63 results on '"Xianjin Du"'
Search Results
2. Retraction notice to: Macrophage SAMSN1 protects against sepsis-induced acute lung injury in mice [Redox Biol. 56 (2022) 102432]
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Wanli Jiang, Chengtai Ma, Jiawei Bai, and Xianjin Du
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Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Published
- 2024
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3. Corrigendum to 'Macrophage SAMSN1 protects against sepsis-induced acute lung injury in mice' [Redox Biol. 56 (2022) 102432]
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Wanli Jiang, Chengtai Ma, Jiawei Bai, and Xianjin Du
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Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Published
- 2024
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4. Click‐hydrogel delivered aggregation‐induced emissive nanovesicles for simultaneous remodeling and antibiosis of deep burn wounds
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Xu Chen, Meijiao Zhao, Qihu Xie, Sitong Zhou, Xiaoping Zhong, Judun Zheng, Ronghua Yang, Xianjin Du, Jinyu Xia, and Yuhui Liao
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aggregation‐induced emission ,burn wounds ,nanovesicles ,Chemistry ,QD1-999 ,Biology (General) ,QH301-705.5 - Abstract
Abstract As a high‐risk trauma, deep burns are always hindered in their repair process by decreased tissue regeneration capacity and persistent infections. In this study, we developed a simultaneous strategy for deep burn wounds treatment using functional nanovesicles with antibacterial and tissue remodeling properties, delivered via a click‐chemistry hydrogel. An aggregation‐induced emission photosensitizer of 4‐(2‐(5‐(4‐(diphenylamino)phenyl)thiophen‐2‐yl)vinyl)‐1‐(2‐hydroxyethyl) pyridin‐1‐ium bromide (THB) with excellent photodynamic properties was first prepared, and then combined with readily accessible adipose stem cells‐derived nanovesicles to generate the THB functionalized nanovesicles (THB@ANVs). The THB@ANVs showed strong antibacterial activity against Gram‐positive bacteria (up to 100% killing rate), and also beneficial effects on tissue remodeling, including promoting cell migration, cell proliferation, and regulating immunity. In addition, we prepared a click‐hydrogel of carboxymethyl chitosan for effective delivery of THB@ANVs on wounds. This hydrogel could be injected to conform to the wound morphology while responding to the acidic microenvironment. In vivo evaluations of wound healing revealed that the THB@ANVs hydrogel dressing efficiently accelerated the healing of second‐degree burn wounds by reducing bacterial growth, regulating inflammation, promoting early angiogenesis, and collagen deposition. This study provides a promising candidate of wound dressing with diverse functions for deep burn wound repair.
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- 2024
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5. Macrophage SAMSN1 protects against sepsis-induced acute lung injury in mice
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Wanli Jiang, Chengtai Ma, Jiawei Bai, and Xianjin Du
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Acute lung injury ,AMPKα2 ,Inflammation ,Oxidative stress ,SAMSN1 ,Medicine (General) ,R5-920 ,Biology (General) ,QH301-705.5 - Abstract
Objective: Inflammation and oxidative stress contribute to the progression of sepsis-induced acute lung injury (ALI). SAM domain, SH3 domain and nuclear localization signals 1 (SAMSN1) is a signaling adaptor protein, and mainly regulates inflammatory response of various immune cells. The present study generates macrophage-specific SAMSN1-knockout (Samsn1MKO) and SAMSN1-transgenic (Samsn1MTG) mice to investigate its role and mechanism in sepsis-induced ALI. Methods: Samsn1MKO and Samsn1MTG mice were exposed to lipopolysaccharide (LPS) instillation or cecal ligation and puncture (CLP) surgery to induce sepsis-induced ALI. Bone marrow transplantation, cellular depletion and non-invasive adoptive transfer of bone marrow-derived macrophages (BMDMs) were performed to validate the role of macrophage SAMSN1 in sepsis-induced ALI in vivo. Meanwhile, BMDMs were isolated from Samsn1MKO or Samsn1MTG mice to further clarify the role of SAMSN1 in vitro. Results: Macrophage SAMSN1 expression was increased in response to LPS stimulation, and negatively correlated with LPS-induced ALI in mice. Macrophage SAMSN1 deficiency exacerbated, while macrophage SAMSN1 overexpression ameliorated LPS-induced inflammation, oxidative stress and ALI in mice and in BMDMs. Mechanistically, we found that macrophage SAMSN1 overexpression prevented LPS-induced ALI though activating AMP-activated protein kinase α2 (AMPKα2) in vivo and in vitro. Further studies revealed that SAMSN1 directly bound to growth factor receptor bound protein 2-associated protein 1 (GAB1) to prevent its protein degradation, and subsequently enhanced protein kinase A (PKA)/AMPKα2 activation in a protein tyrosine phosphatase, non-receptor type 11 (PTPN11, also known as SHP2)-dependent manner. Moreover, we observed that macrophage SAMSN1 overexpression diminished CLP-induced ALI in mice. Conclusion: Our study documents the protective role of macrophage SAMSN1 against sepsis-induced inflammation, oxidative stress and ALI through activating AMPKα2 in a GAB1/SHP2/PKA pathway, and defines it as a promising biomarker and therapeutic target to treat sepsis-induced ALI.
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- 2022
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6. Expert consensus on prevention and cardiopulmonary resuscitation for cardiac arrest in COVID-19
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Wei Song, Jie Wei, Xiangdong Jian, Deren Wang, Yanhong Ouyang, Yuanshui Liu, Xianjin Du, Ying Chen, Yingqi Zhang, Heping Xu, Shuming Xianyu, Qiong Ning, Xiang Li, Xiaotong Han, Feng Zhan, Tao Yu, Wenteng Chen, Jun Zhang, Wenwei Cai, Sheng’ang Zhou, Shengyang Yi, Yu Cao, Xiaobei Chen, Shunjiang Xu, Zong’an Liang, Duohu Wu, Fen Ai, Zhong Wang, Qingyi Meng, Yuhong Mi, Sisen Zhang, Rongjia Yang, Shouchun Yan, Wenbin Han, Yong Lin, Chuanyun Qian, Wenwu Zhang, Yan Xiong, Jun Lv, Baochi Liu, Yan Cao, Xiaojun He, Xuelian Sun, Yufang Cao, and Tian’en Zhou
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sars-cov-2 ,covid-19 ,cardiac arrest ,cpr ,nosocomial infection ,personal protective equipment ,Arctic medicine. Tropical medicine ,RC955-962 - Abstract
Background: Cardiopulmonary resuscitation (CPR) strategies in COVID-19 patients differ from those in patients suffering from cardiogenic cardiac arrest. During CPR, both healthcare and non-healthcare workers who provide resuscitation are at risk of infection. The Working Group for Expert Consensus on Prevention and Cardiopulmonary Resuscitation for Cardiac Arrest in COVID-19 has developed this Chinese Expert Consensus to guide clinical practice of CPR in COVID-19 patients. Main recommendations: 1) A medical team should be assigned to evaluate severe and critical COVID-19 for early monitoring of cardiac-arrest warning signs. 2) Psychological counseling and treatment are highly recommended, since sympathetic and vagal abnormalities induced by psychological stress from the COVID-19 pandemic can induce cardiac arrest. 3) Healthcare workers should wear personal protective equipment (PPE). 4) Mouth-to-mouth ventilation should be avoided on patients suspected of having or diagnosed with COVID-19. 5) Hands-only chest compression and mechanical chest compression are recommended. 6) Tracheal-intubation procedures should be optimized and tracheal-intubation strategies should be implemented early. 7) CPR should be provided for 20-30 min. 8) Various factors should be taken into consideration such as the interests of patients and family members, ethics, transmission risks, and laws and regulations governing infectious disease control. Changes in management: The following changes or modifications to CPR strategy in COVID-19 patients are proposed: 1) Healthcare workers should wear PPE. 2) Hands-only chest compression and mechanical chest compression can be implemented to reduce or avoid the spread of viruses by aerosols. 3) Both the benefits to patients and the risk of infection should be considered. 4) Hhealthcare workers should be fully aware of and trained in CPR strategies and procedures specifically for patients with COVID-19.
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- 2021
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7. Extracorporeal Membrane Oxygenation in Severe Acute Respiratory Distress Syndrome Caused by Chlamydia psittaci: A Case Report and Review of the Literature
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Lu Wang, Zhaokun Shi, Wei Chen, Xianjin Du, and Liying Zhan
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Chlamydia psittaci (C. psittaci) ,pneumonia ,extracorporeal membrane oxygenation (ECMO) ,next-generation sequencing (NGS) ,infection ,Medicine (General) ,R5-920 - Abstract
Background: Infection of Chlamydia psittaci (C. psittaci) could lead to serious clinical manifestations in humans, including severe pneumonia with rapid progression, adult respiratory distress syndrome (ARDS), sepsis, multiple organ dysfunction syndromes (MODS), and probably death. Implementation of extracorporeal membrane oxygenation (ECMO) in the patient with severe ARDS gives a promising new method for recovery.Case Presentation: We report our successful use of venovenous (VV) ECMO in a 48-year-old man who manifested with severe respiratory distress syndrome, acute kidney injury, and septic shock caused by a diagnosis of pneumonia. After the combination of therapy including anti-infection, mechanical ventilation, and continuous renal replacement therapy (CRRT), acute inflammatory syndrome developed. However, his respiratory status rapidly deteriorated. Then, venoarterial (VA)-ECMO support was placed on the patient as suddenly slowing of the heart rate. Harlequin (North-South) syndrome occurred after ECMO initiation. A series of the process could not relieve hypoxia in the upper body. At last, transition to VV-ECMO improved hypoxia. The duration of VV-ECMO was 7 days and the mechanical ventilation was weaned on the next day. On the day of ECMO weaning, nanopore targeted sequencing (NTS) of bronchoalveolar lavage fluid (BALF) reported the presence of C. psittaci. After 19 days of critical systemic rehabilitation and combination therapy, the patient fully recovered from C. psittaci.Conclusion: This is the first reported case of the patient receiving ECMO for C. psittaci pneumonia. ECMO puts the lungs on temporary rest, promotes the recovery of pulmonary function, and also wins time for finding the pathogens, which is crucial in the treatment of rare pathogens.
