Littérature scientifique sur le sujet « Linea cellulare »
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Articles de revues sur le sujet "Linea cellulare"
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Triulzi, F. « Anomalie della linea mediana ». Rivista di Neuroradiologia 7, no 2 (avril 1994) : 187–98. http://dx.doi.org/10.1177/197140099400700207.
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Un moderno approccio alle malformazioni congenite della linea mediana non può non considerare le recenti acquisizioni della embriologia sperimentale. Già più di 40 anni or sono il famoso neuropatologo PI Yakovlev sottolineava l'importanza delle aree mediobasali del prosencefalo embrionario nella genesi delle malformazioni della linea mediana. Attualmente questa affermazione è stata confermata dalla conoscenza della esatta posizione anatomica nell'embrione di 22–24 settimane di gestazione delle future regioni della linea mediana. La adeno e la neuroipofisi, l'ipotalamo il chiasma ed il piatto commissurale sono tutti compresi in una ristretta regione nella parte medio-rostrale del tuba neurale. Le principali anomalie della linea mediana quali: la oloprosencefalia, l'agenesia del corpo callosa e del setto pellucida, potrebbero essere causate da interruzioni nelle differenti fasi di induzione di questa regione. Il meccanismo di regolazione genetica della differenziazione cellulare del sistema nervosa centrale è stato in parte chiarito in questi ultimi anni. Esso procede attraverso un processo di segmentazione all'interno del quale la parte mediobasale del tuba neurale potrebbe rappresentare il segmento più rostrale. A sua volta neuroipofisi, ipotalamo etc, potrebbero rappresentare dei sottosegmenti di questo segmento principale. Una mancata attivazione dei geni che regolano la differenziazione dei diversi segmenti e sottosegmenti potrebbe quindi essere alla base di gran parte delle malformazioni della linea mediana.
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De Angeli, S., S. Buoro, C. Favretti, M. Bonini, A. Fandella et G. Anselmo. « Crescita e morfologia della linea cellulare prostatica umana U285 trattata con mepartricina, finasteride e suramina : Confronto tra i farmaci ». Urologia Journal 61, no 1_suppl (janvier 1994) : 178–83. http://dx.doi.org/10.1177/039156039406101s54.
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The aim of this study was to compare the effects of mepartricin on the proliferation and morphology of U285 cells with those induced by suramin and finasteride, both substances which have been investigated previously. Proliferation was evaluated by the FRAME Cytotoxicity Test, exposing the cells to increasing doses of mepartricin, between 0.1 μg/ml and 5 μg/ml, from the moment of seeding for 24 hours. The morphology was evaluated by scanning electron microscope (SEM). The FRAME Test showed a statistically significant decrease (p<0.05) in proliferation at all times of observation and at all doses in those cultures exposed to mepartricin right from seeding. Those where treatment was given 24 hours later, only showed this decrease with the highest doses. SEM highlighted the reduced capacity of the cells to proliferate, confirming data from the FRAME Test. These results therefore indicate that mepartricin has an anti-proliferation effect both in the Lag phase and the logarithmic growth phase. This behaviour differs from that of suramin and finasteride, which have less marked effect on cellular growth.
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Wang, Hongliang, Fabio Squina, Fernando Segato, Andrew Mort, David Lee, Kirk Pappan et Rolf Prade. « High-Temperature Enzymatic Breakdown of Cellulose ». Applied and Environmental Microbiology 77, no 15 (17 juin 2011) : 5199–206. http://dx.doi.org/10.1128/aem.00199-11.
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ABSTRACTCellulose is an abundant and renewable biopolymer that can be used for biofuel generation; however, structural entrapment with other cell wall components hinders enzyme-substrate interactions, a key bottleneck for ethanol production. Biomass is routinely subjected to treatments that facilitate cellulase-cellulose contacts. Cellulases and glucosidases act by hydrolyzing glycosidic bonds of linear glucose β-1,4-linked polymers, producing glucose. Here we describe eight high-temperature-operating cellulases (TCel enzymes) identified from a survey of thermobacterial and archaeal genomes. Three TCel enzymes preferentially hydrolyzed soluble cellulose, while two preferred insoluble cellulose such as cotton linters and filter paper. TCel enzymes had temperature optima ranging from 85°C to 102°C. TCel enzymes were stable, retaining 80% of initial activity after 120 h at 85°C. Two modes of cellulose breakdown, i.e., with endo- and exo-acting glucanases, were detected, and with two-enzyme combinations at 85°C, synergistic cellulase activity was observed for some enzyme combinations.
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Maeda, Ayaka, Daisuke Tatsumi et Mitsuhiro Morita. « Linear and Nonlinear Rheological Properties of Tunicate Cellulose Solution ». Nihon Reoroji Gakkaishi 45, no 2 (2017) : 107–12. http://dx.doi.org/10.1678/rheology.45.107.
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Feng, Chun-Hsiung, Ming-Shaung Ju, Chou-Ching Lin et H. M. Lan. « QUASI-LINEAR VISCOELASTIC PROPERTIES OF PC-12 CELLS(3A1 Cellular & ; Tissue Engineering & ; Biomaterials I) ». Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2007.3 (2007) : S167. http://dx.doi.org/10.1299/jsmeapbio.2007.3.s167.
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Beyisa Benti Diro, Tadessa Daba et Temam Gemeda Genemo. « Production and characterization of cellulase from mushroom (Pleurotus ostreatus) for effective degradation of cellulose ». International Journal of Biological and Pharmaceutical Sciences Archive 2, no 1 (30 août 2021) : 135–50. http://dx.doi.org/10.53771/ijbpsa.2021.2.1.0066.
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Cellulases are a group of hydrolytic enzymes capable of hydrolyzing the most abundant organic polymer that means cellulose to smaller sugar components including glucose subunits. The aim of this study was to screen cellulase producing oyster mushroom collected from Eucalyptus tree bark to evaluate the in vitro production of cellulase by Pleurotus ostreatus using different lignocellulosic substrates, and to characterize the cellulase produced with respect to changes in pH, temperature, and concentration of substrates. A total of ten mushroom specimens were randomly collected from Eucalyptus tree bark in the premise of Holetta Agricultural Research Center campus. All of the collected mushroom specimens were identified morphologically and biochemically as Pleurotus ostreatus and also screened for their ability to produce cellulase by detecting and measuring zone of hydrolysis on commercial media containing Carbxymethyl Cellulose (CMC) as the sole carbon source. These mushroom specimens were cultivated using both solid state fermentation and submerged fermentation systems supplemented with different lignocellulosic substrates (wheat straw, teff straw, bean straw, wood fiber and Eucalyptus tree bark) to identify the most suitable medium for the production of cellulase. The highest enzyme production was obtained on bean straw and wheat straw which resulted in 0.191 U/ml, 0.868 U/ml and 0.389 U/ml; and 0.216 U/ml, 0.444 U/ml, and 0.245 U/ml of FPase, CMCase, and β-glucosidase in solid state fermentation. The lowest values were, however, obtained in media containing wood fiber in both solid state fermentation and submerged fermentation. Comparison of the lignocellulosic substrates revealed that wheat straw was selected for further growth parameter optimization. The production of cellulase was higher at the 5th day of incubation period, and the optimum pH and incubation temperature required for maximum cellulase production were 4 and 30°C, respectively. Sucrose and Yeast extract at 1% concentration were found to be the most preferred carbon and nitrogen sources for cellulase production by Pleurotus ostreatus. The optimum pH and temperature for cell_free cellulase activity on were found to be 4 and 50°C, respectively. Generally the cellulases produced by Pleurotus ostreatus were stable and active at temperatures ranging from 20-50°C. These characteristics hopefully would make this enzyme potentially attractive in a variety of industrial applications including animal feed treatments. There was a linear relationship between cellulase and its substrate concentration for there was an increase in activity with increase in substrate concentration. The relationship between rate of reaction and substrate concentration depended on the affinity of the enzyme for its substrate. Finally the cellulase was tested for its ability to saccharify agricultural wastes and the results showed the highest release of sugars from wheat straw.
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Hayes, Alethea M., Aijun Wang, Benjamin M. Dempsey et David L. McDowell. « Mechanics of linear cellular alloys ». Mechanics of Materials 36, no 8 (août 2004) : 691–713. http://dx.doi.org/10.1016/j.mechmat.2003.06.001.
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Manzini, Giovanni, et Luciano Margara. « Invertible Linear Cellular Automata overZm : ». Journal of Computer and System Sciences 56, no 1 (février 1998) : 60–67. http://dx.doi.org/10.1006/jcss.1997.1535.
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Manzini, Giovanni, et Luciano Margara. « Attractors of Linear Cellular Automata ». Journal of Computer and System Sciences 58, no 3 (juin 1999) : 597–610. http://dx.doi.org/10.1006/jcss.1998.1609.
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Martı´n del Rey, A., et G. Rodrı´guez Sánchez. « Reversibility of linear cellular automata ». Applied Mathematics and Computation 217, no 21 (juillet 2011) : 8360–66. http://dx.doi.org/10.1016/j.amc.2011.03.033.
Texte intégralThèses sur le sujet "Linea cellulare"
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CROCE, NICOLETTA. « Modulazione dell'espressione di BDNF nella linea cellulare umana di glioblastoma da parte della paroxetina ». Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1232.
