Academic literature on the topic 'Cellules C26'
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Journal articles on the topic "Cellules C26"
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COSTA, CÉSAR S. B., JULIANO R. M. VICENTI, JOAQUÍN A. MORÓN-VILLARREYES, et al. "Extraction and characterization of lipids from Sarcocornia ambigua meal: a halophyte biomass produced with shrimp farm effluent irrigation." Anais da Academia Brasileira de Ciências 86, no. 2 (2014): 935–43. http://dx.doi.org/10.1590/0001-3765201420130022.
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Sarcocornia ambigua is a perennial glasswort, native of South America and a potential new seed-oil crop and forage for direct irrigation with salt water. Small seeds develop inside fertile segments of its cylindrical leafless shoots and, at the harvest, seeds are typically mixed with remnant cellulose material difficult to separate. This work evaluated different extraction methods and the composition of total esterified fatty acids in a meal of ground fertile shoots of S. ambigua, seeking for an alternative primary matter and larger yield of total lipids. The highest lipid yield was obtained with a chloroform:methanol mixture (2:1)(v/v) (5.2% of dry weight). The most abundant polyunsaturated fatty acids in the meal were linoleic acid (C18:2; 21.4%) and oleic acid (C18:1; 18.3%). Fifty six percent of the lipids in S. ambigua meal were saturated and palmitic acid (C16:0) was the main fraction (19.8%). Long-chain fatty acids (≥ C20) represented 29.5% of the lipids. Most abundant long-chain fatty acids were behenic acid (C22:0; 7.1%), lignoceric acid (C24:0; 5.3%) and montanic acid (C28:0; 4.0%). The percentage of saturated lipids in S. ambigua meal was higher than that of vegetable oils with a MUFA nutritional profile and some of these lipids have known bioactive properties.
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Markowski, Adam R., Agnieszka U. Błachnio-Zabielska, Karolina Pogodzińska, Anna J. Markowska, and Piotr Zabielski. "Diverse Sphingolipid Profiles in Rectal and Colon Cancer." International Journal of Molecular Sciences 24, no. 13 (2023): 10867. http://dx.doi.org/10.3390/ijms241310867.
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Colorectal cancer is a heterogenous group of neoplasms showing a variety of clinical and pathological features depending on their anatomical location. Sphingolipids are involved in the formation and progression of cancers, and their changes are an important part of the abnormalities observed during carcinogenesis. Because the course of rectal and colonic cancer differs, the aim of the study was to assess whether the sphingolipid profile is also different in tumors of these two regions. Using a combination of ultra-high-performance liquid chromatography combined with triple quadrupole mass spectrometry, differences in the amounts of cellular sphingolipids were found in colorectal cancer. Sphingosine content was higher in rectal cancer than in adjacent healthy tissue, while the content of two ceramides (C18:0-Cer and C20:0-Cer) was lower. In colon cancer, a higher content of sphingosine, sphinganine, sphingosine-1-phosphate, and two ceramides (C14:0-Cer and C24:0-Cer) was found compared to healthy tissue, but there was no decrease in the amount of any of the assessed sphingolipids. In rectal cancer, the content of sphinganine and three ceramides (C16:0-Cer, C22:0-Cer, C24:0-Cer), as well as the entire pool of ceramides, was significantly lower compared to colon cancer. The S1P/Cer ratio in rectal cancer (S1P/C18:1-Cer, S1P/C20:0-Cer, S1P/C22:0-Cer, S1P/C24:1-Cer) and in colon cancer (S1P/C18:0-Cer, S1P/C18:1-Cer, S1P/C20:0-Cer) was higher than in adjacent healthy tissue and did not differ between the two sites (rectal cancer vs. colonic cancer). It seems that the development of colorectal cancer is accompanied by complex changes in the metabolism of sphingolipids, causing not only qualitative shifts in the ceramide pool of cancer tissue but also quantitative disturbances, depending on the location of the primary tumor.
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Albouery, Mayssa, Alexis Bretin, Bénédicte Buteau, et al. "Soluble Fiber Inulin Consumption Limits Alterations of the Gut Microbiota and Hepatic Fatty Acid Metabolism Caused by High-Fat Diet." Nutrients 13, no. 3 (2021): 1037. http://dx.doi.org/10.3390/nu13031037.
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Diet shapes the gut microbiota which impacts hepatic lipid metabolism. Modifications in liver fat content are associated with metabolic disorders. We investigated the extent of dietary fat and fiber-induced alterations in the composition of gut microbiota and hepatic fatty acids (FAs). Mice were fed a purified low-fat diet (LFD) or high-fat diet (HFD) containing non-soluble fiber cellulose or soluble fiber inulin. HFD induced hepatic decreases in the amounts of C14:0, C16:1n-7, C18:1n-7 and increases in the amounts of C17:0, C20:0, C16:1n-9, C22:5n-3, C20:2n-6, C20:3n-6, and C22:4n-6. When incorporated in a LFD, inulin poorly affected the profile of FAs. However, when incorporated in a HFD, it (i) specifically led to an increase in the amounts of hepatic C18:0, C22:0, total polyunsaturated FAs (PUFAs), total n-6 PUFAs, C18:3n-3, and C18:2n-6, (ii) exacerbated the HFD-induced increase in the amount of C17:0, and (iii) prevented the HFD-induced increases in C16:1n-9 and C20:3n-6. Importantly, the expression/activity of some elongases and desaturases, as well as the gut microbiota composition, were impacted by the dietary fat and fiber content. To conclude, inulin modulated gut microbiota and hepatic fatty acid composition, and further investigations will determine whether a causal relationship exists between these two parameters.
