Encapsulating TiO2 into Polyvinyl Alcohol Coated Polyacrylonitrile Composite Beads for the Effective Removal of Methylene Blue

In this work, novel nanocomposite beads based on polyvinyl alcohol (PVA) coated polyacrylonitrile (PAN) with encapsulation of TiO2 nanoparticles (PPT) were developed successfully via a novel green synthetic method and its methylene blue (MB) removal ability by adsorption was also investigated. As-prepared nanocomposite beads were characterized by different techniques such as Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), scanning electron microscopy (SEM) and thermogravimetric analysis (TGA). TiO2 nanoparticles were encapsulated into the composite beads to endow the composite beads with photocatalytic ability and enhance its adsorption capacity for MB. Batch experiments with several variables such as TiO2 nanoparticle content, pH of the solution, contact time and initial MB concentration were carried out. The adsorption kinetic study revealed that the MB adsorption process agreed well with pseudo-second order model and showed 3-stage intraparticle diffusion model. The adsorption isotherm study indicated that the MB adsorption process could also be better described by Langmuir isotherm model. According to Langmuir isotherm equation, the maximum adsorption capacity and removal rate for MB was 242.13 mg g-1 and 98.4%, respectively. Moreover, the stability and reusability of as-prepared PPT beads were further explored and results demonstrated that PPT could be reused at least five times with negligible loss of sorption capacity and removal rate. Therefore, PPT is expected to be a potential candidate for effluents treatment.</div

Table_1_The Implicated Roles of Cell Adhesion Molecule 1 (CADM1) Gene and Altered Prefrontal Neuronal Activity in Attention-Deficit/Hyperactivity Disorder: A “Gene–Brain–Behavior Relationship”?.docx

Background: Genes related to cell adhesion pathway have been implicated in the genetic architecture of attention-deficit/hyperactivity disorder (ADHD). Cell adhesion molecule 1, encoded by CADM1 gene, is a protein which facilitates cell adhesion, highly expressed in the human prefrontal lobe. This study aimed to evaluate the association of CADM1 genotype with ADHD, executive function, and regional brain functions.Methods: The genotype data of 10-tag single nucleotide polymorphisms of CADM1 for 1,040 children and adolescents with ADHD and 963 controls were used for case–control association analyses. Stroop color–word interference test, Rey–Osterrieth complex figure test, and trail making test were conducted to assess “inhibition,” “working memory,” and “set-shifting,” respectively. A subsample (35 ADHD versus 56 controls) participated in the nested imaging genetic study. Resting-state functional magnetic resonance images were acquired, and the mean amplitude of low-frequency fluctuations (mALFF) were captured.Results: Nominal significant genotypic effect of rs10891819 in “ADHD-alone” subgroup was detected (P = 0.008) with TT genotype as protective. The results did not survive multiple testing correction. No direct genetic effect was found for performance on executive function tasks. In the imaging genetic study for the “ADHD-whole” sample, rs10891819 genotype was significantly associated with altered mALFF in the right superior frontal gyrus (rSFG, peak t = 3.85, corrected P Conclusions: Our study offered preliminary evidence to implicate the roles of CADM1 in relation to prefrontal brain activities, inhibition function, and ADHD, indicating a potential “gene–brain–behavior” relationship of the CADM1 gene. Future studies with larger samples may specifically test these hypotheses generated by our exploratory findings.</p

Ori decreases mitochondrial dysfunction in the hippocampus of Aβ_1–42 induced AD mice.

<p>(A) Representative images of western blotting of cytochrome c, Bax and Bcl-2. (B) Quantitative analysis of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0104745#pone-0104745-g005" target="_blank">Figure 5A</a>. n = 6 mice per group. *P<0.05, **P<0.01 vs. control group; #P<0.05, ##P<0.01 vs. Aβ_1–42 induced AD mice.</p

Effects of Ori on the protein levels of iNOS and COX-2 in Aβ_1–42 induced AD mice.

<p>(A) Representative images of western blotting showing Ori inhibited the expression of iNOS and COX-2 in Aβ_1–42 induced AD mice. (B) Quantitative analysis of iNOS and COX-2 expression. n = 3 mice per group. *P<0.05, **P<0.01 vs. control group; #P<0.05, ##P<0.01 vs. Aβ_1–42 induced AD mice.</p

Ori reduces the inflammatory factors in Aβ_1–42 induced AD mice.

