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The authors utilize a model of activity-dependent neuronal plasticity to study the interplay between synaptogenesis, neuronal death, and neurogenesis on the resulting pattern of neuronal connectivity.
In this study, we utilize a model of low-dose toxin-induced hypoinsulinemia and hyperglycemia that is commonly used to study type I diabetes.
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Joachim et al. [11] detects obstacles utilizing a model of human color vision.
In order to investigate the number of chains and the contact resistance between the particles in the CM, we utilized a model of the effective electric resistance.
To demonstrate effective repression of HIF-1α in these cell lines, we utilized a model of ambient hypoxia.
To test our hypothesis, we utilized a model of canine obesity based on feeding dogs a hypercaloric, high-fat diet to induce the development of insulin resistance.
We utilized a model of mesangial proliferative glomerulonephritis, known as anti-Thy1-induced glomerulonephritis (Thy1 GN), which exhibits sclerosis in the glomeruli.
To test this hypothesis, we measured water intake, urine output, body water stable isotope ratios, and blood glucose values utilizing a model of streptozotocin (STZ -induced diabeteSTZ -induced
By utilizing a model of streptozotocin (STZ -induced diabeteSTZ -inducedx case of aberrant water homeostasis, we diabetesase than untreated dindexes mellitus results in distincaseofbinaberrantor signatures, of the hydrogen (δ2H) and oxygen (δ18O) isotope ratios in body water.
We next utilized a model of chronic DSS-induced colitis to further evaluate the role of IL-25.
We utilized a model of arteriogenesis in the rat hindlimb that allowed us to identify and isolate a single collateral vessel early after induction of collateral growth [ 8].
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