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Tobin, V., M. Le Gall, M. Romero, A. Leturque, and E. Brot-Laroche. "C26 - L’insuline est un inhibiteur de la localisation apicale de GLUT2 dans les entérocytes : une étude in vivo chez la souris et in vitro dans les cellules CACO-2/TC7." Gastroentérologie Clinique et Biologique 30, no. 1 (2006): 86. http://dx.doi.org/10.1016/s0399-8320(06)73108-6.
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Detzner, Johanna, Charlotte Püttmann, Gottfried Pohlentz, et al. "Primary Human Colon Epithelial Cells (pHCoEpiCs) Do Express the Shiga Toxin (Stx) Receptor Glycosphingolipids Gb3Cer and Gb4Cer and Are Largely Refractory but Not Resistant towards Stx." International Journal of Molecular Sciences 22, no. 18 (2021): 10002. http://dx.doi.org/10.3390/ijms221810002.
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Shiga toxin (Stx) is released by enterohemorrhagic Escherichia coli (EHEC) into the human intestinal lumen and transferred across the colon epithelium to the circulation. Stx-mediated damage of human kidney and brain endothelial cells and renal epithelial cells is a renowned feature, while the sensitivity of the human colon epithelium towards Stx and the decoration with the Stx receptor glycosphingolipids (GSLs) globotriaosylceramide (Gb3Cer, Galα1-4Galβ1-4Glcβ1-1Cer) and globotetraosylceramide (Gb4Cer, GalNAcβ1-3Galα1-4Galβ1-4Glcβ1-1Cer) is a matter of debate. Structural analysis of the globo-series GSLs of serum-free cultivated primary human colon epithelial cells (pHCoEpiCs) revealed Gb4Cer as the major neutral GSL with Cer (d18:1, C16:0), Cer (d18:1, C22:1/C22:0) and Cer (d18:1, C24:2/C24:1) accompanied by minor Gb3Cer with Cer (d18:1, C16:0) and Cer (d18:1, C24:1) as the dominant lipoforms. Gb3Cer and Gb4Cer co-distributed with cholesterol and sphingomyelin to detergent-resistant membranes (DRMs) used as microdomain analogs. Exposure to increasing Stx concentrations indicated only a slight cell-damaging effect at the highest toxin concentration of 1 µg/mL for Stx1a and Stx2a, whereas a significant effect was detected for Stx2e. Considerable Stx refractiveness of pHCoEpiCs that correlated with the rather low cellular content of the high-affinity Stx-receptor Gb3Cer renders the human colon epithelium questionable as a major target of Stx1a and Stx2a.
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Detzner, Johanna, Elisabeth Krojnewski, Gottfried Pohlentz, et al. "Shiga Toxin (Stx)-Binding Glycosphingolipids of Primary Human Renal Cortical Epithelial Cells (pHRCEpiCs) and Stx-Mediated Cytotoxicity." Toxins 13, no. 2 (2021): 139. http://dx.doi.org/10.3390/toxins13020139.
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Human kidney epithelial cells are supposed to be directly involved in the pathogenesis of the hemolytic–uremic syndrome (HUS) caused by Shiga toxin (Stx)-producing enterohemorrhagic Escherichia coli (EHEC). The characterization of the major and minor Stx-binding glycosphingolipids (GSLs) globotriaosylceramide (Gb3Cer) and globotetraosylceramide (Gb4Cer), respectively, of primary human renal cortical epithelial cells (pHRCEpiCs) revealed GSLs with Cer (d18:1, C16:0), Cer (d18:1, C22:0), and Cer (d18:1, C24:1/C24:0) as the dominant lipoforms. Using detergent-resistant membranes (DRMs) and non-DRMs, Gb3Cer and Gb4Cer prevailed in the DRM fractions, suggesting their association with microdomains in the liquid-ordered membrane phase. A preference of Gb3Cer and Gb4Cer endowed with C24:0 fatty acid accompanied by minor monounsaturated C24:1-harboring counterparts was observed in DRMs, whereas the C24:1 fatty acid increased in relation to the saturated equivalents in non-DRMs. A shift of the dominant phospholipid phosphatidylcholine with saturated fatty acids in the DRM to unsaturated species in the non-DRM fractions correlated with the GSL distribution. Cytotoxicity assays gave a moderate susceptibility of pHRCEpiCs to the Stx1a and Stx2a subtypes when compared to highly sensitive Vero-B4 cells. The results indicate that presence of Stx-binding GSLs per se and preferred occurrence in microdomains do not necessarily lead to a high cellular susceptibility towards Stx.
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Guo, Tianyao, Zhigui Duan, Jia Chen, et al. "Pull-down combined with proteomic strategy reveals functional diversity of synaptotagmin I." PeerJ 5 (February 8, 2017): e2973. http://dx.doi.org/10.7717/peerj.2973.
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Synaptotagmin I (Syt I) is most abundant in the brain and is involved in multiple cellular processes. Its two C2 domains, C2A and C2B, are the main functional regions. Our present study employed a pull-down combined with proteomic strategy to identify the C2 domain-interacting proteins to comprehensively understand the biological roles of the C2 domains and thus the functional diversity of Syt I. A total of 135 non-redundant proteins interacting with the C2 domains of Syt I were identified. Out of them, 32 and 64 proteins only bound to C2A or C2B domains, respectively, and 39 proteins bound to both of them. Compared with C2A, C2B could bind to many more proteins particularly those involved in synaptic transmission and metabolic regulation. Functional analysis indicated that Syt I may exert impacts by interacting with other proteins on multiple cellular processes, including vesicular membrane trafficking, synaptic transmission, metabolic regulation, catalysis, transmembrane transport and structure formation, etc. These results demonstrate that the functional diversity of Syt I is higher than previously expected, that its two domains may mediate the same and different cellular processes cooperatively or independently, and that C2B domain may play even more important roles than C2A in the functioning of Syt I. This work not only further deepened our understanding of the functional diversity of Syt I and the functional differences between its two C2 domains, but also provided important clues for the further related researches.
