Publications by authors named "Shuyang Zhao"

17 Publications

  • Page 1 of 1

Lung Gene Expression Analysis Web Portal Version 3: Lung-at-a-Glance.

Am J Respir Cell Mol Biol 2021 01;64(1):146-149

Cincinnati Children's Hospital Medical Center Cincinnati, Ohio and.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1165/rcmb.2020-0308LEDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7781007PMC
January 2021

OX-HDL: A Starring Role in Cardiorenal Syndrome and the Effects of Heme Oxygenase-1 Intervention.

Diagnostics (Basel) 2020 Nov 20;10(11). Epub 2020 Nov 20.

Department of Medicine, New York Medical College, Valhalla, NY 10595, USA.

In this review, we will evaluate how high-density lipoprotein (HDL) and the reverse cholesterol transport (RCT) pathway are critical for proper cardiovascular-renal physiology. We will begin by reviewing the basic concepts of HDL cholesterol synthesis and pathway regulation, followed by cardiorenal syndrome (CRS) pathophysiology. After explaining how the HDL and RCT pathways become dysfunctional through oxidative processes, we will elaborate on the potential role of HDL dysfunction in CRS. We will then present findings on how HDL function and the inducible antioxidant gene heme oxygenase-1 (HO-1) are interconnected and how induction of HO-1 is protective against HDL dysfunction and important for the proper functioning of the cardiovascular-renal system. This will substantiate the proposal of HO-1 as a novel therapeutic target to prevent HDL dysfunction and, consequently, cardiovascular disease, renal dysfunction, and the onset of CRS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/diagnostics10110976DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7699797PMC
November 2020

Spontaneous self-intercalation of copper atoms into transition metal dichalcogenides.

Sci Adv 2020 Feb 14;6(7):eaay4092. Epub 2020 Feb 14.

Department of Materials Science and NanoEngineering, Rice University, Houston, TX 77005, USA.

Intercalated transition metal dichalcogenides (TMDs) have attracted substantial interest due to their exciting electronic properties. Here, we report a unique approach where copper (Cu) atoms from bulk Cu solid intercalate spontaneously into van der Waals (vdW) gaps of group IV and V layered TMDs at room temperature and atmospheric pressure. This distinctive phenomenon is used to develop a strategy to synthesize Cu species-intercalated layered TMD compounds. A series of Cu-intercalated 2H-NbS compounds were obtained with homogeneous distribution of Cu intercalates in the form of monovalent Cu (I), occupying the tetrahedral sites coordinated by S atoms within the interlayer space of NbS. The Fermi level of NbS shifts up because of the intercalation of Cu, resulting in the improvement of electrical conductivity in the -direction. On the other hand, intercalation of Cu into vdW gaps of NbS systematically suppresses the superconducting transition temperature () and superconducting volume fraction.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1126/sciadv.aay4092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7021499PMC
February 2020

Activation of natural killer cells by rituximab in granulomatosis with polyangiitis.

Arthritis Res Ther 2019 12 11;21(1):277. Epub 2019 Dec 11.

Department of Hematology, Oncology and Rheumatology, Internal Medicine V, University Hospital of Heidelberg, Heidelberg, Germany.

Objective: In the last few years, anti-CD20 antibody rituximab profoundly changed the therapeutic landscape of granulomatosis with polyangiitis (GPA). Here, we investigated whether natural killer (NK) cells may play a role in rituximab's mechanism of action in GPA.

Methods: B cell depletion, NK cell degranulation, and the expression of CD69 and CD16 on NK cells were measured in a series of in vitro experiments using peripheral blood mononuclear cells (PBMCs). In vivo activation of NK cells was investigated in patients receiving rituximab infusions. Cells were analyzed by seven-color flow cytometry.

Results: NK cells from GPA patients were activated by immobilized rituximab. Also soluble rituximab activated NK cells, provided that B cells were present. NK cells degranulated and expressed the activation marker CD69 while CD16 expression was decreased. This activation of NK cells by soluble rituximab was accompanied by a reduction of B cells. The next-generation anti-CD20 antibody obinutuzumab showed stronger effects compared to rituximab on both the reduction of B cells and the activation of NK cells. Finally, we found that rituximab led to the activation of NK cells in vivo, provided that B cells were not depleted due to prior rituximab infusions.

