Relevant bibliographies by topics / Cytomix

Academic literature on the topic 'Cytomix'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Cytomix"

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Nelin, Leif D., Hilary A. White, Yi Jin, Jennifer K. Trittmann, Bernadette Chen, and Yusen Liu. "The Src family tyrosine kinases src and yes have differential effects on inflammation-induced apoptosis in human pulmonary microvascular endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 9 (May 1, 2016): L880—L888. http://dx.doi.org/10.1152/ajplung.00306.2015.

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Endothelial cells are essential for normal lung function: they sense and respond to circulating factors and hemodynamic alterations. In inflammatory lung diseases such as acute respiratory distress syndrome, endothelial cell apoptosis is an inciting event in pathogenesis and a prominent pathological feature. Endothelial cell apoptosis is mediated by circulating inflammatory factors, which bind to receptors on the cell surface, activating signal transduction pathways, leading to caspase-3-mediated apoptosis. We hypothesized that yes and src have differential effects on caspase-3 activation in human pulmonary microvascular endothelial cells (hPMVEC) due to differential downstream signaling effects. To test this hypothesis, hPMVEC were treated with siRNA against src (siRNAsrc), siRNA against yes (siRNAyes), or their respective scramble controls. After recovery, the hPMVEC were treated with cytomix (LPS, IL-1β, TNF-α, and IFN-γ). Treatment with cytomix induced activation of the extracellular signal-regulated kinase (ERK) pathway and caspase-3-mediated apoptosis. Treatment with siRNAsrc blunted cytomix-induced ERK activation and enhanced cleaved caspase-3 levels, while treatment with siRNAyes enhanced cytomix-induced ERK activation and attenuated levels of cleaved caspase-3. Inhibition of the ERK pathway using U0126 enhanced cytomix-induced caspase-3 activity. Treatment of hPMVEC with cytomix induced Akt activation, which was inhibited by siRNAsrc. Inhibition of the phosphatidylinositol 3-kinase/Akt pathway using LY294002 prevented cytomix-induced ERK activation and augmented cytomix-induced caspase-3 cleavage. Together, our data demonstrate that, in hPMVEC, yes activation blunts the ERK cascade in response to cytomix, resulting in greater apoptosis, while cytomix-induced src activation induces the phosphatidylinositol 3-kinase pathway, which leads to activation of Akt and ERK and attenuation of apoptosis.
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Rodriguez, Luis A., Arezoo Mohammadipoor, Lucero Alvarado, Robin M. Kamucheka, Amber M. Asher, Leopoldo C. Cancio, and Ben Antebi. "Preconditioning in an Inflammatory Milieu Augments the Immunotherapeutic Function of Mesenchymal Stromal Cells." Cells 8, no. 5 (May 15, 2019): 462. http://dx.doi.org/10.3390/cells8050462.

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Multipotent mesenchymal stromal cells (MSCs) have emerged as potent therapeutic agents for multiple indications. However, recent evidence indicates that MSC function is compromised in the physiological post-injury milieu. In this study, bone marrow (BM)- and adipose-derived (AD)-MSCs were preconditioned in hypoxia with or without inflammatory mediators to potentiate their immunotherapeutic function in preparation for in vivo delivery. Human MSCs were cultured for 48 h in either normoxia (21% O2) or hypoxia (2% O2) with or without the addition of Cytomix, thus creating 4 groups: (1) normoxia (21%); (2) Cytomix-normoxia (+21%); (3) hypoxia (2%); and (4) Cytomix-hypoxia (+2%). The 4 MSC groups were subjected to comprehensive evaluation of their characteristics and function. Preconditioning did not alter common MSC surface markers; nonetheless, Cytomix treatment triggered an increase in tissue factor (TF) expression. Moreover, the BM-MSCs and AD-MSCs from the +2% group were not able to differentiate to chondrocytes and osteoblasts, respectively. Following Cytomix preconditioning, the metabolism of MSCs was significantly increased while viability was decreased in AD-MSCs, but not in BM-MSCs. MSCs from both tissues showed a significant upregulation of key anti-inflammatory genes, increased secretion of IL-1 receptor antagonist (RA), and enhanced suppression of T-cell proliferation following the Cytomix treatment. Similarly, following a lipopolysaccharide challenge, the Cytomix-treated MSCs suppressed TNF-α secretion, while promoting the production of IL-10 and IL-1RA. These preconditioning approaches facilitate the production of MSCs with robust anti-inflammatory properties. AD-MSCs preconditioned with Cytomix under normoxia appear to be the most promising therapeutic candidates; however, safety concerns, such as thrombogenic disposition of cells due to TF expression, should be carefully considered prior to clinical translation.
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Scharte, Marion, Xiaonan Han, Daniel J. Bertges, Mitchell P. Fink, and Russell L. Delude. "Cytokines induce HIF-1 DNA binding and the expression of HIF-1-dependent genes in cultured rat enterocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 3 (March 1, 2003): G373—G384. http://dx.doi.org/10.1152/ajpgi.00076.2002.

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Cellular adaptation to hypoxia depends, in part, on the transcription factor hypoxia-inducible factor-1 (HIF-1). Normoxic cells exposed to an inflammatory milieu often manifest phenotypic changes, such as increased glycolysis, that are reminiscent of those observed in hypoxic cells. Accordingly, we investigated the effects of cytomix, a mixture containing IFN-γ, TNF, and IL-1β on the expression of HIF-1-dependent proteins under normoxic and hypoxic conditions. Incubation of intestine-derived epithelial cells (IEC-6) under 1% O2increased HIF-1 DNA binding and expression of aldolase A, enolase-1, and VEGF mRNA. Incubation of normoxic cells with cytomix for 48 h also markedly increased HIF-1 DNA binding and expression of mRNAs for these proteins. Incubation of hypoxic cells with cytomix did not inhibit HIF-1 DNA binding or upregulation of HIF-1-dependent genes in response to hypoxia. Neither cytomix nor hypoxia increased steady-state levels of HIF-1α mRNA. Incubation of IEC-6 cells with cytomix induced nitric oxide (NO·) biosynthesis, which was blocked if the cultures containedl- NG-(1-iminoethyl)lysine hydrochloride (l-NIL). Treatment with l-NIL, however, failed to significantly alter aldolase A, enolase-1, and VEGF mRNA levels in normoxic cytomix-treated cells. Proinflammatory cytokines activate the HIF-1 pathway and increase expression of glycolytic genes in nontransformed rat intestinal epithelial cells, largely through an NO·-independent mechanism.
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Zhu, Y. K., X. D. Liu, C. M. Sköld, T. Umino, H. J. Wang, J. R. Spurzem, T. Kohyama, R. F. Ertl, and S. I. Rennard. "Synergistic neutrophil elastase-cytokine interaction degrades collagen in three-dimensional culture." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 4 (October 1, 2001): L868—L878. http://dx.doi.org/10.1152/ajplung.2001.281.4.l868.