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Detzner, Johanna, Anna-Lena Klein, Gottfried Pohlentz, et al. "Primary Human Renal Proximal Tubular Epithelial Cells (pHRPTEpiCs): Shiga Toxin (Stx) Glycosphingolipid Receptors, Stx Susceptibility, and Interaction with Membrane Microdomains." Toxins 13, no. 8 (2021): 529. http://dx.doi.org/10.3390/toxins13080529.
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Tubular epithelial cells of the human kidney are considered as targets of Shiga toxins (Stxs) in the Stx-mediated pathogenesis of hemolytic–uremic syndrome (HUS) caused by Stx-releasing enterohemorrhagic Escherichia coli (EHEC). Analysis of Stx-binding glycosphingolipids (GSLs) of primary human renal proximal tubular epithelial cells (pHRPTEpiCs) yielded globotriaosylceramide (Gb3Cer) and globotetraosylceramide (Gb4Cer) with Cer (d18:1, C16:0), Cer (d18:1, C22:0), and Cer (d18:1, C24:1/C24:0) as the dominant lipoforms. Investigation of detergent-resistant membranes (DRMs) and nonDRMs, serving as equivalents for the liquid-ordered and liquid-disordered membrane phase, respectively, revealed the prevalence of Gb3Cer and Gb4Cer together with cholesterol and sphingomyelin in DRMs, suggesting lipid raft association. Stx1a and Stx2a exerted strong cellular damage with half-maximal cytotoxic doses (CD50) of 1.31 × 102 pg/mL and 1.66 × 103 pg/mL, respectively, indicating one order of magnitude higher cellular cytotoxicity of Stx1a. Surface acoustic wave (SAW) real-time interaction analysis using biosensor surfaces coated with DRM or nonDRM fractions gave stronger binding capability of Stx1a versus Stx2a that correlated with the lower cytotoxicity of Stx2a. Our study underlines the substantial role of proximal tubular epithelial cells of the human kidney being associated with the development of Stx-mediated HUS at least for Stx1a, while the impact of Stx2a remains somewhat ambiguous.
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Markowski, Adam R., Arkadiusz Żbikowski, Piotr Zabielski, et al. "The Effect of Silencing the Genes Responsible for the Level of Sphingosine-1-phosphate on the Apoptosis of Colon Cancer Cells." International Journal of Molecular Sciences 24, no. 8 (2023): 7197. http://dx.doi.org/10.3390/ijms24087197.
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Sphingosine-1-phosphate (S1P) and ceramides (Cer) are engaged in key events of signal transduction, but their involvement in the pathogenesis of colorectal cancer is not conclusive. The aim of our study was to investigate how the modulation of sphingolipid metabolism through the silencing of the genes involved in the formation (SPHK1) and degradation (SGPL1) of sphingosine-1-phosphate would affect the sphingolipid profile and apoptosis of HCT-116 human colorectal cancer cells. Silencing of SPHK1 expression decreased S1P content in HCT-116 cells, which was accompanied by an elevation in sphingosine, C18:0-Cer, and C18:1-Cer, increase in the expression and activation of Caspase-3 and -9, and augmentation of apoptosis. Interestingly, silencing of SGLP1 expression increased cellular content of both the S1P and Cer (C16:0-; C18:0-; C18:1-; C20:0-; and C22:0-Cer), yet inhibited activation of Caspase-3 and upregulated protein expression of Cathepsin-D. The above findings suggest that modulation of the S1P level and S1P/Cer ratio regulates both cellular apoptosis and CRC metastasis through Cathepsin-D modulation. The cellular ratio of S1P/Cer seems to be a crucial component of the above mechanism.
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Al-Qarawi, AA, EF Abd Allah, and Hashem Abeer. "Effect of Ephedra alata Decne. on lipids metabolism of Aspergillus flavus Link." Bangladesh Journal of Botany 42, no. 1 (2013): 45–50. http://dx.doi.org/10.3329/bjb.v42i1.15823.
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In Aspergillus flavus Link, the total lipid, sterols, neutral lipids, phospholipids and fatty acid content decreased significantly with the application of different concentrations of Ephedra alata Decne. extrtact. Gas chromatographic analysis revealed the presence of 12 fatty acids namely, (caprylic (C8), capric (C10), lauric (C12), myristic (C14), palmitic (C16), palmitoleic (C16:1), stearic (C18), oleic (C18:1), linoleic (C18:2), ? linolenic (C18:3), arachidic (C20) and arachidonic (C20:4) with total un-saturation per cent 69.78 in the cellular lipids of A. flavus. The use of E. alata extracts induced significant alteration in fatty acid profile towards increment saturation. DOI: http://dx.doi.org/10.3329/bjb.v42i1.15823 Bangladesh J. Bot. 42(1): 45-49, 2013 (June)
Dissertations / Theses on the topic "Cellules C26"
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Chaouki, Ghita. "Etude du rôle de la voie de signalisation eIF2αATF4 au cours des états inflammatoires, dans le cadre du stress mitochondrial et de l’anorexie associée à la pathologie". Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2022. http://www.theses.fr/2022UCFAC109.
