Publications by authors named "Y Kong"

3,740 Publications

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Flower-like Spherical α-Ni(OH)2 Derived NiP2 as Superior Anode Material of Sodium Ion Batteries.

Chem Asian J 2021 Jun 11. Epub 2021 Jun 11.

South China University of Technology, College of Environment and Energy, Wushan Road 381, 51064, Guangzhou, CHINA.

Transition metal phosphides (TMPs) are promising anode candidates for sodium-ion batteries, due to their high theoretical specific capacity and working potential. However, the low conductivity and excessive volume variation of TMPs during insertion/extraction of sodium ions results in a poor rate performance and long-term cycling stability, largely limiting their practical application. In this paper, the NiP 2 nanoparticles encapsulated in three-dimensional graphene (NiP 2 @rGO) were obtained from the flower-like sphericalα-Ni(OH) 2 by phosphating and carbon encapsulation processes. When used as a sodium-ion batteries anode material, NiP 2 @rGO composite shows excellent cycling performance (117 mA h g -1 at 10 A g -1 after 8000 cycles). The outstanding electrochemical performance of NiP 2 @rGO is ascribed to the synergistic effect of the rGO and NiP 2 core. The rGO wrapped on the NiP 2 nanoparticles build a conductive way, improving ionic and electronic conductivity. The effective combination of NiP 2 nanoparticles with graphene greatly reduces the NiP 2 nanoparticles aggregation and pulverization during the discharge/charge process. This paper may shed light on the construct of high-performance anode material for sodium ion batteries and to other electrode materials.
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http://dx.doi.org/10.1002/asia.202100387DOI Listing
June 2021

Activation of Autophagic Flux Blunts Cardiac Ischemia/Reperfusion Injury.

Circ Res 2021 Jun 11. Epub 2021 Jun 11.

Internal Medicine, UT Southwestern Medical Center, UNITED STATES.

Reperfusion injury accounts for up to half of myocardial infarct size, and meaningful clinical therapies targeting it do not exist. We have reported previously that autophagy is reduced during reperfusion and that HDAC inhibition enhances cardiomyocyte autophagy and blunts ischemia/reperfusion (I/R) injury when administered at the time of reperfusion. However, whether inducing autophagy per se, as opposed to other effects triggered by HDAC inhibition, is sufficent to protect against reperfusion injury is not clear. We set out to test whether augmentation of autophagy using a specific autophagy-inducing peptide, Tat-Beclin, protects the myocardium through reduction of reactive oxygen species (ROS) during reperfusion injury. Eight to twelve-week-old, wild-type, C57BL6 mice and drug-inducible cardiomyocyte-specific ATG7 knockout mice (to test the dependency on autophagy) were randomized into two groups: exposed to a control Tat-Scrambled (TS) peptide or a Tat-Beclin (TB) peptide. Each group was subjected to I/R surgery (45min coronary ligation, 24h reperfusion). Infarct size, systolic function, autophagic flux, and ROS were assayed. Cultured neonatal rat ventricular myocytes (NRVMs) were exposed to TB during simulated ischemia/reperfusion injury. ATG7 knockdown by siRNA in NRVMs was used to evaluate the role of autophagy. TB treatment at reperfusion reduced infarct size by 20% (absolute reduction; 50% relative reduction) and improved contractile function. Improvement correlated with increased autophagic flux in the border zone with less oxidative stress. ATG7 KO mice did not manifest TB-promoted cardioprotection during I/R. In NRVMs subjected to I/R, TB reduced cell death by 41% and reduced I/R-induced ROS generation. Conversely, ATG7 knockdown in NRVMs abolished these beneficial effects of TB on cell death and ROS reduction. Induction of autophagy at the time of reperfusion is sufficient to mitigate myocardial reperfusion injury by reducing ROS and cell death. Maintenance of appropriate autophagic flux may emerge as a viable clinical therapy to reduce reperfusion injury in acute myocardial infarction.
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http://dx.doi.org/10.1161/CIRCRESAHA.120.318601DOI Listing
June 2021

Androgen receptor inhibition alleviated inflammation in experimental autoimmune myocarditis by increasing autophagy in macrophages.

Eur Rev Med Pharmacol Sci 2021 May;25(10):3762-3771

Department of Cardiology, the Second Hospital of Shandong University, Jinan, China.

Objective: Experimental autoimmune myocarditis (EAM) is characterized by pronounced macrophage infiltration, cardiac necrosis, and cardiac fibrosis. Our previous studies have demonstrated that suppressed androgen receptor (AR) enables anti-inflammation to promote tissue repair by decreasing M1 macrophages and increasing M2 macrophages in an EAM model. Given that autophagy mediates inflammatory response in macrophages, we investigated whether AR inhibition executes its protective role in inflammation through the autophagy pathway in EAM.

