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1
المؤلفون: Hong-jun Zhu, Hong-lei Zhao, Yi-pu Xie, Xu Zhang
المصدر: Journal of Hydrodynamics. 34:329-353
مصطلحات موضوعية: Mechanics of Materials, Mechanical Engineering, Modeling and Simulation, Condensed Matter Physics
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::ec6578dff43ed25778dac13d086ad2acTest
https://doi.org/10.1007/s42241-022-0031-6Test -
2
المؤلفون: Guang-Hui Yu, Chun-Lei Yang, Hong-Lei Zhao, Ai-Xuan Yu, Gen Zhang, Dong-Ying Du, Zhong-Min Su
المصدر: Inorganic Chemistry. 61:5318-5325
مصطلحات موضوعية: Inorganic Chemistry, Alcohols, Humans, Physical and Theoretical Chemistry, Coloring Agents, Carbon, Metal-Organic Frameworks
الوصف: Herein, a N-rich metal-organic framework (MOF) with four kinds of cages, Zn
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3fd1cc6d4e7f539320760a572b075d1aTest
https://doi.org/10.1021/acs.inorgchem.2c00023Test -
3
المؤلفون: Ying Liu, Yi Ming Yin, Xue Peng Li, Hong Lei Zhao, Jianrong Li, Yong Xia Xu
المصدر: Key Engineering Materials. 841:317-321
مصطلحات موضوعية: biology, Chemistry, Mechanical Engineering, 010401 analytical chemistry, 04 agricultural and veterinary sciences, biology.organism_classification, 040401 food science, 01 natural sciences, 0104 chemical sciences, Turbot, 0404 agricultural biotechnology, Quality (physics), Mechanics of Materials, General Materials Science, Food science, Maxima, Flavor
الوصف: The effect of super-chilling at -2°C compared with ice storage at 0°C on flavor quality changes of turbot (Psetta maxima) was investigated. Changes in total volatile basic nitrogen (TVB-N), sensory attributes and volatile compounds were periodically examined for 20 days. Results demonstrated that super-chilling retarded the increases of TVB-N values and maintained better sensory quality compared to the ice storage. Additionally, GC-MS analysis showed super-chilling could more effectively maintain the characteristic volatiles responsible for fresh fish flavor and reduce the contents of putrid compounds such as TMA and acetic acid.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::9c578934f34148c37bd840ee053919d1Test
https://doi.org/10.4028/www.scientific.net/kem.841.317Test -
4
المؤلفون: Ying Luo, Yun-Ling Hao, Ming-Jie Fu, Bao-Quan Wu, Wei Liu, Hong-Lei Zhao, Jin-Jie Liang, Hong-Cheng Fang, Xie-Hui Chen, Xiao-Li Li
المصدر: American Journal of Physiology-Cell Physiology. 315:C380-C388
مصطلحات موضوعية: Male, 0301 basic medicine, MAPK3, Physiology, Down-Regulation, Apoptosis, Myocardial Reperfusion Injury, PC12 Cells, Sevoflurane, Rats, Sprague-Dawley, 03 medical and health sciences, Cell Line, Tumor, microRNA, Animals, Medicine, Myocytes, Cardiac, Myocardial infarction, Protein kinase B, PI3K/AKT/mTOR pathway, L-Lactate Dehydrogenase, business.industry, Cell Biology, medicine.disease, Rats, MicroRNAs, 030104 developmental biology, Ischemic Preconditioning, Myocardial, Cancer research, Mitogen-Activated Protein Kinases, Phosphatidylinositol 3-Kinase, business, Proto-Oncogene Proteins c-akt, Reperfusion injury, Signal Transduction, medicine.drug
الوصف: Recent studies have uncovered the vital roles played by microRNAs in regulating cardiac injury. Among them, the cardiac enriched microRNA-1 (miR-1) has been extensively studied and proven to be detrimental to cardiac myocytes. Hence, the current study aimed to explore whether miR-1 affects myocardial ischemia-reperfusion injury (MIRI) in rats undergoing sevoflurane preconditioning and the underlying mechanism. After successful model establishment, rats with MIRI were transfected with mimics or inhibitors of miR-1, or siRNA against MAPK3, and then were injected with sevoflurane. A luciferase reporter gene assay was conducted to evaluate the targeting relationship between miR-1 and MAPK3. