Relevant bibliographies by topics / In Vitro Liver Models

Academic literature on the topic 'In Vitro Liver Models'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "In Vitro Liver Models"

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ERKEKOĞLU, Pınar, and Belma KOÇER GÜMÜŞEL. "In Vitro Liver Models in Toxicology." Journal of Literature Pharmacy Sciences 8, no. 1 (2019): 1–17. http://dx.doi.org/10.5336/pharmsci.2018-61664.

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Guillouzo, Andre. "Liver Cell Models in in Vitro Toxicology." Environmental Health Perspectives 106 (April 1998): 511. http://dx.doi.org/10.2307/3433803.

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Guillouzo, A. "Liver cell models in in vitro toxicology." Environmental Health Perspectives 106, suppl 2 (April 1998): 511–32. http://dx.doi.org/10.1289/ehp.98106511.

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Witek, Rafal P., and Jessica A. Bonzo. "Perspective on In Vitro Liver Toxicity Models." Applied In Vitro Toxicology 4, no. 3 (September 2018): 229–31. http://dx.doi.org/10.1089/aivt.2018.29017.wit.

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Soldatow, Valerie Y., Edward L. LeCluyse, Linda G. Griffith, and Ivan Rusyn. "In vitro models for liver toxicity testing." Toxicol. Res. 2, no. 1 (2013): 23–39. http://dx.doi.org/10.1039/c2tx20051a.

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van Grunsven, Leo A. "3D in vitro models of liver fibrosis." Advanced Drug Delivery Reviews 121 (November 2017): 133–46. http://dx.doi.org/10.1016/j.addr.2017.07.004.

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Ye, Shicheng, Jochem W. B. Boeter, Louis C. Penning, Bart Spee, and Kerstin Schneeberger. "Hydrogels for Liver Tissue Engineering." Bioengineering 6, no. 3 (July 5, 2019): 59. http://dx.doi.org/10.3390/bioengineering6030059.

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Bioengineered livers are promising in vitro models for drug testing, toxicological studies, and as disease models, and might in the future be an alternative for donor organs to treat end-stage liver diseases. Liver tissue engineering (LTE) aims to construct liver models that are physiologically relevant. To make bioengineered livers, the two most important ingredients are hepatic cells and supportive materials such as hydrogels. In the past decades, dozens of hydrogels have been developed to act as supportive materials, and some have been used for in vitro models and formed functional liver constructs. However, currently none of the used hydrogels are suitable for in vivo transplantation. Here, the histology of the human liver and its relationship with LTE is introduced. After that, significant characteristics of hydrogels are described focusing on LTE. Then, both natural and synthetic materials utilized in hydrogels for LTE are reviewed individually. Finally, a conclusion is drawn on a comparison of the different hydrogels and their characteristics and ideal hydrogels are proposed to promote LTE.
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Vinken, M. "Liver-based in vitro models for toxicity testing." Toxicology Letters 295 (October 2018): S7. http://dx.doi.org/10.1016/j.toxlet.2018.06.029.

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Garcia, Martha C., Margaret Amankwa-Sakyi, and Thomas J. Flynn. "Cellular glutathione in fatty liver in vitro models." Toxicology in Vitro 25, no. 7 (October 2011): 1501–6. http://dx.doi.org/10.1016/j.tiv.2011.05.011.

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Van de Bovenkamp, M., G. M. M. Groothuis, D. K. F. Meijer, and P. Olinga. "Liver fibrosis in vitro: Cell culture models and precision-cut liver slices." Toxicology in Vitro 21, no. 4 (June 2007): 545–57. http://dx.doi.org/10.1016/j.tiv.2006.12.009.

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Dissertations / Theses on the topic "In Vitro Liver Models"

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Vu, Lucas Trung. "Proteomic Analysis of Three Dimensional Organotypic Liver Models." Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/77033.