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- 2021
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8. Normothermic ex vivo Heart Perfusion Combined With Melatonin Enhances Myocardial Protection in Rat Donation After Circulatory Death Hearts via Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis
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Jun Lu, Liwei Xu, Zifeng Zeng, Chuqing Xue, Jiale Li, Xiong Chen, Pengyu Zhou, Shaoyan Lin, Yuhui Liao, Xianjin Du, Ronghua Yang, and Shaoyi Zheng
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donation after circulatory death ,normothermic ex vivo heart perfusion ,melatonin ,heart preservation ,ischemia/reperfusion injury ,pyroptosis ,Biology (General) ,QH301-705.5 - Abstract
ObjectiveThe adoption of hearts from donation after circulatory death (DCD) is a promising approach for the shortage of suitable organs in heart transplantation. However, DCD hearts suffer from serious ischemia/reperfusion injury (IRI). Recent studies demonstrate that nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis is a novel target to ameliorate myocardial IRI. Melatonin is shown to inhibit NLRP3 inflammasome-mediated pyroptosis. Therefore, this study is designed to verify the hypothesis that melatonin can protect the heart graft preserved with ex vivo heart perfusion (EVHP) against myocardial IRI via inhibiting NLRP3 inflammasome-mediated pyroptosis in a rat model of DCD.MethodsDonor-heart rats were randomly divided into three groups: (1) Control group: non-DCD hearts were harvested from heart-beating rats and immediately preserved with allogenic blood-based perfusate at constant flow for 105 min in the normothermic EVHP system; (2) DCD-vehicle group; and (3) DCD-melatonin group: rats were subjected to the DCD procedure with 25 min of warm ischemia injury and preserved by the normothermic EVHP system for 105 min. Melatonin (200 μmol/L) or vehicle was perfused in the cardioplegia and throughout the whole EVHP period. Cardiac functional assessment was performed every 30 min during EVHP. The level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis of heart grafts submitted to EVHP were evaluated.ResultsTwenty five-minute warm ischemia injury resulted in a significant decrease in the developed pressure (DP), dP/dtmax, and dP/dtmin of left ventricular of the DCD hearts, while the treatment with melatonin significantly increased the DP, dP/dtmax of the left ventricular of DCD hearts compared with DCD-vehicle group. Furthermore, warm ischemia injury led to a significant increase in the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis in the hearts preserved with EVHP. However, melatonin added in the cardioplegia and throughout the EVHP period significantly attenuated the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis compared with DCD-vehicle group.ConclusionEVHP combined with melatonin post-conditioning attenuates myocardial IRI in DCD hearts by inhibiting NLRP3 inflammasome-mediated pyroptosis, which might expand the donor pool by the adoption of transplantable DCD hearts.
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- 2021
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9. Artificial Intelligence for Clinical Decision Support in Sepsis
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Miao Wu, Xianjin Du, Raymond Gu, and Jie Wei
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sepsis ,artificial intelligence ,machine learning ,deep learning ,early prediction ,Medicine (General) ,R5-920 - Abstract
Sepsis is one of the main causes of death in critically ill patients. Despite the continuous development of medical technology in recent years, its morbidity and mortality are still high. This is mainly related to the delay in starting treatment and non-adherence of clinical guidelines. Artificial intelligence (AI) is an evolving field in medicine, which has been used to develop a variety of innovative Clinical Decision Support Systems. It has shown great potential in predicting the clinical condition of patients and assisting in clinical decision-making. AI-derived algorithms can be applied to multiple stages of sepsis, such as early prediction, prognosis assessment, mortality prediction, and optimal management. This review describes the latest literature on AI for clinical decision support in sepsis, and outlines the application of AI in the prediction, diagnosis, subphenotyping, prognosis assessment, and clinical management of sepsis. In addition, we discussed the challenges of implementing and accepting this non-traditional methodology for clinical purposes.
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- 2021
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10. The Role of Gut Microbiota in Tumor Immunotherapy
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Miao Wu, Jiawei Bai, Chengtai Ma, Jie Wei, and Xianjin Du
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Tumor immunotherapy is the fourth therapy after surgery, chemotherapy, and radiotherapy. It has made great breakthroughs in the treatment of some epithelial tumors and hematological tumors. However, its adverse reactions are common or even more serious, and the response rate in some solid tumors is not satisfactory. With the maturity of genomics and metabolomics technologies, the effect of intestinal microbiota in tumor development and treatment has gradually been recognized. The microbiota may affect tumor immunity by regulating the host immune system and tumor microenvironment. Some bacteria help fight tumors by activating immunity, while some bacteria mediate immunosuppression to help cancer cells escape from the immune system. More and more studies have revealed that the effects and complications of tumor immunotherapy are related to the composition of the gut microbiota. The composition of the intestinal microbiota that is sensitive to treatment or prone to adverse reactions has certain characteristics. These characteristics may be used as biomarkers to predict the prognosis of immunotherapy and may also be developed as “immune potentiators” to assist immunotherapy. Some clinical and preclinical studies have proved that microbial intervention, including microbial transplantation, can improve the sensitivity of immunotherapy or reduce adverse reactions to a certain extent. With the development of gene editing technology and nanotechnology, the design and development of engineered bacteria that contribute to immunotherapy has become a new research hotspot. Based on the relationship between the intestinal microbiota and immunotherapy, the correct mining of microbial information and the development of reasonable and feasible microbial intervention methods are expected to optimize tumor immunotherapy to a large extent and bring new breakthroughs in tumor treatment.
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- 2021
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11. MEG3 Alleviated LPS-Induced Intestinal Injury in Sepsis by Modulating miR-129-5p and Surfactant Protein D
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Xianjin Du, Dan Tian, Jie Wei, Chen Yan, Peng Hu, Xu Wu, and Wenbin Yang
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Pathology ,RB1-214 - Abstract
Sepsis and intestinal injury triggered by sepsis are common in intensive care units, which can contribute to a high mortality. lncRNAs can modulate gene expression, and they are closely involved in multiple diseases, including sepsis. In our present study, we investigated the biological function of MEG3 in sepsis, especially during the intestinal injury. Currently, we observed that in LPS-induced sepsis mouse models, the intestinal injury was triggered. Meanwhile, we reported that MEG3 was greatly decreased in vivo, with an increase of miR-129-5p and inhibition of SP-D. Then, MEG3 was overexpressed, and we found that its overexpression repressed the intestinal injury via downregulating miR-129-5p in sepsis mice. Moreover, TNF-α and IL-6 expression was elevated in intestinal tissues compared to the control groups. MEG3 restrained the activation of TNF-α and IL-6, in sepsis models. Subsequently, to induce the inflammatory injury of sepsis, human colorectal Caco2 cells were treated with 10 ng/ml LPS. 10 ng/ml LPS significantly inhibited Caco2 cell proliferation and increased the apoptosis. Additionally, MEG3 was decreased whereas miR-129-5p was obviously increased in Caco2 cells incubated with LPS. Interestingly, we showed that MEG3 repressed cell apoptosis partly and enhanced Caco2 cell proliferation. miR-129-5p overexpression could reverse the effect of MEG3 in vitro. Previously, we proved SP-D was reduced in sepsis and it depressed the intestinal injury in vivo. Finally, the correlation among MEG3, miR-129-5p, and SP-D was predicted and confirmed in our investigation. These findings indicated that MEG3 might be a potential target for intestinal damage caused by sepsis via regulating miR-129-5p and SP-D.
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- 2020
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12. miR-199a-5p Exacerbated Intestinal Barrier Dysfunction through Inhibiting Surfactant Protein D and Activating NF-κB Pathway in Sepsis
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Xianjin Du, Dan Tian, Jie Wei, Chen Yan, Peng Hu, Xu Wu, Wenbin Yang, and Zhanyong Zhu
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Pathology ,RB1-214 - Abstract
Sepsis is a severe disease, which results from the excessive inflammatory response to the infection. Dysfunction of intestinal barrier is a crucial problem in various pathological conditions. Meanwhile, microRNAs exhibit significant roles in the modulation of many diseases, including sepsis. Multiple investigations indicate that miR-199a-5p participates in different human diseases. Nevertheless, little is known on the roles of miR-199a-5p in sepsis. Herein, we evaluated the mechanism of miR-199a-5p on the intestinal barrier dysfunction in sepsis. Intestinal mucosa permeability indicators including D-lactic acid, DAO, and FD-40 levels were determined, and they were greatly increased in sepsis. Then, we proved that miR-199a-5p was induced in sepsis mice tissues and isolated intestinal epithelial cells. Moreover, miR-199a-5p increased D-lactic acid, DAO, and FD-40 while inhibition of miR-199a-5p exhibited a reversed process. Additionally, we observed that miR-199a-5p affected the oxidative damage and inflammation in the intestine tissues from sepsis mice. The content of MDA was elevated whereas SOD was remarkably repressed in the miR-199a-5p mimic group. IL-6, IL-1β, and TNF-α were induced by miR-199a-5p overexpression while IL-10 was reduced by miR-199a-5p. Subsequently, surfactant protein D (SP-D) was predicted as the target of miR-199a-5p. The activation of NF-κB has been identified in sepsis. Herein, we demonstrated that inhibitor of miR-199a-5p contributed to IEC injury via targeting SP-D and inactivating the NF-κB pathway. These revealed miR-199a-5p exacerbated the intestinal barrier dysfunction via inhibiting SP-D and activating the NF-κB pathway in sepsis.
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- 2020
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13. MicroRNA-21 Contributes to Acute Liver Injury in LPS-Induced Sepsis Mice by Inhibiting PPARα Expression
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Xianjin Du, Miao Wu, Dan Tian, Jianlin Zhou, Lu Wang, and Liying Zhan
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Biology (General) ,QH301-705.5 - Abstract
The severity of sepsis may be associated with excessive inflammation, thus leading to acute liver injury. MicroRNA-21 is highly expressed in the liver of a variety of inflammation-related diseases, and PPARα is also proved to participate in regulating inflammation. In the present study, the LPS-induced sepsis model was established. We found that microRNA-21 expression was upregulated in the liver of sepsis mice, and microRNA-21 inhibition significantly reduced the liver injury. The expression of liver injury markers, inflammation cytokines, and PPARα in the septic mice was higher than in antagomir-21 treated septic mice. In addition, we also found that PPARα is the target gene of microRNA-21; PPARα antagonist GW6471 could reverse the effect of antagomir-21. In conclusion, our study illustrated that microRNA-21 exacerbate acute liver injury in sepsis mice by inhibiting PPARα expression.
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- 2020
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14. LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way
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Xiaohui Gong, Xianjin Du, Yong Xu, and Wenze Zheng
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Linc00037 ,LncRNA ,Clear cell renal cell carcinoma ,EGFR ,Physiology ,QP1-981 ,Biochemistry ,QD415-436 - Abstract
Background/Aims: LINC00037 has previously been reported to be up-regulated in clear cell renal cell carcinoma (ccRCC), however, the underlying mechanism remained unknown. In this study, we designed to investigate the functional role of LINC00037 in ccRCC Methods: LINC00037 knockdown and re-expressing 786-O and A498 cells were established. CCK8 assay and EdU assay were performed to evaluate the proliferation rates of ccRCC cells. Flow cytometry assay was performed to detect the cell apoptosis and cell cycle. Subcutaneous injection xenotransplantation mouse model was used to observe the role of LINC00037 in tumor growth in vivo. Mass spectrometry (MS) was performed to find the interacting partner of LINC00037 and RNA immunoprecipitation (RIP) was carried out to validate their interaction. Results: We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR. Conclusion: LINC00037 could inhibit proliferation of ccRCC in an epidermal growth factor receptor-dependent way.
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- 2018
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15. Cooperative advertising and coordination in a supply chain: the role of Nash bargaining fairness concerns.
