Relevant bibliographies by topics / CELLULAR AND SYSTEMIC RESPONSES

Academic literature on the topic 'CELLULAR AND SYSTEMIC RESPONSES'

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Published: 11 September 2023

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Journal articles on the topic "CELLULAR AND SYSTEMIC RESPONSES"

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Galluzzi, Lorenzo, Takahiro Yamazaki, and Guido Kroemer. "Linking cellular stress responses to systemic homeostasis." Nature Reviews Molecular Cell Biology 19, no. 11 (October 10, 2018): 731–45. http://dx.doi.org/10.1038/s41580-018-0068-0.

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da Silva, Paulo F. L., and Björn Schumacher. "DNA damage responses in ageing." Open Biology 9, no. 11 (November 2019): 190168. http://dx.doi.org/10.1098/rsob.190168.

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Ageing appears to be a nearly universal feature of life, ranging from unicellular microorganisms to humans. Longevity depends on the maintenance of cellular functionality, and an organism's ability to respond to stress has been linked to functional maintenance and longevity. Stress response pathways might indeed become therapeutic targets of therapies aimed at extending the healthy lifespan. Various progeroid syndromes have been linked to genome instability, indicating an important causal role of DNA damage accumulation in the ageing process and the development of age-related pathologies. Recently, non-cell-autonomous mechanisms including the systemic consequences of cellular senescence have been implicated in regulating organismal ageing. We discuss here the role of cellular and systemic mechanisms of ageing and their role in ageing-associated diseases.
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Ermolaeva, Maria A., Alexander Dakhovnik, and Björn Schumacher. "Quality control mechanisms in cellular and systemic DNA damage responses." Ageing Research Reviews 23 (September 2015): 3–11. http://dx.doi.org/10.1016/j.arr.2014.12.009.

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Qiu, Jin, Lin Yan, Jianbo Chen, Crystal Y. Chen, Ling Shen, Norman L. Letvin, Barton F. Haynes, et al. "Intranasal Vaccination with the Recombinant Listeria monocytogenes ΔactA prfA*Mutant Elicits Robust Systemic and Pulmonary Cellular Responses and Secretory Mucosal IgA." Clinical and Vaccine Immunology 18, no. 4 (January 26, 2011): 640–46. http://dx.doi.org/10.1128/cvi.00254-10.

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ABSTRACTWe previously showed that recombinant (r)Listeria monocytogenescarrying ΔactAand a selectedprfA*mutation (r-ListeriaΔactA prfA*) secreted >100-fold more immunogen in broth culture than wild-type r-Listeriaor r-ListeriaΔactAand elicited much greater cellular and humoral immune responses than r-ListeriaΔactAafter intravenous vaccination of mice. Here, we conducted comparative studies evaluating vaccine-elicited immune responses in systemic and mucosal sites after intranasal, intravenous, intraperitoneal, or subcutaneous immunization of mice with r-ListeriaΔactA prfA*vaccine candidates. Intranasal vaccination of mice with r-ListeriaΔactA prfA* vaccine candidates elicited a robust gamma interferon-positive (IFN-γ+) cellular response in systemic sites, although intravenous or intraperitoneal immunization was more efficient. Surprisingly, intranasal vaccination elicited an appreciable pulmonary IFN-γ+cellular response that was nonstatistically higher than the magnitude induced by the intravenous route but was significantly greater than that elicited by subcutaneous immunization. Furthermore, although intranasal r-ListeriaΔactA prfA*delivery induced poor systemic IgG responses, intranasal vaccination elicited appreciable secretory immunogen-specific IgA titers that were similar to or higher in mucosal fluid than those induced by subcutaneous and intravenous immunizations. Thus, intranasal vaccination with r-ListeriaΔactA prfA*appears to be a useful approach for eliciting robust systemic and pulmonary cellular responses and measurable secretory mucosal IgA titers.
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Donina, S. A., A. N. Naikhin, G. D. Petukhova, I. B. Barantseva, T. V. Chirkova, Е. P. Grigor’eva, А. R. Rekstin, and L. G. Rudenko. "SYSTEMIC ANTIBODY AND CELLULAR IMMUNE RESPONSES IN INFLUENZA INFECTION AND POSTSVACCINATION." Medical Immunology (Russia) 8, no. 1 (July 21, 2014): 31. http://dx.doi.org/10.15789/1563-0625-2006-1-31-36.

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Prabhakar, Nanduri R., Ganesh K. Kumar, Jayasri Nanduri, and Gregg L. Semenza. "ROS Signaling in Systemic and Cellular Responses to Chronic Intermittent Hypoxia." Antioxidants & Redox Signaling 9, no. 9 (September 2007): 1397–404. http://dx.doi.org/10.1089/ars.2007.1732.

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Littauer, Elizabeth Q., E. Stein Esser, Olivia Q. Antao, Dahnide T. Williams, Richard W. Compans, and Ioanna Skountzou. "Systemic dysregulation of cellular immune responses to H1N1 infection during pregnancy." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 208.20. http://dx.doi.org/10.4049/jimmunol.196.supp.208.20.

