Academic literature on the topic 'DNA extracellulare'

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Journal articles on the topic "DNA extracellulare"

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Šuláková, Martina, Jarmila Pazlarová, Rikke Louise Meyer, and Kateřina Demnerová. "Distribution of extracellular DNA in Listeria monocytogenes biofilm." Czech Journal of Food Sciences 37, No. 6 (December 31, 2019): 409–16. http://dx.doi.org/10.17221/9/2019-cjfs.

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Extracellular DNA (eDNA) is an abundant matrix component that protects biofilm from environmental stress, facilitate horizontal gene transfer, and serve as a source of nutrients. eDNA is also found in Listeria monocytogenes biofilm, but it is unknown to which extent its importance as a matrix component varies in terms of phylogenetic relatedness. This study aims to determine if these variations exist. Biofilm forming capacity of ten L. monocytogenes strains of different phylogenetic lineages and serotypes was examined using crystal violet assay at 37°C and 22°C. eDNA content was evaluated fluorometrically at 37°C and at 22°C, then the 3D structure of biofilm was studied by confocal laser scanning microscopy (CLSM). Biofilm forming capacity differed significantly between the culturing conditions and was higher at 37°C than at ambient temperature. eDNA signal distribution was found to be influenced by strain and lineage. CLSM images revealed information about spatial distribution in the biofilm. The information about the eDNA spatial organisation in the biofilm contributes to the understanding of the role of eDNA in a biofilm formation.
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Masola, V., S. Granata, M. Proglio, G. Gambaro, A. Lupo, and G. Zaza. "Eparanasi: un nuovo biomarker di fibrosi e un potenziale target farmacologico per ridurre la progressione del danno renale cronico." Giornale di Clinica Nefrologica e Dialisi 24, no. 2 (January 26, 2018): 10–15. http://dx.doi.org/10.33393/gcnd.2012.1131.

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Il trattamento poli-farmacologico ha determinato, nel corso degli anni, un significativo rallentamento della progressione della malattia renale cronica verso lo stadio di uremia terminale, ma siamo ancora distanti dallo sviluppo di interventi terapeutici in grado di bloccare questo inesorabile e irreversibile processo. Studi clinico-patologici hanno chiaramente dimostrato che il principale elemento coinvolto nel danno renale è la fibrosi tubulo-interstiziale e che il meccanismo patogenetico alla base di questa condizione ha inizio in larga parte nel compartimento tubulare. In particolare, il processo di transizione epitelio-mesenchimale gioca un ruolo importante nella genesi del danno cronico. Durante questo processo, le cellule epiteliali tubulari subiscono un incremento significativo di markers di superficie di natura mesenchimale e, grazie al rimodellamento del citoscheletro e alla degradazione della membrana basale, sono in grado di migrare nell'interstizio dove svolgono un ruolo chiave nel processo patogenetico. In questo contesto, sembra avere un ruolo chiave l'enzima eparanasi, una endo-β-D-glucuronidasi che taglia le catene dell'eparan-solfato a livello di siti specifici intracatena, e partecipa attivamente alla degradazione e al rimodellamento della matrice extracellulare. La degradazione dei vari costituenti dell'ECM, inclusi i proteoglicani eparan-solfato fa-vorisce il rilascio di fattori trofici quali il FGF-2 che induce l'espressione dei marcatori mesenchimali alfa-SMA, VIM e FN, porta alla degradazione della membrana basale mediante la secrezione di metalloproteinasi della matrice ed aumenta la motilità cellulare. L'epressione dell'eparanasi è regolata da fattori di trascrizione, dalla metilazione del DNA e da varie molecole endogene. L'importanza di questo enzima è stata confermata clinicamente dal riscontro di una sua iperespressione in preparati istologici di biopsie effettuate in soggetti affetti da nefropatie croniche (per esempio, nefropatia diabetica). Pertanto visto l'importante ruolo dell'eparanasi sono in fase di standardizzazione numerose strategie per inibire la sua espressione genica e/o la sua attività enzimatica. Infine, è stato proposto il suo possibile utilizzo come biomarker di progressione del danno tubulo-interstiziale da utilizzare routinariamente in ambito nefrologico.
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Weitzman, Jonathan B. "Extracellular DNA." Genome Biology 3 (2002): spotlight—20020227–01. http://dx.doi.org/10.1186/gb-spotlight-20020227-01.

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Xu, Yu, Yanhua Yu, Bowen Yang, Jingjiao Hui, Cai Zhang, Hua Fang, Xiaoyun Bian, Min Tao, Yipeng Lu, and Zhenglu Shang. "Extracellular Mitochondrial Components and Effects on Cardiovascular Disease." DNA and Cell Biology 40, no. 9 (September 1, 2021): 1131–43. http://dx.doi.org/10.1089/dna.2021.0087.

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Silver, Lee, and Gianluca Gallo. "Extracellular Muscle Myosin II Promotes Sensory Axon Formation." DNA and Cell Biology 24, no. 7 (July 2005): 438–45. http://dx.doi.org/10.1089/dna.2005.24.438.

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Chang, Xiulin, Liaoqiong Fang, Jin Bai, and Zhibiao Wang. "Characteristics and Changes of DNA in Extracellular Vesicles." DNA and Cell Biology 39, no. 9 (September 1, 2020): 1486–93. http://dx.doi.org/10.1089/dna.2019.5005.

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Ermakov, Aleksei V., Svetlana V. Kostyuk, Marina S. Konkova, Natalya A. Egolina, Elena M. Malinovskaya, and Natalya N. Veiko. "Extracellular DNA Fragments." Annals of the New York Academy of Sciences 1137, no. 1 (August 2008): 41–46. http://dx.doi.org/10.1196/annals.1448.024.