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Xianjin Du, Shan Jiang, Shaokun Tao, and Shulei Wang
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- 2024
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16. Click-Chemistry Hydrogel Delivery Aggregation-Induced Emission-Active Nanovesicles Enables 'One-Stop' Remodeling and Antibiosis on Deep Scald Wound
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Xu Chen, Meijiao Zhao, Qihu Xie, Sitong Zhou, Yanan Qianzuo, Xiaoping Zhong, Judun Zheng, Ronghua Yang, Xianjin Du, Jinyu Xia, and Yuhui Liao
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The serve burn or scald wounds always face persistent infections and self-repair function decline caused by serious tissue necrosis, leading to delayed healing or even sepsis. In this work, we proposed a click-chemistry hydrogel delivery system of antibacterial and tissue remodeling function nanovesicles for deep scald wound treatment. An hydrophilic photodynamic aggregation-induced emission photosensitizer 4-(2-(5-(4-(diphenylamino)phenyl)thiophen-2-yl)vinyl)-1-(2-hydroxyethyl) pyridin-1-ium bromide (THB) was firstly encapsulated into nanovesicles derived from easily accessible adipose stem cells (ANVs) to create THB@ANVs, which exhibits enhanced bacteria-targeting property and multiple tissue remodeling effects. To deliver THB@ANVs, an injectable click-chemistry hydrogel of carboxymethyl chitosan was used to form a wound treatment system for deep scald wounds. The hydrogel can well matching the wound morphology and respond to the acidic microenvironment of the wound to accelerate sustained release. In vivo wound healing evaluations show that the composite hydrogel can efficiently accelerate wound healing by reducing the number of bacteria, promoting early angiogenesis, and regulating immune reaction. This study provides a simple, low-cost, and effective “one-stop” strategy with diverse functions and wide applicability for scald wound remodeling and antibiosis.
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- 2023
17. Emergency Treatment and Photoacoustic Assessment of Spinal Cord Injury Using Reversible Dual‐Signal Transform‐Based Selenium Antioxidant
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Zhisheng Ji, Judun Zheng, Yanming Ma, Hongyi Lei, Weiqiang Lin, Jialin Huang, Hua Yang, Guowei Zhang, Bin Li, Bowen Shu, Xianjin Du, Jian Zhang, Hongsheng Lin, and Yuhui Liao
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Biomaterials ,General Materials Science ,General Chemistry ,Biotechnology - Published
- 2023
18. Knockdown of miR-129-5p alleviates intestinal barrier dysfunction induced by ischemia/reperfusion injury via targeting surfactant protein D
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Miao Wu, Jiawei Bai, Chengtai Ma, Jie Wei, and Xianjin Du
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An increasing number of microRNAs (miRs) have been shown to serve crucial roles in intestinal ischemia/reperfusion (II/R) injury. The aim of the present study was to examine the effects of miR-129-5p on II/R injury in vitro and in vivo. It was revealed that the expression level of miR-129-5p was upregulated, whereas SP-D expression was downregulated in the intestinal tissues of I/R mice. Serum levels of diamine oxidase, FD-4 and D-lactic acid, which are commonly used indicators of intestinal mucosal permeability, were significantly decreased following miR-129-5p knockdown. By contrast, ZO-1 and E-cadherin expression levels were increased following miR-129-5p knockdown, as determined using IHC, which improved the function of the epithelial barrier. In addition, Caco-2 cells were exposed to hypoxia/reoxygenation, which can trigger II/R injury. miR-129-5p expression was increased, whereas SP-D expression was decreased by H/R exposure in vitro. Knockdown of miR-129-5p increased ZO-1 and E-cadherin expression in Caco-2 cells. Moreover, overexpression of SP-D improved the function of the epithelial barrier, as indicated by increased transepithelial electrical resistance values and decreased paracellular flux of FD-4. It was also found that liver and lung injury triggered by II/R was attenuated by miR-129-5p knockdown. Collectively, the present study suggested that miR-129-5p knockdown mitigated II/R injury by targeting SP-D.
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- 2022
19. PTPN2 negatively regulates macrophage inflammation in atherosclerosis
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Xiaorong Hu, Jianlei Cao, Xianjin Du, Ruisong Ma, Yongzhen Fan, and Xinyong Cai
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STAT3 Transcription Factor ,Aging ,Mice, Knockout, ApoE ,THP-1 Cells ,p38 mitogen-activated protein kinases ,Interleukin-1beta ,Inflammation ,macrophage ,Protein tyrosine phosphatase ,Systemic inflammation ,p38 Mitogen-Activated Protein Kinases ,Mice ,Cell Movement ,medicine ,Animals ,Humans ,Macrophage ,Secretion ,RNA, Messenger ,STAT3 ,Cell Proliferation ,Protein Tyrosine Phosphatase, Non-Receptor Type 2 ,biology ,Interleukin-6 ,Cell growth ,business.industry ,Macrophages ,Transcription Factor RelA ,U937 Cells ,Cell Biology ,Atherosclerosis ,Interleukin-12 ,Cancer research ,biology.protein ,PTPN2 ,medicine.symptom ,business ,Signal Transduction ,Research Paper - Abstract
Atherosclerosis is the main cause of cardiovascular disease. Systemic inflammation is one important characteristic in atherosclerosis. Pro-inflammatory macrophages can secrete inflammatory factors and promote the inflammation of atherosclerosis. It has a great value for the treatment of atherosclerosis by inhibiting the release of inflammatory factors in macrophages. However, the detailed mechanism of this process is still unclear. In this study, we constructed an APOE-/- mice model of atherosclerosis to research the molecular mechanism of atherosclerosis. Protein tyrosine phosphatase non-receptor type 2 (PTPN2), an anti-inflammatory gene, was dramatically decreased in inflammatory mice. Deletion of PTPN2 could significantly induce monocytes toward M1 phenotype of macrophages, enhance the secretion of IL-12 and IL-1, and promote cell proliferation, invasion and metastasis. Mechanism research showed that PTPN2-mediated p65/p38/STAT3 de-phosphorylation could block the process of macrophage inflammation. In vivo experiments showed that PTPN2 may effectively inhibit the inflammatory response during atherosclerosis. In conclusion, we uncovered the negative role of PTPN2 in the occurrence of atherosclerosis, and this study provides a new potential target for atherosclerosis treatment.
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- 2020
20. CircSAMD4A aggravates H/R‐induced cardiomyocyte apoptosis and inflammatory response by sponging miR‐138‐5p
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Xianjin Du, Yongzhen Fan, Xiaorong Hu, Xinyong Cai, Ruisong Ma, and Jianlei Cao
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0301 basic medicine ,Myocardial Infarction ,Apoptosis ,Myocardial Reperfusion Injury ,Inflammation ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Western blot ,Annexin ,medicine ,Animals ,Myocytes, Cardiac ,MTT assay ,Viability assay ,Hypoxia ,TUNEL assay ,medicine.diagnostic_test ,Chemistry ,RNA, Circular ,Cell Biology ,Molecular biology ,MicroRNAs ,030104 developmental biology ,Real-time polymerase chain reaction ,030220 oncology & carcinogenesis ,Molecular Medicine ,medicine.symptom - Abstract
Hypoxia/reoxygenation (H/R)-induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R-induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/R-induced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/R-induced H9C2 cells to investigate its' function in AMI. The levels of circSAMD4A and miR-138-5p were detected by real-time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V-FITC were used to determine apoptosis. The expression of Bcl-2 and Bax proteins was detected by Western blot. IL-1β, TNF-α and IL-6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up-regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R-induced apoptosis and inflammation. MiR-138-5p was down-regulated in H/R-induced H9C2 cells. circSAMD4A was a targeted regulator of miR-138-5p. CircSAMD4A inhibited the expression of miR-138-5p to promote H/R-induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR-138-5p to promote H/R-induced apoptosis and inflammatory response.
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- 2020
21. Circular RNA circANKRD36 regulates Casz1 by targeting miR‐599 to prevent osteoarthritis chondrocyte apoptosis and inflammation
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Jianlin Zhou, Qiong-jie Hu, Hao Peng, Shuang Deng, Hongsong Fang, and Xianjin Du
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0301 basic medicine ,Interleukin-1beta ,Apoptosis ,Inflammation ,Osteoarthritis ,Chondrocyte ,Casz1 ,miR‐599 ,03 medical and health sciences ,Chondrocytes ,0302 clinical medicine ,Western blot ,In vivo ,Circular RNA ,medicine ,Humans ,circANKRD36 ,Aged ,Aged, 80 and over ,Gene knockdown ,Base Sequence ,medicine.diagnostic_test ,business.industry ,RNA, Circular ,Original Articles ,Cell Biology ,Middle Aged ,medicine.disease ,DNA-Binding Proteins ,MicroRNAs ,osteoarthritis ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Cancer research ,Molecular Medicine ,Original Article ,medicine.symptom ,business ,Transcription Factors - Abstract
Osteoarthritis (OA) is an ageing‐related disease characterized by articular cartilage degradation and joint inflammation. circRNA has been known to involve in the regulation of multiple inflammatory diseases including OA. However, the mechanism underlying how circRNA regulates OA remains to be elucidated. Here, we report circANKRD36 prevents OA chondrocyte apoptosis and inflammation by targeting miR‐599, which specifically degrades Casz1. We performed circRNA sequencing in normal and OA tissues and found the expression of circANKRD36 is decreased in OA tissues. circANKRD36 is also reduced in IL‐1β–treated human chondrocytes. FACS analysis and Western blot showed that the knockdown of circANKRD36 promotes the apoptosis and inflammation of chondrocytes in IL‐1β stress. We then found miR‐599 to be the target of circANKRD36 and correlate well with circANKRD36 both in vitro and in vivo. By database analysis and luciferase assay, Casz1 was found to be the direct target of miR‐599. Casz1 helps to prevent apoptosis and inflammation of chondrocytes in response to IL‐1β. In conclusion, our results proved circANKRD36 sponge miR‐599 to up‐regulate the expression of Casz1 and thus prevent apoptosis and inflammation in OA.
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- 2020
22. Severe pneumonia with thrombocytopenia caused by Chlamydia psittaci: A case and literature review
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Zhaokun Shi, Lu Wang, Wei Chen, Xianjin Du, and Liying Zhan
- Abstract
Background: Severe pneumonia caused by Chlamydia psittaci is a rare infectious disease associated with living environment. The causes of thrombocytopenia were infection, leukemia, idiopathic thrombocytopenia and many other factors. The determination of platelet parameters could reflect the compensatory situation of bone marrow and provide a basis reason of thrombocytopenia identification. Case presentation: Based on the patient’s symptoms, exposure history, computerized tomography(CT)and next-generation sequencing, a preliminary diagnosis of the patient were made, at the same time other infections are excluded. We reported a case of severe pneumonia with severe thrombocytopenia caused by Chlamydia psittaci. During the treatment, he was diagnosed as parrot fever and secondary immune thrombocytopenia. Anti-infection and rising platelet with Doptelet treatment were in effect. The presence of high fever, feeling faint, gastrointestinal symptoms, images of chest CT and platelet reduction, Chlamydia psittaci might be considered as a priority reason of this case, other infections and hematology disorders excluded.Conclusion: This is the first reported case of Chlamydia psittaci-induced thrombocytopenia associated with bone marrow changes and treatment. The efficacy of mokexin in the treatment of thrombocytopenia may be further generalized.
