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Libros sobre el tema "In vitro gut model"

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Publicado: 6 de julio de 2024

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1

1947-, McQueen Charlene A., ed. In vitro toxicology: Model systems and methods. Caldwell, N.J: Telford Press, 1989.

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2

Husain, Irfana Shaheen. The development of an in vitro caries model. [Toronto: Faculty of Dentistry, University of Toronto], 1992.

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3

Starkey, Rosalind F. Cellular interactions in an in vitro model of implantation. Manchester: Universityof Manchester, 1993.

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4

Kulkeaw, Kasem. Emergence of In Vitro 3D Systems to Model Human Malaria. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-0691-8.

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5

Falk Symposium (94th 1996 Freiburg, Germany). The gut as a model in cell and molecular biology. Dordrecht: Kluwer Academic Publishers, 1997.

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6

Mahendra, Ahalya. The role of ILK in an in vitro model of renal branching morphogenesis. Ottawa: National Library of Canada, 2003.

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7

Amin, Iqbal Ibn. Quantitative studies on early invasive events of salmonella typhimurium in functioning gut in vitro in the context ofgastroenteritis. Birmingham: University of Birmingham, 1993.

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8

Carter, Kevin. In-vitro investigation of electric toothbrushes and development of an artificial plaque model system. Birmingham: University of Birmingham, 2000.

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9

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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10

Lai, Laura R. B. Protein oxidation occurs in cardiomyocytes exposed to an in vitro model of hypoxia/reperfusion injury. Ottawa: National Library of Canada, 1996.

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11

Ozolins, Terence Robert S. Interspecies co-culture of embryos and maternal hepatocytes: An in vitro model of phenytoin embryotoxicity. Ottawa: National Library of Canada, 1990.

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12

Salmon, Michael. Transferrin receptor bearing cells in rheumatoid arthritis and an in vitro model of lymphocyte activation. Birmingham: University of Birmingham, 1986.

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13

Chakravertty, Aashish. The interaction between human cytomegalovirus and polymorphonuclear leukocytes using an in vitro model of study. Ottawa: National Library of Canada, 2000.

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14

Yeh, John Sho-Ju. The preparation, development, and analysis of an in vitro cadaveric model of cervical spine sagittal motion. Birmingham: University of Birmingham, 2001.

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15

Vičanová, Jana. Skin barrier: Reconstructed epidermis as in vitro model for studies on the stratum corneum barrier formation. [Leiden: University of Leiden, 1998.

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16

Graziano, Victor M. A. The ferret: A potential in vitro small animal model for the study of osteogenesis and osteoclasis. [Toronto: University of Toronto, Faculty of Dentistry], 1998.

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17

Davis, Penelope Lyn. Studies on human papillomavirus type I structural proteins and a model for virus replication in vitro. Birmingham: University of Birmingham, 1992.

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18

Patel, Dharmendra Sumantbhai. The development of an in vitro mucosal model predictive of bioadhesive agents in the mouth: A thesis. Portsmouth: School of Pharmacy and Biomedical Sciences, 1998.

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19

Moelleken, Brent Roderick Wilfred. Tamoxifen - 5-fluorouracil synergy in human breast cancer cell lines: Correlating in vitro synergy with the current estrogen receptor model. [New Haven: s.n.], 1985.

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20

Galligan, Ethel. An investigation of the radioprotective effect of dietary antioxidants on normal tissue and tumour radiosensitivity: In vitro and in an in vivo murine model. [s.l: The Author], 1997.

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21

OHOLO Conference (31st 1986 Tiberias, Israel). Model systems in neurotoxicology: Alternative approaches to animal testing : proceedings of the 31st OHOLO Conference, held in Tiberias, Israel, November 3-7, 1986. Editado por Shahar Abraham y Goldberg Alan M. New York: Liss, 1987.

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22

Personnat, Lyndia. In vitro model of intracochlear drug delivery. 2014.

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23

McQueen, A. In Vitro Toxicology: Model Systems and Methods. Taylor & Francis Group, 1989.

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24

McQueen, A. In Vitro Toxicology: Model Systems and Methods. CRC, 1989.

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25

Ryczko, Michael. XEN cells: An in vitro model of extraembryonic endoderm. 2007.

