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1
Lunde, Robert C. (Robert Charles). "The Country Mouse and the City Mouse." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc501094/.
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The purpose of this play is to dramatize the fable of a city mouse and her cousin in the country, and the differences in their lifestyles. Through visits to each other's respective homes, the mice discover that there is more to life than what their own environment has to offer.
2
Murray, Patricia Ann. "Early mouse development." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366681.
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The five manuscripts presented here concern events that occur during the early stages of mouse development, beginning with differentiation of primitive endoderm and ending with formation of the proamniotic cavity. The main focus of the work has been the role of the basement membrane in early development, with particular reference to its role in the regulation of epiblast and extraembryonic endodermal cell differentiation, parietal endodermal cell migration and programmed cell death (manuscripts 1, 3 and 4). HOW"9ver,the critical role played by the basement membrane in these processes prompted an investigation into the mechanisms regulating the deposition of this specialised extracellular matrix (manuscript 2). Central to all four manuscripts has been the use of an extremely good in vitro model system, the embryoid body. Embryoid bodies are derived from embryonic stem cells of the mouse blastocyst, and their development closely resembles that of the periimplantation embryo. Of particular use, has been the availability of LAMC1-/- ES cells that are unable to express the laminin y1 chain (manuscript 5). This defect renders the cells incapable of assembling a functional laminin type-1 trimer, which is necessary for basement membrane deposition. Hence, embryoid bodies derived from LAMC1-/- ES cells lack basement membranes, allowing the role of the basement membrane in early development to be analysed.
3
Diament, Adam Louis. "A genetic dissection of mouse obesity genes with congenic mouse models /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2004. http://uclibs.org/PID/11984.
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Van, Zant Jeffrey L. Wooten Michael Conrad. "Molecular ecology of Peromyscus polionotus." Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Spring/doctoral/VAN_ZANT_50.pdf.
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Bielohuby, Maximilian. "The mouse adrenal gland." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-76065.
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Beierbach, Elaine. "Lobulation in mouse cerebellum." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ64940.pdf.
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Arnold, Tessa Jean. "The Mouse Magnetic Compass." Thesis, Virginia Tech, 2015. http://hdl.handle.net/10919/53833.
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All five classes of vertebrates use the geomagnetic field for spatial orientation. The geomagnetic field can be used to derive both 'map' and 'compass' information. There is evidence for two different mechanisms used to sense the magnetic field, the radical pair mechanism (RPM) and the magnetite based mechanism (MBM). C57BL/6 laboratory mice can rely on directional information from the magnetic field to position their nests and to solve a water maze task.
The primary objective of this research was to characterize the magnetic compass of C57BL/6 laboratory mice in the plus water maze task. These experiments explored sources of variation in magnetic responses and investigated the underlying magnetic compass orientation mechanism in C57BL/6 mice. The results provide evidence that the mouse magnetic compass is sensitive to low-level radiofrequency fields, consistent with the use of the RPM for magnetic orientation. Surprisingly, the results also suggest that C57BL/6 mice have a polarity sensitive compass, consistent with the use of a MBM for magnetic orientation.
These experiments confirm that mice have a specialized magnetic compass sense. Furthermore, despite the controlled environment in which these laboratory experiments were conducted, a variety of factors can increase the variability in the response. Future experiments are needed to further characterize the mouse magnetic compass, as there is a possibility of a hybrid magnetic response where both magnetoreception mechanisms could be used for spatial orientation.Master of Science
8
Rastogi, Ravi. "POSITION CONCORDANT - HAPTIC MOUSE." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1699.
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Haptic mice, computer mice modified to have a tactile display, have been developed to enable access to computer graphics by individuals who are blind or visually impaired. Although these haptic mice are potentially very helpful and have been frequently used by the research community, there are some fundamental problems with the mouse, limiting its acceptance. In this paper we have identified the problems and have suggested solutions using one haptic mouse, the VT Player. We found that our modified VT Player showed significant improvement both in terms of the odds of obtaining a correct responses and the time to perform the tasks.
9
Bertenyi, Katalin K. A. "The use of transgenic mouse Muta Mouse to study 1,8-dinitropyrene-induced mutagenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0031/MQ27042.pdf.
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10
Clemente, Emily. "Investigation of gene expression patterns in normal juvenile mouse testis and infertile mouse models." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597769.
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This thesis details the use of a series of cDNA libraries corresponding to several testis cell-types derived from juvenile mouse testes to investigate (i) the first wave of spermatogenesis in the wild-type mouse and four germ cell depleted mouse models where mutations have abrogated spermatogenesis at different points in the pathway (ii) mouse mutants with progressive deletions on the Y chromosome that perturb spermiogenesis (the final maturation stages of spermatogenesis). The gene expression patterns generated were validated by extensive comparison to existing data in the literature and the use of real time reverse-transcription PCR and RNA in situ hybridisation (ISH). This analysis permitted (i) the establishment of thousands of gene expression patterns that were associated with the appearance of particular germ cell-types at different stages of the first wave; (ii) the classification of genes into groups associated with spermatogenic stages and somatic or germ cell lineages, this allowing key genes and molecular pathways active at different stages of the spermatogenic pathway to be identified; (iii) the identification from the study of the Yq deleted models, of new genes mapped to the Y chromosome and other candidate genes with a potential role in the infertility phenotypes associated with these Yq deletions. The study has identified differential gene expression of a large number of novel genes active in spermatogenesis. This underlines the potential of such genome based approaches to identify novel genes that will help to provide a better understanding of the genetic networks underlying germ cell development. The value of such a study lies in the scope to unravel causes of infertility and the contribution that this can make to the development of therapies.
11
Alsén, Per. "Immunohistochemical evaluation of antibodies for staining of mouse spinal cord and mouse neuronal cells." Thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-204738.
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Bertenyi, Katalin K. A. (Katalin Kinga Alexandra) Carleton University Dissertation Biology. "The Use of the transgenic mouse MutaTM mouse to study 1,8- dinitropyrene-induced mutagenesis." Ottawa, 1997.
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13
Huo, Yongliang. "Mouse model of Cooley's anemia." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2010r/huo.pdf.
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14
Yamada, Hiroyuki. "Molecular Clocks in Mouse Skin." 京都大学 (Kyoto University), 2010. http://hdl.handle.net/2433/120505.
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15
Widen, Cecilia, and n/a. "Energetics of Mouse Papillary Muscle." Griffith University. School of Physiotherapy and Exercise Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070228.121312.
