Micturition defects and altered bladder function in the klotho mutant mouse model of aging
JavierSeptember 20, 20200 Comments
Introduction and objectives: Symptoms associated with detrusor underactivity (DU) or an underactive bladder (UAB) can greatly affect a person’s quality of life and growing old is a major etiologic factor DU and UAB. Klotho gene has been associated with suppression several phenotypes of aging, and there is a moderate klotho expression in the bladder. Considering this, we hypothesized that klotho gene involved in the regulation of bladder function. Thus, we examined the genetic model of premature aging rodents with hypomorphic klotho expression to changes in bladder function.
Methods: Klotho mutant mice designated as a preclinical model of aging. Men and women have urinary klotho mice were measured at weeks 4, 6, and 8 through metabolic cages and test place void. Histology is rated at 4, 6, and 8 weeks. Lastly, the contraction of the bladder was assessed using bladder tissue bath lines. All the animals are gender- and age-matched wild-type littermates for analysis.
Result: the Void and bladder contraction test klotho mutant mice revealed that, similar to other aging models, has risen to cancel the frequency and decreased urinary volume per micturition event. In vitro contractile response to electrical stimulation is weaker and subtypes of muscarinic receptor expression is reduced in the mutant mice klotho bladder. These data suggest that bladder klotho mutant mice have impaired bladder function.
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Conclusion: Klotho mutant mice recapitulate many of the characteristics of a dysfunctional bladder older, including bladder function changes. Given the short timeframe for bladder dysfunction and robustness of the model, this model will provide new insight to encourage the study of aging bladder.
Micturition defects and altered bladder function in the klotho mutant mouse model of aging
Landscape metabolism of Genetically Engineered Mutant Rat Glioma Model IDH1
Understanding metabolic reprogramming aggressive brain tumor has potential applications for the treatment and imaging biomarkers. However, little is known about the nutritional requirements of isocitrate dehydrogenase 1 (IDH1) mutant glioma.
The IDH1 mutation involve acquisitions neomorphic enzymatic activity that produces D-2-hydroxyglutarate of α-ketoglutarate. In order to gain insight into this metabolism of malignant brain tumor, we performed metabolic profiling orthotopic tumor and contralateral area for glioma IDH1 mutant mouse model; as well as to test the use of glucose and glutamine in supplying major metabolic pathways such as glycolysis and the tricarboxylic acid (TCA).
We also revealed that the main substrate 2-hydroxyglutarate is glutamine in this model, and how the re-routing of this destructive utilization in the TCA. Our 13C tracing analysis, along with hyperpolarized magnetic resonance experiments, expressing the same glycolytic pathway active in both areas (tumor and contralateral) of the brain. Therefore, we describe the reprogramming of the central carbon metabolism associated with IDH1 mutations in genetically engineered mouse models that reflect tumor biology encountered in patients with glioma.
Bone is one of the sites most frequently in lung cancer metastatic non-small cell (NSCLC). Osimertinib, with and without bevacizumab (BV), has been studied in patients with advanced NSCLC. However, the efficacy of drugs on bone metastases of NSCLC has not been studied. H1975 human NSCLC cell lines, expressing red fluorescent protein (H1975-RFP), it orthotopically injected into the tibia of nude mice. established mouse models were randomized into four treatment groups of nine rats: Control; BV only; osimertinib only; osimertinib and BV combination.
