Relevant bibliographies by topics / Inbred rat

Academic literature on the topic 'Inbred rat'

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Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Inbred rat"

1

Thomas, Michael A., Chin-Fu Chen, Michael I. Jensen-Seaman, Peter J. Tonellato, and Simon N. Twigger. "Phylogenetics of rat inbred strains." Mammalian Genome 14, no. 1 (January 1, 2003): 61–64. http://dx.doi.org/10.1007/s00335-002-2204-5.

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Kuramoto, Takashi, Satoshi Nakanishi, and Tadao Serikawa. "Functional polymorphisms in inbred rat strains and their allele frequencies in commercially available outbred stocks." Physiological Genomics 33, no. 2 (April 2008): 205–11. http://dx.doi.org/10.1152/physiolgenomics.00222.2007.

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Polymorphisms that have been proven to influence gene functions are called functional polymorphisms. It is significant to know the distribution of functional polymorphisms in the rat, widely used in animal models for human diseases. In this study, we assessed 16 functional polymorphisms consisting of 3 coat color and 13 disease-associated genes in 136 rat strains, as a part of the genetic profiling program of the National Bio Resource Project for the Rat (NBRP-Rat). Polymorphisms of Cdkn1a, Fcgr3, Grp10, Lss, and Fdft1, which were proven to function in prostate tumorigenesis, glomerulonephritis, hyperphagia, and cholesterol biosynthesis, were shared among various inbred strains. These findings indicated that most rat strains harbored the disease-associated alleles and suggested that many unidentified functional polymorphisms might exist in inbred rat strains. The functional polymorphisms shared in inbred strains were also observed within outbred stocks available commercially. Therefore, this implies that experimental plans based on either rat inbred strains or outbred stocks need to be carefully designed with a full understanding of the genetic characteristics of the animals. To select the most suitable strains for experiments, the NBRP-Rat will periodically improve and update the genetic profiles of rat strains.
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Kren, V., T. W. Kurtz, D. Krenova, V. Bila, M. Printz, and P. Pravenec. "Rat genome mapping using recombinant inbred strains." Transplantation Proceedings 29, no. 3 (May 1997): 1768. http://dx.doi.org/10.1016/s0041-1345(97)00048-1.

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Schlick, Nancy E., Michael I. Jensen-Seaman, Kimberly Orlebeke, Anne E. Kwitek, Howard J. Jacob, and Jozef Lazar. "Sequence analysis of the complete mitochondrial DNA in 10 commonly used inbred rat strains." American Journal of Physiology-Cell Physiology 291, no. 6 (December 2006): C1183—C1192. http://dx.doi.org/10.1152/ajpcell.00234.2006.

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Rat remains a major biomedical model system for common, complex diseases. The rat continues to gain importance as a model system with the completion of its full genomic sequence. Although the genomic sequence has generated much interest, only three complete sequences of the rat mitochondria exist. Therefore, to increase the knowledge of the rat genome, the entire mitochondrial genomes (16,307–16,315 bp) from 10 inbred rat strains (that are standard laboratory models around the world) and 2 wild rat strains were sequenced. We observed a total of 195 polymorphisms, 32 of which created an amino acid change (nonsynonymous substitutions) in 12 of the 13 protein coding genes within the mitochondrial genome. There were 11 single nucleotide polymorphisms within the tRNA genes, six in the 12S rRNA, and 12 in the 16S rRNA including 3 insertions/deletions. We found 14 single nucleotide polymorphisms and 2 insertion/deletion polymorphisms in the D-loop. The inbred rat strains cluster phylogenetically into three distinct groups. The wild rat from Tokyo grouped closely with five inbred strains in the phylogeny, whereas the wild rat from Milwaukee was not closely related to any inbred strain. These data will enable investigators to rapidly assess the potential impact of the mitochondria in these rats on the physiology and the pathophysiology of phenotypes studied in these strains. Moreover, these data provide information that may be useful as new animal models, which result in novel combinations of nuclear and mitochondrial genomes, are developed.
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Pohlová, Irena, Josef Zicha, Vladimir Křen, Jaroslav Kuneš, and Michal Pravenec. "Renal renin activity is associated with alterations of the renin gene in recombinant inbred rat strains." Clinical Science 84, no. 2 (February 1, 1993): 129–32. http://dx.doi.org/10.1042/cs0840129.