Texte intégralRésumé :
Brain-derived Neurotrophic factor (BDNF) è la neurotrofina più espressa nel sistema nervoso dei mammiferi. Esso è stato estesamente studiato, così come altre neurotrofine come il Fattore di Crescita del Nervo (NGF), poiché è in stretta relazione con lo sviluppo neuronale e la sua plasticità, in particolar modo nei cambiamenti a lungo termine e nella sua morfologia. Durante lo sviluppo BDNF supporta la sopravvivenza ed il differenziamento delle popolazioni neuronali del sistema nervoso centrale e periferico ed inoltre prende parte alla crescita ed alla morfologia assonale, agendo anche come modulatore del dolore. Il ruolo di questa proteina nella plasticità sinaptica è stata collegata all’osservazione di una regolazione reciproca tra la sua espressione e la plasticità sinaptica. Il gene BDNF si estende per circa 70 kb all’interno del cromosoma 11p4. Esso mostra una grande complessità a causa dell’uso di promotori alternativi, di meccanismi di splicing alternativo e della presenza di siti di poliadenilazione. Per quanto riguarda la sua espressione, BDNF mostra una diffusa presenza nel sistema nervoso degli adulti, con il più alto livello di mRNA e proteina nell’ippocampo, amigdala, corteccia cerebrale e ipotalamo. Studi recenti hanno suggerito che BDNF è coinvolto in un ampio numero di malattie nell’uomo. Infatti è stato associato a differenze nell’esito di test di intelligenza ed altre funzioni cognitive, influenzando la personalità e la memoria ed essendo relazionabile a malattie neurodegenerative come la schizofrenia, l’Alzheimer, disordini bipolari e depressione. In particolare, diversi studi hanno evidenziato una stretta correlazione tra i livelli di BDNF e la depressione, suggerendo che questa malattia potrebbe essere causata da una diminuzione dei livelli di questa proteina nel cervello. È stato anche notato che gli effetti negativi sull’umore potrebbero essere contrastati inibendo il riassorbimento dei neurotrasmettitori come la serotonina, che sono capaci di aumentare l’espressione di BDNF. Infatti l’inibizione del loro riassorbimento dagli assoni provocano l’accumulo di queste molecole nello spazio sinaptico, avendo così più tempo di agire sui neuroni e sulle cellule gliali. Gli SSRI (Selective-Serotonine Reuptake Inhibitors) inibiscono selettivamente ed estesamente il riassorbimento della serotonina, determinando un incremento della neurotrasmissione serotonergica. Comunque, l’efficacia di questi antidepressivi non può essere solamente spiegata tramite la loro azione sul sistema monoaminergico, perciò il motivo di azione dei farmaci antidepressivi rimane largamente sconosciuto, in particolar modo gli adattamenti molecolari e cellulari che giustificano la loro azione terapeutica. È stato scoperto che gli antidepressivi sono anche capaci di agire sulle cellule gliali di ratto ed è possibile che una riduzione di queste cellule e della loro azione di supporto ai neuroni è coinvolta nella fisiopatologia di differenti malattie psichiatriche. Per investigare gli effetti della paroxetina sull’espressione di BDNF e sul rilascio di questa proteina da parte di cellule non neuronali, sono state usate linee cellulari di glioblastoma-astrocitoma, U-87 MG. Esse sono state trattate con paroxetina ad una concentrazione di 7 μM per differenti intervalli di tempo (6, 12, 24, 48 ore). L’espressione dell’mRNA e del miR-30a-5p è stata analizzata attraverso una retrotrascrizione e una PCR Real Time. È stata anche studiata la concentrazione di BDNF nelle cellule e nel terreno di crescita attraverso un saggio ELISA, per determinare la sintesi della proteina ed il suo rilascio a seguito del trattamento con paroxetina. È stato osservato che l’espressione dell’mRNA di BDNF è significativamente aumentata durante le prime 6 ore di trattamento con paroxetina rispetto alle cellule non trattate. Nelle cellule trattate questa overespressione conduce ad un picco di produzione a 12 ore di incubazione ed, in particolare, nella sua secrezione nel mezzo cellulare dopo 24 ore, mentre nelle cellule non trattate questo rilascio è stato notato solo dopo 48 ore. L’espressione del miR-30a-5p, che controlla la traduzione di BDNF, raggiunge un picco a 12 ore. Questi risultati conducono all’ipotesi che il trattamento di questa linea cellulare non neuronale con paroxetina aumenta l’espressione di BDNF, manifestatasi in una maggiore sintesi e rilascio di proteina. Queste cellule non sono capaci di produrre serotonina o altri neurotrasmettitori poichè esse sono cellule non neuronali. La paroxetina sembra agire su queste cellule in modo simile ai neuroni, per questo si potrebbe supporre che tale effetto sia dovuto all’utilizzo di una via alternativa indipendente dal sistema neuronale monoaminergico. L’aumentata e prolungata induzione di BDNF attraverso gli antidepressivi potrebbe promuovere la sopravvivenza neuronale e proteggere i neuroni, così come le cellule della glia, dagli effetti dannosi dello stress. Ciò potrebbe contribuire a spiegare l’azione terapeutica degli antidepressivi suggerendo nuove strategie per l’intervento farmacologico.Brain-derived neurotrophic factor (BDNF) is the most widely expressed neurotrophin in the mammalian nervous system. It has been widely studied, like other neurotrophins such as nerve growth factor, because it is in close relationship with neuronal development and plasticity, in particular with long-lasting changes in synaptic relations and morphology. During development BDNF supports the survival and the differentiation of neuronal populations of the peripheral and central nervous systems and takes part in axonal growth and, also acting as a central modulator of pain. The role of this protein in synaptic plasticity has been linked to the observation of a reciprocal regulation between BDNF expression and synaptic activity. The human BDNF gene spans ~70 kb within the 11p14 chromosome. It displays a great complexity due to alternative promoters usage, alternative splicing mechanisms and the presence of alternative polyadenylation sites. Concerning its expression, BDNF displays a widespread distribution pattern in the nervous systems of adults, with the highest levels of mRNA and protein in the hippocampus, amygdala, cerebral cortex and hypothalamus. Recent studies have suggested that BDNF is involved in a number of traits and human disorders. In fact it has been associated with differences in performance of intelligence tests and other cognitive functions, influencing personality and memory and being related to neurodegenerative diseases such as, Alzheimer’s disease, bipolar disorders and depression. In particular, many studies have highlighted a tight connection between BDNF levels and depression, suggesting that this disease could be caused by a decrease of the protein in the brain. It has been noticed that negative effects on mood could be lowered by inhibiting the reuptake of neurotransmitters, such as serotonin, that are able to increase the expression of BDNF. In fact, the inhibition of reuptake from axons causes these molecules to accumulate into the synaptic space thus having more time to act on neurons and glial cells. The SSRIs (selective serotonin reuptake inhibitors) selectively and powerfully inhibit serotonin reuptake resulting in a potentiation of serotonergic neurotransmission. However, the efficacy of these antidepressants cannot be only explained by their actions on the monoaminergic system and hence the mechanism of action of antidepressant drugs remain largely unknown, in particular the molecular and cellular adaptations that underlie the therapeutic action of these drugs. It has been found that antidepressants are also able to act on glial cells in rat models and it is possible that a reduction of these cells and their neuron-supporting action is involved in the pathophysiology of different psychiatric deseases. To investigate the effects of paroxetine on BDNF expression and on the release of protein in non-neural cells, we used a human glioblastoma-astrocytoma cell line, U-87 MG. Cultured cells were treated with the antidepressant at the final concentration of 7 µM for different time lengths (6, 12, 24, 48 hours). Expression of BDNF mRNA and miR-30-5p were analyzed by reverse transcription Real-Time PCR. We also studied BDNF concentration in the cultured cells and the medium through Enzyme-Linked Immunosorbent Assay, in order to detect protein synthesis and release induced by treatment. We observed that BDNF mRNA expression was significantly increased in the first 6 hours of paroxetine treatment with respect to non treated cells. In treated cells, this overexpression led to an increase in protein production after 12 hours of incubation and, in particular, in the release of BDNF protein in the culture medium already after 24 hours, while in non treated cells we observed BDNF protein in medium only after 48 hours. miR expression reaches a peak at 12 hours. Our results suggested that paroxetine treatment in this non-neuronal cell line increases BDNF expression, resulting in greater protein synthesis and release. These cells are not able to produce serotonin or other neurotransmitters because they are non-neuronal cells. Paroxentine seems to affect these non-neuronal cells in a similar manner to neuronal cells, but one would suspect that the effect occurs via an alternative pathway, independent from the neuronal monoaminergic system. The enhanced and prolonged induction of BDNF by antidepressants could promote neuronal survival, and protect neurons, such as glial cells, from the damaging effects of stress. This could contribute to explain therapeutic action of antidepressants suggesting new strategies of pharmacological intervention.
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CARIA, PAOLA. « Isolamento e caratterizzazione biologico-molecolare di cellule tumorali simil-staminali da una linea cellulare derivata da un carcinoma papillare tiroideo ». Doctoral thesis, Università degli Studi di Cagliari, 2012. http://hdl.handle.net/11584/266064.