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Proteolytic degradation of extracellular matrix is thought to play an important role in many lung disorders. In the current study, human lung fibroblasts were cast into type I collagen gels and floated in medium containing elastase, cytomix (combination of tumor necrosis factor-α, interleukin-1β, and interferon-γ), or both. After 5 days, gel collagen content was determined by measuring hydroxyproline. Elastase alone did not result in collagen degradation, but in the presence of fibroblasts, elastase reduced hydroxyproline content to 75.2% ( P < 0.01), whereas cytomix alone resulted in reduction of hydroxyproline content to 93% ( P < 0.05). The combination of elastase and cytomix reduced hydroxyproline content to 5.2% ( P < 0.01). α1-Proteinase inhibitor blocked this synergy. Gelatin zymography and Western blot revealed that matrix metalloproteinase (MMP)-1, -3, and -9 were induced by cytomix and activated in the presence of elastase. Tissue inhibitor of metalloproteinase (TIMP)-1 and -2 were also induced by cytomix but were cleaved by elastase. We conclude that a synergistic interaction between cytomix and elastase, mediated through cytokine induction of MMP production and elastase-induced activation of latent MMPs and degradation of TIMPs, can result in a dramatic augmentation of collagen degradation. These findings support the notion that interaction among inflammatory mediators secreted by mononuclear cells and neutrophils can induce tissue cells to degrade extracellular matrix. Such a mechanism may contribute to the protease-anti-protease imbalance in emphysema.
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Thompson, David C., Stephanie E. Porter, Alison K. Bauer, Kumuda C. Das, Brandon Ou, Lori Dwyer-Nield, Carl W. White, and Alvin M. Malkinson. "Cytokine-induced nitric oxide formation in normal but not in neoplastic murine lung epithelial cell lines." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 6 (June 1, 1998): L922—L932. http://dx.doi.org/10.1152/ajplung.1998.274.6.l922.

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Cytomix, a mixture of interferon-γ, tumor necrosis factor-α, and interleukin-1β, induces nitric oxide (NO) production in lung epithelial cell lines. It is not known whether neoplastic transformation alters a cell’s ability to form NO in response to cytokines. The present study investigated NO formation in two murine lines of immortalized “normal” (nontumorigenic) lung epithelial cells of alveolar type II origin, E10 and C10, and their sibling spontaneous transformants, E9 and A5. Nontumorigenic cells elaborated much more NO after cytomix exposure than did their tumorigenic counterparts. NO production was prevented by inhibiting protein synthesis and NO synthase and attenuated by dexamethasone. Northern and Western blot analyses of inducible NO synthase (iNOS) demonstrated cytomix-induced induction of iNOS only in nontumorigenic cells. The deficiency in NO production in tumorigenic cells was not associated with reduced iNOS mRNA stability or with differences in cytomix-induced nuclear factor-κB activation. Although cytomix caused a greater production of NO in E10 cells than in E9 cells, the same treatment induced equivalent proliferation in both cell lines. These results indicate a specific deficiency in cytokine-induced NO synthesis in transformed murine lung epithelial cells relative to their normal progenitor cells and provide a model for investigating iNOS regulation.
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Liu, Shiguang, Donna B. Stolz, Penny L. Sappington, Carlos A. Macias, Meaghan E. Killeen, Jyrki J. Tenhunen, Russell L. Delude, and Mitchell P. Fink. "HMGB1 is secreted by immunostimulated enterocytes and contributes to cytomix-induced hyperpermeability of Caco-2 monolayers." American Journal of Physiology-Cell Physiology 290, no. 4 (April 2006): C990—C999. http://dx.doi.org/10.1152/ajpcell.00308.2005.

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High-mobility group box 1 (HMGB1), a cytokine-like proinflammatory protein, is secreted by activated macrophages and released by necrotic cells. We hypothesized that immunostimulated enterocytes might be another source for this mediator. Accordingly, Caco-2 cells or primary mouse intestinal epithelial cells (IECs) were incubated with “cytomix” (a mixture of TNF, IL-1β, and IFN-γ) for various periods. HMGB1 in cell culture supernatants was detected by Western blot analysis and visualized in Caco-2 cells with the use of fluorescence confocal and immunotransmission electron microscopy. Caco-2 cells growing on filters in diffusion chambers were stimulated with cytomix for 48 h in the absence or presence of anti-HMGB1 antibody, and permeability to fluorescein isothiocyanate-dextran (average molecular mass, 4 kDa; FD4) was assessed. Cytomix-stimulated Caco-2 cells secreted HMGB1 into the apical but not the basolateral compartments of diffusion chambers. Although undetectable at 6 and 12 h after the start of incubation with cytomix, HMGB1 was present in supernatants after 24 h of incubation. HMGB1 secretion by Caco-2 monolayers also was induced when the cells were exposed to FSL-1, a Toll-like receptor (Tlr)-2 agonist, or flagellin, a Tlr5 agonist, but not lipopolysaccharide, a Tlr4 agonist. Cytomix also induced HMGB1 secretion by primary IECs. Cytoplasmic HMGB1 is localized within vesicles in Caco-2 cells and is secreted, at least in part, associated with exosomes. Incubating Caco-2 cells with cytomix increased FD4 permeation, but this effect was significantly decreased in the presence of anti-HMGB1 antibody. Collectively, these data support the view that HMGB1 is secreted by immunostimulated enterocytes. This process may exacerbate inflammation-induced epithelial hyperpermeability via an autocrine feedback loop.
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Subasinghe, Wasanthi, Ismail Syed, and Anjaneyulu Kowluru. "Phagocyte-like NADPH oxidase promotes cytokine-induced mitochondrial dysfunction in pancreatic β-cells: evidence for regulation by Rac1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 1 (January 2011): R12—R20. http://dx.doi.org/10.1152/ajpregu.00421.2010.