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The overall aim of this Thesis was to characterise the energetic properties of the mouse papillary muscle as this preparation could become a useful model to study alterations of energetic aspects of cardiac pathologies and heart-focussed genetic changes. Measurements of resting and active metabolism of the papillary muscles were made in vitro using the myothermic technique. In the first study the mechanism underlying impaired contractility of post-ischaemic rat papillary muscle was investigated. The rat preparation is well established and was used to develop protocols and approaches that could later be used as the basis for studies with mouse papillary muscle. The muscles were exposed to simulated ischaemia for 60 min and change in energetics was studied 30 min into the reperfusion phase. The work output was reduced to 66 ± 3% of the pre-ischaemia value and the enthalpy output decreased to 71 ± 3% of pre-ischaemia value. However, there was no change in either initial, 19 ± 3%, or net mechanical efficiency, 9.0 ± 0.9%. These data, in combination with studies of Ca2+ handling, suggests that the reduced work output was caused by attachment of fewer cross-bridges in each twitch, but with no change in work generated by each cross-bridge. The following two studies involved characterisation of the energetics of the mouse papillary muscle and included measurements of resting and active metabolism. The resting metabolic rate varied with muscle size but the mean initial value was tilda 25 mW g-1 and the estimated steady value tilda 5 mW g-1 . The resting metabolic rate declined exponentially with time towards a steady value, with a time constant of 18 ± 2 min. There was no alteration in isometric force output during this time. The magnitude of resting metabolism depended inversely on muscle mass, more than doubled following a change in substrate from glucose to pyruvate and was increased 2.5-fold when the osmolarity of the bathing solution was increased by addition of 300 mM sucrose. Addition of 30 mM BDM affected neither the time course of the decline in metabolic rate nor the eventual steady value. The energy requirements associated with contractile activity were tilda7 mJ g-1 twitch-1 at a contraction frequency of 1 Hz. The enthalpy output was not affected by changing substrate from glucose to pyruvate but did decrease with an increase in temperature. The enthalpy output was partitioned into force-dependent and force-independent components using BDM to selectively inhibit cross-bridge cycling. The force-independent enthalpy output was 18.6 ± 1.9% of the initial enthalpy output. Muscle initial efficiency was &tilda32% and net efficiency tilda 17% when shortening at a realistic velocity. The enthalpy output decreased with increased contraction frequency but was independent of shortening velocity. On the basis of these values, it was calculated that the twitch energetics were consistent with ATP splitting by half the cross-bridges and the pumping of one Ca 2+ into the SR for every three cross-bridge cycles. The lack of influence of shortening velocity on energy cost supports the idea that the amount of energy to be used is determined early in a twitch and is not greatly influenced by events that occur during the contraction. The suitability of the mouse papillary muscle as a model to study ischaemia and reperfusion damage was also assessed. This preparation is excellent for studying muscle specific changes in work and enthalpy output; however, due to the long-term instability and variability amongst preparations, the suitability of this preparation in prolonged experiments remains uncertain.
16
Deconinck, Anne E. "Mouse models of neuromuscular disease." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320277.
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Barber, K. A. "Immunomodulation in the NOD mouse." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596341.
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A CD8+ T cell clone was generated by priming non-diabetic NOD mice with C2, a Kd-binding, 10-mer peptide (WYIPQSLRGV) derived from the large isoform of GAD. This clone (αC2.4) lyses NOD fibroblast targets transfected with a construct encoding human GAD67. This molecule is entirely homologous with mouse and rate GAD67 at the C2 region and as such this observation indicates that C2 is a naturally processed epitope. The object of this project was to investigate the role of the C2 epitope and altered peptide ligand (APL) derivatives in IDDM pathogenesis in the NOD mouse, with the ultimate aim of modifying disease by induction of antigen specific tolerance. Adoptive transfers into neonatal NOD and NOD-scid recipients have shown αC2.4 not to cause disease. Neither do these cells home to the pancreas. Surface marker characterization demonstrated that αC2.4 did not express β7 integrin, a horning receptor thought to play a key role in infiltration of the pancreas by autoreactive cells. However, administration of the C2 peptide was shown to reduce the incidence of spontaneous but not cyclophospamide induced disease, although this effect was dependent on the route of administration. Knowledge of the specificity of the CD8+T cell clone allowed investigation of the nature of T cell recognition of peptide/MHC as a basis for the search for an APL. Three residues of positions 5, 7 and 8 of the C2 peptide were shown to be critical for recognition of peptide/MHC by αC2.4. On the basis of these findings variant peptides were synthesized and screened by antagonistic properties. None was identified with the ability to alter recognition of C2/MHC by αC2.4. Cytokine intervention has been shown to be an important approach for immune modulation in IDDM in the NOD mouse. The aim of this aspect of the project was to use recombinant retroviral vector technology to modify islet specific T cell clones for targeted expression of immunosuppressive cytokines. Transduction of T cells was achieved although the efficiency of this process was limited. This approach may prove useful in altering the local cytokine milieu towards a non-pathogenic Th2 environment.
18
Legge, M. "Determinants in preimplantation mouse development." Thesis, University of Essex, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235442.
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19
Stechman, Michael James. "Genetic mouse models of nephrolithiasis." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/1116/.
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Nephrolithiasis is a common disorder of multifactorial aetiology. Although most patients have a family history, the underlying genetic causes are largely unknown. To identify novel genes for nephrolithiasis, large-scale radiological and biochemical screens of male mice derived from an N-ethyl-N-nitrosourea-mutagenesis (ENU) programme were performed. This identified models for genetic renal calcification (Rcalc1) and genetic hypercalciuria (Hcalc1). Rcalc1, an ENU-induced mutant with renal opacities on X-ray and histological renal papillary calcification, exhibited autosomal dominant transmission with reduced penetrance. Linkage analysis mapped the Rcalc1 locus to a ~1.1-Mbp region on mouse chromosome 17A3.3, a novel calcification locus containing 30 genes. Urine and plasma biochemistry did not identify a biochemical abnormality associated with Rcalc1, but cDNA microarrays identified transcriptional alterations in genes involved in apoptosis and lipid metabolism. Hcalc1, an ENU-mutant with 24-hour urinary calcium 10x normal, renal stones and diffuse renal calcification on histological analysis, was found to be due to a dominant Ser682Pro transient receptor potential subfamily V, member 5 (Trpv5) mutation. Trpv5 is involved in Vitamin D-mediated renal calcium reabsorption. In summary, this work has identified two novel ENU mouse models for autosomal dominant renal calcification which will further contribute to the study of the genetic basis of renal stones.
