Publications by authors named "Yongzhen Zhai"

7 Publications

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Successful treatment of acute-on-chronic liver failure secondary to alcoholic cirrhosis with glucocorticoids and albumin: a case report.

Daru 2021 Nov 24. Epub 2021 Nov 24.

Department of Infectious Disease, Shengjing Hospital of China Medical University, No.39 of Huaxiang Road, Tiexi District, Shenyang, 110022, Liaoning Province, China.

Glucocorticoids are used as a first-line treatment for severe alcoholic hepatitis, and albumin reduces both the number of hospitalizations and mortality in patients with decompensated cirrhosis. However, for acute-on-chronic liver failure (ACLF), there is no definitive evidence that glucocorticoid therapy is beneficial. In this case report, we describe a male patient who developed into ACLF based on alcoholic cirrhosis, whose symptoms and clinical indicators continued to deteriorate after initial symptomatic treatment. The patient's condition gradually improved after low-dose glucocorticoid therapy, and long-term albumin supplementation resulted in a satisfactory outcome.
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http://dx.doi.org/10.1007/s40199-021-00420-wDOI Listing
November 2021

Clinical characteristics and peripheral immunocyte subsets alteration of 85 COVID-19 deaths.

Aging (Albany NY) 2021 03 12;13(5):6289-6297. Epub 2021 Mar 12.

Department of Infectious Disease, Shengjing Hospital of China Medical University, Shenyang 110004, China.

Objectives: To retrospectively evaluate the clinical and immunological characteristics of patients who died of COVID-19 and to identify patients at high risk of death at an early stage and reduce their mortality.

Results: Total white blood cell count, neutrophil count and C-reactive protein were significantly higher in patients who died of COVID-19 than those who recovered from it (p < 0.05), but the total lymphocyte count, CD4 + T cells, CD8 + T cells, B cells and natural killer cells were significantly lower when compared in the same groups. Multiple logistic regression analysis showed that increased D-dimer, decreased CD4 + T cells and increased neutrophils were risk factors for mortality. Further multiple COX regression demonstrated that neutrophil ≥ 5.27 × 109/L increased the risk of death in COVID-19 patients after adjustment for age and gender. However, CD4 + T cells ≥ 260/μL appeared to reduce the risk of death.

Conclusion: SARS-CoV-2 infection led to a significant decrease of lymphocytes, and decreased CD4 + T cell count was a risk factor for COVID-19 patients to develop severe disease and death.

Methods: This study included 190 hospitalized COVID-19 patients from January 30, 2020 to March 4, 2020 in Wuhan, China, of whom 85 died and 105 recovered. Two researchers independently collected the clinical and laboratory data from electronic medical records.
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http://dx.doi.org/10.18632/aging.202819DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993687PMC
March 2021

3-Methyladenine-enhanced susceptibility to sorafenib in hepatocellular carcinoma cells by inhibiting autophagy.

Anticancer Drugs 2021 04;32(4):386-393

Department of Infectious Disease, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.

As an effective targeted therapy for advanced hepatocellular carcinoma (HCC), sorafenib resistance has been frequently reported in recent years, with the activation of autophagy by cancer cells under drug stress being one of the crucial reasons. Sorafenib treatment could enhance autophagy in HCC cells and autophagy is also considered as an important mechanisms of drug resistance. Therefore, the inhibition of autophagy is a potential way to improve the sensitivity and eliminate drug resistance to restore their efficacy. To determine whether autophagy is involved in sorafenib resistance and investigate its role in the regulation of HepG2 cells' (an HCC cell line) chemosensitivity to sorafenib, we simultaneously treated HepG2 with sorafenib and 3-Methyladenine (3-MA) (a common autophagy inhibitor). First, by performing cell counting kit 8 cell viability assay, Hoechst 33342 apoptosis staining, and Annexin V-fluorescein isothiocyanate/propidium iodide apoptosis kit detection, we found that both sorafenib and 3-MA effectively inhibitted the proliferative activity of HepG2 cells and induced their apoptosis to a certain extent. This effect was significantly enhanced after these two drugs were combined, which was also confirmed by the increased expression of apoptosis-related proteins. Subsequently, by using AAV-GFP-LC3 transfection methods and transmission electron microscopy, we found that both the number and activity of autophagosomes in HepG2 cells in sorafenib and 3-MA group were significantly reduced, suggesting that autophagy activity was inhibited, and this result was consistent with the expression results of autophagy-related proteins. Therefore, we conclude that 3-MA may attenuate the acquired drug resistance of sorafenib by counteracting its induction of autophagy activity, thus enhancing its sensitivity to advanced HCC therapy.
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http://dx.doi.org/10.1097/CAD.0000000000001032DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7952045PMC
April 2021