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Reactive oxygen species (ROS) are important mediators of cellular signal transduction cascades such as proliferation, migration, and apoptosis. Chronic exposure of isolated β-cells to proinflammatory cytokines elevates intracellular oxidative stress leading to the demise of pancreatic β-cells culminating in the onset of diabetes. Although the mitochondrial electron transport chain is felt to be the primary source of ROS, several lines of recent evidence suggest that phagocyte-like NADPH oxidase plays a central role in cytokine-mediated ROS generation and apoptosis of β-cells. However, the precise mechanisms underlying the regulation of NADPH oxidase remain unknown. To address this, insulin-secreting INS 832/13 cells were treated with cytomix (IL-1β, IFN-γ, and TNF-α; 10 ng/ml each) for different time intervals (0–24 h). A significant, time-dependent increase in NADPH oxidase activation/intracellular ROS production, p47phox subunit, but not p67phox subunit, expression of the phagocyte-like NADPH oxidase were demonstrable under these conditions. Furthermore, siRNA-p47phox transfection or exposure of INS 832/13 cells to apocynin, a selective inhibitor of NADPH oxidase, markedly attenuated cytomix-induced ROS generation in these cells. Cytomix-mediated mitochondrial dysfunction in INS 832/13 cells was evident by a significant loss of mitochondrial membrane potential (MMP) and upregulated caspase 3 activity. Cytomix treatment also caused a transient (within 15 min) activation of Rac1, a component of the NADPH oxidase holoenzyme. Furthermore, GGTI-2147 and NSC23766, known Rac1 inhibitors, not only attenuated the cytomix-induced Rac1 activation but also significantly prevented loss of MMP (NSC23766 > GGTI-2147). However, NSC23766 had no effect on cytomix-induced NO generation or caspase 3 activation, suggesting additional regulatory mechanisms might underlie these signaling steps. Together, these findings suggested that Rac1-mediated regulation of phagocyte-like NADPH oxidase contributes to cytokine-mediated mitochondrial dysfunction in the β-cell.
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Burke-Gaffney, A., and P. G. Hellewell. "Endogenous nitric oxide limits cytokine-induced damage of murine lung epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 4 (April 1, 1997): L707—L713. http://dx.doi.org/10.1152/ajplung.1997.272.4.l707.

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This study investigated whether endogenous nitric oxide (NO) limits cytokine-induced damage to the murine lung epithelial cell line LA-4. NO production was assessed as nitrite using the Griess reaction, and cell damage was assessed using ethidium homodimer-1. Cytotoxicity was first detected after a 24-h incubation with a combination of tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma (cytomix). Nitrite production increased to 78.0 +/- 0.5 nmol/10(6) cells at 24 h. Coincubation of LA-4 with cytomix and NO synthase inhibitors, aminoguanidine (3-1,000 microM) and N(G)-monomethyl-L-arginine (10-1,000 microM), but not N(G)-monomethyl-D-arginine, or a soluble guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazole [4,3-a] quinoxalin-1-one, reduced cytomix-induced nitrite production and increased cytotoxicity up to twofold (24 h). Removal of L-arginine from the medium increased damage; reintroduction of 1,000 microM L-arginine, but not D-arginine, reversed this. In aminoguanidine-treated cells, replacement of NO with an NO donor, S-nitrosoglutathione (30 microM), reversed, in part, the cell damage observed in aminoguanidine/cytomix-treated cells. These results suggest that endogenous NO limits cytokine-induced lung epithelial damage.
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Panas, Donna, Fadi H. Khadour, Csaba Szabó, and Richard Schulz. "Proinflammatory cytokines depress cardiac efficiency by a nitric oxide-dependent mechanism." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 3 (September 1, 1998): H1016—H1023. http://dx.doi.org/10.1152/ajpheart.1998.275.3.h1016.

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Proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interferon-γ; Cytomix) depress myocardial contractile work partially by stimulating expression of inducible nitric oxide (NO) synthase (iNOS). Because NO and peroxynitrite inhibit myocardial O2 consumption (MV˙o 2), we examined whether this mechanism contributes to reduced cardiac work. In control isolated working rat hearts, cardiac work was stable for 60 min, followed by a decline from 60 to 120 min, without change in MV˙o 2. Cardiac efficiency (work/MV˙o 2) was therefore reduced from 60 to 120 min. Cytomix shortened the onset (within 20–40 min) and enhanced the depression in cardiac work and efficiency and inhibited MV˙o 2 after 80 min. Mercaptoethylguanidine (MEG), an iNOS inhibitor and peroxynitrite scavenger, or the glucocorticoid dexamethasone (Dex) abolished the effects of Cytomix. iNOS expression was increased 10-fold by Cytomix and abolished by Dex but not MEG. That cytokine-induced depression in cardiac work precedes the reduction in MV˙o 2 suggests, at least in the early response, that NO and/or peroxynitrite may not impair heart function by inhibiting mitochondrial respiration but reduce the heart’s ability to utilize ATP for contractile work.
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Supinski, Gerald S., Alexander P. Alimov, Lin Wang, Xiao-Hong Song, and Leigh A. Callahan. "Calcium-dependent phospholipase A2 modulates infection-induced diaphragm dysfunction." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 10 (May 15, 2016): L975—L984. http://dx.doi.org/10.1152/ajplung.00312.2015.

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Calpain activation contributes to the development of infection-induced diaphragm weakness, but the mechanisms by which infections activate calpain are poorly understood. We postulated that skeletal muscle calcium-dependent phospholipase A2 (cPLA2) is activated by cytokines and has downstream effects that induce calpain activation and muscle weakness. We determined whether cPLA2 activation mediates cytokine-induced calpain activation in isolated skeletal muscle (C2C12) cells and infection-induced diaphragm weakness in mice. C2C12 cells were treated with the following: 1) vehicle; 2) cytomix (TNF-α 20 ng/ml, IL-1β 50 U/ml, IFN-γ 100 U/ml, LPS 10 μg/ml); 3) cytomix + AACOCF3, a cPLA2 inhibitor (10 μM); or 4) AACOCF3 alone. At 24 h, we assessed cell cPLA2 activity, mitochondrial superoxide generation, calpain activity, and calpastatin activity. We also determined if SS31 (10 μg/ml), a mitochondrial superoxide scavenger, reduced cytomix-mediated calpain activation. Finally, we determined if CDIBA (10 μM), a cPLA2 inhibitor, reduced diaphragm dysfunction due to cecal ligation puncture in mice. Cytomix increased C2C12 cell cPLA2 activity ( P < 0.001) and superoxide generation; AACOCF3 and SS31 blocked increases in superoxide generation ( P < 0.001). Cytomix also activated calpain ( P < 0.001) and inactivated calpastatin ( P < 0.01); both AACOCF3 and SS31 prevented these changes. Cecal ligation puncture reduced diaphragm force in mice, and CDIBA prevented this reduction ( P < 0.001). cPLA2 modulates cytokine-induced calpain activation in cells and infection-induced diaphragm weakness in animals. We speculate that therapies that inhibit cPLA2 may prevent diaphragm weakness in infected, critically ill patients.
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Dissertations / Theses on the topic "Cytomix"

