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Characteristics and Risk Factors for Pediatric Sepsis

Current medical Science 2024年第3期44卷 648-656页

作者： Yong-bing ZHU Tong-lin LIU Qi DAI Shu-fan LIU Peng XIONG Hao HUANG Yi YUAN Tian-nan ZHANG Yu CHEN Department of Pediatric Intensive Care Unit Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China

Objective Sepsis is considered a major cause of health loss in children and had high mortality and ***,there is no reliable model for predicting the prognosis of pediatric patients with *** study aimed to analyze the clinical characteristics of sepsis in children and assess the risk factors associated with poor prognosis in pediatric sepsis patients to identify timely interventions and improve their *** This study analyzed the clinical indicators and laboratory results of septic patients hospitalized in the Pediatric Intensive Care Unit of tongji hospital,tongji medical college,Huazhong University of Science and Technology,China,from January 1,2019,to December 31,*** factors for sepsis were identified by logistic regression *** A total of 355 children with sepsis were enrolled,with 333 children(93.8%)in the good prognosis group,and 22 children(6.2%)in the poor prognosis *** them,there were 255 patients(71.8%)in the sepsis group,and 100 patients(28.2%)in the severe sepsis *** length of hospital stay in the poor prognosis group was longer than that in the good prognosis group(P0.05),and the platelet(PLT),albumin(ALB),and hemoglobin(Hb)levels were lower in the poor prognosis group(P<0.01).The IL-8 levels in the severe sepsis group were higher than those in the sepsis group(P<0.05).Multiple logistic regression analysis suggested that lower Hb levels,ALB levels,peak PLT counts,and higher IL-1βlevels were independent risk factors for poor prognosis in children with *** Lower Hb,ALB,and PLT counts and elevated IL-1βare independent risk factors for poor prognosis in children with sepsis.

关键词： pediatric sepsis inflammation severity prognosis risk factors

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High Hydrostatic Pressure Exacerbates Bladder Fibrosis through Activating Piezo1

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当代医学科学（英文） 2024年第4期44卷 718-725页

作者： Bo-lang DENG Dong-xu LIN Zhi-peng LI Kang LI Peng-yu WEI Chang-cheng LUO Meng-yang ZHANG Quan ZHOU Zheng-long YANG Zhong CHEN Department and Institute of Urology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Rehabilitation Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China School of Mechanical Science and Engineering Huazhong University of Science and TechnologyWuhan 430074China

Objective:Bladder outlet obstruction(BOO)results in significant fibrosis in the chronic stage and elevated bladder ***1 is a type of mechanosensitive(MS)channel that directly responds to mechanical *** identify new targets for intervention in the treatment of BOO-induced fibrosis,this study investigated the impact of high hydrostatic pressure(HHP)on Piezo1 activity and the progression of bladder ***:Immunofluorescence staining was conducted to assess the protein abundance of Piezo1 in fibroblasts from obstructed rat *** fibroblasts were cultured under normal atmospheric conditions(0 cmH2O)or exposed to HHP(50 cmH2O or 100 cmH2O).Agonists or inhibitors of Piezol,YAP1,and ROCK1 were used to determine the underlying ***:The Piezo1 protein levels in fibroblasts from the obstructed bladder exhibited an elevation compared to the control *** significantly promoted the expression of various pro-fibrotic factors and induced proliferation of ***,the protein expression levels of Piezol,YAP1,ROCK1 were elevated,and calcium influx was increased as the pressure *** effects were attenuated by the Piezol inhibitor *** Piezo1 activator Yoda1 induced the expression of pro-fibrotic factors and the proliferation of fibroblasts,and elevated the protein levels of YAP1 and ROCK1 under normal atmospheric conditions in ***,these effects could be partially inhibited by YAP1 or ROCK ***:The study suggests that HHP may exacerbate bladder fibrosis through activating Piezo1.

关键词： Piezo1 bladder outlet obstruction fibrosis high hydrostatic pressure

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TRPC6 Knockout Alleviates Renal Fibrosis through PI3K/AKT/GSK3B Pathway

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Current medical Science 2024年第3期44卷 589-602页

作者： An-bang SUN Fang-hua LI Lin ZHU Xi-xi ZENG Min ZHU Qing-hua LEI Yan-hong LIAO Department of Anatomy School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Department of Transfusion Medicine Wuhan Hospital of Traditional Chinese and Western MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Department of Nephrology The First Affiliated Hospital of Zhengzhou UniversityZhengzhou450052China Department of Thoracic Surgery Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China National Basic medical Teaching Demonstration Center Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Key Laboratory of Neurological Diseases of Ministry of Education Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China

