Myocardial infarction followed by reperfussion in a langendorff perfussion system

Myocardial infarction followed by reperfussion in a langendorff perfussion system

X-linked genetic disease resulting in deficiency of the enzyme lysosomal hydrolase Galactosidase A (α-GalA). This enzymatic defect causes cellular accumulation in multiple tissues, but especially in endothelial cells, and in plasma, of neutral glycosphingolipids, particularly globotriosylceramide (Gb3), it causes a very varied and multisystemic clinical symptoms, with cardiac, renal and neurological involvement. Primary cultures of aortic endothelial cells are also derived form this colony for their in vitro use.

Condral defect of 10mm2 surgically generated in the loading area of the medial and lateral femoral condyle

In DBA/2 J mice, mutations in two genes (GpnmbR150X and Tyrp1b) lead to iris disease with features of human iris atrophy and pigment dispersion syndrome. This strain of mice is used as an experimental model of POAG (primary open-angle glaucoma), as they develop a chronic progressive increase in IOP that causes retinal ganglion cell death. The increase in IOP in these animals begins at 10 months of age, and the pressure remains elevated until death. These animal models are very useful in elucidating the glaucoma pathogenesis and to identify potential therapeutic targets

Measurement of intraocular pressure (IOP), reading is obtained from the central cornea of each eye. is measured with a rebound tonometer (Tonolab, Icare, Espoo, Finland) specific adapted by mice or rat

Pterional craniotomy and subsequent surgical occlusion of both branches of the middle cerebral artery

Human PBMC.s will be inoculated intraperitoneally.

Model generated by mouse kidney androgen-regulated protein (KAP) cDNA cloned into pKAP2 vector, microinjected into 1-cell–fertilized B6SJL F2 embryos.

1 cycle of 2.5% DSS in drinking water ad libitum for 5 days, followed by 7 days of regular water to mimic the acute phase of the disease