20
Hong, Karen H. (Karen Hsiao-Ying) 1971. "Mouse modifiers of intestinal tumorigenesis." Thesis, Massachusetts Institute of Technology, 2001. http://hdl.handle.net/1721.1/8585.
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Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Biology, 2001.Includes bibliographical references.
Colorectal cancer involves a series of molecular alterations as a normal cell progresses to malignancy. A large body of evidence points to the mutation of the APC gene as the pivotal event initiating intestinal tumorigenesis. Apdmin, an induced mutation in mouse homologue of APC, was identified several years ago by Moser et al., providing a genetic model system to study this process. We used the Apdmin system to identify additional genes influencing tumorigenesis. One of these genes,. Mom1 (Modifier of Min-1), involves the effect of genetic background on the Apdmin phenotype. On C57BL/6 (B6), the strain on which Apdmin arose, mice develop approximately 100 tumors. However, B6 X AKR Fl hybrids develop five-fold fewer tumors. Mom1 was identified as the major locus controlling this variation and localized to a 15 cM region on distal mouse chromosome 4 by Dietrich et al. To positionally clone Mom1, Gould et al created a B6.Mom1 AKR congenic strain isolating Mom1 from other AKR resistance factors. Separated from other loci, a single copy of Mom1 AKR reduced tumor number by 50% and two copies produced a 70% reduction. We have used recombinant lines derived from B6.Mom1 AKR to mapMom1 to a 4-cM interval containing one candidate gene, the group IIA secretory phospholipase a2 (sPLA2-IIA). Only tumor prone Mom1 strains, such as B6, contain a mutation in sPLA2-IIA abolishing expression. In order to rigorously measure the effect of sPLA2-IIA on the Apdmin tumor phenotype, we have created and analyzed transgenic lines that restore sPLA2-IIA expression. While we conclude that sPLA2-IIA is indeed protective, tumor number is only reduced by approximately 30%, suggesting that sPLA2-IIA is only part of Mom1. Analysis of additional Moml AKR recombinant strains containing and lacking sPLA2-IIA also implicates a separate distal modifier that accounts for the remaining resistance. To further probe how phospholipases impinge on intestinal cancers, we have studied tumorigen-sis in mice lacking group IV cytosolic phospholipase a2 (cPLA2). Crossing ApcMin into this background produces an 83% reduction in tumor number in ApcMin, cPLA2 -/- homozygotes, suggesting that cPLA2 expression promotes tumorigenesis, most likely via the production of arachidonic acid for downstream eicosanoid synthesis.
by Karen H. Hong.
Ph.D.
21
Tam, Mandy Chi-Mun. "Genomic analysis of mouse tumorigenesis." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/37454.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2006.Includes bibliographical references.
The availability of the human and mouse genome sequences has spurred a growing interest in analyzing mouse models of human cancer using genomic techniques. Comparative genomic studies on mouse and human tumors can be valuable in two major ways: in validating mouse models and in identifying genes that are common to mouse and human tumorigenesis. Many analytic tools have emerged in recent years for human genome mining. Some of these tools have been translated to the murine versions. The work in this thesis described the application of two new whole-genome analytic techniques to study mouse tumorigensis: Representational Oligonucleotide Microarray Analysis (ROMA) for tumor DNA copy number asessment and single nucleotide polymorphism (SNP) genotyping using the SNaPshotM system (Applied Biosystems) to detect loss of heterozygosity (LOH) in mouse tumors. The murine version of ROMA was tested on DNA from early-stage KrasGJ2D-derived lung cancers and metastatic retinoblastoma in mice with retinal-specific Rb and p130 deletions. We were interested in identifying the additional genetic lesions that got positively selected during tumorigenesis of these mice.
(cont.) Several recurrent chromosomal copy number gains and losses were observed in the DNA of KrasGJ2D-derived lung tumors. In addition, a focal amplification of the murine N-Myc locus was detected in the metastatic retinoblastomas, demonstrating the capability of ROMA to detect copy number changes at a single-gene resolution. For genome-wide allelotyping, a panel of 147 mouse SNPs were individually validated in 129S4/SvJae vs. C57BL/6J strains and were chosen as markers in the genotyping panel. We worked out a multiplex protocol to genotype the SNPs in an efficient manner. Through this protocol, we generated low-density global LOH maps of lung tumors from mice expressing KrasG12D. LOH that spanned entire chromosomes was seen in a subset of the tumors. A loss of the wild-type p53 allele was also observed in some cases.
by Mandy Chi-Mun Tam.
Ph.D.
22
Kelly, Robert George. "Hypervariable minisatellites in mouse DNA." Thesis, University of Leicester, 1990. http://hdl.handle.net/2381/34433.
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Hypervariable minisatellite loci provide highly informative genetic markers in mammalian genomes. Hybridisation probes based on a G-rich core sequence simultaneously detect many minisatellite loci in human DNA, generating individual specific and highly variable DNA fingerprints with a wide range of applications. Human minisatellite probes cross-hybridise to mouse DNA, generating DNA fingerprints as complex and variable as those of man. Inbred strains of mice have strain-specific DNA fingerprints which can be analysed using recombinant inbred strains. Analysis of the BXD recombinant inbred series using human minisatellite probes 33.6 and 33.15 revealed that the cross- hybridising loci show variation in germline stability; one locus in particular, Ms6-hm, detected by probe 33.6, exhibited multiallelism across the BXD strains, and heterozygosity among contemporary C57BL/6J inbred mice. Ms6-hm alleles were cloned from C57BL/6J DNA by cross-hybridisation to probe 33.6; on propagation in E.coli the majority of minisatellite repeat units were lost. DNA sequence analysis revealed that Ms6-hm consists of a homogeneous array of the repeat unit GGGCA which has evolved by amplification from within a member of the MT (mouse transcript) family of interspersed repetitive elements. Ms6-hm is flanked by two additional, diverged, MT elements, and there is further evidence that MT elements may be associated with other unstable regions of the mouse genome. Multiallelism and heterozygosity at Ms6-hm (which maps near brown on chromosome 4) result from a high germline mutation rate to new length alleles (2.5% per gamete). Mice mosaic for cells carrying common non-parental Ms6-hm alleles in somatic tissue, and in some cases also in the germline, provide evidence for additional, early developmental, mutation events at this locus. Such somatic mutant Ms6-hm alleles provide innocuous and informative markers with which to analyse the lineage relationships of cells in early mouse development. In four mosaic mice the fraction of cells containing the non-parental allele has been shown to be indistinguishable in different adult tissues, suggesting that the mutation events preceded the allocation of the somatic lineages, and that the same pool of primitive ectoderm cells contributes equally to all somatic tissues. Under low-stringency hybridisation conditions the minisatellite repeat array of Ms6-hm cross-hybridises to other unstable minisatellite loci in the mouse genome to generate a novel and highly individual specific DNA fingerprint; at least one cross-hybridising locus is also somatically unstable during early mouse development.
