The New Zealand Black (NZB) mouse chromosome 13 (c13) is linked to development of autoimmunity. B6 mice containing a portion of NZBc13 (B6.NZBc13 (c13)) develop a lupus phenotype that includes: autoantibody production, increased B and T cell activation, and marginal zone B cell and myeloid dendritic cell expansions. c13 mice have a B cell intrinsic dsRNA-sensing defect, leading to increased TLR3 expression and survival. The role of the aberrant dsRNA sensing in the generation of the c13 autoimmune phenotype was assessed by generating c13 mice with TLR3 knocked out (c13.TLR3KO). Marginal zone B cell expansion and B cell activation were attenuated in c13.TLR3KO mice, but other cellular phenotypes were not affected. Autoantibody production was partially reduced. These results indicate that altered dsRNA-sensing contribute to a portion of the altered cellular phenotypes in c13 mice, but that other susceptibility loci in the c13 interval are required for full development of autoimmunity.

No description available.

No description available.

The New Zealand Black (NZB) mouse chromosome 13 (c13) is linked to development of autoimmunity. B6 mice containing a portion of NZBc13 (B6.NZBc13 (c13)) develop a lupus phenotype that includes: autoantibody production, increased B and T cell activation, and marginal zone B cell and myeloid dendritic cell expansions. c13 mice have a B cell intrinsic dsRNA-sensing defect, leading to increased TLR3 expression and survival. The role of the aberrant dsRNA sensing in the generation of the c13 autoimmune phenotype was assessed by generating c13 mice with TLR3 knocked out (c13.TLR3KO). Marginal zone B cell expansion and B cell activation were attenuated in c13.TLR3KO mice, but other cellular phenotypes were not affected. Autoantibody production was partially reduced. These results indicate that altered dsRNA-sensing contribute to a portion of the altered cellular phenotypes in c13 mice, but that other susceptibility loci in the c13 interval are required for full development of autoimmunity.

Multiple-mouse MRI (MMMRI) accelerates biomedical research by imaging multiple mice simultaneously. To date, MMMRI has been explored in three ways: shielded transmit-receive coils, shielded transmits coil with separate unshielded receive coils; and finally shielded transmit-receive coils with independent gradient coils. However alternative transmit coil configurations and possible benefits of eliminating shielding have not yet been explored. The goal of this thesis is to test possible radiofrequency configurations with and without shielding for the purpose of improving image quality for MMMRI. Results demonstrate that using an unshielded transmit-receive coil array provided a 20% improvement over an identical shielded coil. A new unshielded 7-coil MMMRI array is presented, minimizing the ghosting between image overlap using mutual inductance minimization and a sensitivity encoding (SENSE) reconstruction. The final array provided high resolution images (90µm) of up to seven live mice simultaneously with appropriate signal-to-noise for automated analysis.

No description available.

Zugl.: Giessen, Universiẗat, Diss., 2008.

Thesis (M.Med.Sc.)--University of Hong Kong, 2003. / Includes bibliographical references (leaves 48-55). Also available in print.

Thesis(M Tech(Biomedical Technology))--Cape Peninsula University of Technology, 2009 / This thesis provides the first scientific evidence of the photoprotective properties of rooibos and honeybush herbal tea extracts and to some extent, two major honeybush polyphenols, hesperidin and mangiferin. These properties were demonstrated using in vivo models by: Providing evidence for the inhibition of tumour promotion by ultraviolet B (UVB) radiation in a two-stage skin carcinogenesis mouse model. Topical application of polyphenol-rich extracts of rooibos and honeybush prior to UVB tumour promotion of 7,12-dimethylbenz[a]anthracene (DMBA)-initiated mouse skin, inhibited the formation of tumours. The rooibos and honeybush extracts decreased the incidence and volume of the tumours. Topical application of hesperidin and mangiferin were less effective than the honeybush extracts as only the tumour volume was decreased, but not the incidence. Providing evidence for the inhibition of photodamage of the skin by UVB exposure in a mouse model. Topical application of polyphenolic rich extracts of honeybush prior to UVB irradiation of mouse skin reduced erythema, peeling, oedema and hyperplasia. The depletion of antioxidant enzymes catalase and superoxide dismutase (SOD) was prevented. The extracts protected the skin from oxidative and direct DNA damage, and reduced lipid peroxidation. The induction of cyclooxygenase-2 (COX-2) and ornithine decarboxylase (ODC) was also reduced. Topical application of the polyphenols hesperidin and mangiferin showed reduced protective effects compared to the extracts. Suggesting the possible mechanisms by which honeybush and the polyphenols protect against photocarcinogenesis such as reducing tumour promotion, inflammation and oxidative stress. Suggesting the benefits of including honeybush and rooibos as cosmeceuticals in skin care products and sunscreens as part of the strategy for preventing skin cancer. Discussing the recommendations for further study such as investigating more specific chemopreventive activities of these two South African herbal teas and their polyphenols, dose response studies and clinical evaluations.

archives@tulane.edu / BRCA1 faithfully repairs damaged DNA by promoting homology-directed repair (HDR). Loss of Brca1 and other HDR genes are incompatible with embryonic viability and cause severe genomic instability. Cells lacking BRCA1 are sensitive to cellular stresses such as DNA damage caused by ionizing radiation (IR). Homozygous loss of Brca1 is embryonic lethal in mice, and the few tissue-specific knockouts generated develop abnormally. Therefore, we created an inducible Cre mouse model to study Brca1 loss in all adult mouse tissues allowing for examination of viability, longevity, and stress response in the absence of HDR and the importance of HDR in different tissues of an adult mouse. After validating the inducible Cre system using a reporter allele in mice, we generated mice with alleles of the inducible Cre system and floxed Brca1 alleles. Cre was induced in adult mice at ten weeks of age, resulting in extensive, widespread deletion of Brca1. Contrary to the embryonic lethality observed in all previously tested germline Brca1 knockout mouse models, adult mice with Brca1 deletion displayed no overt phenotypes. Brca1Δ/Δ mice showed extensive, widespread deletion of Brca1 and survived up to 1 year after Brca1 recombination. Targeted, high-depth sequencing of recombined tissues indicated mutations accumulated in both the mammary gland and the intestine. However, only the mammary gland had an HDR deficiency signature. Next, we examined Brca1Δ/Δ mice survival after exposure to ionizing radiation and mitomycin C (MMC). Surprisingly, Brca1Δ/Δ mice responses are DNA damage specific. Brca1Δ/Δ mice deficient for HDR showed no increased sensitivity to IR but died four to eight days following MMC exposure. Our results show that BRCA1 is not required for long-term viability or DNA double-strand break repair, but BRCA1 is essential for DNA crosslink repair to maintain viability in an adult mouse. / 1 / JoyOlayiwola