- Published
- 2022
23. Extracorporeal Membrane Oxygenation in Severe Acute Respiratory Distress Syndrome Caused by Chlamydia psittaci: A Case Report and Review of the Literature
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Liying Zhan, Lu Wang, Wei Chen, Zhaokun Shi, and Xianjin Du
- Subjects
Mechanical ventilation ,ARDS ,Medicine (General) ,Respiratory distress ,Septic shock ,business.industry ,medicine.medical_treatment ,Case Report ,General Medicine ,Chlamydia psittaci (C. psittaci) ,medicine.disease ,infection ,Sepsis ,Pneumonia ,surgical procedures, operative ,R5-920 ,Anesthesia ,extracorporeal membrane oxygenation (ECMO) ,medicine ,Extracorporeal membrane oxygenation ,Medicine ,pneumonia ,Renal replacement therapy ,business ,next-generation sequencing (NGS) - Abstract
Background: Infection of Chlamydia psittaci (C. psittaci) could lead to serious clinical manifestations in humans, including severe pneumonia with rapid progression, adult respiratory distress syndrome (ARDS), sepsis, multiple organ dysfunction syndromes (MODS), and probably death. Implementation of extracorporeal membrane oxygenation (ECMO) in the patient with severe ARDS gives a promising new method for recovery.Case Presentation: We report our successful use of venovenous (VV) ECMO in a 48-year-old man who manifested with severe respiratory distress syndrome, acute kidney injury, and septic shock caused by a diagnosis of pneumonia. After the combination of therapy including anti-infection, mechanical ventilation, and continuous renal replacement therapy (CRRT), acute inflammatory syndrome developed. However, his respiratory status rapidly deteriorated. Then, venoarterial (VA)-ECMO support was placed on the patient as suddenly slowing of the heart rate. Harlequin (North-South) syndrome occurred after ECMO initiation. A series of the process could not relieve hypoxia in the upper body. At last, transition to VV-ECMO improved hypoxia. The duration of VV-ECMO was 7 days and the mechanical ventilation was weaned on the next day. On the day of ECMO weaning, nanopore targeted sequencing (NTS) of bronchoalveolar lavage fluid (BALF) reported the presence of C. psittaci. After 19 days of critical systemic rehabilitation and combination therapy, the patient fully recovered from C. psittaci.Conclusion: This is the first reported case of the patient receiving ECMO for C. psittaci pneumonia. ECMO puts the lungs on temporary rest, promotes the recovery of pulmonary function, and also wins time for finding the pathogens, which is crucial in the treatment of rare pathogens.
- Published
- 2021
24. Normothermic ex vivo Heart Perfusion Combined With Melatonin Enhances Myocardial Protection in Rat Donation After Circulatory Death Hearts via Inhibiting NLRP3 Inflammasome-Mediated Pyroptosis
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Chuqing Xue, Pengyu Zhou, Jun Lu, Jiale Li, Zifeng Zeng, Xianjin Du, Ronghua Yang, Shaoyan Lin, Xiong Chen, Yuhui Liao, Shaoyi Zheng, and Liwei Xu
- Subjects
QH301-705.5 ,medicine.medical_treatment ,Ischemia ,Heart preservation ,donation after circulatory death ,melatonin ,Pharmacology ,ischemia/reperfusion injury ,medicine.disease_cause ,Melatonin ,Cell and Developmental Biology ,heart preservation ,medicine ,Biology (General) ,Original Research ,Heart transplantation ,business.industry ,pyroptosis ,Pyroptosis ,Inflammasome ,Cell Biology ,medicine.disease ,normothermic ex vivo heart perfusion ,business ,Reperfusion injury ,Oxidative stress ,Developmental Biology ,medicine.drug - Abstract
ObjectiveThe adoption of hearts from donation after circulatory death (DCD) is a promising approach for the shortage of suitable organs in heart transplantation. However, DCD hearts suffer from serious ischemia/reperfusion injury (IRI). Recent studies demonstrate that nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis is a novel target to ameliorate myocardial IRI. Melatonin is shown to inhibit NLRP3 inflammasome-mediated pyroptosis. Therefore, this study is designed to verify the hypothesis that melatonin can protect the heart graft preserved with ex vivo heart perfusion (EVHP) against myocardial IRI via inhibiting NLRP3 inflammasome-mediated pyroptosis in a rat model of DCD.MethodsDonor-heart rats were randomly divided into three groups: (1) Control group: non-DCD hearts were harvested from heart-beating rats and immediately preserved with allogenic blood-based perfusate at constant flow for 105 min in the normothermic EVHP system; (2) DCD-vehicle group; and (3) DCD-melatonin group: rats were subjected to the DCD procedure with 25 min of warm ischemia injury and preserved by the normothermic EVHP system for 105 min. Melatonin (200 μmol/L) or vehicle was perfused in the cardioplegia and throughout the whole EVHP period. Cardiac functional assessment was performed every 30 min during EVHP. The level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis of heart grafts submitted to EVHP were evaluated.ResultsTwenty five-minute warm ischemia injury resulted in a significant decrease in the developed pressure (DP), dP/dtmax, and dP/dtmin of left ventricular of the DCD hearts, while the treatment with melatonin significantly increased the DP, dP/dtmax of the left ventricular of DCD hearts compared with DCD-vehicle group. Furthermore, warm ischemia injury led to a significant increase in the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis in the hearts preserved with EVHP. However, melatonin added in the cardioplegia and throughout the EVHP period significantly attenuated the level of oxidative stress, inflammatory response, apoptosis, and NLRP3 inflammasome-mediated pyroptosis compared with DCD-vehicle group.ConclusionEVHP combined with melatonin post-conditioning attenuates myocardial IRI in DCD hearts by inhibiting NLRP3 inflammasome-mediated pyroptosis, which might expand the donor pool by the adoption of transplantable DCD hearts.
- Published
- 2021
25. Artificial Intelligence for Clinical Decision Support in Sepsis
- Author
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Xianjin Du, Miao Wu, Raymond Gu, and Jie Wei
- Subjects
Multiple stages ,Medicine (General) ,Review ,Clinical decision support system ,Sepsis ,sepsis ,03 medical and health sciences ,0302 clinical medicine ,R5-920 ,Early prediction ,Medicine ,030212 general & internal medicine ,Mortality prediction ,early prediction ,business.industry ,Critically ill ,Health technology ,deep learning ,030208 emergency & critical care medicine ,General Medicine ,medicine.disease ,artificial intelligence ,Optimal management ,machine learning ,Artificial intelligence ,business - Abstract
Sepsis is one of the main causes of death in critically ill patients. Despite the continuous development of medical technology in recent years, its morbidity and mortality are still high. This is mainly related to the delay in starting treatment and non-adherence of clinical guidelines. Artificial intelligence (AI) is an evolving field in medicine, which has been used to develop a variety of innovative Clinical Decision Support Systems. It has shown great potential in predicting the clinical condition of patients and assisting in clinical decision-making. AI-derived algorithms can be applied to multiple stages of sepsis, such as early prediction, prognosis assessment, mortality prediction, and optimal management. This review describes the latest literature on AI for clinical decision support in sepsis, and outlines the application of AI in the prediction, diagnosis, subphenotyping, prognosis assessment, and clinical management of sepsis. In addition, we discussed the challenges of implementing and accepting this non-traditional methodology for clinical purposes.
- Published
- 2021
26. Managing a Dual-Channel Supply Chain with Fairness and Channel Preference
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Weijie Zhao and Xianjin Du
- Subjects
021103 operations research ,Article Subject ,General Mathematics ,Supply chain ,05 social sciences ,0211 other engineering and technologies ,General Engineering ,02 engineering and technology ,Engineering (General). Civil engineering (General) ,Preference ,Dual (category theory) ,Product (business) ,Microeconomics ,0502 economics and business ,QA1-939 ,Business ,TA1-2040 ,050203 business & management ,Mathematics ,Communication channel - Abstract
This paper investigates a dual-channel supply chain in which a manufacturer sells the product via an offline retailer or online store. The manufacturer sets the wholesale and online price, and the retailer decides the retail price with the retailer’s fairness preference and consumer’s online channel preference. Through investigating the combined impacts of fairness preference and channel preference on the enterprises’ operational strategies, this paper obtains some meaningful results. If a manufacturer thinks over the fairness preference, he decreases the wholesale price to mitigate a loss of retailer and benefit the supply chain design. The manufacturer intends to set up the online channel with a lower acceptance as the fairness preference grows. However, the gains from enhanced online channel acceptance cannot compensate for the manufacturer’s loss by the fairness effect that benefits the retailer. Moreover, the manufacturer cannot neglect the retailer’s fairness preference generating a “lose-lose” case for both members.
- Published
- 2021
27. Equilibrium decisions on pricing and innovation that impact reference price dynamics
- Author
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Yu Li, Xiuli He, Xianjin Du, Shaokun Tao, and Suresh Sethi
- Subjects
Control and Optimization ,Supply chain management ,Applied Mathematics ,Strategy and Management ,Supply chain ,Reference price ,Investment (macroeconomics) ,Atomic and Molecular Physics, and Optics ,Purchasing ,Microeconomics ,Stackelberg competition ,Price ratio ,Economics ,Business and International Management ,Electrical and Electronic Engineering ,Construct (philosophy) - Abstract
Previous studies have confirmed that reference prices play an essential role in consumer purchasing decisions, and some researchers have suggested that reference prices are positively influenced by innovation. Therefore, we construct an interactive effect of innovation and reference price to study their combined impact on supply chain decisions. We model a supply chain, where a manufacturer determines the innovation level and the wholesale price while the retailer controls the retail price, as a dynamic Stackelberg game. We show that the interactive effect causes the steady-state wholesale and retail prices to increase, thus motivating the manufacturer to increase innovation investment. We see that the retail price and the level of innovation increase in reference price effect whereas they decrease in consumer memory. The centralized firm has a higher steady-state innovation level and innovation/price ratio and lower steady-state retail price compared to the decentralized supply chain. Consumers also benefit from the interactive effect as well as from centralization. Finally, we use numerical analysis to demonstrate our results and offer some managerial implications.
- Published
- 2022
28. miR-199a-5p Exacerbated Intestinal Barrier Dysfunction through Inhibiting Surfactant Protein D and Activating NF-κB Pathway in Sepsis
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Wenbin Yang, Xianjin Du, Peng Hu, Chen Yan, Xu Wu, Zhanyong Zhu, Dan Tian, and Jie Wei
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Article Subject ,Immunology ,Surfactant protein D ,Inflammation ,NF-κB ,Cell Biology ,Transfection ,medicine.disease ,medicine.disease_cause ,Sepsis ,chemistry.chemical_compound ,Intestinal mucosa ,chemistry ,Apoptosis ,Cancer research ,medicine ,Pathology ,RB1-214 ,medicine.symptom ,Oxidative stress - Abstract
Sepsis is a severe disease, which results from the excessive inflammatory response to the infection. Dysfunction of intestinal barrier is a crucial problem in various pathological conditions. Meanwhile, microRNAs exhibit significant roles in the modulation of many diseases, including sepsis. Multiple investigations indicate that miR-199a-5p participates in different human diseases. Nevertheless, little is known on the roles of miR-199a-5p in sepsis. Herein, we evaluated the mechanism of miR-199a-5p on the intestinal barrier dysfunction in sepsis. Intestinal mucosa permeability indicators including D-lactic acid, DAO, and FD-40 levels were determined, and they were greatly increased in sepsis. Then, we proved that miR-199a-5p was induced in sepsis mice tissues and isolated intestinal epithelial cells. Moreover, miR-199a-5p increased D-lactic acid, DAO, and FD-40 while inhibition of miR-199a-5p exhibited a reversed process. Additionally, we observed that miR-199a-5p affected the oxidative damage and inflammation in the intestine tissues from sepsis mice. The content of MDA was elevated whereas SOD was remarkably repressed in the miR-199a-5p mimic group. IL-6, IL-1β, and TNF-α were induced by miR-199a-5p overexpression while IL-10 was reduced by miR-199a-5p. Subsequently, surfactant protein D (SP-D) was predicted as the target of miR-199a-5p. The activation of NF-κB has been identified in sepsis. Herein, we demonstrated that inhibitor of miR-199a-5p contributed to IEC injury via targeting SP-D and inactivating the NF-κB pathway. These revealed miR-199a-5p exacerbated the intestinal barrier dysfunction via inhibiting SP-D and activating the NF-κB pathway in sepsis.