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1. A structural alteration within the first intron of the renin gene in spontaneously hypertensive rats was demonstrated to co-segregate with blood pressure in some sets of F2 hybrids or recombinant inbred strains. There is no evidence as to whether restriction fragment length polymorphism of the renin gene is associated with any of the changes in the renin tissue level. For this reason we have determined renal renin activity in spontaneously hypertensive, Wistar-Kyoto and Brown Norway rats as well as in 22 recombinant inbred strains derived from F2 hybrids of spontaneously hypertensive and Brown Norway rats. 2. At the age of 4 months significantly lower renal renin activity was observed in spontaneously hypertensive rats than in both normotensive rat strains, Wistar-Kyoto and Brown Norway. The presence of the spontaneously hypertensive rat allele in recombinant inbred strains was associated with a substantially lower renal renin activity as compared with recombinant inbred strains bearing the Brown Norway rat allele. There was no relationship between renal renin activity and the polymorphism in either the angiotensinogen gene or the angiotensin-converting enzyme gene. 3. There was a borderline correlation between blood pressure and renal renin activity in recombinant inbred strains. Nevertheless, additional comparisons within recombinant inbred strains bearing the spontaneously hypertensive rat allele of the renin gene failed to reveal any significant relationship between blood pressure level and renal renin activity. 4. Our data suggest that the restriction fragment length polymorphism marking the renin gene of the spontaneously hypertensive rat is accompanied by an alteration in the renin-angiotensin system at the renal level. The mechanisms by which structural abnormalities of the renin gene might influence the renin level in the kidney remain to be investigated.
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Bell, R. G. "Variation in responsiveness toTrichinella spiralisinfection in inbred rat strains." Parasitology 105, no. 1 (August 1992): 125–30. http://dx.doi.org/10.1017/s0031182000073777.

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An analysis of interstrain variation between 12 inbred and 4 congenic rat strains in the expression of immunity againstTrichinella spiralisis reported. All rat strains expressed strong rapid expulsion which resulted in the elimination of 88–98% of a challenge infection of muscle larvae. In contrast, substantial interstrain variation in the rate of adult worm expulsion in the primary infection as evident. By day 10 after infection, BUF and YO strains had < 50 worms left in the intestine whereas BI and WKA strain rats had barely begun rejection, with approximately 1000 worms present in the gut for both strains. All other rat strains fell within these extremes in a continuous gradation. There was no clustering of rat strains into phenotypic groups with comparable worm burdens as seen with mice. The number of muscle larvae that established after the primary infection showed less variation than had adult worm burden in the primary infection and there was only a weak correlation of muscle larvae burden with numbers of intestinal adults present at 10 days. Comparison of MHC matched or MHC-disparate rat strains on a PVG background suggested that non-MHC genes determined the principal adult worm rejection characteristics of a given strain. The absence of phenotypic variation in the expression of rapid expulsion in rats reinforces the biological distinction between rat rapid expulsion and the ‘rapid expulsion’ defined for mice
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Woo, Lynn L., Adonis Hijaz, Hui Q. Pan, Mei Kuang, Raymond R. Rackley, and Margot S. Damaser. "Simulated childbirth injuries in an inbred rat strain." Neurourology and Urodynamics 28, no. 4 (April 2009): 356–61. http://dx.doi.org/10.1002/nau.20644.

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Sprott, R. L., and I. Ramirez. "Current Inbred and Hybrid Rat and Mouse Models." ILAR Journal 38, no. 3 (January 1, 1997): 104–9. http://dx.doi.org/10.1093/ilar.38.3.104.

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Leyten, R., J. P. A. M. Vroemen, N. Blanckaert, and K. P. M. Heirwegh. "The congenic normal R/APfd and jaundiced R/APfd-j/j rat strains: a new animal model of hereditary non-haemolytic unconjugated hyperbilirubinaemia due to defective bilirubin conjugation." Laboratory Animals 20, no. 4 (October 1, 1986): 335–42. http://dx.doi.org/10.1258/002367786780808758.