23
Wiltschko, Alexander Bame. "The Structure of Mouse Behavior." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493569.
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Complex animal behaviors are likely built from simpler modules, but their systematic identification in mammals remains a significant challenge. Here we use depth imaging to show that three-dimensional (3D) mouse pose dynamics are structured at the sub-second timescale by using a newly developed 3D imaging and machine learning-based automated phenotyping system, which we term Motion Sequencing (MoSeq). Computational modeling of these fast postural dynamics effectively describes mouse behavior as a series of reused and stereotyped modules with defined transition probabilities, which collectively encapsulate the underlying structure of mouse behavior within a given experiment.
By deploying MoSeq in a variety of experimental contexts, we show that it unmasks strategies employed by the brain to generate specific adaptations to changes in the environment, and captures both predicted and previously-hidden phenotypes induced by genetic, neural, and pharmacological manipulations. We directly compare the predictive power of behavioral representations built by MoSeq against traditional measurements of behavior, including speed, length, and allocentric position, and demonstrate MoSeq is able to discriminate between subtle pharmacological manipulations of behavior, while traditional methods are not. This work demonstrates that mouse body language is built from identifiable components and is organized in a predictable fashion; deciphering this language establishes a framework for characterizing the influence of environmental cues, genes, neural activity and pharmacology on behavior.Medical Sciences
24
Watiti, Tom Wanjala. "Vision-based virtual mouse system." To access this resource online via ProQuest Dissertations and Theses @ UTEP, 2009. http://0-proquest.umi.com.lib.utep.edu/login?COPT=REJTPTU0YmImSU5UPTAmVkVSPTI=&clientId=2515.
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25
Widen, Cecilia. "Energetics of Mouse Papillary Muscle." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367649.
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The overall aim of this Thesis was to characterise the energetic properties of the mouse papillary muscle as this preparation could become a useful model to study alterations of energetic aspects of cardiac pathologies and heart-focussed genetic changes. Measurements of resting and active metabolism of the papillary muscles were made in vitro using the myothermic technique. In the first study the mechanism underlying impaired contractility of post-ischaemic rat papillary muscle was investigated. The rat preparation is well established and was used to develop protocols and approaches that could later be used as the basis for studies with mouse papillary muscle. The muscles were exposed to simulated ischaemia for 60 min and change in energetics was studied 30 min into the reperfusion phase. The work output was reduced to 66 ± 3% of the pre-ischaemia value and the enthalpy output decreased to 71 ± 3% of pre-ischaemia value. However, there was no change in either initial, 19 ± 3%, or net mechanical efficiency, 9.0 ± 0.9%. These data, in combination with studies of Ca2+ handling, suggests that the reduced work output was caused by attachment of fewer cross-bridges in each twitch, but with no change in work generated by each cross-bridge. The following two studies involved characterisation of the energetics of the mouse papillary muscle and included measurements of resting and active metabolism. The resting metabolic rate varied with muscle size but the mean initial value was tilda 25 mW g-1 and the estimated steady value tilda 5 mW g-1 . The resting metabolic rate declined exponentially with time towards a steady value, with a time constant of 18 ± 2 min. There was no alteration in isometric force output during this time. The magnitude of resting metabolism depended inversely on muscle mass, more than doubled following a change in substrate from glucose to pyruvate and was increased 2.5-fold when the osmolarity of the bathing solution was increased by addition of 300 mM sucrose. Addition of 30 mM BDM affected neither the time course of the decline in metabolic rate nor the eventual steady value. The energy requirements associated with contractile activity were tilda7 mJ g-1 twitch-1 at a contraction frequency of 1 Hz. The enthalpy output was not affected by changing substrate from glucose to pyruvate but did decrease with an increase in temperature. The enthalpy output was partitioned into force-dependent and force-independent components using BDM to selectively inhibit cross-bridge cycling. The force-independent enthalpy output was 18.6 ± 1.9% of the initial enthalpy output. Muscle initial efficiency was &tilda;32% and net efficiency tilda 17% when shortening at a realistic velocity. The enthalpy output decreased with increased contraction frequency but was independent of shortening velocity. On the basis of these values, it was calculated that the twitch energetics were consistent with ATP splitting by half the cross-bridges and the pumping of one Ca 2+ into the SR for every three cross-bridge cycles. The lack of influence of shortening velocity on energy cost supports the idea that the amount of energy to be used is determined early in a twitch and is not greatly influenced by events that occur during the contraction. The suitability of the mouse papillary muscle as a model to study ischaemia and reperfusion damage was also assessed. This preparation is excellent for studying muscle specific changes in work and enthalpy output; however, due to the long-term instability and variability amongst preparations, the suitability of this preparation in prolonged experiments remains uncertain.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
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au, efilipov@murdoch edu, and Emilija Filipovska-Naumovska. "Development of methods for detection and eradication of mouse parvovirus from a laboratory mouse colony." Murdoch University, 2007. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20070918.145210.
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The mouse parvovirus designated MPV can infect laboratory mice and affect the humoral and cellular immune response of infected mice, reducing their value for biomedical and medical research. The development and maintenance of MPV-free mouse colonies for biomedical research is therefore essential and requires routine monitoring of the infection status of mice, using serological surveillance procedures.
Recent experience in the Animal Resources Centre (ARC), a major supplier of mice to the medical research community in Australia, was that MPV infection was present but was not detectable with the serological tests that were then in routine use.
This thesis reports the development of a polymerase chain reaction (PCR) assay for the detection of the MPV in the ARC mouse colonies, the genetic characteristics of the strain of MPV detected, the development of a recombinant virus protein that provided a suitable antigen for enzyme-linked immunosorbent assay (ELISA) and a Western immunoblot (WIB) assay for the detection of MPV antibodies, and use of these various assays to determine aspects of the epidemiology and pathogenicity of the infection that were critical to the eradication of virus infection and future immunological surveillance to ensure the absence of infection.
The recombinant protein produced as an antigen was a biotinylated fusion protein, a truncated capsid protein of the strain of MPV detected in the ARC, and was produced using the PinpointTM vector and with expression in Escherichia coli. The protein was produced as an insoluble intracellular product within inclusion bodies and was solubilised using urea and purified. The purified protein was utilised as an antigen for ELISA and the WIB assays to detect virus antibody in infected mice.
