Visualization 1: Highly photorefractive hybrid liquid crystal device for a video-rate holographic display

Visualization 1 blue running horse Originally published in Optics Express on 18 April 2016 (oe-24-8-8824

Summary results of meta-analysis by hemostatic markers.

<p>AF, atrial fibrillation; MPV, mean platelet volume; PF-4, platelet factor 4; BTG, β-thromboglobulin; P-sel, P-selectin; Fib, fibrinogen; TAT, thrombin—antithrombin; F1+2, prothombin fragments 1+2; AT- III, Antithrombin III; tPA, tissue plasminogen activator; PAI-1, plasminogen activator inhibitor-1; vWf, vonWillebrand factor; sTM, soluble thrombomodulin; SMD, standardized mean difference; CI, confidence interval.</p><p>Summary results of meta-analysis by hemostatic markers.</p

Association between fibrinolytic function makers and AF.

<p>A. Tissue-type plasminogen activator and AF; B. Plasminogen activator inhibitor-1 and AF. Forest plots of SMD and overall SMD with 95% CI between AF cases and controls. Black diamonds indicate the SMD, with the size of the square inversely proportional to its variance, and horizontal lines represent the 95% CI. The pooled results are indicated by the black hollow diamond. AF, atrial fibrillation; tPA, tissue-type plasminogen activator; PAI-1, plasminogen activator inhibitor-1; SMD, standardized mean difference.</p

Association between coagulation activation markers and AF.

<p>A. D-dimer and AF; B. fibrinogen and AF; C. Thrombin-antithrombin and AF; D. Prothrombin fragment 1+2 and AF; E. Antithrombin- III and AF. Forest plots of SMD and overall SMD with 95% CI between AF cases and controls. Black diamonds indicate the SMD, with the size of the square inversely proportional to its variance, and horizontal lines represent the 95% CI. The pooled results are indicated by the black hollow diamond. AF, atrial fibrillation; TAT, thrombin-antithrombin; F1+2, prothrombin fragment 1+2; AT- III, antithrombin- III; PAF, paroxysmal AF; PeAF, persistent AF; PtAF, permanent AF; CAF, chronic AF; aAF, acute AF; SMD, standardized mean difference.</p

Association between endothelial function markers and AF.

<p>A. Von Willebrand factor and AF; B. Soluble thrombomodulin and AF. Forest plots of SMD and overall SMD with 95% CI between AF cases and controls. Black diamonds indicate the SMD, with the size of the square inversely proportional to its variance, and horizontal lines represent the 95% CI. The pooled results are indicated by the black hollow diamond. AF, atrial fibrillation; vWf, von Willebrand factor; sTM, soluble thrombomodulin; PAF, paroxysmal AF; PeAF, persistent AF; PtAF, permanent AF; CAF, chronic AF; aAF, acute AF; SMD, standardized mean difference.</p

Association between platelet activation markers and AF.

<p>A. platelet count and AF; B. Mean platelet volume and AF; C. Platelet factor-4 and AF; D. β-thromboglobulin and AF; E. P-selectin and AF. Forest plots of SMD and overall SMD with 95% CI between AF cases and controls. Black diamonds indicate the SMD, with the size of the square inversely proportional to its variance, and horizontal lines represent the 95% CI. The pooled results are indicated by the black hollow diamond. AF, atrial fibrillation; MPV, mean platelet volume; PF-4, platelet factor-4; BTG, β-thromboglobulin; PAF, paroxysmal AF; PeAF, persistent AF; PtAF, permanent AF; CAF, chronic AF; SMD, standardized mean difference.</p

Flow diagram of the literature search and study selection.

<p>Flow diagram of the literature search and study selection.</p

HMGB1-Promoted and TLR2/4-Dependent NK Cell Maturation and Activation Take Part in Rotavirus-Induced Murine Biliary Atresia

<div><p>Recent studies show that NK cells play important roles in murine biliary atresia (BA), and a temporary immunological gap exists in this disease. In this study, we found high-mobility group box-1 (HMGB1) and TLRs were overexpressed in human and rotavirus-induced murine BA. The overexpressed HMGB1 released from the nuclei of rotavirus-infected cholangiocytes, as well as macrophages, activated hepatic NK cells via HMGB1-TLRs-MAPK signaling pathways. Immature NK cells had low cytotoxicity on rotavirus-injured cholangiocytes due to low expression of TLRs, which caused persistent rotavirus infection in bile ducts. HMGB1 up-regulated the levels of TLRs of NK cells and promoted NK cell activation in an age-dependent fashion. As NK cells gained increasing activation as mice aged, they gained increasing cytotoxicity on rotavirus-infected cholangiocytes, which finally caused BA. Adult NK cells eliminated rotavirus-infected cholangiocytes shortly after infection, which prevented persistent rotavirus infection in bile ducts. Moreover, adoptive transfer of mature NK cells prior to rotavirus infection decreased the incidence of BA in newborn mice. Thus, the dysfunction of newborn NK cells may, in part, participate in the immunological gap in the development of rotavirus induced murine BA.</p></div

Expression of HMGB1, TLR2 and TLR4 in livers of infants with biliary atresia (BA) and in bile ducts of mice challenged with RRV.

<p>(<b>A</b>) Paraffin sections of liver tissues from infants at the time of operation for congenital dilation of the bile duct (CDB) (N = 5) or BA (N = 9) immunostained with anti-HMGB1, anti-TLR2 or anti-TLR4 antibody. Brown staining represents positive signals. The scale bar = 20 µm. (<b>B</b>) Protein levels of HMGB1, TLR2 and TLR4 detected by western blotting in liver tissues from patients with CDB or BA. The protein levels are normalized to β-actin. (<b>C</b>) mRNA levels of HMGB1, TLR2 and TLR4 detected by realtime RT-PCR. The data are normalized to <i>GAPDH</i>. (<b>D</b>) All mice were injected with 50 µl vehicle medium or 50 µl RRV supernatant intraperitoneally within 12 hours after birth and were euthanized 7 days later. Paraffin sections of livers were immunostained with anti-HMGB1, anti-TLR2 or anti-TLR4 antibody. The scale bar = 15 µm. (<b>E, F</b> and <b>G</b>) mRNA levels of HMGB1, TLR2 and TLR4 in livers were detected by realtime RT-PCR. The data are normalized to <i>GAPDH</i>. *<i>p</i><0.05, **<i>p</i><0.01; N = 7–16 mice per group. The values were expressed as mean ± SD.</p

Expression of total and phosphorylated p38, ERK and JNK.

<p>(<b>A</b>) Specific bands of p38, p-p38, ERK, p-ERK, JNK and p-JNK of NK cells derived from adult wild-type B10 mice and <i>Tlr4</i>^−/− mice were detected. NK cells were stimulated with HMGB1 or un-stimulated. (<b>B</b>–<b>G</b>) Fold changes of total and phosphorylated p38, ERK and JNK of NK cells derived from wild-type B10 mice and <i>Tlr4</i>^−/− mice were quantified. (<b>H</b>) Specific bands of p38, p-p38, ERK, p-ERK, JNK and p-JNK of NK cells derived from adult wild-type B6 mice and <i>Tlr2</i>^−/− mice were detected. (<b>I</b>–<b>N</b>) Relative protein levels of total and phosphorylated p38, ERK and JNK of NK cells derived from wild-type B6 mice and <i>Tlr2</i>^−/− mice were quantified. *<i>p</i><0.05, **<i>p</i><0.01; N = 5 mice per group. The protein levels are normalized to internal β-Tubulin controls and expressed as mean ± SD.</p