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In this paper the production of the R/APfd-j/j strain which is congenic with the R/APfd strain is reported. The R/APfd-j/j completely lacks hepatic bilirubin UDP-glucuronyltransferase activity, as do our GUNNXR/Pfd-j/j rat strain and various other stocks of GUNN rats (j/j) described in the literature. Our recombinant inbred strain GUNNXR/Pfd-j/j was produced from non-inbred GUNN (j/j) rats. This GUNNXR/Pfd-j/j rat was used as a donor of the jaundice gene j, the R/APfd rat serving as the recipient. After eight backcross-intercross cycles (16 generations) the R/APfd-j/j strain was obtained which is congenic with the R/APfd strain. Congenicity was demonstrated by various techniques including transplantation of skin tissue, strain-specific tumour cells and hepatocytes, the mixed lymphocyte reaction, and comparison of biochemical markers. The potential of the novel inbred strain of jaundiced rat, R/APfd-j/j, and the corresponding control strain R/APfd for biochemical and clinical studies of bilirubin metabolism are briefly discussed.
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Power, D. A., C. Cunningham, and G. R. D. Catto. "The role of RT1 antigen differences in semi-allogeneic rat pregnancy." Clinical Science 72, no. 1 (January 1, 1987): 37–45. http://dx.doi.org/10.1042/cs0720037.

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1. The immunological mechanisms involved in sustaining normal semi-allogeneic pregnancies and in the enhancement of organ allografts were investigated in inbred rats. 2. The antigenic targets for alloantibodies formed after leucocyte transfusions and multiple allogeneic pregnancies were defined by the EA rosette inhibition (EAI) assay in several congenic and recombinant inbred rat strains. 3. Alloantibodies produced by leucocyte immunization (conventionally induced antisera) were directed only to RT1-encoded (major histocompatibility complex, MHC) antigens. Both RT1A (class I MHC) and either RT1B, D (class II MHC) or RT1C (Qa-like) antigens were targets for these alloantibodies; responses to the latter three antigens could not be separated with available congenic recombinant inbred rat strains. 4. Alloantibodies produced as a consequence of multiple semi-allogeneic pregnancies (pregnancy-induced antisera) were directed only to RT1A antigens. 5. Allogeneic pregnancies in which the paternal strain differed from the maternal strain only at the RT1A gene locus produced suppression of a subsequent maternal immune response.
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Dissertations / Theses on the topic "Inbred rat"

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Grieve, Ian C. "Quantitative trait analysis in a panel of recombinant inbred rat strains." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/5617.

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Expression quantitative trait loci (eQTLs) are generated by the combined use of microarray technology to measure gene expression and genetic linkage analysis to map the expression traits to the genome. This thesis describes co-expression and quantitative trait transcript (QTT) analysis carried out on a dataset consisting of thousands of cis- and trans-eQTLs. These were mapped in 29 rat Recombinant Inbred strains derived from a cross between the Spontaneously Hypertensive Rat (SHR), a widely used model of the human metabolic syndrome, and the normotensive Brown Norway (BN). Gene expression data from four tissues relevant to the metabolic syndrome and cardiovascular disease were analysed: fat, kidney, adrenal gland and left ventricle. By systematically applying a rigorous statistical methodology to the eQTL dataset, a consistent, distinct correlation structure was observed. Co-expression of groups of transcripts linked to a common region of the genome, referred to as trans-eQTL clusters, was investigated. Some of these cluster-forming groups were found to remain significantly correlated after the effect of genotype was accounted for, and functionally enriched. An example of successful application of QTT analysis to the dataset is described. This contributed to the identification of Ogn as a regulator of left ventricular mass in rodents and subsequent implication of the homologue of Ogn in a related role in humans. Correlation of a further 103 physiological traits with cis-eQTLs in each of the four tissues was also carried out; analysis which potentially informs a wide range of hypotheses concerning relevant phenotypes. Together, the findings described here demonstrate the utility of a systematic computational approach using correlation-based methodologies in combination with appropriate statistical techniques to inform the genetic analysis of complex traits. These findings indicate the importance of understanding potential confounding factors in eQTL analysis, as well as the potential of the eQTL approach to stimulate gene discovery.
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Ghosh, Sumona. "Effect of exercise training on metabolic intermediate phenotypes in inbred rat strains." Connect to Online Resource-OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1182807006.

