Relevant bibliographies by topics / Mice – Physiology

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Mice – Physiology'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 January 2023

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Journal articles on the topic "Mice – Physiology"

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Modaresi, Mehrdad, and Mansoureh Emadi. "The Effects of Rosemary Extract on Spermatogenesis and Sexual Hormones of Mice under Heat Stress." Trends Journal of Sciences Research 3, no. 2 (September 7, 2018): 69–74. http://dx.doi.org/10.31586/physiology.0302.02.

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Choudhury, Chinmoy, Meenakshi Bawari, and G. D. Sharma G. D. Sharma. "Biochemical Screening of The Effect of a Plant Extract on Albino Mice Physiology." International Journal of Scientific Research 2, no. 8 (June 1, 2012): 38–39. http://dx.doi.org/10.15373/22778179/aug2013/13.

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James, Jeanne F., Timothy E. Hewett, and Jeffrey Robbins. "Cardiac Physiology in Transgenic Mice." Circulation Research 82, no. 4 (March 9, 1998): 407–15. http://dx.doi.org/10.1161/01.res.82.4.407.

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Kale, Ajit, Ivo Amende, Katrina Piskorski, Victor Chu, Jose M. Otero, Peter Mueller, and Thomas G. Hampton. "Non-invasive Physiology in Conscious Mice." Alternatives to Laboratory Animals 32, no. 1_suppl (January 2004): 195–201. http://dx.doi.org/10.1177/026119290403201s33.

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VERKMAN, A. S. "Lessons on Renal Physiology from Transgenic Mice Lacking Aquaporin Water Channels." Journal of the American Society of Nephrology 10, no. 5 (May 1999): 1126–35. http://dx.doi.org/10.1681/asn.v1051126.

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Abstract. Several aquaporin-type water channels are expressed in kidney: AQP1 in the proximal tubule, thin descending limb of Henle, and vasa recta; AQP2, AQP3, and AQP4 in the collecting duct; AQP6 in the papilla; and AQP7 in the proximal tubule. AQP2 is the vasopressin-regulated water channel that is important in hereditary and acquired diseases affecting urine-concentrating ability. It has been difficult to establish the roles of the other aquaporins in renal physiology because suitable aquaporin inhibitors are not available. One approach to the problem has been to generate and analyze transgenic knockout mice in which individual aquaporins have been selectively deleted by targeted gene disruption. Phenotype analysis of kidney and extrarenal function in knockout mice has been very informative in defining the role of aquaporins in organ physiology and addressing basic questions regarding the route of transepithelial water transport and the mechanism of near isoosmolar fluid reabsorption. This article describes new renal physiologic insights revealed by phenotype analysis of aquaporin-knockout mice and the prospects for further basic and clinical developments.
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Sieck, Gary C. "Physiology in Perspective: Of Mice and Men." Physiology 34, no. 1 (January 1, 2019): 3–4. http://dx.doi.org/10.1152/physiol.00049.2018.

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Lindsey, Merry L., Zamaneh Kassiri, Jitka A. I. Virag, Lisandra E. de Castro Brás, and Marielle Scherrer-Crosbie. "Guidelines for measuring cardiac physiology in mice." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 4 (April 1, 2018): H733—H752. http://dx.doi.org/10.1152/ajpheart.00339.2017.

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Cardiovascular disease is a leading cause of death, and translational research is needed to understand better mechanisms whereby the left ventricle responds to injury. Mouse models of heart disease have provided valuable insights into mechanisms that occur during cardiac aging and in response to a variety of pathologies. The assessment of cardiovascular physiological responses to injury or insult is an important and necessary component of this research. With increasing consideration for rigor and reproducibility, the goal of this guidelines review is to provide best-practice information regarding how to measure accurately cardiac physiology in animal models. In this article, we define guidelines for the measurement of cardiac physiology in mice, as the most commonly used animal model in cardiovascular research.Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/guidelines-for-measuring-cardiac-physiology-in-mice/ .
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Gordon, C. J. "Thermal physiology of laboratory mice: Defining thermoneutrality." Journal of Thermal Biology 37, no. 8 (December 2012): 654–85. http://dx.doi.org/10.1016/j.jtherbio.2012.08.004.

