF1v3 et AIF1v1, étaient significativement surexprimés chez les lignées cellulaires lymphoblastoides (LCLs) des soeurs BRCAX atteintes comparativement à leurs soeurs non-atteintes. Nos études d’expression génique ont par la suite révélé que ces deux isoformes étaient majoritairement exprimées dans les tumeurs mammaires les moins sévères et que cette expression provenait du microenvironnement tumoral, AIF1v1 étant majoritairement exprimé par les lymphocytes et AIF1v3 par les macrophages. Nous avons également démontré l’effet d’un traitement à l’acide gras oméga- 3 docosahexaénoïque (DHA) sur la réduction de l’expression des deux isoformes dans des LCLs d’individus BRCAX. Pour finir, nos données montrent que l’expression des isoformes de AIF1 dans les tumeurs et le tissu adipeux mammaires corrélait avec les paramètres cliniques et métaboliques des patientes. Ainsi, les données et connaissances obtenues à travers cette étude représentent une avancée considérable pour la communauté scientifique et la recherche sur le cancer puisqu’il s’agit de la première étude portant sur AIF1v1 et son implication dans le BC, le microenvironnement tumoral et la réaction inflammatoire.<br>Breast cancer (BC) represents one of the most common and dangerous cancers in terms of mortality and incidence among women worldwide. It is even more recurrent in developed countries including Canada [2]. BC is a complex and multifactorial disorder, its severity and response to treatment differs from case to case and its diagnosis can be tricky due to the heterogeneity of the pathology. Thus, this project aims to study a potential BC risk factor that can be used for diagnosis and treatment of BC patients. Allograft Inflammatory Factor-1 (AIF1) is a protein involved in many inflammatory diseases that has also been associated with cancer, however, in most studies, only one isoform has been analyzed. Our analyses of the transcriptional profile of individuals from French Canadian families with high risk of BC (BRCA1/BRCA2 or not-BRCA1/2 (BRCAX)) identified significantly and differentially expressed transcripts between the different groups. Among them, two AIF1 splice variants were highly overexpressed in the BRCAX lymphoblastoid cell lines (LCLs) of the affected sister comparatively with her non-affected sister. Our gene expression analysis revealed that both isoforms were mostly expressed in the least aggressive BC and this expression resulted from the tumor microenvironment, AIF1v1 being mostly expressed by lymphocytes and AIF1v3 by activated macrophages. We also demonstrated the effect of docosahexaenoic omega-3 fatty acids (DHA) on the downregulation of AIF1 isoforms expression in BRCAX LCLs. Lastly, our data showed that AIF1 isoforms expression in breast tumors and breast adipose tissue correlated with metabolic and clinical parameters of BC patients. Ultimately, all data and information resulting from this study represent a major breakthrough for the scientific community and the cancer research field since it is the first study on AIF1v1 and its involvement in BC, breast tumor microenvironment and inflammatory reaction.
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Azzouz, Doua. "Antigènes leucocytaires humains, microchimérisme et auto-anticorps dans la sclérodermie systémique." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4035.