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REZOAGLI, EMANUELE. "Optimization of the Therapeutic Potential of Umbilical Cord-Mesenchymal Stem Cells for Staphylococcus Aureus Induced Pneumonia." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263058.

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Introduzione: la sindrome da distress respiratorio acuto (ARDS) rappresenta il 10% di tutti i ricoveri in terapia intensiva e il 23% dei pazienti ventilati meccanicamente. Le cause più comuni di ARDS includono polmonite e sepsi. Ad oggi non esiste alcun trattamento per l'ARDS. Le cellule staminali mesenchimali (MSC) stanno emergendo come un trattamento promettente dell'ARDS per tre motivi: proprietà immunomodulatorie; antimicrobiche e di rigenerazione tissutale. Uno dei motivi per cui le MSC non sono ancora utilizzate nella terapi dell’ARDS in clinica è dovuto alla variabilità di risposta biologica. Un potenziale strategia per ottimizzarne l’azione è la preattivazione per-trattamento. Ad oggi, non sono disponibili informazioni sul ruolo delle MSC nel trattamento delle ARDS polmonare indotta da batteri Gram +. S. aureus è un batterio Gram + associato a più del 40% di casi di polmonite nosocomiale e con tassi di mortalità>50%. Obiettivi 1. Caratterizzare l'espressione delle citochine delle MSC da cordone ombelicale (UC) e il ruolo del loro mezzo di coltura su una linea cellulare monocitica umana; 2. stabilire un nuovo modello di polmonite batterica gram + usando un ceppo di S. aureus da isolato umano; valutare 3. il potenziale ruolo terapeutico di UC-MSC con e senza preattivazione ​​(serie 1) e 4. di UC-MSC preattivate a basso dosaggio (serie 2) nel trattamento di ARDS indotta da S. aureus nel ratto. Metodi: Gli esperimenti in vitro hanno quantificato il profilo pro/antiinfiammatorio delle citochine derivanti da UC-MSC naïve e preattivate con citomix (TNF-α; IL-1β; e IFN- γ [50 ng / mL ciascuno]) tramite ELISA. Modelli di lesione cellulare in vitro sono stati sviluppati. Cellule THP-1 sono state trattate con mezzo di coltura da MSC per determinarne l'espressione e l'effetto sulla fagocitosi. Ratti (Sprague Dawley) maschi adulti sono stati utilizzati per gli esperimenti. Gli animali sono stati sottoposti a instillazione intratracheale di S. aureus Newman per indurre la ARDS polmonare. Nella serie 1, gli animali sono stati randomizzati, entro 2 ore dall'infezione, alla somministrazione endovenosa di: (1) veicolo (soluzione salina tamponata con fosfato (PBS)); (2) 1x107 / kg di UC-MSC; e (3) 1x107 / kg di UC-MSC pre-attivati ​​per 24 ore. Nella serie 2, abbiamo randomizzato gli animali alla somministrazione endovenosa di: (1) veicolo (soluzione salina tamponata con fosfato (PBS)); (2) 2x106 / kg e (3) 5x106 / kg di UC-MSC pre-attivate per 24 ore con citomix (TNF-α; IL-1β; e IFN- γ [50 ng / mL ciascuno]). I confronti tra i gruppi sono stati testati per le differenze nella carica batterica e nella conta dei globuli bianchi nel lavaggio broncoalveolare (BAL) e in parametri fisiologici a 48h dal danno.
Risultati: le cellule preattivate esprimono un profilo pro/antiinfiammatorio differente rispetto alle UC-MSC naïve in vitro. L'instillazione endotracheale di S. aureus Newman ha indotto il primo modello di ARDS nel ratto usando un tale ceppo batterico. Le UC-MSC naïve hanno trattato parzialmente la lesione polmonare. Al contrario, la preattivazione di UC-MSC con cytomix per 24 ore ha permesso di aumentare significativamente la clearance batterica, ridurre gli infiltrati di cellule polmonari e migliorare l'ossigenazione (PaO2/FiO2 medio>300 (FiO2=1) (serie 1). Questi risultati sono stati confermati nella serie 2, in cui le UC-MSC preattivate hanno dimostrato il loro ruolo terapeutico nella attenuazione dell'ALI anche a basse dosi (2x106/kg).
Conclusioni: la terapia con UC-MSC preattivate ​ ha ridotto la gravità dell'ARDS indotta da S. aureus anche a bassa dose di 2x106 / kg come visibile dalla riduzione della carica batterica e degli infiltrati di cellule infiammatorie polmonari e migliorando compliance respiratoria e ossigenazione arteriosa. L'uso di UC-MSC pre-attivate ​​può rappresentare un trattamento potenzialmente rilevante nell’ARDS polmonare indotta da gram+.
Introduction: Acute respiratory distress syndrome accounts for 10% of all ICU admissions and 23% of all mechanically ventilated patients. The most common causes of ARDS include pneumonia and sepsis. There remains currently no specific treatment for ARDS. Mesenchymal stem cells (MSCs) are emerging as a promising strategy for the treatment of ARDS for three main reasons: immune-modulatory properties, anti-microbial effects and tissue regeneration capabilities. With all of these listed qualities, why aren’t MSCs a current therapy in patients with ARDS? One reason for this, is that MSCs present a strong biological variability in-vivo. A possible approach to overcoming this in-consistency in the potential of MSCs is to prime them before administration. No information is available on the role of MSCs in the treatment of pulmonary ARDS induced by Gram positive bacteria. Staphylococcus aureus Newman is a clinically relevant Gram positive bacterium which is associated with >40% health care pneumonia cases and with mortality rates of >50%. Objectives 1. To characterize the cytokine expression of umbilical cord (UC) MSCs and the role of conditioned media on a human monocytic cell line; 2. to establish a new model of gram positive bacterial pneumonia using a clinically relevant strain of S. Aureus from a human isolate; to evaluate 3. the potential therapeutic role of naïve and preactivated UC-MSCs (Series 1) and 4. of low dose preactivated UC-MSCs (Series 2) freshly harvested from culture in the treatment of acute lung injury in a new model of Rodent S. aureus–induced ARDS. Methods: Cellular assays involved cytokine expression of naïve and preactivated UC-MSCs with cytomix (TNF-α; IL-1β; and IFN- γ [50 ng/mL each]) was measured using ELISA. In-vitro chemical and inflammatory injury assays were carried out. THP-1 cells were treated with conditioned media from primed and naïve MSCs to determine cytokine expression and effect on percentage phagocytosis. Adult male Sprague Dawley rats were used for in-vivo experiments. Animals underwent intratracheal instillation of S. aureus Newman to induce pulmonary ARDS. In series 1, animals were randomized, within 2 hours post infection, to intravenous administration of: (1) vehicle (phosphate buffered saline (PBS)); (2) 1x107/kg fresh UC-MSCs; and (3) 1x107/kg fresh UC-MSCs preactivated for 24 hours. In series 2, we randomized animals, within 2 hours post infection, to intravenous administration of: (1) vehicle (phosphate buffered saline (PBS)); (2) 2x106/kg and (3) 5x106/kg fresh UC-MSCs preactivated for 24 hours with cytomix (TNF-α; IL-1β; and IFN- γ [50 ng/mL each]). Comparisons among the groups were tested for differences in bacterial load and white blood cell count in the bronchoalveolar lavage (BAL), and arterial oxygenation after 48 hours. Results: Primed UC-MSCs variably expressed a different pro/anti-inflammatory profile compared to naïve UC-MSCs in vitro. Endotracheal instillation of S. aureus Newman induced the first model of ARDS in rats using such a bacterium strain. Fresh naïve UC-MSCs did not treat the lung injury. In contrast, the preactivation of fresh UC-MSCs with cytomix for 24 hours allowed to significantly increase the pulmonary bacterial clearance, reduce the lung cell infiltrates and to improve oxygenation with an average PaO2/FiO2 ratio above 300 at an FiO2 of 1.0 (series 1). These results were confirmed in series 2, where preactivated UC-MSCs demonstrated their therapeutic role in the decrease of ALI even at the low dose of 2x106/kg. Conclusions: Fresh preactivated UC-MSCs therapy decreased the severity of S. aureus induced ARDS even at the low dose of 2x106/kg by the reduction of bacterial load and white blood cell infiltrates into the lungs, and leading to the increase of arterial oxygenation. The use of preactivated UC-MSCs may represent a potential clinically relevant treatment of acute lung injury in patients with gram positive induced ARDS.
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Dy, Eric David. "Development of a cytomic force transducer for experimental mechanobiology." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1750740721&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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Fergusson, Ronald John. "Treatment of human lung cancer with interferon and cytoxic agents." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/23889.

