简介：Salmeterol是长行动的β；激活adenylatecyclase的2收缩筋，引起长持续的bronchodilation并且被用于许多年到控制气喘。然而，很少信息都不关于salmeterol的immunoregulatory效果是可得到的。我们发现salmeterol减少在表示了肿瘤坏死factor-alpha，interleukin-1和interleukin-6的质问变应原的老鼠的一个模型的支持inflammatorycytokines的生产。树枝状的房间(DC)是介绍抗原的房间并且在航线充当哨兵。我们发现了那salmeterol(10−5mol/l)减少了lipopolysaccharide引起的发炎(0.1µ；g/ml)在激活的鼠科的骨头导出髓的DC。而且，西方的污点证明这保护的效果被禁止通过原子factor-kappaB发信号部分调停(NF-κ；B)，激活mitogen的蛋白质kinase(MAPK)小径和津贴的戏剧性地减少的层次。我们建议salmeterol由modulatingDC调整导致变应原的气喘的发炎。在结论，我们提供DC是为对气喘的salmeterol的行动负责的目标免疫者房间的证据。

简介：全身的煽动性的反应症候群(先生)和得分系统的概念被骨头的杂志在1992定义。先生在四(发烧或降低体温，tachypnea，心悸亢进，和白细胞增多)被描述为二的出现或更多的临床的标准。Anearly在病人的全身的发炎的诊断和评价对治疗有用选举。这篇论文考察获得系统的先生的申请，它广泛地与严重损害和批评外科的疾病为批评照顾病人的大组被验证了。最近的研究在批评照顾病人作为不利结果的一个重要预兆的参数记录了先生分数。而且，一些研究也给我们上的一个建议岩山引出超载全身的反应。

简介：客观：与严重煽动性的反应症候群(先生)在创伤的病人调查甲状腺荷尔蒙的引申。方法：有严重先生的五十个创伤的病人被注册并且根据他们是否介绍了multiorgandysfunction症候群(MODS)把组划分了成二。甲状腺荷尔蒙大小被拿，包括totaltriiodothyronine(TT3)，全部的甲状腺素(TT4)，免费triiodothyronine(FT3)，免费甲状腺素(FT4)和甲状腺刺激荷尔蒙(TSH)。尖锐生理学和长期的健康评估Ⅱ(APACHEⅡ)20根据临床的数据被计算。恢复或恶化的结果被记录，以及从到时间甲状腺荷尔蒙的先生的发作的时间的长度被测量。结果：Euthyroid病了的症候群(S字)在45cases.TT3水平被介绍否定地与APACHEH分数被相关(r=-0.330,P<0。05)，并且TT3/TT4value否定地与先生的持续时间被相关(r=-0.316,P<0.05)。没有MODS，在MODS病人的TT3，TT4和FT3levels是比那些显著地低的(P<0.05)。没有MODS，给低TT4或FT4的MODS病人比那些经常铺平更多(P<0.05)。与在正常TSH组的病人相比，有有的减少的TSH的病人降低T3，T4，恢复率和更高的APACHEⅡ分数，MODS发生，但是二个组之间没有差别(P>0.05).Conclusions：有严重先生的损伤病人有高可能性得到S字，它更经常并且严重地发生在MODS病人。它在甲状腺轴上显示出先生的影响。Withthe坚持和先生的恶化，有甲状腺荷尔蒙的进步减小。