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Rao, Shobha, and A. S. Verkman. "Analysis of organ physiology in transgenic mice." American Journal of Physiology-Cell Physiology 279, no. 1 (July 1, 2000): C1—C18. http://dx.doi.org/10.1152/ajpcell.2000.279.1.c1.

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The increasing availability of transgenic mouse models of gene deletion and human disease has mandated the development of creative approaches to characterize mouse phenotype. The mouse presents unique challenges to phenotype analysis because of its small size, habits, and inability to verbalize clinical symptoms. This review describes strategies to study mouse organ physiology, focusing on the cardiovascular, pulmonary, renal, gastrointestinal, and neurobehavioral systems. General concerns about evaluating mouse phenotype studies are discussed. Monitoring and anesthesia methods are reviewed, with emphasis on the feasibility and limitations of noninvasive and invasive procedures to monitor physiological parameters, do cannulations, and perform surgical procedures. Examples of phenotype studies are cited to demonstrate the practical applications and limitations of the measurement methods. The repertoire of phenotype analysis methods reviewed here should be useful to investigators involved in or contemplating the use of mouse models.
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Gassmann, Max, and Thierry Hennet. "From Genetically Altered Mice to Integrative Physiology." Physiology 13, no. 2 (April 1998): 53–57. http://dx.doi.org/10.1152/physiologyonline.1998.13.2.53.

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Transgenic and gene-targeted mice permit the study of the function(s) of the single gene(s) in a whole organism, thereby relating molecular biology and integrative physiology. To demonstrate the potential of transgenic models, we present in this review some physiologically relevant information obtained from genetically engineered mice.
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Dissertations / Theses on the topic "Mice – Physiology"

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Muir, Eric R. "Magnetic resonance imaging of retinal physiology and anatomy in mice." Diss., Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/37268.

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MRI can provide anatomical, functional, and physiological images at relatively high spatial resolution and is non-invasive and does not have depth limitation. However, the application of MRI to study the retina is difficult due to the very small size of the retina. This thesis details the development of MRI methods to image blood flow (BF), anatomy, and function of the retina and choroid, and their application to two diseases of the retina: diabetic retinopathy and retinal degeneration. A unique continuous arterial spin labeling technique was developed to image BF in mice and tested by imaging cerebral BF. This method was then applied to image layer-specific BF of the retina and choroid in mice, and to acquire BF functional MRI of the retina and choroid in response to hypoxic challenge. Additionally blood oxygen level dependent functional MRI of the mouse retina and choroid in response to hypoxic challenge was obtained using a balanced steady state free precession sequence which provides fast acquisition, has high signal to noise ratio, and does not have geometric distortion or signal dropout artifacts. In a mouse model of diabetic retinopathy, MRI detected reduced retinal BF in diabetic animals. Visual function in the diabetic mice, as determined by psychophysical tests, was also reduced. Finally, in a mouse model of retinal degeneration, BF and anatomical MRI detected reductions of retinal BF and the thickness of the retina. The studies detailed in this thesis demonstrate the feasibility of layer-specific MRI to study BF, anatomy, and function, in the mouse retina. Further, these methods were shown to provide a novel means of studying animal models of retinal disease in vivo.
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Fust, Anita. "Lung mechanics in mice : effect of decorin deficiency." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80268.

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Decorin is required for the normal fibrillogenesis and spatial arrangement of collagen. As collagen is important in determining the elastic behaviour of the lung, we hypothesized that lung tissue mechanics would be altered in decorin deficient (Dcn-/-) mice. Complex impedance, pressure-volume curves, and length-stress curves of lung parenchyma were measured in C57BL/6 mice, 6 Dcn-/- and 6 wildtype ( Dcn+/+), both in vivo and in vitro. Immunohistochemistry and Western blotting were performed to identify decorin and biglycan in the lung tissues. In vivo, airway resistance was decreased and lung compliance was increased in Dcn-/- mice. In vitro, length-stress curves showed increased compliance in the Dcn-/- mice. Immunohistochemistry showed decorin staining in the airway and vessel walls of Dcn+/+ but not Dcn-/- mice; Western blots showed that biglycan levels were not different in the Dcn-/- mice. These data support a critical role for decorin in the formation of the lung collagen network. Lack of decorin alters lung tissue mechanical behaviour. Additionally, the data from Dcn+/+ mice were compared to those from other species, and is consistent with the evidence in the literature that mouse lungs differ structurally from other species. Finally, differences observed in vivo vs. in vitro suggest that measurements made in the strip more accurately reflect lung tissue properties.
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何存邦 and Tsun-bond Horace Ho. "Aldose reductase deficient mice develop nephrogenic diabetesinsipidus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31222663.

