Relevant bibliographies by topics / MRC5 Cell

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Academic literature on the topic 'MRC5 Cell'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "MRC5 Cell"

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Kim, Ji-Young, Mi-Jin An, Geun-Seup Shin, et al. "Mercury Chloride but Not Lead Acetate Causes Apoptotic Cell Death in Human Lung Fibroblast MRC5 Cells via Regulation of Cell Cycle Progression." International Journal of Molecular Sciences 22, no. 5 (2021): 2494. http://dx.doi.org/10.3390/ijms22052494.

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Heavy metals are important for various biological systems, but, in excess, they pose a serious risk to human health. Heavy metals are commonly used in consumer and industrial products. Despite the increasing evidence on the adverse effects of heavy metals, the detailed mechanisms underlying their action on lung cancer progression are still poorly understood. In the present study, we investigated whether heavy metals (mercury chloride and lead acetate) affect cell viability, cell cycle, and apoptotic cell death in human lung fibroblast MRC5 cells. The results showed that mercury chloride arrested the sub-G1 and G2/M phases by inducing cyclin B1 expression. In addition, the exposure to mercury chloride increased apoptosis through the activation of caspase-3. However, lead had no cytotoxic effects on human lung fibroblast MRC5 cells at low concentration. These findings demonstrated that mercury chloride affects the cytotoxicity of MRC5 cells by increasing cell cycle progression and apoptotic cell death.
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Siczkowski, M., J. E. Davies, and L. L. Ng. "Activity and density of the Na+/H+ antiporter in normal and transformed human lymphocytes and fibroblasts." American Journal of Physiology-Cell Physiology 267, no. 3 (1994): C745—C752. http://dx.doi.org/10.1152/ajpcell.1994.267.3.c745.

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The turnover number for the sodium-hydrogen exchanger isoform 1 (NHE-1) has been determined in human lymphocytes and MRC5 fibroblasts and in their virally transformed counterparts. Using fluorometric methods, we have determined the intracellular pH and Na+/H+ antiport activity of these cells. Intracellular pH was elevated in both lines of transformed cells. In contrast, Na+/H+ antiport activity was apparently unchanged in simian virus 40-transformed MRC5 fibroblasts (MRC5 SV1 TV1 28.9 +/- 5.2 mM/min compared with MRC5 fibroblasts 26.5 +/- 5.3 mM/min) but slightly increased in Epstein-Barr virus-transformed lymphoblasts (16.7 +/- 1.0 mM/min compared with lymphocytes 13.5 +/- 2.3 mM/min, P < 0.05). With the use of specific antisera to NHE-1, viral transformation was associated with a decreased number of NHE-1 molecules per cell in fibroblasts (from 441,504 +/- 53,428 to 64,745 +/- 7,151 sites/cell, P < 0.001) but an increased number in lymphocytes (from 14,066 +/- 3,100 to 22,474 +/- 4,050 sites/cell, P < 0.01). The NHE-1 density per cell yielded very similar turnover numbers for NHE-1 in the untransformed cells (lymphocytes, 3,161 +/- 833 cycles/s; MRC5 fibroblasts, 3,026 +/- 441 cycles/s), which were significantly elevated in the transformed cells (lymphoblasts, 8,471 +/- 1,177 cycles/s; MRC5 SV1 TV1, 10,521 +/- 2,299 cycles/s, P < 0.001 compared with untransformed cells). We conclude that viral transformation has different effects on Na+/H+ antiport activity and NHE-1 density per cell in different cell types, but the turnover number of NHE-1 is significantly increased after viral transformation, which correlates with the increased proliferation rate of these transformed cells.
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Mandron, Marie, Hélène Martin, Béatrice Bonjean, Jacqueline Lulé, Eric Tartour, and Christian Davrinche. "Dendritic cell-induced apoptosis of human cytomegalovirus-infected fibroblasts promotes cross-presentation of pp65 to CD8+ T cells." Journal of General Virology 89, no. 1 (2008): 78–86. http://dx.doi.org/10.1099/vir.0.83278-0.

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An efficient host response to human cytomegalovirus (HCMV) infection may depend on rapid sensing of the infection by the innate immune response prior to deployment of viral immunosubversive functions. Control of HCMV dissemination could be ensured by apoptosis of cells immediately following infection. In the present report, it is demonstrated that changes in the ratio of c-FLIP to FLICE contributed to early sensitivity of HCMV-infected MRC5 fibroblasts to tumour necrosis factor alpha (TNF-α), providing an innate response to infection. Dendritic cells (DCs) co-cultured with HCMV-infected MRC5 cells acquired the ability to secrete TNF-α in an amount sufficient to kill infected fibroblasts. Blockage of TNF-α binding to its receptor on MRC5 cells with soluble TNF-R reduced the number of dead, HCMV-infected fibroblasts ingested by DCs, thus highlighting the impact of the apoptotic state of infected cells for efficient loading of DCs. Those DCs loaded with antigens available early in infection, such as input virion-associated pp65, could then engage antigen processing for cross-presentation to specific CD8+ T cells. Cross-presentation was impaired when MRC5 cells were treated with the pan-caspase inhibitor ZVAD before co-culture with DCs. Altogether, our data suggest that the innate killing capacity of DCs at the early stage of infection plays a role in the activation of anti-HCMV CD8+ T cells.
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Peristeris, Platon, Alexandre Gaspar, Pascal Gros, Philippe Laurent, Hélène Bernon, and Jacques Bienvenu. "Effects of serum amyloid A protein on lymphocytes, HeLa, and MRC5 cells in culture." Biochemistry and Cell Biology 67, no. 7 (1989): 365–70. http://dx.doi.org/10.1139/o89-057.

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A major human acute phase protein, the serum amyloid A protein, has been tested in vitro for its effect on lymphocyte proliferation, the formation of E-stable rosettes, as well as the growth of HeLa and MRC5 cell cultures. Serum amyloid A protein has been found to be markedly inhibitory at 30, 100, 200, and 300 μg/mL, and is a very potent inhibitor of in vitro biological functions.Key words: serum amyloid A protein, lymphocytes, HeLa cells, MRC5 cells.
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Giatromanolaki, Alexandra, Maria Liousia, Stella Arelaki, et al. "Differential effect of hypoxia and acidity on lung cancer cell and fibroblast metabolism." Biochemistry and Cell Biology 95, no. 3 (2017): 428–36. http://dx.doi.org/10.1139/bcb-2016-0197.

