A Guided Mode Resonance Aptasensor for Thrombin Detection

Recent developments in aptamers have led to their widespread use in analytical and diagnostic applications, particularly for biosensing. Previous studies have combined aptamers as ligands with various sensors for numerous applications. However, merging the aptamer developments with guided mode resonance (GMR) devices has not been attempted. This study reports an aptasensor based home built GMR device. The 29-mer thrombin aptamer was immobilized on the surface of a GMR device as a recognizing ligand for thrombin detection. The sensitivity reported in this first trial study is 0.04 nm/μM for thrombin detection in the concentration range from 0.25 to 1 μM and the limit of detection (LOD) is 0.19 μM. Furthermore, the binding affinity constant (Ka) measured is in the range of 106 M−1. The investigation has demonstrated that such a GMR aptasensor has the required sensitivity for the real time, label-free, in situ detection of thrombin and provides kinetic information related to the binding

Optical Design of an LED Lighting Source for Fluorescence Microscopes

In this study, we reveal an LED light source model applied in fluorescence microscopes. This optical model is composed of a confocal total internal reflection lens array system (CTLAS) with a nine-LED array. The CTLAS optical system that we designed consists of a total internal reflection (TIR) lens array and a confocal system. The electrical power of the nine-LED array is 7.9 watts, which is lower than traditional light sources, such as the original 120-watt halogen lamps used in fluorescence microscopes (Zeiss, Axio Imager 2). We have successfully applied the CTLAS system to an Axio Imager 2 fluorescence microscope to observe the vascular bundle organization, modified with Cy3 fluorescence molecules, and have found that in the process of system assembly, the fabrication errors of optical lenses could have a critical effect on the CTLAS system. The results of our experiment show that, in order to achieve the same illuminance as that of the halogen lamp, the displacement error tolerances of the lateral x-axis and the longitudinal z-axis must be controlled within 1.3 mm and 1.7 mm, respectively

Performance Enhancement of Vanadium Redox Flow Battery by Treated Carbon Felt Electrodes of Polyacrylonitrile using Atmospheric Pressure Plasma

A high-performance carbon felt electrode for all-vanadium redox flow battery (VRFB) systems is prepared via low-temperature atmospheric pressure plasma treatment in air to improve the hydrophilicity and surface area of bare carbon felt of polyacrylonitrile and increase the contact potential between vanadium ions, so as to reduce the overpotential generated by the electrochemical reaction gap. Brunauer-Emmett-Teller (BET) surface area of the modified carbon felt is, significantly, five times higher than that of the pristine felt. The modified carbon felt exhibits higher energy efficiency (EE) and voltage efficiency (VE) in a single cell VRFB test at the constant current density of 160 mA cm−2, and also maintains good performance at low temperatures. Moreover, the cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) analysis results show that the resistance between electrolyte and carbon felt electrode decreased. As a result, owing to the increased reactivity of the vanadium ion on the treated carbon felt, the efficiency of the VRFB with the plasma-modified carbon felt is much higher and demonstrates better capacity under a 100-cycle constant current charge-discharge test

Role of Macrophage CCAAT/Enhancer Binding Protein Delta in the Pathogenesis of Rheumatoid Arthritis in Collagen-Induced Arthritic Mice

<div><h3>Background</h3><p>The up-regulation of CCAAT/enhancer binding protein delta (CEBPD) has frequently been observed in macrophages in age-associated disorders, including rheumatoid arthritis (RA). However, the role of macrophage CEBPD in the pathogenesis of RA is unclear.</p> <h3>Methodology and Principal Findings</h3><p>We found that the collagen-induced arthritis (CIA) score and the number of affected paws in <em>Cebpd^−/−</em> mice were significantly decreased compared with the wild-type (WT) mice. The histological analysis revealed an attenuated CIA in <em>Cebpd^−/−</em> mice, as shown by reduced pannus formation and greater integrity of joint architecture in affected paws of <em>Cebpd^−/−</em> mice compared with WT mice. In addition, immunohistochemistry analysis revealed decreased pannus proliferation and angiogenesis in <em>Cebpd^−/−</em> mice compared with WT mice. CEBPD activated in macrophages played a functional role in promoting the tube formation of endothelial cells and the migration and proliferation of synoviocytes. <em>In vivo</em> DNA binding assays and reporter assays showed that CEBPD up-regulated <em>CCL20</em>, <em>CXCL1</em>, <em>IL23A</em> and <em>TNFAIP6</em> transcripts through direct binding to their promoter regions. CCL20, IL23A, CXCL1 and TNFAIP6 contributed to the migration and proliferation of synoviocytes, and the latter two proteins were involved in tube formation of endothelial cells. Finally, two anti-inflammatory chemicals, inotilone and rosmanol, reduced the expression of CEBPD and its downstream targets and mitigated the above phenomena.</p> <h3>Conclusions and Significance</h3><p>Collectively, our findings suggest that CEBPD and its downstream effectors could be biomarkers for the diagnosis of RA and potentially serve as therapeutic targets for RA therapy.</p> </div

Metabolic Syndromes as Important Comorbidities in Patients of Inherited Retinal Degenerations: Experiences from the Nationwide Health Database and a Large Hospital-Based Cohort