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Gobbett, Troy A. "Characterization of phosphofructokinase-M gene expression in preimplantation mouse embryos through the use of competitive reverse transcription-polymerase chain reaction." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1133725.

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The preimplantation mouse embryo undergoes many metabolic changes as development proceeds. One major change is the switch from a pyruvate based metabolism, to a glucose based metabolism. The phosphofructokinase enzyme is the regulatory enzyme of glycolysis and is thought to be a major contributor in controlling the block to glycolysis in early preimplantation mouse embryos. This study was undertaken to construct a system that would allow detection of RNA for the highly glycolytically active subunit (muscletype) of the phosphofructokinase (PFK) enzyme. A muscle specific mutant PFK plasmid was generated to provide mutant internal control RNA. Using this internal control, initial reverse transcriptionpolymerase chain reaction data collected from early embryo stages suggest that the muscle type PFK subunit RNA is not expressed in the preimplantation mouse at the 1-cell or blastocyst stages. This result suggests that PFK activity detected at the later morula and blastocyst stages must be from either a different PFK subunit or a novel embryonic form of PFK.
Department of Biology
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Martin, Emily P. "Expression of glutamate dehydrogenase and glutamine synthetase RNA in preimplantation mouse embryos." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1117849.

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Glutamine serves as a major energy source for all stages of preimplantation mouse embryo development, whether the embryos are raised in vivo or in vitro from the one-cell stage. Glutamate dehydrogenase (GDH) and glutamine synthetase (GS) are enzymes that are involved in the metabolism of glutamine. GDH catalyzes the conversion of glutamate into a-ketoglutarate, a primary component of the tricarboxylic acid cycle. GS catalyzes the conversion of glutamate to glutamine. The expression of GDH RNA and GS RNA were analyzed in preimplantation mouse embryos using reverse transcription (RT) with an oligo dT primer followed by Polymerase Chain Reaction (PCR) amplification of GDH and GS cDNAs using gene specific primers. Data show that GDH RNA is expressed in mouse embryos grown in vivo at the one-cell, two-cell, eight-cell, and blastocyst stages of development. GS RNA is not expressed at the one-cell stage, but first appears at the two-cell stage and is expressed at the eight-cell and blastocyst stages. Semiquantitative PCR analysis using a globin internal standard demonstrated that GS RNA is present at high levels at the two-cell stage and declines by 51 % by the blastocyst stage. These results suggest that, within the preimplantation mouse embryo, GDH RNA is expressed by both the maternal genome as well as the embryonic genome, while GS RNA is only expressed by the embryonic genome. This study provides an explanation for why glutamine is utilized as an energy source during preimplantation development, which allows for a better understanding of glutamine metabolism and its role during early mouse development.
Department of Biology
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Waclaw, Ronald Raymond. "Expression of cell cycle regulatory proteins cyclin B1, cyclin E, and cdk2 during the first three cell cycles of preimplantation mouse embryo development using indirect immunofluorescence." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1125042.

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The cell cycle is a highly regulated process driven by endogenous factors that have regulatory functions. Certain proteins such as cyclins and cyclin-dependent kinases (cdks) are needed to progress through the four phases of the cell cycle. Cell cycle regulatory proteins have been characterized in somatic cells and exhibit phase specific expression patterns. However, the changes in expression of these proteins have not been characterized in early cleavage stage mouse embryos. This study utilized indirect immunofluorescence microscopy to determine the expression pattern of cell cycle regulators cyclin B 1, cyclin E, and CDK2 during the first three cell cycles of preimplantation mouse embryo development. Results suggest unique and specific patterns of expression for all three cell cycle regulators at different stages of the cell cycle. In G1 of the first cell cycle, cyclin E is expressed at high levels, whereas cyclin B 1 and CDK2 are expressed at moderate levels. During DNA synthesis (S phase), CDK2 levels slightly increase. However, cyclin B 1 and cyclin E levels begin to decline in S and continue to decrease to minimal levels in G2. CDK2 expression follows a similar trend during G2, decreasing considerably. During the second cell cycle, cyclin B 1 and CDK2 show staining patterns similar to the first cell cycle. The expression of cyclin E is maintained at a moderate level throughout the entire second cell cycle. Cyclin B 1, cyclin E, and CDK2 are all expressed at moderate levels during GI of the third cell cycle. During S phase, cyclin B 1 and CDK2 are maintained at moderate levels, but cyclin E is decreased to minimal levels. The expression of all three proteins was minimal during G2. This study provides baseline information on the unique expression patterns of cell cycle regulators in early mouse embryos. The determination of cell cycle protein expression will allow for a better understanding of the complex mechanisms in the division process during preimplantation mouse embryo development.
Department of Biology
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Danilovich, Natalia. "Ovarian development and function in follitropin receptor knockout (FORKO) mice." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37647.