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The prognosis for patients with lung cancer remains extremely poor. Newer, more effective treatment regimens are required. In this thesis, the effectiveness of combining human recombinant interferon alpha with various estalished cytotoxic agents was assessed in laboratory models of human lung cancer and a clinical study. The majority of the experimental work was performed on a series of human bronchial carcinoma xenografts established in immune deprived CBA mice. Interferon alone had no cytotoxic effect but appeared to potentiate the activity of various anti-cancer agents in non-small cell tumours. No such effect was seen in two small cell xenografts. Further studies suggested that the dosing schedules of each agent in the combination was important in producing positive effects. The exact mechanisms by which interferon may interact with cytotoxic drugs remains unexplained. It was shown that the results obtained in the xenograft model were not mediated through increased toxicity to the host or by modulation of cell cycle distribution within the tumour cells. Assessment of interferon/drug combinations was also performed using in-vitro models of lung cancer. Significant synergistic interactions were not demonstrated. A pilot clinical study investigating the potential of combined treatment with interferon and Cisplatinum was performed in a group of patients with non-small cell lung cancer. The toxicity of the treatment was predictable and an encouraging response rate was seen.
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Campos, Alexandre Rosa. "Application of proteomics and cytomics in human neutrophils functional studies." reponame:Repositório Institucional da UnB, 2007. http://repositorio.unb.br/handle/10482/1077.

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Dissertação (mestrado)—Universidade de Brasília, Faculdade de Medicina, 2007.
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Biomedical research commonly starts by raising a hypothesis to solve a problem. In this context, scientists select the most appropriate method(s) to answer the question and solve a common dilemma. Over the past decade, we have witnessed a revolution of new technologies in molecular biology – the Omics Science. Highscale technologies such as metabolomics, cytomics, genomics and proteomics are changing the way we study complex biological systems. Current approaches to understanding the functional diversity of an organism preferentially strive for a systems biology approach whereby first the phenotypic classification of a specific cytome is achieved prior to an attempt to perform proteomic analysis. In this context, to better understand the features that involve neutrophil activation and programmed cell death in the pathological and healthy states, this study proposes the integration of cell biology approaches such as flow cytometry with a very robust proteomics platform in an attempt to integrate data at the molecular level with phenotypic data of neutrophils. The application of subcellular fractionation method using digitonin detergent extraction to enrich cytosolic proteins from neutrophils was found reproducible, simple to perform, and inexpensive. ________________________________________________________________________________________ ABSTRACT
Pesquisas biomédica comumente começa com a elaboração de uma hipotese para resolver um problema. Nesse contexto, cientistas selecionam o(s) metodo(s) mais apropriado(s) para responder a questão e solucionar um dilema. Nos últimas anos, nós temos testemunhado uma revolução de novas tecnologias em biologia molecular – a ciência -Omica. Tecnologias de alta-escala tais como metabolômica, citômica, genômica e proteômica estão mudando o modo que estudamos sistemas biológicos complexos. Métodos contemporâneos para o entendimento da diversidade funcional em um dado organismo preferencialmente abordam uma visão de biologia de sistemas onde primeiro a classificação fenótipa de um citoma é alcançado antes de uma tentativa de caracterizar o proteoma de tal célula. Dentro desse contexto, e para proporcionar um melhor entendimento dos componentes envolvidos na ativação e morte celular programada dos neutrófilos nos estados patológicos e sano, esse estudo propõe a integração de métodos em biologia celular tal como citometria de fluxo com uma robusta plataforma proteômica em uma tentativa de integrar dados a nível molecular com dados fenótipicos de neutrófilos. Fracionamento subcelular usando um método de extração e enriquecimento de proteínas citosólicas com o detergente digitonina foi otimizado nesse trabalho, e encontrado ser altamente reprodutível, fácil de realizar, e de baixo custo.
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Strzelczyk, Barbara. "Cytokin mRNA profil i perifera mononukleära celler hos barn med födoämnesallergi." Thesis, Umeå universitet, Biomedicinsk laboratorievetenskap, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-58649.

