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RAGE and its ligand HMGB1 modulate chronic intermittent hypoxia induced renal injury via MAPK signaling pathways

RAGE and its ligand HMGB1 modulate chronic intermittent hypo...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： XuWu HuanLu ZilongLiu ShanqunLi Department of Pulmonary Medicine Center of snoring and Sleep Apnea MedicineZhongshan Hospital of Fudan UniversityShanghai200032China

目的 Chronic kidney disease is a severe comorbidity in patients with obstructive sleep apnea, which is caused by chronic intermittent hypoxia (CIH) triggered deleterious inflammatory response and tissue *** for advanced glycation end product (RAGE) and its ligand high mobility group box 1 (HMGB1) express on wide range of renal cells and mediate a variety of inflammatory responses in renal diseases.方法 In an attempt to understand the deleterious participation of RAGE/HMGB1 in CIH-injured kidney, we performed renal function test and histological *** also investigated RAGE/HMGB1 expression and downstream effector nuclear factor kappa B (NF-kB) signaling pathways by western blot as well as serum levels of proinflammatory cytokines quantified by ***, RAGE neutralizing antibodies, was administered intravenously before each hypoxia cycle to be evaluated the protective effect.结果 HE staining showed a pronounced inflammatory cell infiltration was more observed in *** illustrated that HMGB1 was detected both in the nuclei and diffuse cytoplasm of CIH rats, contrast to control group that only nuclei of tubule *** CIH-induced inflammation consequently accelerated renal dysfunction, leading to activation of NF-kb and recruitment of apoptosis measured by TUNEL *** addition improved renal function, as expected to attenuate the number of TUNEL-positive cells by 37％.Further,enhanced activation of RAGE and NF-kB accompanied phosphorylation of ERK and p-38 that peaked after CIH exposure, but all of which decreased with sRAGE treatment except ***-6 and TNF-a were shown to be increased (118.28±18.98 pg/ml and 125.16±13.04 pg/ml respectively, P＜0.0001) after CIH exposure, meanwhile exhibited significantly decreased in sRAGE-treated group (84.75±11.99 pg/ml and 69.29±10.49 pg/ml, P＜0.0001).All of the upregulated proinflammatory cytokines could be reversed by sRAGE administration except circulatory HMGB1 (P=0.43) and

关键词： Obstructive sleep apnea Chronic intermittent hypoxia RAGE Renal injury

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Isolated nocturnal hypoxemia in interstitial lung disease

Isolated nocturnal hypoxemia in interstitial lung disease

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： ShuyiGu Shanghai Pulmonary Hospital Tongji University School of Medicine

目的 To observe the isolation nocturnal hypoxemia in patients with interstitial lung disease (ILD) about pulmonary function, arterial blood gas, sleep and other effects.方法 In the present study, we analyzed 23 ILD patients (male 11, female 12) who diagnosed with isolation nocturnal hypoxemia at Shanghai Pulmonary Hospital between September 2015 and February *** patients ranged in age from 29 to 79 years with a mean age of 57 ± 12 *** function, arterial blood gas, polysomnography (PSG) *** were classified into groups according to the night minimum blood oxygen saturation (SPO2) group.结果 23 patients were classified into 3 groups, group A (14 cases) ： 85％≤SPO2＜90％;(2) group B (4 cases) ： 80％≤SPO2＜85％;(3) group C (5 cases), 80％≤SPO2＜85％.The lowest SPO2 at night of patients in group A is(88±2.09)％, group B patients is(82±1.71)％, and group C patients is(63±4.98)％, (P ＜ 0.001).FVC％ and FEV1％ in group C were (55.86±12.02)％ and (58.80±12.94)％, significantly less than those in group A [(79.50±10.80)％ and(86.10±10.14)％], (P=0.026, P=0.019).DLco％ in group A was (75.33±12.24)％, much higher than that in group B (62.22±12.05)％ and group C (43.46±16.96)％, (P=0.008).Among patients with 60％≤DLco％＜80％, the night minimum SPO2 was(84±8.72)％.That in patients with 40％≤DLco％＜60％ is (80±12.38)％, and in patients with DLco％＜40％ is (66±7.78)％.Night SPO2 value of ILD patients who suffered severe diffuse hypofunction was significantly lower than that of patients who with mild diffuse hypofunction (P = 0.029).结论 In ILD patients, isolation hypoxemia was correlation with pulmonary functions, especially the diffuse function.