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Recent reports have shown that tumor growth is supported by a specific subpopulation of stem cells, known as cancer stem cells (CSCs) or tumor-initiating cells. This cells have stem-like features, such as self renewal,multipotency, high migration capacity, drug resistance and aberrant differentiation. CSCs have been detected in several kind of tumors and in cancer cell lines grown as non-adherent spheres in serum–free medium under intense stimulation whit growth factors. Presence of cancer stem-like cells in thyroid differentiated carcinoma has not yet fully investigated and the literature on such issue is still limited. The objective of this study was to identify and characterize CSCs from a cancer cell line from papillary thyroid carcinoma (B-CPAP) and a cell line, derived from human thyroid follicular cells (N-THY-ORI 3-1), as control.
Thyrospheres from B-CPAP cells could be propagated up to ten generations, whereas those from N-THY-ORI 3-1 lasted only for four generations. The “stemness” profile was evaluated by functional assays and RT-PCR. B-CPAP sphere forming efficiency (SFE) and self renewal increased exponentially at every generation with maximum value at the 8th. By contrast, N-THY-ORI 3-1 SFE and self renewal progressively decreased along generations. RT-PCR showed mRNA expression of stem cell markers (Oct 4, Nanog, ABCG2) and early and thyroid late differentiation markers (PAX8, TTF1, Tg) in B-CPAP thyrosphere. In particular, ABCG2 expression significantly increased in thyrospheres at 9th generation. On the contrary, PAX8, TTF1 and Tg showed a decrease in thyrosphere along the generation of spheres, while p63 maintained the same expression in all samples. Thyrospheres from non tumorigenic cell line were positive for mRNA expression of stem cell markers (Oct4, Nanog, ABCG2,) and PAX8. In this cell line, Nanog and ABCG2 mRNA expression increased along the generations. To isolate stem-like cells in tumor and normal thyrospheres, we used the fluorescent dye PKH26. The single cells suspensions from thyrospheres were then FACS sorted. According to fluorescent intensity we selected two populations: the brightest fluorescent cells (PKH26 high), which constitute the putative stem cell population and the dimmest fluorescent cells (PKH26 low), which represent proliferating and differentiated cells. Both populations were able to form sphere, but only PKH26 high formed secondary spheres. The molecular analysis showed a higher stem cell marker mRNA expression in PKH26 high compare to PKH26 low cells. On the contrary TTF-1, PAX8 and Tg mRNA were more expressed in PKH26 low cells. Take together, our data show, for the first time, that B-CPAP and N-THY-ORI 3-cell lines contain cells with features and properties of stem cell.
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Sammarini, Giulia <1989>. « Alterazione di pathway epigenetici come meccanismo di resistenza ad Imatinib in una linea cellulare di CML ». Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amsdottorato.unibo.it/8550/1/Tesi%20Dottorato_Sammarini.pdf.
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La CML è una patologia mieloproliferativa risultante dall’espansione policlonale di cellule staminali Il trattamento d’elezione è imatinib (IM). Nonostante il successo di IM nel giro di 18-24 mesi, circa il 30% dei pazienti sviluppa resistenza secondaria. Lo scopo del mio progetto è stato quello di indagare i possibili meccanismi genetici ed epigenetici (come la deregolazione dei miRNA e la metilazione aberrante del DNA) per determinare in che modo possano contribuire all’insorgenza di resistenza. Sono state allestite culture cellulari di K562 resistenti ad IM (da 0,05 fino a 3 µM). I miRNA sono stati analizzati per identificare un profilo caratteristico del processo di resistenza, mentre per gli mRNA sono state ricercate alterazioni nell’espressione dei geni addetti al trasporto dei farmaci. Per quanto riguarda il DNA, è stato valutato come variano i livelli di metilazione durante il processo di acquisizione della resistenza analizzando oltre 850.000 siti CpG.
Dall’analisi dell’espressione dei trasportatori dei farmaci, è emerso che geni della famiglia dei trasportatori ABC sono sovraespressi nelle cellule resistenti. Per quanto riguarda i miRNA, è emerso che 6 miRNA sono significativamente deregolati: miR-193b-3p, miR-486-5p, miR-512-3p, miR-517a-3p, miR-365a-3p, miR-372-3p. Questi modulano geni appartenenti al pathway di segnalazione di ErbB e PI3K/Akt, coinvolti nei processi di vitalità cellulare, apoptosi, metabolismo e tumorigenesi. Per quanto riguarda la metilazione è stato osservato che, con l’incremento della dose somministrata, il numero di geni metilati aumenta notevolmente e, che in particolare, i geni PTPRF, TP73, ARHGEF10, FHDC1, DUSP6, PLD6 e MIR548H4 sono significativamente ipermetilati nelle cellule resistenti.
Conclusioni. Data la recente attenzione rivolta verso il ruolo dei meccanismi epigenetici nell’insorgenza di resistenza, è possibile che un profiling genetico ed epigenetico, che tenga conto di come interagiscono fra loro i trasportatori di efflusso, i miRNA e la metilazione del DNA, possa rappresentare una svolta per la terapia mirata.CML is a myeloproliferative disorder resulting from polyclonal stem cell expansion. The standard treatment is imatinib (IM). Despite the success of IM, within 18-24 months about 30% of patients develop secondary resistance. The aim of my project was to investigate possible genetic and epigenetic mechanisms (as the deregulation of miRNAs and aberrant DNA methylation), to determine how they can contribute to the resistance mechanism. Cell cultures of K562 resistant to IM (0.05 -3 μM) were set up. MiRNA, RNA and DNA were isolated. The miRNAs were analysed with a preformed tool to identify a profiling of the resistance process, while for mRNA alterations in the expression of the genes involved in the transport of drugs were sought. Regarding DNA, we analysed how methylation levels vary during the development of resistance by analyzing over 850,000 CpG sites. From the analysis of the drug transporters, it has emerged that many of the superfamily genes of the ABC transporters are overexpressed in the cells that have acquired resistance. Among these, worthy of note are ABCG2, ABCA3 and ABCC1. Comparing the miRNA expressions to the different concentrations with untreated, we observed that 6 miRNAs are significantly deregulated: miR-193b-3p, miR-486-5p, miR-512-3p, miR-517a-3p, miR-365a -3p, miR-372-3p. These miRNAs modulate genes belonging to the ErbB signaling pathway, involved in the processes of modulation of cell viability, apoptosis, and tumorigenesis mechanism. Regarding methylation, it has been observed that the number of methylated genes increases considerably and the PTPRF, TP73, ARHGEF10, FHDC1, DUSP6, PLD6 and MIR548H4 genes are significantly hypermethylated in resistant cells. Given the recent attention to the role of epigenetic mechanisms in the onset of resistance, it is possible that a genetic and epigenetic profiling, which takes into account how the efflux transporters, miRNAs and DNA methylation interact, can represent a carried out for target therapy.
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MONGUZZI, ERIKA. « EFFETTO DELLA GLIADINA SUL BILANCIO OSSIDATIVO E DANNO AL DNA NELLA LINEA CELLULARE CACO-2 E IN PAZIENTI CELIACI ». Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/490822.
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In recent years a significant increase of gluten-related disorders (GRDs) has been observed. Two factors seem at the basis of this increase. The first set would be related to the diffusion of serological tests. The second set of data associated with the increased prevalence of CD and GRDs could be related to an increase in the global consumption of wheat in recent decades; Cereals that contain gluten are widely consumed and current wheat varieties have a higher content in gluten compared to the past due to changes directed by both technology and nutritional reasons.
In the past, classification of GRDs was very simple, because CD and Dermatitis Herpetiformis (DH) were the only known diseases with a well-documented role of gluten in their pathogenesis.
Increasing complexity in the nomenclature and clinical presentation of GRDs has led to the development of a consensus document by a panel of experts on new classification including: CD, Non-Coeliac Gluten Sensitivity (NCGS), Wheat Allergy (WA) DH, and gluten ataxia (GA) although there can show considerable overlap in the clinical presentation.
Each gluten-related disorder exhibits a specific pathophysiological response to gluten ingestion. Gluten is the main structural protein complex of wheat with equivalent toxic proteins found in other cereals, including rye and barley. The toxic protein fractions of gluten include gliadins and glutenins, with gliadins containing monomeric proteins and glutenins containing aggregated proteins.
In wheat allergy (WA) and celiac disease (CD) the reaction to gluten is mediated by T-cell activation in the gastrointestinal mucosa. However, in WA it is the cross-linking of immunoglobulin (Ig)E by repeat sequences in gluten peptides (for example, serine-glutamine-glutamine -glutamine-(glutamine-) proline-proline-phenylalanine) that triggers the release of chemical mediators, such as histamine, from basophils and mast cells. Whereas in CD it is characterized as a chronic duodenal inflammation in which the increased secretion of inflammatory cytokines may in turn derange intestinal permeability and produce large amounts of reactive oxygen species (ROS), altering the redox state at the cellular level.
Oxidative stress has been defined as the imbalance between the production of ROS and the antioxidant defenses of the cells in favor of the oxidants, leading to potential damage. ROS are produced during the cellular metabolic processes; if the production of ROS overwhelms a cell’s antioxidant (AO) capability, a condition known as oxidative stress occurs.