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26

Katz, Sherri. Nebulized therapies for childhood pulmonary hypertension: An in vitro model. 2006.

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27

Test No. 431: In Vitro Skin Corrosion: Human Skin Model Test. OECD, 2004. http://dx.doi.org/10.1787/9789264071148-en.

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28

Séguin, Cheryle Ann. The development of an in vitro model of nucleus pulposus degeneration. 2005.

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29

Brant, Janet Ann. Development of an in vitro model of peritonitis complicating continuous ambulatory peritonealdialysis. 1996.

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30

(Editor), F. Halter, D. Winton (Editor) y N. A. Wright (Editor), eds. The Gut as a Model in Cell and Molecular Biology (Falk Symposium). Springer, 1997.

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31

Stroke-in-a-dish: An in vitro model of microglial activation and stroke. Ottawa: National Library of Canada, 1998.

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32

Frantseva, Marina. Mechanisms of free radical formation and toxicity in an in vitro model of ischemia. 1999.

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33

Striedter, Georg. Model Systems in Biology. The MIT Press, 2022. http://dx.doi.org/10.7551/mitpress/14366.001.0001.

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How biomedical research using various animal species and in vitro cellular systems has resulted in both major successes and translational failure. In Model Systems in Biology, comparative neurobiologist Georg Striedter examines how biomedical researchers have used animal species and in vitro cellular systems to understand and develop treatments for human diseases ranging from cancer and polio to Alzheimer's disease and schizophrenia. Although there have been some major successes, much of this “translational” research on model systems has failed to generalize to humans. Striedter explores the history of such research, focusing on the models used and considering the question of model selection from a variety of perspectives—the philosophical, the historical, and that of practicing biologists. Striedter reviews some philosophical concepts and ethical issues, including concerns over animal suffering and the compromises that result. He traces the history of the most widely used animal and in vitro models, describing how they compete with one another in a changing ecosystem of models. He examines how therapies for bacterial and viral infections, cancer, cardiovascular diseases, and neurological disorders have been developed using animal and cell culture models—and how research into these diseases has both taken advantage of and been hindered by model system differences. Finally, Striedter argues for a “big tent” biology, in which a diverse set of models and research strategies can coexist productively.
34

Mashregi, Mariam. Accelerated cytotoxic mechanism screening of isoniazid and phenylhydrazine using an in vitro hepatocyte inflammation model. 2006.

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35

Adams, Mark. An in vitro assessment of the mouse as an experimental model for the polymorphic oxidation of metoprolol. 1990.

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36

Bartoszewicz, Lola. Signal transduction mechanisms involved in stretch-induced elastin production in an in-vitro chick aortic organ culture model. 1995.

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37

(Editor), Anna M. Wobus y Kenneth R. Boheler (Editor), eds. Embryonic Stem Cells As a Developmental Model in Vitro (Cells Tissues Organs, Volume 165, Number 3-4, 1999). S Karger Pub, 1999.

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38

Portwine, Carol Ann. Identification and characterization of Li-Fraumeni syndrome families: Molecular and in vitro analysis and development of an in vivo model. 2002.

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39

Facca, Joseph Bruno. "In vitro" characterization of the maximum and mean frequency wave forms of the CW Doppler spectrum from a corotid artery model using DFT analysis and ensemble averaging. 1986.

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40

Lefer, Allan M., K. Schror, P. H. Hinderling y F. III Smith E. Drug Distribution in the Body: In Vitro Prediction and Physiological Interpretation/the Cat As an in Vivo Model for Myocardial Ischemia and Infarction ... in Pharmacology and Clinical Pharmacology). Vch Pub, 1989.

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41

Hong, Jaan. Investigation of Incompatibility Reactions Caused by Biomaterials in Contact With Whole Blood Using a New in Vitro Model (Comprehensive Summaries of Uppsala ... from the Faculty of Medicine, 1049). Uppsala Universitet, 2001.

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42

Hayashi, Inki. The modulatory effects of folate deficiency on mRNA and/or protein expression of the genes involved in folate metabolism and one-carbon transfer reactions using an in vitro folate deficient model of colorectal cancer. 2005.