The outbreak of MPV infection in the ARC was used as an unique opportunity for assessment of the seroprevalence of MPV-1 infection in a large laboratory mouse colony and to utilise this data to determine the sampling size needed to reliably detect MPV-1 infection within such large laboratory mouse colonies. An overall seroprevalence of 16.5% was detected using the developed serological tests, but considerable variation in prevalence was detected in different mouse strains.
The response to MPV infection of 4 different but common strains of mice was determined as a basis for developing appropriate surveillance procedures and the selection of appropriate sentinel animals. The effect of infection of these strains at different ages was also investigated. Virus replication was detected in tissues of all the mice strains infected (outbred ARC(s) and inbred C57BL/6JArc, BALB/c and BALB/c-Foxn1nu/Arc) as juveniles and adults, with the exception of C57BL/6JArc inoculated as adults. However, while seroconversion in mice inoculated as juveniles and adults was detected in ARC(s) and C57BL/6JArc mice, it was not detected in BALB/c mice. The high rate of seroconversion to MPV, the early and prolonged development of an immune response, and the lack of age differences in their susceptibility indicated that ARC(s) mice would provide reliable sentinels for the detection of MPV.
The genomic nucleotide sequence of the ARC strain, excluding the terminal palindromic regions and the predicted amino acid sequences of the non-structural and structural proteins was determined. This strain was very similar (98-99% nucleotide identity) to the previously described MPV strains MPV-1a, MPV-1b and MPV -1c. The similarity suggested there were unlikely to be significant antigenic differences in the proteins of the ARC strain and those strains of MPV reported previously.
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Helstrom, Brian S. "Mouse methods of rotation in a two-dimensional space, comparisons using a two-ball mouse." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq35893.pdf.
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陳醒覺 and Sing-kwok Chan. "Mouse preproendothelin-1 gene: transgenic mouse models to study tissue-specific and developmental expression andregulation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31236571.
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Filipovska-Naumovska, Emilija. "Development of methods for detection and eradication of mouse parvovirus from a laboratory mouse colony." Thesis, Filipovska-Naumovska, Emilija (2007) Development of methods for detection and eradication of mouse parvovirus from a laboratory mouse colony. PhD thesis, Murdoch University, 2007. https://researchrepository.murdoch.edu.au/id/eprint/676/.
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The mouse parvovirus designated MPV can infect laboratory mice and affect the humoral and cellular immune response of infected mice, reducing their value for biomedical and medical research. The development and maintenance of MPV-free mouse colonies for biomedical research is therefore essential and requires routine monitoring of the infection status of mice, using serological surveillance procedures.
Recent experience in the Animal Resources Centre (ARC), a major supplier of mice to the medical research community in Australia, was that MPV infection was present but was not detectable with the serological tests that were then in routine use.
This thesis reports the development of a polymerase chain reaction (PCR) assay for the detection of the MPV in the ARC mouse colonies, the genetic characteristics of the strain of MPV detected, the development of a recombinant virus protein that provided a suitable antigen for enzyme-linked immunosorbent assay (ELISA) and a Western immunoblot (WIB) assay for the detection of MPV antibodies, and use of these various assays to determine aspects of the epidemiology and pathogenicity of the infection that were critical to the eradication of virus infection and future immunological surveillance to ensure the absence of infection.
The recombinant protein produced as an antigen was a biotinylated fusion protein, a truncated capsid protein of the strain of MPV detected in the ARC, and was produced using the PinpointTM vector and with expression in Escherichia coli. The protein was produced as an insoluble intracellular product within inclusion bodies and was solubilised using urea and purified. The purified protein was utilised as an antigen for ELISA and the WIB assays to detect virus antibody in infected mice.
The outbreak of MPV infection in the ARC was used as an unique opportunity for assessment of the seroprevalence of MPV-1 infection in a large laboratory mouse colony and to utilise this data to determine the sampling size needed to reliably detect MPV-1 infection within such large laboratory mouse colonies. An overall seroprevalence of 16.5% was detected using the developed serological tests, but considerable variation in prevalence was detected in different mouse strains.
The response to MPV infection of 4 different but common strains of mice was determined as a basis for developing appropriate surveillance procedures and the selection of appropriate sentinel animals. The effect of infection of these strains at different ages was also investigated. Virus replication was detected in tissues of all the mice strains infected (outbred ARC(s) and inbred C57BL/6JArc, BALB/c and BALB/c-Foxn1nu/Arc) as juveniles and adults, with the exception of C57BL/6JArc inoculated as adults. However, while seroconversion in mice inoculated as juveniles and adults was detected in ARC(s) and C57BL/6JArc mice, it was not detected in BALB/c mice. The high rate of seroconversion to MPV, the early and prolonged development of an immune response, and the lack of age differences in their susceptibility indicated that ARC(s) mice would provide reliable sentinels for the detection of MPV.
The genomic nucleotide sequence of the ARC strain, excluding the terminal palindromic regions and the predicted amino acid sequences of the non-structural and structural proteins was determined. This strain was very similar (98-99% nucleotide identity) to the previously described MPV strains MPV-1a, MPV-1b and MPV -1c. The similarity suggested there were unlikely to be significant antigenic differences in the proteins of the ARC strain and those strains of MPV reported previously.
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Filipovska-Naumovska, Emilija. "Development of methods for detection and eradication of mouse parvovirus from a laboratory mouse colony." Filipovska-Naumovska, Emilija (2007) Development of methods for detection and eradication of mouse parvovirus from a laboratory mouse colony. PhD thesis, Murdoch University, 2007. http://researchrepository.murdoch.edu.au/676/.
Full textAbstract:
The mouse parvovirus designated MPV can infect laboratory mice and affect the humoral and cellular immune response of infected mice, reducing their value for biomedical and medical research. The development and maintenance of MPV-free mouse colonies for biomedical research is therefore essential and requires routine monitoring of the infection status of mice, using serological surveillance procedures.
Recent experience in the Animal Resources Centre (ARC), a major supplier of mice to the medical research community in Australia, was that MPV infection was present but was not detectable with the serological tests that were then in routine use.
This thesis reports the development of a polymerase chain reaction (PCR) assay for the detection of the MPV in the ARC mouse colonies, the genetic characteristics of the strain of MPV detected, the development of a recombinant virus protein that provided a suitable antigen for enzyme-linked immunosorbent assay (ELISA) and a Western immunoblot (WIB) assay for the detection of MPV antibodies, and use of these various assays to determine aspects of the epidemiology and pathogenicity of the infection that were critical to the eradication of virus infection and future immunological surveillance to ensure the absence of infection.