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La voie de signalisation eIF2α-ATF4 est activée dans les cellules en réponse à un large éventail de stress cellulaires. Son activation conduit à une inhibition de la synthèse protéique globale et la régulation de l’expression de gènes cibles du facteur de transcription ATF4. Cette voie est sollicitée en réponse au déficit en acides aminés indispensables, au stress mitochondrial, au stress du réticulum endoplasmique ou encore aux infections virales. Elle déclenche des mécanismes adaptatifs, à l’échelle cellulaire (tels que l’inhibition de la synthèse protéique et l’augmentation du niveau d’autophagie) et de l’organisme entier (comme la régulation du métabolisme, l’inflammation, l’immunité et la prise alimentaire). Les résultats précédents générés par notre laboratoire ainsi que les données de la littérature nous ont amenés à étudier le rôle de la signalisation eIF2α-ATF4 dans deux contextes différents. Dans une première partie, nous avons exploré le rôle de la signalisation eIF2α-ATF4 dans l’anorexie associée aux pathologies cataboliques inflammatoires (sepsis et cancer). Nous avons émis l’hypothèse que cette voie de signalisation pourrait contribuer à l’inhibition de prise alimentaire par une action directe au niveau central et/ou en stimulant l’expression de cytokines anorexigènes, dont GDF15, en périphérie (foie, intestin). Nous avons utilisé deux modèles expérimentaux reproduisant une anorexie associée à la pathologie chez la souris : un modèle d’inflammation systémique aigue de type sepsis (administration unique de lipopolysaccharide bactérien) et un modèle de souris porteuses d’une tumeur de cellules de carcinome de colon C26. Ces deux modèles ont été caractérisés en phase précoce de l’anorexie, par une inflammation aux niveaux périphérique et central (hypothalamus), une augmentation des niveaux circulants d’IL-6 et de GDF15, une profonde modification du métabolisme des acides aminés, et une activation de la voie de signalisation eIF2α-ATF4 dans l’hypothalamus et dans le foie. Ensuite, la réponse de modèles inductibles de perte de fonction d’ATF4 a été testée dans le modèle de sepsis. L’invalidation d’ATF4 au niveau du foie et de l’intestin n’a pas eu d’impact ni sur l’anorexie, ni sur l’induction de la production de GDF15. L’invalidation constitutive de GDF15 a également été sans effet sur l’inhibition de prise alimentaire induite par l’administration de LPS. Le rôle de la fonction ATF4 au niveau central n’a pas pu être testée et devra faire l’objet d’expérimentations futures. L’analyse des échantillons des souris invalidées pour la fonction d’ATF4 au niveau hépatique nous permettra d’évaluer son implication dans les réorientations du métabolisme des AA (transport, biosynthèse, autophagie). Dans le modèle de cancer C26, le passage du stade de pré-anorexie au stade de début d’anorexie a été associé à une activation de la voie signalisation eIF2αATF4 aux niveaux hépatique et hypothalamique, et une approche fonctionnelle pharmacologique sera prochainement mise en place à l’aide de l’ISRIB (ISR Inhibitor) pour étudier son implication dans la régulation de l’appétit et du métabolisme des AA (dans ce modèle les invalidations géniques ne sont pas possibles). Dans une deuxième partie, nous nous sommes intéressés au dysfonctionnement mitochondrial, qui représente une menace majeure pour l'homéostasie cellulaire, favorise l'apparition de nombreux troubles métaboliques et joue un rôle crucial dans la pathogenèse du sepsis. Compte-tenu du rôle joué par la voie de signalisation eIF2α-ATF4 dans la réponse adaptative au stress mitochondrial, nous avons cherché à savoir si un prétraitement activateur de cette voie pourrait être un moyen d'augmenter la résilience du pool mitochondrial lors d'événements stressants ultérieurs. (...)<br>The eIF2α-ATF4 signaling pathway is activated in cells in response to a wide range of cellular stresses. Its activation leads to the inhibition of the global protein synthesis and the regulation of the transcription factor ATF4 target genes expression. This pathway is activated in response to essential amino acid deficiency, mitochondrial stress, endoplasmic reticulum stress or viral infections. Its activation triggers adaptive mechanisms, both at the cellular level (such as inhibition of protein synthesis and increased autophagy) and at the whole organism level (such as regulation of metabolism, inflammation, immunity and food intake). Previous results generated by our laboratory as well as data from the scientific literature led us to investigate the role of eIF2α-ATF4 signaling in two different contexts. Firstly, we explored the role of eIF2α-ATF4 signaling in anorexia associated with catabolic inflammatory pathologies (sepsis and cancer). We hypothesized that this signaling pathway could contribute to the inhibition of food intake by its direct action at the central level and/or by stimulating the expression of anorectic cytokines, including GDF15, in the periphery (liver, intestine). We used two experimental models reproducing pathology-associated anorexia in mice: a sepsis model of acute