[Analysis of a Typical Ozone Pollution Process in Guangzhou in Winter].

This study focused on an ozone pollution event occurring in winter (January) in Guangzhou. Various influencing factors were analyzed, including various atmospheric trace gases, meteorological conditions during the whole pollution process, as well as the characteristics of the main O3 precursor volatile organic compounds (VOCs). The main sources of VOCs and the O3 formation regime were analyzed using an array of tools:the ozone potential formation (OFP), positive matrix factorization (PMF) model, and empirical kinetic modeling approach (EKMA) curve. Feasible strategies for O3 control were suggested. The results showed that O3 and NO2 exceeded the corresponding standards in this winter pollution event, when the concentrations of PM10 and PM2.5 were also high, differing from the air pollution characteristics in summer and autumn. Low boundary layer height (<75 m) and high atmospheric stability at night exacerbated the accumulation of ozone precursors and fine particles. Meteorological conditions such as the increased daytime temperature (5℃), stronger solar radiation (10%), and low horizontal wind speed (<1 m·s-1) favored photochemical reactions and promoted the formation of ozone and fine particles. VOCs were mainly composed of alkanes, and the proportions of alkanes and alkynes in winter were higher than those in the other seasons. Aromatics (xylenes and toluene) and propylene were the key VOCs species leading to O3 formation. The main VOCs sources were vehicle exhaust (22.4%), solvent usage (20.5%), and industrial emissions (17.9%); however, the source with highest OFP was identified as solvent usage. O3 formation in this event was in the VOCs-limited regime, and reducing O3 precursors in the VOCs/NOx ratio of 3:1 was effective and feasible for O3 control. This study explored the causes of an O3 pollution event in winter, which will serve as reference for the synergistic control of O3 and PM2.5 in heavy pollution seasons.

Anionic lanthanide metal-organic frameworks with magnetic, fluorescence, and proton conductivity properties and selective adsorption of a cationic dye.

Two novel microporous anionic lanthanide metal-organic frameworks (Ln-MOFs), namely {[(CH3)2NH2][Ln(bptc)]·2H2O}n (Ln = Gd (1) and Dy (2), H4bptc = biphenyl-3,3',5,5'-tetracarboxylic acid) with a new 4,8-connected topology have been synthesized and structurally characterized. Ln-MOF 1 shows a significant magnetocaloric effect with -ΔSmaxm = 26.37 J kg-1 K-1 at 2 K for ΔH = 7 T, and a high proton conductivity of 1.02 × 10-4 S cm-1 at 323 K and 90% RH. Moreover, Ln-MOF 1 shows specific selective adsorption of the cationic dye Rhodamine B. Ln-MOF 2 exhibits field-induced slow magnetic relaxation with an energy barrier (Ueff) of 48.19 K, characteristic emission of Dy3+, and selective adsorption of Rhodamine B. Therefore, 2 is a multifunctional Ln-MOF with magnetic, fluorescence and selective adsorption properties.

Stable terbium metal-organic framework with turn-on and blue-shift fluorescence sensing for acidic amino acids (L-aspartate and L-glutamine) and cations (Al3+ and Ga3+).

A terbium-based metal-organic framework, namely {[Tb2(ADIP)(H2ADIP)(HCOOH)(H2O)2]·2DMF·2H2O}n (Tb-MOF, H4ADIP = 5,5'-(anthracene-9,10-diyl) diisophthalic acid), was synthesized and characterized. The single-crystal structure analysis shows that the Tb-MOF crystallizes in the C2/C space group in the monoclinic system and its asymmetric unit contains two TbIII ions, one ADIP4-, one H2ADIP2-, one coordinating formic acid and two coordination water molecules. Tb-MOF has a three-dimensional porous structure with a porosity of 41.5%. Tb-MOF is a highly selective and sensitive fluorescence turn-on and blue-shift sensor for L-aspartate (Asp), L-glutamine (Glu), Al3+ and Ga3+with detection limits of 0.25, 0.23, 0.069 and 0.079 µM, respectively. Experimental studies and theoretical calculations show that the sensing process is mainly attributed to the energy transfer and the absorbance caused enhancement (ACE) mechanism. Therefore, Tb-MOF is a good multi-response fluorescence sensor for acidic amino acids and Al3+, Ga3+cations.

Exploration of IRES Elements within the ORF of the Coxsackievirus B3 Genome.