Effect of Oxide Particles on Microstructure and Mechanical Properties of the 45 Carbon Structural Steel.

Materials (Basel) 2020 Mar 9;13(5). Epub 2020 Mar 9.

School of Materials Science & Engineering, Hebei University of Technology, Tianjin 300130, China.

Striking difference in density between the oxide and the steel results in difficulty in preparing oxide dispersion strengthened steel with large size parts or materials. In this research, AlO and TiO particles were initially milled with the 20 steel, and then the mixture was heated to a molten state to form a master alloy, which was used as a raw material for further preparation of the object steel. It was found that homogeneous distribution of the oxide particles was obtained in the mass production of the steel. Moreover, the obtained 45 carbon structural steel presents fine microstructures, together with improved mechanical properties, especially the impact ductility. This should be attributable to the transformation from the introduced micro-size oxide particles to the nano ones, which act as heterogeneous nucleants that play an important role in grain refinement and dispersion strengthening for the steel, during the remelting of the master alloy.
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http://dx.doi.org/10.3390/ma13051232DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7085093PMC
March 2020

Enhancement of autophagy as a strategy for development of new DNA vaccine candidates against Japanese encephalitis.

Vaccine 2019 09 6;37(37):5588-5595. Epub 2019 Aug 6.

Department of Infectious Disease, The Shengjing Hospital of China Medical University, Shenyang 110004, China. Electronic address:

For decades, an on-going concerted effort has been made to develop a universal DNA vaccine to combat the looming threat of a potential outbreak of the emerging Japanese encephalitis virus (JEV) infection. However, effective strategies are urgently required to counter poor immunogenicity and insufficient long-term protection. Recent reports have confirmed the critical role of autophagy in antigen presentation, long-term immune memory and immune responses against JEV. In this study, JEV prM and E protein with strong immunogenicity were fused with microtubule-associated protein 1 light chain 3 (LC3) encoding gene to construct an autophagy-mediated pJME-LC3 DNA vaccine. Researches indicated significant increase of autophagosomes or LC3 Ⅱ expression in pJME-LC3 transfected cells. Furthermore, prME-LC3 fused protein was observed co-localized with GFP-LC3 to autophagosomes, which means it was successfully targeted to autophagosomes. After immunizing with pJME-LC3, mice were detected highest proportion of CD3CD8 T lymphocytes, CD8 effector memory T cells (TEMs) and JEV specific cytotoxic T lymphocyte (CTL) activity to eliminate JEV. pJME-LC3 also enhanced IgG2a antibody in serum and cytokines IFN-γ, IL-12 produced by splenocytes, thus skew toward Th1 type immune response by activating the JAK2/STAT1 signaling pathway and upregulating expression of transcription factor T-bet. Notably, mice immunized with pJME-LC3 showed highest survival rate and long-lasting neutralizing antibody when challenged with virulent JEV, which were consistent with augment in percentage of CD4 central memory T cells (TCMs). In brief, our studies suggested that autophagy can be used as a optimization strategy to enhance JEV specific immune response and long-term immune memory. Our attempt will contribute towards future efforts to develop an efficacious JEV vaccine.
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http://dx.doi.org/10.1016/j.vaccine.2019.07.093DOI Listing
September 2019

Immune-enhancing effect of nano-DNA vaccine encoding a gene of the prME protein of Japanese encephalitis virus and BALB/c mouse granulocyte-macrophage colony-stimulating factor.

Mol Med Rep 2015 Jul 4;12(1):199-209. Epub 2015 Mar 4.