Objective Renal fibrosis is the ultimate pathway of various forms of acute and chronic kidney ***,the knockout of transient receptor potential channel 6(TRPC6)has shown promise in alleviating renal ***,the regulatory impact of TRPC6 on renal fibrosis remains *** In vivo,TRPC6 knockout(TRPC6−/−)mice and age-matched 129 SvEv(WT)mice underwent unilateral renal ischemia-reperfusion(uIR)injury surgery on the left renal pedicle or sham *** and serum were collected on days 7,14,21,and 28 after *** vitro,primary tubular epithelial cells(PTECs)were isolated from TRPC6−/−and WT mice,followed by treatment with transforming growth factorβ1(TGFβ1)for 72 *** anti-fibrotic effect of TRPC6−/−and the underlying mechanisms were assessed through hematoxylin-eosin staining,Masson staining,immunostaining,qRT-PCR,and Western *** Increased TRPC6 expression was observed in uIR mice and PTECs treated with TGFβ***6−/−alleviated renal fibrosis by reducing the expression of fibrotic markers(Col-1,α-SMA,and vimentin),as well as decreasing the apoptosis and inflammation of PTECs during fibrotic progression both in vivo and in ***,we found that the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)/glycogen synthase kinase 3 beta(GSK3β)signaling pathway,a pivotal player in renal fibrosis,was down-regulated following TRPC6 *** These results suggest that the ablation of TRPC6 may mitigate renal fibrosis by inhibiting the apoptosis and inflammation of PTECs through down-regulation of the PI3K/AKT/GSK3β*** TRPC6 could be a novel therapeutic strategy for preventing chronic kidney disease.

关键词： transient receptor potential channel 6 ischemia-reperfusion injury renal fibrosis renal tubular epithelial cells

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Immunomodulation of Proton-activated G Protein-coupled Receptors in Inflammation

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Current medical Science 2024年第3期44卷 475-484页

作者： Min-shan LI Xiang-hong WANG Heng WANG Department of Otolaryngology-Head and Neck Surgery Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Institute of Allergy and Clinical Immunology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China Hubei Clinical Research Center for Nasal Inflammatory Diseases Wuhan430030China

Proton-activated G protein-coupled receptors(GPCRs),initially discovered by Ludwig in 2003,are widely distributed in various *** receptors have been found to modulate the immune system in several inflammatory diseases,including inflammatory bowel disease,atopic dermatitis,and ***-activated GPCRs belong to the G protein-coupled receptor family and can detect alternations in extracellular *** detection triggers downstream signaling pathways within the cells,ultimately influencing the function of immune *** this review,we specifically focused on investigating the immune response of proton-activated GPCRs under inflammatory conditions.

关键词： proton-activated G protein-coupled receptors inflammation immunomodulation disease

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Clinical applications of stem cell-derived exosomes

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Signal Transduction and Targeted Therapy 2024年第2期9卷 621-651页

作者： Fei Tan Xuran Li Zhao Wang Jiaojiao Li Khawar Shahzad Jialin Zheng Department of ORL-HNS Shanghai Fourth People’s Hospitaland School of MedicineTongji UniversityShanghaiChina Plasma Medicine and Surgical Implants Center Tongji UniversityShanghaiChina The Royal college of Surgeons in Ireland DublinIreland The Royal college of Surgeons of England LondonUK Center for Translational Neurodegeneration and Regenerative Therapy Tongji Hospital affiliated to Tongji University School of MedicineShanghaiChina Shanghai Frontiers Science Center of Nanocatalytic Medicine Tongji UniversityShanghaiChina

Although stem cell-based therapy has demonstrated considerable potential to manage certain diseases more successfully than conventional surgery,it nevertheless comes with inescapable drawbacks that might limit its clinical *** to stem cells,stem cell-derived exosomes possess numerous advantages,such as non-immunogenicity,non-infusion toxicity,easy access,effortless preservation,and freedom from tumorigenic potential and ethical *** can inherit similar therapeutic effects from their parental cells such as embryonic stem cells and adult stem cells through vertical delivery of their pluripotency or *** a thorough search and meticulous dissection of relevant literature from the last five years,we present this comprehensive,up-to-date,specialty-specific and disease-oriented review to highlight the surgical application and potential of stem cell-derived *** derived from stem cells(e.g.,embryonic,induced pluripotent,hematopoietic,mesenchymal,neural,and endothelial stem cells)are capable of treating numerous diseases encountered in orthopedic surgery,neurosurgery,plastic surgery,general surgery,cardiothoracic surgery,urology,head and neck surgery,ophthalmology,and obstetrics and *** diverse therapeutic effects of stem cells-derived exosomes are a hierarchical translation through tissue-specific responses,and cell-specific molecular signaling *** this review,we highlight stem cell-derived exosomes as a viable and potent alternative to stem cell-based therapy in managing various surgical *** recommend that future research combines wisdoms from surgeons,nanomedicine practitioners,and stem cell researchers in this relevant and intriguing research area.