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La Sclérodermie Systémique (ScS) est une maladie auto-immune rare et complexe, cliniquement divisée en deux sous-groupes : la ScS cutanée diffuse (dc-ScS) et la ScS cutanée limitée (lc-ScS). Les anticorps anti-topoisomérase et anti-centromère (ATA et ACA) sont respectivement les marqueurs de chaque sous-groupe. Beaucoup d'études ont analysé les gènes des Antigènes leucocytaires humains (HLA), fort facteur de risque, dans plusieurs groupes ethniques de patients atteints de ScS. La plupart des allèles de susceptibilité HLA-DRB1 (*11:01, *11:04, *15:01, *08:02…) et DQB1 (*03:01, *03:02, *06:01 and *06:02) ont en commun une séquence d'acides aminés, respectivement 67FLEDR71 et 71TRAELDT77 sur leurs chaînes &#946;. Pour la première fois, nous évaluons le risque relatif conféré par une ou deux doses de 67FLEDR71 et/ou une ou deux doses de 71TRAELDT77 chez des patients Caucasiens Français atteints de SSc. Nous montrons que le motif 67FLEDR71 est fortement associé à la dc-ScS et encore plus à la production d'ATA, alors que l'association de 71TRAELDT77 est plus faible dans les deux sous-groupes. Notre groupe a montré récemment dans la polyarthrite rhumatoïde (PR) que les patients qui n'ont pas les allèles de susceptibilité à la PR peuvent acquérir ces allèles via les cellules fœtales et/ou maternelles, aussi appelé Microchimérisme (Mc). Nous avons testé la même hypothèse dans la ScS. Contrairement à la PR, nos résultats n'ont pas démontré un tel transfert de susceptibilité via le Mc dans la SSc. Finalement, la présence d'auto-anticorps, liée à un génotype HLA, est précieuse au diagnostic et /ou pronostic de la maladie (ex : ACA ou ATA)<br>Systemic sclerosis (SSc) is a rare and complex autoimmune disease clinically divided into two subgroups: diffuse cutaneous (dcSSc) and limited cutaneous (lcSSc). Anti-topoisomerase and anti-centromere antibodies (ATA and ACA) are respectively markers of each subset. Many studies have analyzed Human Leukocyte Antigen (HLA) genes, the strongest genetic risk factor, in several ethnic groups in patients with SSc. Most common HLA-DRB1 (*11:01, *11:04, *15:01, *08:02…) and HLA-DQB1 (*03:01, *03:02, *06:01 and *06:02) susceptibility alleles have in common an amino acid sequence, respectively 67FLEDR71 and 71TRAELDT77 on their &#946; chains. For the first time, we evaluate the relative risk conferred by one or two 67FLEDR71 and/or one or two 71TRAELDT77 motives among Caucasian French patients with SSc. We show that 67FLEDR71 motif is highly associated with dcSSc and even more with ATA production, whereas 71TRAELDT77 association is weaker in both subgroups. Our group has recently shown in Rheumatoid Arthritis (RA) that patients who lack the RA HLA susceptibility that it could be transferred to patients via fetal and/or maternal cells, also called microchimerism (Mc). We test the same hypothesis in SSc. Contrary to RA, our results fail to demonstrate such transfer of HLA susceptibility via Mc in SSc. Finally linked to a particular HLA genotype is the presence of autoantibodies, helpful for disease diagnosis and/or prognosis (i.e. ACA or ATA). Patients who do not have these markers are difficult to diagnose or classify. By ProtoArray® technique, we identify 6 new auto-antigens in the plasmas of SSc patients
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Vahsen, Nicola. "Functional analysis of the apoptosis-inducing factor (AIF)." [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=981721702.

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Bassem, Yehia Khaled, and Vahab Abdowod. "Analys av indikatorerna AIT, AIF, SAIDI och SAIFI i lokalnätet." Thesis, Högskolan Väst, Avdelningen för Industriell ekonomi, Elektro- och Maskinteknik, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:hv:diva-13584.