and systemic inflammation (single administration of bacterial lipopolysaccharide) and a model of mice carrying a C26 colon carcinoma cell tumor. Both models were characterized in the early phase of anorexia by inflammation at the peripheral and central (hypothalamus) levels, increased circulating levels of IL-6 and GDF15, profound alterations in amino acid metabolism, and activation of the eIF2αATF4 signaling pathway in the hypothalamus and liver. Afterwards, the response of inducible models of ATF4 loss-of-function was tested in the sepsis model. ATF4 knock-out in the liver and intestine had no impact on either anorexia or the induction of GDF15 production. Constitutive invalidation of GDF15 also had no effect on the inhibition of food intake induced by LPS administration. The role of ATF4 function at the central level could not be tested and should be the subject of future experiments. The analysis of samples from mice knocked-out for ATF4 at the hepatic level, will allow us to evaluate ATF4 involvement in the reorientation of AA metabolism (transport, biosynthesis, autophagy). In the C26 cancer model, the transition from pre-anorexia to early anorexia was associated with an activation of the eIF2α-ATF4 signaling pathway at the hepatic and hypothalamic levels, and a pharmacological approach using ISRIB (ISR Inhibitor) will soon be implemented to study the involvement of the ISR in the regulation of appetite and AA metabolism (in this model, genes knock-out is not possible) Secondly, we focused on mitochondrial dysfunction, which represents a major threat to cellular homeostasis, promotes the development of many metabolic disorders and plays a crucial role in the pathogenesis of sepsis. Given the role played by the eIF2α-ATF4 signaling pathway in the adaptive response to mitochondrial stress, we investigated whether a pretreatment activating this pathway could be a way to increase the resilience of the mitochondrial pool during subsequent stressful events. We demonstrated in mice that a pretreatment activating the GCN2-eIF2α-ATF4 pathway upstream of inflammatory stress (LPS administration) counteracted some of the effects of this stress on mitochondrial homeostasis in the liver, an organ playing a major role in the metabolic and immune response to endotoxic stress. These results are presented as an article that will be submitted soon for publication
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Allen, Frederick Jr. "CCL3 Augments Antitumor Responses in CT26 by Enhancing Cellular Trafficking and Interferon-Gamma Expression." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1513124234665339.
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Filali-Ansary, Aziz. "Régulation de l'incorporation du cholestérol venant de liposomes ou de lipoprotéines, de la biosynthèse d'hormones stéroïdes en C21 et de leurs hydroxylations dans des cellules corticosurrénaliennes de rats transformées par l'oncogène Ha-rasEJ et dans les cellules de la lignée Y1." Dijon, 1990. http://www.theses.fr/1990DIJOS051.
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Ce travail a porté sur l'étude d'une nouvelle lignée de cellules corticosurrénaliennes de rats nouveau-nés transformées par l'oncogène Ha-rasEJ. Celui-ci a été introduit dans les cellules à l'aide d'un liposome refermant un plasmide contenant le gène considéré. Nous avons recherché les propriétés de ces cellules GM1 vis-à-vis de l'incorporation du cholestérol apporté par les liposomes et les lipoprotéines et vis-à-vis de la biosynthèse des stéroïdes en C21. Nous avons aussi utilisé les cellules de la lignée Y1; 1) la levée de l'inhibition des mitoses dans les cellules transformées GM1 a permis de cultiver ces cellules par passages successifs en subcultures pendant 18 mois; 2) les liposomes de petite taille contenant le cholestérol et l'oléate de cholestéryle ont permis le transfert de l'oléate de cholestéryle aux cellules Y1; cette incorporation est activée par la protéine de transfert des esters de cholestéryle ou CETP; 3) les liposomes contenant le cholestérol non estérifié ont permis le transfert de ce dernier aux cellules GM1. Les cardiolipines utilisées pour fabriquer les liposomes sont responsables d'une stéroïdogenèse 3 fois plus intense dans ces cellules qu'avec les liposomes de phosphatidylcholines; 4) les cellules GM1 incorporent le cholestérol des LDL et celui des HDL ; la vitesse maxima d'incorporation est plus grande avec les LDL mais les HDL ont une affinité plus élevée pour les cellules GM1 et sont une source plus efficace de cholestérol pour la biosynthèse des stéroïdes en C21 ; 5) les cellules GM1 expriment l'activité corticostérone 18-hydroxylase et 18-déhydrogénase.
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Bezine, Maryem. "Implication du canal potassium Kv3.1 dans la lipotoxicité du 7-cétocholestérol, 24S-hydroxycholestérol et de l’acide tétracosanoïque sur des cellules nerveuses 158N et BV-2 : Etude des relations entre Kv3.1, homéostasie potassique et métabolisme peroxysomal dans la maladie d’Alzheimer." Thesis, Bourgogne Franche-Comté, 2017. http://www.theses.fr/2017UBFCI010/document.