The impairment of redox equilibrium proved to cause severe damage in proteins, lipids and DNA. In the last decade several studies showed that gluten exposure reflects in an intracellular oxidative imbalance, characterized by: increased levels of lipid peroxidation products (4-hydroxy-2(E)-nonenal (4-HNE)), increased oxidized (GSSG)/reduced (GSH) glutathione ratio and decreased number of protein-bound sulfhydryl groups.
Finally, ROS can induce the formation of oxidative DNA lesion products (8-oxodG), which is considered as a mutagenicity marker. Oxidative damage can lead to single or double-strand breaks, point and frameshift mutations and chromosome abnormalities. There is considerable circumstantial evidence that oxidative DNA damage may play an important role not only in carcinogenesis, being used as a predictive marker of cancer development, but also in aging. Nowadays, studies concerning oxidative damage on DNA have not been developed with regard to CD.
The aim of this study was to investigate a possible gliadin-induced genotoxic damage and its correlation with oxidative stress in vitro and in vivo.
The in vitro models consist of Caco-2 cell line of heterogeneous human epithelial colorectal adenocarcinoma cells generally used for this type of study. Whereas the in vivo model has been used serum and duodenal biopsies of patients.
For this study the Caco-2 cells have been exposed for maximum 24h to increasing concentrations (250µg/mL‒1000µg/mL) of digested gliadin (PT gliadin). Starting from a 500µg/mL dose (with a 12-hour contact time), an increase of reactive oxygen species (ROS) (DCFDA probe) was observed. The alkaline Comet assay showed DNA damage at a concentration of 1000 g/mL after 24h, characterized by a significant increase of DNA in the tail. Furthermore, the enzyme-modified Comet assay showed oxidative damage mainly with endonuclease-III, calculated as ∆ tail moment after 24h treatment at 1000µg/mL. Moreover, immunohistochemistry ɣ-H2AX detection (focal phosphorylation of histone H2AX at serine 139 to generate ɣ-H2AX in response to double-strand breaks) demonstrated an increase of the number of foci at 500µg/mL and 1000 µg/mL as genotoxic signature. The transglutaminase type 2 (TG2) activity was evaluated by western blot and ELISA method. The results show an increase of the enzyme expression in the chromatin and cytoskeleton at different doses (250, 500, and 1000µg/mL) compatible with apoptosis, as confirmed by annexin V (cytofluorometric staining method). Has been observed an increase of apoptotic cells starting from a 250 µg/ml dose.
The oxidative stress has been evaluated through the analysis of biomarkers into the serum of patients: naïve celiac disease (nCD), celiac patient responders, undergoing to gluten free diet at least 12 months (CD-GDF), refractory celiac patient non responders, undergoing to gluten free diet at least 12 months (RCD) and healthy subjects (CTRL). The results demonstrated that Total Antioxidant Capacity (TAC) appeared to be significantly decreased in patients RCD respect to CD-GDF (p<0.05) and to CTRL (p<0.001). Plasmatic concentrations of TBARS, assessed as marker of lipid peroxidation and protein carbonyls (PC), assessed as marker of protein oxidation, were found significantly increased in RCD respect to CD-GDF, while the plasma levels of CD-GDF resulted similar to CTRL in both plasma biomarkers.
Whereas the genotoxic damage was confirmed in vivo at the duodenal biopsy of celiac patients by means of H2AX e 8-OHG immunohistochemistry.
In conclusion digested gliadin induces an increase of ROS production in Caco-2 cells with an alteration of the cellular redox state. Moreover, the high concentration of ROS induces DNA damage and the stimulation of the apoptotic process. This mechanism seems present also in vivo as demonstrated by the findings from CD patients.
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PERRONE, DONATELLA. « Le cancer stem cells nei tumori della regione testa-collo : studio in vitro ed in vivo della linea cellulare HEP2 ». Doctoral thesis, Università di Foggia, 2014. http://hdl.handle.net/11369/331740.
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Abstract
Recenti evidenze scientifiche hanno proposto un nuovo modello di tumorigenesi, secondo il quale l’origine di un tumore dipende da un accumulo sequenziale e stocastico di mutazioni all’interno di una popolazione cellulare eterogenea costituente uno specifico tessuto. Benché le cellule tumorali spesso esibiscono un largo numero di mutazioni, solo una piccola sottopopolazione risulta cruciale per lo sviluppo ed il mantenimento del tumore. Studi condotti a tale riguardo hanno evidenziato che il cancro origina e viene mantenuto da cellule che posseggono caratteristiche di staminalità, ossia capacità di auto-rinnovamento e di differenziazione. Questa sottopopolazione di cellule cancerose è stata definita come “cellule staminali tumorali” (o cancer stem cells, CSCs) e ad oggi è ritenuta principale responsabile della progressione neoplastica e possibile causa dell’eterogeneità del tumore.
Le CSCs rappresentano, dunque, un modello utile per studiare i meccanismi alla base dell’oncogenesi, prerequisito fondamentale per perseguire l’obiettivo ultimo di individuazione di nuovi target molecolari specifici per terapie topiche nel trattamento dei tumori HNSCC. In quest‘ottica è risultato interessante affrontare uno studio volto all’identificazione e alla caratterizzazione molecolare e fenotipica delle cellule staminali cancerose nel tumore della regione testa-collo (Head and neck squamous cell carcinoma, HNSCC). Tale ricerca è stata condotta a carico delle Hep-2, una linea cellulare continua e ben differenziata di carcinoma laringeo umano. Mediante uno specifico protocollo di crescita, la coltura cellulare di Hep-2 è stata arricchita in cancer stem cells. Successivamente, il potenziale tumorigenico delle Hep-2 arricchite in CSCs è stato valutato mediante analisi in vivo.
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DUGNANI, ERICA. « Identificazione e validazione di potenziali marcatori biologici nell’adenocarcinoma duttale del pancreas ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/76153.
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Introduzione. L’adenocarcinoma duttale (PDAC) rappresenta circa l’85% delle neoplasie maligne pancreatiche. È un tipo di neoplasia molto aggressiva e ha prognosi infausta. Il PDAC è una malattia con una elevata mortalità, spesso diagnosticata in uno stadio avanzato per il quale esistono poche e inefficaci terapie. L’alta incidenza di ricadute locali unita alla precoce metastatizzazione sono le caratteristiche cliniche più tipiche di questo tumore. Inoltre la nota resistenza del tumore alla chemio e alla radioterapia limita l’efficacia di questi approcci terapeutici.
Scopo. Identificare e validare nuovi marcatori biologici associati a caratteristiche di aggressività dell’adenocarcinoma pancreatico al fine di utilizzarli per comprendere proprietà biologiche del tumore stesso o in clinica per una corretta valutazione prognostica.
Metodi e risultati. Abbiamo studiato n=17 linee cellulari umane immortalizzate di PDAC per alcune caratteristiche di aggressività cellulare: per la clonogenicità e la chemioresistenza alla gemcitabina in vitro e, in vivo, per la capacità di crescita in topi immunocompromessi (CD1-nude). Tutte le 17 linee cellulari sono state caratterizzate per l’espressione di classi di marcatori molecolari: recettori delle chemochine (CCR1-CCR10; CXCR1-CXCR6; CX3CR1; XCR1) e putativi marcatori staminali tumorali (ESA+CD24+CD44+; CD133+, CXCR4+) mediante citometria a flusso, secrezione di fattori solubili (n=48) tramite la tecnologia luminex e l’espressione di geni (n=11) coinvolti nello sviluppo pancreatico con Real Time PCR. Usando l’analisi statistica inter-linea (regressione lineare o di cox) abbiamo cercato una correlazione tra i fenotipi biologici e le caratteristiche di malignità cellulare individuando nuovi marcatori. Questi marcatori sono stati validati su tessuti tumorali primari in casistiche di pazienti affetti da PDAC: l’espressione del marcatore identificato è stata correlata con l’esisto clinico della neoplasia.
In una prima analisi inter-linea n=35 fattori sono risultati statisticamente associati ad una o più caratteristiche di aggressività. È seguita una classificazione per priorità che, avvalendosi della sola correlazione con la tumorigenicità in vivo, ha ridotto a n=20 i fattori di rischio da validare. Abbiamo quindi approfondito lo studio su 4 marcatori molecolari di sviluppo pancreatico (ISL1, PDX1, PAX6, KRT19), sui fenotipi staminali e su 2 recettori delle chemochine (CCR5, CXCR3).
L’espressione genica dell’mRNA di ISL1, PDX1, PAX6 e KRT19 è stata valutata in sezioni criostatiche di n=42 resezioni chirurgiche di pazienti affetti da PDAC. Non sono emerse correlazioni significative tra l’espressione di questi fattori e la sopravvivenza globale. Tuttavia alti livelli dell’mRNA di KRT19 predicono una progressione più precoce e di tipo metastatico. Più elevati livelli di PDX1 e PAX6 sono associati con una più alta probabilità di recidiva locale. Inoltre combinando i marcatori è stato individuato un fenotipo più aggressivo correlato con una minor sopravvivenza: si tratta dei pazienti che esprimono ad elevati livelli sia PDX1 che KRT19.