Conclusion: B cell-bound rituximab activates NK cells in GPA. While NK cells therefore participate in rituximab's mechanism of action in humans, their potential may be more efficiently exploited, e.g., by Fc engineering of therapeutic antibodies.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s13075-019-2054-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6907269PMC
December 2019

Cutibacterium acnes Type II strains are associated with acne in Chinese patients.

Antonie Van Leeuwenhoek 2020 Mar 19;113(3):377-388. Epub 2019 Oct 19.

Biochip Center, College of Basic Medicine, China Medical University, Shenyang, 110000, China.

Acne is a common inflammatory skin disease, especially in adolescents. Certain Cutibacterium acnes subtypes are associated with acne, although more than one subtype of C. acnes strains may simultaneously reside on the surface of the skin of an individual. To better understand the relationship between the genomic characteristics of C. acnes subtypes and acnes, we collected 50 C. acnes strains from the facial skin of 10 people (5 healthy individuals, 5 patients with acne) in Liaoning, China and performed whole genome sequencing of all strains. We demonstrated that the six potential pathogenic C. acnes strains were all Type II subtype, and discovered 90 unique genes of the six strains related to acne using pan-genome analysis. The distribution of 2 of the 90 genes was identified by PCR in bacterial cultures collected from the facial skin of 171 individuals (55 healthy individuals, 52 patients with mild acne and 64 patients with moderate to severe acne). Both the genes were significantly associated with acne (Chi square test, P < 0.01). We conclude that Type II strains are associated with acne in Chinese patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10482-019-01344-xDOI Listing
March 2020

In Situ X-ray Absorption Spectroscopic Investigation of the Capacity Degradation Mechanism in Mg/S Batteries.

Nano Lett 2019 05 3;19(5):2928-2934. Epub 2019 Apr 3.

i-Lab, Suzhou Institute of Nano-Tech and Nano-Bionics , Chinese Academy of Sciences , Suzhou , Jiangsu 215123 , China.

The Mg/S battery is attractive because of its high theoretical energy density and the abundance of Mg and S on the earth. However, its development is hindered by the lack of understanding to the underlying electrochemical reaction mechanism of its charge-discharge processes. Here, using a unique in situ X-ray absorption spectroscopic tool, we systematically study the reaction pathways of the Mg/S cells in Mg(HMDS)-AlCl electrolyte. We find that the capacity degradation is mainly due to the formation of irreversible discharge products, such as MgS and MgS, through a direct electrochemical deposition or a chemical disproportionation of intermediate polysulfide. In light of the fundamental understanding, we propose to use TiS as a catalyst to activate the irreversible reaction of low-order MgS and MgS, which results in an increased discharging capacity up to 900 mAh·g and a longer cycling life.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acs.nanolett.8b05208DOI Listing
May 2019

MicroRNA-34a-5p suppresses tumorigenesis and progression of glioma and potentiates Temozolomide-induced cytotoxicity for glioma cells by targeting HMGA2.

Eur J Pharmacol 2019 Jun 6;852:42-50. Epub 2019 Mar 6.

Department One of Neurosurgery, Zhoukou Central Hospital, Zhoukou, Henan, China.

Glioma is a frequently diagnosed brain tumors and Temozolomide (TMZ) is a common chemotherapeutic drug for glioma. High mobility group AT-hook 2 (HMGA2) was reported to be linked with glioma pathogenesis and Temozolomide (TMZ)-induced cytotoxicity. Our present study aimed to further search for the upstream regulatory microRNAs (miRNAs) of HMGA2 in glioma. RT-qPCR assay was conducted to measure the expression of HMGA2 mRNA and microRNA-34a-5p (miR-34a-5p). HMGA2 protein expression was examined by western blot assay. Cell proliferative ability and cell viability was assessed by CCK-8 assay. Cell migratory and invasive capacities were estimated by Transwell migration and invasion assay. Bioinformatics analysis and luciferase reporter assay was conducted to investigate the potential interaction between miR-34a-5p and HMGA2. Mouse xenograft experiments were performed to further test the roles of TMZ, miR-34a-5p and HMGA2, alone or in combination, in glioma tumorigenesis in vivo. We found HMGA2 expression was notably upregulated in glioma tissues and cells, and associated with glioma grade and poor prognosis. HMGA2 knockdown or miR-34a-5p overexpression inhibited migration, invasion, proliferation and enhanced TMZ-induced cytotoxicity in glioma cells. Moreover, HMGA2 was a target of miR-34a-5p. And, miR-34a-5p expression was remarkably reduced in glioma tissues and cells. MiR-34a-5p exerted its function through targeting HMGA2 in glioma cells. HMGA2 knockdown or miR-34a-5p overexpression inhibited tumor growth and enhanced TMZ-mediated anti-tumor effect in glioma xenograft models. We concluded MiR-34a-5p suppressed tumorigenesis and progression of glioma and potentiated TMZ-induced cytotoxicity for glioma cells by targeting HMGA2, deepening our understanding on molecular basis of HMGA2 in glioma.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ejphar.2019.03.005DOI Listing
June 2019

