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We hypothesized that the novel environment differentially increased the stress level of aged GLE male mice, which subsequently altered dopaminergic signaling and decreased locomotor activity.
Other established model systems include xenografts from primary tumors or osteosarcoma cell lines in immunodeficient nude mice, which subsequently develop into tumors resembling osteosarcoma[ 13- 15].
Mice were administered exogenous leptin, which, through its action on the sweet taste receptor, suppressed the neuronal activation to sweet stimuli in normal mice, which subsequently reduced their consumption of sweet solutions.
In their in vivo study pieces of human mammary gland were transplanted onto immune-compromised mice, which subsequently were treated with E2 and progesterone at the adequate doses of follicular or luteal phase of woman's menstrual cycle.
After validation of cytotoxicity with NIR exposure up to 8 J/cm in vitro, we employed an orthotopic breast cancer model of bilateral MDA-MB-468luc tumors in female athymic mice, which subsequently received a panitumumab-IR700 conjugate in vivo.
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Furthermore, the influence of senescent cells in aging of an organism was also shown by reactivating telomerase in mouse tissues, which subsequently "became rejuvenated" (Jaskelioff et al. 2011, Bernardes de Jesus et al. 2012).
NSCLC cells were also subcutaneously transplanted into the left thigh of nude mice, which were subsequently raised for 2 weeks.
To complete cyclical transmission, flies were fed on anesthetized NMRI mice, which were subsequently monitored for parasitaemia.
In order to determine the protective efficacy of antibody, J8-DT, DT or PBS antisera were passively transferred into naïve mice, which were subsequently challenged with M1 GAS.
During week six of therapy, metabolic cages were used to collect urine samples from all mice, which were subsequently analyzed for urine protein (Upro) and creatine levels by UT Southwestern Medical Center's mouse metabolic phenotyping core.
Additionally, biosynthesis of fatty acid is likely, at least in part, to also be regulated by NPY neuron specific Y2 signalling, as evident by altered expression levels of acetyl-CoA carboxylase (ACC) in skeletal muscle of female mice, which could subsequently inversely influence expression of CPT1.
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