简介：有免疫力的房间，特别地巨噬细胞，在导致组织缺氧的煽动性的反应起关键作用。小GTPaseRhoB被许多刺激很快通常导致并且被描述了为细胞骨架组织和泡和膜受体trafficking的一个重要管理者。然而，RhoB是否涉及导致组织缺氧的煽动性的反应，是未知的。这里，我们在巨噬细胞在RhoB表示的RhoB和机制和意义的表示上调查了组织缺氧的效果。我们显著地发现了那组织缺氧upregulated在老鼠的RAW264.7房间，鼠标腹巨噬细胞，和怒气的RhoB的表达式。RhoB的导致组织缺氧的表示被组织缺氧可诱导的factor-1(HIF-1)的一个特定的禁止者显著地堵住，c6月N终端kinase(JNK)，或细胞外信号的调整蛋白质kinase(英皇家空军之阶级最低之兵)，显示那激活组织缺氧的HIF-1，JNK，和英皇家空军之阶级最低之兵被组织缺氧涉及RhoB的upregulation。RhoB表示击倒不仅interleukin-1贝它(IL-1)的显著地压制的基础生产，interleukin6(IL-6)，并且在normoxia而且更多的肿瘤坏死因素alpha(TNF-)显著地减少了这些cytokines的刺激组织缺氧的生产。而且，我们证明RhoB增加了NF-Btranscriptional的原子factor-kappaB(NF-B)活动，和抑制活动显著地减少了IL-1，IL-6，和TNF-的增加RhoB的mRNA层次。最后，我们证明RhoB提高了房间粘附并且在normoxia和组织缺氧禁止了房间移植。一起拿，这些结果建议RhoB在巨噬细胞和煽动性的反应的导致组织缺氧的激活起一个重要作用。

简介：为了成功地感染，招待房间并且躲避主机免疫者反应，一个类型III分泌物系统(T3SS)被伤寒通常使用细菌的病原体象enteropathogenicEscherichiacoli(EPEC)那样。最近的调查结果表明了各种各样的受动器通过T3SS被注入主人房间并且在煽动性的发信号的小径上施加禁止的效果，破坏对这些病原体的有免疫力的回答。这里，我们考察针对探讨EPEC受动器蛋白质调制的几条重要煽动性的发信号小径的调整的最近的研究，例如原子factor-B(NF-B)和激活mitogen的蛋白质kinase(MAPK)小径，它在这块未经勘探的地和帮助里提供卓见进未完成的工作为EPEC受动器在煽动性的发信号的网络识别新奇位置。

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简介：AIM:Tostudytheeffectsofglutamine(Gin)onthechangeofintestinalpermeabilityanditsrelationshiptosystemicinflammatoryresponseinearlyabdominalpostoperativepatients.METHODS:Aprospective,randomized,double-blindandcontrolledtrialwastaken.TwentypatientsundergoingabdominalsurgerywererandomizedintoGingroup(oraladministrationofglutamine,30g/d,for7d,n=10)andplacebogroup(oraladministrationofplacebo,30g/d,for7d,n=-10).Temperaturesandheartratesofallpatientsweredailyrecorded.Whitebloodcellcounts(WBC)andbiochemicalvariablesweremeasuredbeforeoperationand4and7dalterdrugadministration.Serumconcentrationsofglutamine,endotoxin,diamineoxidaseandmalondialdehydeandurinelactulose/mannito(L/M)ratioweremeasuredbeforeand7dalterdrugadministration.RESULTS:Thepatientsinthe2groupswerecomparablepriortodrugadministration.SerumGinconcentrationwassignificantlydecreasedintheplacebogroupandincreasedintheGingroup7dalterdrugadministration.UrineL/MratiowassignificantlyincreasedintheplacebogroupanddecreasedintheGingroup.Theserumconcentrationofendotoxin,diamineoxidaseandmalondialdehydewassignificantlydecreasedintheGingroupcomparedwiththoseintheplacebogroup.Temperatures,heartratesandWBCcountsweresignificantlylowerintheGingroupthanthoseintheplacebogroup.CONCLUSION:Gutisoneofthesourcesofsystemicinflammatoryresponseinabdominalpostoperativepatientsandglutaminecandecreaseintestinalpermeability,maintainintestinalbarrierandattenuatesystemicinflammatoryresponseinearlypostoperativepatients.

简介：Hypertonicsaline(HS)hasbeenappliedinseveralmedicalareassuchaspneumology(asthma,cysticfibrosisandbronchiolytis),endocrinology(hyponatremia)andespeciallyinemergencymedicine,intraumaticandinflammatory/infectiousdisorders.Itmaybecomposedof

简介：ＥＸＣＥＳＳＩＶＥＦＵＮＣＴＩＯＮＳＯＦＡＣＬＡＳＳＯＦＳＵＰＥＲＰＲＯＣＥＳＳＥＳＺｈａｏＸｕｅｌｅｉ（赵学雷）（ＩｎｓｔｉｔｕｔｅｏｆＭａｔｈｅｍａｔｉｃｓ，ＳｈａｎｔｏｕＵｎｉｖｅｒｓｉｔｙ，Ｓｈａｎｔｏｕ５１５０６３，Ｃｈｉｎａ）Ａｂｓｔｒａ...