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Energimarknadsinspektionen (EI) är en tillsynsmyndighet för el, fjärrvärme och naturgas, där en av myndighetens uppgifter är att kontrollera elnätbolagens distribution av el och om distributionen är av god kvalité. God leveranssäkerhet bestäms utifrån EI:s föreskrifter och allmänna råd i publikationen EIFS 2013:1. Varje år rapporterar elnätsbolag in avbrottsdata till EI som används för att mäta och analysera leveranssäkerheten i det svenska elnätet. Energimarknadsinspektionen använder etablerade indikatorer som beskriver leveranssäkerheten i distributionsnätet i Sverige. Indikatorerna som idag används är SAIDI och SAIFI som är kundviktade index som beskriver medelavbrottstiden och medelavbrottsfrekvensen för ett specifikt nät. Under 2019 överväger EI att införa två indikatorer som skall ersätta de nuvarande indexen SAIDI och SAIFI, indikatorerna benämns AIT och AIF. Enligt EI ska dessa indikatorer ge en mer rättvis bild av leveranssäkerheten än vad SAIDI och SAIFI ger, då de nya indikatorerna tar hänsyn till kundernas effektuttag. Detta arbete syftar till att utreda hur de nya indikatorerna AIT och AIF påverkar mätningen av leveranssäkerheten i GENAB:s nät, där leveranssäkerhetsindikatorerna beräknas på olika typer av nät för att sedan jämföras. Därefter undersöks hur de övervägda leveranssäkerhets-indikatorerna kan förbättras med hjälp av ökad automation i nätet. Utifrån resultatet av undersökningarna kan slutsatsen dras att en övergång till AIT och AIF kommer att medföra att indikatorernas medelavbrottstid och medelavbrottsfrekvens ökar för kunderna per år i GENAB:s nät.<br>Swedish Energy Markets Inspectorate (EI) is a regulatory authority for electricity, district heating and natural gas, where one of their tasks is to control the company's power distribution quality. A good electrical delivery reliability is determined on the basis of EI:s regulations and general advice in the publication EIFS 2013:1. Every year, the power distribution companies reports data to EI of the disturbances they have had in their networks, which is used to measure and analyse the electrical delivery reliability in the Swedish electricity grid. EI uses established indicators that describe the electrical delivery reliability of the distribution networks in Sweden. The indicators used today are named SAIDI and SAIFI, which are customer-weighted indices that describe the average interruption duration and the average interruption frequency for a specific network. In the beginning of 2019, EI will consider introducing two indicators to replace the current SAIDI and SAIFI indices, the indicators are being defined as AIT and AIF. According to EI, these indicators will be better than SAIDI and SAIFI as they take into consideration the customer's expected power consumption during the power outage. The purpose of this report is to investigate how the new indicators AIT and AIF affects the delivery reliability indicators in GENAB:s network, where these indicators are exercised on different types of networks and then compared. How the network can be made more efficient in the future by means of automation in the network is investigated based on the results on the indicators. From the results and investigations, it can be concluded that the transition to AIT and AIF will result in an increase of the indicator´s interruption time and the number of interruptions for customers per year in GENAB:s network.
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Landshamer, Stefan. "Role of Bid and AIF in glutamate induced neuronal cell death." Diss., [S.l.] : [s.n.], 2007. http://edoc.ub.uni-muenchen.de/archive/00006586.

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Mallett, Ross A. History Australian Defence Force Academy UNSW. "The Interplay between Technology, Tactics and Organisation in the First AIF." Awarded by:University of New South Wales - Australian Defence Force Academy. School of History, 1999. http://handle.unsw.edu.au/1959.4/38710.

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The purpose of this thesis is to investigate the interplay between the technology, tactics and organisation of the First AIF. Warfare in the twentieth warfare is characterised by the presence of certain technologies that give it a distinctive nature and which first appeared in the Great War. It was in the Great War that the highly dispersed form of tactics that we know today emerged. Thus, it is a natural starting point not only for the examination of warfare in the era of technology but for considering the nature of technological change itself. My Australian perspective enabled issues to be looked at to a depth that would not be possible in a work of this length with a broader view. I have argued that the Great War was characterised by the problem of trench warfare, and I have traced the progress of tactical, technological and organisational developments that ultimately supplied the solutions. I have also shown how the Great War was not only a war of technology in which new technologies were introduced and developed, but also one which saw the spread of new ways of thinking about military technology. In preparing this thesis, I have inspected the actual battlefields in France, Belgium and Turkey. I have drawn on a broad range of published material, but the thesis is largely based upon the primary documents found in the Australian War Memorial and Australian National Archives.
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Poulin, Éric. "Modélisation pharmacocinétique combinée IRM-TEP." Mémoire, Université de Sherbrooke, 2012. http://hdl.handle.net/11143/6351.