Improving a Mg/S Battery with YCl Additive and Magnesium Polysulfide.

Adv Sci (Weinh) 2019 Feb 12;6(4):1800981. Epub 2018 Dec 12.

i-lab Suzhou Institute of Nano-Tech and Nano-Bionics Chinese Academy of Science Suzhou Jiangsu 215123 China.

Rechargeable magnesium/sulfur (Mg/S) batteries are widely regarded as one of the alternatives to lithium-ion batteries. However, a key factor restricting their application is the lack of suitable electrolyte. Herein, an electrolyte additive that can reduce the polarization voltage is developed and 98.7% coulombic efficiency is realized. The as-prepared Mg-ion electrolyte exhibits excellent Mg plating/stripping performance with a low overpotential of 0.11 V for plating process, and high anodic stability up to 3.0 V (vs Mg/Mg). When it is coupled with magnesium polysulfide, which has high reactivity and is homogeneously distributed on carbon matrix, the Mg/S cells deliver a good cycling stability with a high discharge capacity over 1000 mAh g for more than 50 cycles.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/advs.201800981DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6382296PMC
February 2019

Enhanced Sulfur Redox and Polysulfide Regulation via Porous VN-Modified Separator for Li-S Batteries.

ACS Appl Mater Interfaces 2019 Feb 5;11(6):5687-5694. Epub 2019 Feb 5.

College of Energy, Soochow Institute for Energy and Materials InnovationS (SIEMIS), Key Laboratory of Advanced Carbon Materials and Wearable Energy Technologies of Jiangsu Province , Soochow University , Suzhou , Jiangsu 215006 , P. R. China.

Lithium-sulfur (Li-S) batteries have now emerged as the next-generation rechargeable energy storage system because of the high energy density and theoretical capacity. However, the notorious "lithium polysulfide (LiPS) shuttle" and sluggish kinetics in sulfur redox have posted great threat to their practical applications. Herein, we develop a VN-modified separator as an effective promoter to regulate the LiPSs and accelerate the electrochemical kinetics of Li-S batteries. Benefiting from the dense packing structure and polar surface of porous VN, the VN-modified separator favorably synergizes bifunctionality of physical confinement and chemical entrapment toward LiPSs while affording smooth lithium-ion migration. In addition, the superb electrical conductivity of VN also propels the LiPS conversion. With these advantages, thus-integrated batteries with VN-modified separator exhibit an average capacity decay of 0.077% per cycle at 1 C for 800 cycles. A reasonable areal capacity of 4.2 mAh cm is achieved even with a high sulfur mass loading of 3.8 mg cm at 0.2 C. The present work offers a rational strategy to regulate the LiPS behavior and guide the sulfur redox kinetics toward effective and long-life Li-S batteries.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acsami.8b22014DOI Listing
February 2019

JAK-STAT signaling mediates the senescence of bone marrow-mesenchymal stem cells from systemic lupus erythematosus patients.

Acta Biochim Biophys Sin (Shanghai) 2017 Mar;49(3):208-215

Department of Immunology, Medical College, Nantong University, Nantong 226001, China.