关键词： Isolated nocturnal hypoxemia interstitial lung disease pulmonary function tests

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Effectsofhome-basedlowerlimbresistancetraininginstableCOPD patientsonmusclestrengthandfunctionalstatus:aquasiexperiment research

Effectsofhome-basedlowerlimbresistancetraininginstab...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： YI Chen FirstAffiliatedHospitalofSoochowUniversity

目的 Thisstudyaimedtoidentifytheeffectofhome-basedlowerlimbstrengthtrainingtraininginpatientswithstablechronic obstructivepulmonarydisease(COPD).Wetriedtoprovidescientificevidenceforthedevelopmentofsimple,safeandfeasible home-basedlowerlimbstrengthtraininginterventionsforstableCOPDpatients. 方法(1)Home-basedlowerlimbstrengthtraininginclude：Sixsetsoflowerlimbtraining(including：straightlegliftingexercises, pronehipextensionexercises,thighabductionexercises,posteriormusclegroupexercises,priorandposteriormusclegroup exercises,standingcalfraise),usingthemethodofself-gravityresistanceandThera-bandresistance,8～12RM,20～30min/session, 3sessions/week,foradurationof12weeks.(2)Weconducteda12-weekrandomizedcontrolled***whometour inclusioncriteriawererandomizedintotheinterventiongroup(n=25)andthecontrolgroup(n=22).Interventiongroupreceived routinepulmonaryrehabilitationguidanceandhome-basedlowerlimbstrengthtrainingwhilecontrolgroupreceivedroutine pulmonaryrehabilitation***groupsreceivedscheduledtelephonevisits,andinterventiongrouphadadditional homevisitsif***musclestrength,fiverepetitionsit-to-standtest,six-minutewalkdistance,ModifiedMedical ResearchCouncildyspneascale,qualityoflifewerecomparedatenrollmentandat12weeks. 结果 ***wasnostatisticallysignificantdifferencebetweenthecontrolgroupandtheexperimentalgroupinbaselinedata(P＞ 0.05).***week12,comparedwithatbaseline,improvementsinallindexesofmusclestrength(isometricextensormusclepeak torgue,isometricextensormusclepeakTQ/BW,isokineticextensormusclepeaktorgue,extensormusclepeakTQ/BW)inthe interventiongroupyieldedstatisticalsignificance(P＜0.05).Improvementinisometricextensormusclepeaktorgueinthecontrol groupindicatedstatisticalsignificance(P=0.017),nosign

关键词： Pulmonarydisease,chronicobstructive Home-based LowerLimb Strengthtraining

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Emodin attenuates bleomycin-induced pulmonary fibrosis in mice through a PPARγ-dependent pathway

Emodin attenuates bleomycin-induced pulmonary fibrosis in mi...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： TaoZhu Chun-yanYe WeiZhang MinXiao Xiao-ling Wu Hua-pengYu Fu-qiangWen ZhuJiang Hospital of Southern Medical University Division of Pulmonary Diseases State Key Laboratory ZhuJiang Hospital of Southern Medical University Respiratory Medicine First Affiliated Hospital of Chengdu Medical College Division of Pulmonary Diseases State Key Laboratory of Biotherapy of ChinaDepartment of Respiratory

