ABSTRACT.Purpose: The purpose of this study was to evaluate the ability of different methods to induce choroidal neovascularization (CNV) in the domestic pig. Methods: A total of 26 Danish landrace pigs was used. A sample of 22 eyes in 12 pigs underwent retinal photocoagulation with a xenon lamp, six eyes in four pigs underwent retinal photocoagulation with a diode laser, and mechanical rupture of Bruch's membrane (BM) was induced in 12 pigs following surgical debridement of the retinal pigment epithelium without damage to the neuroretina. Results: All 12 pigs (100%) in the group with mechanical rupture of BM developed CNV. The induced membranes were morphologically similar to CNV membranes in humans. Induced CNV was found in 13 of 22 (54%) xenon lamp-treated animals and in five of six (83%) diode laser-treated animals. The CNV in these groups was small and the morphology of the induced lesions was dominated by retinal gliosis and retinal neovascularization, probably due to a marked destruction of the neuroretina. Conclusions: Surgical debridement of the retinal pigment epithelium followed by mechanical rupture of BM is a reproducible method of producing CNV in the domestic pig, whereas photocoagulation gives rise to glially derived subretinal fibrovascular membranes and primarily retinal neovascularization.
Therapeutic options are urgently needed for non‐alcoholic fatty liver disease (NAFLD), but development is time‐consuming and costly. In contrast, drug repurposing offers the advantages of re‐applying compounds that are already approved, thereby reducing cost. Acetylsalicylic acid (ASA) and pentoxifylline (PTX) have shown promise for treatment of NAFLD, but have not yet been tested in combination. Guinea pigs were fed a high‐fat diet for 16 weeks and then continued on the diet while being treated with ASA, PTX or ASA+PTX for 8 weeks. Chow‐fed animals served as healthy controls. Guinea pigs were CT scanned before intervention start and at intervention end. Animals without steatosis (ie NAFLD) at week 16 were excluded from the data analysis. ASA and PTX alone or in combination did not improve hepatic steatosis, ballooning, inflammation or fibrosis nor did the treatments affect liver enzymes (aminotransferases and alkaline phosphatase) or circulating lipids. Liver triglyceride levels, relative liver weight and hepatic mRNA expression of monocyte chemoattractant protein 1, interleukin 8 and platelet‐derived growth factor b were nominally decreased. Thus, in the current study, treatment with ASA and PTX alone or in combination for 8 weeks did not ameliorate NASH or hepatic fibrosis in guinea pigs.
Fabry's disease, angiokeratoma corporis diffusum, is an X-linked inborn error of glycosphingolipid metabolism due to lack of activity of the lysosomal enzyme, alpha-galactosidase A, resulting in progressive intracellular deposition of neutral glycosphingolipids in various tissues, including vascular endothelial - and smooth muscle cells. Occlusions of the retinal vessels are rare. We present a case of central retinal artery occlusion in a 25-year-old male with Fabry's disease, documented by fluorescein- and indocyanine green angiography performed by scanning laser opththalmoscopy.
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