PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11932829

Latex aneurysms: a technical note.

J Klisch·J Zitt·M Schumacher
View original source ↗Export metadata ↓

Abstract

We describe a new technique for manufacturing latex tubings with thin-walled aneurysms. The physical characteristics of the latex model with its compliance simulates important details such as shape, size, neck and the thin wall of an aneurysm. Therefore important aspects of neuroendovascular therapy could be simulated and investigated in-vitro.

Explore related subjects

AneurysmEmbolization, TherapeuticHumansIntracranial AneurysmLatexModels, AnatomicJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Klisch, J Zitt, M Schumacher. 2002. Latex aneurysms: a technical note.. https://doi.org/10.1055/s-2002-23575

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Mechanistic insights into Claudin-14 dysfunction implicated in veins of Galen malformation.

Claudin-14 (CLDN14) is a key component of tight junctions (TJs) critical for maintaining paracellular barrier function. Variants of CLDN14 have been linked to Vein of Galen malformations (VOGMs), a rare cerebrovascular disorder; however, the molecular mechanisms underlying their pathogenicity remain unknown. Here, we investigate the mechanistic effects of two VOGM-associated mutations, A113P and V143M, using reinforcement-learning driven enhanced sampling molecular dynamics simulations combined with DiffNets-based deep learning and independent trajectory-wide structural analyses. Our analysis reveals that A113P induces broader structural disruption of CLDN14, perturbing paracellular sealing, pore symmetry, and inter-protomer communication, whereas V143M induces structural rearrangements centred around TM3 and the TM3-ECL2 region. In both cases, mutation-specific alterations are observed in structural stability and interfacial organization across oligomeric assemblies. Notably, these effects are qualitatively consistent across different modelled architectures, despite variability in local responses. In the absence of experimentally resolved structures, the structural perturbations reported here provide a mechanistic understanding of how VOGM-associated variants may influence CLDN14 structure and dynamics.

Aneurysm↗
PubMed2003

Brain vascular malformations in the fetus: diagnosis and prognosis.

UNLABELLED: DIAGNOSIS OF BRAIN VASCULAR MALFORMATIONS IN THE FETUS: Vein of Galen aneurysms can be diagnosed in utero. Other malformations are not seen. Ultrasound makes the diagnosis by showing a "cystic" structure in the posterior fossa. Colour Doppler shows the high flow. PROGNOSIS: The prognosis can be established by MRI. Bad prognosis factors are brain atrophy, cardiac insufficiency and complexity of the malformation. If these factors are absent, postnatal treatment by embolisation can be scheduled.

Aneurysm↗
PubMed2003

Aortic dissection precedes formation of aneurysms and atherosclerosis in angiotensin II-infused, apolipoprotein E-deficient mice.

OBJECTIVE: We sought to define the temporal characteristics of angiotensin II (AngII)-induced abdominal aortic aneurysms (AAAs) and to provide mechanistic insight into the development of this vascular pathology in apolipoprotein E-deficient (apoE-/-) mice. METHODS AND RESULTS: Male apoE-/- mice were infused with AngII for 1 to 56 days. Suprarenal arteries were sequentially sectioned, and cellular features were defined by histologic and immunocytochemical techniques. The initial identified event was medial accumulation of macrophages in regions of elastin degradation. Subsequent medial dissection was associated with luminal dilation and thrombus formation. Thrombi were usually constrained by adventitial tissue, although approximately 10% of mice died due to rupture. Thrombi led to profound inflammation that was characterized by infiltration of macrophages and T and B lymphocytes. Remodeling of the tissues was associated with regeneration of elastin fibers and reendothelialization of the dilated luminal surface. Aneurysmal tissue underwent profound neovascularization. Atherosclerotic lesions were only detected after development of the aneurysms. CONCLUSIONS: The initial event in AngII-induced AAA is a focal dissection in the suprarenal region. The progression of AAA precedes the development of overt atherosclerotic lesions.

Aneurysm↗