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In vitro liver models that closely mimic the in vivo microenvironment are central for understanding hepatic functions and intercellular communication processes. Bottom-up shotgun proteomic analysis of the hepatic cells can lend insight into such processes. This technique employs liquid chromatography-tandem mass spectrometry (LC-MS/MS) for relative quantification of protein abundances by measuring intensities of their corresponding peptides. Organotypic 3D liver models have been developed in our laboratory that consist of hepatocytes and liver sinusoidal endothelial cells (LSECs) separated by a polyelectrolyte multilayer (PEM), which serves as a mimic for the Space of Disse. Each component within these models is easily separable allowing for systematic evaluation of the cells and PEMs. In this study, proteomes of hepatocytes from PEM containing models, cultured with and without LSECs, were compared to those from monolayers. Changes in core metabolism were evaluated among all culture conditions. Overall, all cultures were ketogenic and performed gluconeogenesis. The presence of the PEM led to increases in proteins associated with mitochondrial-based β-oxidation and peroxisomal proteins. The PEMs also limited production of structural proteins, which are linked to dedifferentiation of hepatocytes, suggesting that cell-ECM interactions are essential for maintenance of their liver-like state. The presence of LSECs increased levels of carboxylesterases and other phase I and phase II detoxification enzymes suggesting that intercellular signaling mediates enzyme abundance. Taken together, these results suggest that the cell-cell (from the LSECs) and cell-ECM (from the PEMs) interactions exert different, yet crucial effects, and both are required for the preservation of metabolic liver functions and differentiated phenotypes. Changes in the PEMs as a result of cell culture were also evaluated but exhibited minimal differences at this time point. Proteomes of LSECs monolayers were also characterized. Enzymes related to the metabolism of amino acids, lipids, oxidative phosphorylation and phase I and phase II detoxification processes were all identified in LSECs monolayers highlighting their role in these processes. Characterization of 3DHL LSECs was not possible due to ion suppression resulting from the presence of excess contaminant proteins. Nonetheless, this study provides a foundation in which LSECs from 3D liver models can be compared against in future studies.
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Granitzny, Anne [Verfasser]. "In vitro/ex vivo liver models for the prediction of idiosyncratic drug-induced liver injury / Anne Granitzny." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2017. http://d-nb.info/1150192496/34.

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Tirnitz-Parker, Janina Elke Eleonore. "Primary culture and immortal cell lines as in vitro models to evaluate the role of TWEAK signalling in hepatic oval cells /." Connect to this title, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0039.

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Heslop, James. "Investigating novel methods of enhancing in vitro models of drug induced liver injury." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2053229/.

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Drug induced liver injury (DILI) is a major cause of patient morbidity and mortality inferring considerable burdens onto healthcare and pharmaceutical sectors. As a consequence, substantial resources are directed towards triaging potentially dangerous new compounds at all stages of drug development. However, despite these efforts, hepatotoxic compounds remain the greatest cause of post-marketing drug withdrawal. One of the major factors preventing efficacious screening of new compounds is the lack of a truly representative in vitro model of hepatotoxicity. This thesis describes our efforts to utilise innovative and emerging techniques to further understand and develop in vitro models of hepatotoxicity. One such technique is the generation of hepatocyte-like cells from induced pluripotent stem cells (iPSCs). iPSC-derived hepatocyte-like cells offer a reproducible, physiologically-relevant, genotypically normal and population-representative model of hepatotoxicity; however, current differentiation protocols are not capable of producing hepatocyte-like cells beyond a relatively immature phenotype, limiting their use for toxicological studies. As part of the cellular reprogramming process the epigenome of the somatic cell undergoes dramatic changes; however, the studies have shown that this ‘resetting’ of the epigenome to a pluripotent state is an imperfect process, resulting in an altered differentiation propensity skewed towards the lineage of origin. We evaluated if using human hepatocytes as the starting cell type and utilising the inherent ‘epigenetic memory’ associated with iPSCs could enhance the maturity of hepatocyte-like cells. Despite a trend towards improvement in phenotype, no significant differences were found between isogenic hepatocyte-derived and fibroblast-derived iPSCs. The further development of hepatocyte-like cells is limited by the inability of current culture systems to adequately support the hepatic phenotype. Once placed into culture, primary human hepatocytes, the gold standard model of hepatotoxicity, quickly lose the metabolic qualities required for modelling drug induced liver injury. Thus, without a culture system which supports the hepatic phenotype, the differentiation of hepatocyte-like cells will remain sub-optimal. Using iTRAQ proteomics we attempted to identify the driving factors responsible for the process of hepatocyte dedifferentiation. Our results identified numerous novel factors, including HSF2, SMARCB1, ZEB1 and FOXO1 which may drive the selective loss of metabolic phenotype. The proteomic assessment of hepatocyte dedifferentiation also highlighted the loss of Nrf2-related proteins during culture. Further investigation of Nrf2 in hepatocytes revealed a potentially negative relationship between Nrf2 induction and the key metabolic enzyme, CYP3A4. Furthermore, Nrf2 gene and protein expression was shown to increase during hepatocyte-like cell differentiation. Taken together, these results suggest that Nrf2 may negatively regulate the hepatic phenotype, potentially preventing the establishment of a mature phenotype during hepatocyte-like cell differentiation. A mechanistic evaluation of Nrf2 during differentiation and dedifferentiation is therefore required to gain a fuller insight into the role it plays in the maintenance and acquisition of the hepatic phenotype. In summary, this thesis presents our contribution to the further understanding, development and enhancement of in vitro hepatotoxicity models, using innovative techniques to assess the impact of epigenetic memory on HLC differentiation, identifying novel influencing factors driving the loss of phenotype in hepatocyte culture systems and evaluating the influence of Nrf2 on the hepatic phenotype during differentiation and dedifferentiation.
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Chang, Robert Chao Sun Wei. "Biofabrication of three-dimensional liver cell-embedded tissue constructs for in vitro drug metabolism models /." Philadelphia, Pa. : Drexel University, 2009. http://hdl.handle.net/1860/3069.