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were employed to evaluate the expressions of miR-1, MAPK3, phosphatidylinositol 3-kinase (PI3K), and Akt. Additionally, the concentration of lactate dehydrogenase (LDH) was determined. Cell apoptosis and viability were assessed using TUNEL and cell counting kit-8 assays, and the ischemic area at risk and infarct size were detected using Evans blue and triphenyltetrazolium chloride staining. MAPK3 was found to be the target gene of miR-1. miR-1 expressed at a high level whereas MAPK3 expressed at a low level in MIRI rats. Overexpressing miR-1 or silencing MAPK3 blocked the PI3K/Akt pathway to increase cell apoptosis, ischemic area at risk, and infarct area but decreased cell viability and increased LDH concentration. In contrast, miR-1 downregulation abrogated the effects induced by miR-1 mimics or siRNA against MAPK3. These findings indicate that inhibition of miR-1 promotes MAPK3 to protect against MIRI in rats undergoing sevoflurane preconditioning through activation of the PI3K/Akt pathway.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::093e2d0482b6e5869abee8efd24318c3Test
https://doi.org/10.1152/ajpcell.00310.2017Test -
5
المؤلفون: Wen-Qin Guo, Lingyue Zhao, Hong-Lei Zhao, Xie-Hui Chen
المصدر: JACC. Heart failure. 7(3)
مصطلحات موضوعية: Heart Failure, medicine.medical_specialty, Adrenergic receptor, business.industry, Adrenergic beta-Antagonists, 030204 cardiovascular system & hematology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Heart failure, Internal medicine, medicine, Cardiology, Humans, In patient, 030212 general & internal medicine, Cardiology and Cardiovascular Medicine, business, Adrenergic alpha-Antagonists, Cohort study
الوصف: Jackevicius et al. [(1)][1] performed a propensity score–matched cohort study to evaluate the safety of alpha-blockers (ABs) in patients with heart failure (HF). They concluded that HF patients treated with ABs had a lower rate of HF hospitalizations and all-cause mortality than patients who were
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a7d17cfa9bdb36cd23269d2c854dd68dTest
https://pubmed.ncbi.nlm.nih.gov/30819387Test -
6
المؤلفون: Hong-Lei Zhao, Xie-Hui Chen
المصدر: International journal of cardiology. 279
مصطلحات موضوعية: Drug, medicine.medical_specialty, Ticagrelor, business.industry, media_common.quotation_subject, Drug-Eluting Stents, Clopidogrel, Text mining, Internal medicine, Cardiology, Medicine, Humans, Acute Coronary Syndrome, Cardiology and Cardiovascular Medicine, business, Platelet Aggregation Inhibitors, medicine.drug, media_common
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::71127edb0501e0d105700107f838e1e5Test
https://pubmed.ncbi.nlm.nih.gov/29801763Test -
7
المؤلفون: Yun-Ling Hao, Xie-Hui Chen, Li Xie, Zhi-Ye Wu, Wu-Hua Ou, Ying Luo, Rui-Shuang Liu, Bao-Quan Wu, Zhi-Ling Zhang, Wen-Min Xu, Li-Mei Liu, Hong-Lei Zhao, Yong-Kang Lu
المصدر: Experimental Cell Research. 398:112389
مصطلحات موضوعية: 0301 basic medicine, Ischemia, Apoptosis, Pharmacology, Biology, Protective Agents, medicine.disease_cause, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, parasitic diseases, medicine, Animals, Humans, Hydrogen Sulfide, Receptor, Cells, Cultured, Cardioprotection, chemistry.chemical_classification, Reactive oxygen species, TUNEL assay, Cystathionine gamma-Lyase, Endothelial Cells, Cell Biology, medicine.disease, Rats, Disease Models, Animal, Oxidative Stress, 030104 developmental biology, chemistry, Reperfusion Injury, 030220 oncology & carcinogenesis, Receptors, Calcium-Sensing, Reperfusion injury, Oxidative stress
الوصف: Ischemia-reperfusion (I/R) injury is a multifactorial process triggered when an organ is subjected to transiently reduced blood supply. The result is a cascade of pathological complications and organ damage due to the production of reactive oxygen species following reperfusion. The present study aims to evaluate the role of activated calcium-sensing receptor (CaR)-cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway in I/R injury. Firstly, an I/R rat model with CSE knockout was constructed. Transthoracic echocardiography, TTC and HE staining were performed to determine the cardiac function of rats following I/R Injury, followed by TUNEL staining