Materials And Methods: To determine whether AR inhibition can perform its anti-inflammatory effects by upregulating autophagy, we pre-treated mice with 3-methyl adenine (3-MA), a pharmacological inhibitor of autophagy. Immunofluorescence assay and Western blot were used to detect autophagy levels and autophagy activity in five different groups. Immunofluorescence marked F4/80 and LC3 to illustrate the autophagy level in macrophages. TUNEL assays were used to detect the apoptosis level in heart tissue of five different groups.

Results: We demonstrated that AR inhibition resolves injury with sustained inhibition of inflammatory cytokines associated with enhanced autophagy, especially in macrophages. Increased LC3II/I expression corroborated complete autolysosome formation detected by electron microscopy and correlated with degradation of SQSTM1/p62 in the AR inhibition group by Western blot. These effects could be reversed within 3-MA, a pharmacological inhibitor of autophagy. Specifically, pharmacological inhibition of autophagy increased apoptosis and inflammation, which could be attenuated by AR inhibition.

Conclusions: AR inhibition alleviates the inflammatory response and tissue apoptosis by enhancing autophagy, especially in macrophages.
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http://dx.doi.org/10.26355/eurrev_202105_25944DOI Listing
May 2021

Kidney Biopsy in Patients With Monoclonal Gammopathy: A Multicenter Retrospective Cohort Study.

Front Med (Lausanne) 2021 24;8:687149. Epub 2021 May 24.

State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Guangdong Provincial Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.

To analyze the clinical characteristics and renal pathological manifestations of patients with monoclonal gammopathy (MG) and kidney injury. This was a multicenter retrospective cohort study conducted at four tertiary hospitals in China. The study population comprised patients with MG admitted from January 1 2013 to December 31 2020. Hospitalization records, laboratory data, and kidney biopsy reports of all patients were collected from the electronic hospital information systems. The study outcomes included kidney disease progression and major hemorrhagic complications after kidney biopsy. We identified 1,164 patients with MG, 782 (67.2%) of whom had underlying kidney injury. Of 101 patients who underwent kidney biopsy, 16 had malignant neoplasms. Amyloid nephropathy was the most common finding ( = 34, 33.7%), followed by membranous nephropathy ( = 18, 17.8%) and membranoproliferative nephritis ( = 8, 7.9%). Among 85 patients with non-malignant hematologic conditions who underwent kidney biopsy, 43 had MG of renal significance (MGRS) related lesions and 42 had MG-unrelated lesions. The risk of kidney disease progression was higher in patients with kidney injury than in patients without kidney injury. Among patients with MG and kidney injury, only 12.9% underwent kidney biopsy and more than 40% of these patients had MG-unrelated lesions. A kidney biopsy is safe and essential to maximize the possibility of correct diagnosis for patients with clinically suspected MG of renal significance (MGRS).
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http://dx.doi.org/10.3389/fmed.2021.687149DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8180861PMC
May 2021

CHOP Regulates Endoplasmic Reticulum Stress-Mediated Hepatoxicity Induced by Monocrotaline.

Front Pharmacol 2021 24;12:685895. Epub 2021 May 24.

College of Veterinary Medicine, Northwest A&F University, Yangling, China.

Monocrotaline (MCT), a pyrrolizidine alkaloid, is the major toxin in , which causes cell apoptosis in humans and animals. It has been reported that the liver is a vulnerable target of MCT. However, the exact molecular mechanism of the interaction between endoplasmic reticulum (ER) stress and liver injury induced by MCT is still unclear. In this study, the cytotoxicity of MCT on primary rat hepatocytes was analyzed by a CCK-8 assay and Annexin V-FITC/PI assay. Protein expression was detected by western blotting and immunofluorescence staining. As a result, MCT significantly decreased the cell viability and mediated the apoptosis of primary rat hepatocytes. Meanwhile, MCT could also induce ER stress in hepatocytes, indicated by the expression of ER stress-related proteins, including GRP78, p-IRE1α, ATF6, p-eIF2α, ATF4, and CHOP. Pretreatment with 4-PBA, an inhibitor of ER stress, or knockdown of CHOP by siRNA could partly enhance cell viability and relieve the apoptosis. Our findings indicate that ER stress is involved in the hepatotoxicity induced by MCT, and CHOP plays an important role in this process.
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http://dx.doi.org/10.3389/fphar.2021.685895DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8181757PMC
May 2021