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Regan, Sophie Louise. "In Vitro and In Vivo models for the investigation of drug bioactivation and drug-induced liver injury." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510967.

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Brabyn, Caroline Jane. "Development and characterization of an in vitro model for liver homeostasis." Thesis, University of Ottawa (Canada), 1994. http://hdl.handle.net/10393/6906.

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The major objective of this work was the development of an in vitro model for liver homeostasis which would allow the future study of early events in cell proliferation and cell death. The model which was set up involves growing T51B rat liver epithelial cells with a single dose of 1nM epidermal growth factor (EGF). This results in a period of hyperplasia where the cells reach double the control cell numbers two days after EGF addition. This is then followed by a decrease in cell numbers and the cell density returns to around the confluent control level five days after EGF addition. The model was investigated to ascertain whether the decrease in cell numbers three to five days after EGF addition was due to an increase in apoptosis. The results from light and electron microscopy studies, from the electrophoresis of T51B cell DNA and from the quantification of nuclear fragmentation indicated that the cells do die via an increase in apoptosis. The electron microscopy studies also show that healthy T51B cells can phagocytose apoptotic bodies. This suggests that the model is more physiological than other in vitro models of apoptosis. Cell growth studies and EGF binding studies were carried out in order to try to determine which events, if any, are EGF specific. The results from these studies suggest that occupancy of the low affinity binding site of the EGF receptor is responsible for the hyperproliferation seen when the T51B cells are grown with high doses of EGF. These studies also suggest that the apoptosis could be triggered by the down-regulation of the receptor, in a manner analogous to the removal of a trophic hormone in other systems. Thus this work describes the development and characterization of an in vitro model of liver homeostasis which closely parallels in vivo systems where animals are given mitogenic stimuli, and it also provides a good system for studying the role of EGF in cell proliferation and apoptosis.
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Douglas, O. "An evaluation of in vitro models for the assessment of mitochondrial toxicity within Drug Induced Liver Injury (DILI)." Thesis, University of Liverpool, 2017. http://livrepository.liverpool.ac.uk/3012327/.

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Drug Induced Liver Injury (DILI) is of major concern to both clinicians and the pharmaceutical industry due to the attrition of lead compounds during preclinical development and the incidence of hepatotoxicity and/or the withdrawal of drugs post marketing. It has been hypothesised that drug-induced mitochondrial dysfunction (DIMD) could be a causative factor of DILI. The nucleoside analogue fialuridine (FIAU) was withdrawn from use following a clinical trial in 1993 in which 5 patients died of hepatic failure. Subsequent research has shown that FIAU induces toxicity via mitochondrial DNA damage. However, current in vitro screening methods do not identify these compounds as toxic and thus this poses a problem to pre-clinical safety assessments. Three methods of metabolic modification, utilising glucose or galactose supplemented media and 2DG were compared to define and monitor mitochondrial toxicity induced by FIAU, and positive control adefovir (ADEF), in HepG2 (human hepatocellular carcinoma) cells. The structural isomer of fialuridine, (FIAU 2’ epimer) was included as a negative control. Mitochondrial toxicity could not be demonstrated in HepG2 cells over a 7-day period by any of these drugs. The HepaRG line is evident to be more hepatocyte-like than HepG2 cells and therefore can overcome the limitations of the widely used HepG2 cells. It is hypothesised that their increased primary human hepatocyte (PHH) like phenotypic characteristics may be more suitable for drug toxicity studies. Here, the utility of HepaRG based models in the detection of mitotoxicants was compared with previous research using a HepG2 model. Bioenergetic phenotyping revealed that the HepaRG line is less metabolically active when compared to HepG2 cells. HepaRG cells have the capacity to undergo metabolic modification using a short term glucose/galactose switch method and thus detect compounds with mitochondrial liabilities (EC50-ATPglu/EC50-ATPgal >2). Following the assessment of 12 hepatotoxins it was concluded that the HepaRG line offered no increased sensitivity for the detection of mitotoxicants compared with HepG2 cells. However, their stability in culture over extended periods (1 to 4 weeks) may be advantageous for the study of delayed toxicity. Therefore, HepaRG cells were further utilised in the assessment of FIAU induced mitochondrial toxicity, using an acute metabolic screen. Mitochondrial toxicity in the absence of cell death was demonstrated following 2-week drug incubation. The measurement of cellular respiration (using Seahorse technology) demonstrated a dose-dependent decrease in mitochondrial respiration in the absence of a decrease in mitochondrial mass. Further studies demonstrated significant drug-dependent decreases in the expression of nuclear encoded complex II, mitochondria-encoded complex IV, plus a decrease in mitochondrial DNA (mtDNA). The studies have demonstrated that the HepaRG cell model is a suitable model for the study of mitochondrial toxicity induced by nucleoside antivirals with evidence indicating that the mechanism of action via effects upon mitochondrial DNA matches the clinical mechanism of hepatotoxicity. Further studies utilising HepaRG were performed to assess the chemical and molecular pathways of toxicity induced by paracetamol. The studies provided evidence that HepaRG cells have the metabolic capacity for the turnover of parent compound to the toxic metabolite NAPQI. Furthermore, acute metabolic screening demonstrated that following short term incubations the parent compound paracetamol contains a mitochondrial liability in the absence of NAPQI-induced GSH depletion. The studies within this thesis have highlighted that the HepaRG line is suitable for the detection of mitotoxicants in which toxicity is delayed or which is mediated via CYP P450 catalysed-metabolites. Additionally, the studies provide much evidence as to the power of in vitro screening models in providing fine and detailed mechanistic information.
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Sams, Craig. "In vitro human liver metabolism of some industrial solvents and pesticides and incorporation of metabolic parameters into mathematical models." Thesis, University of Sheffield, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434530.