关键词： viable stem capable

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LncRNA MEG3 Inhibits the Epithelial-mesenchymal Transition of Bladder Cancer Cells through the Snail/E-cadherin Axis

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当代医学科学（英文） 2024年第4期44卷 726-734页

作者： Liang WANG Ping WANG Bing LIU Hui ZHANG Cheng-cheng WEI Ming XIONG Gang LUO Miao WANG Department of Urology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Department of Clinical Laboratory Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430022China Department of Urology The Central Hospital of WuhanTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430014China

Objective:This study aimed to investigate the role of the long noncoding RNA(lncRNA)maternally expressed gene 3(MEG3)in the epithelial-mesenchymal transition(EMT)of bladder cancer cells and the potential ***:Cell invasion,migration,and wound healing assays were conducted to assess the effects of MEG3 on the invasive and migratory capabilities of bladder cancer *** expression levels of E-cadherin were measured using Western blotting,RT-qPCR,and dual luciferase reporter *** immunoprecipitation and pull-down assays were performed to investigate the interactions between MEG3 and its downstream ***:MEG3 suppressed the invasion and migration of bladder cancer cells and modulated the transcription of *** binding of MEG3 to the zinc finger region of the transcription factor Snail prevented its ability to transcriptionally repress ***,MEG3 suppressed the phosphorylation of extracellular regulated protein kinase(ERK),c-Jun N-terminal kinase(JNK),and P38,thereby decreasing the expression of Snail and stimulating the expression of ***:MEG3 plays a vital role in suppressing the EMT in bladder cancer cells,indicating its potential as a promising therapeutic target for the treatment of bladder cancer.

关键词： Snail bladder cancer epithelial-mesenchymal transition long noncoding RNA maternally expressed gene 3

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Fibroblast-localized lncRNA CFIRL promotes cardiac fibrosis and dysfunction in dilated cardiomyopathy

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Science China(Life Sciences) 2024年第6期67卷 1155-1169页

作者： Shuai Yuan Xudong Zhang Jiabing Zhan Rong Xie Jiahui Fan Beibei Dai Yanru Zhao Zhongwei Yin Qian Liu Dao Wen Wang Huaping Li Chen Chen Division of Cardiology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders Wuhan 430030China Department of Forensic Medicine Tongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China

CFIRL is a long noncoding RNA(lnc RNA),we previously identified as the most significantly upregulated lnc RNA in the failing hearts of patients with dilated cardiomyopathy(DCM).In this study,we determined the function of CFIRL and its role in ***-time polymerase chain reaction and in situ hybridization assays revealed that CFIRL was primarily localized in the nucleus of cardiac fibroblasts and robustly increased in failing *** knockdown or fibroblast-specific knockout of CFIRL attenuated transverse aortic constriction(TAC)-induced cardiac dysfunction and fibrosis in *** of CFIRL in vitro promoted fibroblast proliferation and aggravated angiotensin II-induced differentiation to *** knockdown attenuated these ***,RNA pull-down assay and gene expression profiling revealed that CFIRL recruited ENO1,a newly identified noncanonical transcriptional factor,to activate ***-6 exerted a paracrine effect on cardiomyocytes to promote cardiac hypertrophy,which can be prevented by CFIRL *** findings uncover the critical role of CFIRL,a fibroblast-associated lnc RNA,in heart failure by facilitating crosstalk between fibroblasts and *** knockdown might be a potent strategy to prevent cardiac remodeling in heart failure,particularly in DCM.

关键词： lncRNA fibroblast fibrosis dilated cardiomyopathy heart failure

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The role of innate immunity in diabetic nephropathy and their therapeutic consequences

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Journal of Pharmaceutical Analysis 2024年第1期14卷 39-51页

作者： Min Yang Chun Zhang Department of Nephrology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430022China

Diabetic nephropathy (DN) is an enduring condition that leads to inflammation and affects a substantial number of individuals with diabetes worldwide. A gradual reduction in glomerular filtration and emergence of proteins in the urine are typical aspects of DN, ultimately resulting in renal failure. Mounting evidence suggests that immunological and inflammatory factors are crucial for the development of DN. Therefore, the activation of innate immunity by resident renal and immune cells is critical for initiating and perpetuating inflammation. Toll-like receptors (TLRs) are an important group of receptors that identify patterns and activate immune responses and inflammation. Meanwhile, inflammatory responses in the liver, pancreatic islets, and kidneys involve inflammasomes and chemokines that generate pro-inflammatory cytokines. Moreover, the activation of the complement cascade can be triggered by glycated proteins. This review highlights recent findings elucidating how the innate immune system contributes to tissue fibrosis and organ dysfunction, ultimately leading to renal failure. This review also discusses innovative approaches that can be utilized to modulate the innate immune responses in DN for therapeutic purposes.