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Au cours des dernières années, des modalités d'imagerie comme la tomographie d'émission par positrons (TEP) et l'imagerie par résonance magnétique (IRM) ont été utilisées pour caractériser le microenvironnement tumoral et prédire la réponse au traitement durant la thérapie. La TEP est reconnue pour sa fonctionnalité et elle est utilisée avec une multitude de radiotraceurs. Par contre, sa résolution spatiale est limitée. L'IRM apporte une localisation anatomique précise et une information sur la perfusion des tissus. La modélisation pharmacocinétique augmente le potentiel de ces deux modalités en permettant des études quantitatives. Cependant, ces analyses quantitatives nécessitent l'acquisition de plusieurs images successives afin de suivre la distribution d'un agent de contraste (AC) en IRM et d'un radiotraceur en TEP. Plusieurs types d'analyse pharmacocinétique en IRM et en TEP requièrent la concentration de l'agent en fonction du temps dans le sang, nommée fonction d'entrée artérielle (AIF). Toutefois, cette dernière est difficile à mesurer. En IRM, pour la modélisation, il existe un compromis à faire entre la résolution spatiale et la résolution temporelle. Dans ce mémoire, une approche pour convertir l'AIF d'une modalité à l'autre est proposée pour le petit animal. L'AC gadolinium-acide diéthylène-triamine penta-acétique (Gd-DTPA) en IRM et le radiotraceur [indice supérieur 18] F-fluorodésoxyglucose (FDG) en TEP ont été utilisés. Un modèle mathématique a été développé pour effectuer la conversion et comparer les AIFs. Afin d'évaluer l'efficacité de la méthode, les paramètres pharmacocinétiques ont été calculés pour l'AIF obtenue par prélèvements sanguins et par notre méthode de conversion. Aucune différence statistique n'a été trouvée entre les paramètres des deux méthodes. Ces résultats suggèrent donc qu'une seule AIF serait nécessaire pour faire la modélisation dans les deux modalités. Une méthode qui optimise le temps d'acquisition d'images de même que la résolution spatiale en IRM a été proposée afin d'obtenir une quantification tumorale plus juste. Le temps d'acquisition a été réduit d'un facteur 3,2 avec une perte négligeable (1,5%) de résolution spatiale. Il a également été démontré qu'il est possible d'utiliser la méthode de région de référence combinée avec notre méthode de conversion d'AIF afin de faire la modélisation dans les deux modalités. Il s'agit, à notre connaissance, du premier travail évaluant la synergie entre les acquisitions IRM et TEP combinées. Ce travail pourrait donc avoir un impact significatif sur l'exploitation des deux modalités d'imagerie.
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Courtin, Laurine. "Optimisation de la transformation à froid des tubes de gaine en acier austénitique 15-15TI AIM1." Thesis, Poitiers, 2015. http://www.theses.fr/2015POIT2277/document.

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Afin de faire face aux besoins croissants en énergie, les réacteurs de 4ème génération sont envisagés mondialement. Un premier prototype de réacteur à neutrons rapides à caloporteur sodium (appelé ASTRID) est à l'étude au CEA. Le matériau de référence retenu pour le gainage combustible du premier coeur est l'acier austénitique 15-15Ti - AIM1 (Austenitic Improved Material). L’objectif de la thèse est d’étudier des voies d’optimisation de la gamme de mise en forme à froid du gainage permettant d’améliorer la résistance au gonflement. Les investigations portent principalement sur les conditions de transformation à froid et les traitements thermiques appliqués au cours de la mise en forme (notamment lors du dernier traitement d’hypertrempe). Les effets de ces paramètres sont étudiés en lien avec la microstructure (notamment l’affinement structural, l’état de précipitation, la remise en solution des éléments d’addition et l’arrangement des dislocations).La démarche adoptée se divise en trois étapes principales :- une analyse des gammes de fabrication mises en oeuvre par le passé ainsi qu’une étude des conditions d’étirage à froid et des traitements thermiques appliqués ;- une évaluation de nouveaux procédés de mise en forme tels que le laminage à pas de pèlerin et le martelage visant à valider la fabrication des tubes finis selon les spécifications requises ;- une optimisation des gammes de fabrication à froid et de la microstructure du matériau final. Les résultats de caractérisation de la microstructure et du comportement mécanique permettent d’envisager favorablement l’utilisation d’un procédé alternatif tel que le laminage à pas de pèlerin pour fabriquer les tubes de gaine<br>In order to face the next century energy demand growth, the worldwide development of the 4th generation of nuclear reactors is considered. The construction of a sodium-cooled fast reactor prototype (ASTRID) is currently envisaged at the CEA. The reference material selected for the fuel cladding of its first core is the 15-15Ti-AIM1 austenitic steel (Austenitic Improved Material).The goal of this PhD thesis work is to investigate the different ways of optimization for the coldworking steps undergone by the claddings during their manufacture in order to improve their swelling resistance. The main investigations are focused on the conditions of the cold-working steps and the thermal treatments applied throughout the shaping of the claddings, especially of the last solution annealing treatment. The effects of these parameters on the microstructure are investigated (structural refinement, precipitation and the additive elements dissolution and arrangement of the dislocations).This study is divided into three main steps:- an analysis of the fabrication routes applied in the past along with the study of the “coldwork” and the thermal treatments conditions;- an assessment of new shaping processes, such as the “cold-pilgering” and the hammering, in order to verify the conformity of the manufactured tubes with respect to the required specifications.- an attempt of optimization of the cold-work routes and the microstructure of the final material. The results of microstructure characterization and the mechanical behavior allow envisaging favorably the use of an alternative process such as the cold pilgering to manufacture claddings
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Bakelar, Jeremy W. "Binding Interactions of (R)- and (S)-hydroxypropyl-CoM Dehydrogenases and the Zinc Knuckle Proteins Air1 and Air2." DigitalCommons@USU, 2015. https://digitalcommons.usu.edu/etd/4273.