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Abstract The 2009 H1N1 flu pandemic demonstrated that pregnant women infected with influenza were at risk for severe respiratory distress and premature-rupture-of-membranes (PROM), leading to high incidence of hospitalization, preterm births and small for gestation age (SGA) neonates. We utilize a syngeneic BALB/c pregnant mouse model which recapitulates clinical phenotypes shown during influenza infection of pregnant women. Pregnant mice sublethally infected (0.5xLD50) with pandemic H1N1 A/California/07/09 showed higher viral titers and delayed viral clearance relative to non-pregnant mice, and increased incidence of stillbirths and SGA offspring. Lymphocytes isolated at days 7 and 14 from lungs and spleens of infected pregnant and non-pregnant female mice were analyzed for H1N1 A/Ca/07/09 specific IL-4 and IFN-γ responses. Pregnancy delayed influenza-specific cytokine secretion at the site of infection, indicating systemic dysregulation of anti-viral responses. Lymphocytes from draining mediastinal lymph nodes, spleens and lungs were used to quantify activation of B cells in germinal centers (GC), maturation into antibody secreting cells and memory B cells, and mucosal homing to lung tissue following infection. Pregnancy decreased maturation of GC+ B cells in the spleen and migration of plasma cells from the spleen to the lungs. Infected pregnant mice generated equivalent serum influenza-specific neutralizing antibody titers and increased IgA antibody secreting cells (ASC) in the lungs 6 weeks post-infection relative to infected non-pregnant mice, indicating a potential role in pregnancy favoring the development of mucosal immunity in response to prolonged viral exposure.
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Waickman, Adam T., Joseph Lu, Corey Chase, Hengsheng Fang, Erinn McDowell, Erin Bingham, Jeffrey Bogart, Stephen Graziano, Stephen J. Thomas, and Teresa Gentile. "Systemic Cancer Therapy Does Not Significantly Impact Early Vaccine-Elicited SARS-CoV-2 Immunity in Patients with Solid Tumors." Vaccines 10, no. 5 (May 9, 2022): 738. http://dx.doi.org/10.3390/vaccines10050738.

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mRNA vaccines have been shown to be safe and effective in individuals with cancer. It is unclear, however, if systemic anti-cancer therapy impacts the coordinated cellular and humoral immune responses elicited by SARS-CoV-2 mRNA vaccines. To fill this knowledge gap, we assessed SARS-CoV-2 mRNA vaccine-elicited immunity in a cohort of patients with advanced solid tumors either under observation or receiving systemic anti-cancer therapy. This analysis revealed that SARS-CoV-2 mRNA vaccine-elicited cellular and humoral immunity was not significantly different in individuals with cancer receiving systemic anti-cancer therapy relative to individuals under observation. Furthermore, even though some patients exhibited suboptimal antibody titers after vaccination, SARS-CoV-2 specific cellular immune responses were still detected. These data suggest that antibody titers offer an incomplete picture of vaccine-elicited SARS-CoV-2 immunity in cancer patients undergoing active systemic anti-cancer therapy, and that vaccine-elicited cellular immunity exists even in the absence of significant quantities of SARS-CoV-2 specific antibodies.
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Lillard, James W., Udai P. Singh, Prosper N. Boyaka, Shailesh Singh, Dennis D. Taub, and Jerry R. McGhee. "MIP-1α and MIP-1β differentially mediate mucosal and systemic adaptive immunity." Blood 101, no. 3 (February 1, 2003): 807–14. http://dx.doi.org/10.1182/blood-2002-07-2305.

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AbstractMacrophage inflammatory protein-1α (MIP-1α) and MIP-1β are distinct but highly homologous CC chemokines produced by a variety of host cells in response to various external stimuli and share affinity for CCR5. To better elucidate the role of these CC chemokines in adaptive immunity, we have characterized the affects of MIP-1α and MIP-1β on cellular and humoral immune responses. MIP-1α stimulated strong antigen (Ag)–specific serum immunoglobulin G (IgG) and IgM responses, while MIP-1β promoted lower IgG and IgM but higher serum IgA and IgE antibody (Ab) responses. MIP-1α elevated Ag-specific IgG1 and IgG2b followed by IgG2a and IgG3 subclass responses, while MIP-1β only stimulated IgG1 and IgG2b subclasses. Correspondingly, MIP-1β produced higher titers of Ag-specific mucosal secretory IgA Ab levels when compared with MIP-1α. Splenic T cells from MIP-1α– or MIP-1β–treated mice displayed higher Ag-specific Th1 (interferon-γ [IFN-γ]) as well as selective Th2 (interleukin-5 [IL-5] and IL-6) cytokine responses than did T cells from control groups. Interestingly, mucosally derived T cells from MIP-1β–treated mice displayed higher levels of IL-4 and IL-6 compared with MIP-1α–treated mice. However, MIP-1α effectively enhanced Ag-specific cell-mediated immune responses. In correlation with their selective effects on humoral and cellular immune responses, these chemokines also differentially attract CD4+ versus CD8+ T cells and modulate CD40, CD80, and CD86 expressed by B220+ cells as well as CD28, 4-1BB, and gp39 expression by CD4+ and CD8+ T cells in a dose-dependent fashion. Taken together, these studies suggest that these CC chemokines differentially enhance mucosal and serum humoral as well as cellular immune responses.
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Mineo, Tiago Wilson Patriarca, and Rosangela Zacarias Machado. "Neospora caninum modulates canine systemic cellular immune responses during acute oral infection." Veterinary Immunology and Immunopathology 128, no. 1-3 (March 2009): 300–301. http://dx.doi.org/10.1016/j.vetimm.2008.10.192.

