An Amphiphilic Star-Shaped Polymer (Star-PEG-PCL2) used as a Stationary Phase for GC.

A star-shaped polymer (Star-PEG-PCL2) was synthesized with PCL and PEG and used as a stationary phase for gas chromatography. The statically coated Star-PEG-PCL2 column exhibited an efficiency of 2260 plates/m determined by naphthalene at 120 °C and moderate polarity. The Star-PEG-PCL2 column showed high resolution performance for isomers of a wide ranging polarity, including methylnaphthalenes, halogenated benzenes, nitrobenzene, phenols, and anilines, and displayed dual-nature selectivity for a mixture of 17 analytes. Also, the Star-PEG-PCL2 column exhibited good separation performance and column inertness for Grob test mixture and a series of cis-/trans-isomers. In addition, it exhibited advantageous separation performance over the commercial HP-35 and PEG-20M columns for chloroaniline and bromoaniline isomers through its unique three-dimensional framework. In conclusion, it has good potential as a new stationary phase for separating a variety of analytes because of its special structure and excellent separation performance.

Synthesis, Crystal Structure and Separation Performance of p-tert-butyl(tetradecyloxy)calix[6]arene.

This work describes the investigation of separation performance of the p-tert-butyl(tetradecyloxy)calix[6]arene (C6A-C10-OH) as stationary phase for gas chromatography (GC) separations. Its structure was characterized by IR, 1H NMR, 13C NMR, MS and single-crystal X-ray diffraction analysis. The C6A-C10-OH column shows good separation capacity for aliphatic, aromatic and cis-/trans- isomers. Especially, it exhibits multiple molecular recognition interactions for the analytes with a wide range of polarity, including dispersion, π-π, H-bonding and dipole-dipole interactions. The present work provides experimental and theoretical basis for the designing of the new calixarene stationary phases in GC analyses.

Histone deacetylase­2: A potential regulator and therapeutic target in liver disease (Review).

Histone acetyltransferases are responsible for histone acetylation, while histone deacetylases (HDACs) counteract histone acetylation. An unbalanced dynamic between histone acetylation and deacetylation may lead to aberrant chromatin landscape and chromosomal function. HDAC2, a member of class I HDAC family, serves a crucial role in the modulation of cell signaling, immune response and gene expression. HDAC2 has emerged as a promising therapeutic target for liver disease by regulating gene transcription, chromatin remodeling, signal transduction and nuclear reprogramming, thus receiving attention from researchers and clinicians. The present review introduces biological information of HDAC2 and its physiological and biochemical functions. Secondly, the functional roles of HDAC2 in liver disease are discussed in terms of hepatocyte apoptosis and proliferation, liver regeneration, hepatocellular carcinoma, liver fibrosis and non­alcoholic steatohepatitis. Moreover, abnormal expression of HDAC2 may be involved in the pathogenesis of liver disease, and its expression levels and pharmacological activity may represent potential biomarkers of liver disease. Finally, research on selective HDAC2 inhibitors and non­coding RNAs relevant to HDAC2 expression in liver disease is also reviewed. The aim of the present review was to improve understanding of the multifunctional role and potential regulatory mechanism of HDAC2 in liver disease.

Emerging Roles for NLRC5 in Immune Diseases.

Innate immunity activates the corresponding immune response relying on multiple pattern recognition receptors (PRRs) that includes pattern recognition receptors (PRRs), like NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and C-type lectin receptors (CLRs), which could accurately recognize invasive pathogens. In particular, NLRs belong to a large protein family of pattern recognition receptors in the cytoplasm, where they are highly correlated with activation of inflammatory response system followed by rapid clearance of invasive pathogens. Among the NLRs family, NLRC5, also known as NOD4 or NOD27, accounts for a large proportion and involves in immune responses far and wide. Notably, in the above response case of inflammation, the expression of NLRC5 remarkably increased in immune cells and immune-related tissues. However, the evidence for higher expression of NLRC5 in immune disease still remains controversial. It is noted that the growing evidence further accounts for the participation of NLRC5 in the innate immune response and inflammatory diseases. Moreover, NLRC5 has also been confirmed to exert a critical role in the control of regulatory diverse signaling pathways. Together with its broad participation in the occurrence and development of immune diseases, NLRC5 can be consequently treated as a potential therapeutic target. Nevertheless, the paucity of absolute understanding of intrinsic characteristics and underlying mechanisms of NLRC5 still make it hard to develop targeting drugs. Therefore, current summary about NLRC5 information is indispensable. Herein, current knowledge of NLRC5 is summarized, and research advances in terms of NLRC5 in characteristics, biological function, and regulatory mechanisms are reviewed.

NLRC5 promotes cell proliferation via regulating the NF-κB signaling pathway in Rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease and the pathogenesis remains unclear. Previous studies suggested that fibroblast-like synoviocytes (FLSs) play an important role in RA pathogenesis, including the injury of cartilage, the hyperplasia of the synovium and the release of inflammatory cytokines. We used complete Freund's adjuvant (CFA) induced rats as animal models for studying the RA pathogenesis. NLRC5 as the largest member of the NLR family has been reported to play a critical role in regulating immune responses. Increasing evidence suggests that NLRC5 is an pivotal negative modulator of inflammatory pathways. We investigated the mechanisms and signaling pathways of NLRC5 in RA progression. Significantly increased expression of NLRC5 was found in AA rats synovial tissues and cells. And high expression of inflammatory cytokine and cell proliferation of FLSs accompanied with NLRC5 overexpression, but inhibited in cells with NLRC5 silencing treatment. Interestingly, we found that overexpression of NLRC5 also coordinated the activation of NF-κB signaling pathway. These results suggested that NLRC5 promotes RA progression via the NF-κB signaling pathway potentially.

Novel "signal-on" electrochemiluminescence biosensor for the detection of PSA based on resonance energy transfer.

Here, we propose a simple and novel "signal-on" electrochemiluminescence (ECL) biosensor based on resonance energy transfer (RET) for detection of prostate specific antigen (PSA). The system is composed of Multi-walled carbon nanotubes (MWCNT), polyamidoamine (PAMAM) dendrimer and Au nanoparticles (NPs) film on glassy carbon electrode (GCE) to improve the electron transfer, provide abundant amine group for the immobilization of biomolecules, and amplify the ECL signal. After that, Au nanorods (Au NRs) labeled peptide is modified on electrode surface to serve as ECL-RET acceptor due to the excellent overlap between the ECL emission spectrum of Ru(bpy)32+ and the absorption spectrum of Au NRs, leading to the significant decrement of ECL signal. Upon the sensing cleavage of peptide with PSA, both Au NRs and peptide are released from electrode surface, resulting in the high recovery efficiency of ECL signal. The proposed approach exhibits a wide linear range from 0.1pg/mL to 10ng/mL with a detection limit of 0.03pg/mL. Results revealed that the recoveries were in a range from 95% to 108%, indicating good accuracy of the proposed method for PSA detection. In addition, the proposed biosensor exhibited well specificity for the detection of PSA.