简介：AbstractBackground:The first-line treatment for lung cancer is surgical resection, and one-lung ventilation (OLV) is the most basic anesthetic management method in lung surgery. During OLV, inflammatory cytokines are released in response to the lung tissue damage and promote local and contralateral lung damage through the systemic circulation. We designed a randomized, prospective study to evaluate the effect of the urinary trypsin inhibitor (UTI) ulinastatin on the inflammatory response after video-assisted thoracic lobectomy in patients with lung cancer.Methods:Adult patients aged 19 to 70 years, who were scheduled for video-assisted thoracic lobectomy surgery to treat lung cancer between May 2020 and August 2020, were enrolled in this randomized, prospective study. UTI (300,000 units) mixed with 100 mL of normal saline in the ulinastatin group and 100 mL of normal saline in the control group was administered over 1 h after inducing anesthesia.Results:The baseline (T0) interferon-γ (IFN-γ)/interleukin-4 (IL-4) ratio was not different between the groups (6941.3 ± 2778.7 vs. 6954.3 ± 2752.4 pg/mL, respectively; P > 0.05). The IFN-γ/IL-4 ratio was significantly higher in ulinastatin group at 30 min after entering the recovery room than control group (20,148.2 ± 5054.3 vs. 6674.0 ± 2963.6, respectively; adjusted P < 0.017). Conclusion: Administering UTI attenuated the anti-inflammatory response, in terms of INF-γ expression and the IFN-γ/IL-4 ratio, after video-assisted thoracic surgery in lung cancer patients.Trial registration:Clinical Research Information Service of Korea National Institute of Health (CRIS), KCT0005533.

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简介：BackgroundCoronarymicroembolization(CME)ischaracterizedbydistalmicrovascularocclusion.However,theinflammatorymechanismsandtherapeutictargetsofCMEarelargelyunknown.MethodsAtotalof11GuangxiBamaminiatureswinesweredividedintotwogroups:sham(n=5)andCME(n=6).MicrosphereswereinjectedintotheleftanteriordescendingarteryoftheCMEgrouptomakeananimalmodelofCME.TheexpressionsofmicroRNA-146a(miR-146a)andIRAK1,TRAF6,andAUF1inthemyocardiumweredetectedbyqPCR.ResultsIntheCMEgroup,microspheres,microinfarction,andinflammatorycellinfiltrationwerefoundunderanopticalmicroscope.TheexpressionlevelsofmiR-146awerelowinbothgroups.AfterCME,theexpressionlevelsofIRAK1,TRAF6,andAUF1intheCMEgroupwereupregulatedcomparedwiththoseintheshamgroup(P<0.01;P<0.05;P<0.05,respectively).ConclusionsAUF1,IRAK1andTRAF6,butnotmiR-146a,couldbeinvolved,inmyocardiuminflammationfollowingCME.

简介：Airwaydiseasesarethemostcommonlydescribedlungmanifestationsofinflammatoryboweldisease(IBD).However,thesimilaritiesindiseasepathogenesisandthesharingofimportantenvironmentalriskfactorsandgeneticsusceptibilitysuggestthatthereisacomplexinterplaybetweenIBDandairwaydiseases.RecentevidenceofIBDoccurrenceamongpatientswithairwaydiseasesandthehigherthanestimatedprevalenceofsubclinicalairwayinjuriesamongIBDpatientssupportthehypothesisofatwo-wayassociation.Futureresearcheffortsshouldbedirectedtowardfurtherexplorationofthisassociation,asairwaydiseasesarehighlyprevalentconditionswithasubstantialpublichealthimpact.