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Helg, Andreas Gabriel. "Allopyranosyl-Nukleinsäure : Synthese, Paarungseigenschaften und Struktur von Guanin-/Cytosin-enthaltenden Oligonukleotiden /." [S.l.] : [s.n.], 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10464.

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Letort, Gaelle. "Exploration par simulations numériques de l'auto-organisation du cytosquelette sous conditions géométriquement contrôlées." Thesis, Université Grenoble Alpes (ComUE), 2015. http://www.theses.fr/2015GREAS048/document.

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Le cytosquelette joue un rôle essentiel dans de nombreux processus cellulaires (division, adhésion, migration, morphogenèse..). Un de ses principaux constituants, les filaments d'actine, des polymères semi flexibles polarisés, forme des réseaux dont les architectures spécifiques permettent au cytosquelette de réaliser ses fonctions physiologiques. Un enjeu majeur en biologie cellulaire est de comprendre comment les cellules peuvent former une telle variété d'organisations à partir de la même entité de base, les monomères d'actine. Nous avons découvert récemment que limiter la nucléation des filaments d'actine à des géométries définies suffit à contrôler la formation de différentes organisations (Reymann et al, 2010). Néanmoins, les paramètres principaux permettant d'expliquer comment ces contraintes géométriques déterminent l'organisation collective des filaments n'ont pas été identifiés. Pour comprendre les lois physiques régissant ce phénomène, j'ai développé des simulations numériques du système expérimental en utilisant le logiciel Cytosim. J'ai pu ainsi montrer que la géométrie, les interactions stériques entre filaments, leurs propriétés mécaniques, et l'efficacité de la nucléation sont les paramètres clés contrôlant la formation de structures. Cette étude propose une base solide pour comprendre l'organisation cellulaire de l'actine en identifiant un système minimal de composants suffisant pour simuler l'émergence de différentes organisations d'actine (réseau branché, faisceaux de filaments parallèles ou antiparallèles). Avec cet outil, nous pouvons à présent prédire, étant donnée une géométrie de nucléation, quelles structures en émergeront.Nous avons alors combiné nos deux méthodes in-vitro et in-silico pour étudier comment le couplage entre l'architecture des réseaux et leur composition biochimique contrôle la réponse contractile. La connectivité entre les filaments en est un facteur crucial. En effet, un réseau peu connecté se déforme seulement localement, et n'instaure pas de comportement global. Une structure fortement connectée est très rigide, les moteurs moléculaires ne peuvent donc pas la déformer efficacement. La contraction d'une structure n'est donc possible que pour des valeurs de connectivité intermédiaires. L'amplitude de cette contraction est alors déterminée par l'organisation des filaments. Ainsi nous avons pu expliquer comment l'architecture mais aussi la connectivité des réseaux gouverne leur contractilité.Finalement, les microtubules sont aussi des acteurs essentiels aux processus cellulaires. Étant longs et rigides, ils servent de senseurs de la forme cellulaire et organisent les organites. Leur distribution spatiale, facteur majeur pour l'organisation cellulaire, est contrôlée dans un grand nombre de types cellulaires par la position du centrosome, un organite qui nuclée la plupart des microtubules. La capacité du centrosome à trouver le centre de la cellule dans de nombreuses conditions physiologiques est particulièrement étonante. Il peut aussi adopter une position décentrée lors de processus cellulaires spécifiques. Des mécanismes pouvant potentiellement expliquer le positionnement du centrosome ont été proposés (Manneville et al., 2006; Zhu et al, 2010), mais ce phénomène reste dans sa plus grande partie inexpliqué. J'ai utilisé les simulations pour explorer différents mécanismes pouvant le contrôler selon différentes conditions. Ces résultats permettent de disposer d'une base théorique pour présumer des mécanismes intervenant dans un système donné. Ils peuvent aussi permettre de valider ou réfuter des hypothèses sur les phénomènes mis en jeu et aider à l'élaboration de nouveaux systèmes expérimentaux.Les simulations que j'ai développées aident ici à étudier des comportements spécifiques, en apportant de nouveaux éclairages sur les comportements collectifs du cytosquelette. Elles pourraient être utilisées comme un outil prédictif ou adaptées pour l'étude d'autres systèmes expérimentaux
The cytoskeleton plays a crucial role in cellular processes, including cell division, adhesion, migration and morphogenesis. One of its main compenent, the actin filaments, a polarised semi-flexible polymer, contributes to these processes by forming specific collective architectures, whose structural organisations are essential to perform their functions. A major challenge in cell biology is to understand how the cell can form such a variety of organisations by using the same basic entity, the actin monomers. Recently we discovered that limiting actin nucleation to specific regions was sufficient to obtain actin networks with different organization (Reymann et al., 2010). However, our understanding of the general parameters involved in geometrically-driven actin assembly was limited. To understand mechanistically how spatially constraining actin nucleation determines the emergent actin organization, I performed detailed simulations of the actin filament system using Cytosim, a simulation tool dedicated to cytoskeleton system. I found that geometry, actin filaments local interactions, bundle rigidity, and nucleation efficiency are the key parameters controlling the emergent actin architecture. This study sets the foundation for our understanding of actin cellular organization by identifying a reduced set of components that were sufficient to realistically reproduce in silico the emergence of the different types of actin organization (branched actin network, parallel or anti parallel actin bundles). We can now predict for any given nucleation geometry which structures will form.Being able to control the formation of specific structures in-vitro and in-silico, we used the combination of both methods to study how the interplay between actin network architecture and its biochemical composition affects its contractile response. We highlighted the importance of the connectivity between filaments in the structures. Indeed, a loosely connected network cannot have a global behavior, but undergoes only local deformations. A highly connected network will be too rigid to be efficiently deformed by molecular motors. Only for an intermediate range of network connectivity the structures will contract, with an amplitude that depends notably on actin filaments organisation. This work explains how architecture and connectivity govern actin network contractility.Finally, the microtubules are also essential actors of cellular processes. Being long and rigid, they serve as sensors of the cellular shape and can organize the position of organelles in the cytoplasm. Their spatial distribution in the cell is thus a crucial cellular feature. this distribution is determined in a vast number of cell types by the position of the centrosome, an organelle that nucleates the majority of microtubules. Quite strinkingly, the centrosome is able to find the center of the cell in a lot of different physiological conditions, but can nonetheless adopt a decentered position in specific cellular processes. How this positioning is controled is not yet fully understood, but a few potential mechanims have been proposed (Manneville et al., 2006; Zhu et al., 2010). I used the simulations to explore different mechanisms taht can explain the position of the centrosome under different conditions. These results offer theorical considerations as a basis to assess which mechanism might prevail in a specific experimental system and may help to design new experimental setups.The simulations that I developed helped to study some specific behavior, by giving new insights into cytoskeleton collective organisations. These simulations can be further used as predictive tool or adapted to other experimental systems
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Feldhaus, Beatrix. "Periventrikuläre Leukomalazie Untersuchung Cytokin-induzierter Schädigungen von Oligodendrocyten-Vorläuferzellen und Protektion durch Corticoide /." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968797806.