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This study examined the metabolic response of lung cancer cells and normal lung fibroblasts to hypoxia and acidity. GLUT1 and HXKII mRNA/protein expression was up-regulated under hypoxia in the MRC5 fibroblasts and in the A549 and H1299 lung cancer cell lines, indicating intensified glucose absorption and glycolysis. Under hypoxia, the LDHA mRNA and LDH5 protein levels increased in the cancer cells but not in the fibroblasts. Acidity suppressed the above-mentioned hypoxia effect. PDH-kinase-1 (PDK1 mRNA and protein) and inactive phosphorylated-PDH protein levels were induced under hypoxia in the cancer cells, whereas these were reduced in the MRC5 lung fibroblasts. In human tissue sections, the prevalent expression patterns supported the contrasting metabolic behavior of cancer cells vs. tumor fibroblasts. The monocarboxylate/lactate transporter 1 (MCT1) was up-regulated in all the cell lines under hypoxic conditions, but it was suppressed under acidic conditions. The mitochondrial DNA (mtDNA) content per cell decreased significantly in the A549 cancer cell line under hypoxia, but it increased in the MRC5 fibroblasts. Taking into account these findings, we suggest that, under hypoxia, cancer cells intensify the anaerobic direction in glycolysis, while normal fibroblasts prefer to seek energy by intensifying the aerobic use of the available oxygen.
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Ng-Blichfeldt, John-Poul, Tristan de Jong, Rosa K. Kortekaas та ін. "TGF-β activation impairs fibroblast ability to support adult lung epithelial progenitor cell organoid formation". American Journal of Physiology-Lung Cellular and Molecular Physiology 317, № 1 (2019): L14—L28. http://dx.doi.org/10.1152/ajplung.00400.2018.

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Transforming growth factor-β (TGF-β)-induced fibroblast-to-myofibroblast differentiation contributes to remodeling in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis, but whether this impacts the ability of fibroblasts to support lung epithelial repair remains little explored. We pretreated human lung fibroblasts [primary (phFB) or MRC5 cells] with recombinant human TGF-β to induce myofibroblast differentiation, then cocultured them with adult mouse lung epithelial cell adhesion molecule-positive cells (EpCAM+) to investigate their capacity to support epithelial organoid formation in vitro. While control phFB and MRC5 lung fibroblasts supported organoid formation of mouse EpCAM+ cells, TGF-β pretreatment of both phFB and MRC5 impaired organoid-supporting ability. We performed RNA sequencing of TGF-β-treated phFB, which revealed altered expression of key Wnt signaling pathway components and Wnt/β-catenin target genes, and modulated expression of secreted factors involved in mesenchymal-epithelial signaling. TGF-β profoundly skewed the transcriptional program induced by the Wnt/β-catenin activator CHIR99021. Supplementing organoid culture media recombinant hepatocyte growth factor or fibroblast growth factor 7 promoted organoid formation when using TGF-β pretreated fibroblasts. In conclusion, TGF-β-induced myofibroblast differentiation results in Wnt/β-catenin pathway skewing and impairs fibroblast ability to support epithelial repair likely through multiple mechanisms, including modulation of secreted growth factors.
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Dai, Yu-heng, Xiao-qing Li, Da-peng Dong, Hai-bo Gu, Cheng-ying Kong та Zhihao Xu. "P27 Promotes TGF-β-Mediated Pulmonary Fibrosis via Interacting with MTORC2". Canadian Respiratory Journal 2019 (19 вересня 2019): 1–9. http://dx.doi.org/10.1155/2019/7157861.

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Pulmonary fibrosis (PF), a progressive and life-threatening pulmonary disease, is the main pathological basis of interstitial lung disease (ILD) which includes the idiopathic pulmonary fibrosis (IPF). No effective therapeutic strategy for pulmonary fibrosis has been established. TGF-β signaling has emerged as the vital regulator of PF; however, the detailed molecular mechanisms of TGF-β in PF were uncertain. In the present study, we proved that inhibition of MTORC2 suppresses the expression of P27 in MRC5 and HLF cells. And in bleomycin-induced PF model, the expression of α-SMA and P27 was upregulated. Moreover, TGF-β application increased the level of α-SMA, vimentin, and P27 in MRC5 and HLF cells. Furthermore, P27 overexpression advanced the cell cycle process and promoted the proliferation of MRC5 and HLF cells. Finally, the rescue experiment showed that MTORC2 knockdown reversed P27 overexpression-induced cell cycle acceleration and proliferation. Thus, our results suggest that P27 is involved in TGF-β-mediated PF, which was regulated by MTORC2, providing a novel insight into the development of PF.
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Abdalla, Ashraf N., Usama Shaheen, Qasem M. A. Abdallah, et al. "Proapoptotic Activity of Achillea membranacea Essential Oil and Its Major Constituent 1,8-Cineole against A2780 Ovarian Cancer Cells." Molecules 25, no. 7 (2020): 1582. http://dx.doi.org/10.3390/molecules25071582.

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Among the hundreds of reported Achillea species, A. membranacea (Labill.) DC. is one of the six that grow in Jordan. Many species of this genus are used in folk medicine to treat a variety of ailments and several biological and pharmacological activities have been ascribed to their essential oil (EO). For this study, the EO obtained from a specimen of A. membranacea grown in Jordan was analyzed by GC-MS. Ninety-six compounds were detected, of which oxygenated monoterpenes was the predominant class (47.9%), followed by non-terpene derivatives (27.9%), while sesquiterpenes represented 14.2% of the total composition. The most abundant compound in the EO was 1,8-cineole (21.7%). The cytotoxic activity of the EO was evaluated against three cancer cell lines (MCF7, A2780 and HT29), and one normal fibroblast cell line (MRC5) by MTT assay. Significant growth inhibition was observed in EO-exposed A2780 and HT29 cells (IC50 = 12.99 and 14.02 μg/mL, respectively), while MCF7 and MRC5 were less susceptible. The EO induced apoptosis and increased the preG1 events in A2780 cells. 1,8-Cineole, the major constituent of the EO, exhibited submicromolar cytotoxicity against A2780 cells, and was 42 times more selective against MRC5 cells. Its cytotoxicity against A2780 cells was comparable with that of doxorubicin, but 1,8-cineole was more selective for MRC5 normal cells. Interestingly, 1,8-cineole enhanced apoptosis in A2780, and caused a remarkable dose-dependent increase in preG1 events. Thus, 1,8-cineole has demonstrated promising cytotoxic and proapoptotic properties.
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Koulaouzidou, Elisabeth A., Maria Helvatjoglu-Antoniades, George Palaghias, Artemis Karanika-Kouma, and Dimitrios Antoniades. "Cytotoxicity of Dental Adhesives In Vitro." European Journal of Dentistry 03, no. 01 (2009): 03–09. http://dx.doi.org/10.1055/s-0039-1697399.