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This work is focused on understanding protein function by describing how paralogous proteins with overlapping and distinct functions interact with their substrates and with other proteins. Two model systems are the subject of this research: (1) the stereospecific dehydrogenases R- and S-HPCDH, and (2) the zinc knuckle proteins Air1 and Air2. R- and S-HPCDH are homologous enzymes that are central to the metabolism of propylene and epoxide in the soil bacterium Xanthobacter autotrophicus. The bacterium produces R- and S-HPCDH simultaneously to facilitate transformation of R- and S-enantiomers of epoxypropane to a common achiral product 2-ketopropyl-CoM (2-KPC). Both R- and S-HPCDH are highly stereospecific for their respective substrates as each enzyme displays less than 0.5% activity with the opposite substrate isomer. Presented here are substrate-bound x-ray crystal structures of S-HPCDH. Comparisons to the previously reported product-bound structure of R-HPCDH reveal structural differences that provide each enzyme with a distinct substrate binding pocket. These structures demonstrate how chiral discrimination by R- and S-HPCDH results from alternative binding of the distal end of substrates within each substrate binding pocket, providing a structural basis for stereospecificity displayed by R- and S-HPCDH. Air1 and Air2 are homologous eukaryotic proteins that individually function within a trimeric protein complex called TRAMP. In the nucleus, TRAMP participates in RNA surveillance, processing, and turnover by stimulating the 3’-5’ exonucleolytic degradation of targeted RNAs by the nuclear exosome. Previous studies have indicated that within TRAMP Air1 and Air2 provide crucial protein-protein interactions that link the individual subunits of the complex. However, the mechanistic details of these protein-protein interactions are poorly understood. The work in this dissertation has characterized a previously unknown binding interface between Air2 and another TRAMP component, the helicase Mtr4. This interaction may explain how helicase activity is modulated in TRAMP. In addition to TRAMP protein interactions, preliminary studies have identified a small region of Air1 that is required for modulating the activity of a protein that is not found in TRAMP, the methyltransferase Hmt1. Collectively, these studies provide important characterization of Air1 and Air2 protein-binding interactions, and establish a foundation for future research efforts aimed at exploring Air protein function.
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Apostolova, Nadezda. "Mitochondrial role of Apoptosis-Inducing Factor (AIF): Oxidative Phosphorylation and Reactive Oxygen Species." Doctoral thesis, Universitat de València, 2008. http://hdl.handle.net/10803/9775.