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Ni, Jia-Hao, and Wan-Xi Yang. "Extracellular and Intracellular Skeletons: How Do They Involve in Apoptosis." DNA and Cell Biology 41, no. 2 (February 1, 2022): 80–90. http://dx.doi.org/10.1089/dna.2021.0613.

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Hua, Yanqiu, Xiulin Chang, Liaoqiong Fang, and Zhibiao Wang. "Subgroups of Extracellular Vesicles: Can They Be Defined by “Labels?”." DNA and Cell Biology 41, no. 3 (March 1, 2022): 249–56. http://dx.doi.org/10.1089/dna.2021.0488.

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MUKHERJEE, ANIL B., ELEONORA CORDELLA-MIELE, and LUCIO MIELE. "Regulation of Extracellular Phospholipase A2 Activity: Implications for Inflammatory Diseases." DNA and Cell Biology 11, no. 3 (April 1992): 233–43. http://dx.doi.org/10.1089/dna.1992.11.233.

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Dissertations / Theses on the topic "DNA extracellulare"

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Shields, Robert Colquhoun. "Extracellular DNA in head and neck biofilms." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2498.

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Extracellular DNA (eDNA) is a ubiquitous component of the extracellular matrix of microbial biofilms. It has a number of functions that include a role as an adhesin during biofilm attachment, and facilitating matrix stability in mature biofilms. Increasingly, deoxyribonuclease (DNase) enzymes have been shown to reduce the colonisation of many microbial biofilms, both bacterial and fungal. Biofilms are estimated to be responsible for around 60% of bacterial infections, including many chronic diseases. The aim of this work was to determine the role of eDNA in chronic mixed-species biofilm infections, and to explore the potential of DNase enzymes for biofilm control. This included three major areas of research, focusing on chronic rhinosinusitis, tracheoesophageal speech valves (TESVs), and dental plaque. An important aspect was to test the efficacy of a novel bacterial nuclease, NucB, isolated from a seaweed-associated strain of Bacillus licheniformis, against microbial biofilms. The colonisation of speech valves by micro-organisms was studied using scanning electron microscopy (SEM). In keeping with previous observations, these biofilms were co-aggregations of fungal and bacterial species. Using confocal laser scanning microscopy, eDNA was observed in the biofilm matrix. Extracellular DNA was extracted and quantified from TESV biofilms. All six biofilms studied had detectable nucleic acids, as measured by NanoDrop spectrophotometry. The eDNA was apparently heavily degraded, and produced smears by agarose gel electrophoresis. Nevertheless, eDNA appeared to be providing biofilm stability since micro-organisms were liberated from the surface of the valves following treatment with NucB in over 60% of the TESVs tested. To assess the role of eDNA in biofilms associated with chronic rhinosinusitis, ‘obstructive mucin’ and sinus mucosa biopsy samples collected during functional endoscopic sinus surgery at the Freeman Hospital, Newcastle, were analysed for the presence of biofilms and biofilm-forming micro-organisms. An average of 3.75 bacterial species per patient were cultured from obstructive mucin. The most commonly isolated micro-organisms were Staphylococcus aureus, coagulase-negative staphylococci and α-haemolytic streptococci. Micro-organisms were not detected by transmission electron microscopy of the obstructive mucin and this material appeared to originate through a host inflammatory response. However, bacteria were visualised on the surface of sinus mucosa using a peptide nucleic acid fluorescence in situ hybridization (PNA-FISH) universal bacteria probe. Twenty-four bacterial isolates were iv assessed for their ability to form biofilms in a microtitre plate model. All micro-organisms tested formed biofilms, and 14 of 22 were susceptible to NucB. In total, 15 of 24 microbial species produced eDNA that was detectable by agarose gel electrophoresis. By SEM, cellular colonisation was lower in treated samples and, in the case of Streptococcus constellatus FH20 stringy, matrix-like material was not present after DNase treatment. The role of eDNA in matrix stability and initial biofilm attachment was also studied in oral bacteria. Streptococcus gordonii DL1, Streptococcus mutans GS-5, Fusobacterium nucleatum 25586 and Actinomyces oris MG1 were examined using DNase treatment, CLSM, and eDNA extraction. Of these species, all except S. gordonii appeared to rely on high molecular weight (HMW) eDNA for biofilm attachment and biofilm stability. Although S. gordonii did not produce detectable HMW eDNA, nucleic acids were detectable by NanoDrop spectrophotometry. Furthermore, this species produces an extracellular nuclease which may degrade the HMW eDNA in the conditions used to culture biofilms. Interestingly, four S. mutans strains differed in their sensitivity to DNase treatment. Oral biofilms were also modelled in a BioFlux microfluidics device using flowing human saliva. Mixed-species biofilms and single species biofilms of S. mutans UA159 and S. gordonii DL1 were cultured using this technique, to determine whether this model would allow more realistic experiments for DNase testing. Finally, the extracellular nuclease, SsnA, of S. gordonii DL1 was characterised. A nuclease-deficient mutant did not produce extracellular nuclease activity on DNase Test agar or during a Forster Resonance Energy Transfer (FRET) assay. Nuclease activity was cell-wall-associated as predicted from the predicted amino acid sequence of SsnA. Allelic exchange mutagenesis determined that ssnA expression was regulated by CcpA in response to repressing sugars. However, in planktonic culture non-repressing carbon sources also inhibited enzyme activity during a FRET assay. Further experiments using acidic buffers replicated the inhibition of SsnA without the presence of sugars. SsnA was purified as a GST-tagged fusion protein in an Escherichia coli protein expression system, and had anti-biofilm activity against S. mutans GS-5. However, this species is strongly acidogenic and therefore it is hypothesised that although SsnA may be a competition biofilm factor, acid production by S. mutans may reduce its efficacy in vivo. In conclusion, this thesis has provided strong evidence for the role of eDNA in facilitating biofilm formation and mature biofilm stability of clinically relevant v biofilms. Nucleic acids were present in biofilms associated with a chronic infection, medical implant biofouling and dental plaque. A variety of DNase enzymes (NucB, DNase I, and SsnA) were capable of reducing biofilm colonisation. Given the adhesive function of eDNA in biofilm matrices it is proposed that DNase enzymes may be beneficial for controlling healthcare-related biofilms.
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Fisher, Mark. "Intra and extracellular responses to DNA damage." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/214106/1/Mark_Fisher_Thesis.pdf.

