Rabbit Anti-Human PSMA1 Polyclonal Antibody

Objective: Studies of regenerative therapies have focused on the paracrine effects of mesenchymal stem cells, but little has been revealed about the humoral factors of periodontal ligament (PDL) stem cells. The aim of this study was to identify and compare the secretory factors of human permanent- and deciduous teeth PDL cells (P-PDL and D-PDL cells, respectively) in order to understand the characteristics of these cells and their potential applications in regenerative therapies. Design: Conditioned media were collected from P-PDL and D-PDL cells (P-PDL-CM and D-PDL-CM, respectively). These media were analyzed with high-performance liquid-chromatography-coupled electrospray ionization tandem mass spectrometry and a cytokine membrane assay. In addition, Western blot analysis was performed to verify the differences between the two media. Results: Cytokines related to neurogenesis (NT-3 and NT-4) and angiogenesis-related cytokines (EGF and IGF-1) were identified in P-PDL-CM. The expression levels of immune-response-related cytokines (interleukins I, II, and IV) and secreted proteins related to tissue degradation and catalytic activities (matrix metallopeptidase 1 (MMP1), Proteasome subunit, alpha type, 1 (PSMA1), and cullin 7 (CUL7)) were higher in D-PDL-CM. Vasorin (VASN) was expressed more strongly in P-PDL-CM, but tudor domain containing 7 (TDRD7) was expressed more strongly in D-PDL-CM in Western blot analysis. Conclusion: The cytokine expressions of the two cell types showed different patterns, especially in neurogenesis and immune responses. P-PDL cells are more suitable candidates for applications in regenerative therapies. (C) 2016 Elsevier Ltd. All rights reserved.

Papillary thyroid carcinoma (PTC) is most common among all thyroid cancers. Multiple genomic alterations occur in PTC, and gene rearrangements are one of them. Here we screened 14 tumors for novel fusion transcripts by RNA-Seq. Two samples harboring RET/PTC1 and RET/PTC3 rearrangements were positive controls whereas the remaining ones were negative regarding the common PTC alterations. We used Sanger sequencing to validate potential fusions. We detected 2 novel potentially oncogenic transcript fusions: TG-FGFR1 and TRIM33-NTRK1. We detected 4 novel fusion transcripts of unknown significance accompanying the TRIM33-NTRK1 fusion: ZSWIM5-TP53BP2, TAF4B-WDR1, ABI2-MTA3, and ARID1B-PSMA1. Apart from confirming the presence of RET/PTC1 and RET/PTC3 in positive control samples, we also detected known oncogenic fusion transcripts in remaining samples: TFG-NTRK1, ETV6-NTRK3, MKRN1-BRAF, EML4-ALK, and novel isoform of CCDC6-RET.