Publications by authors named "Z Liu"

56,057 Publications

A Portable Micro-Gas Chromatography with Integrated Photonic Crystal Slab Sensors on Chip.

Biosensors (Basel) 2021 Sep 9;11(9). Epub 2021 Sep 9.

Department of Electrical Engineering, University of Texas at Arlington, Arlington, TX 76019, USA.

The miniaturization of gas chromatography (GC) systems has made it possible to utilize the analytical technique in various on-site applications to rapidly analyze complex gas samples. Various types of miniaturized sensors have been developed for micro-gas chromatography (µGC). However, the integration of an appropriate detector in µGC systems still faces a significant challenge. We present a solution to the problem through integration of µGC with photonic crystal slab (PCS) sensors using transfer printing technology. This integration offers an opportunity to utilize the advantages of optical sensors, such as high sensitivity and rapid response time, and at the same time, compensate for the lack of detection specificity from which label-free optical sensors suffer. We transfer printed a 2D defect free PCS on a borofloat glass, bonded it to a silicon microfluidic gas cell or directly to a microfabricated GC column, and then coated it with a gas responsive polymer. Realtime spectral shift in Fano resonance of the PCS sensor was used to quantitatively detect analytes over a mass range of three orders. The integrated µGC-PCS system was used to demonstrate separation and detection of a complex mixture of 10 chemicals. Fast separation and detection (4 min) and a low detection limit (ng) was demonstrated.
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http://dx.doi.org/10.3390/bios11090326DOI Listing
September 2021

Epigallocatechin gallate (EGCG) attenuates staphylococcal alpha-hemolysin (Hla)-induced NLRP3 inflammasome activation via ROS-MAPK pathways and EGCG-Hla interactions.

Int Immunopharmacol 2021 Sep 22;100:108170. Epub 2021 Sep 22.

College of Food Science and Engineering, Jilin University, Changchun 130062, China. Electronic address:

Alpha-hemolysin (Hla), the virulence factor secreted by Staphylococcus aureus (S. aureus), plays a critical role in infection and inflammation, which is a severe health burden worldwide. Therefore, it is necessary to develop a drug against Hla. Epigallocatechin gallate (EGCG), a polyphenol extracted from green tea, has excellent anti-inflammatory activity. In this study, we investigated the inhibitory effect of EGCG on Hla-induced NLRP3 inflammasome activation in vitro and in vivo and elucidated the potential molecular mechanism. We found that EGCG attenuated the hemolysis of Hla by inhibiting its secretion. Besides, EGCG significantly decreased overproduction of ROS and activation of MAPK signaling pathway induced by Hla, thereby markedly attenuating the expression of NLRP3 inflammasome-related proteins in THP-1 cells. Notably, EGCG could spontaneously bind to Hla with affinity constant of 1.71 × 10 M, thus blocking the formation of the Hla heptamer. Moreover, Hla-induced expression of NLRP3, ASC and caspase-1 protein and generation of IL-1β and IL-18 in the damaged liver tissue of mice were also significantly suppressed by EGCG in a dose-dependent manner. Collectively, EGCG could be a promising candidate for alleviating Hla-induced the activation of NLRP3 inflammasome, depending on ROS mediated MAPK signaling pathway, and inhibition of Hla secretion and heptamer formation. These findings will enlighten the applications of EGCG to reduce the S. aureus infection by targeting Hla in food and related pharmaceutical fields.
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http://dx.doi.org/10.1016/j.intimp.2021.108170DOI Listing
September 2021

Associations of perinatal exposure to PM with gestational weight gain and offspring birth weight.

Environ Res 2021 Sep 22:112087. Epub 2021 Sep 22.

Department of Epidemiology, University of Washington, Seattle, WA, 98195, USA.

Background: PM have been associated with weight change in animal models and non-pregnant populations. Evidence of associations between PM and gestational weight gain (GWG), an important determinant of course and outcomes of pregnancy, and subsequent birth outcomes is limited.

Methods: The study was conducted among a subset of participants from the Omega Study, a prospective pregnancy cohort. Exposure to PM (μg/m) was ascertained for participants (N = 855) based on their residential address using a validated national spatiotemporal model. Adjusted multivariable linear regression models were used to estimate associations of trimester-specific and pregnancy-month PM exposures with early (<20 weeks gestation), late (≥20 weeks gestation), and total GWG and infant birth weight. Stratified models and product terms were used to examine whether pre-pregnancy BMI (ppBMI) and infant sex modified the associations.