Department of Infectious Diseases, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

Plasmid-encoded granulocyte-macrophage colony-stimulating factor (GM‑CSF) is an adjuvant for genetic vaccines; however, how GM-CSF enhances immunogenicity remains to be elucidated. In the present study, it was demonstrated that injection of a plasmid encoding the premembrane (prM) and envelope (E) protein of Japanese encephalitis virus and mouse GM-CSF (pJME/GM-CSF) into mouse muscle recruited large and multifocal conglomerates of macrophages and granulocytes, predominantly neutrophils. During the peak of the infiltration, an appreciable number of immature dendritic cells (DCs) appeared, although no T and B-cells was detected. pJME/GM-CSF increased the number of splenic DCs and the expression of major histocompatibility complex class II (MHCII) on splenic DC, and enhanced the antigenic capture, processing and presentation functions of splenic DCs, and the cell-mediated immunity induced by the vaccine. These findings suggested that the immune-enhancing effect by pJME/GM-CSF was associated with infiltrate size and the appearance of integrin αx (CD11c)+cells. Chitosan-pJME/GM-CSF nanoparticles, prepared by coacervation via intramuscular injection, outperformed standard pJME/GM-CSF administrations in DC recruitment, antigen processing and presentation, and vaccine enhancement. This revealed that muscular injection of chitosan‑pJME/GM-CSF nanoparticles may enhance the immunoadjuvant properties of GM-CSF.
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http://dx.doi.org/10.3892/mmr.2015.3419DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438877PMC
July 2015

Hepatitis B virus X protein modulates apoptosis in human renal proximal tubular epithelial cells by activating the JAK2/STAT3 signaling pathway.

Int J Mol Med 2013 May 7;31(5):1017-29. Epub 2013 Mar 7.

Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

Hepatitis B virus X protein (HBx) is a multifunctional protein, and it activates multiple signal transduction pathways in multiple types of cells and regulates the process of cell apoptosis. In the present study, we mainly investigated the correlation between HBx and renal tubular epithelial cell apoptosis in hepatitis B virus-associated glomerulonephritis (HBVGN) and the possible signaling mechanism. Cell apoptosis in nephridial tissues of patients with HBVGN were determined by the TUNEL method. HBx, p-STAT3 and STAT3 levels in nephridial tissues were determined by immunohistochemical assay, and a correlation analysis between HBx expression levels and apoptosis index in nephridial tissues was conducted. The activation of the JAK2/STAT3 signaling pathway in HK-2 cells and the expression of the apoptosis-related proteins Bax and Bcl-2 were determined by western blot analysis following transfection with the HBx eukaryotic expression vector. Cellular proliferation activity was determined by the CCK‑8 method, and cell apoptosis was determined with HO33342 staining using transmission electron microscopy and Annexin V/PI double staining flow cytometry. The results revealed that the apoptosis index in nephridial tissues of patients with HBVGN was significantly higher when compared to that of the control group, and p-STAT3 expression levels in HBVGN nephridial tissues were significantly increased. In the control group, no HBx expression was observed in the nephridial tissues, whereas HBx expression was found in the nephridial tissues of 86% of the patients with HBVGN. The HBx expression levels had a linear correlation with the apoptosis index in the nephridial tissues. After target gene HBx infection, expression levels of both p-JAK2 and p-STAT3 in human proximal HK-2 cells were significantly increased, and the Bax/Bcl-2 ratio was also significantly increased. At the same time, cellular proliferation of HK-2 cells was significantly inhibited, and the rate of apoptosis was increased. After incubation with AG490, the JAK2/STAT3 signaling pathway was partially blocked, which caused a decrease in the Bax/Bcl-2 ratio and reduced cell apoptosis caused by HBx. In conclusion, HBx upregulates the Bax/Bcl-2 ratio by activating the JAK2/STAT3 signaling pathway to cause renal tubular epithelial cell apoptosis, and it is possibly involved in the pathogenic mechanism of nephridial tissue damage caused by HBV.
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http://dx.doi.org/10.3892/ijmm.2013.1295DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658604PMC
May 2013
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