- Published
- 2020
29. MicroRNA-21 Contributes to Acute Liver Injury in LPS-Induced Sepsis Mice by Inhibiting PPARα Expression
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Lu Wang, Miao Wu, Liying Zhan, Xianjin Du, Dan Tian, and Jianlin Zhou
- Subjects
0301 basic medicine ,Liver injury ,Acute liver injury ,Article Subject ,business.industry ,QH301-705.5 ,Antagonist ,Inflammation ,Pharmacology ,medicine.disease ,Sepsis ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Downregulation and upregulation ,030220 oncology & carcinogenesis ,Drug Discovery ,microRNA ,medicine ,Pharmacology (medical) ,medicine.symptom ,Target gene ,Biology (General) ,business ,Research Article - Abstract
The severity of sepsis may be associated with excessive inflammation, thus leading to acute liver injury. MicroRNA-21 is highly expressed in the liver of a variety of inflammation-related diseases, and PPARα is also proved to participate in regulating inflammation. In the present study, the LPS-induced sepsis model was established. We found that microRNA-21 expression was upregulated in the liver of sepsis mice, and microRNA-21 inhibition significantly reduced the liver injury. The expression of liver injury markers, inflammation cytokines, and PPARα in the septic mice was higher than in antagomir-21 treated septic mice. In addition, we also found that PPARα is the target gene of microRNA-21; PPARα antagonist GW6471 could reverse the effect of antagomir-21. In conclusion, our study illustrated that microRNA-21 exacerbate acute liver injury in sepsis mice by inhibiting PPARα expression.
- Published
- 2020
30. Application of CRISPR/Cas9 technology in sepsis research
- Author
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Xianjin Du, Jie Wei, Niandan Hu, and Miao Wu
- Subjects
Gene Editing ,0303 health sciences ,Cas9 ,Gene Transfer Techniques ,Computational biology ,Biology ,medicine.disease ,Sepsis ,03 medical and health sciences ,0302 clinical medicine ,Genome editing ,030220 oncology & carcinogenesis ,medicine ,CRISPR ,Humans ,Clustered Regularly Interspaced Short Palindromic Repeats ,CRISPR-Cas Systems ,030304 developmental biology - Abstract
CRISPR/Cas9, as a new genome-editing tool, offers new approaches to understand and treat diseases, which is being rapidly applied in various areas of biomedical research including sepsis field. The type II prokaryotic CRISPR/Cas system uses a single-guide RNA (sgRNA) to target the Cas9 nuclease to a specific genomic sequence, which is introduced into disease models for functional characterization and for testing of therapeutic strategies. This incredibly precise technology can be used for therapeutic research of gene-related diseases and to program any sequence in a target cell. Most importantly, the multifunctional capacity of this technology allows simultaneous editing of several genes. In this review, we focus on the basic principles, advantages and limitations of CRISPR/Cas9 and the use of the CRISPR/Cas9 system as a powerful tool in sepsis research and as a new strategy for the treatment of sepsis.
- Published
- 2019
31. Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling
- Author
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Yan Zhou, Ming Deng, Shi-qing Liu, Xianjin Du, Bin He, Jianghua Ming, Guirong Wang, Yaming Li, and Jianlin Zhou
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,MAP Kinase Signaling System ,p38 mitogen-activated protein kinases ,Biophysics ,Down-Regulation ,Apoptosis ,Inflammation ,Nitric Oxide ,Biochemistry ,Article ,Chondrocyte ,Rats, Sprague-Dawley ,03 medical and health sciences ,Chondrocytes ,Osteoarthritis ,medicine ,Animals ,Humans ,Protein kinase A ,Molecular Biology ,Cells, Cultured ,Chemistry ,Cartilage ,Surfactant protein D ,Cell Biology ,Pulmonary Surfactant-Associated Protein D ,Rats ,Cell biology ,030104 developmental biology ,medicine.anatomical_structure ,Immunology ,medicine.symptom - Abstract
Innate immune molecule surfactant protein D (SP-D), a member of the C-type lectin protein family, plays an indispensable role in host defense and the regulation of inflammation in the lung and other tissues. Osteoarthritis (OA) is a degenerative disease of cartilage, with inflammation that causes pathologic changes and tissue damage. However, it is unknown whether there exist SP-D expression and its potential role in the pathogenesis of OA. In this study, we examined SP-D expression and explored its biological function in a sodium nitroprusside (SNP)-stimulated rat chondrocytes and surgically-induced rat OA model. We found SP-D expression in both human and rat articular chondrocytes, with higher level in normal chondrocytes compared to in OA chondrocytes. Furthermore, In vivo study demonstrated that recombinant human SP-D (rhSP-D) ameliorated cartilage degeneration in surgically-induced rat OA model. In vitro cell culture study showed that rhSP-D markedly inhibited the expression of caspase-3 as an apoptosis biomarker, and decreased phosphorylation of p38 mitogen-activated protein kinase (MAPK), which resulted in maintaining normal nuclear morphology and increasing mitochondrial membrane potential in SNP-stimulated rat chondrocytes. Collectively, these findings indicate that SP-D expresses in articular chondrocytes and suppresses SNP-stimulated chondrocyte apoptosis and ameliorates cartilage degeneration via suppressing p38 MAPK activity.
- Published
- 2018
32. LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way
- Author
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Yong Xu, Xianjin Du, Xiaohui Gong, and Wenze Zheng
- Subjects
0301 basic medicine ,Clear cell renal cell carcinoma ,Cell cycle checkpoint ,Physiology ,EGFR ,Transplantation, Heterologous ,Mice, Nude ,Apoptosis ,lcsh:Physiology ,Flow cytometry ,lcsh:Biochemistry ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Epidermal growth factor ,Cell Line, Tumor ,medicine ,Animals ,Humans ,lcsh:QD415-436 ,Epidermal growth factor receptor ,RNA, Small Interfering ,Carcinoma, Renal Cell ,Cell Proliferation ,Mice, Inbred BALB C ,Linc00037 ,medicine.diagnostic_test ,biology ,lcsh:QP1-981 ,Cell growth ,Chemistry ,Cell Cycle Checkpoints ,Cell cycle ,medicine.disease ,Kidney Neoplasms ,LncRNA ,Up-Regulation ,ErbB Receptors ,030104 developmental biology ,Tumor progression ,030220 oncology & carcinogenesis ,Disease Progression ,Cancer research ,biology.protein ,RNA Interference ,RNA, Long Noncoding - Abstract
Background/Aims: LINC00037 has previously been reported to be up-regulated in clear cell renal cell carcinoma (ccRCC), however, the underlying mechanism remained unknown. In this study, we designed to investigate the functional role of LINC00037 in ccRCC Methods: LINC00037 knockdown and re-expressing 786-O and A498 cells were established. CCK8 assay and EdU assay were performed to evaluate the proliferation rates of ccRCC cells. Flow cytometry assay was performed to detect the cell apoptosis and cell cycle. Subcutaneous injection xenotransplantation mouse model was used to observe the role of LINC00037 in tumor growth in vivo. Mass spectrometry (MS) was performed to find the interacting partner of LINC00037 and RNA immunoprecipitation (RIP) was carried out to validate their interaction. Results: We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR. Conclusion: LINC00037 could inhibit proliferation of ccRCC in an epidermal growth factor receptor-dependent way.
- Published
- 2018
33. The upstream innovation with an overconfident manufacturer in a supply chain
- Author
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Huimin Zhan, Xiaoxuan Zhu, Xianjin Du, and Xiuli He
- Subjects
Upstream (petroleum industry) ,021103 operations research ,Information Systems and Management ,business.industry ,Strategy and Management ,Supply chain ,05 social sciences ,0211 other engineering and technologies ,02 engineering and technology ,Management Science and Operations Research ,Profit (economics) ,Cognitive bias ,0502 economics and business ,business ,050203 business & management ,Industrial organization ,Downstream (petroleum industry) ,Overconfidence effect - Abstract
Overconfidence is a common, pervasive cognitive bias that is of great practical importance in decision-making and widely recognized as an influential factor to consider in operations management. In this paper, we consider overconfidence bias in a supply chain innovation scenario, which consists of an innovative upstream supplier and an overconfident downstream manufacturer overestimating the impact of innovation to enhance demand. We investigate the influence of the manufacturer’s overconfidence on supplier innovation and supply chain profits under the wholesale price contract and the cost-sharing contract settings. Our results suggest that while the overconfidence is detrimental to the supplier’s innovation under a wholesale price contract, it is beneficial to the supplier’s innovation under a cost-sharing contract, and even more beneficial than in the centralized case. We also find that, under a wholesale price contract the manufacturer’s profit can be higher than under a cost-sharing contract when the level of overconfidence exceeds a certain threshold. Interestingly, we further find that the supplier’s unawareness of overconfidence benefits both biased supply chain members under a wholesale price contract but shows the opposite effect for a cost-sharing contract. Our results offer insights into overconfidence bias in operations management and provide practical decision-making advice for supply chain members.
- Published
- 2021
34. CircSAMD4A aggravates H/R-induced cardiomyocyte apoptosis and inflammatory response by sponging miR-138-5p.
- Author
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Xiaorong Hu, Ruisong Ma, Jianlei Cao, Xianjin Du, Xinyong Cai, and Yongzhen Fan
- Subjects
CIRCULAR RNA ,PYROPTOSIS ,MYOCARDIAL infarction ,INFLAMMATION ,MYOCARDIAL injury ,BCL-2 proteins - Abstract
Hypoxia/reoxygenation (H/R)-induced myocardial cell injury is the main cause of acute myocardial infarction (AMI). Many proofs show that circular RNA plays an important role in the development of AMI. The purpose of this study was to investigate the role of circSAMD4A in H/R-induced myocardial injury. The levels of circular SAMD4A (circSAMD4A) were detected in the heart tissues of AMI mice and H/Rinduced H9C2 cells, and the circSAMD4A was suppressed in AMI mice and H/Rinduced H9C2 cells to investigate its' function in AMI. The levels of circSAMD4A and miR-138-5p were detected by real-time quantitative PCR, and MTT assay was used to detect cell viability. TUNEL analysis and Annexin V-FITC were used to determine apoptosis. The expression of Bcl-2 and Bax proteins was detected by Western blot. IL-1β, TNF-β and IL-6 were detected by ELISA kits. The study found that the levels of circSAMD4A were up-regulated after H/R induction and inhibition of circSAMD4A expression would reduce the H/R-induced apoptosis and inflammation. MiR-138-5p was down-regulated in H/R-induced H9C2 cells. circSAMD4A was a targeted regulator of miR-138-5p. CircSAMD4A inhibited the expression of miR-138-5p to promote H/R-induced myocardial cell injury in vitro and vivo. In conclusion, CircSAMD4A can sponge miR-138-5p to promote H/R-induced apoptosis and inflammatory response. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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35. An Image Mosaic Algorithm Based on Improved ORB
- Author
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Lin Li and Xianjin Du
- Subjects
Matching (graph theory) ,Computer science ,Feature (computer vision) ,Feature extraction ,ComputingMethodologies_IMAGEPROCESSINGANDCOMPUTERVISION ,Image scaling ,Hamming distance ,Rotation (mathematics) ,Algorithm ,ComputingMethodologies_COMPUTERGRAPHICS ,Orb (optics) ,k-nearest neighbors algorithm - Abstract
Due to the lack of scale invariance in ORB (Oriented FAST and Rotated BRIEF) algorithm, image mosaic in complex scenes, high mismatch rate, and easy to produce mosaic seams in synthetic images, etc. In this paper, an improved ORB algorithm for image mosaic based on BRISK feature extraction is proposed. Firstly, the FAST9-16 of BRISK algorithm is introduced to detect corner points and solve the scale invariance problem. Then ORB algorithm is used to describe feature points, and Hamming distance is used to roughly match image features. Then KNN algorithm and PROSAC (Progressive Sample Consensus) algorithm are used to refine and purify the matching points to further improve the accuracy. Finally, image seamless fusion and mosaic are completed by gradual-in-gradual-out weighted average fusion. The experimental results show that the proposed algorithm has good performance in image scaling, rotation and illumination intensity. It is a real-time image mosaic method with high accuracy and good mosaic effect.
