Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions •
The aim of this study is to present the mid-term outcomes of Pulsta valve. The Pulsta valve is a Self-expandable knitted nitinol-wire stent mounted with a treated tri-leaflet α-Gal-free porcine pericardial valve for percutaneous pulmonary valve implantation (PPVI) in patients with native right ventricular outflow tract (RVOT) lesions. A multi-center clinical trial using Pulsta valve® was designed for patients with severe pulmonary regurgitation (PR) in the native RVOT in multiple centers in South Korea and 25 patients were enrolled. Before PPVI, severe PR (mean PR fraction: 45.5 ± 6.9%) and enlarged RV volume (mean indexed RV end-diastolic volume; 169.7 ± 13.0 ml/m ) was present. The mean age was 21.6 ± 6.6 years old. All patients were successfully implanted with 26, 28, or 32 mm diameter of Pulsta valve loaded on the 18 or 20 French delivery catheters. At 6 months follow up, indexed RV end-diastolic volume was decreased to 126.9 ± 16.9 ml/m . At mean 33.1 ± 14.3 months follow-up, the mean value of mean pressure gradient in Pulsta valve was 6.5 ± 3.0 mmhg without significant PR. There was no serious device-related adverse event. A multi-center clinical trial was completed successfully with planned Pulsta valve implantation and demonstrated good mid-term effectiveness without device-related serious adverse events.
Mast cells play important roles via FcεRI-mediated activation in allergic asthma. A nonpolymorphic MHC I-like molecule CD1d, which is mainly expressed in APCs, presents glycolipid Ag to iTCR on iNKT cells and modulates allergic responses. This study aimed to investigate the role of CD1d on IgE production and mast cell activation related to allergic asthma. Bone marrow-derived mast cells (BMMCs) from C57BL/6 Wild type (WT) or KO (CD1d(-/-)) mice were activated with Ag/Ab (refer to WT-act-BMMCs and KO-act-BMMCs, respectively) or α-Galactosylceramide (WT-αGal-BMMCs, KO-αGal-BMMCs) in the presence of iNKT cells. WT, KO or BMMC-transferred KO mice were sensitized and/or challenged by OVA or α-Gal to induce asthma. KO-act-BMMCs reduced intracellular Ca(2+) levels, expression of signaling molecules (Ras, Rac1/2, PLA2, COX-2, NF-κB/AP-1), mediator release (histamines, leukotrienes and cytokines/chemokines), and total IgE levels versus the corresponding WT-BMMCs. KO mice reduced total and OVA-specific serum IgE levels, number of mast cells, recruiting molecules (CCR2/CCL2, VCAM-1, PECAM-1), expression of tryptase, c-kit, CD40L and cytokine mRNA, co-localization of c-kit and CD1d or iNKT cells in BAL cells or lung tissues, and PCA responses, compared with the corresponding WT mice. BMMC-transferred KO-both mice showed the restoration of all allergic responses versus KO-both mice (Ag/Ab reaction plus α-Gal). KO-αGal-BMMCs or KO-αGal mice did not show any responses. Our data suggest that CD1d-expressed mast cells may function as APC cells for iNKT cells and exacerbate airway inflammation and remodeling through up-regulating IgE production via B cell Ig class switching and mediator release in mast cells of OVA-challenged mice.