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Dissertations / Theses on the topic "CELLULAR AND SYSTEMIC RESPONSES"

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Rasid, Orhan. "NK cells and systemic inflammation : compartmentalization and memory responses." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB078.

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L'inflammation systémique est une réaction qui implique l’ensemble de l’organisme suite une agression sévère, potentiellement mortelle, illustrée par le syndrome de réponse inflammatoire systémique (SIRS). De nombreux acteurs cellulaires et moléculaires contribuent au développement de cette cascade inflammatoire parmi lesquels les cellules NK jouent un rôle clé. Malgré l'accumulation de preuves sur l’existence de propriétés spécifiques à chaque organe en réponse à l'inflammation systémique, en termes de cellules NK, on sait peu de choses sur la dynamique compartimentalisée de l’activation des cellules NK pendant un SIRS. En outre, le statut immunitaire des cellules NK après la résolution d’un SIRS est également mal connu. Dans le présent travail, nous avons étudié les réponses des cellules NK provenant de différents organes en utilisant un modèle d’endotoxinémie murine. Nous avons caractérisé la réponse des cellules NK au sein de la rate, du poumon, de la moelle osseuse, de la cavité péritonéale, et dans la circulation. Nous avons trouvé que, malgré une dynamique similaire de la réponse dans les différents organes, les réponses des cellules NK sont compartimentalisées avec des seuils différent et spécifiques. A l’aide de transferts adoptifs, nous avons constaté que la réactivité des cellules NK spécifiques d'organes peut refléter le compartiment d’origine lors des phases initiales de l'inflammation. Cependant, les cellules NK ont la capacité de s’adapter rapidement à leur nouvel environnement et d'ajuster leurs niveaux de réponse à ceux des cellules NK résidentes. Ainsi, cette étude fournit une preuve de concept qui confirme la compartimentalisation de la réponse des cellules NK lors de l'inflammation systémique. Dans une deuxième partie, nous avons analysé le statut des cellules NK à différents moments après une endotoxinémie. Les réponses des cellules NK au sein d’une préparation de cellules de la rate sont fortement supprimées en réponse à une restimulation in vitro, 14 jours après l'endotoxinémie. Cependant, nous avons montré que la réactivité intrinsèque des cellules NK est en fait augmentée après l'injection d’endotoxine, aboutissant à des cellules NK présentant des caractéristiques de cellules NK mémoires. Des expériences de transfert adoptif ont confirmé les propriétés de mémoire des cellules NK après endotoxinémie. Nos résultats accroissent la connaissance concernant le rôle des cellules NK dans un contexte d'inflammation systémique, révélant des réponses compartimentalisés et l’induction d’une mémoire suite à l’endotoxinémie. L'observation selon laquelle les cellules NK développent des propriétés de mémoire après une inflammation systémique dans le contexte d'un environnement suppressif est d’une grande nouveauté et ce phénomène est rapporté pour la première fois
Systemic inflammation is whole-body reaction to a triggering insult that often results in life threatening illness like systemic inflammatory response syndrome (SIRS). Contributing to the development of this inflammatory cascade are numerous cellular and molecular players, among which, NK cells have been shown to play a key role. Despite accumulating evidence on the organ-specific properties of both systemic inflammation and NK cells, little is known about the compartmentalized dynamics of NK cell activation during SIRS. Furthermore, the status of NK cells after the resolution of SIRS is also poorly characterized. In the present work, we investigated NK responses in different organs using a mouse model of endotoxinemia and characterized the compartmentalized response of spleen, lung, bone marrow, peritoneal and circulating NK cells. We found that despite similar dynamics of response in different organs, NK cells responses, are compartmentalized with seemingly specific thresholds of maximum activation. Using a series of adoptive transfers, we found that while organ-specific NK cell responsiveness can affect the initial phases of inflammation, these cells have the capacity to quickly adapt to a new environment and adjust their response levels to that of resident NK cells. Thus, this study provides proof of concept data on the compartmentalization of the NK cell responses during systemic inflammation. In a second part, we assessed the status of NK cells at different times after endotoxemia. NK cells responses in the context of whole spleen preparations were severely suppressed in response to in vitro restimulation at 14 days after endotoxemia. However, intrinsic NK cell responsiveness was increased after endotoxemia, showing characteristics of NK cell memory. Adoptive transfer experiments confirmed memory properties of NK cells after endotoxemia. Overall, these results expand on the role of NK cells in the context of systemic inflammation revealing compartmentalized responses during and memory properties following endotoxemia. The observation that NK cells develop memory properties after systemic inflammation in the context of a suppressive environment is of the highest novelty and the first one to report such a phenomenon
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Finan-Marchi, Amanda Rose. "THE SYSTEMIC STEM CELL RESPONSE TO CARDIAC PRESSURE OVERLOAD." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1333897602.

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Daba, Alina. "Insights on systemic and cellular iron homeostasis: hepcidin responses to oral and parenteral iron loading and an alternative mechanism for ferritin mRNA translation." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107735.