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ABSTRACTObjectives: The purpose of this study was to evaluate the cytotoxic effect of six dental adhesives (Admira Bond, Clearfil Liner Bond 2V, ED Primer II, Fuji Bond LC, Gluma Comfort Bond, and NanoBond) applied to cell cultures.Methods: The experiments were performed on two cell lines, rat pulp cells (RPC-C2A) and human lung fibroblasts (MRC5). Samples of the adhesives were light-cured and placed in culture medium for 24 hours. The extraction media was applied on the RPC-C2A and the MRC5 cells. Complete medium was used as a control. Cytotoxicity was evaluated with a modified sulforhodamine B (SRB) assay after 24 hours of exposure.Results: The cell survival of RPC-C2A cells exposed to Fuji Bond LC, NanoBond, Clearfil Liner Bond 2V, ED Primer II, Admira Bond and Gluma Comfort Bond was 73%, 67%, 50%, 20%, 18% and 5% respectively, relative to the cell survival with the control medium. In the MRC5 cell line, the relative survival was 98%, 80%, 72%, 41%, 19% and 7% after exposure to NanoBond, Fuji Bond LC, Clearfil Liner Bond 2V, ED Primer II, Admira Bond and Gluma Comfort Bond, respectively.Conclusions: Different types of dental adhesives showed different cytotoxic effects on cells in vitro. The self-etch adhesives were superior in terms of cytotoxicity. The different cytotoxic effects of dental adhesives should be considered when selecting an appropriate adhesive for operative restorations. (Eur J Dent 2009;3:3-9)
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Boulos, Areen, Jean-Marc Rolain, and Didier Raoult. "Antibiotic Susceptibility of Tropheryma whipplei in MRC5 Cells." Antimicrobial Agents and Chemotherapy 48, no. 3 (2004): 747–52. http://dx.doi.org/10.1128/aac.48.3.747-752.2004.

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ABSTRACT Whipple's disease is considered a rare chronic disease with a broad spectrum of clinical manifestations. Several antibiotics have been used for the treatment of this disease, and the current reference treatment was determined empirically on the basis of only a few clinical observations. Patients should be treated for months, and many relapse after antibiotic withdrawal. We report here the first extensive study on the susceptibilities of three reference strains of Tropheryma whipplei to antibiotic in cell culture by using a real-time PCR assay as previously described. We found that doxycycline, macrolides, ketolides, aminoglygosides, penicillin, rifampin, teicoplanin, chloramphenicol, and trimethoprim-sulfamethoxazole were active, with MICs ranging from 0.25 to 2 μg/ml. Vancomycin was somewhat active at an MIC of 10 μg/ml. We found heterogeneity in the susceptibility to imipenem, with one strain being susceptible and the two other strains being resistant. Cephalosporins, colimycine, aztreonam, and fluoroquinolones were not active. We also demonstrated that a combination of doxycycline and hydroxychloroquine was bactericidal. This combination has been shown to be active in the treatment of patients suffering from chronic infections with Coxiella burnetii, a bacterium that is also found intracellularly in acidic vacuoles. We believe, then, that this combination therapy should be further evaluated in clinical trials for the treatment of Whipple's disease.
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Dissertations / Theses on the topic "MRC5 Cell"

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Igor, Đan. "Radiobiološki efekti niskih pre-iradijacionih doza jonizujućeg zračenja na humane ćelijske linije HT29 i MRC5." Phd thesis, Univerzitet u Novom Sadu, Medicinski fakultet u Novom Sadu, 2016. https://www.cris.uns.ac.rs/record.jsf?recordId=100268&source=NDLTD&language=en.