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Le potassium (K+) est impliqué dans la régulation de l’excitabilité cellulaire, la régulation du cycle cellulaire, la viabilité cellulaire, la neuroprotection et le maintien des fonctions microgliales et oligodendrocytaires. Le dysfonctionnement des canaux potassiques, décrit dans plusieurs maladies neurodégénératives comme la Maladie d’Alzheimer (MA), la sclérose en plaques (SEP), la maladie de Parkinson et la maladie de Huntington, pourrait être une potentiel cible thérapeutique. Les mécanismes toxiques sous-jacents de ces pathologies neurodégénératives impliquent des oxystérols, dérivés oxydés du cholestérol, et des acides gras en relation avec le métabolisme peroxysomal. Le 7-cétocholestérol (7KC), le 24S-hydroxycholestérol (24S-OHC) et l'acide tétracosanoïque (C24: 0), souvent trouvés à des taux élevés au niveau du cerveau et dans le plasma de patients atteints de maladies neurodégénératives (MA, maladie de Nieman-Pick, SEP, maladie de Parkinson, maladie de Huntington et X-ALD conduisent une rupture de l’équilibre Redox qui aboutirait à la neurodégénérescence. Dans ce contexte, il est intéressant de déterminer l’éventuelle connexion entre environnement lipidique et homéostasie potassique. L’étude in vitro a été réalisée sur des olygodendrocytes murins 158N et les cellules microgliale BV-2. Nous avons montré que la lipotoxicité du 7KC, 24S-OHC et C24:0 implique une rétention du K+ faisant intervenir les canaux potassium voltage dépendant (Kv). Ces résultats ont montré que l'inhibition des canaux Kv conduisant à une augmentation la [K+]i contribue à la cytotoxicité du 7KC, 24S-OHC et C24:0. Nous nous sommes focalisés sur le canal Kv3.1b. La retention du K+ induite par les oxystérols (7KC et 24S-OHC) serait sous le contrôle de Kv3.1b. L’étude clinique réalisée sur du plasma de MA a révélé une corrélation négative entre le taux d’acide docosahexaénoïque (DHA) et la concentration de K+. Chez les souris transgéniques J20, modèle de la MA, l’étude de la topographie d’expression de Kv3.1b et d’Abcd3, au niveau de l’hippocampe et du cortex, a montré une baisse de l’expression de ces deux marqueurs. Dans leur ensemble, les résultats obtenus ont établi des relations entre lipotoxicité, métabolisme peroxysomal et altération de l’homéostasie potassique dans la neurodégénérescence et suggèrent une possible modulation de l’expression et de l’activité de kv3.1b dans la physiopathologie des maladies neurodégénératives<br>Potassium (K+) is involved in the regulation of cellular excitability, cell cycle regulation, cell viability, neuroprotection and maintenance of microglial and oligodendrocytic functions. Potassium dysfunction, described in several neurodegenerative diseases such as Alzheimer's Disease (AD), multiple sclerosis (MS), Parkinson's disease and Huntington's disease, may be a potential therapeutic target. The underlying toxic mechanisms of these neurodegenerative pathologies involve oxysterols, which are oxidized cholesterol derivatives, and fatty acids including those associated with peroxisomal metabolism. 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC) and tetracosanoic acid (C24:0), often found at increased levels in the brain and plasma of patients with neurodegenerative diseases (Nieman-Pick disease, MS, Parkinson's disease, Huntington's disease and X-ALD) lead to a breakdown of the redox equilibrium leading to neurodegeneration. In this context, it is interesting to determine the possible connection between the lipid environment and potassium homeostasis The in vitro study was carried out on 158N murine oligodendrocytes and microglial BV-2 cells. We have shown that the lipotoxicity of 7KC, 24S-OHC and C24:0 implies retention of K+ involving the voltage dependent potassium channels (Kv). These results have shown that inhibition of Kv channels lead to an increase in [K +] i contributing to the cytotoxicity of 7KC, 24S-OHC and C24:0. The retention of K+ induced by oxysterols (7KC and 24S-OHC) would be under the control of Kv3.1b. A clinical study, on plasma of patients with Alzheimer’s disease, revealed a negative correlation between docosahexaenoic acid (DHA) and K+ concentration. In the J20 mice, a transgenic model of Alzheimer’s disease, the expression of Kv3.1b and Abcd3 was decreased in the hippocampus and cortex. Overall, the results obtained established relationships between lipotoxicity, peroxisomal metabolism and potassium homeostasis in neurodegeneration and suggest a possible modulation of the expression and activity of kv3.1b in the pathophysiology of neurodegenerative diseases. So, modulation of Kv3.1 could constitute a new therapeuthic approach against some neurodegenerative diseases
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MATIGNON, Christophe. "Etude de la détonation de deux mélanges stoechiométriques (CH4/H2/O2/N2 et CH4/C2H6/O2/N2) Influence de la proportion relative des deux combustibles et de la température initiale élevée." Phd thesis, Université de Poitiers, 2000. http://tel.archives-ouvertes.fr/tel-00010305.
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Ce travail traite de la détonation de mélanges réactifs gazeux à deux combustibles de détonabilité très différente xH2+(1–x)CH4 et xC2H6+(1–x)CH4 stoechiométriques dans l'oxygène et dilués avec de l'azote dans des proportions variant de l'oxygène pur à l'air. Les paramètres de l'étude sont la proportion relative x des combustibles, la dilution en azote B=O2/N2 et les conditions initiales de température et de pression. Cette étude s'inscrit dans le cadre général de l'amélioration des conditions de sécurité des procédés chimiques. Nous avons traité le problème par la comparaison de la mesure de la taille caractéristique de la structure tridimensionnelle cellulaire de la détonation autonome et stationnaire avec la longueur d'induction chimique calculée dans les hypothèses du modèle ZND au moyen de plusieurs schémas détaillés de cinétique chimique. Les résultats obtenus pour les mélanges à un combustible montrent que la détonabilité du méthane diminue en fonction de la température initiale quelle que soit B, et que celle de l'éthane et de l'hydrogène diminue à B=0 mais augmente à B=3,76 (air) (l'inversion de comportement en fonction de la température initiale se produit pour B=2 pour l'éthane, et pour B=1 pour l'hydrogène). Les résultats obtenus pour les mélanges à deux combustibles montrent que leur détonabilité est à chaque fois influencée par le combustible le plus lourd, c'est à dire que la détonabilité des mélanges H2/CH4 est plutôt gouvernée par CH4 alors que celle des mélanges C2H6/CH4 est plutôt gouvernée par C2H6. Avec l'oxygène pur (B=0), l'augmentation de la température initiale désensibilise ces mélanges. Au delà d'une certaine valeur de B, on observe une inversion de détonabilité en fonction de x.