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Essaouiba, Amal. "Development of a liver-pancreas in vitro model using microfluidic organ-on-chip technologies." Thesis, Compiègne, 2020. http://www.theses.fr/2020COMP2573.

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Le diabète mellitus, également désigné comme la maladie du siècle, est une pathologie mortelle qui affecte le système endocrinien. Les mécanismes liés à la rupture de la boucle de rétroaction, qui régule le métabolisme et induit le diabète, ne sont pas entièrement connus. La compréhension des mécanismes d'action de l'insuline est donc essentielle pour le développement de stratégies thérapeutiques efficaces afin du lutter contre cette maladie. Par conséquent, il est impératif de trouver un modèle robuste et fiable, capable de surmonter les limites de la culture cellulaire traditionnelle en 2D et de l'expérimentation animale, pour la recherche sur le diabète. L'objectif de cette thèse est de développer un nouveau modèle de co‐culture foie‐pancréas en utilisant des systèmes microphysiologiques avancés (MPs) afin d’aborder plus efficacement le mécanisme impliqué dans la régulation endocrinienne hépatique et pancréatique. Ce travail met en évidence la capacité des systèmes multi‐organes sur puce qui combinent la compartimentation avancée des cellules en 3D, la microfluidique et la technologie des cellules souches pluripotentes induites (iPSC), pour atteindre une complexité biologique élevée et des fonctions rarement reproduites par une seule de ces technologies d’ingénierie tissulaire
Diabetes mellitus (DM) or the so called disease of the century is a life threatening dysfunction that affects the endocrine system. The mechanisms underlying the break in the feedback loop that regulates the metabolism and the consequent diabetes induction are not fully known. Understanding the mechanisms of insulin action is therefore crucial for the further development of effective therapeutic strategies to combat DM. Accordingly, it is imperative to find a robust and reliable model for diabetes research able to overcome the limitations of traditional 2D in vitro cell culture and animal experimentation. The aim of this thesis is to develop a new liver‐pancreas co‐culture model using advanced microphysiological systems (MPs) to tackle more effectively the mechanism involving the hepatic and pancreatic endocrine regulation. This work highlights the power of multi organ‐on‐chip systems that combines the advanced 3D‐cell compartmentalization, microfluidics and induced pluripotent stem cells (iPSC) technology to achieve a high biological complexity and functions that are rarely reproduced by only one of these tissue engineering technologies
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Books on the topic "In Vitro Liver Models"

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Ozolinš, Terence Robert Stanislavs. Interspecies co-culture of embryos and maternal hepatocytes: An in vitro model of phenytoin embryotoxicity. Toronto, Ont: Faculty of Pharmacy, University of Toronto, 1990.

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Rogiers, Vera, and Mathieu Vinken. Protocols in in vitro hepatocyte research. New York: Humana Press, 2015.

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Stock, Peggy, and Bruno Christ, eds. In Vitro Models for Stem Cell Therapy. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1225-5.

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Aura, Anna-Marja. In vitro digestion models for dietary phenolic compounds. [Espoo, Finland]: VTT Technical Research Centre of Finland, 2005.

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Khademhosseini, Alireza. In vitro study of bone marrow derived progenitor cells in liver-like microenvironments. Ottawa: National Library of Canada, 2001.