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This dissertation examines the ovarian development and function in genetically modified mice that lack FSH receptor (FSH-R) signaling. We propose that a complete or partial loss of FSH-R causes ovarian insufficiency resulting in estrogen deficiency and premature aging in female mice.
Targeted disruption of FSH-R caused a gene dose related endocrine and gametogenic abnormality in female mice. The resulting FOllitropin R&barbelow;eceptor K&barbelow;nockO&barbelow;ut (FORKO) mutants were acyclic and infertile due to ovulatory defects, even with very high levels of FSH. Lack of FSH-R signaling in females caused a severe ovarian underdevelopment, producing estrogen deficiency. As a consequence, the null mutants developed obesity and skeletal abnormalities. The expression of nuclear estrogen receptor(s) alpha and beta genes and the corresponding proteins in the ovary and uterus of FORKO mice were maintained intact, as estrogen administration induced uterine growth and decreased accumulation of the adipose tissue. By 12 months of age, 92% of FORKO animals developed ovarian neoplasms of sex cord-stromal type similar to pathology observed in women. Our results showed, for the first time, that the loss of the FSH-R signaling mechanisms predisposes the ovary to molecular and structural changes causing tumor formation.
In contrast to acyclic and infertile FORKO (-/-) females, a phenotype of FORKO mice with a partial (+/-) disruption of the receptor gene exhibits irregular cyclicity and reduced fertility, undergoing early reproductive senescence. Our findings also demonstrate that the loss of a single allele of the FSH receptor gene causes a premature exhaustion of gonadal reserves accompanied by age-related changes in the hypothalamic-pituitary axis.
The study concludes that the FSH receptor signaling offers a protective mechanism, which gradually weakens upon reproductive senescence (menopause in women); therefore this knockout constitutes a unique and promising animal model for studying the physiology and molecular mechanisms of gonadal receptors and hormones.
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Johnson, Marjorie Isabelle. "Alterations in fast and slow-twitch muscles of genetically dystrophic mice with special reference to parvalbumin." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/27358.

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Muscular dystrophy is a genetic disease which affects the morphology, physiology and biochemical nature of the muscle fiber. This study was designed to examine the progressive effects of muscular dystrophy on the differentiation process of skeletal muscle. Chapter 1 examines the neonatal development of muscle spindles and their intrafusal fibers in the soleus and extensor digitorum longus (EDL) of genetically dystrophic mice according to histochemical, quantitative, and ultrastructural parameters. Despite alterations in the surrounding extrafusal fibers, muscle spindles and their intrafusal fibers appeared enzymatically and histologically unaffected in incipient stages of murine dystrophy. In the second chapter the distribution and concentration of parvalbumin (PV), a calcium-binding protein, in 32 and 2-week-old dystrophic mice was mapped by immunohistochemical and biochemical procedures. The number of parvalbumin-immunoreactive fibers was significantly reduced in the adult dystrophic EDL but slightly increased in the adult dystrophic soleus. No differences between strains were observed in the 2-week samples. These findings were supported by routine myosin ATPase histochemistry. Parvalbumin was isolated on SDS-PAGE gels and the concentration of PV was estimated by a RIA. These results confirmed the immunohistochemical data in that PV content was dramatically reduced in the adult dystrophic EDL and significantly increased in the dystrophic soleus. No changes were detected in the samples of the 2-week-old muscles. The similarity in the distribution and content of PV between the fast and slow dystrophic muscles at 32 weeks of age suggests an alteration in the distribution and phenotypic expression of fiber types in muscular dystrophy and supports the hypothesis that dystrophy alters the normal differentiation process of skeletal muscle.
Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
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許芝盛 and Chi-shing Hui. "The acute and subchronic toxic effects of dichloroacetonitrile inmice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31970205.