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The apoptotic function of Apoptosis-inducing factor (AIF) is well documented in theliterature, but its physiological role in the mitochondrion is less certain. Using a smallinterfering RNA (siRNA) strategy, we studied whether modulation of AIF expression incultured cells influenced the production of reactive oxygen species (ROS). We foundthat siAIF-transfected cells had reduced AIF protein levels and this was paralleled by asignificant increase in ROS. We tested the generality of this response by using twodifferent human cell lines, the hepatoma cell line Hep3B and cervix carcinoma lineHeLa, and also by employing a mouse ES AIF-KO cell line. The increased ROS weremitochondrial in origin as a similar silencing strategy in cells devoid of a functioningmitochondrial electron transport chain (ETC) did not result in a ROS-increase. Theaugmented ROS levels were sufficient to activate Hypoxia-inducible factor 1&#945; (HIF-1&#945;),a ROS-sensitive transcription factor, and this effect could be reversed usingantioxidants, both the broad-range general antioxidant (N-acetyl cysteine) and aspecific mitochondrial-targeted antioxidant (MitoQ), proving the implication of ROS inthe HIF-1&#945; stabilization. We also studied another two redox-sensitive transcriptionfactor and thus observed up-regulation in the expression of Nuclear factor (erythroidderived2)-like 2 (Nrf2), however without major changes in Nuclear factor-kappa B(NF-&#954;B) levels. Examination of the cellular oxygen consumption rate revealed that AIFdepletedcells had a major impairment of respiration, at Complex I in the ETC. Westernblot analysis also showed a loss of Complex I 39 and 20 kDa subunits. Studies usingthe antioxidants mentioned above, revealed that the respiratory competence could beregained in AIF-silenced cells. However, neither of the antioxidant treatments we usedcould recover Complex I assembly. Studies of the energetic state of siAIF cells showedthat despite a 30% decrease in the overall intact cell respiration, these cells maintainnormal basal levels of ATP, presumably due to a higher glycolytic capacity and a lowerproliferation rate. Moreover, we analyzed the expression of another redox-activeprotein, thioredoxin, by Western blot and found that the mitochondrial isoform, Trx2,was significantly decreased when AIF was silenced. Preliminary co-immunoprecipitationanalyses and proteomic studies failed to show any direct correlation between AIF andTrx2 at the protein level.Our results lead us to the conclusion that the defect in respiration in siAIF cells isdownstream of Complex I protein loss and is presumably due to ROS-mediateddamage to the ETC. This suggests an integral mitochondrial function of AIF, as a redoxmodifier and chaperone-like molecule, necessary for Complex I assembly. Additionalstudies are required to define the detailed mechanism of the AIF enzymatic activity inthe mitochondrion and to establish its binding partners.<br>La función proapoptótica del Factor Inductor de Apoptosis (AIF) está biendocumentada, sin embargo su papel fisiológico en la mitocondria es menos conocido.Empleando la metodología de interferencia por ARN, estudiamos si la modulación de laexpresión proteica de AIF en cultivo celular modifica la producción celular de especiesreactivas de oxígeno (ROS). Observamos que el silenciamiento de AIF estaba seguidopor un incremento significativo en los niveles de las ROS. Estas ROS fueronmitocondriales de origen, puesto que el silenciamiento de AIF en células que carecende la cadena de transporte electrónico funcional (ETC) en la mitocondria no llevó a unincremento de ROS. Este incremento fue suficiente para activar el Factor inducible porhipoxia (HIF-1&#945;), efecto que se puede revertir usando los antioxidantes, N-AcetilCisteina y MitoQ, demostrando así la implicación de los ROS en la estabilización deHIF1-&#945;. Los análisis del consumo de oxigeno celular mostraron que las células de AIFsilenciado sufren una disminución en la respiración celular, al nivel del Complejo I de laETC, acompañada por una disminución significativa en la expresión de sus subunidades39 y la 20kDa. Tratamientos con los antioxidantes previamente nombrados mostraronque la tasa de respiración se puede recuperar, no siendo así con la expresión delComplejo I de la ETC. Estudios del estado energético de las células siAIF mostraronque a pesar de la disminución de 30% en la tasa de la respiración celular, estas célulasmantienen niveles normales de ATP, como resultado de un incremento en la capacidadglucolítica y una reducción en la tasa de proliferación. Posteriormente, analizamos laexpresión de la proteína tioredoxina y observamos una disminución significativa en laisoforma mitocondrial, la tioredoxina 2 (Trx2), aunque los análisis preliminares de coinmunoprecipitacióny proteómica no mostraron la existencia de una correlacióndirecta entre las proteínas AIF y Trx2.Concluyendo, nuestros resultados sugieren que el defecto de la respiración celular esposterior al defecto en el Complejo I, probablemente como consecuencia al daño de laETC por ROS. Esta observación apunta a un papel integrador de AIF en la mitocondria,como modulador del estatus redox y necesario para el ensamblaje del Complejo I.
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Books on the topic "Aif1"

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Dürschke, Oliver. Koevolution von AIFM- und OGAW-Regime. Springer Fachmedien Wiesbaden, 2021. http://dx.doi.org/10.1007/978-3-658-34263-0.