Previous studies have revealed that bone marrow-mesenchymal stem cells (BM-MSCs) from systemic lupus erythematosus (SLE) patients exhibited early signs of senescence, which may participate in the development of SLE. However, the molecular mechanisms about this phenomenon have not been fully elucidated. In the current study, we aimed to investigate whether Janus kinase (JAK)-signaling transducers and activators of transcription (STAT) signaling mediated the senescence of BM-MSCs from SLE patients. Twelve female SLE patients and healthy subjects were enrolled in the study. All BM-MSCs were isolated by density gradient centrifugation. Western blot analysis was used to test the expression of JAK-STAT signaling molecules. We observed the activity of β-gal of cells, the changes of cytoskeletal structure by F-actin staining, and the distribution of cell cycle by flow cytometry. BM-MSCs from SLE patients showed prominent features of senescence, and abnormal activation of JAK-STAT signaling transduction, high level of phosphorylated JAK2, and STAT3. After stimulation of IFN-γ in normal MSCs, JAK-STAT signaling was activated. The cell volume and the number of senescence-associated β-galactosidase (SA-β-gal) positive in SLE BM-MSCs were increased. The organization of cytoskeleton was nearly disordered. The rate of cell proliferation was decreased. AG490, the inhibitor of JAK2, and knockdown of STAT3 in BM-MSCs, could significantly reverse the senescence. In summary, our study indicated that JAK-STAT signaling pathway may play a critical role in the senescence of SLE BM-MSCs.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/abbs/gmw134DOI Listing
March 2017

Overexpression of HOXC8 is Associated With Poor Prognosis in Epithelial Ovarian Cancer.

Reprod Sci 2016 07 13;23(7):944-54. Epub 2016 Jan 13.

Department of Oncology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, People's Republic of China

Homeobox C8 (HOXC8) is a transcription factor that has been reported as a potential driver oncogene in several tumors and involved in the regulation of many cancer-related proteins. In this study, we investigated the expression and role of HOXC8 in ovarian cancer. Western blot and immunohistochemistry analyses were performed to detect the expression of HOXC8. Kaplan-Meier curve showed that high expression of HOXC8 was related to poor prognosis of patients with epithelial ovarian cancer (EOC). Starvation and refeeding assay were used to assess cell cycle, suggesting that HOXC8 played a critical role in EOC cell proliferation. HOXC8 depletion by small interfering RNA inhibited cell proliferation, migration, and induced apoptosis in EOC cells. Moreover, HOXC8 knockdown increased the expression of ZAC1. Owing to the overexpression of HOXC8, our findings implied that HOXC8 is involved in the progression of EOC and could be a potential therapeutical approach of EOC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/1933719115625845DOI Listing
July 2016

Reduction in Autophagy by (-)-Epigallocatechin-3-Gallate (EGCG): a Potential Mechanism of Prevention of Mitochondrial Dysfunction After Subarachnoid Hemorrhage.

Mol Neurobiol 2017 01 7;54(1):392-405. Epub 2016 Jan 7.

Department of Neurosurgery, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan, 453100, China.

Mitochondrial dysfunction and subsequent autophagy, which are common features in central nervous system (CNS) disorders, were found to contribute to neuronal cell injury after subarachnoid hemorrhage (SAH). (-)-Epigallocatechin-3-gallate (EGCG), the main biological active of tea catechin, is well known for its beneficial effects in the treatment of CNS diseases. Here, the ability of EGCG to rescue cellular injury and mitochondrial function following the improvement of autophagic flux after SAH was investigated. As expected, EGCG-protected mitochondrial function depended on the inhibition of cytosolic Ca concentration ([Ca]) influx via voltage-gated calcium channels (VGCCs) and, consequently, mitochondrial Ca concentration ([Ca]) overload via mitochondrial Ca uniporter (MCU). The attenuated [Ca] and [Ca] levels observed in the EGCG-treated group likely lessened oxyhemoglobin (OxyHb)-induced mitochondrial dysfunction, including mitochondrial membrane potential depolarization, mitochondrial membrane permeability transition pore (mPTP) opening, reactive oxygen species (ROS), and cytochrosome c (cyt c) releasing. Subsequently, EGCG can restore the disrupted autophagy flux after SAH both at the initiation and formation stages by regulating Atg5, LC3B, and Becn-1 (Beclin-1) mRNA expressions. Thus, precondition EGCG resulted in autophagosomes and more autolysosomes compared with SAH group. As a result, EGCG pre-treatment increased the neurological score and decreased cell death. This study suggested that the mitochondrial dysfunction and abnormal autophagy flux synergistically contribute to SAH pathogenesis. Thus, EGCG can be regarded as a new pharmacological agent that targets both mitochondria and altered autophagy in SAH therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12035-015-9629-9DOI Listing
January 2017

Spy1 participates in the proliferation and apoptosis of epithelial ovarian cancer.

J Mol Histol 2016 Feb 7;47(1):47-57. Epub 2015 Dec 7.

Department of Oncology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, People's Republic of China.