Objective: This study aimed to identify internal ribosome entry sites (IRESs) in the open reading frame (ORF) of the Coxsackievirus B3 (CVB3) genome. Methods: The sequences of P1, P2, or P3 of the CVB3 genome or the truncated sequences from each antithymocyte globulin (ATG) to the end of the P1, P2, or P3 gene were inserted into the pEGFP-N1 vector. After transfection, possible IRES-dependent green fluorescent protein (GFP)-fused proteins were detected by anti-GFP western blotting. The sequences of possible IRESs were inserted into specific Fluc/Rluc bicistronic vectors, in which the potential IRESs were determined according to the Fluc/Rluc activity ratio. Expression of Fluc and Rluc mRNA of the bicistronic vector was detected by RT-qPCR. Results: After transfection of full length or truncated sequences of the P1, P2, or P3 plasmids, six GFP-fused protein bands in P1, six bands in P2 and nine bands in P3 were detected through western blotting. Two IRESs in VP2 (1461-1646 nt) and VP1 (2784-2983 nt) of P1; one IRES in 2C (4119-4564 nt) of P2; and two IRESs in 3C (5634-5834 nt) and 3D (6870-7087 nt) of P3 were identified according to Fluc/Rluc activity ratio. The cryptic promoter was also excluded by RT-qPCR. Conclusion: Five IRESs are present in the CVB3 coding region.

Linc00299/miR-490-3p/AURKA axis regulates cell growth and migration in atherosclerosis.

Long non-coding RNA (lncRNA) plays a crucial role in regulating various cellular processes in atherosclerosis. The present study identified the regulation of Linc00299, via miR-490-3p targeting Aurora kinase A (AURKA), on migration and proliferation of endothelial cells and vascular smooth muscle cells (VSMCs) during atherosclerosis. The expression of RNAs was assessed by real-time PCR. The proliferation, apoptosis and migration were detected using MTT assay, Annexin V/PI staining and Transwell system, respectively. Bindings of Linc00299/miR-490-3p and subsequent miR-490-3p/AURKA were verified by luciferase and biotin pull-down assays. The protein expression of AURKA was detected by Western blotting. Expressions of Linc00299 and miR-490-3p were upregulated and downregulated in atherosclerosis patients, respectively. Both Linc00299 knockdown and miR-490-3p overexpression suppressed cell proliferation, increased apoptosis and inhibited migration of VSMCs and HUVECs. Linc00299 directly bound to miR-490-3p which targeted AURKA. The regulation of Linc00299 on expression of AURKA and proliferation and migration of VSMCs were dependent on miR-490-3p. Atherosclerosis-increased Linc00299 acts as a sponge of miR-490-3p to upregulate AURKA, and as a result increases proliferation and migration in VSMCs and HUVECs. Our study reveals an important effect of Linc00299/miR-490-3p/AURKA axis on regulating cell proliferation and migration in atherosclerosis.

Coxsackievirus B3 Infection Triggers Autophagy through 3 Pathways of Endoplasmic Reticulum Stress.

OBJECTIVE: Autophagy is a highly conserved intracellular degradation pathway. Many picornaviruses induce autophagy to benefit viral replication, but an understanding of how autophagy occurs remains incomplete. In this study, we explored whether coxsackievirus B3 (CVB3) infection induced autophagy through endoplasmic reticulum (ER) stress. METHODS: In CVB3-infected HeLa cells, the specific molecules of ER stress and autophagy were detected using Western blotting, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy. Then PKR-like ER protein kinase (PERK) inhibitor, inositol-requiring protein-1 (IRE1) inhibitor, or activating transcription factor-6 (ATF6) inhibitor worked on CVB3-infected cells, their effect on autophagy was assessed by Western blotting for detecting microtubule-associated protein light chain 3 (LC3). RESULTS: CVB3 infection induced ER stress, and ER stress sensors PERK/eIF2α, IRE1/XBP1, and ATF6 were activated. CVB3 infection increased the accumulation of green fluorescent protein (GFP)-LC3 punctuation and induced the conversion from LC3-I to phosphatidylethanolamine-conjugated LC3-1 (LC3-II). CVB3 infection still decreased the expression of mammalian target of rapamycin (mTOR) and p-mTOR. Inhibition of PERK, IRE1, or ATF6 significantly decreased the ratio of LC3-II to LC3-I in CVB3-infected HeLa cells. CONCLUSION: CVB3 infection induced autophagy through ER stress in HeLa cells, and PERK, IRE1, and ATF6a pathways participated in the regulation of autophagy. Our data suggested that ER stress may inhibit mTOR signaling pathway to induce autophagy during CVB3 infection.

Identification of the internal ribosome entry sites (IRES) of prion protein gene.

Many studies demonstrated that there are several type bands of prion protein in cells. However, the formation of different prion protein bands is elusive. After several low molecular weight bands of prion protein appeared in SMB-S15 cells infected with scrapie agent Chandler, we think that IRES-dependent translation mechanism induced by prion is involved in the formation of prion protein bands. Then we designed a series of pPrP-GFP fusing plasmids and bicistronic plasmids to identify the IRES sites of prion protein gene and found 3 IRES sites inside of PrP mRNA. We also demonstrated that cap-independent translation of PrP was associated with the ER stress through Tunicamycin treatment. We still found that only IRE1 and PERK pathway regulated the IRES-dependent translation of PrP in this study. Our results indicated, we found that PrP gene had an IRES-dependent translation initiation mechanism and we successfully identified the IRESs inside of the prion protein gene.