- Published
- 2019
36. miR-199a-5p Exacerbated Intestinal Barrier Dysfunction through Inhibiting Surfactant Protein D and Activating NF
- Author
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Xianjin, Du, Dan, Tian, Jie, Wei, Chen, Yan, Peng, Hu, Xu, Wu, Wenbin, Yang, and Zhanyong, Zhu
- Subjects
Inflammation ,Mucous Membrane ,NF-kappa B p50 Subunit ,Apoptosis ,Pulmonary Surfactant-Associated Protein D ,Transfection ,Permeability ,Mice, Inbred C57BL ,Mice ,MicroRNAs ,Oxidative Stress ,HEK293 Cells ,Gene Expression Regulation ,Sepsis ,Animals ,Humans ,Intestinal Mucosa ,Research Article - Abstract
Sepsis is a severe disease, which results from the excessive inflammatory response to the infection. Dysfunction of intestinal barrier is a crucial problem in various pathological conditions. Meanwhile, microRNAs exhibit significant roles in the modulation of many diseases, including sepsis. Multiple investigations indicate that miR-199a-5p participates in different human diseases. Nevertheless, little is known on the roles of miR-199a-5p in sepsis. Herein, we evaluated the mechanism of miR-199a-5p on the intestinal barrier dysfunction in sepsis. Intestinal mucosa permeability indicators including D-lactic acid, DAO, and FD-40 levels were determined, and they were greatly increased in sepsis. Then, we proved that miR-199a-5p was induced in sepsis mice tissues and isolated intestinal epithelial cells. Moreover, miR-199a-5p increased D-lactic acid, DAO, and FD-40 while inhibition of miR-199a-5p exhibited a reversed process. Additionally, we observed that miR-199a-5p affected the oxidative damage and inflammation in the intestine tissues from sepsis mice. The content of MDA was elevated whereas SOD was remarkably repressed in the miR-199a-5p mimic group. IL-6, IL-1β, and TNF-α were induced by miR-199a-5p overexpression while IL-10 was reduced by miR-199a-5p. Subsequently, surfactant protein D (SP-D) was predicted as the target of miR-199a-5p. The activation of NF-κB has been identified in sepsis. Herein, we demonstrated that inhibitor of miR-199a-5p contributed to IEC injury via targeting SP-D and inactivating the NF-κB pathway. These revealed miR-199a-5p exacerbated the intestinal barrier dysfunction via inhibiting SP-D and activating the NF-κB pathway in sepsis.
- Published
- 2019
37. MEG3 Alleviated LPS-Induced Intestinal Injury in Sepsis by Modulating miR-129-5p and Surfactant Protein D
- Author
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Chen Yan, Jie Wei, Xu Wu, Xianjin Du, Dan Tian, Peng Hu, and Wenbin Yang
- Subjects
0301 basic medicine ,Lipopolysaccharides ,Male ,Article Subject ,Immunology ,Apoptosis ,Pharmacology ,Sepsis ,03 medical and health sciences ,Mice ,0302 clinical medicine ,In vivo ,Intensive care ,Pathology ,Medicine ,RB1-214 ,Animals ,Humans ,Cell Proliferation ,MEG3 ,Inflammation ,business.industry ,Cell growth ,Surfactant protein D ,Epithelial Cells ,Cell Biology ,medicine.disease ,Flow Cytometry ,Pulmonary Surfactant-Associated Protein D ,In vitro ,Mice, Inbred C57BL ,MicroRNAs ,030104 developmental biology ,030220 oncology & carcinogenesis ,RNA, Long Noncoding ,Caco-2 Cells ,business ,Research Article - Abstract
Sepsis and intestinal injury triggered by sepsis are common in intensive care units, which can contribute to a high mortality. lncRNAs can modulate gene expression, and they are closely involved in multiple diseases, including sepsis. In our present study, we investigated the biological function of MEG3 in sepsis, especially during the intestinal injury. Currently, we observed that in LPS-induced sepsis mouse models, the intestinal injury was triggered. Meanwhile, we reported that MEG3 was greatly decreased in vivo, with an increase of miR-129-5p and inhibition of SP-D. Then, MEG3 was overexpressed, and we found that its overexpression repressed the intestinal injury via downregulating miR-129-5p in sepsis mice. Moreover, TNF-α and IL-6 expression was elevated in intestinal tissues compared to the control groups. MEG3 restrained the activation of TNF-α and IL-6, in sepsis models. Subsequently, to induce the inflammatory injury of sepsis, human colorectal Caco2 cells were treated with 10 ng/ml LPS. 10 ng/ml LPS significantly inhibited Caco2 cell proliferation and increased the apoptosis. Additionally, MEG3 was decreased whereas miR-129-5p was obviously increased in Caco2 cells incubated with LPS. Interestingly, we showed that MEG3 repressed cell apoptosis partly and enhanced Caco2 cell proliferation. miR-129-5p overexpression could reverse the effect of MEG3 in vitro. Previously, we proved SP-D was reduced in sepsis and it depressed the intestinal injury in vivo. Finally, the correlation among MEG3, miR-129-5p, and SP-D was predicted and confirmed in our investigation. These findings indicated that MEG3 might be a potential target for intestinal damage caused by sepsis via regulating miR-129-5p and SP-D.
- Published
- 2019
38. miR-182-5p contributes to intestinal injury in a murine model of Staphylococcus aureus pneumonia-induced sepsis via targeting surfactant protein D
- Author
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Chen Yan, Wenbin Yang, Xianjin Du, Miao Wu, Peng Hu, Dan Tian, Jie Wei, Xu Wu, and Tailang Yin
- Subjects
0301 basic medicine ,Staphylococcus aureus ,Physiology ,Cell Survival ,Clinical Biochemistry ,Inflammation ,Apoptosis ,medicine.disease_cause ,Microbiology ,Sepsis ,03 medical and health sciences ,Gene Knockout Techniques ,Mice ,0302 clinical medicine ,Immune system ,Pneumonia, Staphylococcal ,medicine ,Animals ,Intestinal Mucosa ,Cells, Cultured ,business.industry ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,Surfactant protein D ,Epithelial Cells ,Cell Biology ,Oncogenes ,medicine.disease ,Pulmonary Surfactant-Associated Protein D ,Mice, Inbred C57BL ,Pneumonia ,Disease Models, Animal ,MicroRNAs ,030104 developmental biology ,Terminal deoxynucleotidyl transferase ,030220 oncology & carcinogenesis ,Tumor necrosis factor alpha ,medicine.symptom ,business ,Signal Transduction - Abstract
Sepsis is a severe clinical disease, which is resulted from the excessive host inflammation response to the infection. Growing evidence indicates that Staphylococcus aureus pneumonia is a significant cause of sepsis, which can lead to intestinal injury, inflammation, and apoptosis. Studies have shown that miR-182-5p can serve as a tumor oncogene or a tumor suppressive microRNA in various cancers, however, its biological role in sepsis is still uninvestigated. Here, we reported that miR-182-5p was obviously increased in S. aureus pneumonia mice models. Loss of miR-182-5p inhibited intestinal damage and intestinal apoptosis as indicated by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. In addition, we observed the lack of miR-182-5p altered the local inflammatory response to pneumonia in the intestine. Elevated tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were observed in intestinal tissue of pneumonia groups compared with the shams. Furthermore, miR-182-5p knockout (KO) pneumonia group demonstrated decreased levels of intestinal TNF-α and IL-6. Primary murine intestinal epithelial cells were isolated and cultured in our investigation. We exhibited downregulation of miR-182-5p repressed intestinal epithelial cells apoptosis and rescued the cell viability. Meanwhile, miR-182-5p caused elevated cell apoptosis and reduced cell proliferation. Moreover, the surfactant protein D (SP-D) binds with the bacterial pathogens and remove the pathogens and apoptotic bodies, which exhibits important roles in modulating immune responses. It was displayed in our study that SP-D was greatly decreased in pneumonia mice models. SP-D was predicted as a downstream target of miR-182-5p. These data concluded that miR-182-5p promoted intestinal injury in S. aureus pneumonia-induced sepsis via targeting SP-D.
- Published
- 2019
39. NEAT1 promotes myocardial ischemia-reperfusion injury via activating the MAPK signaling pathway
- Author
-
Chen Yan, Xianjin Du, Xu Wu, Xiaorong Hu, Peng Hu, Dan Tian, Jie Wei, and Wenbin Yang
- Subjects
0301 basic medicine ,MAPK/ERK pathway ,Physiology ,MAP Kinase Signaling System ,Clinical Biochemistry ,Down-Regulation ,Apoptosis ,Myocardial Reperfusion Injury ,Pharmacology ,Cell Line ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Downregulation and upregulation ,Lactate dehydrogenase ,medicine ,Animals ,RNA, Messenger ,Protein kinase A ,chemistry.chemical_classification ,Reactive oxygen species ,biology ,Chemistry ,Cell Biology ,medicine.disease ,Mice, Inbred C57BL ,030104 developmental biology ,030220 oncology & carcinogenesis ,Gene Knockdown Techniques ,biology.protein ,Cytokines ,Creatine kinase ,RNA, Long Noncoding ,Inflammation Mediators ,Reactive Oxygen Species ,Reperfusion injury - Abstract
Myocardial ischemia-reperfusion (IR) injury is a common cardiovascular problem, which remains a major cause of death in the world. Emerging evidence has suggested that long noncoding RNAs are crucial players in myocardial injury. However, the functional involvement of nuclear enriched abundant transcript 1 (NEAT1) in myocardial IR injury remains poorly investigated. Our study focused on the mechanism of NEAT1 in myocardial IR injury. Here, we reported a crucial role for NEAT1 in exacerbating cardiac IR injury. NEAT1 was greatly increased in myocardial IR injury mice models. As exhibited knockdown of NEAT1 resulted in attenuated myocardial IR injury in vivo. In addition, we found that NEAT1 was dramatically induced by hypoxia/reoxygenation in H9c2 cells. Lactate dehydrogenase (LDH), malondialdehyde, reactive oxygen species levels, and endoplasmic reticulum stress-regulated cardiomyocyte apoptosis were inhibited by the downregulation of NEAT1. Here, it was shown that knockdown of NEAT1 was able to repress tumor necrosis factor-α, interleukin-1β, and IL-6 expression. The silence of NEAT1 protected against IR injury via decreasing troponin levels, cardiocytes apoptosis, creatine kinase, and lactate LDH release in vivo. Meanwhile, the mitogen-activated protein kinase (MAPK) signaling was involved in NEAT1-mediated myocardial IR injury. In summary, our data indicated that NEAT1 contributed to myocardial IR injury via activating the MAPK pathway.