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Demaret, Henri. L' AIFV: En service à la Force terrestre belge. De Krijger, 1997.

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Effenberger, Susanne Johanna. Spezial-AIF zur Investition in PPP-Immobilien. Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16500-0.

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Arshad, Maqbūl. Aif. Bī. Aī.: Pakistan men̲ Amrikī k̲h̲ufiyah idāre ... Faikṭ Pablīkeshanz, 2004.

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Against the sun: The AIF in Malaya, 1941-42. Allen & Unwin, 1998.

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Kapitalbeteiligungsrecht: Kommentar zum Private-equity-Recht : WKBG, UBGG, Risikobegrenzungsgesetz, Nebengesetze und AIFM-Richtlinie. Schäffer-Poeschel, 2009.

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Doneley, Bob. Black over blue: The 25th Battalion, AIF at war, 1915-1918. USQ Press, 1997.

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John, Edwards. Never a backward step: A history of the first 33rd Battalion, AIF. Bettong Books, 1996.

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Austin, Ronald J. Our dear old battalion: The story of the 7th Battalion, AIF, 1914-1919. Slouch Hat Publications, 2004.

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Turrell, A. N. Never unprepared: A history of the 26th Australian infantry battalian (AIF) 1939-1946. 26th Battalion Reunion Association, 1992.

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Book chapters on the topic "Aif1"

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Modjtahedi, Nazanine, and Guido Kroemer. "AIFM1." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_174.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, et al. "AIB1." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_9000.

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Modjtahedi, Nazanine, and Guido Kroemer. "AIFM1." In Encyclopedia of Signaling Molecules. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_174-1.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, et al. "AIF." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_174.

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, et al. "AIF." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4043.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, et al. "aIF6 in Archae." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100054.

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Haentjens, Matthias, and Pierre De Gioia Carabellese. "UCITS and AIFs." In European Banking and Financial Law Statutes. Routledge, 2017. http://dx.doi.org/10.4324/9781315172507-4.

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Effenberger, Susanne Johanna. "Spezial-AIF." In Spezial-AIF zur Investition in PPP-Immobilien. Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16500-0_4.

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Ide, Risako. "Aisatsu." In Handbook of Pragmatics. John Benjamins Publishing Company, 2007. http://dx.doi.org/10.1075/hop.11.ais1.

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Effenberger, Susanne Johanna. "Modellierung des Spezial-AIFs." In Spezial-AIF zur Investition in PPP-Immobilien. Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-16500-0_5.

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Conference papers on the topic "Aif1"

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Azzouz, DF, M. El Haddad, S. Kanaan, et al. "FRI0114 Allograft inflammatory factor 1 (AIF1) polymorphisms RS4711274 (G/A) and RS2269475 (C/T) may predict etanercept plus methotrexate response in french caucasian patients with rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4872.

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HIRAOKA, Tomotaka, and Hirosuke YAMAMOTO. "Dynamic AIFV Coding." In 2018 International Symposium on Information Theory and Its Applications (ISITA). IEEE, 2018. http://dx.doi.org/10.23919/isita.2018.8664267.

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TORRES-BLANC, C., E. E. CASTIÑEIRA, and S. CUBILLO. "MEASURING CONTRADICTION BETWEEN TWO AIFS." In Proceedings of the 8th International FLINS Conference. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812799470_0041.

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Sumigawa, Kentaro, and Hirosuke Yamamoto. "Coding of binary AIFV code trees." In 2017 IEEE International Symposium on Information Theory (ISIT). IEEE, 2017. http://dx.doi.org/10.1109/isit.2017.8006709.