Results: Average monthly PM exposure during the first, second, and third trimesters were 7.3 μg/m, 7.9 μg/m, and 7.7 μg/m, respectively. Higher third trimester PM exposure was associated with higher late (0.40 kg per 5 μg/m (McDowell et al., 2018); 95%CI: 0.12, 0.67) and total (0.35 kg; 95%CI: 0.01, 0.70) GWG among participants with normal ppBMI. Higher second month PM exposure was associated with lower early (-0.70 kg; 95%CI: 1.22, -0.18), late (-0.84 kg; 95% CI: 1.54, -0.14), and total (-1.70 kg; 95%CI: 2.57, -0.82) GWG among participants with overweight/obese ppBMI. Product terms between PM and ppBMI were significant for second month PM exposure and early (p-value = 0.01) and total GWG (p-value<0.01). Higher third trimester PM exposure was associated with higher birth weight, though higher fourth month PM exposure was associated with lower birth weight, particularly among those with normal ppBMI and male infants.

Conclusions: Associations of PM with GWG vary by exposure window and ppBMI, while associations of PM with birth weight potentially vary by exposure window, ppBMI and infant sex. Further exploration of associations between PM and maternal/child health outcomes are needed.
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http://dx.doi.org/10.1016/j.envres.2021.112087DOI Listing
September 2021

Mast cells-derived exosomes worsen the development of experimental cerebral malaria.

Acta Trop 2021 Sep 22:106145. Epub 2021 Sep 22.

Guangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, P. R. China; Department of Pathogen Biology and Immunology, School of Life Sciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, P. R. China. Electronic address:

Cerebral malaria (CM) is the most severe neurological complication caused by Plasmodium falciparum infection. The accumulating evidence demonstrated that mast cells (MCs) and its mediators played a critical role in mediating malaria severity. Earlier studies identified that exosomes were emerging as key mediators of intercellular communication and can be released from several kinds of MCs. However, the potential functions and pathological mechanisms of MCs-derived exosomes (MCs-Exo) impacting on CM pathogenesis remain largely unknown. Herein, we utilized an experimental CM (ECM) model (C57BL/6 mice infected with P. berghei ANKA strain), and then intravenously (i.v.) injected MCs-Exo into P. berghei ANKA-infected mice to unfold this mechanism and investigate the effect of MCs-Exo on ECM pathogenies. We also used an in vitro model by investigating the pathogenesis development of brain microvascular endothelial cells line (bEnd.3 cells) co-cultured with P. berghei ANKA blood-stage soluble antigen (PbAg) after MCs-Exo treatment. The higher numbers of MCs and levels of MCs degranulation were observed in skin, cervical lymph node, and brain of ECM mice than those of the uninfected mice. Exosomes were successfully isolated from culture supernatants of mouse MCs line (P815 cells) and characterized by spherical vesicles with the diameter of 30-150 nm, and expression of typical exosomal markers (e.g., CD9, CD63, and CD81). The i.v. injection of MCs-Exo dramatically elevated incidence of ECM in the P. berghei ANKA-infected mice, exacerbated liver and brain histopathological damage, promoted Th1 cytokine response, aggravated brain vascular endothelial activation and blood brain barrier breakdown in ECM mice. In addition, the treatment of MCs-Exo led to the decrease of cells viability and mRNA levels of Ang-1, ZO-1, and Claudin-5, but increase of mRNA levels of Ang-2, CCL2, CXCL1, and CXCL9 in bEnd.3 cells co-cultured with PbAg in vitro. Taken together, our data indicated that MCs-Exo could worsen pathogenesis of ECM in mice.
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http://dx.doi.org/10.1016/j.actatropica.2021.106145DOI Listing
September 2021

Integrated analysis reveals distinct molecular, clinical, and immunological features of B7-H3 in acute myeloid leukemia.

Cancer Med 2021 Sep 25. Epub 2021 Sep 25.

Zhenjiang Clinical Research Center of Hematology, Jiangsu, China.

The role of B7-H3 in acute myeloid leukemia (AML) is not fully understood. Two previous studies investigating its expression and significances in AML are partially different. In this study, we aimed to systematically characterize the genomic and immune landscape in AML patients with altered B7-H3 expression using multi-omics data in the public domain. We found significantly increased B7-H3 expression in AML compared to either other hematological malignancies or healthy controls. Clinically, high B7-H3 expression was associated with old age, TP53 mutations, wild-type WT1 and CEBPA, and the M3 and M5 FAB subtypes. Moreover, we observed that increased B7-H3 expression correlated significantly with a poor outcome of AML patients in four independent datasets. Gene set enrichment analysis (GSEA) revealed the enrichment of the "EMT" oncogenic gene signatures in high B7-H3 expressers. Further investigation suggested that B7-H3 was more likely to be associated with immune-suppressive cells (macrophages, neutrophils, dendritic cells, and Th17 cells). B7-H3 was also positively associated with a number of checkpoint genes, such as VISTA (B7-H5), CD80 (B7-1), CD86 (B7-2), and CD70. In summary, we uncovered distinct genomic and immunologic features associated with B7-H3 expression in AML. This may lead to a better understanding of the molecular mechanisms underlying B7-H3 dysregulation in AML and to the development of novel therapeutic strategies.
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http://dx.doi.org/10.1002/cam4.4284DOI Listing
September 2021
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