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Siu, Kwan-yin, and 蕭君言. "The development and characterization of a knockout model for secretin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40887674.

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Books on the topic "Mice – Physiology"

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Immunology of nude mice. Boca Raton, Fla: CRC Press, 1989.

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D, Hoit Brian, and Walsh Richard A. 1946-, eds. Cardiovascular physiology in the genetically engineered mouse. Norwell, MA: Kluwer Academic Publishers, 1998.

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Janet, Rossant, and Tam Patrick P. L, eds. Mouse development: Patterning, morphogenesis, and organogenesis. San Diego: Academic Press, 2002.

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Dewar, A. D. The physiology of the extra-uterine and other weight changes of pregnancy: Studies in the laboratory mouse. Edinburgh: Durham Academic Press, 2001.

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Rola jąder nadskrzyżowaniowych (SCN) w regulacji okołodobowej rytmiki aktywności lokomotorycznej myszy: Wpływ czynników farmakologicznych i uszkodzeń SCN. Kraków: Wydawn. Uniwersytetu Jagiellońskiego, 1997.

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Lamoreux, M. Lynn. The colors of mice: A model genetic network. Chichester, West Sussex: Wiley-Blackwell, 2010.

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

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Lynn, Lamoreux M., ed. The colors of mice: A model genetic network. Chichester, West Sussex: Wiley-Blackwell, 2010.

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McGarry, Michael P. Mouse hematology: A laboratory manual. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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McGarry, Michael P. Mouse hematology: A laboratory manual. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2010.

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Book chapters on the topic "Mice – Physiology"

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Bullard, Daniel C. "Knockout Mice in Inflammation Research." In Physiology of Inflammation, 381–401. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4614-7512-5_18.

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Ma, Tonghui, and Alan S. Verkman. "Gastrointestinal Phenotype of Aquaporin Knockout Mice." In Molecular Biology and Physiology of Water and Solute Transport, 151–57. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-1203-5_21.

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Garcia, Kristen, Marcus Hock, Vikrant Jaltare, Can Uysalel, Kimberly J. McCabe, Abigail Teitgen, and Daniela Valdez-Jasso. "Investigating the Multiscale Impact of Deoxyadenosine Triphosphate (dATP) on Pulmonary Arterial Hypertension (PAH) Induced Heart Failure." In Computational Physiology, 77–90. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-05164-7_7.

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Abstract2-deoxy-ATP (dATP) is a myosin activator known to improve cardiac contractile force [1]. In vitro studies have shown that dATP alters the calcium transient profile in addition to the kinetics of the cross-bridge cycle [2]. Furthermore, in vivo studies of transgenic mice with increased production of dATP show elevated left ventricular systolic function [3]. Pulmonary arterial hypertension (PAH) is a rare disease of the pulmonary vasculature in which pressure overload in the right ventricle results in reduced contractile function and right heart failure [4]. We hypothesize that dATP may have a therapeutic effect on PAH-induced heart failure, by improving contractile function and restoring cardiac output and ejection fraction. However, because the effects of dATP cannot easily be assessed experimentally, we propose using a computational multiscale modeling approach to predict cardiac function. By altering parameters in an existing multiscale biventricular cardiac model [5], we were able to reproduce end-systolic and end-diastolic pressures and volumes that reflect the PAH condition, as well as healthy hearts. dATP was simulated by adjusting parameters in the model at the molecular and cellular levels based on experimental data [1], allowing us to predict the effects of dATP on PAH at the organ level. Our results show that the molecular effects of dATP can increase cardiac output and restore ejection fraction in PAH conditions, though at the cost of elevated mean arterial pressure, and may provide a new approach to treating this disease. Our multiscale modeling approach paves the way for further studies mapping out cardiovascular mechanics. As novel therapeutics continue to be discovered, their application and mechanism can be further explored through these computational models.
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Vatner, Stephen F., Gen Takagi, Kuniya Asai, and Richard P. Shannon. "Cardiovascular Physiology in Mice: Conscious Measurements and Effects of Anesthesia." In Developments in Cardiovascular Medicine, 257–75. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1653-8_17.