The recombinant protein produced as an antigen was a biotinylated fusion protein, a truncated capsid protein of the strain of MPV detected in the ARC, and was produced using the PinpointTM vector and with expression in Escherichia coli. The protein was produced as an insoluble intracellular product within inclusion bodies and was solubilised using urea and purified. The purified protein was utilised as an antigen for ELISA and the WIB assays to detect virus antibody in infected mice.
The outbreak of MPV infection in the ARC was used as an unique opportunity for assessment of the seroprevalence of MPV-1 infection in a large laboratory mouse colony and to utilise this data to determine the sampling size needed to reliably detect MPV-1 infection within such large laboratory mouse colonies. An overall seroprevalence of 16.5% was detected using the developed serological tests, but considerable variation in prevalence was detected in different mouse strains.
The response to MPV infection of 4 different but common strains of mice was determined as a basis for developing appropriate surveillance procedures and the selection of appropriate sentinel animals. The effect of infection of these strains at different ages was also investigated. Virus replication was detected in tissues of all the mice strains infected (outbred ARC(s) and inbred C57BL/6JArc, BALB/c and BALB/c-Foxn1nu/Arc) as juveniles and adults, with the exception of C57BL/6JArc inoculated as adults. However, while seroconversion in mice inoculated as juveniles and adults was detected in ARC(s) and C57BL/6JArc mice, it was not detected in BALB/c mice. The high rate of seroconversion to MPV, the early and prolonged development of an immune response, and the lack of age differences in their susceptibility indicated that ARC(s) mice would provide reliable sentinels for the detection of MPV.
The genomic nucleotide sequence of the ARC strain, excluding the terminal palindromic regions and the predicted amino acid sequences of the non-structural and structural proteins was determined. This strain was very similar (98-99% nucleotide identity) to the previously described MPV strains MPV-1a, MPV-1b and MPV -1c. The similarity suggested there were unlikely to be significant antigenic differences in the proteins of the ARC strain and those strains of MPV reported previously.
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Kim, Na-Hyun. "Introducing Deache mouse : An alternative computer mouse design for people with fine motor skill impairments." Thesis, Umeå universitet, Institutionen för informatik, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-160907.
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Ruotsalainen, H. (Heli). "Lysyl hydroxylases:characterization of mouse lysyl hydroxylases and generation of genetically modified lysyl hydroxylase 3 mouse lines." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514277392.
Full textAbstract:
Abstract
Lysyl hydroxylase (EC 1.14.11.4, procollagen-lysine, 2-oxyglutarate, 5-dioxygenase, Plod) catalyzes the hydroxylation of certain lysine residues in collagens and in other proteins with collagenous domains. Three lysyl hydroxylase isoforms have been cloned from human and rat. The importance of lysyl hydroxylase 1 in collagen biosynthesis is demonstrated by the heritable disorder, Ehlers-Danlos syndrome type VI, which is characterized by joint laxity, progressive scoliosis, muscle hypotonia, scleral fragility and rupture of the ocular globe. An alternatively spliced form of lysyl hydroxylase 2 seems to function as a telopeptide lysyl hydroxylase. Lysyl hydroxylase 3 has three enzyme activities, lysyl hydroxylase, hydroxylysyl galactosyltransferase (EC 2.4.1.50), and galactosylhydroxylysyl glucosyltransferase (EC 2.4.1.66) activities that have been demonstrated earlier with in vitro experiments.
In this thesis study, the cDNAs of mouse lysyl hydroxylase isoforms 1, 2 and 3 were cloned and characterized and the gene structures of lysyl hydroxylase 2, Plod2, and lysyl hydroxylase 3, Plod3, were determined. Mouse lysyl hydroxylase isoforms were found to be highly homologous to the corresponding human isoforms and they were approximately 60% identical with each other. The mouse Plod3 gene has 19 exons as do the human PLOD1 and PLOD3 genes, and mouse Plod2, like the human PLOD2, has 20 exons including one alternatively spliced extra exon. The mouse isoforms were also found to have distinct tissue distributions. Phylogenetic analysis revealed that the lysyl hydroxylase genes have evolved from an ancestral gene through two gene duplication events. Lysyl hydroxylase 3 was demonstrated to be the oldest isoform, which is further supported by the association of glycosyltransferase activities with lysyl hydroxylase 3 and with the only lysyl hydroxylase of Caenorhabditis elegans.
The roles of the different enzyme activities of lysyl hydroxylase 3 were determined in vivo by generating three genetically modified lysyl hydroxylase 3 mouse lines. The analysis of these mouse lines demonstrated that lysyl hydroxylase 3 possesses at least lysyl hydroxylase and glucosyltransferase activities in vivo and it functions as the main, if not the only glucosyltransferase during embryogenesis. The absence of lysyl hydroxylase 3 and, especially, its glucosyltransferase activity results in the abnormal glycosylation of type IV collagen, and thus causes a severe basement membrane defect leading to death during early development. By contrast, lysyl hydroxylase activity had no effect on embryonic development, but caused changes in the structure of the epidermal basement membrane and changes in collagen fibril organization and probably in their interactions.
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Al-Janabi, Tamara. "Making a mouse model for schizophrenia : using the mouse to model the schizophrenia susceptibility gene ZNF804A." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/42404/.
Full textAbstract:
Schizophrenia is a complex disorder, with several genes putatively associated with the pathogenesis of the disorder. A large genome-wide association study (O’Donovan et al. 2008) identified ZNF804A as a candidate gene for schizophrenia (meta-analysis p = 1.61 x 10-7). The association of the gene with schizophrenia (and bipolar disorder) has since been successfully replicated several times, confirming the association (Riley et al., 2010; Steinberg et al., 2010; Zhang et al., 2010, Williams et al., 2011). The aim of this thesis is to create and provide preliminary assessments of a mouse model of the murine form of ZNF804A, Zfp804a. A mutagenised DNA archive derived from mice treated with N-ethyl-N-nitrosourea (ENU) held at the MRC Mammalian Genetics Unit, Harwell, was screened for mutations in Zfp804a. Two mutations (C59X and C417Y) were selected for re-derivation based upon the estimated impact upon the protein. The mutations were backcrossed onto a C57Bl/6J background for three successive generations using a panel of genetic markers to aid selection for the highest level of C57Bl/6J congenicity (and therefore speed up the backcrossing process). G4 mice were tested in the study. Preliminary assessments of the fourth generation intercross cohort revealed, most notably, that the mice breed well, have no gross physical deficits and that male Zfp804aC59X/C59X mutants appeared less anxious than other groups in the elevated plus maze and performed better than other groups on the RotaRod. Initial indications show that Zfp804a may indeed influence behaviour and cognition however further work is necessary to expand upon these findings with larger samples.
