OBJECTIVETo assess the embolic effects and biocompatibility of Eudragit mixture, a new liquid embolic agent.

METHODSIn vitro, the viscosity and precipitation time of Eudragit mixtures at several concentrations were measured to study the best proportion of components of the mixture. In vivo, a branch of the right external carotid artery was embolized with Eudragit mixture in 12 rabbits, and with n-butyl cyanoacrylate in another 12 rabbits for a comparative study of the general, angiographic and histopathologic changes between the two groups.

RESULTSEudragit mixture containing 7.5 g Eudragit, 50 ml absolute ethanol and 50 ml iopromide was shown in vitro to have good properties including rapid precipitation and soft elastic sponge formation upon contact with blood; in vivo, to be nontoxic, nonadherent to the microcatheter and able to embolize the vascular lumen completely without later recanalisation.

CONCLUSIONEudragit mixture is an effective, nontoxic, safe and promising liquid embolic agent.

Animals ; Carotid Artery Thrombosis ; pathology ; physiopathology ; therapy ; Cerebral Angiography ; Chemical Precipitation ; Embolism ; therapy ; Embolization, Therapeutic ; methods ; Enbucrilate ; therapeutic use ; Male ; Polymethacrylic Acids ; chemistry ; therapeutic use ; Rabbits ; Viscosity

Medium spiny neurons (MSNs) in the striatum, which can be divided into D1 and D2 MSNs, originate from the lateral ganglionic eminence (LGE). Previously, we reported that Six3 is a downstream target of Sp8/Sp9 in the transcriptional regulatory cascade of D2 MSN development and that conditionally knocking out Six3 leads to a severe loss of D2 MSNs. Here, we showed that Six3 mainly functions in D2 MSN precursor cells and gradually loses its function as D2 MSNs mature. Conditional deletion of Six3 had little effect on cell proliferation but blocked the differentiation of D2 MSN precursor cells. In addition, conditional overexpression of Six3 promoted the differentiation of precursor cells in the LGE. We measured an increase of apoptosis in the postnatal striatum of conditional Six3-knockout mice. This suggests that, in the absence of Six3, abnormally differentiated D2 MSNs are eliminated by programmed cell death. These results further identify Six3 as an important regulatory element during D2 MSN differentiation.