La nostra strategia di screening ha mostrato essere fattori di rischio per lo sviluppo tumorale nel topo, non i classici fenotipi staminali descritti in letteratura (ESA+/CD24+/CD44+, CD133+, CD133+/CXCR4+) ma la combinazione ESA+/CD24-/CD44+ e la sola espressione di CXCR4 ed ESA: tuttavia la validazione clinica, condotta su una coorte di 39 pazienti affetti da adenocarcinoma duttale, non ha confermato che questi marcatori, né i classici già descritti, correlino in maniera statisticamente significativa con la sopravvivenza o con la progressione nel tempo e nemmeno con il sito di recidiva. Il fenotipo ESA+/CD24+/CD44- è invece risultato un fattore di rischio prognostico indipendente sia per la sopravvivenza (HR=4,166 p=0,001) che per la progressione (HR=2,208 p=0,019).
CCR5 e CXCR3 sono risultati espressi su tessuti tumorali processati a fresco (n=6) ed analizzati in citometria a flusso a fronte di una negatività del pancreas di donatori d’organo (n=10). Essi sono espressi rispettivamente nell’11,9% e nel 17,6% delle cellule CA19.9+ del tumore, mentre solo nello 0,4% e il 0,34% nel tessuto sano. L’aumentata espressione di CCR5 e CXCR3 sembra essere una caratteristica tipica del PDAC.
Conclusioni. La nostra strategia ha identificato marcatori biologici capaci di distinguere differenti comportamenti clinici del tumore in termini di progressione e sede di recidiva. La differente espressione di questi predittori potrebbe essere la causa di differenze biologiche che hanno un effetto sui meccanismi di progressione e diffusione tumorale. Al fine di confermare i nostri risultati stiamo realizzando un tissue microarray di resezioni chirurgiche di pazienti affetti da adenocarcinoma duttale. Inoltre in futuro il modello statistico sviluppato potrà essere applicato per testare ogni nuovo potenziale marcatore; caratterizzata la sua espressione sulle linee cellulari, si procederà con l’analisi inter-linea per verificare se sia un potenziale indicatore di aggressività in vitro o in vivo nel modello murino; quindi si potrà confermare il suo reale ruolo diagnostico, prognostico o predittivo in ambito clinico.
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SCATURRO, Anna Lisa. « Sintesi, caratterizzazione e nuove strategie formulative per la somministrazione di nuovi derivati dopaminici nella terapia della malattia di Parkinson ». Doctoral thesis, Università degli Studi di Palermo, 2014. http://hdl.handle.net/10447/91186.
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AMARU', JESSICA. « Fisiopatologia dei recettori della somatostatina nei tumori ipofisari GH-secernenti ». Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1046906.
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First-generation somatostatin receptor ligands (fg-SRLs), such as octreotide (OCT), represent the first-line medical therapy in acromegaly. Fg-SRLs show a preferential binding affinity for somatostatin receptor subtype-2 (SST2), while the second-generation ligand, pasireotide (PAS), has high affinity for multiple SSTs (SST5 > SST2 > SST3 > SST1). Whether PAS acts via SST2 in somatotroph tumors, or through other SSTs (e.g., SST5), is a matter of debate. In this light, the combined treatment OCT+PAS could result in additive/synergistic effects. We evaluated the efficacy of OCT and PAS (alone and in combination) on growth hormone (GH) secretion in primary cultures from human somatotroph tumors, as well as on cell proliferation, intracellular signaling and receptor trafficking in the rat GH4C1 cell line. The results confirmed the superimposable efficacy of OCT and PAS in reducing GH secretion (primary cultures), cell proliferation, cAMP accumulation and intracellular [Ca2+] increase (GH4C1 cells), without any additive effect observed for OCT+PAS. In GH4C1 cells, co-incubation with a SST2-selective antagonist reversed the inhibitory effect of OCT and PAS on cell proliferation and cAMP accumulation, while both compounds resulted in a robust internalization of SST2 (but not SST5). In conclusion, OCT and PAS seem to act mainly through SST2 in somatotroph tumor cells in vitro, without inducing any additive/synergistic effect when tested in combination.
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Dempsey, Benjamin. « Thermal properties of linear cellular alloys ». Thesis, Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/17968.
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Hayes, Alethea M. « Compression behavior of linear cellular steel ». Thesis, Georgia Institute of Technology, 2001. http://hdl.handle.net/1853/32857.
Texte intégralLivres sur le sujet "Linea cellulare"
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K, Kamrani Ali, Parsaei H. R et Liles Donald H, dir. Planning, design, and analysis of cellular manufacturing systems. Amsterdam : Elsevier, 1995.
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Productivity Development Team (Productivity Press), dir. Cellular manufacturing : One-piece flow for workteams. Portland, OR : Productivity Press, 1999.
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Hughes, Marija Matich. Computers, antennas, cellular telephones and power lines health hazards. Washington, D.C : Hughes Press, 1996.
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B, Roninson Igor, dir. Molecular and cellular biology of multidrug resistance in tumor cells. New York : Plenum Press, 1991.
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Arichika, Namikawa, et Raedler Elisabeth, dir. Cleavage lines of the skin. Basel : Karger, 1986.
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Bear, Greg. Dead lines. New York : Ballantine Books, 2004.
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Bear, Greg. Dead lines. New York : Ballantine Books, 2004.
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Bear, Greg. Dead Lines. New York : Random House Publishing Group, 2004.
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Richard, Barrett, dir. Templates for the solution of linear systems : Building blocks for iterative methods. Philadelphia : SIAM, 1994.
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San Francisco (Calif.). Office of the Controller. Audits Division. Airport Commission : Concession audit of Action Cellular Rent-A-Phone, Inc. San Francisco : Office of the Controller, 2003.
Trouver le texte intégralChapitres de livres sur le sujet "Linea cellulare"
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Ceccherini-Silberstein, Tullio, et Michel Coornaert. « Linear Cellular Automata ». Dans Springer Monographs in Mathematics, 283–342. Berlin, Heidelberg : Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-14034-1_8.
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Garzon, Max. « Linear Cellular Automata ». Dans Models of Massive Parallelism, 39–62. Berlin, Heidelberg : Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-77905-3_3.
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Hadeler, Karl-Peter, et Johannes Müller. « Linear Cellular Automata ». Dans Springer Monographs in Mathematics, 287–334. Cham : Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53043-7_10.
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Sutner, K. « Linear Cellular Automata and de Bruijn Automata ». Dans Cellular Automata, 303–19. Dordrecht : Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-015-9153-9_12.
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Sutner, Klaus. « Linear Cellular Automata and Decidability ». Dans Automata, Universality, Computation, 259–76. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-09039-9_12.
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Cardell, Sara Díaz, et Amparo Fúster-Sabater. « Modelling Through Linear Cellular Automata ». Dans SpringerBriefs in Mathematics, 45–63. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-12850-0_3.
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Katz, Sheldon. « Cellular decompositions and line bundles ». Dans Enumerative Geometry and String Theory, 77–93. Providence, Rhode Island : American Mathematical Society, 2006. http://dx.doi.org/10.1090/stml/032/06.
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Fasler-Kan, Elizaveta, Nijas Aliu, Kerstin Wunderlich, Sylvia Ketterer, Sabrina Ruggiero, Steffen Berger et Peter Meyer. « The Retinal Pigment Epithelial Cell Line (ARPE-19) Displays Mosaic Structural Chromosomal Aberrations ». Dans Cellular Heterogeneity, 305–14. New York, NY : Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7680-5_17.
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Patra, Narayan. « On-line Frequency Reallocation for Call Requests in Linear Wireless Cellular Networks ». Dans Lecture Notes in Networks and Systems, 1097–107. Singapore : Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-0146-3_106.
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Hasselbaink, Danny M., Theo H. M. Roemen et Ger J. van der Vusse. « Protein acylation in the cardiac muscle like cell line, H9c2 ». Dans Cellular Lipid Binding Proteins, 101–12. Boston, MA : Springer US, 2002. http://dx.doi.org/10.1007/978-1-4419-9270-3_14.
Texte intégralActes de conférences sur le sujet "Linea cellulare"
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Tavsanoglu, Vedat. « Jacobi's Iterative Method for Solving Linear Equations and the Simulation of Linear CNN ». Dans 2006 10th International Workshop on Cellular Neural Networks and Their Applications. IEEE, 2006. http://dx.doi.org/10.1109/cnna.2006.341622.
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« The Effect of Allicin on ZNF703 Gene Expression in GCC Lines ». Dans International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916405.
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Popovici, Adriana, et Dan Popovici. « Dilatability to Quantum Linear Cellular Automata ». Dans 12th International Symposium on Symbolic and Numeric Algorithms for Scientific Computing (SYNASC 2010). IEEE, 2010. http://dx.doi.org/10.1109/synasc.2010.28.
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Arnoux, D., B. Boutière, N. Pourreau-Schneider, P. Martin et J. Sampol. « PLASMINOGEN ACTIVATORS (t-PA and u-PA) IN HUMAN NEOPLASTIC CELL LINES AND THEIR MODULATION BY BASEMENT MEMBRANE COMPONENTS ». Dans XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643190.
