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Furthermore, the real interaction of DNA with the encapsulated curcumin is confirmed by the interaction of the adenine and cytosine nucleotides. This has been verified through zeta potential measurements. Moreover, our prepared nanocapsules has presented a high percentage recovery of DNA and RNA (96-101%). Finally, stability results have illustrated a high photostability of encapsulated curcumin, indicating that proposed nanocapsules can be considered as a stable sensor during measurement time.PURPOSE To evaluate the clinical and radiological outcomes for patients who undergone posterior-only lumbosacral hemivertebrectomy with short fusion with minimum two year follow-up. METHODS From 2005 to 2016, a consecutive series of 16 paediatrics scoliosis due to lumbosacral hemivertebrae were included in this study. They were treated by one stage posterior hemivertebrae resection with bilateral or unilateral short fusion. Coronal and sagittal parameters and pelvic obliquity were measured at pre-operatively, immediate post-operatively and at final follow-up. The outcome and efficacy of the correction were investigated. RESULTS The mean age was 10.4 ± 3.4 years (3-15 years). The mean follow-up period was 38.8 ± 16.2 months (24-79 months). The mean segmental scoliosis was 35.4 ± 9.2 and 7.7 ± 5.4 pre-operatively and post-operatively (78.4% correction rate) and 8.2 ± 5.0 (77%) at the latest follow-up. The compensatory coronal curve of 28.6 ± 16.1 was spontaneously corrected to 8.0 ± 8.4 in post-operatively 12.0 ± 8.4 at final follow-up. Trunk shift was significantly improved on both coronal (RTS 86.1%) and sagittal plane (68.7%) after the surgery and kept stable during the follow-up. Sacral tilt of 14.2 ± 5.3 was significantly improved to 4.7 ± 3.6 at final follow-up. There was no significant difference between bilateral and unilateral instrumentation groups (P > 0.05). One case had implants failure, and the incidence rate is 6.3%. CONCLUSIONS Early posterior hemivertebrectomy with short fusion is effective in the treatment of lumbosacral hemivertebrae. It can achieve good coronal curve correction, sacral tilt, and trunk shift improvement. No neurological complications were found. Importantly, it can prevent secondary structural deformities and potentially save fusion level.PURPOSE The different mechanisms that trigger the autoimmune attack to the thyroid between Hashimoto's thyroiditis (HT) and Graves' disease (GD) are still unclear. The aim of this study was to recognize thyroid antigens specific CD8+ T-cell epitopes and explore the relationship between these epitopes and thyroid autoantibodies, duration and classification in these two diseases. METHODS Free thiiodothyronine, free tetraiodothyronine, thyroid-stimulating hormone, TgAb, and TPOAb were all measured by immunochemiluminometric assays, while TRAb was tested by radioimmunoassay. HLA class I peptide affinity algorithms were applied to predict candidate thyroid autoantigen peptides that blind to HLA-A*0201. The ELISpot assay was used to detect Tg-, TPO-, and TSHR-specific CD8+ T cells. RESULTS We demonstrated that TG-6 was a novel HLA-A*0201-restricted CTL epitope in GD. TG-6, TG-7, TG-10, TG-11, and TPO-6 were immunodominant in GD patients compared with HT patients (TG-6 38.5 vs. 8%, P = 0.034; TG-7, TG-10, TG-11, and TPO-6 23.1 vs. 0%, P = 0.034). The immunodominance of TG-6 in GD patients was more evident than healthy controls (HC) (TG-6 35.8 vs. 0%, P = 0.011), but there was no statistically significant difference between HT patients and HC. Subgroup analyses revealed the T-cell responsiveness to TG-6 was stronger in TgAb-negative HT patients (0 vs. 40%, P = 0.033). However, there was no correlation showed for TPOAb, TRAb, medication and duration in both HT and GD patients. CONCLUSIONS We report for the first time that both diseases, HT and GD, recognize different antigen-specific CD8-positive T cells. Tg maybe the dominant thyroid autoantigen contributing to breaking tolerance in GD. It could improve our knowledge of autoimmune thyroid diseases pathogenesis as well as offer new therapeutical tools in terms of peptide vaccine therapy.Across the Bilateria, FGF/FGFR signaling is critical for normal development, and in both Drosophila and vertebrates, docking proteins are required to connect activated FGFRs with downstream pathways. While vertebrates use Frs2 to dock FGFR to the RAS/MAPK or PI3K pathways, the unrelated protein, downstream of FGFR (Dof/stumps/heartbroken), fulfills the corresponding function in Drosophila. Selleckchem MRT68921 To better understand the evolution of the signaling pathway downstream of FGFR, the available sequence databases were screened to identify Frs2, Dof, and other key pathway components in phyla that diverged early in animal evolution. While Frs2 homologues were detected only in members of the Bilateria, canonical Dof sequences (containing Dof, ankyrin, and SH2/SH3 domains) were present in cnidarians as well as bilaterians (but not in other animals or holozoans), correlating with the appearance of FGFR. Although these data suggested that Dof coupling might be ancestral, gene expression analysis in the cnidarian Hydra revealed that Dof is not upregulated in the zone of strong FGFRa and FGFRb expression at the bud base, where FGFR signaling controls detachment. In contrast, transcripts encoding other, known elements of FGFR signaling in Bilateria, namely the FGFR adaptors Grb2 and Crkl, which are acting downstream of Dof (and Frs2), as well as the guanyl nucleotide exchange factor Sos, and the tyrosine phosphatase Csw/Shp2, were strongly upregulated at the bud base. Our expression analysis, thus, identified transcriptional upregulation of known elements of FGFR signaling at the Hydra bud base indicating a highly conserved toolkit. Lack of transcriptional Dof upregulation raises the interesting question, whether Hydra FGFR signaling requires either of the docking proteins known from Bilateria.It has been recently reported by our group that GM1-oligosaccharide added to neuroblastoma cells or administered to mouse experimental model mimics the neurotrophic and neuroprotective properties of GM1 ganglioside. In addition to this, differently from GM1, GM1-oligosaccharide is not taken up by the cells, remaining solubilized into the extracellular environment interacting with cell surface proteins. Those characteristics make GM1-oligosaccharide a good tool to study the properties of the endogenous GM1, avoiding to interfere with the ganglioside natural metabolic pathway. In this study, we show that GM1-oligosaccharide administered to mice cerebellar granule neurons by interacting with cell surface induces TrkA-MAP kinase pathway activation enhancing neuron clustering, arborization and networking. Accordingly, in the presence of GM1-oligosaccharide, neurons show a higher phosphorylation rate of FAK and Src proteins, the intracellular key regulators of neuronal motility. Moreover, treated cells express increased level of specific neuronal markers, suggesting an advanced stage of maturation compared to controls.
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