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Iron is vital for all living organisms, but due to its ability to readily accept or donate electrons, it is also potentially toxic. Finely tuned mechanisms have evolved to control iron homeostasis at the systemic and cellular level. The peptide hormone hepcidin controls systemic iron homeostasis by binding to and degrading the iron exporter, ferroportin, leading to decreased iron efflux from duodenal enterocytes, macrophages and hepatocytes into the blood stream. Cellular iron homeostasis is regulated by the IRE / IRP system, which controls the levels of proteins involved in iron uptake, utilization, export and storage in a coordinated manner. Excess intracellular iron is stored and detoxified in ferritin. In this work, we study how an excess of iron is managed at the systemic and cellular level. In chapter II, we hypothesize that dietary and parenteral iron loading have differential effects on body iron status and hepcidin expression in mice. We perform time – course experiments and compare the effects of dietary and parenteral iron loading on circulating and tissue iron parameters. We show that dietary iron overload exceeds the capacity of hepcidin to lower body iron levels, and parenteral iron loading elicits a delayed hepcidin response. We provide evidence that circulating holo – transferrin and hepatocytic iron are the sole iron signals for hepcidin activation. In chapter III, we examine how an excess of iron is managed at the cellular level. We hypothesize that ferritin might benefit from an alternative, IRES - dependent mechanism of translation. We inhibit global or ferritin - specific cap – dependent translation initiation and challenge the cells with iron. We show that ferritin by – passes both the global and the specific inhibition of translation. We then test for the presence of an IRES in the 5'UTR of ferritin mRNA and further validate this sequence.
Le fer est vital pour tous les organismes vivants, cependant étant donné son habilité à donner ou accepter des électrons facilement, il a aussi le potentiel d'être toxique. Des mécanismes très précis ont évolué pour contrôler l'homéostasie du fer aux niveaux systémique et cellulaire. L'hormone peptidique, hepcidine, contrôle l'homéostasie du fer au niveau systémique par la dégradation de la ferroportine, l'exportateur cellulaire du fer. En conséquence, l'efflux du fer des entérocytes, des macrophages et des hépatocytes vers la circulation diminue. Au niveau cellulaire, le système IRE / IRP contrôle, d'une manière coordonnée, les niveaux des protéines impliquées dans l'acquisition, l'utilisation, l'exportation et le stockage du fer. L'excès de fer est stocké dans la ferritine. Dans ce travail, nous examinons comment l'excès de fer est géré aux niveaux systémique et cellulaire. Dans le chapitre II, nous émettons l'hypothèse que les surcharges orale et parentérale en fer ont des effets différents sur l'homéostasie systémique du fer et sur l'expression de l'hepcidine chez les souris. Nous comparons les effets des surcharges orale et parentérale en fer aux niveaux circulatoire et tissulaire. Nous démontrons que la surcharge orale en fer excède la capacité hypoferrémique de l'hepcidine alors que la surcharge parentérale en fer induit une réponse retardée de l'hepcidine. Nous apportons aussi la preuve que la holo – transferrine circulatoire et le fer hépatocytaire sont les signaux uniques de l'activation ferrique de l'hepcidine. Dans le chapitre III, nous examinons comment l'excès de fer est géré au niveau cellulaire. Nous émettons l'hypothèse que la ferritine bénéficie d'un mécanisme alternatif de traduction, dépendant d'une séquence IRES. Nous inhibons l'initiation de la traduction dépendante de la coiffe 5' globalement, ou spécifiquement pour la ferritine, et traitons les cellules avec une source de fer. Nous démontrons que la ferritine surpasse le blocage global ou spécifique de la traduction dépendante de la coiffe 5'. Nous testons la présence d'une séquence IRES dans l'extrémité 5' de l'ARNm et par la suite nous la validons.
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Hughes, Phillipa Jane. "Cellular responses to aluminium." Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262389.

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Zhao, Ming-Hui. "Characterisation of autoimmune responses in systemic vasculitis." Thesis, Anglia Ruskin University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259510.

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Calay, Ediz Suha. "Cellular and Systemic Metabolic Adaptations to Energy Status." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11547.

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Roberts, Tara Laurine. "Cellular responses to immunostimulatory DNA /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18175.pdf.

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Lidehäll, Anna Karin. "Cellular Immune Responses to Cytomegalovirus." Doctoral thesis, Uppsala University, Department of Oncology, Radiology and Clinical Immunology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8578.

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Cytomegalovirus (CMV) is a widespread infection affecting 50-90% of the human population. A typical silent primary infection is followed by life-long persistence in the host under control by virus-specific CD8 (“killer”) and CD4 (“helper”) T cells. Although harmless in most people, CMV may cause disease and sequelae in patients with deficient cellular immunity, such as AIDS patients, recipients of organ transplants and children who have acquired the virus before birth. In this thesis we have characterized the cellular immunity to CMV in immunocompetent subjects, in patients receiving transplants and in infants.

In healthy individuals with latent CMV, the frequencies of CMV-specific CD8 T cells varied considerably between the donors. Within the same individual, the changes over time were usually small. In patients with primary, symptomatic CMV infection, the frequencies of CMV-specific CD8 T cells peaked within the first month after the appearance of symptoms. The frequencies then declined to levels similar to those in latently infected CMV carriers. The CD4 T-cell function followed the same pattern, but with lower peak values.

Immunosuppressed renal transplant patients with latent CMV had CMV-specific CD4 cell function similar to healthy controls. The frequencies of CMV-specific CD8 T cells were also comparable, but their function was impaired. When renal transplant recipients were investigated longitudinally, we found that their CMV-specific T cells decreased rapidly after transplantation. Whereas the frequencies and function of CD8 T cells rebounded within 3 months, CD4 T-cell recovery was impaired during the entire first year after transplantation.