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Lödige, Inga. "Untersuchungen zur Rolle des Kernexportes des Transkriptionsfaktors STAT1 in der Cytokin-abhängigen Geninduktion." [S.l.] : [s.n.], 2006. http://www.diss.fu-berlin.de/2006/527/index.html.

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Schießer, Stefan. "Synthese neuer Cisplatin-N-Lost-Konjugate und epigenetisch relevanter C5-modifizierter Cytosin Derivate." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-167750.

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Books on the topic "Cytomix"

1

Taylor, Patricia May. Cytoxic T-cells in influenza. Uxbridge: Brunel University, 1985.

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Sanderson, Brandon. Cytonic. Delacorte Press, 2021.

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Sanderson, Brandon, and Suzy Jackson. Cytonic. Audible Studios on Brilliance Audio, 2022.

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Sanderson, Brandon. Cytonic. Random House Publishing Group, 2021.

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Sanderson, Brandon. Cytonic. Random House Children's Books, 2021.

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Bamidele, Ganiyu. Cytorux. Independently Published, 2019.

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Sanderson, Brandon. Cytonic. Random House Children's Books, 2021.

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Sanderson, Brandon. Citónica / Cytonic. Ediciones B, 2022.

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Sanderson, Brandon. Cytonic: The Third Skyward Novel. Orion Publishing Group, Limited, 2022.

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Sanderson, Brandon. Cytonic: The Third Skyward Novel. Orion Publishing Group, Limited, 2021.

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Book chapters on the topic "Cytomix"

1

Arnemann, J. "5-Methyl-Cytosin." In Springer Reference Medizin, 1635. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3522.

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Arnemann, J. "5-Methyl-Cytosin." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_3522-1.

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Thomas, Philip, and Michael Fenech. "Buccal Micronucleus Cytome Assay." In Methods in Molecular Biology, 235–48. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-409-8_17.

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Krauseneck, P., D. Dommasch, P. Dienst, U. Bogdahn, L. Kappos, D. Seybold, and H. G. Mertens. "Intrathekale Verträglichkeit von Cytosin-Arabinosid." In Kardiovaskuläre Erkrankungen und Nervensystem Neurotoxikologie Probleme des Hirntodes, 500–504. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-46521-5_108.

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Arendt, Thomas, Birgit Belter, Martina K. Brückner, Uwe Ueberham, Markus Morawski, and Attila Tarnok. "A Cytomic Approach Towards Genomic Individuality of Neurons." In Neuromethods, 81–106. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7280-7_5.

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Gerstner, A. O. H., and G. Valet. "Cytomics and Predictive Medicine for Oncology." In An Omics Perspective on Cancer Research, 183–99. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2675-0_10.

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O’Connor, José-Enrique, Guadalupe Herrera, Francisco Sala-de-Oyanguren, Beatriz Jávega, and Alicia Martínez-Romero. "Cytomics of Oxidative Stress: Probes and Problems." In Single Cell Analysis, 83–118. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4499-1_4.

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Thomas, Philip, and Michael Fenech. "Erratum to: Buccal Micronucleus Cytome Assay." In Methods in Molecular Biology, E1. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-409-8_22.

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Thomas, Philip, and Michael Fenech. "Cytokinesis-Block Micronucleus Cytome Assay in Lymphocytes." In Methods in Molecular Biology, 217–34. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60327-409-8_16.

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DeBernardi, Maria A., Stephen M. Hewitt, and Andres Kriete. "Automated Confocal Imaging and High-Content Screening for Cytomics." In Handbook Of Biological Confocal Microscopy, 809–17. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-45524-2_46.

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Conference papers on the topic "Cytomix"

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Tárnok, Attila, Anja Mittag, and Dominik Lenz. "Clinical cytomics." In Biomedical Optics 2006, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2006. http://dx.doi.org/10.1117/12.645024.

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Tarnok, Attila, and Guenther K. Valet. "Cytomics in predictive medicine." In Biomedical Optics 2004, edited by Gerald E. Cohn, Warren S. Grundfest, David A. Benaron, and Tuan Vo-Dinh. SPIE, 2004. http://dx.doi.org/10.1117/12.528200.

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Tárnok, Attila, and Arkadiusz Pierzchalski. "Cytomics in regenerative medicine." In Biomedical Optics (BiOS) 2008, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2008. http://dx.doi.org/10.1117/12.761495.

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Dy, E., and C. M. Ho. "Development of a Cytomic Force Transducer for Experimental Mechanobiology." In 2009 IEEE 22nd International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2009. http://dx.doi.org/10.1109/memsys.2009.4805401.

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Guzzi, Pietro H., and Mario Cannataro. "CytoMCL: A Cytoscape plugin for fast clustering of protein interaction networks." In 2012 25th IEEE International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2012. http://dx.doi.org/10.1109/cbms.2012.6266325.