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Pastrakuljic, Aleksandra. In vitro activities associated with CYP1A1 and CYP1A2 in normal human liver specimens. Ottawa: National Library of Canada, 1996.

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Mahmood, Tahir. Models of tissue bonding to bioactive glass in vitro. [Toronto: Faculty of Dentistry, University of Toronto], 2000.

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Brevini, Tiziana A. L., Alireza Fazeli, and Kursad Turksen, eds. Next Generation Culture Platforms for Reliable In Vitro Models. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1246-0.

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Dranitsaris, George. In vitro biotransformation of theophylline and resorufin analogues in normal and diseased human liver. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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Bishop, Kate. Liver-enriched transcription factors and the maintainance of the differentiated hepatocyte phenotype in vitro. Birmingham: University of Birmingham, 2003.

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Book chapters on the topic "In Vitro Liver Models"

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Thurman, R. G., P. E. Ganey, S. A. Belinsky, J. G. Conway, and M. Z. Badr. "In Vitro Models of Liver Toxicity." In Handbook of Experimental Pharmacology, 99–117. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61013-4_5.

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Chayama, Kazuaki, and C. Nelson Hayes. "Unmet Needs in Basic Research: In Vitro and In Vivo Models." In Hepatitis B Virus and Liver Disease, 25–43. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4843-2_2.

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Hayes, C. Nelson, and Kazuaki Chayama. "Unmet Needs in Basic Research of Hepatitis B Virus Infection: In Vitro and In Vivo Models." In Hepatitis B Virus and Liver Disease, 29–49. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-3615-8_2.

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Solaipriya, S., N. Mahalakshmi, R. Prajitha, and V. Sivaramakrishnan. "In Vivo, Ex Vivo, and In Vitro Models Systems for Liver Cancer Research." In Handbook of Animal Models and its Uses in Cancer Research, 1–21. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1282-5_19-1.

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Wiggins, Benjamin G., Konstantinos Aliazis, Scott P. Davies, Gideon Hirschfield, Patricia F. Lalor, Gary Reynolds, and Zania Stamataki. "In Vitro and Ex Vivo Models to Study T Cell Migration Through the Human Liver Parenchyma." In Methods in Molecular Biology, 195–214. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6931-9_14.

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O’Connor, Sean, and Paul Cohen. "In Vitro Approaches to Model and Study Communication Between Adipose Tissue and the Liver." In Thermogenic Fat, 151–58. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6820-6_15.

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Mortimore, Glenn E., and Charles M. Schworer. "Application of Liver Perfusion as an in vitro Model in Studies of Intracellular Protein Degradation." In Ciba Foundation Symposium 75 - Protein Degradation in Health and Disease, 281–305. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720585.ch17.

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López-Márquez, Arístides, Ainhoa Martínez-Pizarro, Belén Pérez, Eva Richard, and Lourdes R. Desviat. "Modeling Splicing Variants Amenable to Antisense Therapy by Use of CRISPR-Cas9-Based Gene Editing in HepG2 Cells." In Methods in Molecular Biology, 167–84. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2010-6_10.

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AbstractThe field of splice modulating RNA therapy has gained new momentum with FDA approved antisense-based drugs for several rare diseases. In vitro splicing assays with minigenes or patient-derived cells are commonly employed for initial preclinical testing of antisense oligonucleotides aiming to modulate splicing. However, minigenes do not include the full genomic context of the exons under study and patients’ samples are not always available, especially if the gene is expressed solely in certain tissues (e.g. liver or brain). This is the case for specific inherited metabolic diseases such as phenylketonuria (PKU) caused by mutations in the liver-expressed PAH gene.Herein we describe the generation of mutation-specific hepatic cellular models of PKU using CRISPR/Cas9 system, which is a versatile and easy-to-use gene editing tool. We describe in detail the selection of the appropriate cell line, guidelines for design of RNA guides and donor templates, transfection procedures and growth and selection of single-cell colonies with the desired variant, which should result in the accurate recapitulation of the splicing defect.
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Wahba, R., C. Bangard, R. Kleinert, S. Rösgen, K. J. Lackner, A. H. Hölscher, and D. L. Stippel. "Electro-physiological parameters of hepatic radiofrequency ablation — a comparison of in vitro vs. in vivo porcine liver model." In Deutsche Gesellschaft für Chirurgie, 85–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_34.

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Levya, Elliot B., Kevin Cleary, Filip Banovac, Daigo Tanaka, Sheng Xu, David Lindisch, and Neil Glossop. "Evaluation of a magnetic tracking-guided needle placement system featuring respiratory gating in an in vitro liver model." In CARS 2002 Computer Assisted Radiology and Surgery, 329–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56168-9_54.