Book chapters on the topic "Cellules C26"
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O’Neill, C. M., and R. J. Mathias. "Regeneration of Plants from Protoplasts of Arabidopsis Thaliana CV. Columbia L. (C24), Via Direct Embryogenesis." In Current Issues in Plant Molecular and Cellular Biology. Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0307-7_52.
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Sharma, Sunny, and Karl-Dieter Entian. "Chemical Modifications of Ribosomal RNA." In Ribosome Biogenesis. Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2501-9_9.
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AbstractCellular RNAs in all three kingdoms of life are modified with diverse chemical modifications. These chemical modifications expand the topological repertoire of RNAs, and fine-tune their functions. Ribosomal RNA in yeast contains more than 100 chemically modified residues in the functionally crucial and evolutionary conserved regions. The chemical modifications in the rRNA are of three types—methylation of the ribose sugars at the C2-positionAbstract (Nm), isomerization of uridines to pseudouridines (Ψ), and base modifications such as (methylation (mN), acetylation (acN), and aminocarboxypropylation (acpN)). The modifications profile of the yeast rRNA has been recently completed, providing an excellent platform to analyze the function of these modifications in RNA metabolism and in cellular physiology. Remarkably, majority of the rRNA modifications and the enzymatic machineries discovered in yeast are highly conserved in eukaryotes including humans. Mutations in factors involved in rRNA modification are linked to several rare severe human diseases (e.g., X-linked Dyskeratosis congenita, the Bowen–Conradi syndrome and the William–Beuren disease). In this chapter, we summarize all rRNA modifications and the corresponding enzymatic machineries of the budding yeast.
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Kelley, Brian. "Software-Defined Radio for Advanced Gigabit Cellular Systems." In Wireless, Networking, Radar, Sensor Array Processing, and Nonlinear Signal Processing. CRC Press, 2009. http://dx.doi.org/10.1201/9781420046052-c22.
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"11. Metabotropic Transmission: Receptors and G Proteins." In Molecular and Cellular Physiology of Neurons. Harvard University Press, 2015. http://dx.doi.org/10.4159/harvard.9780674735644.c16.
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"15. Mechanoreceptors." In Molecular and Cellular Physiology of Neurons. Harvard University Press, 2015. http://dx.doi.org/10.4159/harvard.9780674735644.c21.
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"16. Photoreceptors and Olfactory Receptor Neurons." In Molecular and Cellular Physiology of Neurons. Harvard University Press, 2015. http://dx.doi.org/10.4159/harvard.9780674735644.c22.
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"Appendix: Symbols Used." In Molecular and Cellular Physiology of Neurons. Harvard University Press, 2015. http://dx.doi.org/10.4159/harvard.9780674735644.c23.
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"References." In Molecular and Cellular Physiology of Neurons. Harvard University Press, 2015. http://dx.doi.org/10.4159/harvard.9780674735644.c24.
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"Index." In Molecular and Cellular Physiology of Neurons. Harvard University Press, 2015. http://dx.doi.org/10.4159/harvard.9780674735644.c25.
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"Vitamin B5: Pantothenate." In The Chemical Biology of Human Vitamins. The Royal Society of Chemistry, 2018. http://dx.doi.org/10.1039/bk9781788014649-00161.
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Vitamin B5 is the simple acid pantothenic acid (from the Greek pantos, meaning widespread). B5 needs to undergo five enzymatic steps to be converted to coenzyme A, in which the terminal thiol of a cysteamine moiety is the key reactive atom, once dissociated to the thiolate anion. The thiolate serves as nucleophile towards a variety of acids to yield acyl thioesters (acyl-CoAs). These are the cellular acylating agents in metabolic pathways. The two-carbon acyl group in acetyl CoA is doubly activated: as electrophile at C1 and as nucleophile at C2, and so ideally set up for C–C bond formations in fatty acid and steroid biosynthetic pathways, as well as the first step in the citrate metabolic cycle.
Conference papers on the topic "Cellules C26"
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Benedicto, Aitor, Joana Marquez, Elvira Olaso, and Beatriz Arteta. "Abstract B10: LFA-1/ICAM-1 interaction switches on an orchestrated prometastatic microenvironmental shift during experimental liver metastasis of colon C26 cancer cells." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b10.
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Guagchinga Moreno, Genesis Yulisa, Andrea Carolina Serrano Larrea, Frank Alexis, and Javier Santamaría. "Cellulose-based beads as a possible method for drug release in the treatment of Leishmaniasis disease." In VIII Congreso Internacional de Investigación REDU. Medwave, 2022. http://dx.doi.org/10.5867/medwave.2022.s1.ci26.
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Alande, C., and C. Landric. "Autotransplantation de germes dentaires au centre hospitalier de Pau : une série de cas." In 66ème Congrès de la SFCO. EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603008.