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43

Selgrath, James Patrick. Observations on defined tissue, contractile region, tubular vessel, and blood islet formation in enzymatically formed trophoblastic vesicles, and the use of trophoblastic vesicles as a model system for the evaluation of embryonic cell metabolism in vitro. 1987.

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44

Merl, Dan, Joseph Lucas, Joseph Nevins, Haige Shen y Mike West. Trans-study projection of genomic biomarkers in analysis of oncogene deregulation and breast cancer. Editado por Anthony O'Hagan y Mike West. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780198703174.013.6.

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This article focuses on the use of Bayesian concepts and methods in the trans-study projection of genomic biomarkers for the analysis of oncogene deregulation in breast cancer. The objective of the study is to determine the extent to which patterns of gene expression associated with experimentally induced oncogene pathway deregulation can be used to investigate oncogene pathway activity in real human cancers. This is often referred to as the in vitro to in vivo translation problem, which is addressed using Bayesian sparse factor regression analysis for model-based translation and refinement of in vitro generated signatures of oncogene pathway activity into the domain of human breast tumour tissue samples. The article first provides an overview of the role of oncogene pathway deregulation in human cancers before discussing the details of modelling and data analysis. It then considers the findings based on biological evaluation and Bayesian pathway annotation analysis.
45

Woolf, Eric C. y Adrienne C. Scheck. Ketogenic Diet as Adjunctive Therapy for Malignant Brain Cancer. Editado por Jong M. Rho. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0013.

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Malignant brain tumors are devastating, and increased survival requires new therapeutic modalities. Metabolic dysregulation results in an increased need for glucose in tumor cells, suggesting that reduced tumor growth could be achieved with decreased glucose availability either through pharmacological means or use of a high-fat, low-carbohydrate ketogenic diet (KD). KD provides increased blood ketones to support energy needs of normal tissues and has been shown to reduce tumor growth, angiogenesis, inflammation, peritumoral edema, migration, and invasion. Furthermore, this diet can enhance the activity of radiation and chemotherapy in a mouse model of glioma, thus increasing survival. In vitro studies indicate that increasing ketones in the absence of glucose reduction can also inhibit cell growth and potentiate the effects of radiation. Thus, emerging data provide strong support for the use of KD in the treatment of malignant gliomas and thus far has led to a limited number of clinical trials.
46

Kawamura, Masahito. Ketogenic Diet in a Hippocampal Slice. Editado por Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0021.

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The hippocampus is thought to be a good experimental model for investigating epileptogenesis in and/or antiepileptic therapy for temporal lobe epilepsy. The hippocampus is also a useful target for researching the ketogenic diet. This chapter focuses on electrophysiological recordings using hippocampal slices and introduces their use for studying the anticonvulsant effects underlying ketogenic diets. The major difficulty in using hippocampal slices is the inability to precisely reproduce the in vivo condition of ketogenic diet feeding in this in vitro preparation. Three different approaches are reported to reproduce diet effects in the hippocampal slices: (1) direct application of ketone bodies, (2) mimicking the ketogenic diet condition with whole-cell patch-clamp technique, and (3) hippocampal slices from ketogenic diet–fed animals. Significant results have been found with each of these methods. These three approaches are useful tools to elucidate the underlying anticonvulsant mechanisms of the ketogenic diet.
47

Dickenson, Donna. The Commodification of Women’s Reproductive Tissue and Services. Editado por Leslie Francis. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199981878.013.6.

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Although the term “commodification” is sometimes criticized as imprecise or overused, in fact it has a complex philosophical ancestry and can never be used too much because the phenomena that it describes are still gaining ground. The issues that commodification raises in relation to reproductive technologies include whether it is wrong to commodify human tissues generally and gametes particularly, and whether the person as subject and the person as object can be distinguished in modern biomedicine. This chapter examines three areas in which commodification is a serious concern for important reproductive technologies: the sale of eggs for in vitro fertilization and research, the banking of umbilical cord blood, and the use of gestational surrogates both domestically and internationally. In each example, the commodification of women’s reproductive labor is masked by the manner in which “the lady vanishes” under a gift model, ignoring the true economic value of their labor and opening up the possibility of exploitation by commercial interests.
48

Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.
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