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Radioterapija (RT) je jedan od najvažnijih modaliteta lečenja solidnih malignih tumora i koristi je vi&scaron;e od 50% pacijenata (52,3%) sa malignim tumorima. Nauka koja proučava efekte elektromagnetnog zračenja na biolo&scaron;ke sisteme naziva se radiobiologija. Radiobiologija se fokusira na odgovor ćelija, tkiva i organizma kao celine na jonizujuće zračenje i proučava mehanizme radiobiolo&scaron;kog odgovora. Izlaganje ćelija niskim dozama JZ koje su nakon određenog vremenskog intervala praćene uobičajenim radioterapijskim dozama naziva se radioadaptivno zračenje. Adaptivni odgovor u sebi može da sadrži nekoliko fenomena: hiperradiosenzitaciju/radiorezistenciju, &ldquo;bystander&rdquo; efekat i radioadaptivni efekat u užem smislu. O molekularnim mehanizmima koji stoje iza navedenih efekata ne zna se dovoljno. U ovom radu ispitivan je odgovor malignih i zdravih ćelija na različite modalitete jonizujućeg zračenja u cilju boljeg poznavanja puteva ćelijske smrti i preživljavanja. Potpuno razumevanje molekularnih puteva koji vode u apoptozu ili u preživljavanje ćelija nakon izlaganja jonizujućem zračenju moglo bi koristiti u iznalaženju novih i efikasnijih strategija i modaliteta lečenja malignih tumora u cilju njihove potpune eredikacije. U istraživanju su kori&scaron;tene dve humane ćelijske linije ćelijska linija humanog kolorektalnog karcinoma HT-29 i ćelijska linija humanih fetalnih fibroblasta pluća MRC-5. Ćelije su zračene u dva režima različitim pre-iradijacionim dozama(0,03; 0,05 i 0,07Gy) i istom kurativnom dozom (2Gy) tokom 4 dana. Vi&scaron;ekratna primena niskih doza JZ nije značajno smanjila vijabilnost HT-29 ćelija, dok su dve radioadaptivne doze (0,05+2Gy i 0,07+2Gy), adekvatne doze JZ za radioterapijski postulat po&scaron;tede zdravih ćelija i bolji antitumorski efekat u odnosu na neradioadaptivno zračenje od 2Gy u toku 4 dana. Pokazana je mogućnost modulisanja ćelijskog odgovora na JZ uz pomoć niskih doza JZ koje su praćene dozom od 2Gy (radioadaptivni tip zračenja) u oba dizajnirana režima zračenja. Stepen o&scaron;tećenja hromozoma za većinu isporučenih doza pokazao dozno zavisni trend. Dozno-zavisno o&scaron;tećenje naslednog materijala izazvano radioadaptivnim zračenjem potvrđuje hipotezu da je stepen o&scaron;tećenja zdravih, MRC-5, ćelija manji nego u ćelijama kolorektalnog adenokarcinoma. Fragmentacija DNK je zabeležena za pojedine doze JZ u obe ćelijske linije, a uočena je i razlika u odgovoru zdrave i tumorske ćelijske linije. Detekcijom mutacija primarne sekvence fragmenta p53 gena pokazano je da se broj mutacija povećava sa povećanjem doze JZ. Oba režima radioadaptivnog zračenja, u obe ćelijske linije izazivaju vi&scaron;i nivo ekspresije p53. Ekspresija p38 MAPK proteina u HT-29 ćelijama bila je niža za sve isporučene doze JZ u odnosu na nezračene ćelije. U MRC-5 ćelijama, povi&scaron;ena ekspresija p38 MAPK utvrđena je samo u uzorcima koji su jednokratno primili samo niske doze JZ i dozu od 2Gy dnevno tokom 4 dana, u odnosu na nezračenu kontrolu. Razlike u ekspresiji ispitivanih proteina dobijene nakon primene dva režima radioadaptivnog zračenja posledica su delovanja niskih pre-iradijacionih doza JZ na modulisanje radiobiolo&scaron;kog odgovora obe ćelijske linije. Nivo ekspresije Bcl-2 i Bax proteina i njihov međusobni odnos, u obe ćelijske linije, su odraz različitog radiobiolo&scaron;kog odgovora ispitivanih ćelija koji zavisi od primenjenog režima zračenja.<br>Radiotherapy (RT) is one of the most important treatment modality for solid malignant tumors and it is applied in more than 50% of the patients (52.3%). Radiobiology id scientific discipline which studies the effects of electromagnetic irradiation on biological systems. Radiobiology focuses on the response of the cells, tissues and the organism as a whole to ionizing radiation and studying the mechanisms of radiobiological response. Exposure of cells to low-dose irradiation (priming dose) followed by challenging doses is called radioadaptive radiation. Adaptive response is described as several phenomena: hyperradiosensitivity / radiorezistence, &quot;bystander&quot; effect and radioadaptive effect in sensu strict. Molecular mechanisms underlying the above effects are not sufficiently known. In this study, the response of malignant and healthy cells on various modalities of ionizing radiation is explored in order to improve knowledge of pathways of cell death and survival. Fully understanding the molecular pathways leading to apoptosis or cell survival after exposure to ionizing radiation may be used in finding new and more effective strategies and modalities for the treatment of malignant tumors. The study used two human cell lines: human colorectal cancer HT-29 cell line and the human fetal lung fibroblast MRC-5. The cells were irradiated in two modalities using different pre-irradiation doses (0.03, 0.05 and 0,07Gy) and the same challenging dose (2Gy) for 4 days. Everyday use of low-dose did not significantly reduce the viability of HT-29 cells, while two radioadaptive doses (0.05 + 2Gy and 0.07+2Gy), are adequate doses for sparing healthy cells with better anti-tumor effects. The possibility of modulating the cellular response to the ionizing radiation was shown using low-doses followed by 2Gy (radioadaptive radiation) in both designed regimes of radiation. The level of chromosomal damage showed a dose-dependent trend. Dose-dependent damage to the genetic material caused by radiation confirms the hypothesis that the degree of damage to MRC-5 cells is smaller than the HT29 cells. DNA fragmentation differed between HT29 and MRC-5 cells. Detection of mutations in p53 gene fragment sequence increased with increasing doses. Both irradiation modalities, in both cell lines induce a higher level of p53 expression. Expression of p38 MAPK protein in the HT-29 cells was lower for all delivered doses compared to nonirradiated. In MRC-5 cells, increased expression of the p38 MAPK was found only in the samples that had only received on first day low-doses compared to the control nonirradiated cells. Differences in the expression of the tested proteins reflect different molecular mechanisms activated in normal and tumor cells. The level of Bcl.2 and Bax expression also reflected different radiobiological responses between normal and tumor cells, which depended on the applied irradiation regime.
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Arigony, Ana Lúcia Vargas. "Avaliação do efeito do micronutriente ferro (Fe) na viabilidade celular e estabilidade genômica de culturas celulares de fibroblasto pulmonar (MRC5) e hepatorcarcinoma (HepG2) humanos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/78152.