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Pirogov, Aleksey, Anna Prikhodko, Evgeniya Afanas'eva, and Yuliy Perelman. "COMPARATIVE ASSESSMENT OF AIRWAY CELLULAR INFLAMMATION IN PATIENTS WITH BRONCHIAL ASTHMA IN RESPONSE TO HYPOSMOLAR AND COLD STIMULES." 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_5fe01d9c45b256.10926397.

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An approach is presented to the study of cellular inflammation using cytological analysis of sputum in patients with bronchial asthma with different types of airway reaction to bronchoprovocation with cold air and distilled water. When the airways are hyperresponsive to hypoosmolar and cold stimuli, it has been established the activation of the neutrophilic component of bronchial granulocytes. Cold airway hyperresponsiveness is associated with an increase in neutrophil content and a concomitant decrease in the number of macrophages in the inflammatory pattern of the bronchi. An increase in sputum cytosis is inherent in a positive airway response to a hypoosmolar test with an unexpressed dynamics of the level of bronchial eosinophils.
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Bocsi, József, Dominik Lenz, Anja Mittag, Ursula Sauer, Lena Wild, John Hess, Dietmar Schranz, Jörg Hambsch, Peter Schneider, and Attila Tárnok. "Immunological changes following protein losing enteropathy after surgery total cavopulmonary connection (TCPC) by cytomics." In Biomedical Optics (BiOS) 2008, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2008. http://dx.doi.org/10.1117/12.761640.

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López Silva, Brenda A., and Luc Renambot. "CytoViz: an artistic mapping of network measurements as living organisms in a VR application." In Electronic Imaging 2007, edited by Andrew J. Woods, Neil A. Dodgson, John O. Merritt, Mark T. Bolas, and Ian E. McDowall. SPIE, 2007. http://dx.doi.org/10.1117/12.711637.

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Bocsi, Jozsef, Anja Mittag, Arkadiusz Pierzchalski, Pavel Osmancik, Ingo Dähnert, and Attila Tárnok. "Classification and discrimination of pediatric patients undergoing open heart surgery with and without methylprednisolone treatment by cytomics." In SPIE BiOS, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2011. http://dx.doi.org/10.1117/12.876487.

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Bugaev, P. D., and V. N. Melnikov. "Micro fertilizers and growth regulators - as factors of increasing barley yield." In Agrobiotechnology-2021. Publishing house RGAU-MSHA, 2021. http://dx.doi.org/10.26897/978-5-9675-1855-3-2021-82.

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The effectiveness of the use of a tank mixture of siliplant micronutrient with insecticidal mordant Cruiser CS and siliplant micronutrient with growth regulators, micro- and organomineral fertilizers has been revealed. It was found that when seeds were treated with a tank mixture with an insecticidal protectant Kruiser,KS (0.5 l/t) with micro–fertilization Siliplant (60 ml/t), the germination energy of barley seeds increased by 2.2%, laboratory germination – by 4.0% and growth strength – by 4.0% compared with the protectant Kruiser, KS, and when plants were treated in phase 3 with a siliplant with epin extra, the greatest increase in the yield of barley grain of the variety was obtained Mikhailovsky - 0.35-0.41 t/ha. The use of siliplant with cytovit micro-fertilization, where the yield increase was 0.31-0.37 t/ha, siliplant with zircon - yield increase -0.33-0.36 t/ha and siliplant with organomineral fertilizer ecofus, where the yield increase was 0.24-0.34 t/ha, proved to be effective.
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Reports on the topic "Cytomix"

1

Tel-Zur, Neomi, and Jeffrey J. Doyle. Role of Polyploidy in Vine Cacti Speciation and Crop Domestication. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697110.bard.

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1. Abstract: Over the past 25 years, vine cacti of the genera Hylocereus and Selenicereus have been introduced into Israel and southern California as new exotic fruit crops. The importance of these crops lies in their high water use efficiency and horticultural potential as exotic fruit crops. Our collaboration focused on the cytological, molecular and evolutionary aspects of vine cacti polyploidization to confront the agricultural challenge of genetic improvement, ultimately to improve success of vine cacti as commercial fruit crop plants. More specifically, we worked on the: 1- Identification of the putative ancestor(s) of the tetraploid H. megalanthus; 2- Determination of the number of origins of H. megalanthus (single vs. multiple origins of polyploidy); 3- Cytogenetic analysis of BC1 and F1 hybrids; 4- Determination of important agricultural traits and the selection of superior hybrids for cultivation. The plant material used in this study comprised interspecific Hylocereus F1 and first backcross (BC1) hybrids, nine Hylocereus species (58 genotypes), nine Selenicereus species (14 genotypes), and four Epiphyllum genotypes. Two BC1 hexaploids (BC-023 and BC-031) were obtained, a high ploidy level that can be explained only by a fertilization event between one unreduced female gamete from the triploid hybrid and a balanced gamete from the pollen donor, the diploid H. monacanthus. These findings are scientific evidence that support the possibility that “hybridization followed by chromosome doubling” could also occur in nature. Cytomixis, the migration of chromatin between adjacent cells through connecting cytoplasmatic channels, was observed in vine cacti hybrids and may thus imply selective DNA elimination in response to the allopolyploidization process. Evidence from plastid and nrDNA internal transcribed spacers (ITS) sequences support the placement of H. megalanthus within a monophyletic Hylocereus group. Furthermore, both plastid and ITS datasets are most consistent with a conclusion that this tetraploid species is an autopolyploid, despite observations that the species appears to be morphologically intermediate between Hylocereus and Selenicereus. Although the possibility of very narrow allopolyploidly (i.e., derivation from parents that are barely diverged from each other such as closely related species in the same genus) cannot be ruled out entirely based on our data (in part due to the unavailability of Hylocereus species considered to be morphologically the closest relatives of H. megalanthus), the possibility of H. megalanthus representing an intergeneric cross (i.e., Hylocereus × Selenicereus) seems extremely unlikely. Interestingly, the process of homogenization of ITS sequences (concerted evolution) is either incomplete or lacking in both Hylocereus and Selenicereus, and the inclusion of several artificial hybrids in the molecular study revealed the potential for biparental plastid inheritance in Hylocereus. The most important agricultural implication of this research project was the information collected for F1 and BC1 hybrids. Specifically, this project concluded with the selection of four superior hybrids in terms of fruit quality and potential yields under extreme high temperatures. These selected hybrids are self-compatible, avoiding the need for hand cross pollination to set fruits, thus reducing manpower costs. We recently offered these hybrids to growers in Israel for prioritized rapid evaluation and characterization.
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