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Thesis (M.S.)--University of Toledo, 2007.
"In partial fulfillment of the requirements for the degree of Master of Science in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 59-68.
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Ghosh, Sumona. "Effects of Exercise Training on Metabolic Intermediate Phenotypes in Inbred Rat Strains." University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1182807006.

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Garrett, Michael R. "Genetic dissection of hypertension-related renal disease using the Dahl salt-sensitive rat." Connect to Online Resource-OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1175545256.

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Dissertation (Ph.D.)--University of Toledo, 2006.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 89-95, p. 127-131, p. 184-192, p.198-233.
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Ways, Justin Andrew. "An Inbred Rat Model of Exercise Capacity: The Path to Identifying Alleles Regulating Variation in Treadmill Running Performance and Associated Phenotypes." Connect to full text in OhioLINK ETD Center, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1201562803.

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Dissertation (Ph.D.)--University of Toledo, 2007.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 142-183.
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Baker, K. C. "The absorption from the gut and immunomodulatory effects of the sulphated polygalactan food-additive, carrageenan : Studies in the inbred rat." Thesis, University of Reading, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.371432.

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Bossy, Tanya. "Implication of a novel nerve growth factor (NGF) maturation and degradation cascade in the Fischer-344 rat model of age-associated memory deficits." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111573.

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Despite the overwhelming evidence for atrophy of the NGF-dependant Basal Forebrain Cholinergic neurons during aging, there is no persuasive evidence towards a decrease in NGF and/or NGF mRNA content in the brain of aged animals. Previous experiments from our laboratory have shown that NGF is released as a precursor protein and cleaved into the mature form in the extracellular space under the influence of a complex protease cascade. These recent findings have lead us to propose that any alterations in levels and/or activity of this maturation/degradation cascade might affect NGF's biological activity and perhaps lead to cognitive impairments in a subset of aged rats. To investigate this possibility, we measured protein and mRNA levels of the protease cascade players (NGF, pro-NGF, tPA, plasminogen, plasmin, MMP-9, neuroserpin). We found significantly decreased levels of both pro-NGF protein and NGF mRNA, but no difference in the remaining elements of the protease cascade, when comparing aged impaired (Al) to the aged unimpaired (AU) animals. Our second objective was to investigate whether animals trained in the Morris Water Maze would preserve their cognitive status in two additional behavioral paradigms, the Novel Object Location (NOL, spatial memory) and Novel Object Recognition (NOR, nonspatial memory) tasks. We found that both AU and AI animals in the MWM were impaired in the NOL when compared to the young controls, with the AI animals performing significantly worse than the AU in this particular task. In the NOR tasks, AI animals performed significantly worse compared to both young and AU animals. In conclusion, further experiments are required to better understand the implication of the complex protease cascade involved in NGF's maturation and degradation as well as its effect on memory of aged animals. In addition, because the segregation of animals (aged impaired/unimpaired) is a crucial step in aging research, we now have additional behavioral paradigms (NOL/NOR) that confirm the cognitive status of these animals.
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Todd, Derrick James. "Role of the Intestinal Immune System in the Pathogenesis of Autoimmune Diabetes in the BB Rat Model of Type 1 Diabetes Mellitus." eScholarship@UMMS, 2001. https://escholarship.umassmed.edu/gsbs_diss/138.