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Plasminogen activators (PA)may play an important role in the regulation of enzyme activation relative to basement membrane degradation associated with the invasive growth of tumors. In order to acquire a better understanding of the complex cascade reactions leading to the formation of plasmin, we have undertaken a comparative study of urokinase-type (u-PA) and tissue-type (t-PA) plasminogen activators in cellular extracts of 20 human cancer cell lines (13 malignant melanomas, 6 breast adenocarcinomas and 1 vulvar carcinoma). Four malignant cell lines,showing various t-PA or u-PA activity levels, were selected to study the modulation of proteolytic activity by laminin and fibronectin, major components of basal membrane. This study was performed in cellular extracts and conditioned medium. Our results showed that melanoma cells have high t-PA activity preferentially released into the culture medium. On the vulvar cell line, A 431, u-PA activity predominates and is also secreted into the medium. In contrast, breast cancer cells MCF-7 and MDA show u-PA activity, mostly recovered in the cellular extracts. An enhancement of respective PA activities occurs when cells are cultured on fibronectin or laminin, varying with the nature of the cell line.Additional studies are needed to precise interrelation between tumor cells, basement membrane components and PA activities and the potential significance of proteolytic activities as markers of malignancy and invasive capacity.
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« The Effects of Valproic Acid on Viability of MCF-7 Cell Line ». Dans International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916406.
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Nagai, M., K. Tanizaki, Y. Hayasaka, T. Kawashima et T. Shibata. « Microfluidic cellular valve powerd by linear bioactuator ». Dans 2013 Transducers & Eurosensors XXVII : The 17th International Conference on Solid-State Sensors, Actuators and Microsystems (TRANSDUCERS & EUROSENSORS XXVII). IEEE, 2013. http://dx.doi.org/10.1109/transducers.2013.6627113.
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Stanica, George Cosmin, et Petre Anghelescu. « Encryption Algorithm using Linear Hybrid Cellular Automaton ». Dans 2022 International Semiconductor Conference (CAS). IEEE, 2022. http://dx.doi.org/10.1109/cas56377.2022.9934500.
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Santti, Tero, Olli Lahdenoja, Ari Paasio, Mika Laiho et Jonne Poikonen. « Line Detection on FPGA with parallel sensor-level segmentation ». Dans 2014 14th International Workshop on Cellular Nanoscale Networks and their Applications (CNNA). IEEE, 2014. http://dx.doi.org/10.1109/cnna.2014.6888648.
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Caragiannis, Ioannis, Christos Kaklamanis et Evi Papaioannou. « Efficient on-line communication in cellular networks ». Dans the twelfth annual ACM symposium. New York, New York, USA : ACM Press, 2000. http://dx.doi.org/10.1145/341800.341807.
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Mojica, Eduardo, Alain Gauthier et Naly Rakoto-Ravalontsalama. « Canonical piecewise-linear approximation of nonlinear cellular growth ». Dans 2007 46th IEEE Conference on Decision and Control. IEEE, 2007. http://dx.doi.org/10.1109/cdc.2007.4434461.
Texte intégralRapports d'organisations sur le sujet "Linea cellulare"
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Granot, David, Scott Holaday et Randy D. Allen. Enhancing Cotton Fiber Elongation and Cellulose Synthesis by Manipulating Fructokinase Activity. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7613878.bard.
Texte intégralRésumé :
a. Objectives (a) Identification and characterization of the cotton fiber FRKs; (b) Generating transgenic cotton plants overproducing either substrate inhibited tomato FRK or tomato FRK without substrate inhibition; (c) Generating transgenic cotton plants with RNAi suppression of fiber expressed FRKs; (d) Generating Arabidopsis plants that over express FRK1, FRK2, or both genes, as additional means to assess the contribution of FRK to cellulose synthesis and biomass production. b. Background to the topic: Cellulose synthesis and fiber elongation are dependent on sugar metabolism. Previous results suggested that FRKs (fructokinase enzymes that specifically phosphorylate fructose) are major players in sugar metabolism and cellulose synthesis. We therefore hypothesized that increasing fructose phosphorylation may enhance fiber elongation and cellulose synthesis in cotton plants. Accordinlgy, the objectives of this research were: c. Major conclusions and achievements: Two cotton FRKs expressed in fibers, GhFRK2 and GhFRK3, were cloned and characterized. We found that GhFRK2 enzyme is located in the cytosol and GhFRK3 is located within plastids. Both enzymes enable growth on fructose (but not on glucose) of hexose kinase deficient yeast strain, confirming the fructokinase activity of the cloned genes. RNAi constructs with each gene were prepared and sent to the US collaborator to generate cotton plants with RNAi suppression of these genes. To examine the effect of FRKs using Arabidopsis plants we generated transgenic plants expressing either LeFRK1 or LeFRK2 at high level. No visible phenotype has been observed. Yet, plants expressing both genes simultaneously are being created and will be tested. To test our hypothesis that increasing fructose phosphorylation may enhance fiber cellulose synthesis, we generated twenty independent transgenic cotton plant lines overexpressing Lycopersicon (Le) FRK1. Transgene expression was high in leaves and moderate in developing fiber, but enhanced FRK activity in fibers was inconsistent between experiments. Some lines exhibited a 9-11% enhancement of fiber length or strength, but only one line tested had consistent improvement in fiber strength that correlated with elevated FRK activity in the fibers. However, in one experiment, seed cotton mass was improved in all transgenic lines and correlated with enhanced FRK activity in fibers. When greenhouse plants were subjected to severe drought during flowering and boll development, no genotypic differences in fiber quality were noted. Seed cotton mass was improved for two transgenic lines but did not correlate with fiber FRK activity. We conclude that LeFRK1 over-expression in fibers has only a small effect on fiber quality, and any positive effects depend on optimum conditions. The improvement in productivity for greenhouse plants may have been due to better structural development of the water-conducting tissue (xylem) of the stem, since stem diameters were larger for some lines and the activity of FRK in the outer xylem greater than observed for wild-type plants. We are testing this idea and developing other transgenic cotton plants to understand the roles of FRK in fiber and xylem development. We see the potential to develop a cotton plant with improved stem strength and productivity under drought for windy, semi-arid regions where cotton is grown. d. Implications, scientific and agricultural: FRKs are probably bottle neck enzymes for biomass and wood synthesis and their increased expression has the potential to enhance wood and biomass production, not only in cotton plants but also in other feed and energy renewable plants.
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Lillehoj, Hyun, Dan Heller et Mark Jenkins. Cellular and molecular identification of Eimeria Acervulina Merozoite Antigens eliciting protective immunity. United States Department of Agriculture, novembre 1992. http://dx.doi.org/10.32747/1992.7561056.bard.
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Coccidiosis, ubiquitous diseases of poultry, seriously impair the growth and feed utilization of livestock and poultry. Coccidiosis causes over $600 million annual losses world-wide and no vaccine is currently available. The goal of this study was to investigate the cellular and molecular mechanisms controlling protective immune responses to coccidia parasites in order to develop immunological control strategy against coccidiosis. The major findings of this study were: 1) cell-mediated immunity plays a major role in protection against coccidiosis, 2) when different genetic lines showing different levels of disease susceptibility were compared, higher T-cell response was seen in the strains of chickens showing higher disease resistance, 3) early interferon secretion was observed in more coccidia-resistant chicken strains, 4) both sporozoite and merozoite antigens were able to induce interferon production, and 5) chicken monoclonal antibodies which detect immunogenic coccidia proteins have been developed. This study provided a good background work for future studies toward the development of recombinant coccidial vaccine. Availability of chicken monoclonal antibodies which detect immunogenic coccidia proteins will enhance our ability to identify potential coccidial vaccine antigens.
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Pasheva, Evdokia, Maria Petrova, Shazie Yusein-Myashkova, Jordana Todorova et Iva Ugrinova. The Cellular Transloca tion of NF-κB in Breast Cancer Cell Lines Is Affected by HMGB1 Protein but Not by Its Truncated Form. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, août 2020. http://dx.doi.org/10.7546/crabs.2020.08.06.
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Naim, Michael, Andrew Spielman, Shlomo Nir et Ann Noble. Bitter Taste Transduction : Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, février 2000. http://dx.doi.org/10.32747/2000.7695839.bard.
Texte intégralRésumé :
Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.
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Lapidot, Moshe, et Vitaly Citovsky. molecular mechanism for the Tomato yellow leaf curl virus resistance at the ty-5 locus. United States Department of Agriculture, janvier 2016. http://dx.doi.org/10.32747/2016.7604274.bard.