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Conference papers on the topic "In Vitro Liver Models"

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Cozzi, C., G. Polito, L. M. Strambini, and G. Barillaro. "Towards an in-Vitro Liver Lobule Model." In 2015 1st Workshop on Nanotechnology in Instrumentation and Measurement (NANOFIM). IEEE, 2015. http://dx.doi.org/10.1109/nanofim.2015.8425337.

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Gaitantzi, Haristi, Emrullah Birgin, Erik Rasbach, Katja Breitkopf-Heinlein, and Nuh Rahbari. "Generation of human liver organoids – An in vitro model of liver diseases." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740649.

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Gaitantzi, H., C. Cai, S. Asawa, K. Böttcher, M. Ebert, and K. Breitkopf-Heinlein. "Human 3-dimensional liver organoids: in vitro model systems to study liver diseases." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402185.

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Kobayashi, Yo, Akinori Onishi, Hiroki Watanabe, Takeharu Hoshi, Kazuya Kawamura, and Masakatsu G. Fujie. "In vitro validation of viscoelastic and nonlinear physical model of liver for needle insertion simulation." In EMBS International Conference on Biomedical Robotics and Biomechatronics (BioRob 2008). IEEE, 2008. http://dx.doi.org/10.1109/biorob.2008.4762837.

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Alex, Aneesh, BanuPriya Sridharan, Edita Aksamitiene, Chi Zhang, Jindou Shi, Prabuddha Mukherjee, Mantas Zurauskas, et al. "Enhancing liver on a chip Complex In Vitro Model studies using label-free optical imaging." In Visualizing and Quantifying Drug Distribution in Tissue V, edited by Conor L. Evans and Kin Foong Chan. SPIE, 2021. http://dx.doi.org/10.1117/12.2578531.

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Tourlomousis, Filippos, and Robert C. Chang. "Computational Modeling of 3D Printed Tissue-on-a-Chip Microfluidic Devices as Drug Screening Platforms." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-38454.

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Physiological tissue-on-a-chip technology is enabled by adapting microfluidics to create micro scale drug screening platforms that replicate the complex drug transport and reaction processes in the human liver. The ability to incorporate three-dimensional (3d) tissue models using layered fabrication approaches into devices that can be perfused with drugs offer an optimal analog of the in vivo scenario. The dynamic nature of such in vitro metabolism models demands reliable numerical tools to determine the optimum tissue fabrication process, flow, material, and geometric parameters for the most effective metabolic conversion of the perfused drug into the liver microenvironment. Thus, in this modeling-based study, the authors focus on modeling of in vitro 3d microfluidic microanalytical microorgan devices (3MD), where the human liver analog is replicated by 3d cell encapsulated alginate hydrogel based tissue-engineered constructs. These biopolymer constructs are hosted in the chamber of the 3MD device serving as walls of the microfluidic array of channels through which a fluorescent drug substrate is perfused into the microfluidic printed channel walls at a specified volumetric flow rate assuring Stokes flow conditions (Re<<1). Due to the porous nature of the hydrogel walls, a metabolized drug product is collected as an effluent stream at the outlet port. A rigorous modeling approached aimed to capture both the macro and micro scale transport phenomena is presented. Initially, the Stokes Flow Equations (free flow regime) are solved in combination with the Brinkman Equations (porous flow regime) for the laminar velocity profile and wall shear stresses in the whole shear mediated flow regime. These equations are then coupled with the Convection-Diffusion Equation to yield the drug concentration profile by incorporating a reaction term described by the Michael-Menten Kinetics model. This effectively yields a convection-diffusion–cell kinetics model (steady state and transient), where for the prescribed process and material parameters, the drug concentration profile throughout the flow channels can be predicted. A key consideration that is addressed in this paper is the effect of cell mechanotransduction, where shear stresses imposed on the encapsulated cells alter the functional ability of the liver cell enzymes to metabolize the drug. Different cases are presented, where cells are incorporated into the geometric model either as voids that experience wall shear stress (WSS) around their membrane boundaries or as solid materials, with linear elastic properties. As a last step, transient simulations are implemented showing that there exists a tradeoff with respect the drug metabolized effluent product between the shear stresses required and the residence time needed for drug diffusion.
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Watanabe, H., N. Yamazaki, Y. Isobe, XiaoWei Lu, Y. Kobayashi, T. Miyashita, T. Ohdaira, M. Hashizume, and M. G. Fujie. "Validation of accuracy of liver model with temperature-dependent thermal conductivity by comparing the simulation and in vitro RF ablation experiment." In 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6347292.

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Tourlomousis, Filippos, and Robert C. Chang. "2D and 3D Multiscale Computational Modeling of Dynamic Microorgan Devices as Drug Screening Platforms." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-52734.