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Chan, Sing-kwok. "Mouse preproendothelin-1 gene : transgenic mouse models to study tissue-specific and developmental expression and regulation /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19737002.
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Dolan, Jennifer M. "Thyroid Histology and Reproductive Function in the Prairie Deer Mouse and in the White-Footed Mouse." W&M ScholarWorks, 1990. https://scholarworks.wm.edu/etd/1539625585.
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Gormally, Emmanuelle. "An investigation of the mouse mutant tattered." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267899.
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Yu, Tian. "Role of Gli3 in the developing mouse forebrain." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/4382.
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The mammalian forebrain, which consists of the telencephalon and the diencephalon, is responsible for many higher cognitive functions such as thinking, learning and memory. The cerebral cortex, which is important for language and processing information, is located in the dorsal portion of the telencephalon. The basal ganglia, which are important for movement, are located in the ventral telencephalon. Many genes are involved in patterning and the development of the forebrain. One gene that appears to be crucial for forebrain development is Gli3. Gli3 has been shown to work as both a transcriptional activator and a repressor of the Sonic Hedgehog (Shh) signalling pathway in the developing spinal cord and limb buds. In the telencephalon, Shh has been shown to be important for induction of ventral cell fate, but the exact function of Gli3 in the forebrain and the interactions between Gli3 and Shh are still obscure. Previous studies have shown that Gli3 is required for the formation of the cortical hem area of the telencephalon, which does not form in Gli3Xt/Xt mutant mice lacking functional Gli3. The residual dorsal telencephalon of the Gli3Xt/Xt mutants is partially ‘ventralized’. The main aim of this study was to re-examine the developing forebrain of Gli3Xt/Xt mouse mutants to gain insight into the function of Gli3 during forebrain development. In this thesis, the expression of Gli3 mRNA and protein was examined in the E12.5 and E14.5 wild type telencephalon. The highdorsal-to-lowventral expression pattern of Gli3 corresponds to severedorsal-to-mildventral defects observed in the Gli3Xt/Xt mutants. The ratios between the levels of the cleaved and full length isoforms of Gli3 in dorsal and ventral telencephalon resemble those described in dorsal and ventral spinal cord and in the anterior and posterior limb bud, respectively, suggesting Gli3 in the dorsal telencephalon may act as a repressor of the Shh signalling pathway. The total amount and the ratios of the two isoforms of Gli3 protein were examined in Shh and Foxg1 null mice, which lack ventral telencephalon. The results obtained agree with a role of Gli3 as a repressor of the Shh pathway in the dorsal telencephalon. The forebrains of Gli3Xt/Xt mutants were analysed systematically both anatomically and by molecular markers in this thesis. The border between the telencephalon and the diencephalon was delineated in the Gli3Xt/Xt mutants by using a combination of markers expressed in different areas within the forebrain. This lead to the observation that the previously reported ‘ventralization’ only occurred in the very rostral telencephalic sections of the Gli3Xt/Xt mutant embryos, suggesting a possible shape change of the Gli3Xt/Xt telencephalon. To examine the possible causes of the significant size reduction of Gli3Xt/Xt mutant telencephalon compared to wild type telencephalon from E10.5, cell proliferation and cell death properties studies were undertaken. The changes observed were not sufficient to explain the phenotypic differences between the Gli3Xt/Xt mutant and the wild type embryos indicating that they might be the result of an early patterning defect. The dorsal telencephalon is severely reduced in volume at both E12.5 and E10.5, containing cells from adjacent eminentia thalami, probably due to the loss of the dorso-medial telencephalon. Large clusters of eminentia thalami cells were observed at later developmental stages, when the neocortex becomes highly disorganized, forming rosettes comprising mainly neural progenitors. These results suggest Gli3 is important for the formation of an intact telencephalic-diencephalic boundary and for preventing the abnormal location of diencephalic cells in the dorsal telencephalon. The volume of Gli3Xt/Xt ventral telencephalon was increased compared to that of the wild types at E10.5, but became smaller than that of the wild type littermates at E12.5. This might have been the result of a combination of more cells exiting the cell cycle and increased cell death observed in the Gli3Xt/Xt ventral telencephalon at E10.5, suggesting Gli3 regulates cell differentiation and cell death properties at this age and brain region. The significant expansion of rostro-ventral telencephalon observed in the Gli3Xt/Xt mutant might correlate with the expansion of Fgf8 expression and this hypothesis has been tested in this thesis.
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鈴木, 伸之介. "マウス卵母細胞および初期胚におけるエピジェネティック修飾と発生能に関する研究." Kyoto University, 2015. http://hdl.handle.net/2433/199532.
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Suzuki, Shinnosuke. "Studies on the developmental potential and epigenetic modifications of mouse oocytes and preimplantation embryos." Kyoto University, 2015. http://hdl.handle.net/2433/199350.
Full textAbstract:
Kyoto University (京都大学)0048
新制・課程博士
博士(農学)
甲第19026号
農博第2104号
新制||農||1030(附属図書館)
学位論文||H27||N4908(農学部図書室)
31977
京都大学大学院農学研究科応用生物科学専攻
(主査)教授 今井 裕, 教授 久米 新一, 教授 松井 徹
学位規則第4条第1項該当
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JONES, EVAN FIELDING. "DEVELOPMENT OF THE LASER REMOTE MOUSE." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1085766388.
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Böhm, Bernd R. "Quantitative modelling of mouse limb morphogenesis." Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/31967.
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In this thesis we combine quantitative measurements of mouse limb morphogenesis and computer modelling to test a well established theory about the cellular mechanisms promoting limb elongation. A distally directed gradient of cellular proliferation was believed to be the driving mechanism for limb outgrowth. We find that the empirically measured spatial proliferation pattern fails to promote normal development - a reverse engineering algorithm was applied and revealed a proliferation pattern that could indeed carry out normal development. The differences between those patterns is dramatic and suggests that isotopic cellular proliferation alone has very little impact on limb morphogenesis and other – non isotropic - mechanisms need to be involved.En esta tesis tratamos de testar una bien establecida teor´ıa sobre los mecanismos celulares que promueven de la elongaci´on de las extremidades. Para eso combinamos mediciones cuantitativas del proceso morfogen ´etico de la extremidad del rat´on con modelos computacionales. Se cre´ıa que la fuerza conductora del crecimiento de las extremidades era un gradiente en sentido distal del incremento de la proliferaci´on celular. Descubrimos que el patr´on de proliferaci´on celular basado en medidas emp´ıricas no consegu´ıa promover un desarrollo normal, mientras que un algoritmo de ingenier´ıa inversa aplicado al proceso revel´o un patr´on que si podr´ıa. La diferencia entre estos dos patrones es inmensa y sugiere que la proliferaci´on celular isotropica por si sola tiene muy poco impacto sobre la morfog´enesis de las extremidades, indicando as´ı la necesidad de que otros procesos no isotr´opicos se hallen involucrados.