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Micronutrientes, vitaminas e minerais, são indispensáveis para as vias de metabolismo do DNA e, além disso, são tão importantes para a manutenção da vida quanto os macronutrientes. Na ausência dos nutrientes adequados, a instabilidade genômica compromete a homeostase, ocasionando doenças crônicas e certos tipos de câncer. Meios de cultura celular tem por finalidade mimetizar o ambiente in vivo, proporcionando aos modelos in vitro condições adequadas para que se avalie a resposta celular aos diferentes estímulos. O artigo de revisão sumariza e discute os micronutrientes usados na suplementação das culturas celulares e sua influência na a viabilidade celular e a estabilidade genômica, focando nos estudos in vitro previamente realizados. Nestes estudos, os meios de cultura celular incluem certas vitaminas e minerais em concentrações distintas das fisiológicas in vivo. Em muitos meios de cultura comumente usados, a única fonte de micronutrientes é o Soro Fetal Bovino (SFB), o qual contribui com 5-10% da composição final do meio. Atenção insuficiente tem sido direcionada à composição de SFB, micronutrientes e culturas celulares como um todo, ou à influência de micronutrientes na viabilidade e genética de culturas celulares. Estudos adicionais avaliando melhor o papel de micronutrientes no nível molecular e a sua influência na estabilidade genômica de células ainda se fazem necessários. O micronutriente foco dessa tese é o Ferro (Fe), que por sua vez é um micronutriente essencial, sendo requerido para o crescimento, desenvolvimento e condições normais de funcionamento das células. Tanto seu excesso quanto a sua deficiência podem causar estresse oxidativo e dano ao DNA. Uma vez que os meios de cultura usualmente utilizados para culturas celulares têm níveis de Fe abaixo das concentrações encontradas no soro fisiológico humano, os objetivos deste estudo foram a avaliação do papel da suplementação com Fe na viabilidade celular, na produção de espécies reativas de oxigênio (ERO), na atividade da catalase, na integridade genômica, na expressão de proteínas de reparo de DNA que contém clusters Fe/S em sua estrutura (TFIIH e MutyH) e na expressão de receptores de absorção de Fe (CD71 e Nramp2). Duas linhagens celulares – MRC5 (fibroblasto pulmanar humano) e HepG2 (hepatocarcinoma) - e dois tipos de suplementação com Fe foram utilizados, holo-Transferrina (h-Tf) e FeSO4. Ambas suplementações foram capazes de aumentar os níveis intracelulares de Fe e a viabilidade genômica. A suplementação com Fe também aumentou a formação de ERO, sem alterar a atividade da catalase. No entanto, este aumento de ERO não foi acompanhado por genotoxicidade. No que se refere à expressão de proteínas de reparo ao DNA, os resultados sugerem que o pré-tratamento com h-Tf ou FeSO4 não exercem influência direta na expressão de TFIIH ou MutyH. Entretanto, na expressão de receptores de Fe, os resultados preliminares indicam que CD71 é uma via prioritária de absorção de Fe, estando relacionada com a homeostase de Fe, enquanto Nramp2 parece ter um papel secundário. Devido à importância fisiológica da h-Tf na homeostase do Fe e o acúmulo de ERO menos pronunciado, sugere-se que h-Tf seja uma melhor forma para a suplementação de Fe nas culturas in vitro. Estudos adicionais se fazem necessários para a melhor elucidação do papel do Fe na viabilidade celular e estabilidade genômica.<br>Micronutrients, including minerals and vitamins, are indispensable to DNA metabolic pathways and thus are as important for life as macronutrients. Without the proper nutrients, genomic instability compromises homeostasis, leading to chronic diseases and certain types of cancer. Cell-culture media try to mimic the in vivo environment, providing in vitro models used to infer cells’ responses to different stimuli. The review summarizes and discusses studies of cellculture supplementation with micronutrients that can increase cell viability and genomic stability, with a particular focus on previous in vitro experiments. In these studies, the cell-culture media include certain vitamins and minerals at concentrations not equal to the physiological levels. In many common culture media, the sole source of micronutrients is fetal bovine serum (FBS), which contributes to only 5-10% of the media composition. Minimal attention has been dedicated to FBS composition, micronutrients in cell cultures as a whole, or the influence of micronutrients on the viability and genetics of culture cells. Further studies better evaluating micronutrients’ roles at a molecular level and its influence on the genomic stability of cells is still required. The micronutrient focus on this thesis is Iron (Fe), which is an essential micronutrient and is required for growth, development, and normal cellular functioning. Either excess or deficiency of iron can cause oxidative stress and DNA damage Since the cell media commonly used for cell culture has a lower iron concentration than the human serum, this study aimed to evaluate the role of iron supplementation on viability, reactive oxygen species (ROS) production, catalase activity, genome integrity and the expression of iron-bearing DNA repair proteins (TFIIH and MutyH) and proteins associated with iron absorption (CD71 and Nramp2). Two human cell lines – MRC5 (normal lung fibroblast) and HepG2 (hepatocellular carcinoma) and 2 sources of iron - holo-Transferrin (h-Tf) or FeSO4 were used. Both iron supplements were able to increase intracellular iron levels and cell viability. Iron supplementation increased the formation of ROS, but did not alter catalase activity. However, this increase was not accompanied by genotoxicity. Regarding the DNA repair protein expressions, the results suggest that 24h pre-treatment with h-Tf or FeSO4 has no role in the TFIIH or MutyH expressions. Although, in iron receptor proteins expression, the preliminary data could indicate that CD71 is priority related with Fe homeostasis while Nramp2 seems to have a secondary role. Due to h-Tf physiological role in the iron homeostasis and the less pronounced ROS accumulation, h-Tf could be a better iron supplier in vitro. Additional studies are still required to better elucidate the role of Fe in cell viability and genomic stability.
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Yates, Sally A. "The cytotoxic effects of malondialdehyde on human lung fibroblast cells." Thesis, Liverpool John Moores University, 2015. http://researchonline.ljmu.ac.uk/4529/.

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Malondialdehyde (MDA) is a mutagenic and carcinogenic product of lipid peroxidation which has also been found at elevated levels in smokers. MDA reacts with nucleic acid bases to form pyrimidopurinone DNA adducts, of which 3-(2-deoxy-β-D-erythro-pentofuranosyl)pyrimidol[1,2-α]purin-10(3H)-one (M1dG) is the most abundant and has been linked to smoking. Mutations in the TP53 tumour suppressor gene are associated with half of all cancers. This research applied a multidisciplinary approach to investigate the toxic effects of MDA on the human lung fibroblasts MRC5, which have an intact p53 response, and their SV40 transformed counterpart, MRC5 SV2, which have a sequestered p53 response. Both cell lines were treated with MDA (0-1000 µM) for 24 and 48 h and subjected to a variety of analyses to examine cell proliferation, cell viability, cellular and nuclear morphology, apoptosis, p53 protein expression, DNA topography and M1dG adduct detection. For the first time, mutation sequencing of the 5’ untranslated region (UTR) of the TP53 gene in response to MDA treatment was carried out. The main findings were that both cell lines showed reduced proliferation and viability with increasing concentrations of MDA, the cell surface and nuclear morphology were altered, and levels of apoptosis and p53 protein expression appeared to increase. A LC MS-MS method for detection of M1dG adducts was developed and adducts were detected in CT-DNA treated with MDA in a dose-dependent manner. DNA appeared to become more fragmented with increasing MDA concentration, and the number of mutations in the 5’ UTR region of the TP53 gene also increased. The majority of mutations observed were insertions, compared to lung cancer mutation data where the majority were G to T transversions. This was unexpected, suggesting that tobacco smoke compounds have a different role in mutagenesis than endogenous lipid peroxidation. Thus, MDA has been found to have a clear effect on human lung fibroblasts at both the cellular and DNA level.
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Wilkinson, Simon. "Characterisation of human MRCK protein kinase and its signalling role in cancer cells: regulation of cell invasion." Thesis, Institute of Cancer Research (University Of London), 2005. http://publications.icr.ac.uk/9713/.