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The ability to incorporate three-dimensional (3D) hepatocyte-laden hydrogel constructs using layered fabrication approaches into devices that can be perfused with drugs enables the creation of dynamic microorgan devices (DMDs) that offer an optimal analog of the in vivo liver metabolism scenario. The dynamic nature of such in vitro metabolism models demands reliable numerical tools to determine the optimum process, material, and geometric parameters for the most effective metabolic conversion of the perfused drug into the liver microenvironment. However, there is a current lack of literature that integrates computational approaches to guide the optimum design of such devices. The groundwork of the present numerical study has been laid by our previous study [1], where the authors modeled in 2D an in vitro DMD of arbitrary dimensions and identified the modeling challenges towards meaningful results. These constructs are hosted in the chamber of the microfluidic device serving as walls of the microfluidic array of channels through which a fluorescent drug substrate is perfused into the microfluidic printed channel walls at a specified volumetric flow rate assuring Stokes flow conditions (Re<<1). Due to the porous nature of the hydrogel walls, a metabolized drug product is collected at the outlet port. A rigorous FEM based modeling approach is presented for a single channel parallel model geometry (1 free flow channel with 2 porous walls), where the hydrodynamics, mass transfer and pharmacokinetics equations are solved numerically in order to yield the drug metabolite concentration profile at the DMD outlet. The fluid induces shear stresses are assessed both in 3D, with only 27 cells modeled as single compartment voids, where all of the enzymatic reactions are assumed to take place. In this way, the mechanotransduction effect that alters the hepatocyte metabolic activity is assessed for a small scale model. This approach overcomes the numerical limitations imposed by the cell density (∼1012 cells/m3) of the large scale DMD device. In addition, a compartmentalization technique is proposed in order to assess the metabolism process at the subcellular level. The numerical results are validated with experiments to reveal the robustness of the proposed modeling approach and the necessity of scaling the numerical results by preserving dynamic and biochemical similarity between the small and large scale model.
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Hansen, J. B., J. O. Olsen, L. Wilagård, and B. Østerud. "THE EFFECT OF COD LIVER OIL INTAKE ON THE STIMULATION OF BLOOD CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643406.

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In an in vitro model, stimulation of blood cells with a low concentration of lipopolysaccharides (LPS) revealed differences between women and men that possibly could be an explanation to why young women have less coronary heart disease than men (see abstract Hansen et al. “A model to--”).This model was also used to study the effect of intake of cod liver oil (CLO). 40 students (20 men and 20 women) were tested followed by an intake of 25 ml CLO daily for 2 months by 20 of the students.Heparinized blood samples were incubated with 2 ng LPS/ ml for 2 hours followed by isolation of plasma for thromboxane B2 and 6-keto-PG 1α quantitation.After the first 2 months period of CLO drinking we have the following results:The two months of CLO intake had no significant effect pn the thromboplastin induced synthesis in monocytes. In addition platelet aggregation was tested in a whole blood aggregometer using ADP addition to heparinized blood or collagen induced platelet aggregation in citrated whole blood. ADP aggregation was reduced from 75.9 ± 16.8% to 55.4 ± 19% in the CLO group of women, whereas the reduction in the CLO group of men was 70.1 ± 17.1% to 60.9±18.6%. Similar result were found with collagen aggregation (57% to 33% for women and 48% to 30% for men).It is concluded that CLO intake reduces TxA2 production and plateletaggregation without having reduced effect on PGI2 production in whole blood.
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Franich, Andjela, Ivana Vasić, Snežana Rajković, Aleksandar Arsenijević, Marija Milovanović, Nebojša Arsenijević, Jelena Milovanović, and Marija Živković. "CYTOTOXICITY OF CATIONIC DINUCLEAR PLATINUM(II) COMPLEXES IN AN EXPERIMENTAL MODEL OF MOUSE COLON CANCER." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.293f.

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The series of nine dinuclear platinum(II) complexes, [{Pt(L)Cl}2(μ-X)]2+ (where L is two NH3 or bidentantly coordinated diamine ligand – ethylenediamine, en; (±)-1,2-propylenediamine, 1,2-pn; isobutylenediamine, ibn; trans-(±)-1,2-diaminocyclohexane, dach; 1,3-propylenediamine, 1,3-pd; 2,2- dimethyl-1,3-propylenediamine, 2,2-diMe-1,3-pd; (±)-1,3-pentanediamine,1,3-pnd, and X is a bridging pyrazine (pz) or pyridazine (pydz) ligand) have been synthesized and characterized. The antitumor potential of these complexes against CT26 cells were determined by in vitro and in vivo assays. A murine model of heterotopic colon cancer tumor was induced in immunocompetent BALB/c mice for investigating antitumor potential of the Pt(II) complexes in vivo. It was found that complexes Pt1, Pt2 and Pt7 shows significant in vitro cytotoxic activity against mouse colon carcinoma CT26 cells, while all these complexes show moderate apoptotic effect. Complexes Pt1 and Pt7 arrested CT26 cells in G2/M phase of cell cycle, while complexes Pt5 and Pt6 exerted the highest antiproliferative effect which was evaluated by detection of Ki67 expressing cells. Complexes Pt1 and Pt2 performed significant in vivo antitumor effects reducing the growth of primary tumor and the incidence of lung and liver metastases without causing the significant hepato- and nephro- toxicity.
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Reports on the topic "In Vitro Liver Models"