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The intestine is the largest lymphoid organ in the body, challenged constantly by an enonnous quantity and diversity of antigens. Distinct from peripheral lymphocytes, intestinal lymphocytes have evolved unique mechanisms of tolerance and appear to govern mucosal processes such as "chronic physiologic inflammation" and oral tolerance. Failure of mucosal tolerance has been implicated in the pathogenesis of several diseases, including inflammatory bowel disease, celiac disease, and even autoimmune diabetes. One population of intestinal lymphocytes, intraepithelial lymphocytes (IELs), exists within the intestinal epithelium itself and remains poorly characterized. IELs respond to unique activation signals and appear to be in part responsible for the maintenance of epithelial integrity and mucosal tolerance. Type 1 diabetes is one of the most common chronic childhood illnesses and causes significant morbidity and mortality. Type 1 diabetes mellitus is an autoimmune disease that results from immune-mediated destruction of insulin-producing pancreatic beta cells and is characterized by an absolute insulin deficiency. Several animal models are used to study the immunopathogenesis of type 1 diabetes, including the BB rat and NOD mouse. BBDP rats spontaneously develop autoimmune diabetes mellitus and are severely deficient in peripheral T cells. BBDR rats do not spontaneously develop autoimmune diabetes, have nonnal numbers of peripheral T cells, and can be induced to become diabetic by injections of a cytotoxic anti-ART2a mAb and low doses of poly I:C. The cause of autoimmune diabetes in BB rats and humans is still unknown, but both genetic and environmental factors appear to participate. I hypothesize that one important class of environmental factors--diet and enteromicrobial agents--participates in this pathogenic process through the mediation of the gut immune system. In this dissertation, I report a new method for the isolation of rat IELs that is based on the selective removal of intestinal epithelial cells under conditions that leave the basement membrane undisturbed. The yield of rat IELs using this method is 5-10 fold greater than that reported for other methods. Morphological and phenotypic analyses demonstrate that the purified cell population is comprised of IELs and is not contaminated with lamina propria or Peyer's patch lymphocytes. Phenotypic analysis reveals 5 major subsets of IELs, including populations of γδ T and natural killer (NK) cells present at levels not previously detected. I also report that rat intraepithelial NK (IENK) and peripheral NK cells are similar in morphology, in their ability to lyse NK-sensitive targets, and in their ability to suppress a one-way mixed lymphocyte culture. In contrast, IENK cells differ from splenic NK cells phenotypically, and a substantial fraction of IENK cells appear to spontaneously secrete IL-4 and/or IFN-γ. I conclude that rat IELs harbor a large population of NKR-P1A+ CD3-cells that function as NK cells but display an activated phenotype and unusual cytokine profile that clearly distinguish them from splenic NK cells. Their phenotypic and functional characteristics suggest that these distinctive intraepithelial NK cells may participate in the regulation of mucosal immunity. I next demonstrate that, prior to diabetes, both BBDP and ART2a-depleted BBDR rats have a reduced total number of IELs and exhibit a selective deficiency of IENK cell number and function as compared to control BBDR rats. The deficiency of BBDP rat IELs can be corrected by engraftment of bone marrow from histocompatible WF donors. These results suggest 1) that the peripheral lymphopenia in BBDP rats extends to the IEL compartment, particularly to IENK cells, 2) that in BBDR rats the diabetes-inducing treatment depletes IELs, particularly IENK cells, and 3) that the defect in BBDP rat IELs is intrinsic to hematopoietic cells, not intestinal stromal cells. I also establish that, unlike BBDR and WF rats, BBDP rats are also deficient in γδTCR+IELs, a population of T cells that may play a role in normal mucosal tolerance. In addition, I report preliminary data supporting the hypothesis that systemic autoreactivity may be initiated in the intestine; peripheral autoreactive lymphocyte populations appear to emanate first from mesenteric lymph nodes that drain the intestine, and such cells may initiate a type 2 autoimmune phenomenon driven by IL-4. Collectively, my findings support the hypothesis that a failure of mucosal tolerance in BBDP rats, perhaps secondary to deficiencies in one or more IEL subpopulations, participates in the pathogenesis of autoimmune diabetes in these animals by activating peripheral autoreactive T cells. The nature of the autoimmune response in BB rats (driven by IL-4) appears to be distinct from that of NOD mice. Despite the differences between these two well-accepted animal models of autoimmune diabetes, until more is known about the pathogenesis of type 1 DM in humans, lessons learned from both the BB rat and NOD mouse continue to be of tremendous benefit to our understanding of human disease.
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van, Wijngaarden Peter, and petervanwijn@yahoo com au. "Heritable influences in oxygen-induced retinopathy." Flinders University. Medicine, 2006. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20060824.211102.