Texte intégralRésumé :
Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomato that causes extensive crop loss worldwide, including the US and Israel. Genetic resistance in the host plant is considered highly effective in the defense against viral infection in the field. Thus, the best way to reduce yield losses due to TYLCV is by breeding tomatoes resistant or tolerant to the virus. To date, only six major TYLCV-resistance loci, termed Ty-1 to Ty-6, have been characterized and mapped to the tomato genome. Among tomato TYLCV-resistant lines containing these loci, we have identified a major recessive quantitative trait locus (QTL) that was mapped to chromosome 4 and designated ty-5. Recently, we identified the gene responsible for the TYLCV resistance at the ty-5 locus as the tomato homolog of the gene encoding messenger RNA surveillance factor Pelota (Pelo). A single amino acid change in the protein is responsible for the resistant phenotype. Pelo is known to participate in the ribosome-recycling phase of protein biosynthesis. Our hypothesis was that the resistant allele of Pelo is a “loss-of-function” mutant, and inhibits or slows-down ribosome recycling. This will negatively affect viral (as well as host-plant) protein synthesis, which may result in slower infection progression. Hence we have proposed the following research objectives: Aim 1: The effect of Pelota on translation of TYLCV proteins: The goal of this objective is to test the effect Pelota may or may not have upon translation of TYLCV proteins following infection of a resistant host. Aim 2: Identify and characterize Pelota cellular localization and interaction with TYLCV proteins: The goal of this objective is to characterize the cellular localization of both Pelota alleles, the TYLCV-resistant and the susceptible allele, to see whether this localization changes following TYLCV infection, and to find out which TYLCV protein interacts with Pelota. Our results demonstrate that upon TYLCV-infection the resistant allele of pelota has a negative effect on viral replication and RNA transcription. It is also shown that pelota interacts with the viral C1 protein, which is the only viral protein essential for TYLCV replication. Following subcellular localization of C1 and Pelota it was found that both protein localize to the same subcellular compartments. This research is innovative and potentially transformative because the role of Peloin plant virus resistance is novel, and understanding its mechanism will lay the foundation for designing new antiviral protection strategies that target translation of viral proteins. BARD Report - Project 4953 Page 2
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Chejanovsky, Nor, et Bruce A. Webb. Potentiation of pest control by insect immunosuppression. United States Department of Agriculture, juillet 2004. http://dx.doi.org/10.32747/2004.7587236.bard.
Texte intégralRésumé :
Our original aims were to elucidate the mechanisms through which the immunosuppressive insect virus, the Campoletis sonorensis polydnavirus (CsV) promotes replication of a well-characterized pathogenic virus, the Autographa californica multiple nucleopolyhedrovirus (AcMNPV) in hosts that are mildly or non-permissive to virus replication. According to the BARD panels criticism we modified our short-term goals (see below). Thus, in this feasibility study (one-year funding) we aimed to show that: 1. S. littoralis larvae mount an immune response against a baculovirus infection. 2. Immunosuppression of an insect pest improves the ability of a viral pathogen (a baculovirus) to infect the pest. 3. S. littoralis cells constitute an efficient tool to study some aspects of the anti- viral immune response. We achieved the above objectives by: 1. Finding melanized viral foci upon following the baculoviral infection in S . littoralis larvae infected with a polyhedra - positive AcMNPV recombinant that expressed the GFP gene under the control of the Drosophila heat shock promoter. 2. Studying the effect of AcMNPV-infection in S . littoralis immunosuppressed by parasitation with the Braconidae wasp Chelonus inanitus that bears the CiV polydna virus, that resulted in higher susceptibility of S. littoralis to AcMNPV- infection. 3. Proving that S. littoralis hemocytes resist AcMNPV -infection. 4. Defining SL2 as a granulocyte-like cell line and demonstrating that as littoralis hemocytic cell line undergoes apoptosis upon AcMNPV -infection. 5. Showing that some of the recombinant AcMNPV expressing the immuno-suppressive polydna virus CsV- vankyrin genes inhibit baculoviral-induced lysis of SL2 cells. This information paves the way to elucidate the mechanisms through which the immuno- suppressive polydna insect viruses promote replication of pathogenic baculoviruses in lepidopteran hosts that are mildly or non-permissive to virus- replication by: - Assessing the extent to which and the mechanisms whereby the immunosuppressive viruses, CiV and CsV or their genes enhance AcMNPV replication in polydnavirus- immunosuppressed H. zea and S. littoralis insects and S. littoralis cells. - Identifying CiV and CsV genes involved in the above immunosuppression (e.g. inhibiting cellular encapsulation and disrupting humoral immunity). This study will provide insight to the molecular mechanisms of viral pathogenesis and improve our understanding of insect immunity. This knowledge is of fundamental importance to controlling insect vectored diseases of humans, animals and plants and essential to developing novel means for pest control (including baculoviruses) that strategically weaken insect defenses to improve pathogen (i.e. biocontrol agent) infection and virulence.
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Jander, Georg, et Daniel Chamovitz. Investigation of growth regulation by maize benzoxazinoid breakdown products. United States Department of Agriculture, janvier 2015. http://dx.doi.org/10.32747/2015.7600031.bard.
Texte intégralRésumé :
Introduction Previous research had suggested that benzoxazinoids, a class of defensive metabolites found in maize, wheat, rye, and wild barley, are not only direct insect deterrents, but also influence other areas of plant metabolism. In particular, the benzoxazinoid 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxa- zin-3(4H)- one (DIMBOA) was implicated in: (i) altering plant growth by interfering with auxin signaling, and (ii) leading to the induction of gene expression changes and secondary plant defense responses. The overall goal of this proposal was to identify mechanisms by which benzoxazinoids influence other aspects of plant growth and defense. Specifically, the following hypotheses were proposed to be tested as part of an approved BARD proposal: Benzoxazinoid breakdown products directly interfere with auxin perception Global changes in maize and barley gene expression are induced by benzoxazinoid activation. There is natural variation in the maize photomorphogenic response to benzoxazinoids. Although the initial proposal included experiments with both maize and barley, there were some technical difficulties with the proposed transgenic barley experiments and most of the experimental results were generated with maize. Summary of major findings Previous research by other labs, involving both maize and other plant species, had suggested that DIMBOA alters plant growth by interfering with auxin signaling. However, experiments conducted in both the Chamovitz and the Jander labs using Arabidopsis and maize, respectively, were unable to confirm previously published reports of exogenously added DIMBOA effects on auxin signaling. Nevertheless, analysis of bx1 and bx2 maize mutant lines, which have almost no detectable benzoxazinoids, showed altered responses to blue light signaling. Transcriptomic analysis of maize mutant lines, variation in inbred lines, and responses to exogenously added DIMBOA showed alteration in the transcription of a blue light receptor, which is required for plant growth responses. This finding provides a novel mechanistic explanation of the trade-off between growth and defense that is often observed in plants. Experiments by the Jander lab and others had demonstrated that DIMBOA not only has direct toxicity against insect pests and microbial pathogens, but also induces the formation of callose in both maize and wheat. In the current project, non-targeted metabolomic assays of wildtype maize and mutants with defects in benzoxazinoid biosynthesis were used to identify unrelated metabolites that are regulated in a benzoxazinoid-dependent manner. Further investigation identified a subset of these DIMBOA-responsive compounds as catechol, as well as its glycosylated and acetylated derivatives. Analysis of co-expression data identified indole-3-glycerol phosphate synthase (IGPS) as a possible regulator of benzoxazinoid biosynthesis in maize. In the current project, enzymatic activity of three predicted maize IGPS genes was confirmed by heterologous expression. Transposon knockout mutations confirmed the function of the maize genes in benzoxazinoid biosynthesis. Sub-cellular localization studies showed that the three maize IGPS proteins are co-localized in the plastids, together with BX1 and BX2, two previously known enzymes of the benzoxazinoid biosynthesis pathway. Implications Benzoxazinoids are among the most abundant and effective defensive metabolites in maize, wheat, and rye. Although there is considerable with-in species variation in benzoxazinoid content, very little is known about the regulation of this variation and the specific effects on plant growth and defense. The results of this research provide further insight into the complex functions of maize benzoxazinoids, which are not only toxic to pests and pathogens, but also regulate plant growth and other defense responses. Knowledge gained through the current project will make it possible to engineer benzoxazinoid biosynthesis in a more targeted manner to produce pest-tolerant crops without negative effects on growth and yield.
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Cahaner, Avigdor, Susan J. Lamont, E. Dan Heller et Jossi Hillel. Molecular Genetic Dissection of Complex Immunocompetence Traits in Broilers. United States Department of Agriculture, août 2003. http://dx.doi.org/10.32747/2003.7586461.bard.
