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Month-old Mice (month-old + mouse)
Selected AbstractsAged mice have enhanced endocortical response and normal periosteal response compared with young-adult mice following 1 week of axial tibial compressionJOURNAL OF BONE AND MINERAL RESEARCH, Issue 9 2010Michael D Brodt Abstract With aging, the skeleton may lose its ability to respond to positive mechanical stimuli. We hypothesized that aged mice are less responsive to loading than young-adult mice. We subjected aged (22 months) and young-adult (7 months) BALB/c male mice to daily bouts of axial tibial compression for 1 week and evaluated cortical and trabecular responses using micro,computed tomography (µCT) and dynamic histomorphometry. The right legs of 95 mice were loaded for 60 rest-inserted cycles per day to 8, 10, or 12,N peak force (generating mid-diaphyseal strains of 900 to 1900 µ, endocortically and 1400 to 3100 µ, periosteally). At the mid-diaphysis, mice from both age groups showed a strong anabolic response on the endocortex (Ec) and periosteum (Ps) [Ec.MS/BS and Ps. MS/BS: loaded (right) versus control (left), p,<,.05]. Generally, bone formation increased with increasing peak force. At the endocortical surface, contrary to our hypothesis, aged mice had a significantly greater response to loading than young-adult mice (Ec.MS/BS and Ec.BFR/BS: 22 months versus 7 months, p,<,.001). Responses at the periosteal surface did not differ between age groups (p,>,.05). The loading-induced increase in bone formation resulted in increased cortical area in both age groups (loaded versus control, p,<,.05). In contrast to the strong cortical response, loading only weakly stimulated trabecular bone formation. Serial (in vivo) µCT examinations at the proximal metaphysis revealed that loading caused a loss of trabecular bone in 7-month-old mice, whereas it appeared to prevent bone loss in 22-month-old mice. In summary, 1 week of daily tibial compression stimulated a robust endocortical and periosteal bone-formation response at the mid-diaphysis in both young-adult and aged male BALB/c mice. We conclude that aging does not limit the short-term anabolic response of cortical bone to mechanical stimulation in our animal model. © 2010 American Society for Bone and Mineral Research [source] Advanced glycation endproducts and pro-inflammatory cytokines in transgenic Tg2576 mice with amyloid plaque pathologyJOURNAL OF NEUROCHEMISTRY, Issue 2 2003Gerald Münch Abstract Increased expression and altered processing of the amyloid precursor protein (APP) and generation of ,-amyloid peptides is important in the pathogenesis of amyloid plaques in Alzheimer's disease (AD). Transgenic Tg2576 mice overexpressing the Swedish mutation of human APP exhibit ,-amyloid deposition in the neocortex and limbic areas, accompanied by gliosis and dystrophic neurites. However, murine plaques appear to be less cross-linked and the mice show a lower degree of inflammation and neurodegeneration than AD patients. ,Advanced glycation endproducts (AGEs)', formed by reaction of proteins with reactive sugars or dicarbonyl compounds, are able to cross-link proteins and to activate glial cells, and are thus contributing to plaque stability and plaque-induced inflammation in AD. In this study, we analyze the tissue distribution of AGEs and the pro-inflammatory cytokines IL-1, and TNF-, in 24-month-old Tg2576 mice, and compare the AGE distribution in these mice with a younger age group (13 months old) and a typical Alzheimer's disease patient. Around 70% of the amyloid plaque cores in the 24-month-old mice are devoid of AGEs, which might explain their solubility in physiological buffers. Plaque associated glia, which express IL-1, and TNF-,, contain a significant amount of AGEs, suggesting that plaques, i.e. A, as its major component, can induce intracellular AGE formation and the expression of the cytokines on its own. In the 13-month-old transgenic mice, AGEs staining can neither be detected in plaques nor in glial cells. In contrast, AGEs are present in high amounts in both plaques and glia in the human AD patient. The data obtained in this show interesting differences between the transgenic mouse model and AD patients, which should be considered using the transgenic approach to test therapeutical strategies to eliminate plaques or to attenuate the inflammatory response in AD. [source] The effect of Ginkgo biloba on the cerebellum of aging SAMP mouse,A TUNEL, bcl-2, and fMRI studyMICROSCOPY RESEARCH AND TECHNIQUE, Issue 8 2007Maria S.M. Wai Abstract EGb 761, an extract from Ginkgo biloba that possesses neuroprotective properties, was fed to a strain of fast aging mice (SAMP-8) beginning at 3 weeks of age until they were sacrificed at 3 months and 11 months, respectively, along with an age-matched control group without herbal feeding. The aim of the study was to determine (1) the status of apoptosis and the status of bcl-2, a molecule involved in the fate of cells following injury, in the cerebella of these mice and (2) to analyze the functional changes as shown by fMRI images. The data indicated that there were no differences in apoptosis between the mice fed with EGb 761 and the control group at the two time points of 3 and 11 months of age. For bcl-2 positive cells, there was a decrease in density only in the cerebella of 11-month-old mice fed with the herbal extract when compared with controls. Functional studies indicated that while no changes were observed in the 3-month-old mice fed with Ginkgo biloba, an expansion of activated sites, possibly related to "synaptic reorganization and pathway alteration," was observed in the 11-month-old mice. Microsc. Res. Tech., 2007. © 2007 Wiley-Liss, Inc. [source] Hepsin cooperates with MYC in the progression of adenocarcinoma in a prostate cancer mouse modelTHE PROSTATE, Issue 6 2010Srinivas Nandana Abstract BACKGROUND Hepsin is a cell surface protease that is over-expressed in more than 90% of human prostate cancer cases. The previously developed Probasin-hepsin/Large Probasin-T antigen (PB-hepsin/LPB-Tag) bigenic mouse model of prostate cancer demonstrates that hepsin promotes primary tumors that are a mixture of adenocarcinoma and neuroendocrine (NE) lesions, and metastases that are NE in nature. However, since the majority of human prostate tumors are adenocarcinomas, the contribution of hepsin in the progression of adenocarcinoma requires further investigation. METHODS We crossed the PB-hepsin mice with PB-Hi-myc transgenic mouse model of prostate adenocarcinoma and characterized the tumor progression in the resulting PB-hepsin/PB-Hi-myc bigenic mice. RESULTS We report that PB-hepsin/PB-Hi-myc bigenic mice develop invasive adenocarcinoma at 4.5 months. Further, histological analysis of the 12- to 17-month-old mice revealed that the PB-hepsin/PB-Hi-myc model develops a higher grade adenocarcinoma compared with age-matched tumors expressing only PB-Hi-myc. Consistent with targeting hepsin to the prostate, the PB-hepsin/PB-Hi-myc tumors showed higher hepsin expression as compared to the age-matched myc tumors. Furthermore, endogenous expression of hepsin increased in the PB-Hi-myc mice as the tumors progressed. CONCLUSIONS Although we did not detect any metastases from the prostates in either the PB-hepsin/PB-Hi-myc or the PB-Hi-myc mice, our data suggests that hepsin and myc cooperate during the progression to high-grade prostatic adenocarcinoma. Prostate 70: 591,600, 2010. © 2009 Wiley-Liss, Inc. [source] | ||||||||||