目的 Idiopathic pulmonary fibrosis (IPF) is a chronic devastating disease with poor *** pathological processes, including inflammation, epithelial mesenchymal transition (EMT), apoptosis and oxidative stress, are involved in the pathogenesis of *** recent study showed that emodin, the main active component of Radix rhizoma Rhei, could significantly ameliorate inflammation by a PPARγ-dependent ***, the aim of current study was to explore whether emodin could attenuate pulmonary fibrosis in mice, and its involved potential mechanism.方法 A murine model of pulmonary fibrosis was induced by bleomycin (BLM) intratracheal *** day 21, cell counts of total cells, macrophages, neutrophils and lymphocytes, alone with TNF-α in bronchoalveolar lavage fluid (BALF) were *** staining and Masson's trichrome (MT) staining were used to observe the histological *** Ashcroft score and hydroxyproline content of lungs were also ***-β1, α-SMA and PPARγ mRNA and protein were *** of NF-κB was determined by western blotting and ***, shRNA-PPARγ transfection was performed to knockdown PPARγ expression in lung.结果 On day 21 after bleomycin stimulation, emodin reduced the inflammatory cells and TNF-α in BALF, the Ashcroft score and hydroxyproline content of lung, pulmonary pathological alterations, TGF-β1 and α-SMA expression, and the activation of NF-κ***, emodin up-regulated PPARγ expression in ***, we also found that these effects of emodin were noticeably abrogated by shRNA-PPARγ transfection.结论 Taken together, our results indicated that BLM-induced pulmonary fibrosis were potently compromised by emodin very likely through the PPARγ-dependent inactivation of NF-κB in mice.

关键词： Emodin Pulmonary fibrosis Transforming growth factor-β1 (TGF-β1) Alpha-smooth muscle actin (α-SMA)

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PDA联合移动护士站的应用与体会

PDA联合移动护士站的应用与体会

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者：李旭中国医科大学附属盛京医院

目的探讨PDA联合移动护士站在临床工作中的应用效果.随着信息化技术的快速发展及信息化系统在医院的广泛应用,信息技术对改善医疗质量、提高工作效率发挥了重要作用.方法实验组为PDA与移动护士站联合应用,对照组为单纯应用PDA. 选取... 详细信息

目的探讨PDA联合移动护士站在临床工作中的应用效果.随着信息化技术的快速发展及信息化系统在医院的广泛应用,信息技术对改善医疗质量、提高工作效率发挥了重要作用.方法实验组为PDA与移动护士站联合应用,对照组为单纯应用PDA. 选取我院第二呼吸内科MICU病区,2014年1月至2016年1月入院者,将2014年1月至2014年12月入院患者归为对照组,共400例;将2015年1月至2015年12月入院患者归为实验组,共398例.MICU共18张床位,分为6个护理小组,每个护理小组由一名N2能级有重症监护资格证书的护士负责,实行8小时责任工作制,根据患者病情程度每人分管2-4名患者.系统介绍PDA为手持电脑设备,通过无线局域网技术,实现HIS系统在病房的扩展与延伸,通过扫描患者腕带的二维条码信息,准确地完成病人、药品及标本的识别,并可实时录入、修改、查询患者基本信息、生命体征、医嘱数据等;移动护士站为平板电脑与护士处置车为一体的移动医疗设备,电脑本身带有大容量蓄电池并可连接无线网.结果实验组与对照组比较,PDA联合移动护士站使用后,相比于单纯应用PDA,对护士工作效率、满意度及护理文书质量提升有较大帮助,实验组方法有效.结论 PDA小巧轻便,可在床旁录入患者体征及帮助护士对患者进行身份识别,并且准确记录医嘱执行时间等,已在临床中广泛应用,但PDA屏幕偏小,界面简单,不方便重症记录的书写及医嘱执行.增加移动护士站后,相当于将护士站移到了患者床旁,护士可以在操作电脑的同时兼顾患者病情、询问患者主诉,突出危重病人的护理观察重点,及时执行医嘱和书写护理记录,增加了护理记录书写的及时性和真实性,改变盲目执行医嘱的情况.并且电脑屏幕大,书写记录更直观方便,可在记录的同时进行自检.执行医嘱和护理治疗处置,联合PDA身份识别,药品、标本识别确认及执行时间记录,实现了医嘱的闭环管理,增加护理安全性.两种设备各取所长,完成了从医嘱下达到床旁执行全过程的信息采集.同时使用移动护士站后,减少了护士往返于护士站与患者床旁的时间,使护士更专注于护理操作,增加了直接为病人服务的时间,有更多的时间与患者沟通进行心理护理及健康宣教等,从而为患者提供及时、安全、高品质的治疗护理.同时,护理工作得到了患者及临床医师的认可,体现了护士的工作价值,提高了护士的工作积极性,以更大的热情投入于工作中,值得临床中推广.