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Masuda, Tsuyoshi, Kazuhiro Ohmi, Hideki Yamaguchi, Kazuhide Hasegawa, Tomoyasu Sugiyama, Yuzuru Matsuda, Masamitsu Lino, and Yoshiaki Nonomura. "Growing and differentiating characterization of aortic smooth muscle cell line, p53LMAC01 obtained from p53 knock out mice." In Muscle Physiology and Biochemistry, 99–104. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5543-8_13.

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Sipe, J. D., R. Neta, P. Ghezzi, and R. Numerof. "The Physiology of the Acute Phase Serum Amyloid a (SAA) Response in Mice." In Amyloid and Amyloidosis 1990, 71–74. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3284-8_18.

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Burges, Mark E., and Cynthia R. Bishop. "Reproductive Physiology, Normal Neonatology, and Neonatal Disorders of the Small Rodents (Hamsters/Gerbils/Rats/Mice)." In Management of Pregnant and Neonatal Dogs, Cats, and Exotic Pets, 259–72. Chichester, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118997215.ch15.

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Georg, Jutta. "Das Dionysische: Physiologie des Rausches." In »Hat man mich verstanden?«, 99–105. Stuttgart: J.B. Metzler, 2018. http://dx.doi.org/10.1007/978-3-476-04614-7_12.

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Borst, Jannie, Lex Bakker, and Ferry Ossendorp. "γδ T Lymphocytes in Mice and Man: A Review." In Basic Mechanisms of Physiologic and Aberrant Lymphoproliferation in the Skin, 1–16. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1861-7_1.

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Prevot, Vincent. "Puberty in Mice and Rats." In Knobil and Neill's Physiology of Reproduction, 1395–439. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-397175-3.00030-2.

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Conference papers on the topic "Mice – Physiology"

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Rofiqoh, Husnur, Kristanti Wanito Wigati, and Suhartati. "Effect of Exercise on Learning Capability and Memory of Mice (Mus Musculus) Exposed to Monosodium Glutamate (MSG)." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007334801590164.

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Surya Noviyanti, Dini, Bambang Purwanto, and Choesnan Effendi. "Uphill 10° Inclination Angle of Treadmill Concentric Exercises Improves Blood Glucose Levels and Glut-4 Levels in Diabetes Mice Model." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007332700560061.

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Agus Vieya Putri, Daeng, Gadis Meinar Sari, and Tjitra Wardani. "Antioxidant Effect of Dayak Onion Extract (Eleutherine Americana Merr.) on Serum MDA Levels in Mice (Mus Musculus) Exposed by Lead Acetate." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007332300370039.

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Liang, Yun, Keith M. Stantz, Ganapathy Krishnamurthi, Laigao Chen, and Gary D. Hutchins. "Investigation of Contrast-Enhanced In-Vivo Animal Imaging With Micro-CT." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33053.

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Rapid progress in molecular biology, much sparked by the human Genome Project, is opening a new era in medicine and biology. The development of in-vivo micro-imaging technology for small animals (mice and rats) has generated unprecedented opportunities for studying the structural and physiologic properties exhibited by different genes in a cost-effective and low-risk means. This knowledge, in turn, will help guide the study in human genetic system. Micro-computed tomograph (microCT) with resolution on the scale of micrometer is a new technique for obtaining the 3D images of the internal structure of small objects [1,2]. Its biological and medical applications include noninvasively screening animals for genetic mutations and identification as well as monitoring of structural and physiology properties that are linked with specific genes. This paper reports on our preliminary investigation on two aspects of this new imaging technique: (1) an initial experience of instrumentation capability and limitation, and (2) the contrast enhancement strategy necessary for organ-specific anatomic and physiologic studies.
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Milivojević, Nevena, David Caballero, Mariana Carvalho, Marko Živanović, Nenad Filipovic, Rui Reis, and Joaquim Oliveira. "ENGINEERING A MICROFLUDIC PLATFORM AS A PRE-CLINICAL MODEL FOR BIOMEDICAL APPLICATIONS." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.259m.