Viral Contamination Source in Clinical Microbiology Laboratory.

To understand the potential causes of laboratory-acquired infections and to provide possible solutions that would protect laboratory personnel, samples from a viral laboratory were screened to determine the main sources of contamination with six subtypes of Rhinovirus. Rhinovirus contamination was found in the gloves, cuffs of protective wear, inner surface of biological safety cabinet (BSC) windows, and trash handles. Remarkably, high contamination was found on the inner walls of the centrifuge and the inner surface of centrifuge tube casing in the rotor. Spilling infectious medium on the surface of centrifuge tubes was found to contribute to contamination of centrifuge surfaces. Exposure to sodium hypochlorite containing no less than 0.2 g/L available chlorine decontaminated the surface of the centrifuge tubes from Rhinovirus after 2 min.

Coxsackievirus B3 2A protease promotes encephalomyocarditis virus replication.

To determine whether 2A protease of the enterovirus genus with type I internal ribosome entry site (IRES) effect on the viral replication of type II IRES, coxsackievirus B3(CVB3)-encoded protease 2A and encephalomyocarditis virus (EMCV) IRES (Type II)-dependent or cap-dependent report gene were transiently co-expressed in eukaryotic cells. We found that CVB3 2A protease not only inhibited translation of cap-dependent reporter genes through the cleavage of eIF4GI, but also conferred high EMCV IRES-dependent translation ability and promoted EMCV replication. Moreover, deletions of short motif (aa13-18 RVVNRH, aa65-70 KNKHYP, or aa88-93 PRRYQSH) resembling the nuclear localization signals (NLS) or COOH-terminal acidic amino acid motif (aa133-147 DIRDLLWLEDDAMEQ) of CVB3 2A protease decreased both its EMCV IRES-dependent translation efficiency and destroy its cleavage on eukaryotic initiation factor 4G (eIF4G) I. Our results may provide better understanding into more effective interventions and treatments for co-infection of viral diseases.

VEGF promotes cardiac stem cells differentiation into vascular endothelial cells via the PI3K/Akt signaling pathway.

Recent research suggested that cardiac stem cells (CSCs) may have the clinical application for cardiac repair. However, their characteristics and the regulatory mechanisms of their growth and differentiation have not been fully investigated. Vascular endothelial growth factor (VEGF, VEGF-A) is a major regulator of physiological and pathological angiogenesis. But the homing role of VEGF for CSCs is unclear. In this report, CSCs were isolated, purified, and expanded in vitro from rat heart. VEGF, SU5416 (VEGF receptor blocker), and Wortmannin (PI3K/Akt signaling pathway inhibitor) were used for differentiation into vascular endothelial cells (VECs). Real-time qPCR was selected to confirm the role of PI3K/Akt signaling pathway in VECs differentiation from rat CSCs. The result of real-time qPCR demonstrated that PI3K/Akt signaling pathway plays an important role in rat CSCs differentiated into VECs. So, our research provides a theoretical basis and experimental evidence for therapeutic application of rat CSCs to treat cardiac repair.

Oxidative stress and cell-cycle change induced by coexposed PCB126 and benzo(a) pyrene to human hepatoma (HepG2) cells.

Benzo(a)pyrene (BaP) never exists in the environment as a single compound but always coexists with other chemicals. These chemicals may affect the toxicity of BaP. Our previous study confirmed that polychlorinated biphenyls (PCBs), which were recently found coexisting with BaP in various environmental media, dramatically enhanced the genotoxicity of BaP. But the known mechanisms associated with this phenomenon are limited. Because BaP's genotoxicity is highly associated with its ability to induce the oxidative stress, we propose that the coexistence of PCBs may enhance BaP's genotoxicity by affecting BaP-induced oxidative stress. In this study, the HepG2 cells were treated with either BaP (50 µM), 3,3',4,4',5-pentachlorobiphenyl (PCB126) (0.01, 0.1, 1, and 10 nM), or pretreated with PCB126 followed by a coexposure to BaP and PCB126. We found that the exposure to BaP alone effectively increased the level of reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and the percentage of cells in G0/G1 phase, but decreased the percentage of S-phase cells. Compared to BaP alone, coexposure to both BaP and PCB126 effectively enhanced the levels of ROS and MDA as well as the percentage of cells in S phase, but decreased the levels of GSH and percentage of cells in G0/G1 phase. Our findings suggest that increasing oxidative stress and impairing the normal cell-cycle control may be mechanisms by which PCB126 enhances the genotoxity of BaP exposure.