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Retinopathy of prematurity, a disease characterised by aberrant retinal vascular development in premature neonates, is a leading cause of blindness and visual impairment in childhood. This work sought to examine differences in the susceptibility of inbred rat strains to oxygen-induced retinopathy, a model of human retinopathy of prematurity. The overriding aim was to identify genetic factors in rats that might be generalisable to humans. Newborn rats of six different strains were exposed to alternating cycles of hyperoxia and relative hypoxia for fourteen days. Rats were removed to room air and killed for analysis immediately, to assess oxygen-induced retinal vascular attenuation, or four days later to evaluate the extent of hypoxia-induced vasoproliferation. Whole flat-mounted retinae were stained with fluorophore conjugated isolectin GS-IB4, and measurement of vascular area was conducted using fluorescence microscopy and video-image analysis. A hierarchy of susceptibility to the inhibitory effects of cyclic hyperoxia and relative hypoxia on postnatal retinal vascularization was identified for the rat strains studied. Susceptibility to vascular attenuation was predictive of the subsequent risk of vascular morphological abnormalities. Cross-breeding experiments between susceptible and resistant strains demonstrated that the susceptible phenotype was dominantly inherited in an autosomal fashion. These studies confirmed an association between ocular pigmentation and retinopathy risk, however the finding of differential susceptibility amongst albino rat strains implicated factors in addition to those associated with ocular pigmentation. Quantitative real-time reverse transcription-polymerase chain reaction was used to compare the retinal expression of angiogenic factor genes in susceptible and resistant strains with the aim of identifying a genetic basis for the strain difference. Eight angiogenic factor genes were selected for study: vascular endothelial growth factor (VEGF); VEGF receptor 2; angiopoietin 2; Tie2; pigment epithelium-derived factor; erythropoietin; cyclooxygenase-2 and insulin-like growth factor-1. The most notable difference between strains was the expression of vascular endothelial growth factor (VEGF) during the cyclic hyperoxia exposure period - higher VEGF expression was associated with relative resistance to retinopathy. Other differences in retinal angiogenic factor gene expression between strains, such as higher expression of VEGF receptor 2 and angiopoietin 2 in resistant strains, appeared to be secondary to those in VEGF. Following cyclic hyperoxia, the expression pattern of angiogenic factor genes changed - messenger RNA levels of hypoxia-induced genes, including VEGF, VEGF receptor 2, angiopoietin 2 and erythropoietin, were significantly higher in those strains with larger avascular areas, than in those strains that were relatively resistant to retinopathy. These findings provide firm evidence for hereditary risk factors for oxygen-induced retinopathy in the rat. Differences in the regulatory effects of oxygen on VEGF expression appear to be central to the risk of retinopathy. The potential relevance of these hereditary factors is discussed in the context of the human disease.
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Sweeney, Patricia M. "Indirect inbred selection for drying rate in maize hybrids /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487681788253123.

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Books on the topic "Inbred rat"

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Neurobiology of reproduction in the female rat: A fifty-year perspective. Berlin: Springer-Verlag, 1989.

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L, Snyder David, ed. Dietary restriction and aging: Proceedings of the Symposium on the Effects of Dietary Restriction on Aging and Disease in Germfree and Conventional Lobund-Wistar Rats, held in Notre Dame, Indiana, March 27-29, 1988. New York, NY: A.R. Liss, 1989.

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A, Boorman Gary, ed. Pathology of the Fischer rat: Reference and atlas. San Diego: Academic Press, 1990.

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Boorman, Gary A., Scot L. Eustis, Michael R. Elwell, and C. Montgomery. Pathology of the Fischer Rat: Reference and Atlas. Academic Press, 1990.

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Boorman, Gary A., Scot L. Eustis, Michael R. Elwell, and C. Montgomery. Pathology of the Fischer Rat: Reference and Atlas. Academic Press, 1990.

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Everett, Jack W. Neurobiology of Reproduction in the Female Rat: A 50 Year Perspective (Monographs on Endocrinology). Springer, 1990.

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Kenji, Shima, ed. Obesity and NIDDM: Lessons from the OLETF rat. Amsterdam: Elsevieer, 1999.

