In order to allow for a comparative evaluation of the in vivo degeneration of biological and tissue-engineered heart valves and vascular grafts, a small animal model of accelerated cardiovascular calcification is desired. Wistar rats (n = 102; 6 groups) were fed ad libitum with regular chow and 5 different regimens of pro-calcific diet supplemented with combinations of vitamin D (VD), cholesterol (CH) and dicalcium phosphate (PH). Moreover, cryopreserved (n = 7) or detergent-decellularized rat aortic conduit grafts (n = 6) were infrarenally implanted in Wistar rats under severely pro-calcific conditions. The follow-up lasted up to 12 weeks. High-dose application of VD (300,000 IU/kg), CH (2%) and PH (1.5%) resulted in elevated serum calcium and cholesterol levels as well as LDL/HDL ratio. It increased the tissue MMP activity visualized by in situ zymography and caused significantly aggravated calcification of the native aortic valve as well as the aortic wall as assessed by histology and micro-computed tomography. (Immuno)histology and quantitative real-time PCR revealed chondro-osteogenic cell transformation, lipid deposition, nitrosative stress and low-level inflammation to be involved in the formation of calcific lesions. Despite pro-calcific in vivo conditions, decellularization significantly reduced calcification, inflammation and intimal hyperplasia in aortic conduit implants. A well balanced dietary trigger for pathologic metabolic conditions may represent an appropriate mid-term treatment to induce calcifying degeneration of aortic valves as well as vascular structures in the systemic circulation in rats. With respect to experimental investigation focusing on calcifying degeneration of native or prosthetic tissue, this regimen may serve as a valuable tool with a rapid onset and multi-facetted character of cardiovascular degeneration.
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Allergol Immunopathol (Madr)
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Bone and Joint Research Team of Degeneration and Injury, Guangdong Provincial Academy of Chinese Medical Sciences, Guangzhou, China.
Rheumatoid arthritis (RA) is a chronic autoimmune joint disease. Its main pathological manifestations are joint cartilage, bone tissue injury, synovial hyperplasia, and chronic inflammation. At present, the pathogenesis of the disease has not been fully defined, and delaying the disease to improve joint function is the existing treatment.
View Article and Find Full Text PDFDrug Deliv Transl Res
January 2025
School of Pharmacy, Medical Biology Centre, Queen's University Belfast, Belfast, UK.
Glaucoma is an optic neuropathy in which progressive degeneration of retinal ganglion cells and the optic nerve leads to irreversible visual loss. Glaucoma is one of the leading causes of blindness. The pathogenesis of glaucoma is determined by different pathogenetic mechanisms, including increased intraocular pressure, mechanical stress, excitotoxicity, resistance to aqueous drainage and oxidative stress.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory of Clinical Investigation, National Institute on Aging, Intramural Research Program, Baltimore, MD, USA.
Background: Neurite degeneration is increasingly suspected to represent a causal feature of mild cognitive impairment (MCI) and Alzheimer's disease (AD). Therefore, sensitive and specific imaging biomarkers of neuronal degeneration are needed to elucidate the mechanisms underlying cognitive impairment in MCI and AD. However, the recently developed Neurite Orientation Dispersion and Density Imaging (NODDI) MRI technique, used to measure the neurite density index (NDI), has some limitations.
View Article and Find Full Text PDFBackground: Reactive astrogliosis refers to functional and morphological changes in astrocytes that occur with neuronal damage in numerous neurological conditions. PET tracers targeting monoamine oxidase B (MAO-B) are used to visualize reactive astrogliosis in the living brain. [F]SMBT-1, a MAO-B selective PET tracer, was developed by modifying the chemical structure of [F]THK5351.
View Article and Find Full Text PDFBackground: The choroid plexus (ChP) plays a vital role in CSF production and waste clearance. While existing imaging studies have established connections between ChP volume changes and age-related neurodegenerative diseases, a comprehensive investigation into the microstructural and vascular changes associated with aging remains insufficient. This study aims to explore ChP changes in normal aging using diffusion and perfusion MRI in the HCP-Aging dataset to enhance our understanding of age-related microstructural and vascular changes in the ChP.
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