<p>The mRNA levels of IL-1β (A), IL-6 (B), iNOS (C), COX-2 (D), TNF-α (E), MCP-1 (F) and IL-10 (G) were measured in each group by Real-time PCR. GAPDH was used as an internal control. n = 6 mice per group. *P<0.05, **P<0.01 vs. control group; #P<0.05, ##P<0.01 vs. Aβ_1–42 induced AD mice.</p

Ori inhibits Aβ_1–42 induced activation of NF-κB in Aβ_1–42 induced AD mice.

<p>(A) Representative image of western blotting of p65, p-IκBα, IκBα in the cytosolic and p65 in nuclear. (B) Quantitative analysis of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0104745#pone-0104745-g004" target="_blank">Figure 4A</a>. n = 6 mice per group. *P<0.05, **P<0.01 vs. control group; #P<0.05, ##P<0.01 vs. Aβ_1–42 induced AD mice.</p

Ori suppresses glial activation in Aβ_1–42 induced AD mice.

<p>(A) Immunostaining for Iba1 and GFAP in the hippocampus of mice. (B) Quantitative analysis of Iba1 and GFAP staining. n = 6 mice per group. Scale bar  = 50 µm. *P<0.05, **P<0.01 vs. control group; #P<0.05, ##P<0.01 vs. Aβ_1–42 induced AD mice.</p

Ori attenuates learning and memory impairment in Aβ_1–42 induced AD mice in the Morris water maze test.

<p>(A) Escape latency for escape to a submerged platform in the training trails. **P<0.01 vs. control group; ##P<0.01 vs. Ori-treated AD mice. (B) Searching distance for escape to a submerged platform in the training trails. **P<0.01 vs. control group; #P<0.05, ##P<0.01 vs. Ori-treated AD mice. (C) Crossing platform times in the probe trail. **P<0.01 vs. control group; ##P<0.01 vs. Aβ_1–42 induced AD mice. (D) Swimming speed in the training trails. n = 6 mice per group.</p

Effect of Ocular Magnification on Macular Choroidal Thickness Measurements Made Using Optical Coherence Tomography in Children

To evaluate the relationship between ocular magnification correction and macular choroidal thickness (ChT) measurements in children, and to demonstrate when ocular magnification correction is necessary. Chinese children aged 6–9 years with various refractive statuses were included. Swept-source optical coherence tomography was used to measure macular ChT. A self-designed program was adopted to simulate ChT changes in each sector of the ETDRS grid in the macula under various simulated axial lengths (ALs). ChT measurements were not affected for all simulated ALs in over 95% of the individuals in the central fovea. In the inferior, superior, and temporal parafoveal sectors, the extent of AL that may include 95% of the individuals narrowed from approximately 22.0 mm to 27.2 mm. In the nasal parafoveal sector and inferior, superior, and temporal perifoveal sectors, the extent of AL that may include 95% of the individuals became even narrower, from approximately 22.8 mm to 26.0 mm. The narrowest extent was observed in the perifoveal nasal sector, ranging from 23.3 mm to 25.5 mm. The effect of ocular magnification was more significant in hyperopes than in myopes in the inferior parafoveal sector and temporal, superior, and nasal perifoveal sectors. During macular ChT measurements, ocular magnification correction is not necessary in the central fovea. However, ocular magnification should be corrected normally in the nasal perifoveal region and in individuals with ALs shorter than 22.8 mm or longer than 26.0 mm in the remaining macular regions.</p

DG treatment significantly increased the expression of PGC-1α <i>in vitro and in vivo</i>.

<p>Neurons were treated with 2 µM Aβ_1–42 and 0.001 µg/µl DG for the indicated time points, and the mRNA (A) and protein expression (B) of PGC-1α were analyzed by Real-time PCR and western blotting respectively. (C) Quantitative analysis of the relative protein levels of PGC-1α. The relative RNA or protein levels of control neurons were considered 1. Results were shown as the mean± SEM and represented at least three independent experiments. * <i>P</i><0.05 and ** <i>P</i><0.01 for Student's <i>t</i>-test compared with Aβ_1–42-treated, respectively. (D) The expression of PGC-1α of hippocampus of normal mice with saline or DG, and Aβ_1–42-induced AD mice with saline or DG was determined by western blotting. (E) Quantitative analysis of the relative protein levels of PGC-1α. Results were shown as the mean± SEM and represented at least three independent experiments. ** <i>P</i><0.01 for one-way ANOVA followed by Tukey <i>post hoc</i> test compared with control mice; # <i>P</i><0.05 for one-way ANOVA followed by Tukey <i>post hoc</i> test compared with Aβ_1–42-treated AD mice. n = 4 mice per group.</p