关键词： Innate immunity Diabetic nephropathy Inflammation Toll-like receptor Inflammasomes

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Serum LDL Promotes Microglial Activation and Exacerbates Demyelinating Injury in Neuromyelitis Optica Spectrum Disorder

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Neuroscience Bulletin 2024年第8期40卷 1104-1114页

作者： Man Chen Yun‑Hui Chu Wen‑Xiang Yu Yun‑Fan You Yue Tang Xiao‑Wei Pang Hang Zhang Ke Shang Gang Deng Luo‑Qi Zhou Sheng Yang Wei Wang Jun Xiao Dai‑Shi Tian Chuan Qin Department of Neurology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Hubei Key Laboratory of Neural Injury and Functional Reconstruction Huazhong University of Science and TechnologyWuhan 430030China Department of Neurology Hainan General HospitalHainan Affiliated Hospital of Hainan Medical UniversityHaikou 570311China

Neuromyelitis optica spectrum disorder(NMOSD)is an autoimmune inflammatory demyelinating disease of the central nervous system(CNS)accompanied by blood-brain barrier(BBB)*** in microglial lipid metabolism is believed to be closely associated with the neuropathology of ***,there is limited evidence on the functional relevance of circulating lipids in CNS demyelination,cellular metabolism,and microglial ***,we found that serum low-density lipoprotein(LDL)was positively correlated with markers of neurological damage in NMOSD *** addition,we demonstrated in a mouse model of NMOSD that LDL penetrates the CNS through the leaky BBB,directly activating *** activation leads to excessive phagocytosis of myelin debris,inhibition of lipid metabolism,and increased glycolysis,ultimately exacerbating myelin *** also found that therapeutic interventions aimed at reducing circulating LDL effectively reversed the lipid metabolic dysfunction in microglia and mitigated the demyelinating injury in *** findings shed light on the molecular and cellular mechanisms underlying the positive correlation between serum LDL and neurological damage,highlighting the potential therapeutic target for lowering circulating lipids to alleviate the acute demyelinating injury in NMOSD.

关键词： Neuromyelitis optica spectrum disorder Low-density lipoprotein Microglia

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Suppression of MyD88 disturbs gut microbiota and activates the NLR pathway and hence fails to ameliorate DsS-inducedcolitis

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Precision Clinical Medicine 2024年第2期7卷 146-158页

作者： Jun-hua Li Yu Chen Zheng-hao Ye Li-ping Chen Jia-xin Xu Jian Han Lin Xie Shuai Xing De-an Tian Ursula Seidler Jia-zhi Liao Fang Xiao Department of Nephrology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Gastroenterology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Institute of Organ Transplantation Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Department of Gastroenterology Hepatology and EndocrinologyHannover Medical SchoolHannover 30625Germany

Background:Myeloid differentiation factor 88(MyD88)is the core adaptor for Toll-like receptors defending against microbial invasion and initiating a downstream immune response during microbiota-host ***,the role of MyD88 in the pathogenesis of inflammatory bowel disease is *** study aims to investigate the impact of MyD88 on intestinal inflammation and ***:MyD88 knockout(MyD88^(-/-))mice and the MyD88 inhibitor(TJ-M2010-5)were used to investigate the impact of MyD88 on acute dextran sodium sulfate(Dss)-induced *** activity index,colon length,histological score,and inflammatory cytokines were examined to evaluate the severity of *** transcriptome analysis and 16S rDNA sequencing were used to detect the potential ***:In an acute DSS-colitis model,the severity of colitis was not alleviated in MyD88^(-/-)mice and TJ-M2010-5-treated mice,despite significantly lower levels of NF-kB activation being exhibited compared to control ***,16S rDNA sequencing and RNA transcriptome analysis revealed a higher abundance of intestinal Proteobacteria and an up-regulation of the nucleotide oligomerization domain-like receptors(NLRs)signaling pathway in colitis mice following MyD88 *** blockade of the NLRs signaling pathway or elimination of gut microbiota with broad-spectrum antibiotics in DsS-induced colitis mice treated with TJ-M2010-5 ameiorated the disease severity,which was not improved solely by MyD88 *** treatment with broad-spectrum antibiotics,downregulation of the NLR signaling pathway was ***:Our study suggests that the suppression of MyD88 might be associated with unfavorable changes in the composition of gut microbiota,leading to NLR-mediated immune activation and intestinal inflammation.

关键词： microbiota innate immunity myeloid differentiation factor 88,MyD88 inhibitor NOD-like receptor inflammatory bowel disease

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