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This thesis describes the characterisation of human MRCKcc (myotonic dystrophy kinase-related Cdc42-binding kinase) and the signalling role of MRCK in tumour cell invasion. The first results chapter reports the identity and sequence of the human isoform of MRCKa. It is shown that previously reported expression of a sequence known as PK428 in breast tumours with poor prognosis represents MRCKa expression. PK428 is identified as a partial cDNA of the previously uncloned human MRCKa. The cloning of several splice-variants of full-length MRCKa is described. MRCKa expression is also analysed in human tumour samples, but the data are not conclusive enough to establish MRCKa expression as a prognostic marker. Subsequent work details the functional role of MRCKa and MRCK? in mediating invasion of three-dimensional extracellular matrices by tumour cell lines. In tumour cells that exhibit an elongated morphology, abrogation of signalling of both MRCKa/?, by RNA interference, and ROCK (Rhokinase), with the small-molecule inhibitors Y-27632 or HA-1077, results in inhibition of invasion. This is associated with a collapsed cellular morphology and abrogation of phosphorylation of both the myosin targeting subunit (MYPT1) of myosin light chain phosphatase and of myosin light chain (MLC2). Effects on morphology and invasion are recapitulated with blebbistatin, a specific inhibitor of actomyosin contractility. This suggests that MRCK and ROCK have a redundant role in promoting invasion through regulation of myosin activity. In a cell line with a rounded morphology in threedimensional matrices, switching between three morphological states is identified - rounded, elongated and collapsed, in order of decreasing actomyosin contractility. In this cell line, MRCK and ROCK have a redundant role in maintaining the elongated morphology but ROCK alone signals the high level of contractility that drives the rounded morphology.
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Braesch-Andersen, Ken. "Temperature dependence in human Rhinovirus infection of human MRC-5." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-392331.

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Temperature has been known to be an important factor for in vitro studies where human cell cultures are infected with HRV (human Rhinovirus). The mechanisms behind the temperature effect on the struggle between virulence and cellular defense, are still largely unknown and may be a crucial part in finding a treatment to the common cold. In this study we focused on a few cellular key elements in this struggle and observed behavior changes in regards to the pre-infection growth temperature and the temperature during the viral infection. Past studies have focused mainly on the temperature post inoculation, but here we also wanted to correlate virulence to the growth temperatures preceding the viral infection. We found that the growth temperature of the cell did indeed affect its response to the HRV. If the cells had been growing in an optimal body temperature of 37°C before getting virally infected at 33°C, the viability of the cells did decrease in comparison to cells that had been growing in 33°C from before the viral infection. We could also observe a significant temperature dependence regarding IL-8 release upon HRV inoculation. HRV strive to block induction of inflammatory cytokines such as interferons and IL-1. It may be that impaired IL-8 release at lower temperatures will prevent important danger signals alerting the immune system when cytokine signaling is otherwise hampered by viral intervention.
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Chastonay, José de. "Replication of the hepatitis A virus in MRC-5 cells /." [S.l : s.n.], 1985. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Allouche, Farouk. "Role of RANKL in the differentiation of B cell associated stroma in secondary lymphoid organs." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ002.

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RANKL (ligand du récepteur activateur de NF-KB) est un membre de la famille des TNF dont la signalisation passe par RANK et qui joue un rôle important dans la régulation immunitaire. Chez l'adulte, RANKL est exprimé constitutivement par des cellules réticulaires marginales (MRC) des ganglions lymphatiques. Comme les MRCs sont physiquement proches des lymphocytes B (LB) et ont été proposé d’être des précurseurs de cellules dendritiques folliculaires (FDC), RANKL pourrait jouer un rôle dans la différenciation du stroma associé aux LB et dans la réponse humorale. Afin de mieux comprendre la fonction de RANKL exprimé par les MRC, nous avons généré des souris déficitaires pour RANKL dans les cellules stromales. Nous avons constaté que la formation du follicule B était perturbée ainsi que le réseau FDC. Bien que RANKL ne soit pas requis pour la formation des MRC, il est nécessaire pour l'expression de la chimiokine CXCL13 par ces mêmes cellules. Parmi les TNFRSF dont la signalisation est requise pour l’expression de CXCL13 et la différenciation des FDC, le TNFR1 était significativement réduit dans les cellules stromales des souris dépourvues de RANKL stromal. Ainsi, RANKL pourrait constituer une nouvelle cible thérapeutique contre les immunopathologies des LB en agissant sur son stroma<br>RANKL (receptor activator of NF-κB ligand), a member of the TNF family that signals via RANK, plays an important role for immune regulation. In the adult, RANKL is constitutively expressed by marginal reticular cells (MRCs) of the lymph nodes. Because MRCs are positioned in close vicinity to B cells and may be precursors of follicular dendritic cells (FDCs), RANKL could play a role in the differentiation of B cell-associated stroma and the humoral immune response. In order to better understand the role of RANKL expressed by the MRCs, we generated mice with conditional RANKL deficiency in the stromal compartment. We found that the B cell follicle structure was disrupted and FDC network formation was reduced. Although RANKL was not required for MRC formation, it was necessary for the expression of B cell attracting chemokine CXCL13. Among the TNFRSF members known to control CXCL13 expression and FDC formation, we found that TNFR1 was significantly reduced in the RANKL cKO mice. Thus, RANKL may present a novel therapeutic strategy against B cell-mediated immunopathologies by acting on its stroma
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Karki, Surya B. "Non-thermal Miniature Dielectric Barrier Discharge Plasma for Treatment ofLung Carcinoma Cells." University of Toledo / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1523017849495564.