Finally, the frequencies and function of CMV-specific T-cells were investigated in children with congenital and postnatal CMV. CMV-specific CD8 T cells could be detected in even the youngest children, suggesting that these cells can develop early in life. In contrast, CMV specific CD4 T cells were low or absent in the youngest children but increased slowly with age.

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Lidehäll, Anna Karin. "Cellular immune responses to cytomegalovirus /." Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8578.

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Tomkins, C. E. "Cellular responses to genotoxic stress." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362104.

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Books on the topic "CELLULAR AND SYSTEMIC RESPONSES"

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King, William James. Autoimmune cellular responses towards neutrophil granule enzymes in systemic vasculitis. Birmingham: University of Birmingham, 1998.

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M, Berry, and Logan Ann, eds. CNS injuries: Cellular responses and pharmacological strategies. Boca Raton: CRC Press, 1999.

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Feige, U., I. Yahara, R. I. Morimoto, and B. S. Polla, eds. Stress-Inducible Cellular Responses. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-9088-5.

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Dr, Feige U., ed. Stress-inducible cellular responses. Basel: Birkhäuser Verlag, 1996.

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Peter, Downes C., Wolf C. Roland, and Lane David 1952-, eds. Cellular responses to stress. London: Portland, 1999.

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Peter, Downes C., Wolf C. Roland, and Lane David 1952-, eds. Cellular responses to stress. Princeton, N.J: Princeton University Press, 1999.

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Davies, Stuart Matthew. Cellular responses to potential biomaterials. Birmingham: Aston University. Department of Chemical Engineering and Applied Chemistry, 1991.

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Galli, Corrado L., Marina Marinovich, and Alan M. Goldberg, eds. Modulation of Cellular Responses in Toxicity. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79872-6.

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L, Galli C., Marinovich Marina, Goldberg Alan M, North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Study Institute on the Modulation of Cellular Responses in Toxicity (1994 : Ponte di Legno, Italy), eds. Modulation of cellular responses in toxicity. Berlin: Springer, 1995.

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Vitor, Cohen Ricardo, ed. Metabolic and systemic responses following interventional laparoscopy. Austin: R.G. Landes, 1994.

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Book chapters on the topic "CELLULAR AND SYSTEMIC RESPONSES"

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Peng, Yingjie, Guoxiang Yuan, Jeffrey L. Overholt, Ganesh K. Kumar, and Nanduri R. Prabhakar. "Systemic and Cellular Responses to Intermittent Hypoxia: Evidence for Oxidative Stress and Mitochondrial Dysfunction." In Advances in Experimental Medicine and Biology, 559–64. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9280-2_71.

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Rasmussen, Howard, Carlos Isales, Shridar Ganesan, Roberto Calle, and Walter Zawalich. "Ca2+-Cyclic AMP Interactions in Sustained Cellular Responses." In Ciba Foundation Symposium 164 - Interactions Among Cell Signalling Systems, 98–112. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514207.ch7.

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Martínez-A., C., A. de la Hera, M. A. R. Marcos, C. Márquez, M. Alvarez de Mon, and M. L. Toribio. "General Principles of Complex Biological Systems Operating in Immunology. Self-Responses Might Define the Boundaries of the Developing Immune System." In The Semiotics of Cellular Communication in the Immune System, 183–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73145-7_17.

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Rieu, Alain-Marc. "Systemic disruption, systemic responses." In Managing Knowledge, Governing Society, 51–66. London: Routledge, 2021. http://dx.doi.org/10.4324/9781003187004-3.

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Rink, H., T. C. Yang, L. Böhm, R. Govorun, D. Häder, G. Horneck, B. Kaina, et al. "Cellular Responses." In Fundamentals for the Assessment of Risks from Environmental Radiation, 339–44. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4585-5_43.

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Land, Walter Gottlieb. "Cellular Inflammatory Responses." In Damage-Associated Molecular Patterns in Human Diseases, 475–590. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78655-1_22.

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Fischer, Uwe, and Fumio Takizawa. "Cellular Immune Responses." In Principles of Fish Immunology, 141–76. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-85420-1_4.

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Capperauld, Ian. "Cellular Responses to Sutures." In Interaction of Cells with Natural and Foreign Surfaces, 243–57. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2229-0_25.

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Mirkes, P. E. "Cellular Responses to Stress." In Drug Toxicity in Embryonic Development I, 245–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60445-4_9.

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Sietsema, Kathy E. "Exercise Responses in Systemic Conditions." In Clinical Exercise Testing, 264–72. Basel: KARGER, 2002. http://dx.doi.org/10.1159/000062226.

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Conference papers on the topic "CELLULAR AND SYSTEMIC RESPONSES"

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Cruz, Tamara, Alejandra López-Giraldo, Guillaume Noell, Laureano Molins, Manel Juan, Marco Antonio Fernandez, Maria Rosa Faner Canet, and Alvar Agusti. "Pulmonary and systemic cellular immune response network in patients with mild-moderate COPD." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1020.

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Steward, Robert L., Chao-Min Cheng, and Philip R. LeDuc. "Probing Nonlinear Cellular Responses to Integrated Mechanical Signals Through Examining Cell Alignment." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19205.