- Published
- 2018
40. Iron-load exacerbates the severity of atherosclerosis via inducing inflammation and enhancing the glycolysis in macrophages
- Author
-
Xinyong Cai, Changjiang Zhang, Wenwen Fu, Xianjin Du, Xiaorong Hu, and Ruisong Ma
- Subjects
0301 basic medicine ,Male ,medicine.medical_specialty ,Physiology ,Iron ,Clinical Biochemistry ,Macrophage polarization ,Inflammation ,Ferric Compounds ,Severity of Illness Index ,Proinflammatory cytokine ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Macrophage ,Animals ,Interleukin 6 ,biology ,Chemistry ,CD68 ,Macrophages ,Cell Polarity ,Cell Biology ,Atherosclerosis ,Mice, Inbred C57BL ,030104 developmental biology ,Endocrinology ,Phenotype ,030220 oncology & carcinogenesis ,biology.protein ,Ferric ,Female ,medicine.symptom ,Glycolysis ,medicine.drug ,Transforming growth factor - Abstract
Atherosclerosis is still the major cause of morbidity and mortality all over the world. Recently, it has been reported increased levels of tissue iron increase the risk of atherosclerosis. However, the detailed mechanism of iron-induced atherosclerosis progression is barely known. Here, we used apoE-deficient mice models to investigate the effects of low iron diet (
- Published
- 2018
41. Expert consensus on prevention and cardiopulmonary resuscitation for cardiac arrest in COVID-19
- Author
-
Shouchun Yan, Zong’an Liang, Wenteng Chen, Jie Wei, Xiaobei Chen, Baochi Liu, Yu Cao, Shunjiang Xu, Yingqi Zhang, Xuelian Sun, Tian’en Zhou, Wenbin Han, Wenwu Zhang, Shuming Xianyu, Duohu Wu, Xiaotong Han, Deren Wang, Yan Xiong, Yan Cao, Chuanyun Qian, Jun Zhang, Ying Chen, Tao Yu, Rongjia Yang, Yufang Cao, Fen Ai, Jun Lv, Xiangdong Jian, Shengyang Yi, Zhong Wang, Yuanshui Liu, Sisen Zhang, Wei Song, Xianjin Du, Xiaojun He, Heping Xu, Qingyi Meng, Wenwei Cai, Yong Lin, Xiang Li, Yanhong Ouyang, Sheng’ang Zhou, Feng Zhan, Qiong Ning, and Yuhong Mi
- Subjects
medicine.medical_specialty ,Resuscitation ,Coronavirus disease 2019 (COVID-19) ,business.industry ,medicine.medical_treatment ,Risk of infection ,RC955-962 ,Expert consensus ,General Medicine ,sars-cov-2 ,covid-19 ,cardiac arrest ,cpr ,nosocomial infection ,personal protective equipment ,Arctic medicine. Tropical medicine ,Emergency medicine ,Health care ,medicine ,Cardiopulmonary resuscitation ,Infectious disease (athletes) ,business ,Personal protective equipment - Abstract
Background: Cardiopulmonary resuscitation (CPR) strategies in COVID-19 patients differ from those in patients suffering from cardiogenic cardiac arrest. During CPR, both healthcare and non-healthcare workers who provide resuscitation are at risk of infection. The Working Group for Expert Consensus on Prevention and Cardiopulmonary Resuscitation for Cardiac Arrest in COVID-19 has developed this Chinese Expert Consensus to guide clinical practice of CPR in COVID-19 patients. Main recommendations: 1) A medical team should be assigned to evaluate severe and critical COVID-19 for early monitoring of cardiac-arrest warning signs. 2) Psychological counseling and treatment are highly recommended, since sympathetic and vagal abnormalities induced by psychological stress from the COVID-19 pandemic can induce cardiac arrest. 3) Healthcare workers should wear personal protective equipment (PPE). 4) Mouth-to-mouth ventilation should be avoided on patients suspected of having or diagnosed with COVID-19. 5) Hands-only chest compression and mechanical chest compression are recommended. 6) Tracheal-intubation procedures should be optimized and tracheal-intubation strategies should be implemented early. 7) CPR should be provided for 20-30 min. 8) Various factors should be taken into consideration such as the interests of patients and family members, ethics, transmission risks, and laws and regulations governing infectious disease control. Changes in management: The following changes or modifications to CPR strategy in COVID-19 patients are proposed: 1) Healthcare workers should wear PPE. 2) Hands-only chest compression and mechanical chest compression can be implemented to reduce or avoid the spread of viruses by aerosols. 3) Both the benefits to patients and the risk of infection should be considered. 4) Hhealthcare workers should be fully aware of and trained in CPR strategies and procedures specifically for patients with COVID-19.
- Published
- 2021
42. Surfactant Proteins SP-A and SP-D Ameliorate Pneumonia Severity and Intestinal Injury in a Murine Model of Staphylococcus Aureus Pneumonia
- Author
-
Robert N. Cooney, Qinghe Meng, Xianjin Du, Guirong Wang, Linlin Zhang, Osama A. Abdel-Razek, and Asim Sharif
- Subjects
Male ,0301 basic medicine ,Apoptosis ,Critical Care and Intensive Care Medicine ,medicine.disease_cause ,Microbiology ,Sepsis ,03 medical and health sciences ,0302 clinical medicine ,Pulmonary surfactant ,Pneumonia, Staphylococcal ,medicine ,Animals ,Pulmonary Surfactant-Associated Protein D ,Lung ,bcl-2-Associated X Protein ,Pulmonary Surfactant-Associated Protein A ,Mice, Knockout ,Caspase 3 ,business.industry ,Surfactant protein D ,medicine.disease ,Surfactant protein A ,Intestines ,Mice, Inbred C57BL ,Disease Models, Animal ,Pneumonia ,030104 developmental biology ,Proto-Oncogene Proteins c-bcl-2 ,Staphylococcus aureus ,030220 oncology & carcinogenesis ,Immunology ,Emergency Medicine ,Female ,business ,Bronchoalveolar Lavage Fluid ,Signal Transduction - Abstract
Staphylococcus aureus pneumonia is an important cause of sepsis which causes gut injury, inflammation, and apoptosis. The surfactant proteins surfactant protein A (SP-A) and surfactant protein D (SP-D) bind bacterial pathogens and facilitate clearance of pathogens, apoptotic bodies, and modulate immune responses. SP-A and SP-D are expressed in both lung and gut epithelia. We hypothesize SP-A and SP-D regulate pneumonia severity and gut injury during pneumonia.Wild-type (WT) and SP-A and SP-D double knockout (SP-A/D KO) mice were subjected to S. aureus or sham pneumonia. Bronchoalveolar lavage and tissue harvest were performed 24 h later. Pneumonia severity, gut mucosal injury, inflammation, and apoptosis were measured using a combination of histology, immunohistochemistry, cytokine assay, TUNEL assay, quantitative real-time polymerase chain reaction, and Western blot analyses.Pneumonia increased gut inflammation, apoptosis, and mucosal injury in both groups. Pneumonia histology and bacterial growth in bronchoalveolar lavage fluid demonstrate more severe infection in SP-A/D KO mice compared with WT controls. SP-A/D KO mice with pneumonia also demonstrate more severe histologic gut mucosal injury, increased gut apoptosis, elevated caspase-3 levels, and Bax/Bcl-2 mRNA expression compared with WT pneumonia mice. Nuclear factor κB (NF-κB) p65 expression and its nuclear translocation, gut levels of tumor necrosis factor α and interleukin-1β were all increased in SP-A/D KO mice with pneumonia compared with WT controls.These data provide evidence SP-A and SP-D attenuate S. aureus pneumonia severity resulting in decreased intestinal mucosal injury, apoptosis, and inflammation. Improved pulmonary clearance of S. aureus decreased caspase-3 and Bax/Bcl-2 expressions and decreased activation of the NF-κB signaling pathway in intestine represent potential mechanisms for the effects of SP-A and SP-D on gut injury during pneumonia.
- Published
- 2016
43. LncRNA UCA1 sponges miR-206 to exacerbate oxidative stress and apoptosis induced by ox-LDL in human macrophages
- Author
-
Changjiang Zhang, Ruisong Ma, Xianjin Du, Xiaorong Hu, and Wenwen Fu
- Subjects
0301 basic medicine ,CD36 Antigens ,Small interfering RNA ,Physiology ,CD36 ,Clinical Biochemistry ,Apoptosis ,medicine.disease_cause ,Monocytes ,Cell Line ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,medicine ,Humans ,RNA, Small Interfering ,Foam cell ,chemistry.chemical_classification ,Gene knockdown ,Reactive oxygen species ,biology ,Macrophages ,Cell Biology ,Atherosclerosis ,Cell biology ,Lipoproteins, LDL ,MicroRNAs ,Oxidative Stress ,030104 developmental biology ,chemistry ,Gene Expression Regulation ,030220 oncology & carcinogenesis ,biology.protein ,RNA, Long Noncoding ,Oxidative stress ,Foam Cells - Abstract
Long noncoding RNA UCA1 has exerted a significant effect in cardiovascular disease. The biological role of UCA1 in atherosclerosis is unclear. Our study was to identify the potential mechanisms in the progression of atherosclerosis. Here, we observed that ox-LDL increased UCA1 expression greatly in THP-1 cells. Knockdown of UCA1 greatly inhibited CD36 expression, a crucial biomarker in atherosclerosis. Meanwhile, 20 μg/ml ox-LDL induced foam cell formation, which can be reversed by downregulation of UCA1. In addition, TC and TG levels induced by ox-LDL was rescued by UCA1 small interfering RNA. Accumulating studies have indicated that oxidative stress contributes to atherosclerosis progression. Here, we also found that reactive oxygen species, MDA, and THP-1 cell apoptosis were restrained by decreased of UCA1 with an increase of the superoxide dismutase activity. Moreover, miR-206 was predicted as a target of UCA1 and knockdown of UCA1 was able to repress miR-206 expression. Furthermore, overexpression of miR-206 inhibited oxidative stress process and it was reversed by UCA1 upregulation in vitro. In conclusion, we indicated that UCA1 sponged miR-206 to exacerbate atherosclerosis events induced by ox-LDL in THP-1 cells.
- Published
- 2018
44. Incumbent Repositioning with Decision Biases
- Author
-
Brian Wu, Meng Li, and Xianjin Du
- Subjects
Flexibility (engineering) ,Microeconomics ,050208 finance ,Strategy and Management ,0502 economics and business ,05 social sciences ,Economics ,Mental model ,Strategic Choice ,Behavioral strategy ,Business and International Management ,050203 business & management ,Overconfidence effect - Abstract
Incumbent firms often reposition themselves in response to entrants, but when doing so they incur repositioning costs. Incumbent repositioning costs and the associated decision biases have been identified in the economics, operations and strategy literatures as critical aspects of the competitive interactions between incumbents and entrants, but they have received limited attention in game-theoretic treatments at the strategy level. To fill this gap, we develop a strategic mental model to analytically characterize the impacts of repositioning costs and decision biases on firms’ equilibrium strategies and profits. Including these costs and biases changes the nature of strategic dynamics as well as introduces new implications for strategic choice.