observation on apoptosis. Besides, with the attempt to better elucidate how CaR-CSE/H2S affects I/R, in-vitro culture of human coronary artery endothelial cells (HCAECs) was conducted with gadolinium chloride (GdCl3, a CaR agonist), H2O2, siRNA against CSE (siCSE), or W7 (a CaM inhibitor). The interaction between CSE and CaM was subsequently detected. Plasma oxidative stress indexes, H2S and CSE, and apoptosis-related proteins were all analyzed following cell apoptosis. We found that H2S elevation led to the improvement whereas CSE knockdown decreased cardiac function in rats with I/R injury. Moreover, oxidative stress injury in I/R rats with CSE knockout was aggravated, while the increased expression of H2S and CSE in the aortic tissues resulted in alleviated the oxidative stress injury. Moreover, increased H2S and CSE levels were found to inhibit cell apoptotic ability in the aortic tissues after I/R injury, thus attenuating oxidative stress injury, accompanied by inhibited expression of apoptosis-related proteins. In HCAECs following oxidative stress treatment, siCSE and CaM inhibitor were observed to reverse the protection of CaR agonist. Coimmunoprecipitation assay revealed the interaction between CSE and CaM. Taken together, all above-mentioned data provides evidence that activation of the CaR-CSE/H2S pathway may confer a potent protective effect in cardiac I/R injury.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2f662663c7f4cf31edc82191d5e6f8b6Test
https://doi.org/10.1016/j.yexcr.2020.112389Test -
8
المؤلفون: Wei Liu, Jin-Jie Liang, Hong-Lei Zhao, Xie-Hui Chen, Hong-Cheng Fang, Bao-Quan Wu, Zhi-Ling Zhang, Wen-Ying Zhang, Yun-Ling Hao, Ying Luo
المصدر: Journal of cellular physiology. 234(4)
مصطلحات موضوعية: 0301 basic medicine, Male, Programmed cell death, Physiology, Clinical Biochemistry, Notch signaling pathway, Apoptosis, Myocardial Reperfusion Injury, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, medicine, Gene silencing, Animals, Myocytes, Cardiac, Gene Silencing, HES1, Cells, Cultured, Cell Proliferation, Receptors, Notch, Cell growth, Chemistry, Cell Biology, medicine.disease, Mice, Inbred C57BL, Disease Models, Animal, Oxidative Stress, 030104 developmental biology, 030220 oncology & carcinogenesis, Cancer research, Female, Signal transduction, Inflammation Mediators, Apoptosis Regulatory Proteins, Keratin-1, Reperfusion injury, Signal Transduction
الوصف: Myocardial ischemia and reperfusion injury (MIRI) includes major drawbacks, such as excessive formation of free radicals and also overload of calcium, which lead to cell death, tissue scarring, and remodeling. The current study aims to explore whether KRT1 silencing may ameliorate MIRI via the Notch signaling pathway in mouse models. Myocardial tissues were used for the determination of the positive rate of KRT1 protein expression, apoptosis of myocardial cells, creatine kinase (CK) and lactate dehydrogenase (LDH) expression, expression of related biomarkers as well as myocardial infarction area. The transfected myocardial cells were treated with KRT1-siRNA, Jagged1, and DAPT (inhibitor of Notch-1 signaling pathway). The expression of KRT1, NICD, Hes1, Bcl-2, and Bax protein was detected. The MTT assay was applied for cell proliferation and flow cytometry was used for cell apoptosis. Mice with MIRI had a higher positive rate of KRT1 protein expression, apoptosis of myocardial cells, CK and LDH expression, myocardial infarction area, increased expression of MDA, NO, SDH, IL-1, IL-6, TNF-α, CRP, KRT1, Bax protein, CK, and LDH, and decreased expression of SOD, NICD, Hes1, and Bcl-2. The downregulation of KRT1 led to decreased expression of KRT1 and Bax protein, increased expression of NICD, Hes1, and Bcl-2, decreased cell apoptosis, and improved cell proliferation. The inhibition of the Notch signaling pathway leads to reduced expression of Bax, increased expression of NICD, Hes1, and Bcl 2, and also decreased cell apoptosis and increased cell proliferation. Our data conclude that KRT1 silencing is able to make MIRI better by activating the Notch signaling pathway in mice.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1d5279558fd6d5384a69f154f7b25404Test