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Cells are complex systems that continuously receive signals in a variety of forms including both physical and chemical. The ability of cells to integrate these signals and already be hard wired to have coupled responses indicates the complexity at which cells function in terms of signal integration. One of the important areas in signal response is in mechanical stimulation, which has been shown to influence many cellular functions through the cytoskeleton and most often induces various cellular alignment. Most studies generally probe the affects of mechanical stimulation on cell behaviour by one mode of mechanical stimulation, though cells in fact experience multiple modes of mechanical stimulation simultaneously. From this comes the question of how does the cell process these multiple mechanical inputs? In this study we probed the effects of uniaxial stretch and/or shear fluid flow on NIH 3T3 fibroblast behaviour, specifically cell alignment. We used fluorescence microscopy to examine the orientation of the actin cytoskeleton and observed alignment along the direction of force for both uniaxial stretching and shear fluid flow in comparison to cells exposed to both mechanical modes. The cellular response surprisingly revealed an alignment that was neither parallel nor perpendicular to the direction of force. Furthermore, the integration of these 2 modes revealed a nonlinear response to combinations of shear stress and uniaxial stretching. These intriguing results have potential implications in a variety of fields including bioengineering, mechanotransduction, and cell structure.
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Mann, Jennifer, Raymond Lam, and Jianping Fu. "Cellular Response to Stretch by Modulation of Cytoskeletal Tension in Two Distinct Phases." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-54016.

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External forces are increasingly recognized as major regulators of cell structure and function, yet the underlying mechanism by which cells sense force and transduce it into intracellular biochemical signals and behavioral responses (‘mechanotransduction’) is largely undetermined. To aid in the mechanistic study of mechanotransduction, we devised a novel cell stretching device that allows for quantitative control and real-time measurement of mechanical stimuli and cellular biomechanical responses. Using this device, we studied the subcellular dynamic responses of contractile force and adhesion remodeling of vascular smooth muscle cells (VSMCs) to stretch. Our data showed that VSMCs could acutely enhance their contraction to resist rapid cell deformation, but they could also allow slow adaptive inelastic cytoskeletal reorganization in response to sustained cell stretch. Our study may help elucidate the mechanotransduction system in smooth muscle cells, and thus contribute to our understanding of pressure-induced vascular disease processes.
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Li, Lei, Xuetao Shi, Xiaoqing Lv, and Jing Liu. "A Biomimetic Microfluidic Device for the Study of the Response of Endothelial Cells Under Mechanical Forces." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-36430.

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Vascular science is an active area of medicine and biological research. In recent years, intensive research has been focused on the reaction of endothelial cells (ECs) to relevant biological, chemical, or physical cues in vitro. The primary thing of these studies is to make a biomimic environment of ECs which is closer to the in vivo conditions. Here we developed a microfluidic system and fabricated a grooved micropattern thin film to simulate inner blood vessel wall. The micropattern structure was generated by using the elastic biocompatible material poly(dimethylsiloxane) (PDMS). Human umbilical vein endothelial cells (HUVECs) were cultured on the grooved micropattern film. After the cells reached confluence, the thin PDMS film with cells was inserted into the biological grade plastic tube. Then cell culture medium was perfused into the tube and the cellular responses under shear stress and pressure were investigated. The F-actin cytoskeleton and the nuclei of the cells were stained for examination. This microfluidic system provides a convenient and cost-effective platform for the studies of cellular response to mechanical forces. Moreover, this system could also be used for studying cellular responses to drugs under mechanical forces.
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Khatri, Nava Raj, and Paul F. Egan. "Tailored Energy Absorption for 3D Printed Multi-Material Cellular Structures Using ABS and TPU." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-73699.

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Abstract Advances in multi-material 3D printing technologies are enabling the construction of advantageous engineering structures for diverse applications. Multi-material printing allows the combination of contrasting engineering materials in a single part to gain synergistic performance increases. Cellular structure such as honeycomb structures provide high-energy absorption to weights ratio that could benefit through multi-material strategies for tailored responses in applications such as design of helmets and prosthetics. In this study, we investigate the compressive response and the energy absorption for combinations of acrylonitrile butadiene styrene (ABS) and thermoplastic polyurethane (TPU) printed lattices. Results demonstrate energy absorption increases from pure TPU samples of 2.18kN.mm in a non-linear fashion to pure ABS samples of 11.47kN.mm as bands of TPU are added to ABS. Splitting a single band of TPU into multiple bands with the same total thickness changes the behavior of first and second peak before densification. Testing with in-plane loading demonstrated more similar behavior among the differently designed multi-material lattices, with collapsing occurring with sequential failures of unit cell rows. These results demonstrate the feasibility in constructing multi-material lattice systems with ABS and TPU combinations, while highlighting their benefits for enabling controlled energy absorption and deformation responses based on designed material combinations.
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Wang, James H. C., David Stone, Fengyan Jia, Chris Celechovsky, and Savio L. Y. Woo. "Biological Responses of Fibroblasts to Cyclic Stretching: A Novel Culture Model Study." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2573.

