Effects of low level laser therapy on inflammatory and angiogenic gene expression during the process of bone healing: A microarray analysis.
São Carlos, Brazil. In J Photochem Photobiol B, Jan 2016
Microarray analysis demonstrated that LLLT produced an up-regulation of the genes related to the inflammatory process (MMD, PTGIR, PTGS2, Ptger2, IL1, 1IL6, IL8, IL18) and the angiogenic genes (FGF14, FGF2, ANGPT2, ANGPT4 and PDGFD) at 36h and 3days, followed by the decrease of the gene expression on day 7. Immunohistochemical analysis revealed that the subjects that were treated presented a higher expression of COX-2 at 36h after surgery and an increased VEGF expression on days 3 and 7 after surgery.
High-throughput alternative splicing detection using dually constrained correspondence analysis (DCCA).
Sankt Gallen, Switzerland. In J Biomed Inform, Dec 2015
Splicing candidates reveal a series of genes related to carcinogenesis (SFTPB), cell adhesion (STAB2, PCDH15, HABP2), tumor aggressiveness (ARNTL2), apoptosis, proliferation and differentiation (PDE4D, FLT3, IL1R2), cell invasion (ETV1), as well as tumor growth (OLFM4, FGF14), tumor necrosis (AFF3) or tumor suppression (TUSC3, CSMD1, RHOBTB2, SERPINB5), with indication of known alternative splicing in a majority of genes.
Split-luciferase complementation assay to detect channel-protein interactions in live cells.
Galveston, United States. In Methods Mol Biol, 2014
As a response to the urgent need of developing rapid and albeit accurate technologies to survey ion channel molecular complexes, we describe a new application of the split-luciferase complementation assay to study the interaction of the voltage-gated Na + channel with the intracellular fibroblast growth factor 14 and its dynamic regulation in live cells.
Spinocerebellar ataxia 28: a novel AFG3L2 mutation in a German family with young onset, slow progression and saccadic slowing.
Lübeck, Germany. In Cerebellum Ataxias, 2014
METHODS: After excluding repeat expansions in the genes for SCA1-3, 6-8, 10, 12, and 17, Sanger sequencing of the coding regions of TTBK2 (SCA11), KCNC3 (SCA13), PRKCG (SCA14), FGF14 (SCA27) and AFG3L2 (SCA28) was performed.
Autosomal dominant cerebellar ataxia type I: a review of the phenotypic and genotypic characteristics.
Johnson City, United States. In Orphanet J Rare Dis, 2010
To date, 21 subtypes have been identified: SCA1-SCA4, SCA8, SCA10, SCA12-SCA14, SCA15/16, SCA17-SCA23, SCA25, SCA27, SCA28 and dentatorubral pallidoluysian atrophy (DRPLA).
Autosomal dominant cerebellar ataxias: polyglutamine expansions and beyond.
Paris, France. In Lancet Neurol, 2010
All other SCAs are caused by either conventional mutations or large rearrangements in genes with different functions, including glutamate signalling (SCA5/SPTBN2) and calcium signalling (SCA15/16/ITPR1), channel function (SCA13/KCNC3, SCA14/PRKCG, SCA27/FGF14), tau regulation (SCA11/TTBK2), and mitochondrial activity (SCA28/AFG3L2) or RNA alteration (SCA31/BEAN-TK2).
Spinocerebellar Ataxia Type 15
Seattle, United States. In Unknown Journal, 2006
DIAGNOSIS/TESTING: The diagnosis of SCA15 should be considered in individuals in whom the diagnoses of SCA5, SCA6, SCA8, SCA11, SCA12, SCA14, and SCA27 have been excluded by molecular genetic testing (if available) and who fulfill the clinical diagnostic criteria for SCA15.