- Published
- 2018
45. MiR-181a inhibits vascular inflammation induced by ox-LDL via targeting TLR4 in human macrophages
- Author
-
Jing-Min Lu, Yin Sha, and Xianjin Du
- Subjects
0301 basic medicine ,Physiology ,CD36 ,Clinical Biochemistry ,Inflammation ,Apoptosis ,03 medical and health sciences ,0302 clinical medicine ,microRNA ,medicine ,Humans ,Foam cell ,Reporter gene ,biology ,Chemistry ,Tumor Necrosis Factor-alpha ,Macrophages ,Cell Biology ,Atherosclerosis ,Lipoproteins, LDL ,Toll-Like Receptor 4 ,MicroRNAs ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,TLR4 ,biology.protein ,Cancer research ,lipids (amino acids, peptides, and proteins) ,medicine.symptom ,Blood vessel - Abstract
Atherosclerosis is a kind of chronic inflammation disease with lipid accumulation in in blood vessel linings. Increasing evidence has reported that microRNAs can exert crucial roles in atherosclerosis. In previous study, miR-181a has been implicated to be abnormally expressed in atherosclerosis mice, however its detailed function in atherosclerosis remains uninvestigated. Hence, in our current study, we focused on the biological role of miR-181a in atherosclerosis progression. Ox-LDL has been commonly identified as an important atherosclerosis regulator. We observed that ox-LDL induced THP-1 cell apoptosis dose-dependently and time- dependently. Meanwhile, 25 µg/ml ox-LDL can promote foam cell formation and increased miR-181a expression significantly. CD36 has been involved in atherosclerosis progression and it was found that overexpression of miR-181a inhibited its protein levels. Moreover, miR-181a mimics repressed foam cell formation, TC and TG levels induced by ox-LDL dramatically. In addition, miR-181a mimics were able to reverse THP-1 cell apoptosis, increased IL-6, IL-1β, and TNF-α protein expression triggered by 25 µg/ml ox-LDL. TLR4 has been linked to various inflammation-associated diseases. In our present study, TLR4 was indicated as miR-181a target and the binding correlation between them was validated by dual-luciferase reporter assay. In conclusion, these results improves the understanding of atherosclerosis modulated by miR-181a/TLR4 and can contribute to development of new approaches for atherosclerosis.
- Published
- 2017
46. MiR-370 inhibits vascular inflammation and oxidative stress triggered by oxidized low-density lipoprotein through targeting TLR4
- Author
-
Yin Sha, Dan Tian, Xianjin Du, and Jing-Min Lu
- Subjects
0301 basic medicine ,THP-1 Cells ,Inflammation ,medicine.disease_cause ,Biochemistry ,Monocytes ,03 medical and health sciences ,chemistry.chemical_compound ,microRNA ,medicine ,Humans ,Receptor ,Molecular Biology ,Chemistry ,Cell Biology ,Malondialdehyde ,Atherosclerosis ,In vitro ,Lipoproteins, LDL ,Toll-Like Receptor 4 ,MicroRNAs ,Oxidative Stress ,030104 developmental biology ,Gene Expression Regulation ,Cancer research ,TLR4 ,medicine.symptom ,Oxidative stress ,Lipoprotein - Abstract
Atherosclerosis, as a chronic cardiovascular disease, still remains a serious threat to human health. Inflammation and oxidative stress are commonly involved in various stages of atherosclerosis development. MicroRNAs are reported to play important roles in macrophages, which can respond to inflammation and oxidative stress. In our current study, we focused on the biological roles of miR-370 in atherosclerosis. According to the previously research, miR-370 was downregulated in AS mice models. Oxidized low-density lipoprotein (Ox-LDL) is regarded as a crucial regulator of atherosclerosis and we observed that miR-370 was decreased by ox-LDL dose-dependently and time-dependently in THP-1 cells. Then, it was found that miR-370 overexpression was able to inhibit inflammation molecules including IL-6 and IL-1β. Meanwhile, ROS levels, and malondialdehyde (MDA) were also restrained by miR-370 mimics in vitro. Toll-like receptor 4 (TLR4) has been implicated in many inflammation diseases. It can serve as a target of miR-370 and TLR4 expression was greatly increased in ox-LDL-incubated THP-1 cells in a time and dose dependent manner. The negative correlation was validated using a dual-luciferase reporter assay in our study. In conclusion, our present study revealed that miR-370 can reduce inflammatory reaction and inhibit the ROS production by targeting TLR4 in THP-1 cells.
- Published
- 2017
47. Protective effects of glutathione on oxidative injury induced by hydrogen peroxide in intestinal epithelial cells
- Author
-
Robert N. Cooney, James Osei Sarpong, Qinghe Meng, Haitao Ren, Natesh Yepuri, and Xianjin Du
- Subjects
0301 basic medicine ,MAP Kinase Signaling System ,p38 mitogen-activated protein kinases ,Interleukin-1beta ,Drug Evaluation, Preclinical ,Inflammation ,Apoptosis ,Biology ,Cell Line ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Western blot ,medicine ,Animals ,Intestinal Mucosa ,chemistry.chemical_classification ,Reactive oxygen species ,medicine.diagnostic_test ,NF-kappa B ,Glutathione ,Hydrogen Peroxide ,Interleukin-1 beta secretion ,Cell biology ,Rats ,IκBα ,Intestinal Diseases ,Oxidative Stress ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ,Surgery ,medicine.symptom ,Sesquiterpenes - Abstract
Background Reactive oxygen species are increased in multiple gastrointestinal diseases and contribute to their pathogenesis. glutathione (GSH) is an antioxidant that helps to prevent reactive oxygen species–mediated mucosal damage. This study examines the mechanisms by which GSH attenuates hydrogen peroxide (H2O2)–induced injury in intestinal epithelial cells. Methods IEC-6 cells were cultured and treated with H2O2 ± GSH. Inflammation was measured by nuclear factor kappa-B (NF-κB) P65 expression, NF-κB nuclear translocation, iκBα phosphorylation, and interleukin 1 beta secretion. Terminal deoxynucleotidyl transferase–mediated UTP end-labeling staining and cleaved caspase-3 were used to assess apoptosis. The role of P38 mitogen-activated protein kinase (P38 MAPK) signaling was examined using the P38 MAPK agonist U46619 and inhibitor SB203580 in H2O2 and GSH-treated cells. Phosphorylated and total P38 MAPKs and cleaved caspase-3 were measured by Western blot. Data are means ± standard deviation, statistical significance P Results Pretreatment with GSH attenuates the activation of NF-κB and P38 MAPK signaling pathways by H2O2. GSH also decreased H2O2-mediated increases in interleukin 1 beta secretion, cleaved caspase-3 activation, and apoptosis in IEC-6 cells. SB203580 attenuated the increase in apoptosis and cleaved caspase-3 in H2O2-treated cells. The increase in apoptotic index and cleaved caspase-3 observed in U46619-treated cells was also diminished by GSH. Conclusions GSH appears to ameliorate oxidative injury in intestinal epithelial cells by attenuating H2O2-mediated activation of NF-κB and P38 MAPK signaling pathways that regulate intestinal inflammation and apoptosis.
- Published
- 2017
48. Anti-inflammatory effect of exendin-4 postconditioning during myocardial ischemia and reperfusion
- Author
-
Jie Wei, Xianjin Du, and Xiaorong Hu
- Subjects
Agonist ,medicine.drug_class ,Ischemia ,Myocardial Reperfusion Injury ,Inflammation ,Pharmacology ,HMGB1 ,Glucagon-Like Peptide-1 Receptor ,chemistry.chemical_compound ,Lactate dehydrogenase ,Receptors, Glucagon ,Genetics ,medicine ,Animals ,Humans ,HMGB1 Protein ,Creatine Kinase ,Molecular Biology ,L-Lactate Dehydrogenase ,biology ,Interleukin-6 ,Tumor Necrosis Factor-alpha ,Venoms ,business.industry ,Antagonist ,General Medicine ,Malondialdehyde ,medicine.disease ,Peptide Fragments ,Rats ,Gene Expression Regulation ,chemistry ,biology.protein ,Exenatide ,Creatine kinase ,medicine.symptom ,Peptides ,business - Abstract
High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Preconditioning of exendin-4 (Ex), a glucagon-like peptide-1 receptor agonist, has been reported to attenuate myocardial I/R injury. The current study investigated whether Ex postconditioning also attenuated myocardial I/R injury and the potential mechanisms. Anesthetized male rats were subjected to ischemia for 30 min and treated with Ex (5 μg/kg, i.v.) 5 min before reperfusion, in the absence and/or presence of exendin (9–39) (an antagonist of glucagon-like peptide-1 receptor, 5 μg/kg, i.v.), followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), tumor necrosis factor-α, interleukin-6, and infarct size were measured. HMGB1 expression was assessed by immunoblotting. Postconditioning with Ex significantly decreased infarct size and levels of LDH and CK after 4 h reperfusion (all p
- Published
- 2014
49. Ghrelin Attenuates Hydrogen Peroxide-Induced Intestinal Injury in IEC-6 Cells
- Author
-
Xianjin Du, Robert N. Cooney, Qinghe Meng, and Natesh Yepuri
- Subjects
medicine.medical_specialty ,chemistry.chemical_compound ,Endocrinology ,chemistry ,business.industry ,Internal medicine ,Intestinal injury ,medicine ,Surgery ,Ghrelin ,Hydrogen peroxide ,business - Published
- 2018
50. Lefty A attenuates the TGF-β1-induced epithelial to mesenchymal transition of human renal proximal epithelial tubular cells
- Author
-
Pengcheng Luo, Jian-Ping Peng, Li Fang, Jie Zhang, You-Kong Li, and Xianjin Du
- Subjects
medicine.medical_specialty ,Left-Right Determination Factors ,medicine.medical_treatment ,Blotting, Western ,Clinical Biochemistry ,Smad2 Protein ,Biology ,Cell morphology ,Collagen Type I ,Kidney Tubules, Proximal ,Mesoderm ,Transforming Growth Factor beta1 ,Internal medicine ,medicine ,Renal fibrosis ,Humans ,RNA, Messenger ,Smad3 Protein ,Epithelial–mesenchymal transition ,Molecular Biology ,Cells, Cultured ,Reverse Transcriptase Polymerase Chain Reaction ,Growth factor ,Connective Tissue Growth Factor ,Epithelial Cells ,Lefty ,Cell Biology ,General Medicine ,CTGF ,Endocrinology ,Cancer research ,Signal transduction ,Transforming growth factor - Abstract
The epithelial to mesenchymal transition (EMT) is a crucial event for renal fibrosis that can be elicited by TGF-beta1/Smads signaling and its downstream mediator connective tissue growth factor (CTGF). As a distinct member of the TGF-beta superfamily, Lefty A has been shown to be significantly downregulated in the kidneys of patients with severe ureteral obstruction, suggesting its role in renal fibrosis induced by obstructive nephropathy. In order to determine whether Lefty A prevents TGF-beta1-induced EMT, human proximal tubule epithelial cells (HK-2) were stably transfected with Lefty A or control vectors and stimulated with 10 ng/ml TGF-beta1 for 48 h. The results show that stimulation with TGF-beta1 led to EMT including cell morphology changes, Smad2/3 signaling pathway activation, increased alpha-SMA, collagen type I, and CTGF expression, and decreased E-cadherin expression in mock-transfected HK-2 cells. Overexpression of Lefty A efficiently blocked p-Smad2/3 activation and attenuated all these EMT changes induced by TGF-beta1. This finding suggests that Lefty A may serve as a potential new therapeutic target to inhibit or even reverse EMT during the process of renal fibrosis.
- Published
- 2010
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