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Further technological advances are in great need for improving our understanding about critical biological and fundamental pathological processes, such as tissue development and cancer progression, or for the discovery and screening of novel pharmacological drugs. Preclinical experimentation demands for highly reliable and physiologically-relevant systems capable of recapitulating the complex human physiology. Traditional in vitro models, albeit widely employed, fail to reproduce the complexity of the native scenario with cells displaying aberrant gene expressions. Similarly, in vivo animal models, such as mice, poorly mimic the human condition and are ethically questionable. During the last decades, a new paradigm in preclinical modelling has emerged aiming to solve the limitations of the aforementioned methods. The combination of advanced tissue engineering, nanotechnology, and cell biology has resulted in the development of cutting-edge microfluidics-based models with an unprecedented ability to recreate within a microfluidic device the native habitat of cells within a microengineered chip. A diverse variety of micro- and bio-fabrication techniques is available for the development of microfluidic devices. Among all them, UV-photolithography and soft lithography is the considered the gold-standard method for the fabrication of chips due to its simplicity, versatility, and rapid prototyping. In this work, we describe the step-by-step fabrication procedure of a microfluidic chip by UV-photolithography and replica molding and discuss about their potential applications in the biomedical field.
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Van der Heiden, K., H. C. Groen, P. C. Evans, L. Speelman, F. Gijsen, M. de Jong, A. F. W. van der Steen, and J. J. Wentzel. "Non-Invasive Molecular Imaging of Shear Stress-Induced Endothelial Activation and Atherosclerotic Plaque Vulnerability." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80515.

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Atherosclerosis is a lipid- and inflammation driven disease of the larger arteries and is found at specific locations in the arterial tree, i.e. at branches and bends where endothelial cells are exposed to low and low, oscillatory shear stress. Shear stress, the frictional force acting on the endothelial cells as a result of the blood flow, affects endothelial physiology. It determines the location of atherosclerotic lesion development as low and low, oscillatory shear stress induce pro-inflammatory transcription factors but reduce expression and/or activity of anti-inflammatory transcription factors in endothelial cells, rendering the vascular wall vulnerable for inflammation. Consequently, in the presence of atherosclerotic risk factors, such as hypercholesterolemia and diabetes, atherosclerotic lesion development can occur. Although the relationship between low and low, oscillatory shear stress and the prevalence of atherosclerosis has been recognized for several decades, insight into the mechanisms underlying this relationship is still incomplete. The correlation between shear stress and endothelial inflammation was demonstrated by in vitro experiments, in which cultured endothelial cells were exposed to specific flow profiles, and confirmed in vivo by gene expression pattern studies at atherosclerosis-susceptible sites. However, the relationship was not substantiated by direct causal in vivo evidence. Therefore, we developed a method to change the local shear stress field in mice in vivo and studied its effect on the endothelial molecular pathways and resulting atherosclerotic plaque formation. Moreover it allowed us to develop non-invasive molecular imaging strategies to detect vulnerable plaques.
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Daly, J., Z. Yang, J. L. Ingram, R. M. Tighe, and L. G. Que. "Physiologic Response to Chronic House Dust Mite Exposure in Mice Is Dependent on Lot Characteristics." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2950.

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Austin, JM, JA Englert, DF Riascos, RD Brown, B. Ith, DC Christiani, MA Perrella, and RM Baron. "Modeling Physiologic Effects of Chronic Endotoxin Exposure in Mice." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2189.

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Krishnamurthi, Ganapathy, Keith M. Stantz, Rosemary Steinmetz, Gary D. Hutchins, and Yun Liang. "Reproducibility of physiologic parameters obtained using functional computed tomography in mice." In Medical Imaging 2004, edited by Amir A. Amini and Armando Manduca. SPIE, 2004. http://dx.doi.org/10.1117/12.536255.

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Kawachi, N., N. Suzui, S. Ishii, S. Ito, N. S. Ishioka, K. Kikuchi, T. Tsukamoto, T. Kusakawa, and F. Fujimaki. "Molecular imaging for plant physiology: Imaging of carbon translocation to sink organs." In 2009 IEEE Nuclear Science Symposium and Medical Imaging Conference (NSS/MIC 2009). IEEE, 2009. http://dx.doi.org/10.1109/nssmic.2009.5402366.

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