关键词：移动护理信息化闭环管理

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Extensively disturbance of regulatory T cells - Th17 cells balance in stage Ⅱ pulmonary sarcoidosis

Extensively disturbance of regulatory T cells - Th17 cells b...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： JingjingDing JinghongDai HourongCai QianGao YantingWen Department of Respiratory Medicine the Affiliated Drum Tower Hospital of Nanjing University Medical SchoolNanjing

目的 Sarcoidosis is a systemic inflammatory disorder characterized by *** enough evidences correlate the derangement of CD4+ T subsets, which may have an impact on the therapeutic effects of corticosteroids, with the radiographical staging of *** we show the disturbance of CD4+ T subsets in newly diagnosed stage Ⅱ pulmonary sarcoidosis, the most common stage in which corticosteroids treatment is used. 方法 39 newly diagnosed and treatment-na？ve patients, and 9 subjects after corticosteroids treatment were ***4+ CD45RA+ cells, CD4+ CD45RO+ cells, CCR4+ CCR6+ cells, and T regulatory cells (Tregs) were tested by Flow Cytometry ***1/Th2, Tregs/Th17 related cytokines and mRNAs, SAA and CCL20 were also *** activation of PI3K/PTEN/Akt signaling pathway was detected by Western Blot. 结果 Percentages of CD4+CD45RO+ memory T cells and Tregs, serum levels of IL-17A, TGF-β1, IL-6, IFN-γ, IL-10, SAA and CCL20, copies of T-bet, FoxP3, IL-17 and RORc in the periphery were elevated in patients with newly diagnosed stage Ⅱ pulmonary ***, PI3K/Akt signaling pathway was activated in bronchoalveolar lavage cells. 结论 Disturbance of T memory cells, Th1/Th2, and Tregs/Th17 cells, and activation of PI3K/Akt signaling were seen in newly diagnosed stage Ⅱ pulmonary sarcoidosis, which can be partly ameliorated by corticosteroids *** studies are warranted to better understand the role of PI3K/PTEN/Akt signaling pathway in both the various disease stages and the treatment responses of stage Ⅱ sarcoidosis and to validate the possibility of a treatment based on Th17/Tregs and/or PI3K/Akt neutralization.

关键词： Stage Ⅱ pulmonary sarcoidosis Th17 cells Tregs Th1 Th2 PI3K/Akt signaling pathway

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Autocrine IL-34 signaling promotes NSCLC cells invasion and its prognostic role in NSCLC

Autocrine IL-34 signaling promotes NSCLC cells invasion and ...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： zhileilv jinshuo FanqiHuang mengfei Guojieli Hanguorong Hulian ChenyangJin Department of Respiratory Medicine Key Laboratory of Pulmonary Diseases of Health MinistryUnion HospitalTongji Medical CollegeHuazhong University of Science and Technology

