Adenine-induced Model
Adenine-induced Model - Related Videos
09:14
DamID-seq: Genome-wide Mapping of Protein-DNA Interactions by High Throughput Sequencing of Adenine-methylated DNA Fragments
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Cited by 22 •
2016
We describe herein an assay by coupling DNA adenine methyltransferase identification (DamID) to high throughput sequencing (DamID-seq). This improved method provides a higher resolution and a wider dynamic range, and allows analyzing DamID-seq data in conjunction with other high throughput sequencing data such as ChIP-seq, RNA-seq, etc.
09:07
Murine Model of Epicutaneously-Induced Immunomodulation
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2025
The study demonstrates the role of the skin in modulating immune responses in mice through epicutaneous (EC) immunization. EC immunization with a protein antigen can suppress immune responses in contact hypersensitivity or reverse skin-induced suppression when combined with pathogen-associated molecular patterns. EC immunization shows promise as an effective, needle-free approach to immunotherapy.
08:05
Murine Model of Allergen Induced Asthma
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Cited by 51 •
2012
Experimental mouse models of allergic asthma offer new possibilities for studying disease pathogenesis and developing new therapeutics. These models are well suited to measuring factors governing the allergic immune response, airway inflammation, and pulmonary pathophysiology.
10:37
Ferric Chloride-induced Murine Thrombosis Models
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Cited by 65 •
2016
We report a refined procedure of the ferric chloride (FeCl3)-induced thrombosis models on carotid and mesenteric artery as well as vein, characterized efficiently using intravital microscopy to monitor time to occlusive thrombi formation.
02:33
Inducing an Acute Electroconvulsive Seizure in a Rat Model
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2025
Source: Jang, S., et al, Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins. J. Vis. Exp. (2017)This video demonstrates the induction of an acute electroconvulsive seizure (ECS) in a rat model to study seizure-induced neuroplasticity. Researchers apply electrical stimulation via ear-clip electrodes, triggering neuronal hyperexcitability and clonus. This model helps investigate synaptic plasticity, seizure...
FAQs
Adenine is converted into poorly soluble 2,8-dihydroxyadenine, whose crystals accumulate within renal tubules. Their presence can obstruct tubular flow and damage epithelial cells, while the resulting inflammatory response contributes to progressive interstitial fibrosis. This sequence connects the initiating exposure with both functional decline and structural remodeling, allowing investigators to study chronic kidney disease-related changes together.
The model’s adjustable severity is valuable because researchers can examine renal injury across different levels rather than treating kidney disease as a single fixed outcome. That flexibility supports comparisons of dysfunction, tissue remodeling, and systemic consequences, and it helps preclinical studies evaluate whether candidate treatments perform under more or less pronounced disease conditions.
Findings require careful interpretation because injury produced in this model does not fully reproduce human kidney disease. The model can reproduce relevant features, including renal dysfunction, inflammation, fibrosis, and systemic effects of reduced kidney function, but differences from human disease may limit direct clinical translation. Researchers therefore use it as a controlled preclinical tool, not a complete human substitute.
An experimental workflow centers on administering adenine, then examining the resulting renal and systemic changes. Investigators may assess kidney dysfunction, tissue remodeling, and biomarkers while relating those findings to the progression of injury. Because the induction is described as straightforward and severity can be adjusted, the model is practical for organized preclinical comparisons of disease and treatment responses.
Useful readouts include renal dysfunction, tissue remodeling, biomarkers, and systemic effects associated with reduced kidney function. Together, these outcomes provide complementary information: functional measures indicate impaired kidney performance, tissue assessment reveals structural change, and biomarkers can help track disease-related biology or treatment effects. This combination supports evaluation of candidate therapies beyond a single endpoint.
In medicine and nephrology, the model links a reproducible renal injury pattern with broader chronic kidney disease research. It can support studies of complications arising as kidney function declines, investigation of tissue remodeling, and testing of candidate treatments before clinical evaluation. Its value comes from combining controlled induction with outcomes relevant to both kidney pathology and systemic disease.