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J, Hedrich Hans, Adams M, and International Council for Laboratory Animal Science., eds. Genetic monitoring of inbred strains of rats: A manual on colony management, basic monitoring techniques, and genetic variants of the laboratory rat. Stuttgart: Gustav Fischer Verlag, 1990.

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Hedrich, Hans J. Genetic Monitoring of Inbred Strains of Rats: A Manual on Colony Management, Basic Monitoring Techniques, and Genetic Variants of the Laboratory Rat. Gustav Fischer, 1991.

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Festing, Michael F. W. Inbred Strains in Biomedical Research. Palgrave, 2014.

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Book chapters on the topic "Inbred rat"

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Okuyama, Tohru, Kazuo Hashi, Yasutaka Kurokawa, Satoshi Sasaki, and Katsuko Sudo. "Morphological Study on Congenital Hydrocephalus of the Inbred Rat, LEW/Jms." In Annual Review of Hydrocephalus, 9–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-11155-0_6.

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Karlsson, Sandra, and Karin Klinga-Levan. "Expression Analysis of Human Endometrial Adenocarcinoma in an Inbred Rat Model." In Hormonal Carcinogenesis V, 503–9. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_50.

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Yankah, A. C., and H.-U. Wottge. "Immunosuppression in allograft valve surgery. A study on inbred rat model." In Cardiac Valve Allografts, 135–41. Heidelberg: Steinkopff, 1997. http://dx.doi.org/10.1007/978-3-642-59250-8_14.

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Gasser, M., W. Timmermann, and A. Thiede. "Segmental Femoral Artery Allografts: Histomorphological Analysis of the Rejection Response in Inbred Rat Strains." In Organtransplantation in Rats and Mice, 359–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_36.

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Timmermann, W., and A. Thiede. "The Rejection Response to Segmental Grafts of the Femoral Artery in Inbred Rat Strains." In Microsurgical Models in Rats for Transplantation Research, 101–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-61657-0_16.

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Okuyama, Tohru, Kazuo Hashi, Satoshi Sasaki, Katsuko Sudo, and Yasutaka Kurokawa. "Changes in Cerebral Microvasculature in Congenital Hydrocephalus of the Inbred Rat LEW/Jms: Light and electron microscopic examination." In Annual Review of Hydrocephalus, 5–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-11152-9_3.

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Yamada, Hiroshi, Norihiko Tamaki, Takayuki Shirakuni, Hiromitsu Sumiyoshi, Shizuo Oi, Satoshi Matsumoto, and Katsuko Sudo. "The Etiology of the Congenital Hydrocephalus in the Inbred Rat LEW/Jms: Light microscopic study in the embryonic stage." In Annual Review of Hydrocephalus, 4–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-11155-0_2.

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Engemann, R., H. J. Gassel, Th Schang, A. Thiede, and H. Hamelmann. "The Immunogenicity of Isolated Liver Cells: Comparison of Complete Liver Cell Suspensions (LCS) versus Liver Parenchymal Cell Suspensions (LPS) in Two Different Allogeneic Inbred Rat Strain Combinations." In Experimental and Clinical Hepatology, 157–67. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4151-9_22.

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Scheidel, P. H., M. Korell, T. Strowitzki, U. Noss, R. A. Wiedemann, and H. K. Hepp. "Orthotopic Transplantation of the Fallopian Tube, Ovary, and Segment of the Uterus in Inbred Rats." In Microsurgical Models in Rats for Transplantation Research, 295–301. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-61657-0_51.

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Gugenheim, J., D. Houssin, E. Martin, and H. Bismuth. "Decreased Graft Versus Host Reaction After Portal Venous Drainage of Spleen Grafts in Inbred Strains of Rats." In Microsurgical Models in Rats for Transplantation Research, 269–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-61657-0_45.

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Conference papers on the topic "Inbred rat"

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Jo, T., K. Tsuchiya, M. Hassan, S. Siddiqui, H. Ghezzo, and JG Martin. "Investigation of Molecular Regulation in the Airways of Two Highly Inbred Rat Strains." 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.a6042.

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