The blood flow recovery was studied by laser
Doppler imaging. Differential gene expression between these two models was assessed by quantitative real-time polymerase chain reactions (PCR). Inflammatory and progenitor cells recruitment were determined by immunohistochemistry.
Results: We found that hypoxia-related genes increased significantly in the calf, but not in the thigh, after gradual and acute femoral arterial occlusion (P < .05). Shear-stress dependent genes and inflammatory genes were upregulated immediately in the thigh only after acute femoral arterial Occlusion (P < .05). These differences in gene expression were consistent with increased SDF-1 alpha expression, recruitment of macrophages and hemangiocytes, and higher VX-770 clinical trial SRT2104 price blood flow recovery after acute
arterial occlusion than after gradual arterial occlusion (P < .05).
Conclusion: This is the first study to show the mechanisms that regulate blood flow recovery are critically dependent on the rate of arterial occlusion. This novel model of gradual arterial occlusion may more closely resemble the human diseases, and may provide more accurate mechanistic insights for creating novel molecular therapies. (J Vasc Surg 2008;48:1546-58.)”
“Increasing evidence suggests that the inappropriate activation of cyclin-dependent kinases (CDKs) could induce neuronal apoptosis in Alzheimer’s disease (AD), which means that the nearly pharmacological inhibitors of cell-cycle progression may effectively impede the development or progression of AD. Indirubin-3′-monoxime (IMX), a known effective inhibitor of CDKs, has been shown to have therapeutic effects on learning and memory deficits induced by beta-amyloid (A beta) intracerebroventricular infusion in rats. In the present study, we investigated the neuroprotective effects of IMX on A beta(25-35)-induced neuronal apoptosis and its potential mechanisms in human neuroblastoma SH-SY5Y cells. A beta(25-35)-induced apoptosis,
characterized by decreased cell viability, neuronal DNA condensation, and fragmentation, was associated with an increase in tau protein hyperphosphorylation. IMX, however, attenuated A beta(25-35)-induced cell death in a dose-dependent manner. Furthermore, expression of hyperphosphorylation tau protein was significantly decreased with IMX treatment. Our study suggests that IMX may usefully prevent or delay the neuronal loss of AD. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Objective: This experimental study investigated the hemodynamic effect of corrective procedures for arteriovenous access-related ischemia in pulsatile flow.
Methods: Silicone models of an emulated tapered and bifurcated arterial tree of the upper arm and forearm were integrated into a pulsatile flow circuit.