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Dos, Santos Goncalves Marina. "Rôle des exopolysaccharides et de l'ADN extracellulaire dans le développement du biofilm par Klebsiella pneumoniae." Thesis, Clermont-Ferrand 1, 2014. http://www.theses.fr/2014CLF1PP02.

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Le biofilm est défini comme une communauté microbienne adhérant à une surface biotique ou abiotique, et engluée dans une matrice extracellulaire auto-produite. Les biofilms naturels sont composés de plusieurs espèces microbiennes et leurs interactions, qu'elles soient synergiques ou antagonistes, jouent un rôle important dans le développement, la composition et le fonctionnement des consortia impliqués. De plus, ces relations impliquent souvent la production de molécules antagonistes limitant la croissance ou l'adhésion bactérienne. Enfin la composition de la matrice extracellulaire joue un rôle important dans la robustesse du biofilm. Au cours de ce travail, l'étude des interactions au sein de biofilms mixtes constitués par K. pneumoniae et S. epidermidis a permis d'isoler un polysaccharide produit par K. pneumoniae, capable d'inhiber l'adhésion aux surfaces abiotiques de plusieurs autres espèces bactériennes à Gram-négatif et à Gram-positif. La caractérisation physico-chimique de cette molécules de haut poids moléculaire a permis de mettre en évidence qu'elle était composée de galactose, glucose, rhamnose et d'acide glucuronique. Par ailleurs, l'analyse d'extraits de mutants déficients pour la production de capsule a montré que ce polysaccharide correspondait à la capsule de K. pneumoniae. Son mode d'action consisterait à inhiber les interactions initiales entre bactéries et surface. Le suivi dans le temps de la formation de biofilm monospecies par K. pneumoniae avec la technique Biofilm Ring Test® a également permis de mettre en évidence un phénotype original. En effet, la détection initiale d'agrégats bactériens est suivie par une modification apparente de leur structure, qui serait liée à des changements de leur robustesse face aux forces d'aimantation magnétique. La présence d'ADN extracellulaire au sein de la matrice du biofilm pourrait jouer un rôle dans la survenue de ce phénotype comme l'indique les mesures effectuées en présence de l'enzyme DNAse I. En parallèle, l'observation de biofilm formés par K. pneumoniae dans des modèles expérimentaux cinétiques a mis en évidence des décrochements massifs de biomasse au cours de la maturation du biofilm, qui pourraient être corrélées aux modifications internes de robustesse de la matrice. L'ensemble de ces données permet de mieux caractériser les interactions intimes survenant à l'intérieur de biofilms constitués par K. pneumoniae et à terme de mieux caractériser et donc prévenir leur formation et dissémination
Biofilms are defined as microbial communities adhering to biotic or abiotic surfaces and embedded in a self-produced extracellular matrix. Natural biofilms are composed of several microbial species and their interactions, synergistic or antagonistic, play important roles in development, composition and functioning of the consortia. Furthermore, the relationships often involve the production of antagonist molecules that impair competitors' growth or adhesion. The composition and evolution of the extracellular matrix plays also an important role in the biofilms' robustness. In this work, study of the interactions within biofilms formed by K. pneumoniae and S. epidermidis led to the isolation of a polysaccharide produced by K. pneumoniae able to inhibit the adherence to abiotic surfaces of several Gram-negative and Gram-positive bacterial species. The physico-chemical characterization of this high molecular weight molecule showed it was composed of galactose, glucose, rhamnose and glucuronic acid. This data, together with the analysis of extracts from capsule-deficient mutants, indicated that the capsule of K. pneumoniae was responsible for the biofilm inhibition phenotype, probably by inhibiting the initial interactions between bacteria and surface. By monitoring the formation of monospecies biofilm by K. pneumoniae with the Biofilm Ring Test® technique, we were able to detect an original phenotype. Indeed, detection of bacterial aggregates still occurred after a few hours of incubation but in a different way, probably related to changes of the biofilm robustness towards magnetic forces. The presence of extracellular DNA in the matrix of the biofilm is likely to play a role in the occurrence of this phenotype, as indicated by the assays performed in presence of the enzyme DNase I. At the same time, observations of biofilm formed by K. pneumoniae in kinetic experimental models showed massive detachment events during biofilm maturation, which could be correlated to changes in internal strength of the matrix. All these dtat contribute to a better characterization of the intimate interactions occuring within biofilms formed by K. pneumoniae and will ultimately lead to the development of efficient anti-biofilm strategies
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Carrera, Samantha. "Influence of extracellular factors on p53-mediated DNA damage responses." Thesis, University of Leicester, 2013. http://hdl.handle.net/2381/27796.