https://pubmed.ncbi.nlm.nih.gov/30191968Test -
9
المؤلفون: Wen-Qin Guo, Hong-Lei Zhao, Xie-Hui Chen
المصدر: Journal of the American College of Cardiology. 73:532-533
مصطلحات موضوعية: medicine.medical_specialty, business.industry, medicine.medical_treatment, Multivessel disease, 030204 cardiovascular system & hematology, Revascularization, medicine.disease, Culprit, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Intervention (counseling), cardiovascular system, medicine, Cardiology, In patient, cardiovascular diseases, 030212 general & internal medicine, Myocardial infarction, Cardiology and Cardiovascular Medicine, business, Cohort study
الوصف: Rathod et al. [(1)][1] performed a cohort study to investigate the outcomes of complete revascularization compared with culprit vessel–only intervention in subjects with non–ST-segment elevation myocardial infarction and multivessel disease. They concluded that complete coronary
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::fb4548ba210a65f99ef8d500c63eb459Test
https://doi.org/10.1016/j.jacc.2018.11.029Test -
10
المؤلفون: Wen-Ying Zhang, Wei Liu, Bao-Quan Wu, Xie-Hui Chen, Ying Luo, Hong-Lei Zhao, Yun-Ling Hao, Fang Fang, Jin-Jie Liang
المصدر: Life sciences. 208
مصطلحات موضوعية: 0301 basic medicine, Cell, Inflammation, Apoptosis, Myocardial Reperfusion Injury, Protective Agents, Rhodamine 123, p38 Mitogen-Activated Protein Kinases, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, chemistry.chemical_compound, medicine, Animals, Myocytes, Cardiac, Hydrogen Sulfide, General Pharmacology, Toxicology and Pharmaceutics, Phosphorylation, Cells, Cultured, chemistry.chemical_classification, Membrane Potential, Mitochondrial, Reactive oxygen species, TUNEL assay, NF-kappa B, RNA-Binding Proteins, General Medicine, Transfection, Cell biology, Rats, 030104 developmental biology, medicine.anatomical_structure, Glucose, chemistry, Cold Shock Proteins and Peptides, Signal transduction, medicine.symptom, Reactive Oxygen Species, Signal Transduction
الوصف: Aims Hydrogen sulfide (H2S) is a novel signaling molecule with potent cytoprotective actions. In this study, we hypothesize that exogenous H2S may protect cardiac cells against high glucose (HG)-induced myocardial injury and inflammation with the involvement of the CIRP-MAPK signaling pathway. Main methods H9c2 cardiac cells cultured under HG conditions were transfected with siRNA and different inhibitor for detecting the effects of sodium hydrogen sulfide (NaHS) (a H2S donor) on cell biological processes. The cardiac cell viability and LDH activity were determined by CCK-8 and LDH kit. ELISA was employed to measure the levels of inflammatory factors, while 2′,7′-dichlorofluorescein diacetate (DCFH-DA) to evaluate reactive oxygen species (ROS). Mitochondrial membrane potential (MMP) was identified by rhodamine 123 staining. TUNEL staining and Hoechst 33258 staining were employed to observe cardiac cell apoptosis. Besides, we determined the expression of CIRP-MAPK signaling pathway- and apoptosis-related factors by protein immunoblot analysis. Key findings HG culturing induced toxicity, LDH, higher level of inflammatory factors, ROS, MMP, and apoptosis in cardiac cells, attenuated the viability of cardiac cells, and activated the CIRP-MAPK signaling pathway. Notably, CIRP silencing aggravated the above condition. H2S or blockade of the MAPK signaling pathway reversed the above conditions induced by HG. Significance The present study provides evidence for the protective effect of exogenous H2S on HG-induced myocardial injury and inflammation in H9c2 cardiac cells and suggests that the activation of CIRP-MAPK signaling pathway might be one of the mechanisms underlying the protective effect of H2S.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::38a9030250dcad171c6d54d69c387ae9Test
https://pubmed.ncbi.nlm.nih.gov/29857073Test