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Abstract Because of the advantage of better control of experimental conditions, in vitro model systems have been developed to examine the effects of mechanical loading on cells. Previous studies have shown that cyclic stretching causes cells to change orientation, proliferation and gene expression (Buck et al., 1980; Wang et al., 1995; Leung et al., 1976). However, one drawback of these model systems is that they are unable to control cell alignment and shape, and in addition, some provide heterogeneous strains to cells during stretching (See review by Schaffer, 1994). Consequently, cellular responses in these systems may not be similar to those in vivo. For example, tendon and ligament fibroblasts align with collagen fibers in vivo and are hence subjected to stretching along the tissue long axis. In contrast, in many existing systems, cells either randomly orient or orient away from the stretching direction.
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Yao, Jia, Svetlana Atasheva, Cedrick B. Young, and Dmitry M. Shayakhmetov. "Abstract 959: Cellular dynamics of productive anti-tumor response mediating long-term rejection of disseminated lung tumors after systemic therapy with oncolytic adenovirus." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-959.

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Hedjazi, Lotfi, Christophe L. Martin, Sofiane Guessasma, Guy Della Valle, and Rémy Dendievel. "Application of Discrete Element Simulation to the Crushing of a Food Biopolymer Foam for Mastication Modelling." In ASME 2012 11th Biennial Conference on Engineering Systems Design and Analysis. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/esda2012-82953.

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The fragmentation behaviour of brittle airy cereal foods is studied both numerically and experimentally. The food item is subjected to severe compression until densification stage. Experimental evidence of typical cellular material behaviour is pointed out by elasticity, cell collapse and densification regimes. Using an accurate description of the cellular structure determined by X-ray tomography, a numerical approach based on discrete element method is proposed in order to better explain the resulting fragmentation. The approach allows to reproduce the deformation stages and predicted results show good agreement with experimental mechanical responses, in terms of maximum force. Moreover, large size fragments are found to form as a consequence of small rupture events.
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Chiang, Martin Y. M., and Joy Dunkers. "An Analytical Solution for Flexible Substrates Undergoing Small Equibiaxial Strains." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206285.

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Cells can distinguish between different types of mechanical signals, such as stretch (tension), pressure (compression), and shear, to guide mechanosensitive cellular activities. Cell culture systems with controlled delivery of a mechanical input such as substrate strain, hydrostatic pressure, or fluid shear stress are used for the in vitro application of these forces. The work reported here uses a system that imparts equibiaxial loading on a flexible substrate to study cell response to stretch, similar to the Bioflex in the Flexcell [1] family of products. The objective of this study is to introduce an analytical (closed-form) solution of the relationship between the substrate strain and pressure under small strains, less than 2%. The solution is derived from the superposition of two elastic responses induced in the equibiaxial strain culture system after applying pressure.
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Zhou, Yilu, Lauren Resutek, Liyun Wang, and X. Lucas Lu. "Effects of Bisphosphonate on Long-Term Culture of Cartilage Allografts." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14635.

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Zoledronic acid (ZA), an FDA approved bisphosphonate (BP) medicine, is widely used for the treatment of osteoclast-related bone loss diseases [1]. Our previous study has found that systemic administration of ZA could dramatically suppress the development of post-traumatic osteoarthritis (PTOA) in the DMM (destabilization of the medial meniscus) mouse model, a model recapitulating the altered joint loading associated with PTOA [2]. This finding is consistent with a few similar studies using different animal models [3]. However, little is known about the cellular and biochemical mechanisms of BP mediated chondro-protection in PTOA pathogenesis. Studies have shown that PTOA often initiates from the apoptosis and altered metabolism of cartilage chondrocytes. In this study, we will investigate the direct effects of ZA on the metabolisms of chondrocytes using long-term in vitro culture of cartilage allografts. As one of the earliest responses of chondrocytes to mechanical stimulation, intracellular calcium ([Ca 2+] i) signaling is the upstream of numerous mechanotransduction pathways [4]. We hypothesize that the chondro-protective mechanisms of ZA could be represented by the characteristics of [Ca 2+] i signaling of in situ chondrocytes. Our specific aims were to: (i) compare the in situ spontaneous [Ca 2+] i responses of chondrocytes cultured in non-ZA and ZA supplemented environments, and (ii) compare the biomechanical properties of cartilage allografts under the two culture conditions.
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Reports on the topic "CELLULAR AND SYSTEMIC RESPONSES"

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Avni, Adi, and Kirankumar S. Mysore. Functional Genomics Approach to Identify Signaling Components Involved in Defense Responses Induced by the Ethylene Inducing Xyalanase Elicitor. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7697100.bard.

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Plant-microbe interactions involve a large number of global regulatory systems, which are essential for plants to protect themselves against pathogen attack. An ethylene-inducing xylanase (EIX) of Trichoderma viride is a potent elicitor of plant defense responses, like hypersensitive response (HR), in specific cultivars of tobacco (Nicotiana tabacum) and tomato (Lycopersicon esculentum). The central goal of this proposal was to investigate the molecular mechanisms that allow plants to specifically activate defense responses after EIX treatment. We proposed to identify cellular signaling components involved in the induction of HR by the EIX elicitor. The molecular genetic analysis of the signal transduction pathway that modulates hypersensitive responses is an important step in understanding the induction of plant defense responses. The genes that mediate LeEIX2-EIX dependent activation of resistance mechanisms remain to be identified. We used two approaches to identify the cellular signaling components that induce HR mediated by the EIX elicitor. In the first approach, we performed a yeast two-hybrid screening using LeEix2 as bait to identify plant proteins that interact with it. In the second approach, we used virus-induced gene silencing (VIGS) for a high-throughput screen to identify genes that are required for the induction of LeEIX2-EIX mediated HR. VIGS will also be used for functional characterization of genes that will be identified during the yeast two-hybrid screen. This investigation will shed light on cellular processes and signaling components involved in induction of general plant defense against pathogens and will provide the basis for future biotechnological approaches to improve plant resistance to pathogens. Several genes were indentified by the two approaches. We used the VIGS and yeast two hybrid approaches to confirm that activity of the genes initially identified by different procedure. Two genes inhibit the induction of HR by the fungal elicitor in the different systems; Tobacco-Harpin binding protein 1 and cyclopropyl isomerase.
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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.
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Weigelt, Jes, and Anna Kramer. Systemic Challenges, Systemic Responses: Innovating adaptation to climate change through agroecology. TMG Research gGmbH, October 2020. http://dx.doi.org/10.35435/2.2020.2.