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Cells have evolved sophisticated mechanisms to maintain genomic stability after cellular stress. Activation of DNA damage response pathways, and most importantly p53, leads to adaptive responses that can be influenced by different extracellular factors. The aim of this project was to study how extracellular factors modulate p53 cell-fate decisions after DNA damage, with particular interest in oxygen tensions and vitamin A metabolites. First, we focused on how physiological oxygen tensions (5% 02) may influence cellular responses to genotoxic stress. We showed that normal and cancer cells cultured at 5% 02 had a reduction in p53-mediated apoptosis after exposure to different genotoxic stresses. This was not due to a decrease p53 protein levels or its transactivation activity, and the oxidative damage caused by DNA damaging agents was not affected by oxygen tensions. We also found a p53-independent activation of MAPK at 5% 02, which when inhibited restored levels of p53-induced apoptosis. HIF-1α, a transcription factor induced at lower O2 concentrations, was present and active at 5% 02. However, this did not affect MAPK activation and HIF-1α was not involved in the resistance to apoptosis under these conditions, although MAPK was necessary for HIF-1α expression and activation. We next explored the effect of the vitamin A (retinol) pathway on the cellular responses to DNA damage. We showed that Stra6, a retinol-inducible gene, is upregulated by p53 after DNA damage. While overexpression of Stra6 sensitized cells to p53-induced apoptosis independently of the retinoic acid signalling, its inhibition resulted in decreased apoptosis after DNA damage and less induction of oxidative stress. This shows that both oxygen tensions and vitamin A metabolites, through Stra6, are potent modulators of the p53 responses to DNA damage.
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Tursi, Sarah Anne. "Curli-Extracellular DNA Complexes: Pathogenicity and Role in Enteric Biofilms." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/511656.

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Microbiology and Immunology
Ph.D.
The first recorded observation of bacterial biofilms dates back to the 17th century by Antoine Van Leeuwenhoek. Today, biofilms are known as bacteria encapsulated within a self-produced extracellular matrix adherent to biotic or abiotic surfaces. Since the initial discovery of biofilms, research has explored the structure and function of biofilms. Only until recently has the role of biofilms within the medical setting become apparent. Here, we investigate the role of curli-extracellular DNA (eDNA) complexes in disease pathogenicity and explore the ability to target bacterial amyloid curli as a novel anti-biofilm therapeutic target. Biofilms of enteric bacteria, such as Escherichia coli and Salmonella enterica serovar Typhimurium, are composed of various components that act in consortium to fortify the extracellular matrix. One of the main components of enteric biofilms is amyloid curli. Curli, one of the best characterized bacterial amyloids, is a protein with a conserved cross beta sheet structure that forms basket like structures encapsulating the bacteria. Within the biofilm, curli serves to fortify the extracellular matrix, aids in bacterial attachment and protects bacteria from harsh environmental conditions. Extracellular DNA (eDNA) is another integral component of enteric biofilms. Recent reports from our lab has suggested that curli forms irreversible complexes with eDNA. Even with exposure to DNases, co-localized curli and eDNA can be observed. Other components of enteric biofilms include cellulose and Biofilm Associated Protein A. Biofilms of S. Typhimurium have been associated with significant disease pathologies. In addition to identifying the existence of curli-eDNA complexes within S. Typhimurium biofilms, our lab has also reported that curli-eDNA complexes of S. Typhimurium potentiate the autoimmune disease Systemic Lupus Erythematosus (SLE). SLE is an autoimmune disease characterized by the production of type I interferons and autoantibodies, although the etiology remains unknown. Systemically, curli binds to and activates the Toll like Receptor (TLR)1/2 complex leading to a pro-inflammatory response. In these studies we aimed to identify the innate immune mechanisms leading to the autoimmune phenotype following stimulation with curli-eDNA complexes. As TLR9 is activated by unmethylated bacterial DNA CpG DNA sequences leading to the production of type I interferons we hypothesized a potential role for TLR9 in recognizing eDNA of the curli-eDNA complex leading to the generation of the hallmarks of SLE. To investigate this hypothesis, we stimulated wild-type, TLR2 knockout, TLR9 knockout and TLR2-9 double knockout immortalized macrophages with curli-eDNA complexes purified from S. Typhimurium biofilms. We observed a significant reduction in the transcript level of type I interferons (IFN), Ifnβ, Isg15 and Cxcl10, upon stimulation of TLR2 knockout, TLR9 knockout and TLR2-9 double knockout immortalized macrophages implicating a role in TLR9 recognition of the curli-eDNA complex. As there was a significant reduction of type I interferon levels upon stimulation of TLR2 knockout macrophages, we hypothesized that TLR2 may serve as a carrier to bring the curli-eDNA complex into the endosome containing TLR9. To inhibit phagocytosis, we pretreated cells with endocytosis inhibitors and stimulated wild-type macrophages with curli-eDNA complexes. We observed a reduction in the transcript level of Ifnβ suggesting that curli-eDNA complexes gain access to endosomal TLR9 via TLR2 engagement. Finally, to explore the role of TLR2 and TLR9 in the production of autoantibodies, curli-eDNA complexes were intraperitoneal injected twice weekly for six weeks into C57BL/6 wild-type, TLR2 knockout, TLR9 mutant and TLR2 knockout-TLR9 mutant mice. We observed a robust generation of anti-double stranded autoantibodies within the first three weeks, however the production of autoantibodies was significantly decreased and delayed in the TLR2 knockout, TLR9 mutant and TLR2 knockout-TLR9 mutant mice. Overall, these data suggest that curli acts as a carrier for DNA to elicit an autoimmune response via TLR2 and TLR9. Within biofilms of S. Typhimurium, curli is the main proteinaceous component. Biofilms lacking curli destabilize and fail to form mature biofilms. Recent research has shown that in response to the production of host amyloids, the body will generate anti-amyloid antibodies in the serum. Monoclonal antibodies (mAb) generated from serum antibodies have been shown to have pan anti-amyloid properties in vitro and in vivo due to the β-sheet conformational epitope. As amyloids from both human and bacterial origin share a β-sheet conformational structure, we hypothesized as to if the anti-amyloid mAbs can eradicate S. Typhimurium biofilms by targeting curli. We incubated S. Typhimurium biofilms in the presence of various mAbs (ALZ.4A6, ALZ.4GI, ALZ.2C10 and ALZ.3H3) and observed a significant reduction of biofilm thickness and curli content within the biofilm. We deduced that ALZ.3H3 conferred the greatest anti-biofilm response. When we visualized the three-dimensional architecture of biofilms incubated with ALZ.3H3, we observed that ALZ.3H3 induced the formation of a loose architecture compared to untreated biofilms that were dense and compact. The resulting loose biofilm architecture induced by incubation with ALZ.3H3 enhanced the susceptibility of the biofilms to antibiotic exposure and macrophage clearance. We also observed enhanced biofilm eradication in vivo when catheters precoated with S. Typhimurium biofilms were inserted into the back flanks of mice that were percutaneously injected with ALZ.3H3. Both in vitro and in vivo, combination therapy of ALZ.3H3 and antibiotic enhanced biofilm clearance. In summary, we propose a novel anti-biofilm strategy by targeting the amyloid component of the biofilm, thus satisfying an unmet need in the art of biofilm prevention. Overall, these data in summation significantly broadens our understanding of disease pathogenicity and the role of curli-eDNA complexes in S. Typhimurium biofilms. As amyloid-eDNA complexes may be found in other biofilms, these results may extend beyond enteric bacteria proving novel insight into host-microbe interactions and the generation of novel anti-biofilm therapeutics.
Temple University--Theses
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Bußkamp, Holger [Verfasser]. "From New DNA Conjugation Approaches to 3D DNA Networks for an Artificial Extracellular Matrix / Holger Bußkamp." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1112745408/34.