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Hajkova, Petra. "Epigenetic reprogramming in mouse germ cells." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=970526938.
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Carlson, Anne Elizabeth. "Signaling mechanisms of mouse sperm capacitation /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/10539.
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Chapouton, Prisca. "Regionalization of the developing mouse telencephalon." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-11597.
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Lindsay, Elizabeth Anne. "Photodynamic therapy of a mouse glioma." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46889.
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Palidwor, Gareth A. "Tissue-specific codon usage in mouse." Thesis, University of Ottawa (Canada), 2011. http://hdl.handle.net/10393/28932.
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Codon usage bias is due to a combination of biased mutation and selection effects. Isochore-related GC mutational bias has been shown to be the dominant cause of tissue-specific codon bias in adult human tissues and limited evidence for translational selection has been shown. This thesis is a comprehensive evaluation of the relative contribution of selection and mutation to variation in codon usage among different mouse embryonic tissues.
Through a detailed analysis of tissue-specific codon usage in relation to gene expression and gene location of mouse embryonic tissue-specific genes, I found that translational selection is partially responsible for some differences in codon usage among tissue-specific genes. This observation indicates profound impact of selection favouring codon-anticodon adaptation. The characteristic GC biases of tissue-specific gene sets are shown not to be caused by their clustering on the same isochore. Tissue-specific genes are no more clustered on the genome than randomly selected genes.
In mouse, the usage of some G-ending codons decreases with increasing GC bias, while all other G and C-ending codons increase. To understand this counterintuitive observation, we generate a continuous-time Markov chain model of GC-biased synonymous substitution which explains qualitative usage patterns of all codons, including non-linear and sometimes non-monotone codon usage in isoleucine, arginine and leucine. This effect is universal, extending to mouse and human genes as well as plant and prokaryotic genomes.
This work enriched our understanding of the codon-anticodon adaptation theory and extended it to the level of tissue-specific genes. The result suggests the possibility of tissue-specific tRNA pools mediating tissue-specific codon-anticodon adaptation. The methods developed in the thesis can be easily extended to characterize this previously little explored facet of codon-anticodon adaptation.
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Elfving, Anna. "Transcriptional regulation of mouse ribonucleotide reductase." Licentiate thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-41272.
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All living organisms are made of cells and they store their hereditary information in the form of double stranded DNA. In all organisms DNA replication and repair is essential for cell division and cell survival. These processes require deoxyribonucleotides (dNTPs), the building blocks of DNA. Ribonucleotide reductase (RNR) is catalyzing the rate limiting step in the de novo synthesis of dNTPs. Active RNR is a heterodimeric protein complex. In S phase cells, the mouse RNR consists of the R1 and the R2 proteins. The R1/R2 RNR-complex supplies the cell with dNTPs required for DNA replication. Outside S-phase or in non-proliferating cells RNR is composed of R1 and p53R2 proteins. The R1/p53R2 RNR-complex supplies cells with dNTPs required for mitochondrial DNA replication and for DNA repair. An undisturbed dNTP regulation is important since unbalanced dNTP pools results in DNA mutations and cell death. Since unbalanced pools are harmful to the cell, RNR activity is regulated at many levels. The aim of this thesis is to study how the mouse RNR genes are regulated at a transcriptional level. We have focused on the promoter regions of all three mouse RNR genes. Primer extension experiments show that the transcription start of the TATA-less p53R2 promoter colocalizes with an earlier unidentified initiator element (Inr-element). This element is similar to the known Inr-element in the mouse R1 promoter. Furthermore, functional studies of the R1 promoter revealed a putative E2F binding element. This result suggests that the S phase specific transcription of the R1 gene is regulated by a similar mechanism as the R2 promoter which contains an E2F binding site. Finally we have established a method to partially purify the transcription factor(s) binding the upstream activating region in the mouse R2 promoter by phosphocellulose chromatography and affinity purification using oligonucleotides immobilized on magnetic beads. This method will allow us to further study the transcription factors responsible for activating expression of the R2 protein. This method has a potential to be utilized as a general method when purifying unknown transcription factors.
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Tyas, David Anthony. "Generation of a Pax6 reporter mouse." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/27562.
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In order to better understand Pax6 function I generated a novel tool – a ‘Pax6 reporter’ transgenic mouse that expresses GFP under the control of Pax6 regulatory elements. The transgenic mouse was generated from a modified yeast artificial chromosome (YAC) that contains the human PAX6 gene and has been previously demonstrated to rescue loss of endogenous Pax6 in Pax6sey/sey mice. The key advantages of a YAC addition transgenic include that it is already known that Pax6 regulatory elements are present over a 200Kb region and inserting a reporter gene into the endogenous Pax6 would not be independent of the endogenous locus. An expression cassette encoding GFP and an IRES-neoR vector were inserted into the YAC in frame with the normal PAX6 translation start point in exon 4, preserving the rest of the PAX6 locus. This put GFP and neomycin under the control of the PAX6 regulatory elements. The modified YAC was then injected into fertilised mouse oocytes to generate nine lines of transgenic mice. Once generated the expression pattern in each line was analysed at a range of developmental stages by imaging appropriate sections of agarose embedded mouse embryos. This confirmed that the expression was the same as the previously reported Pax6 expression pattern. In addition, the copy number and extent of the YAC incorporated in each of the nine lines was investigated.
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Petersson, Johan. "Notch signaling pathways inthe obese mouse." Thesis, Örebro universitet, Institutionen för medicinska vetenskaper, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-66818.
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Qin, Yinghao. "The Smart Phone as a Mouse." The University of Waikato, 2006. http://hdl.handle.net/10289/2289.
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With the development of hardware, mobile phone has become a feature-rich handheld device. Built-in camera and Bluetooth technology are supported in most current mobile phones. A real-time image processing experiment was conducted with a SonyEricsson P910i smartphone and a desktop computer. This thesis describes the design and implementation of a system which uses a mobile phone as a PC mouse. The movement of the mobile phone can be detected by analyzing the images captured by the onboard camera and the mouse cursor in the PC can be controlled by the movement of the phone.