Browsing by Author "Lin, Bin"

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    A Comparison of the Ligation Torque Expression of a Ribbonwise Bracket–Archwire Combination and a Conventional Combination: A Primary Study
    (Hindawi, 2022-09-28) Lin, Bin; Jiang, Feifei; Chen, Jie; Liang, Jiaxing; Mechanical and Energy Engineering, Purdue School of Engineering and Technology
    Objective: To assess the effect of the third-order mechanics of a new ribbonwise bracket-archwire combination using an orthodontic torque simulator. Material and Methods. An orthodontic torque simulator was used to measure the third-order moment of a maxillary central incisor as it changed from a neutral position to a 40° rotation in 1° increment. A new ribbonwise bracket (Xinya, China) was compared with a conventional ligation bracket (American Orthodontic, U.S.A.). The effects of different archwire sizes (i.e., 0.017″ × 0.025″ and 0.019″ × 0.025″) and materials (i.e., nickel-titanium, titanium-molybdenum alloy, and stainless steel) were analyzed. Paired sample t-tests were conducted to compare the moments between the two bracket types corresponding to each of the archwires. The effects of the stiffness of the bracket-archwire complexes were also assessed. Results: Statistically significant differences (P=0.05) between the moments from the two brackets were found. The ribbonwise bracket-archwire complex generated larger moments when the rotation angle was lower than 30°. The ribbonwise brackets produced moments that could reach a threshold of 5 Nmm more quickly as the angle was increased. The higher the stiffness of the complex, the larger the moment. Conclusion: The ribbonwise bracket-archwire complex reached the moment threshold limits earlier than the conventional complex. When the rotation angle is less than 30°, the ribbonwise bracket-archwire complex generated a greater torque moment in comparison with the conventional complex.
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    Genetically programmed alternative splicing of NEMO mediates an autoinflammatory disease phenotype
    (The American Society for Clinical Investigation, 2022) Lee, Younglang; Wessel, Alex W.; Xu, Jiazhi; Reinke, Julia G.; Lee, Eries; Kim, Somin M.; Hsu, Amy P.; Zilberman-Rudenko, Jevgenia; Cao, Sha; Enos, Clinton; Brooks, Stephen R.; Deng, Zuoming; Lin, Bin; de Jesus, Adriana A.; Hupalo, Daniel N.; Piotto, Daniela G.P.; Terreri, Maria T.; Dimitriades, Victoria R.; Dalgard, Clifton L.; Holland, Steven M.; Goldbach-Mansky, Raphaela; Siegel, Richard M.; Hanson, Eric P.; Pediatrics, School of Medicine
    Host defense and inflammation are regulated by the NF-κB essential modulator (NEMO), a scaffolding protein with a broad immune cell and tissue expression profile. Hypomorphic mutations in inhibitor of NF-κB kinase regulatory subunit gamma (IKBKG) encoding NEMO typically present with immunodeficiency. Here, we characterized a pediatric autoinflammatory syndrome in 3 unrelated male patients with distinct X-linked IKBKG germline mutations that led to overexpression of a NEMO protein isoform lacking the domain encoded by exon 5 (NEMO-Δex5). This isoform failed to associate with TANK binding kinase 1 (TBK1), and dermal fibroblasts from affected patients activated NF-κB in response to TNF but not TLR3 or RIG-I-like receptor (RLR) stimulation when isoform levels were high. By contrast, T cells, monocytes, and macrophages that expressed NEMO-Δex5 exhibited increased NF-κB activation and IFN production, and blood cells from these patients expressed a strong IFN and NF-κB transcriptional signature. Immune cells and TNF-stimulated dermal fibroblasts upregulated the inducible IKK protein (IKKi) that was stabilized by NEMO-Δex5, promoting type I IFN induction and antiviral responses. These data revealed how IKBKG mutations that lead to alternative splicing of skipping exon 5 cause a clinical phenotype we have named NEMO deleted exon 5 autoinflammatory syndrome (NDAS), distinct from the immune deficiency syndrome resulting from loss-of-function IKBKG mutations.
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    Silencing of Kv1.5 Gene Inhibits Proliferation and Induces Apoptosis of Osteosarcoma Cells
    (MDPI AG, 2015-11-11) Wu, Jin; Chen, Zhida; Liu, Qingjun; Zeng, Wenrong; Wu, Xinyu; Lin, Bin; Department of Neurological Surgery, IU School of Medicine
    Kv1.5 (also known as KCNA5) is a protein encoded by the KCNA5 gene, which belongs to the voltage-gated potassium channel, shaker-related subfamily. Recently, a number of studies have suggested that Kv1.5 is overexpressed in numerous cancers and plays crucial roles in cancer development. However, until now, the expression and functions of Kv1.5 in osteosarcoma are still unclear. To characterize the potential biological functions of Kv1.5 in osteosarcoma, herein, we examined the expression levels of Kv1.5 in osteosarcoma cells and tissues using quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemistry assays. Four short hairpin RNAs (shRNAs) targeting Kv1.5 were designed and homologous recombination technology was used to construct pGeneSil-Kv1.5 vectors. In addition, the vectors were transfected into osteosarcoma MG63 cells and Kv1.5 mRNA level was measured by qRT-PCR and the Kv1.5 protein level was examined by western blot. We also examined the effects of Kv1.5 silencing on proliferation, cell cycle and apoptosis of the osteosarcoma cells using CCK-8, colony formation, flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. Our results showed that Kv1.5 was aberrantly expressed in osteosarcoma and that the synthesized shRNA targeting Kv1.5 reduced Kv1.5 mRNA and protein expression effectively. Silencing Kv1.5 expression in the osteosarcoma cells significantly inhibited the proliferation of osteosarcoma cells, induced cell cycle arrest at G0/G1 phase, and induced cell apoptosis through up-regulation of p21, p27, Bax, Bcl-XL and caspase-3 and down-regulation of cyclins A, cyclins D1, cyclins E, Bcl-2 and Bik. In summary, our results indicate that Kv1.5 silencing could suppress osteosarcoma progression through multiple signaling pathways and suggest that Kv1.5 may be a novel target for osteosarcoma therapeutics.