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Susevski, Vanessa. "Development of DNA Aptamers Targeting Breast Cancer Derived Extracellular Vesicles for Biomarker Discovery." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41035.

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Detection of cancer at the early stages greatly increases the chance for successful treatment and favourable prognosis for patients. However, a liquid-based biopsy has yet to be developed for most cancers. Extracellular vesicles (EVs) are an attractive candidate for early cancer detection since their surface proteome mirrors the cell of origin. Thus, there is a need for the development of reliable probes that can detect cancer derived EVs. In this thesis, the VBS-1 aptamer was developed to selectively bind to triple-negative breast cancer cell line derived EVs. Initially, several EV isolation methods were compared and isolated EVs were validated and characterized. Aptamer clones were developed by Systematic Evolution of Ligands by Exponential Enrichment to EVs isolated by differential ultracentrifugation and their binding was validated by flow cytometry. The binding partner of the selected VBS-1 aptamer was identified by LC-MS/MS to be the transmembrane protein ATP1A1. The presence of an ATP1A1-positive EV population was validated by flow cytometry. The selected aptamer may find further application in biosensors for the detection of EVs as cancer biomarkers in biological fluids.
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Rapsinski, Glenn James. "Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA." Diss., Temple University Libraries, 2016. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/273605.

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Microbiology and Immunology
Ph.D.
Salmonella enterica serovar Typhimurium is an important cause of gastroenteritis in the United States and the developing world. Biofilm growth is an significant mechanism, which S. Typhimurium utilizes to contaminate food products and survive in the environment. Biofilms are also an important part of the infectious process for many pathogenic bacteria. As part of the biofilm, S. Typhimurium produces an extracellular matrix consisting of cellulose, extracellular DNA, and most importantly, the amyloid protein curli. Similar to amyloids associated with human diseases, curli is recognized by the innate immune system through Toll-Like Receptors (TLRs). Here, we studied the immune receptors recognizing curli as well as interactions between eDNA and curli during biofilm development in order to glean a better understanding of these complex bacterial communities and the immune response to them. Recently, our lab demonstrated that curli fibers are recognized by the TLR2/TLR1 complex. CD14 has been shown to be a common adaptor protein for TLR2/TLR1 complex in response to one of its ligands, tri-acylated lipopeptide, Pam3CSK4. In order to study the role of CD14 in the immune receptor complex recognizing curli, we utilized HeLa 57A cells, a human cervical cancer cell line that has a stably transfected luciferase reporter for Nf-κB activation. When these cells were transiently transfected with TLR2 and TLR1 together or with the addition of membrane-bound CD14, NfκB activation was enhanced by the presence of CD14 in response to purified curli, GST-tagged curli subunit (GST-CsgA), and the control lipopeptide Pam3CSK4. Soluble CD14 also increased NfκB activation in response to purified curli. Bone marrow derived macrophages (BMDM) from wild type (C57BL/6) mice produced more IL-6 and nitric oxide in response to stimulation with purified curli, GST-CsgA, and Pam3CSK4, than BMDMs deficient in CD14. Binding assays demonstrated direct binding of curli to all members of this hypothesized trimolecular complex, TLR2, TLR1, and CD14. Utilizing synthetic peptides corresponding to the fourth and fifth repeat of the CsgA monomer, CsgA R4-5, and its modified version, CsgA R4-5N122A deficient in forming amyloid fibers, we also showed that binding to CD14, and CD14 enhancement of IL-6 production required the fibrillar amyloid structure of curli. To study interactions between curli and eDNA in biofilms and the resulting immune response generated to composites formed by these ECM components, we analyzed biofilms of GFP expressing S. Typhimurium using confocal laser scanning microscopy (CLSM). Staining for amyloids with Congo Red revealed the presence of curli in the biofilms and staining with propidium iodide demonstrated the presence of extracellular DNA in the biofilms. Co-staining with TOTO-1, a nucleic acid stain, and Congo Red showed co-localization of the fluorescent signal for these molecules within the biofilms. DNase I treatment of the biofilms produced no significant change in biofilm thickness by confocal microscopy signifying that the biofilm, possibly eDNA, was resistant to DNase treatment. This was further confirmed by the presence of DNA in purified curli fibers, which were treated twice with DNase and RNase. Polymerization assays showed acceleration of amyloid polymerization in the presence of DNA from both bacteria and salmon sperm. CLSM of bone marrow derived dendritic cells demonstrated that DCs are able to sample antigens from biofilms. BMDCs also produced robust quantities of proinflammatory cytokines in response to wild type, msbB, and ΔfliCfljB S. Typhimurium biofilms and purified amyloid/DNA composites as measured by ELISA. Using BMDCs deficient in TLR2 and TLR9, we found that this cytokine production was partially dependent on TLR2, but did not require TLR9. Together, these findings significantly broaden our understanding of S. Typhimurium biofilms and the immune response to ECM components present in its biofilms. We now understand that a trimolecular complex of TLR2/TLR1/CD14 is required for full response to curli by innate immune cells. We also discerned that interactions between biofilm components aid biofilm development and create composites that are highly immunogenic. This new information enhances the need to explore the interaction between composite ligands and the immune system rather than only studying ligands individually.
Temple University--Theses
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Apel, Falko. "Recognition of Neutrophil Extracellular Traps by the Cytosolic DNA Sensor cGAS." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/19727.