This study aimed to evaluate the medical and socioeconomic impacts of IRDs using the nationwide health database and a large hospital-based cohort. This retrospective cross-sectional cohort study used data from the nationwide National Health Insurance Research Database (NHIRD). All patients with IRD from January 2012 to December 2016 were selected from the NHIRD and matched with the general population at a ratio of 1:4. All variables, including comorbidities, medications, service utilization, and medical costs, within 1 year from the date of the IRD diagnosis, were analyzed. Disability data were retrieved from the Taiwan Inherited retinal degeneration Project (TIP), a medical center-based database. A total of 4447 and 17,788 subjects from the nationwide database were included in the IRD and control groups, respectively. The Charlson comorbidity index score was higher in the IRD group (0.74:0.52, p &lt; 0.001). Yearly visits to the ophthalmology clinic were more frequent in the IRD group (6.80:1.06, p &lt; 0.001), particularly to tertiary medical centers (p &lt; 0.001). The IRD group showed greater odds ratios (OR) for metabolic syndrome-related comorbidities, including hypertension (OR = 1.18, 95% confidence interval (CI) 1.10 to 1.26) and diabetes (OR = 1.32, 95% CI 1.21 to 1.45), and double the average yearly medical cost (2104.3 vs. 1084.6 USD, p &lt; 0.001) and ten times the yearly ophthalmology cost (369.1 vs. 36.1 USD, p &lt; 0.001). The average disability level was 54.17% for all subjects. This study revealed the large medical and socioeconomic impacts of IRD on not only patients with IRD, but also their family members and the whole society

Cebpd plays an important role in CIA mice.

<p>A, Age- and sex-matched C57BL/6 mice were immunized with chicken CII emulsified in CFA at day 0. The mice were scored every 2–3 days without knowledge of their genotypes. Clinical score of arthritis: the scores for four paws were obtained for each mouse, and the total severity score for the group was divided by the number of animals in the group to obtain an average severity score. B, The rear paws and joints from <i>Cebpd^+/+</i> and <i>Cebpd^−/−</i> mice were stained with hematoxylin and eosin after collagen-induced arthritis. C, Histopathological scores: the score from two ankle joints in each mouse was assessed by two orthopedic surgeons blind to the genotypes of the mice. The average histopathological score in the <i>Cebpd ^−/−</i> group was significantly lower than that of the wild-type group (<i>p = </i>0.016). *<i>p</i><0.05; <i>n = </i>10 for control and <i>n = </i>6 for the experimental group.</p

<i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> genes are responsive to CEBPD activation in THP-1 cells.

<p>A, CEBPD participates in TNFα-induced <i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> transcripts in THP-1 cells. Total RNA was extracted from TNFα-treated THP-1 cells treated with lentiviral shCEBPD (sh-D) or shluciferase (sh-L) for RT-PCR analysis. B, <i>Ccl20</i>, <i>Cxcl1</i>, <i>Il23a</i> and <i>Tnfaip6</i> transcripts in TNFα-treated primary macrophages of WT or <i>Cebpd</i>-deficient mice. Total RNA was extracted from TNFα-treated macrophages of WT or <i>Cebpd</i>-deficient mice for RT-PCR analysis. C, Putative CEBPD-binding motifs in the <i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> reporters. The 5′-flanking regions of human <i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> genes were subcloned into pGL3 basic reporters. (D) CEBPD activates <i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> reporter activities in THP-1 cells. pcDNA3/HA/CEBPD (pcHA/CEBPD) or pcDNA3/HA (pcHA) was cotransfected with the <i>CCL20</i> (−1000 to +50), <i>CXCL1</i> (−970 to +51), <i>IL23A</i> (−1200 to +60) or <i>TNFAIP6</i> (−600 to +76) reporter. The data are presented as the means ± SE of relative luciferase activity from three independent experiments in duplicate. E, CEBPD contributes to TNFα-induced <i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> reporter activities in THP-1 cells. Oligonucleotides of siCEBPD (si-D) or siLacZ (si-C) were cotransfected with various indicated reporters. The lysates of transfectants were harvested after treating with TNFα for 6 h. The data are presented as the means ± SE of relative luciferase activity. The asterisks represent significant differences (*<i>p</i><0.05; Student’s t test). F, CEBPD binds to the 5′-flanking regions of the <i>CCL20</i>, <i>CXCL1</i>, <i>IL23A</i> and <i>TNFAIP6</i> genes <i>in vivo</i>. Chromatin was isolated for ChIP analysis from THP-1 cells with or without TNFα treatment, as described in the Materials and Methods. The locations of the PCR primers in the 5′-flanking regions of <i>CCL20</i> (−344 to −7), <i>CXCL1</i> (−736 to −406), <i>IL23A</i> (−379 to −45) and <i>TNFAIP6</i> (−354 to −6) are presented in the left panel. Chromatin was separately immunoprecipitated with control IgG and CEBPD antibodies and then amplified by PCR with the indicated primers, as shown in the right panel.</p

CCL20, CXCL1, IL23A and TNFAIP6 contribute to the proliferation and migration of rFLS cells, but only CXCL1 and TNFAIP6 increase endothelial cell tube formation.

<p>A, CCL20, CXCL1, IL23A and TNFAIP6 contribute to the proliferation and migration of rFLS cells. The purified rFLS were cultured with the conditioned medium harvested from TNFα-treated THP-1 cells containing the indicated lentivirus, namely shLuciferase (Sh-L), shCCL20 (Sh-CC), shCXCL1 (Sh-CX), shIL23A (Sh-IL) or shTNFAIP6 (Sh-TA). The migration and proliferation assays were conducted using a Boyden chamber assay and a CCK-8 kit, respectively. The results are shown as the means ± SE. The asterisks represent significant differences (*<i>p</i><0.05; Student’s t test). B, The endothelial tube formation assay was conducted using conditioned media harvested from THP-1 cells as described in the Materials and Methods. The results are shown in the upper panel and compared statistically in the lower panel. The number of intersections between branches of assembled endothelial cell networks was counted in the whole field. The data are presented as the means ± SE. The asterisks represent significant differences (*<i>p</i><0.05, **<i>p</i><0.01; Student’s t test).</p