Texte intégralRésumé :
Objectives: (1) Evaluate Immunocompetence-OTL-containing Chromosomal Regions (ICRs), marked by microsatellites or candidate genes, for magnitude of direct effect and for contribution to relationships among multiple immunocompetence, disease-resistance, and growth traits, in order to estimate epistatic and pleiotropic effects and to predict the potential breeding applications of such markers. (2) Evaluate the interaction of the ICRs with genetic backgrounds from multiple sources and of multiple levels of genetic variation, in order to predict the general applicability of molecular genetic markers across widely varied populations. Background: Diseases cause substantial economic losses to animal producers. Emerging pathogens, vaccine failures and intense management systems increase the impact of diseases on animal production. Moreover, zoonotic pathogens are a threat to human food safety when microbiological contamination of animal products occurs. Consumers are increasingly concerned about drug residues and antibiotic- resistant pathogens derived from animal products. The project used contemporary scientific technologies to investigate the genetics of chicken resistance to infectious disease. Genetic enhancement of the innate resistance of chicken populations provides a sustainable and ecologically sound approach to reduce microbial loads in agricultural populations. In turn, animals will be produced more efficiently with less need for drug treatment and will pose less of a potential food-safety hazard. Major achievements, conclusions and implications:. The PI and co-PIs had developed a refined research plan, aiming at the original but more focused objectives, that could be well-accomplished with the reduced awarded support. The successful conduct of that research over the past four years has yielded substantial new information about the genes and genetic markers that are associated with response to two important poultry pathogens, Salmonella enteritidis (SE) and Escherichia coli (EC), about variation of immunocompetence genes in poultry, about relationships of traits of immune response and production, and about interaction of genes with environment and with other genes and genetic background. The current BARD work has generated a base of knowledge and expertise regarding the genetic variation underlying the traits of immunocompetence and disease resistance. In addition, unique genetic resource populations of chickens have been established in the course of the current project, and they are essential for continued projects. The US laboratory has made considerable progress in studies of the genetics of resistance to SE. Microsatellite-marked chromosomal regions and several specific genes were linked to SE vaccine response or bacterial burden and the important phenomenon of gene interaction was identified in this system. In total, these studies demonstrate the role of genetics in SE response, the utility of the existing resource population, and the expertise of the research group in conducting such experiments. The Israeli laboratories had showed that the lines developed by selection for high or low level of antibody (Ab) response to EC differ similarly in Ab response to several other viral and bacterial pathogens, indicating the existence of a genetic control of general capacity of Ab response in young broilers. It was also found that the 10w-Ab line has developed, possibly via compensatory "natural" selection, higher cellular immune response. At the DNA levels, markers supposedly linked to immune response were identified, as well as SNP in the MHC, a candidate gene responsible for genetic differences in immunocompetence of chickens.
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Shomer, Ilan, Ruth E. Stark, Victor Gaba et James D. Batteas. Understanding the hardening syndrome of potato (Solanum tuberosum L.) tuber tissue to eliminate textural defects in fresh and fresh-peeled/cut products. United States Department of Agriculture, novembre 2002. http://dx.doi.org/10.32747/2002.7587238.bard.
Texte intégralRésumé :
The project sought to understand factors and mechanisms involved in the hardening of potato tubers. This syndrome inhibits heat softening due to intercellular adhesion (ICA) strengthening, compromising the marketing of industrially processed potatoes, particularly fresh peeled-cut or frozen tubers. However, ICA strengthening occurs under conditions which are inconsistent with the current ideas that relate it to Ca-pectate following pectin methyl esterase (PME) activity or to formation of rhamnogalacturonan (RG)-II-borate. First, it was necessary to induce strengthening of the middle lamellar complex (MLX) and the ICA as a stress response in some plant parenchyma. As normally this syndrome does not occur uniformly enough to study it, we devised an efficient model in which ICA-strengthening is induced consistently under simulated stress by short-chain, linear, mono-carboxylic acid molecules (OAM), at 65 oC [appendix 1 (Shomer&Kaaber, 2006)]. This rapid strengthening was insufficient for allowing the involved agents assembly to be identifiable; but it enabled us to develop an efficient in vitro system on potato tuber parenchyma slices at 25 ºC for 7 days, whereas unified stress was reliably simulated by OAMs in all the tissue cells. Such consistent ICA-strengthening in vitro was found to be induced according to the unique physicochemical features of each OAM as related to its lipophilicity (Ko/w), pKa, protonated proportion, and carbon chain length by the following parameters: OAM dissociation constant (Kdiss), adsorption affinity constant (KA), number of adsorbed OAMs required for ICA response (cooperativity factor) and the water-induced ICA (ICAwater). Notably, ICA-strengthening is accompanied by cell sap leakage, reflecting cell membrane rupture. In vitro, stress simulation by OAMs at pH<pKa facilitated the consistent assembly of ICAstrengthening agents, which we were able to characterize for the first time at the molecular level within purified insoluble cell wall of ICA-strengthened tissue. (a) With solid-state NMR, we established the chemical structure and covalent binding to cell walls of suberin-like agents associated exclusively with ICA strengthening [appendix 3 (Yu et al., 2006)]; (b) Using proteomics, 8 isoforms of cell wall-bound patatin (a soluble vacuolar 42-kDa protein) were identified exclusively in ICA-strengthened tissue; (c) With light/electron microscopy, ultrastructural characterization, histochemistry and immunolabeling, we co-localized patatin and pectin in the primary cell wall and prominently in the MLX; (d) determination of cell wall composition (pectin, neutral sugars, Ca-pectate) yielded similar results in both controls and ICA-strengthened tissue, implicating factors other than PME activity, Ca2+ or borate ions; (e) X-ray powder diffraction experiments revealed that the cellulose crystallinity in the cell wall is masked by pectin and neutral sugars (mainly galactan), whereas heat or enzymatic pectin degradation exposed the crystalline cellulose structure. Thus, we found that exclusively in ICA-strengthened tissue, heat-resistant pectin is evident in the presence of patatin and suberinlike agents, where the cellulose crystallinity was more hidden than in fresh control tissue. Conclusions: Stress response ICA-strengthening is simulated consistently by OAMs at pH< pKa, although PME and formation of Ca-pectate and RG-II-borate are inhibited. By contrast, at pH>pKa and particularly at pH 7, ICA-strengthening is mostly inhibited, although PME activity and formation of Ca-pectate or RG-II-borate are known to be facilitated. We found that upon stress, vacuolar patatin is released with cell sap leakage, allowing the patatin to associate with the pectin in both the primary cell wall and the MLX. The stress response also includes formation of covalently bound suberin-like polyesters within the insoluble cell wall. The experiments validated the hypotheses, thus led to a novel picture of the structural and molecular alterations responsible for the textural behavior of potato tuber. These findings represent a breakthrough towards understanding of the hardening syndrome, laying the groundwork for potato-handling strategies that assure textural quality of industrially processed particularly in fresh peeled cut tubers, ready-to-prepare and frozen preserved products.
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Sessa, Guido, et Gregory Martin. A functional genomics approach to dissect resistance of tomato to bacterial spot disease. United States Department of Agriculture, janvier 2004. http://dx.doi.org/10.32747/2004.7695876.bard.
Texte intégralRésumé :
The research problem. Bacterial spot disease in tomato is of great economic importance worldwide and it is particularly severe in warm and moist areas affecting yield and quality of tomato fruits. Causal agent of spot disease is the Gram-negative bacterium Xanthomonas campestris pv. vesicatoria (Xcv), which can be a contaminant on tomato seeds, or survive in plant debris and in association with certain weeds. Despite the economic significance of spot disease, plant protection against Xcvby cultural practices and chemical control have so far proven unsuccessful. In addition, breeding for resistance to bacterial spot in tomato has been undermined by the genetic complexity of the available sources of resistance and by the multiple races of the pathogen. Genetic resistance to specific Xcvraces have been identified in tomato lines that develop a hypersensitive response and additional defense responses upon bacterial challenge. Central goals of this research were: 1. To identify plant genes involved in signaling and defense responses that result in the onset of resistance. 2. To characterize molecular properties and mode of action of bacterial proteins, which function as avirulence or virulence factors during the interaction between Xcvand resistant or susceptible tomato plants, respectively. Our main achievements during this research program are in three major areas: 1. Identification of differentially expressed genes during the resistance response of tomato to Xcvrace T3. A combination of suppression subtractive hybridization and microarray analysis identified a large set of tomato genes that are induced or repressed during the response of resistant plants to avirulent XcvT3 bacteria. These genes were grouped in clusters based on coordinate expression kinetics, and classified into over 20 functional classes. Among them we identified genes that are directly modulated by expression of the type III effector protein AvrXv3 and genes that are induced also during the tomato resistance response to Pseudomonas syringae pv. tomato. 2. Characterization of molecular and biochemical properties of the tomato LeMPK3MAP kinase. A detailed molecular and biochemical analysis was performed for LeMPK3 MAP kinase, which was among the genes induced by XcvT3 in resistant tomato plants. LeMPK3 was induced at the mRNA level by different pathogens, elicitors, and wounding, but not by defense-related plant hormones. Moreover, an induction of LeMPK3 kinase activity was observed in resistant tomato plants upon Xcvinfection. LeMPK3 was biochemically defined as a dual-specificity MAP kinase, and extensively characterized in vitro in terms of kinase activity, sites and mechanism of autophosphorylation, divalent cation preference, Kₘand Vₘₐₓ values for ATP. 3. Characteriztion of molecular properties of the Xcveffector protein AvrRxv. The avirulence gene avrRxvis involved in the genetic interaction that determines tomato resistance to Xcvrace T1. We found that AvrRxv functions inside the plant cell, localizes to the cytoplasm, and is sufficient to confer avirulence to virulent Xcvstrains. In addition, we showed that the AvrRxv cysteine protease catalytic core is essential for host recognition. Finally, insights into cellular processes activated by AvrRxv expression in resistant plants were obtained by microarray analysis of 8,600 tomato genes. Scientific and agricultural significance: The findings of these activities depict a comprehensive and detailed picture of cellular processes taking place during the onset of tomato resistance to Xcv. In this research, a large pool of genes, which may be involved in the control and execution of plant defense responses, was identified and the stage is set for the dissection of signaling pathways specifically triggered by Xcv.