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Neutrophile Granulozyten produzieren „Neutrophil Extracellular Traps“ (NETs), ein mit antimikrobiellen Molekülen bestücktes Netzwerk aus Chromatinfasern, das während eines Zelltodprogramms namens „NETosis“ von den sterbenden Neutrophilen ausgestoßen wird. Ihre netzartige Struktur erlaubt es ihnen, eine weitere Verbreitung des Infektionserregers zu verhindern; zudem erzeugen sie eine hohe lokale Konzentration an toxischen Molekülen, die Mikroorganismen töten können. Unter normalen Bedingungen werden NETs von Nukleasen zerkleinert und anschließend von Makrophagen entfernt. Wenn dieser Aufräummechanismus gestört ist, aktivieren NETs das Immunsystem und führen zur Produktion von Autoantikörpern oder entzündungsfördernden Zytokinen. NETs werden mit einer wachsenden Liste von inflammatorischen und Autoimmunerkrankungen in Verbindung gebracht. Wie genau dabei NETs durch das Immunsystem erkannt werden, ist noch nicht bekannt. In der vorliegenden Arbeit zeige ich, dass NETs durch den zytosolischen DNA Sensor „cyclic GMP-AMP synthase“ (cGAS) detektiert werden können und dass dadurch die Expression von Typ I Interferonen (TIIFN) induziert wird. Zu Beginn demonstriere ich, dass NETs durch rekombinantes cGAS erkannt werden und dass mit isolierten NETs stimulierte Immunzellen cGAS-abhängig TIIFN produzieren. Des Weiteren zeige ich, dass Neutrophile, die NETosis begehen, in Nachbarzellen ebenfalls cGAS-anhängig TIIFN induzieren können. Abschließend konnte ich diese Ergebnisse in einem in vivo Mausmodel für systemische NET-Produktion bestätigen. Die vorliegende Arbeit zeigt einen Mechanismus, wie NETs durch das Immunsystem erkannt werden und dadurch sowohl zur Entstehung als auch zur Progression von Krankheiten beitragen kann. Sie ermöglicht dementsprechend die Entwicklung neuer Interventionsstrategien, welche zur Heilung oder Linderung einer Vielzahl von Erkrankungen beitragen können.
The first line of cellular defense of the immune system are neutrophils. They are the most abundant white blood cell, which exert an array of antimicrobial effector functions. Neutrophils release neutrophil extracellular traps (NETs), a composite of chromatin and antimicrobial molecules, into the extracellular space during a form of regulated cell death called NETosis. Their net-like structure prevent further dissemination of the invader and establishes a high local concentration of toxic molecules that mediate pathogen killing. NETs provide a platform for undesired immune activation and contribute to the production of autoantibodies and pro-inflammatory cytokines. NETs are implicated in a growing list of inflammatory and autoimmune diseases, but the exact mechanism how NETs are recognized by the immune system is not fully understood. In this study, I demonstrate that the cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS) senses NETs and induces the production of type I interferons (TIIFN). I first showed that NETs are recognized by recombinant cGAS and that cells treated with isolated NETs produce TIIFN in a cGAS dependent mechanism. Secondly, I demonstrate that neutrophils undergoing NETosis are taken up by neighboring immune cells and induce cGAS-dependent TIIFN expression. Lastly, I confirmed our in vitro results in a mouse model of systemic NET induction. Wildtype mice injected with Concanavalin A significantly upregulate the expression of interferon stimulated genes, while cGAS-/- mice and Cybb-/- mice, which are incapable of producing NETs, fail to induce this response.
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Lawler, Danielle Suzanne. "The role of respiratory viral infection and extracellular DNA in allergic sensitisation." Thesis, Lawler, Danielle Suzanne (2018) The role of respiratory viral infection and extracellular DNA in allergic sensitisation. Honours thesis, Murdoch University, 2018. https://researchrepository.murdoch.edu.au/id/eprint/43144/.

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The correlation between allergic disease and viral infections has been well established. While respiratory viral infections are strongly correlated with the development of allergic asthma, it is not known precisely how viral infection may produce, or alternatively protect, against allergic disease. Furthermore, little is known about the impact of viral infection on IgE sensitisation, due to conflicting and limited research. Recently, neutrophil extracellular traps (NETs) have been observed in viral infections and shown to induce a Th2 response. We aim to explore the link between virus infection and allergy and test if the link is mediated through NETs. We hypothesise that NETs are induced during viral respiratory infections, but that they do not adequately control the viral disease. Instead, they contribute to the development of allergic disease, and their removal will be beneficial to patients. This hypothesis was addressed by sensitising rats to ovalbumin (OVA), during a respiratory viral infection and re-exposing the animals to OVA one week after sensitisation. To test the involvement of NETs, DNase-I was administered during viral infection to degrade NETs. OVA-specific IgE serum levels, along with cellular infiltrates into the airways, were compared between groups to assess allergic sensitisation before and after OVA re-exposure. Although no effect on IgE sensitisation was observed with viral infection, DNase treatment reduced the risk of IgE sensitisation and increased T regulatory cell (Treg) proportions in the airways, which also displayed higher levels of FoxP3. We did not observe a difference between any of the groups in respect to allergic recall response suggesting that the achieved sensitisation was not sufficient to induce clinical disease. Our findings nevertheless suggest that DNase treatment induces a regulatory response, which may protect against allergic disease. Future studies should explore this immunoregulatory response, as a novel strategy for allergy protection.
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Books on the topic "DNA extracellulare"

1

Prohofsky, Earl. Statistical mechanics and stability of macromolecules: Application to bond disruption, base pair separation, melting, and drug dissociation of the DNA double helix. Cambridge [Eng.]: Cambridge University Press, 1995.