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CASTIÑEIRA, E., S. CUBILLO, and W. MONTILLA. "ON THE INCOMPATIBILITY BETWEEN TWO AIFS." In Proceedings of the 8th International FLINS Conference. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812799470_0040.

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Jimenez Arbás, Estíbaliz, Marta María Sánchez Menéndez, and Luisa Ruiz Fernández. "Transversalidad educativa: casos clínicos para el estudio de Geriatría y Patologías Osteoarticulares y su intervención en Autonomía e Independencia Funcional en el Adulto." In IN-RED 2019: V Congreso de Innovación Educativa y Docencia en Red. Editorial Universitat Politècnica de València, 2019. http://dx.doi.org/10.4995/inred2019.2019.10444.

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El objetivo de este proyecto es introducir al alumnado en el conocimiento de la discapacidad a través de casos clínicos en dos asignaturas, Geriatría y Patologías Osteoarticulares (POA) y Autonomía e Independencia Funcional en el Adulto (AIF), para ello dispusieron de material y tutorización para la resolución de los casos durante las clases de POA, por otro lado en AIF desarrollan estrategias de intervención desde la Terapia Ocupacional. Se prepararon cinco casos clínicos en reumatología (artritis reumatoide, colagenosis, espondiloartropatías, artritis cristalinas e infecciosas) y cuatro en traumatología (tendinopatías, artrosis, fracturas y amputaciones). En AIF se eligieron dos casos, mano reumatoide más específicamente un caso clínico de artritis reumatoide y otro caso clínico, una amputación de mano. La innovación metodológica de este poyecto es la transversalidad educativa. Se diseño finalmente una gamificación para la evaluación de conocimientos realizando un scape room.
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"Session AI1: Artificial Intelligence I." In 2019 14th International Conference on Computer Engineering and Systems (ICCES). IEEE, 2019. http://dx.doi.org/10.1109/icces48960.2019.9068187.

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Hiraoka, Tomotaka, and Hirosuke Yamamoto. "Alphabetic AIFV Codes Constructed from Hu- Tucker codes." In 2018 IEEE International Symposium on Information Theory (ISIT). IEEE, 2018. http://dx.doi.org/10.1109/isit.2018.8437915.

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Golin, Mordecai, and Elfarouk Harb. "Polynomial Time Algorithms for Constructing Optimal AIFV Codes." In 2019 Data Compression Conference (DCC). IEEE, 2019. http://dx.doi.org/10.1109/dcc.2019.00031.

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Han, Hong, Xian-Liang Lu, Li-Yong Ren, Bo Chen, and Ning Yang. "AIFD: A Runtime Solution to Buffer Overflow Attack." In 2007 International Conference on Machine Learning and Cybernetics. IEEE, 2007. http://dx.doi.org/10.1109/icmlc.2007.4370697.

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Reports on the topic "Aif1"

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Lahusen, John T. Interaction of AIB1 and BRCA1 in Breast Cancer. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada471237.

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Wilkinson, John C. The AIF/XIAP Axis in Prostate Cancer. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada525568.

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Wilkinson, John. The AIF/XIAP Axis in Prostate Cancer. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada554637.

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Wilkinson, John. The AIF/XIAP Axis in Prostate Cancer. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada545562.

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Oh, Annabell S. EGF Regulation of Nuclear Co-Activator AIB1 Function in Breast Cancer. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada436895.

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Oh, Annabell S., and Anna Riegal. EGF Regulation of Nuclear Co-Activator AIB1 Function in Breast Cancer. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada417856.

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Lauritsen, Kristina J., and Anna T. Riegel. Regulation and Role of Nuclear Receptor Coactivator AIB1 in Breast Cancer. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada417025.

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Murdoch, Fern E. The Role of AIB1 in Estrogen-Dependent Breast Tumor Cell Growth. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada408992.

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Lauritsen, Kristina J. Regulation and Role of Nuclear Receptor Coactivator AIB1 in Breast Cancer. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada407253.

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Marmorstein, Ronen. Structure and Function of AIB1 (Amplified in Breast Cancer-1) Protein. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada408058.

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