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Autotransplantation de germes dentaires au centre hospitalier de Pau : une série de cas Alande C1, Landric C2 1. Interne en Chirurgie Orale, UFR Odontologie, Service ORL et Stomatologie CH Pau 2. Spécialiste en Chirurgie Orale, Assistante hospitalière, CH Pau. INTRODUCTION : L’autotransplantation correspond au déplacement d’un organe fonctionnel (transplant) d’un site donneur vers un site receveur, sur un même patient. Dans le cadre de l’organe dentaire, le transplant est placé dans une alvéole osseuse intrabuccale naturelle ou préparée chirurgicalement. Les indications sont nombreuses : délabrement carieux, expulsion traumatique, défaut d’éruption, agénésie. C’est une technique chirurgicale peu utilisée, pourtant les métaanalyses les plus récentes font état d’un taux de succès compris entre 75 et 91% (1). Ce travail expose une série de 07 transplantations. OBSERVATION : Les 7 transplantations ont été réalisées au Centre Hospitalier de Pau entre aout 2017 et janvier 2018. Les patients étaient initialement adressés par leur dentiste ou leur othodontiste pour des avulsions. Les indications résultaient toutes d’un délabrement carieux de premières molaires maxillaires ou mandibulaires, ces dernières étant non restaurables. Les patients étaient âgés de 17 à 23 ans. Les transplants étaient tous des germes de 3ème molaire incluse situées au stade 7-8 de Nolla. Le même protocole chirurgical a été systématiquement utilisée pour chacun des patients, à savoir : avulsion de la dent délabrée, révision et rinçage alvéolaire, préparation du site receveur, avulsion du germe, temps extra-alvéolaire le plus court possible, positionnement dans le site receveur avec ajustement si nécessaire, mise en sous occlusion par améloplastie, contention. Un soin tout particulier était accordé à la préservation des cellules desmodontales du transplant. Les patients n’ont pas présenté de complication per ou postopératoire. Leur suivi post-opératoire est en cours et est réalisé de façon systématique à 1 semaine, 1 mois, 2 mois avec orthopantomogramme et 6 mois. Pour être considérées comme un succès, les transplantations devaient présenter les critères suivants : poursuite de l’édification radiculaire, absence de mobilité du transplant, absence de signes infectieux cliniques et radiologiques, visualisation radiologique d’un ligament alvéolo-dentaire sans signe d’ankylose. DISCUSSION : De plus en plus d’études tendent à montrer que la préservation des cellules desmodontales est un des facteurs majeurs pour la réussite du traitement (2). Avec l’avènement de la planification 3D (3), ce paramètre pourra être d’avantage contrôlé. Les taux de succès de cette thérapeutique, déjà élevés, pourraient être amenés à augmenter d’avantage. Les transplantations sont aujourd’hui une alternative de choix au traitement implantaire chez les jeunes patients.
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Kurnikova, Irina, Shirin Gulova, Guzal Akhmadullina, Natalia Danilina, and Ikram Mokhammed. "Methods of computer simulation in the development of technology for the functional assessment of the state of the liver in patients." In 14th International Conference on Applied Human Factors and Ergonomics (AHFE 2023). AHFE International, 2023. http://dx.doi.org/10.54941/ahfe1003456.
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Most of the diseases associated with carbohydrate and fat metabolism disorders (type 2 diabetes mellitus, obesity, metabolic syndrome) lead to changes in the structure and function of liver cells, and the formed liver dysfunction negatively affects the further progression of the disease. The process of liver damage develops with varying intensity and does not immediately lead to irreversible consequences; therefore, dysfunction should be detected as early as possible, and the data obtained should be used to assess the current state and predict their reversibility.Study purpose. To create a quantitative assessment method that allows to assess the current functional state of the liver and to determine the reversibility of existing functional disorders and the severity of structural changes, to assess the prognosis of the course of the disease and the effectiveness of restorative measures.Instruments and Data Collection Procedure. Examination of patients, in addition to conventional methods, included an assessment of the absorptive-excretory function of the liver and biliary tract patency using a scintillation gamma camera (Siemens Symbia T16) with subsequent processing on the SUPER-SEGAMS computer system (Hungary). Freshly prepared Bromesida, 99mТс was administered intravenously at the rate of 1.1 MBq per kg of the patient's body weight, with a normal content of bilirubin in blood. Series of scintigrams allow to assess the passage of the drug visually through the blood-liver-ducts-intestine system, to characterize the anatomical features and organic changes in the biliary system. Quantitative analysis of the "activity-time" curves obtained from the areas of interest (the right lobe of the liver - 2 zones, the left lobe of the liver, the common bile duct, the intestinal area, the heart area) makes it possible to study the absorptive-excretory function of the liver.Results. By the method of mathematical modeling, a formula was obtained - the index of the functional activity of hepatocytes:IFAH= (-1,1564 + 0,0653 × BMI - 0,0144 × Tmax) × 100,where:IFAH - index of functional activity of hepatocytes (liver cells);BMI - body mass index (kg/m2)Tmax - indicator of the absorption function of the liver (min) - the time to reach the maximum accumulation of the radiopharmaceutical in the liver. It is an indicator of the function of polygonal liver cells (normal = 8-12 min).Functional activity of hepatocytes: from 0 to 9.9 - normal functional activity of hepatocytes; from 10 to 19.9 - the risk of developing functional disorders; from 20 to 29.9 - reversible dysfunction of hepatocytes (steatosis); more than 30 - irreversible (organic) liver dysfunction (steatohepatitis). With negative IFAH values - the influence of extrahepatic factors, such as diseases that accelerate metabolism at the cellular level (thyrotoxicosis), taking drugs in violation of the prescriptions before these studies.The originality and novelty of the technique are confirmed by the patent – “A method for diagnosing fatty hepatosis” (patent RU 2 578 080 C2 dated February 19, 2016).The method was tested in clinical practice and the data obtained confirmed the high diagnostic accuracy (95%) of the proposed method for calculating the index of IFAH.Conclusion: the discussed method allows doctors to evaluate not only the current functional state of the liver, but also to determine the reversibility of existing functional disorders and the severity of structural changes; also could be used to evaluate the prognosis of the course of the disease and the effectiveness of restorative measures. It is characterized by relative ease of implementation. Only one parameter — Tmax is required, after which the study can be completed.