50 research outputs found

    Effect of Superhydrophobic Surface of Titanium on Staphylococcus aureus

    Get PDF
    Despite the systemic antibiotics prophylaxis, orthopedic implants still remain highly susceptible to bacterial adhesion and resulting in device-associated infection. Surface modification is an effective way to decrease bacterial adhesion. In this study, we prepared surfaces with different wettability on titanium surface based on TiO2 nanotube to examine the effect of bacterial adhesion. Firstly, titanium plates were calcined to form hydrophilic TiO2 nanotube films of anatase phase. Subsequently, the nanotube films and inoxidized titaniums were treated with 1H, 1H, 2H, 2H-perfluorooctyl-triethoxysilane (PTES), forming superhydrophobic and hydrophobic surfaces. Observed by SEM and contact angle measurements, the different surfaces have different characteristics. Staphylococcus aureus (SA) adhesion on different surfaces was evaluated. Our experiment results show that the superhydrophobic surface has contact angles of water greater than 150∘ and also shows high resistance to bacterial contamination. It is indicated that superhydrophobic surface may be a factor to reduce device-associated infection and could be used in clinical practice

    Suppression of MAPK11 or HIPK3 reduces mutant Huntingtin levels in Huntington's disease models.

    Get PDF
    Most neurodegenerative disorders are associated with accumulation of disease-relevant proteins. Among them, Huntington disease (HD) is of particular interest because of its monogenetic nature. HD is mainly caused by cytotoxicity of the defective protein encoded by the mutant Huntingtin gene (HTT). Thus, lowering mutant HTT protein (mHTT) levels would be a promising treatment strategy for HD. Here we report two kinases HIPK3 and MAPK11 as positive modulators of mHTT levels both in cells and in vivo. Both kinases regulate mHTT via their kinase activities, suggesting that inhibiting these kinases may have therapeutic values. Interestingly, their effects on HTT levels are mHTT-dependent, providing a feedback mechanism in which mHTT enhances its own level thus contributing to mHTT accumulation and disease progression. Importantly, knockout of MAPK11 significantly rescues disease-relevant behavioral phenotypes in a knockin HD mouse model. Collectively, our data reveal new therapeutic entry points for HD and target-discovery approaches for similar diseases

    Disruption of RFX family transcription factors causes autism, attention-deficit/hyperactivity disorder, intellectual disability, and dysregulated behavior

    Get PDF
    Purpose We describe a novel neurobehavioral phenotype of autism spectrum disorder (ASD), intellectual disability, and/or attention-deficit/hyperactivity disorder (ADHD) associated with de novo or inherited deleterious variants in members of the RFX family of genes. RFX genes are evolutionarily conserved transcription factors that act as master regulators of central nervous system development and ciliogenesis. Methods We assembled a cohort of 38 individuals (from 33 unrelated families) with de novo variants in RFX3, RFX4, and RFX7. We describe their common clinical phenotypes and present bioinformatic analyses of expression patterns and downstream targets of these genes as they relate to other neurodevelopmental risk genes. Results These individuals share neurobehavioral features including ASD, intellectual disability, and/or ADHD; other frequent features include hypersensitivity to sensory stimuli and sleep problems. RFX3, RFX4, and RFX7 are strongly expressed in developing and adult human brain, and X-box binding motifs as well as RFX ChIP-seq peaks are enriched in the cis-regulatory regions of known ASD risk genes. Conclusion These results establish a likely role of deleterious variation in RFX3, RFX4, and RFX7 in cases of monogenic intellectual disability, ADHD and ASD, and position these genes as potentially critical transcriptional regulators of neurobiological pathways associated with neurodevelopmental disease pathogenesis
    corecore