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Stoner, Terri Dorene. "Indole-3-Carbinol Inhibition of Herpes Simplex Virus Replication." Kent State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=kent1228328838.

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Cunha, Luiz Antônio da. "Avaliação da influência do dipeptídeo N-ß-alanil-L-histidina (L- carnosina) sobre a cinética de expansão de culturas de células diplóides humanas, estirpe MRC-5." Instituto de Tecnologia em Imunobiológicos, 2007. https://www.arca.fiocruz.br/handle/icict/5812.

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Submitted by Priscila Nascimento (pnascimento@icict.fiocruz.br) on 2012-11-14T17:52:45Z No. of bitstreams: 1 luiz-antonio-da-cunha.pdf: 2013128 bytes, checksum: 0e5dc52de1e8d6ce612c04c856313ff7 (MD5)<br>Made available in DSpace on 2012-11-14T17:52:45Z (GMT). No. of bitstreams: 1 luiz-antonio-da-cunha.pdf: 2013128 bytes, checksum: 0e5dc52de1e8d6ce612c04c856313ff7 (MD5) Previous issue date: 2007<br>Fundação Oswaldo Cruz. Instituto de Tecnologia em Imunobiológicos. Rio de Janeiro, RJ, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.<br>Um acordo internacional de transferência de tecnologia, firmado em 2003, entre a FIOCRUZ e a GlaxoSmithKline permitiu o acesso de Bio-Manguinhos a um moderno processo produtivo da vacina tríplice viral (TVV) contra o sarampo, a caxumba e a rubéola. A produção dessa vacina é parte do compromisso de Bio-Manguinhos com o programa nacional de auto-suficiência em imunobiológicos, tido como uma meta prioritária da política de saúde pública do governobrasileiro. A tecnologia aplicada para a produção da TVV envolve o uso de células MRC-5 como substrato celular para a produção de vírus vacinais da rubéola, particularmente da cepa Wistar RA27/3. A estirpe MRC-5 é reconhecida como um dos mais importantes substratos celulares para a produção de vacinas virais, e também tem sido adotada como modelo de estudo para senescência celular in vitro. A senescência celular é um estágio fisiológico complexo pelo qual, invariavelmente, qualquer população de células somáticas normais passa após atingir um determinado número de mitoses. Esseestágio fisiológico é caracterizado nas células diplóides pela contenção da capacidade de se multiplicar e pelo desenvolvimento de alterações morfológicas peculiares, especialmente quando cultivadas in vitro. Com o objetivo de aprimorar omonitoramento de estirpes de células diplóides humanas (HDCS – do inglês Human Diplóide Cells Strains) e contribuir para o estabelecimento da base de conhecimento necessário para a futura aplicação no processo de produção de TVV em Bio-Manguinhos, nós avaliamos culturas de células MRC-5 condicionadas com carnosina, em três diferentes aspectos: cinética de crescimento, propagação da cepa vacinal, Wistar RA27/3, do vírus da rubéola e a expressão do marcador biológico de senescência, a enzima β-galactosidase AS (β-gal AS). A avaliação do potencial antioxidante e antisenescente atribuído a carnosina, um dipeptídeo ubíquo à fisiologia de todos os animais superiores, sobre as células MRC-5 pode contribuir para aprimorar os procedimentos de qualificação e controle de células diplóides associados à produção de vacinas, e aindaservir para o desenvolvimento de novos produtos e a pesquisa científica. Aspectos dacinética de crescimento da cultura de células condicionadas com carnosina, observados neste estudo, são discutidos sob o ponto de vista da teoria do compromisso celular com a senescência. Todas as culturas de células MRC-5 avaliadas demonstraram a expressão da β-gal AS através do uso de X-Gal ou ONPG como substrato. Não encontramos variações no perfil de propagação de cepas vacinais do vírus da rubéola que possam ser associadas ao condicionamento das células MRC-5 com carnosina, nas condições testadas.<br>An international technology transfer agreement established between FIOCRUZ and GlaxoSmithKline in 2003, will provide Bio-Manguinhos with access to a modern manufacturing process for the production of the triple viral vaccine against measles, mumps and rubella (TVV). The production of TVV forms part of the Bio-Manguinhos commitment to the self-sufficiency national programin immunobiologicals, within the Brazilian government public health prioritized policies. The TVV technology employs diploid cells derived from normal human lung tissue(MRC-5) as the substrate for production of the attenuated rubella vaccine virus,Wistar RA27/3. The MRC-5 strain is one of the most important cellular substrates for viral vaccine manufacturing and in addition is widely used as a model for in vitrostudies of cell senescence. Cellular senescence is a physiological stage which normal somatic cells beyond certain duplication level go through, invariably. Such physiological stage is characterized by growth arrest and specific morphological changes, commonly, observed in diploid cells under in vitroculture environment. Aiming to contribute with the human diploid cells strains (HDCS) monitoring study and line up with the establishment of the necessaryknowledge base for the conduction of the TVV production process in Bio-Manguinhos, weevaluated MRC-5 cell cultures conditioned with carnosine under three different aspects: growth kinetics, propagation of the attenuated strain of rubella virus Wistar RA27/3 and the expression of the senescence bio-marker, SA β-Galactosidase. An evaluation of the antioxidant and antisenescence features attributed to carnosine, a dipeptide, ubiquitous to the physiology of all superior animals, over MRC-5 may contribute to the improvement of the qualification and control procedures in production of vaccines, product development and scientific research. Aspects of the growth kineticsof MRC-5 cells conditioned with carnosine observed in this study are discussed in relation to the cellular commitment theory. All MRC-5 tested demonstrated SA β-Galactosidase activity, as verified by enzyme processing of X-Gal or ONPG used as substrate. Additionally, no variations in the propagation profile of the attenuated rubella virus by treating cells with carnosine could be characterized in this study.
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Books on the topic "MRC5 Cell"

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Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Rheumatology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0019.

