ABSTRACT
We report a procedure using a pressure-controllable flute needle to remove subfoveal retention of perfluorocarbon liquid (PFCL) under silicone oil. With a two-port pars plana approach, we used a 27-gauge dental injection needle to create a retinotomy at the farthest edge of the PFCL bubble from the fovea. A 27-gauge flute needle was then inserted into the edge of the subfoveal PFCL to aspirate it with vacuum pressure. Three patients with subfoveal retained PFCL were treated by this procedure within silicone oil tamponade 1 month after the first operation. They promptly underwent successful removal of the PFCL with postoperative retinal reattachment and good visual outcome. This procedure allows safe and early treatment for subfoveal retained PFCL. Many medical institutions around the world could implement this procedure using common dental injection needles and flute needles.
ABSTRACT
Angiotensin II (Ang II) plays a crucial role in the pathogenesis of renal diseases. The objective of the present study was to investigate the possible inflammatory effect of Ang II on glomerular endothelial cells and the underlying mechanism. We isolated and characterized primary cultures of rat glomerular endothelial cells (GECs) and observed that Ang II induced the synthesis of monocyte chemoattractant protein-1 (MCP-1) in GECs as demonstrated by Western blot. Ang II stimulation, at concentrations ranging from 0.1 to 10 µm, of rat GECs induced a rapid increase in the generation of reactive oxygen species as indicated by laser fluoroscopy. The level of p47phox protein, an NAD(P)H oxidase subunit, was also increased by Ang II treatment. These effects of Ang II on GECs were all reduced by diphenyleneiodonium (1.0 µm), an NAD(P)H oxidase inhibitor. Ang II stimulation also promoted the activation of nuclear factor-kappa B (NF-κB). Telmisartan (1.0 µm), an AT1 receptor blocker, blocked all the effects of Ang II on rat GECs. These data suggest that the inhibition of NAD(P)H oxidase-dependent NF-κB signaling reduces the increase in MCP-1 production by GECs induced by Ang II. This may provide a mechanistic basis for the benefits of selective AT1 blockade in dealing with chronic renal disease.