This study focused on determining the role of Spy1 in human epithelial ovarian cancer (EOC). Speedy is a novel cell cycle protein capable of promoting cell proliferation. In this study, western blot and immunohistochemistrical analyses were performed to detect the expression of Spy1 in ovarian cancer. Spy1 protein levels increased with ovarian cancer grade, and Kaplan-Meier curve showed that overexpression of Spy1 was significantly correlated with reduced patient survival. In vitro, Spy1 depletion in ovarian cell lines led to reduced proliferation according to CCK8 and plate colony assays. The expression of Spy1 was positively related to pThr187-p27. Flow cytometry revealed that the reduced expression of Spy1 induced the apoptosis of the EOC cells. In summary, our findings suggested that Spy1 may be a novel independent prognostic predictor of survival for ovarian patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10735-015-9646-zDOI Listing
February 2016

PSMB4 expression associates with epithelial ovarian cancer growth and poor prognosis.

Arch Gynecol Obstet 2016 06 6;293(6):1297-307. Epub 2015 Oct 6.

Department of Pathogen Biology, Medical College, Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226001, People's Republic of China.

Purpose: In this study, we investigated the expression and role of PSMB4 in human epithelial ovarian cancer(EOC).

Methods: Western blot was used to evaluate the expression of PSMB4 in EOC tissues, and immunohistochemical analysis was performed on 115 cases of ovarian cancers. Then, we used Fisher exact test to analyze the correlation between PSMB4 and clinicopathological parameters. Starvation and re-feeding assay was used to assess cell cycle. CCK-8 assay and plate colony formation assay showed the influence of PSMB4 on proliferation of EOC cells.

Results: The expression of PSMB4 in EOC tissues was higher than normal ovary tissues and was significantly associated with clinical pathologic variables. Kaplan-Meier curve showed that high expression of PSMB4 was related to poor prognosis of EOC patients. Starvation and re-feeding assay suggested that PSMB4 played a critical role in EOC cell proliferation. CCK-8 assay and plate colony formation assay showed that EOC cells treated with PSMB4-siRNA reduced cell proliferation of EOC cells. Additionally, PSMB4 knockdown decreased NF-κB activity. PSMB4 also regulated the expression of NF-κB mediated proteins, including cyclin D1, and cyclin E which involved in cell proliferation.

Conclusions: Our findings implied that PSMB4 is involved in the progression of EOC and could serve as potential therapeutical target of EOC. These data suggested that PSMB4 may promote cell proliferation via the NF-κB-target gene in EOC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00404-015-3904-xDOI Listing
June 2016

Network-based stratification analysis of 13 major cancer types using mutations in panels of cancer genes.

BMC Genomics 2015 11;16 Suppl 7:S7. Epub 2015 Jun 11.

Background: Cancers are complex diseases with heterogeneous genetic causes and clinical outcomes. It is critical to classify patients into subtypes and associate the subtypes with clinical outcomes for better prognosis and treatment. Large-scale studies have comprehensively identified somatic mutations across multiple tumor types, providing rich datasets for classifying patients based on genomic mutations. One challenge associated with this task is that mutations are rarely shared across patients. Network-based stratification (NBS) approaches have been proposed to overcome this challenge and used to classify tumors based on exome-level mutations. In routine research and clinical applications, however, usually only a small panel of pre-selected genes is screened for mutations. It is unknown whether such small panels are effective in classifying patients into clinically meaningful subtypes.

Results: In this study, we applied NBS to 13 major cancer types with exome-level mutation data and compared the classification based on the full exome data with those focusing only on small sets of genes. Specifically, we investigated three panels, FoundationOne (240 genes), PanCan (127 genes) and TruSeq (48 genes). We showed that small panels not only are effective in clustering tumors but also often outperform full exome data for most cancer types. We further associated subtypes with clinical data and identified 5 tumor types (CRC-Colorectal carcinoma, HNSC-Head and neck squamous cell carcinoma, KIRC-Kidney renal clear cell carcinoma, LUAD-Lung adenocarcinoma and UCEC-Uterine corpus endometrial carcinoma) whose subtypes are significantly associated with overall survival, all based on small panels.

Conclusion: Our analyses indicate that effective patient subtyping can be carried out using mutations detected in smaller gene panels, probably due to the enrichment of clinically important genes in such panels.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1471-2164-16-S7-S7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4474538PMC
March 2016