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Cao, Cheng J., Gunda Reddy, Desmond I. Bannon, and Mark S. Johnson. In Vitro Study of Hexahydro-1,3,5-Trinitro-1,3,5-Triazine (RDX) Metabolism in Human Liver. Fort Belvoir, VA: Defense Technical Information Center, October 2008. http://dx.doi.org/10.21236/ada638277.

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Abou-Donia, M. B., and A. W. Abu-Quare. In Vitro Metabolism of Pyridostigmine Bromide (PB), DEET and Permethrin, Alone and in Combination by Human Plasma and Liver Microsomes. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada402080.

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Geisbert, Thomas W. Pathogenesis of Ebola Hemorrhagic Fever in Primate Models In Vivo and In Vitro. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ad1012627.

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Casabar, Richard C., Andrew D. Wallace, Ernest Hodgson, and Randy L. Rose. Metabolism of Endosulfan-Alpha by Human Liver Microsomes and its Utility as a Simultaneous In Vitro Probe for CYP2B6 and CYP3A4. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada445178.

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Rothstein, Jeffrey D. Anti-Excitotoxic and Antioxidant TGF-Beta Family Neurotrophic Factors: In Vitro Screening Models of Motor Neuron Degeneration. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada405360.

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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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Lioy, P. J., M. Gallo, P. Georgopoulos, R. Tate, and B. Buckley. Comparison of the bioavailability of elemental waste laden soils using in vivo and in vitro analytical methodology and refinement of exposure/dose models. 1998 annual progress report. Office of Scientific and Technical Information (OSTI), June 1998. http://dx.doi.org/10.2172/13580.

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Spiers, Donald, Arieh Gertler, Harold Johnson, and James Spain. An In Vitro and In Vivo Investigation of the Diverse Biological Activities of Bovine Placental Lactogen. United States Department of Agriculture, August 1993. http://dx.doi.org/10.32747/1993.7568087.bard.

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In order to understand the structure-function relationship of bovine placental lactogen (bPL) and initiate production of material for in vivo testing, 28 different bPL analogues were prepared by either truncation or site-directed mutagenesis. The effect of these mutations was determined by measuring binding capacity, ability to homodimerize extracellular domains (ECDs) of several lactogenic and somatogenic receptors, and by in vitro bioassays. Two analogues were prepared in large amounts for in vivo studies. These studies (a) identified the residues responsible for the somatogenic activity of bPL (K73, G133, T188) and for both lactogenic and somatogenic activity (N-terminus, K185, Y190); (b) allowed preparation of bPL analogues with selectively abolished or reduced somatogenic activity; and (c) provided a tool to understand the kinetic difference between lactogenic and somatogenic receptors. In vivo studies using rodent and dairy models showed that bovine growth hormone (bGH) is superior to bPL in stimulating growth and lactation. Likewise, bGH has greater somatogenic activity in different age groups and thermal environments. Initial studies of bPL analog T188 suggest that its lactogenic potential is superior to bGH. Effective experimental models have now been developed and tested for analysis of new bPL analogs.
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Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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Hawkins, Brian T., and Sonia Grego. A Better, Faster Road From Biological Data to Human Health: A Systems Biology Approach for Engineered Cell Cultures. RTI Press, June 2017. http://dx.doi.org/10.3768/rtipress.2017.rb.0015.1706.

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Traditionally, the interactions of drugs and toxicants with human tissue have been investigated in a reductionist way—for example, by focusing on specific molecular targets and using single-cell-type cultures before testing compounds in whole organisms. More recently, “systems biology” approaches attempt to enhance the predictive value of in vitro biological data by adopting a comprehensive description of biological systems and using computational tools that are sophisticated enough to handle the complexity of these systems. However, the utility of computational models resulting from these efforts completely relies on the quality of the data used to construct them. Here, we propose that recent advances in the development of bioengineered, three-dimensional, multicellular constructs provide in vitro data of sufficient complexity and physiological relevance to be used in predictive systems biology models of human responses. Such predictive models are essential to maximally leveraging these emerging bioengineering technologies to improve both therapeutic development and toxicity risk assessment. This brief outlines the opportunities presented by emerging technologies and approaches for the acceleration of drug development and toxicity testing, as well as the challenges lying ahead for the field.
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