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Chapter 19 covers the basic science and clinical topics relating to rheumatology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers basic science, the synovium, autoantibodies, osteoarthritis, rheumatoid arthritis, septic arthritis, crystal arthropathies, spondyloarthritides, psoriatic arthritis, low back pain, systemic lupus erythematosus, systemic sclerosis, polymyositis/dermatomyositis, Sjögren syndrome, giant cell arteritis/polymyalgia rheumatic, polyarteritis nodosa, Churg-Strauss syndrome (eosinophilic granulomatosis with polyangiitis), granulomatosis with polyangiitis (Wegener), treating systemic vasculitis, relapsing polychondritis, and Behҫet disease.
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Book chapters on the topic "MRC5 Cell"

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Aghaiypour, Khosrow, Javad Baharizadeh, Siavash Sadeghian, and Ashraf Mohammadi. "Systematic Following of Telomerase during MRC5 Population Dubbling and Cell Senescence." In 3rd Kuala Lumpur International Conference on Biomedical Engineering 2006. Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-68017-8_125.

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Jones, W. G., S. D. Fossa, G. M. Mead, et al. "A Randomised Trial of Two Radiotherapy Schedules in the Adjuvant Treatment of Stage I Seminoma (MRC TE18) — Preliminary Report." In Germ Cell Tumours V. Springer London, 2002. http://dx.doi.org/10.1007/978-1-4471-3281-3_53.

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Trabelsi, Khaled, Semy Majoul, Fatma Charfi, and Héla Kallel. "Measles Virus Production in MRC-5 Cells Grown on Microcarriers in a Stirred Bioreactor." In Cells and Culture. Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3419-9_133.

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Fosså, S. D., L. Collette, N. Aaronson, R. de Wit, and J. T. Roberts. "Quality of Life in Patients with Good Prognosis Metastatic Germ Cell Tumours: Comparison of Four Chemotherapy Schedules (EORTC 30941/MRC TE20)." In Germ Cell Tumours V. Springer London, 2002. http://dx.doi.org/10.1007/978-1-4471-3281-3_42.

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Burgener, A., M. Patrick, K. Coombs, D. Moffatt, N. Huzel, and Michael Butler. "The Modification of a Serum-Free Media Formulation for the Production of Reovirus and the Growth of Vero, MRC-5, MDCK and BHK Cell Lines." In Animal Cell Technology: From Target to Market. Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0369-8_44.

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Collins, Arlene R. "Induction of Apoptosis in MRC-5, Diploid Human Fetal Lung Cells after Infection with Human Coronavirus OC43." In Advances in Experimental Medicine and Biology. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_100.

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Johnson, S. E., E. W. Pearson, and W. K. Ing. "Clinical Responses in Humans to Rabies Vaccine Prepared in MRC-5 Diploid Cells from Canadian Seed Virus." In Rabies in the Tropics. Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70060-6_13.

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"Squamous-cell carcinoma of the penis." In Concise Notes in Oncology for MRCP and MRCS. CRC Press, 2018. http://dx.doi.org/10.1201/9781315378381-54.

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"Cell cycle." In Cracking the MRCS Viva. CRC Press, 2006. http://dx.doi.org/10.1201/b13358-62.

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"Anterior Horn Cell Disorders." In Neurology for MRCP. IMPERIAL COLLEGE PRESS, 2011. http://dx.doi.org/10.1142/9781848164635_0013.

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Conference papers on the topic "MRC5 Cell"

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Vara Prasad, K. N. R. Surya, and Vijay K. Bhargava. "Resource optimization for energy efficiency in multi-cell massive MIMO with MRC detectors." In 2016 IEEE Wireless Communications and Networking Conference (WCNC). IEEE, 2016. http://dx.doi.org/10.1109/wcnc.2016.7564657.

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Prasad, K. N. R. Surya Vara, and Vijay K. Bhargava. "Resource optimization for energy efficiency in multi-cell massive MIMO with MRC detectors." In 2016 IEEE Wireless Communications and Networking Conference Workshops (WCNCW). IEEE, 2016. http://dx.doi.org/10.1109/wcncw.2016.7552686.

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Huang, Ying, L. V. Gangming, Shihua Zhu, and Fan Li. "Uplink performance analysis of very large single-cell MU-MIMO system with MRC receiver." In 2013 19th Asia-Pacific Conference on Communications (APCC). IEEE, 2013. http://dx.doi.org/10.1109/apcc.2013.6766034.

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Cheng, Hei Victor, Emil Bjornson, and Erik G. Larsson. "Uplink pilot and data power control for single cell massive MIMO systems with MRC." In 2015 International Symposium on Wireless Communication Systems (ISWCS). IEEE, 2015. http://dx.doi.org/10.1109/iswcs.2015.7454371.

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Dutcher, Janice, May Garrett, George Wilding, et al. "Abstract B213: Pharmacokinetics (PK) and efficacy of axitinib in patients (pts) with sorafenib‐refractory metastatic renal cell carcinoma (mRCC)." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b213.

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ARELLANO-ORDEN, ELENA, FRANCISCO JAVIER SAENZ-CORONILLA, ANA MONTES-WORBOYS, SONIA MOLINA-PINELO, MIGUEL ANGEL DE GREGORIO ARIZA, and FRANCISCO RODRIGUEZ-PANADERO. "COMPARISON BETWEEN IN VITRO CO-CULTURE OF MRC-5 FIBROBLAST CELL LINE WITH DIFFERENT TYPES OF STENTS." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1100.

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Sinha, Arkadeep, Aprill Watanabe, Jordan Winter, Peter Allen, Galen Hostetter, and Brian B. Haab. "Abstract B60: Analysis of the endocytic receptor MRC2 as a target for mesenchymal pancreatic cancer cells." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-b60.

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Tsimafeyeu, Ilya, Rustem Gafanov, Anna Semenova, et al. "Abstract A1: Clinical outcomes in patients with chronic hepatitis C and metastatic renal cell carcinoma (mRCC) after treatment with nivolumab." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a1.

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Kale, Vijaykumar P., Dhimant Desai, Taryn Dick, et al. "Abstract 736: DJ4, a novel ROCK and MRCK inhibitor, potently inhibits migration and invasion of cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-736.

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Farah, Ibrahim O., Veshell L. Lewis, Wellington K. Ayensu, and Joseph A. Cameron. "Abstract 3369: Differential biotherapeutic advantages of honey in targeting the Warburg effect and survival of MRC-5 and A549 cell lines." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3369.

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