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Williams, Bryan R. G. Rapid Detection of Cellular Responses to Biological Agents. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada410758.

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Williams, Bryan R. Rapid Detection of Cellular Responses to Biological Agents. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada421869.

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Weber, Thomas J., Nancy H. Colburn, and Michael K. Bowman. Linking Molecular Events to Cellular Responses at Low Dose Exposures. Office of Scientific and Technical Information (OSTI), June 2000. http://dx.doi.org/10.2172/833477.

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Kadhim, Munira A. Mechanisms underlying cellular responses of cells from haemopoietic tissue to low. Office of Scientific and Technical Information (OSTI), August 2012. http://dx.doi.org/10.2172/1048876.

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Hansen, Peter J., and Amir Arav. Embryo transfer as a tool for improving fertility of heat-stressed dairy cattle. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7587730.bard.

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The overall objective of the current proposal is to develop procedures to improve the pregnancy rate achieved following transfer of fresh or cryopreserved embryos produced in the laboratory into heat-stress recipients. The overall hypothesis is that pregnancy rate in heat-stressed lactating cows can be improved by use of embryo transfer and that additional gains in pregnancy rate can be achieved through development of procedures to cryopreserve embryos, select embryos most likely to establish and maintain pregnancy after transfer, and to enhance embryo competence for post-transfer survival through manipulation of culture conditions. The original specific objectives were to 1) optimize procedures for cryopreservation (Israel/US), 2) develop procedures for identifying embryos with the greatest potential for development and survival using the remote monitoring system called EmbryoGuard (Israel), 3) perform field trials to test the efficacy of cryopreservation and the EmbryoGuard selection system for improving pregnancy rates in heat-stressed, lactating cows (US/Israel), 4) test whether selection of fresh or frozen-thawed blastocysts based on measurement of group II caspase activity is an effective means of increasing survival after cryopreservation and post-transfer pregnancy rate (US), and 5) identify genes in blastocysts induced by insulin-like growth factor-1 (IGF-1) (US). In addition to these objectives, additional work was carried out to determine additional cellular determinants of embryonic resistance to heat shock. There were several major achievements. Results of one experiment indicated that survival of embryos to freezing could be improved by treating embryos with cytochalasin B to disrupt the cytoskeleton. An additional improvement in the efficacy of embryo transfer for achieving pregnancy in heat-stressed cows follows from the finding that IGF-1 can improve post-transfer survival of in vitro produced embryos in the summer but not winter. Expression of several genes in the blastocyst was regulated by IGF-1 including IGF binding protein-3, desmocollin II, Na/K ATPase, Bax, heat shock protein 70 and IGF-1 receptor. These genes are likely candidates 1) for developing assays for selection of embryos for transfer and 2) as marker genes for improving culture conditions for embryo production. The fact that IGF-1 improved survival of embryos in heat-stressed recipients only is consistent with the hypothesis that IGF-1 confers cellular thermotolerance to bovine embryos. Other experiments confirmed this action of IGF-1. One action of IGF-1, the ability to block heat-shock induced apoptosis, was shown to be mediated through activation of the phosphatidylinositol 3-kinase pathway. Other cellular determinants of resistance of embryos to elevated temperature were identified including redox status of the embryo and the ceramide signaling pathway. Developmental changes in embryonic apoptosis responses in response to heat shock were described and found to include alterations in the capacity of the embryo to undergo caspase-9 and caspase-3 activation as well as events downstream from caspase-3 activation. With the exception of IGF-1, other possible treatments to improve pregnancy rate to embryo transfer were not effective including selection of embryos for caspase activity, treatment of recipients with GnRH.and bilateral transfer of twin embryos. In conclusion, accomplishments achieved during the grant period have resulted in methods for improving post-transfer survival of in vitro produced embryos transferred into heat-stressed cows and have lead to additional avenues for research to increase embryo resistance to elevated temperature and improve survival to cryopreservation. In addition, embryo transfer of vitrified IVF embryos increased significantly the pregnancy rate in repeated breeder cows.
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Spitz, Douglas R. Mitochondrial-Derived Oxidants and Cellular Responses to Low Dose/Low LET Ionizing Radiation. Office of Scientific and Technical Information (OSTI), November 2009. http://dx.doi.org/10.2172/967081.

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Scott, Bobby, R., Ph.D. Advanced Computational Approaches for Characterizing Stochastic Cellular Responses to Low Dose, Low Dose Rate Exposures. Office of Scientific and Technical Information (OSTI), June 2003. http://dx.doi.org/10.2172/812039.

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