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Taberlet, Pierre, Aurélie Bonin, Lucie Zinger, and Eric Coissac. DNA extraction. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198767220.003.0005.

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Chapter 5 “DNA extraction” focuses on the particularities and practical constraints associated with the isolation of eDNA from environmental samples. The extraction protocol is indeed crucial in eDNA studies, as it will determine whether extracellular, intracellular, or total DNA is targeted. Chapter 5 describes the main advantages and limitations of the most popular extraction kits aimed at obtaining DNA from soil, sediment, litter, feces, or water. It provides a detailed protocol for DNA extraction from soil samples using a saturated phosphate buffer. This protocol has been optimized for an easy implementation in the field using a mobile laboratory, so the material and consumables necessary are also listed.
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Prohofsky, Earl. Statistical Mechanics and Stability of Macromolecules: Application to Bond Disruption, Base Pair Separation, Melting, and Drug Dissociation of the DNA Double Helix. Cambridge University Press, 2009.

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Prohofsky, Earl. Statistical Mechanics and Stability of Macromolecules: Application to Bond Disruption, Base Pair Separation, Melting, and Drug Dissociation of the DNA Double Helix. Cambridge University Press, 2011.

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Prohofsky, Earl. Statistical Mechanics and Stability of Macromolecules: Application to Bond Disruption, Base Pair Separation, Melting, and Drug Dissociation of the DNA Double Helix. Cambridge University Press, 2005.

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Douglas, Kenneth. Bioprinting. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780190943547.001.0001.

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Abstract: This book describes how bioprinting emerged from 3D printing and details the accomplishments and challenges in bioprinting tissues of cartilage, skin, bone, muscle, neuromuscular junctions, liver, heart, lung, and kidney. It explains how scientists are attempting to provide these bioprinted tissues with a blood supply and the ability to carry nerve signals so that the tissues might be used for transplantation into persons with diseased or damaged organs. The book presents all the common terms in the bioprinting field and clarifies their meaning using plain language. Readers will learn about bioink—a bioprinting material containing living cells and supportive biomaterials. In addition, readers will become at ease with concepts such as fugitive inks (sacrificial inks used to make channels for blood flow), extracellular matrices (the biological environment surrounding cells), decellularization (the process of isolating cells from their native environment), hydrogels (water-based substances that can substitute for the extracellular matrix), rheology (the flow properties of a bioink), and bioreactors (containers to provide the environment cells need to thrive and multiply). Further vocabulary that will become familiar includes diffusion (passive movement of oxygen and nutrients from regions of high concentration to regions of low concentration), stem cells (cells with the potential to develop into different bodily cell types), progenitor cells (early descendants of stem cells), gene expression (the process by which proteins develop from instructions in our DNA), and growth factors (substances—often proteins—that stimulate cell growth, proliferation, and differentiation). The book contains an extensive glossary for quick reference.
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Kirchman, David L. Elements, biochemicals, and structures of microbes. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789406.003.0002.

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Microbiologists focus on the basic biochemical make-up of microbes, such as relative amounts of protein, RNA, and DNA in cells, while ecologists and biogeochemists use elemental ratios, most notably, the ratio of carbon to nitrogen (C:N), to explore biogeochemical processes and to connect up the carbon cycle with the cycle of other elements. Microbial ecologists make use of both types of data and approaches. This chapter combines both and reviews all things, from elements to macromolecular structures, that make up bacteria and other microbes. The most commonly used elemental ratio was discovered by Alfred Redfield who concluded that microbes have a huge impact on the chemistry of the oceans because of the similarity in nitrogen-to-phosphorus ratios for organisms and nitrate-to-phosphate ratios in the deep oceans. Although statistically different, the C:N ratios in soil microbes are remarkably similar to the ratios of aquatic microbes. The chapter moves on to discussing the macromolecular composition of bacteria and other microbes. This composition gives insights into the growth state of microbes in nature. Geochemists use specific compounds, “biomarkers”, to trace sources of organic material in ecosystems. The last section of the chapter is a review of extracellular polymers, pili, and flagella, which serve a variety of functions, from propelling microbes around to keeping them stuck in one place.
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van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.
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Book chapters on the topic "DNA extracellulare"

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Adams, Jr., Ph.D., James D. "Chapter 10. DNA, Nuclear Cell Signaling and Neurodegeneration." In Extracellular and Intracellular Signaling, 175–87. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733434-00175.

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Barroso, Marina Valente, and Josiane Sabbadini Neves. "Detection of Eosinophil Extracellular DNA Traps." In Methods in Molecular Biology, 193–98. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1095-4_16.

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Morozkin, Evgeniy S., Ekaterina M. Loseva, Vladislav A. Mileiko, Kira S. Zadesenets, Nikolay B. Rubtsov, Valentin V. Vlassov, and Pavel P. Laktionov. "Comparative Study of Extracellular DNA by FISH." In Circulating Nucleic Acids in Plasma and Serum, 143–46. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9382-0_19.

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Podgornaya, Olga I., Irina N. Vasilyeva, and Vladimir G. Bespalov. "Heterochromatic Tandem Repeats in the Extracellular DNA." In Advances in Experimental Medicine and Biology, 85–89. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42044-8_16.

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Tani, Katsuji, and Masao Nasu. "Roles of Extracellular DNA in Bacterial Ecosystem." In Nucleic Acids and Molecular Biology, 25–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12617-8_3.

