Novel technique to reduce prolapsed device in atrial septal defect closure.

Objective: Transcatheter closure of atrial septal defect (ASD) has become an alternative treatment to surgical repair. One of the challenges is the prolapse of the left atrial disc during the procedure. Many techniques have been developed to prevent the prolapse but not reduce it. In this study, we present a novel technique, termed push back technique, that help reduce the prolapsed device. Methods: We enrolled 24 patients (8 males, 16 females) between May 2008 and January 2023 who underwent the push back technique during transcatheter closure of ASD in Taichung Veterans General Hospital. We recorded the hemodynamic data, success rate and complications including device embolization/migration, valvular regurgitation, pericardial effusion, and residual shunt. Results: The median age was 6.3 years (1.2-70.5 years) and the median weight was 19.1 kg (7.8-90 kg). Fifteen (62.5%) patients had mild pulmonary hypertension. The median Qp/Qs was 2.54 (1.5-8.8). The median ASD stretched size was 21.2 mm (7.7-35.3 mm). The median device size was 22 mm (8-40 mm). The median fluoroscopy time was 14 min (5-23 min) and median procedure time was 47 min (25-78 min). The push back technique successfully reduced the prolapsed device in 21 (87.5%) patients. There was no complication in all patients. Conclusion: We present a novel push back technique that can successfully reduce the prolapsed device in 87.5% (21/24) patients without complications. It is feasible, safe and effective.

Loss of α1,6-Fucosyltransferase Decreases Hippocampal Long Term Potentiation: IMPLICATIONS FOR CORE FUCOSYLATION IN THE REGULATION OF AMPA RECEPTOR HETEROMERIZATION AND CELLULAR SIGNALING.

Core fucosylation is catalyzed by α1,6-fucosyltransferase (FUT8), which transfers a fucose residue to the innermost GlcNAc residue via α1,6-linkage on N-glycans in mammals. We previously reported that Fut8-knock-out (Fut8(-/-)) mice showed a schizophrenia-like phenotype and a decrease in working memory. To understand the underlying molecular mechanism, we analyzed early form long term potentiation (E-LTP), which is closely related to learning and memory in the hippocampus. The scale of E-LTP induced by high frequency stimulation was significantly decreased in Fut8(-/-) mice. Tetraethylammonium-induced LTP showed no significant differences, suggesting that the decline in E-LTP was caused by postsynaptic events. Unexpectedly, the phosphorylation levels of calcium/calmodulin-dependent protein kinase II (CaMKII), an important mediator of learning and memory in postsynapses, were greatly increased in Fut8(-/-) mice. The expression levels of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPARs) in the postsynaptic density were enhanced in Fut8(-/-) mice, although there were no significant differences in the total expression levels, implicating that AMPARs without core fucosylation might exist in an active state. The activation of AMPARs was further confirmed by Fura-2 calcium imaging using primary cultured neurons. Taken together, loss of core fucosylation on AMPARs enhanced their heteromerization, which increase sensitivity for postsynaptic depolarization and persistently activate N-methyl-d-aspartate receptors as well as Ca(2+) influx and CaMKII and then impair LTP.

Loss of α1,6-fucosyltransferase suppressed liver regeneration: implication of core fucose in the regulation of growth factor receptor-mediated cellular signaling.

Core fucosylation is an important post-translational modification, which is catalyzed by α1,6-fucosyltransferase (Fut8). Increased expression of Fut8 has been shown in diverse carcinomas including hepatocarcinoma. In this study, we investigated the role of Fut8 expression in liver regeneration by using the 70% partial hepatectomy (PH) model, and found that Fut8 is also critical for the regeneration of liver. Interestingly, we show that the Fut8 activities were significantly increased in the beginning of PH (~4d), but returned to the basal level in the late stage of PH. Lacking Fut8 led to delayed liver recovery in mice. This retardation mainly resulted from suppressed hepatocyte proliferation, as supported not only by a decreased phosphorylation level of epidermal growth factor (EGF) receptor and hepatocyte growth factor (HGF) receptor in the liver of Fut8(-/-) mice in vivo, but by the reduced response to exogenous EGF and HGF of the primary hepatocytes isolated from the Fut8(-/-) mice. Furthermore, an administration of L-fucose, which can increase GDP-fucose synthesis through a salvage pathway, significantly rescued the delayed liver regeneration of Fut8(+/-) mice. Overall, our study provides the first direct evidence for the involvement of Fut8 in liver regeneration.