目的 IL-34 is a cytokine charactered by sharing the same receptor M-CSFR with M-CSF and funcitonal overlap with M-CSF.M-CSF/M-CSFR signal pathway has been shown to be participated in *** is necessary to evaluate whether this new cytokine IL-34 functionally overlapping with M-CSF is also involved in *** investigated the expression of IL-34 in NSCLC cells and the association between IL-34 expression and clinical features of NSCLC patients.方法 Expression of IL-34 was detected by immunofluorescence and Western blot in NSCLC cell lines and by immunohistochemistry in NSCLC *** simultaneously estimate the expression patterns of both IL-34 and M-CSF to show the M-CSFR ligands expression patterns in each NSCLC cell lines and *** association between IL-34 expression and clinical features and prognosis was *** assay was applied to investigate the invasive promotional role of IL-34 stimulation.结果 Expression of IL-34 was detected in NSCLC cell lines including A549,H460,H1299,H292,and SK-MES by immunofluorescence and Western *** the functional overlap between IL-34 and M-CSF in M-CSFR signal pathway,IL-34 and M-CSF were simultaneously evaluated in the same clinical specimen by *** are four patterns of expression of IL-34 and M-CSF including IL-34high M-CSFhigh,IL-34high M-CSFlow,IL-34low M-CSFhigh and IL-34low *** expression patterns of IL-34 and M-CSF indicated that it is necessary to evaluate them two cytokines simultaneously as whole M-CSFR *** IL-34 expression was associated with a high degree of regional lymph node metastasis and worse overall survival after 33 months of ***-34 enhanced the invasive activity of NSCLC cells with nearly equivalent efficience of M-CSF结论 IL-34 is expressed in NSCLC cells,and high IL-34 expression was associated with a high degree of regional lymph node metastasis and worse overall ***-34 promotes invasion of NSCLC cell lines in *** in

关键词： IL-34 non-small cell lung cancer NSCLC invasion prognosis

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Association of genetic polymorphisms at TOX3/LOC643714 with risk of lung cancer in a Han Chinese population from southwestern China

Association of genetic polymorphisms at TOX3/LOC643714 with ...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： chaowenjiang Institute of Human Respiratory Disease Xinqiao HospitalThe Third Military Medical UniversityChongqing 400037China

目的 Due to the potential role of TOX3 in banding and unbinding of DNA and alteration of chromatin structure and the molecular and genetic linkage of lung cancer and breast cancer,we deduced that the genetic polymorphisms at the TOX3/LOC643714 locus,one of the first breast cancer regions identified through genome-wide association study(GWAS),might be also associated with lung cancer risk.方法 To test the hypothesis,16 SNPs at the TOX3/LOC643714 locus were evaluated in the case-control study.结果 Pearson's chi-square test or Fisher's exact test revealed that rs9933638,rs12443621,and rs3104746 were associated with lung cancer risk(P=0.000,P=0.000,and P=0.005,respectively),confirmed by the subsequent logistic regression analyses,in which individuals with rs9933638(GG+GA)were displayed to have an elevated lung cancer risk compared with rs9933638AA carriers(OR=1.893,95％CI=1.308-2.741,P=0.001).Similar findings were discovered for rs12443621(OR=1.824,95％CI=1.272-2.616,P=0.001,rs12443621(GG+GA)carriers ***12443621AA carriers),indicating that subjects with allele G of both rs9933638 and rs12443621 were susceptible to lung ***,rs3104746TT carriers showed an increased lung cancer risk compared with rs3104746(TA+AA)carriers(OR=1.665,95％CI=1.243-2.230,P=0.001),demonstrating that individuals with rs3104746TT were susceptible to lung cancer compared with rs3104746(TA+AA)carriers.结论 The findings not only discovered for the first time that the SNPs of the TOX3/LOC643714 locus was associated with lung cancer risk,but also provided new evidences that lung cancer and breast cancer are linked at the molecular and genetic level at least in part,which may help to explore the new carcinogenesis mechanisms.