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Chiang, Wen-Chi, and Tim Tolker-Nielsen. "Extracellular DNA as Matrix Component in Microbial Biofilms." In Nucleic Acids and Molecular Biology, 1–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12617-8_1.

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Šrámková, K., F. Franěk, I. Lüdemann, and R. Pörtner. "Physiological Status of Immobilized Hybridoma Cells: Assessment through Extracellular DNA Analysis." In Animal Cell Technology: Basic & Applied Aspects, 421–25. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5746-9_68.

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Joubert, Vanessa, Franck M. André, Marco Schmeer, Martin Schleef, and Lluis M. Mir. "Increased Efficiency of Minicircles Versus Plasmids Under Gene Electrotransfer Suboptimal Conditions: An Influence of the Extracellular Matrix." In Minicircle and Miniplasmid DNA Vectors, 215–25. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527670420.ch13.

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Lang, Andrew S., and J. Thomas Beatty. "Gene Transfer Agents and Defective Bacteriophages as Sources of Extracellular Prokaryotic DNA." In Nucleic Acids and Molecular Biology, 15–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12617-8_2.

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Dell'anno, Antonio, and Cinzia Corinaldesi. "Section 2 update: Degradation and turnover of extracellular DNA in marine sediments." In Molecular Microbial Ecology Manual, 2137–43. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-2177-0_203.

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Conference papers on the topic "DNA extracellulare"

1

Vasilyeva, Irina, O. Korytov, V. Bespalov, A. Semenov, G. Tochil'nikov, S. Ivanov, and L. Korytova. "EFFECTS OF RADIATION EXPOSURE OF THE BLADDER ON EARLY CHANGES OF EXTRACELLULAR DNA AND OTHER INDICATORS OF PERIPHERAL BLOOD." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9b37c7f8.86673968.

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On the model of radiation cystitis in rats, a decrease in the number of blood cells was found 6 h after local irradiation and an increase in extracellular DNA level was found in 6-24 h with normalization 48 h after exposure. The relative change in the content of extracellular DNA (0 h against 6 h) correlated with changes in triglycerides (0 h against 24 h).
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Wen, Fushi, Alex Shen, Andrew Choi, and Jiaqi Shi. "Abstract 2421: Extracellular DNA in pancreatic cancer metastasis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2421.

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Sabogal Piñeros, Yanaika Shari, Barbara Dierdorp, Tamara Dekker, Els J. M. Weersink, and Rene Lutter. "Extracellular DNA traps in sputum from severe asthma patients." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.623.

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Previtera, Michelle L., Kevin Trout, Uday Chippada, Rene Schloss, and Noshir A. Langrana. "Fibroblast Behavior on Tunable Gels With Decreasing Elasticity." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53251.

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Cells sense and react to various extracellular matrix (ECM) cues including chemical and physical cues. Previous studies in our laboratory and others have used static substrates, where the elastic properties remain unchanged throughout the culture period, to examine the effects of mechanical stiffness on neuron and fibroblast behavior [1–4]. However, in vivo, the ECM is dynamic and alters due to pathological, developmental, and external factors [5]. To study the effects of dynamic ECM changes on cell behavior, we developed a DNA-crosslinked, polyacrylamide gel (DNA gel) that allows us to study how dynamic changes in ECM stiffness affect cell behavior [6, 7].
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Wang, Yi-Chang, Andrew A. Kelso, Yi-Hsuan Chen, Chi-An Hsieh, Wei-Kai Chen, Jeremy M. Stark, Hsing-Jien Kung, and David K. Ann. "Abstract 3722: Extracellular arginine starvation imposes DNA replication fork stall and permits DNA damage tolerance." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3722.

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Beckmann, L., C. Dicke, B. Sievers, and F. Langer. "Myeloperoxidase (MPO) Inhibits the Procoagulant Activity (PCA) of Extracellular DNA." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680100.

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Sadik, Mohamed M., Jianbo Li, Jerry W. Shan, David I. Shreiber, and Hao Lin. "Quantifying the Effects of Extracellular Conductivity on Transport During Electroporation." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53215.

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Electroporation is an effective means to permeabilize the cell membrane and deliver biologically active molecules (such DNA, RNA, dyes, etc…) into the cell cytoplasm, while maintaining cell viability and functionality [1]. Despite extensive research, electroporation still suffers from major drawbacks such as high cell death and low delivery efficiency. In the past, studies focused mainly on permeabilization of the membrane during electroporation while transport of molecules from one side of the membrane to the other has been overlooked. Previous experimental work demonstrated an inverse relation between the electrical conductivity of the extracellular buffer and total concentration delivered into cells [2]. This inverse correlation suggests that additional molecular transport mechanisms, besides diffusion, govern the delivery into cells.
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Shelke, Ganesh V., Su Chul Jang, Yanan Yin, Cecilia Lässer, and Jan Lötvall. "Abstract 939: Cell-free DNA associated with extracellular vesicle: Biomarker or bioactivity." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-939.

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Chen, Xi, and Chengping Hu. "The formation and effects of extracellular DNA traps in a murine asthma model." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa1103.

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Palinkas, Fanni, David Jamieson, Steve Wedge, Daniel Palmer, Helen Reeves, and Ruchi Shukla. "P88 Extracellular vesicle DNA-PK mRNA – a candidate liquid biomarker for hepatocellular carcinoma." In Abstracts of the BSG Annual Meeting, 20–23 June 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-bsg.145.

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Reports on the topic "DNA extracellulare"

1

Button, Julie M. Analysis of cellular and extracellular DNA in fingerprints. Office of Scientific and Technical Information (OSTI), September 2014. http://dx.doi.org/10.2172/1169860.

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The Level of Extracellular DNA as a Stress Marker of Competitive Load. Anna B. Lopatina, Sergei L. Panchenko, September 2016. http://dx.doi.org/10.14526/01_1111_139.

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