关键词： lung cancer risk genetic polymorphisms TOX3/LOC643714 Han Chinese

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Integrated analyses identify the potential cross-talks among miRNAs in IPF

Integrated analyses identify the potential cross-talks among...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： HaihaiLiang ShanshanLiu HongliShan Harbin Medical University

目的 Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and highly lethal fibrotic lung disease with unknown cause or *** some microRNAs (miRNAs) have been confirmed the contribution to the pathophysiological processes of IPF, the roles of miRNAs and intrinsic links between them in fibrotic lung diseases are not yet well understood.方法 We induced pulmonary fibrosis by intratracheally injection of Bleomycin (BLM).Masson's Trichrome stained method was used to evaluate the development of fibrosis and the content of collagen is quantified by Sircol Collagen Assay Kit or Hydroxyproline Assay *** cultured A549 cells and HEK-293 cells, synthesized miR-26a, both with its antisense inhibitor oligonucleotide (AMO-26a) and negative control (NC) were transfected or cotransfected with lipofectamine *** blot was used to examine TGFβ1, Lin28B, E-Cadherin expression and real-time PCR was used to detect miR-26a, let-7d, CollagenⅠ, CollagenⅢ at mRNA levels.结果 In our study, we identified and constructed a regulation network of differentially expressed IPF miRNAs and EMT ***, we found the downregulation of miR-26a and upregulation of Lin28B in mice with experimental pulmonary ***, we found that Lin28B could induce the process of epithelial-mesenchymal transition (EMT) by inhibiting let-7d, whereas inhibition of Lin28B mitigated TGF-β1-induced fibrogenesis and attenuated EMT in both cultured A549 cells and MLE-12 *** addition, inhibition of miR-26a resulted in lung epithelial cells transforming into myofibroblasts in vitro and in vivo, whereas forced expression of miR-26a alleviated TGF-b1- and BLM-induced EMT in A549 cells and in mice, *** importantly, over-expression of miR-26a could simultaneously enhance the expression of let-7d in A549 cells, and further study confirmed that Lin28B was one of the direct targets of miR-26a, which mediates, at least in part, the regulatory effects of miR-26a on the biog

关键词： IPF microRNA-26a Lin28B let-7d EMT

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Blockade of interplay between IL-17A and histone deacetylase-2attenuates house dust mite-induced allergic airway inflammation

Blockade of interplay between IL-17A and histone deacetylase...

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2016中华医学会呼吸病学年会暨第十七次全国呼吸病学学术会议

作者： TianwenLai ChaoZhang YueHu JianLou FengXu FeiLi YingWu ZhaoYun YuanyuanMao ChaoCao WenLi SongminYing ZhihuaChen HuahaoShen Department of Respiratory and Critical Care Medicine Second Affiliated HospitalInstitute of Respiratory DiseasesZhejiang University School ofMedicineHangzhouChina

目的 Histone deacetylase-2(HDAC2)and interleukin(IL)-17A have been implicated in asthma ***,it is not known how HDAC2 regulates airway inflammation and whether IL-17A is pivotal in this *** aimed to elucidate the role of HDAC2 in house dust mite(HDM)-induced allergic airway inflammation,focusing on the link with IL-17A.方法 HDAC2+/-,IL-17A-/-and HDAC2/IL-17A double-deficient(HDAC2+/-IL-17A-/-)mice were used in a model of HDM-induced *** inflammation,mucus production and airway remodeling were *** addition,we evaluated the effects of IL-17A on HDAC2 expression in HDM-stimulated normal human bronchial epithelial(NHBE)cells.结果 HMD exposure decreased HDAC2 expression and increased airway inflammation in lungs of wild-type(WT)mice,which were further augmented in HDAC2+/-*** levels of IL-17A were also significantly higher in HDAC2+/-mice versus WT asthmatic *** contrast to our observations in HDAC2+/-mice,IL-17A-/-mice attenuated HDM-induced airway ***,we observed that HDAC2+/-IL-17A-/-mice reverted a single-deficient animal back to the WT *** with HDM increased expression of cytokines(e.g.,IL-6,IL-8,IL-17A)in NHBE cells and co-stimulation with IL-17A further decreased HDAC2 expression.结论 These findings opens a new option that HDAC2 sets up a vicious circle that links IL-17A responses to allergen exposure and plays a critical role in the amplification of allergic airway ***,targeting their interaction may be a potential therapeutic approach to ameliorate disease progression of allergic asthma.

关键词： Asthma HDAC2 IL-17A

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