简介：AbstractBackground:Endothelial cells play a key role in the cytokine storm caused by influenza A virus. MicroRNA-155 (miR-155) is an important regulator in inflammation. Its role in the inflammatory response to influenza A infection, however, has yet to be elucidated. In this study, we explored the role as well as the underlying mechanism of miR-155 in the cytokine production in influenza A-infected endothelial cells.Methods:Human pulmonary microvascular endothelial cells (HPMECs) were infected with the influenza A virus strain H1N1. The efficiency of H1N1 infection was confirmed by immunofluorescence. The expression levels of proinflammatory cytokines and miR-155 were determined using real-time polymerase chain reaction. A dual-luciferase reporter assay characterized the interaction between miR-155 and sphingosine-1-phosphate receptor 1 (S1PR1). Changes in the target protein levels were determined using Western blot analysis.Results:MiR-155 was elevated in response to the H1N1 infection in HPMECs (24 h post-infection vs. 0 h post-infection, 3.875 ± 0.062 vs. 1.043 ± 0.013, P = 0.001). Over-expression of miR-155 enhanced inflammatory cytokine production (miR-155 mimic vs. negative control, all P < 0.05 in regard of cytokine levels) and activation of nuclear factor kappa B in infected HPMECs (miR-155 mimic vs. negative control, P = 0.004), and down-regulation of miR-155 had the opposite effect. In addition, S1PR1 was a direct target of miR-155 in the HPMECs. Inhibition of miR-155 enhanced the expression of the S1PR1 protein. Down-regulation of S1PR1 decreased the inhibitory effect of the miR-155 blockade on H1N1-induced cytokine production and nuclear factor kappa B activation in HPMECs.Conclusion:MiR-155 maybe modulate influenza A-induced inflammatory response by targeting S1PR1.

简介：目的：讨胃经穴在胃肠实热型肥胖症治疗中的作用。方法：51例胃肠实热型肥胖症患者随机分为两组，治疗组以胃经取穴为主，对照组采用俞募配穴法取穴。隔日治疗1次，1个月为1个疗程，共治疗3个疗程。观察患者的症状、体征的变化，测量治疗前后的肥胖指标及血瘦素、血脂、血糖、ACHE等实验室指标。结果：与对照组相比，胃经组可显著减少各项肥胖指标（P〈0．01）；改善肥胖患者的高瘦素血症（P〈0．05）和脂代谢紊乱（P〈0．05）；逆转肥胖患者的副交感神经功能亢进的失衡状态（P〈0．05）。结论：经穴位可以作用于肥胖发生和发展的多个环节，是治疗胃肠实热型肥胖症的关键而有效的选穴。

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简介：Acriticalfunctionoftheintestinalmucosaistoformabarrierthatseparatesluminalcontentsfromtheinterstitium.Thesinglelayerofintestinalepithelialcells(IECs)servesasadynamicinterfacebetweenthehostanditsenvironment.Cellpolarityandstructuralpropertiesoftheepitheliumiscomplexandisimportantinthedevelopmentofepithelialbarrierfunction.Epithelialcellsassociatewitheachotherviaaseriesofintercellularjunctions.TheapicalmostintercellularjunctionalcomplexreferredtoastheApicalJunctionComplex(AJC)isimportantinnotonlycell-cellrecognition,butalsointheregulationofparacellularmovementoffluidandsolutes.Defectsintheintestinalepithelialbarrierfunctionhavebeenobservedinanumberofintestinaldisorderssuchasinflammatoryboweldisease(IBD).ItisnowbecomingevidentthatanaberrantepithelialbarrierfunctionplaysacentralroleinthepathophysiologyofIBD.Thus,abetterunderstandingoftheintestinalepithelialbarrierstructureandfunctioninhealthyanddiseasestatessuchasIBDwillfosternewideasforthedevelopmentoftherapiesforsuchchronicdisorders.

简介：由模式识别受体(PRR)的病原体的天生的察觉到在在自我和非自我部件之间的天生的辨别起必要作用，导致天生的有免疫力的防卫和煽动性的回答的产生。天生的煽动性的反应的开始，激活和分辨率被相互作用的一个复杂网络在有免疫力、非有免疫力的系统的众多的细胞、分子的部件之中调停。当时一控制并且有益的天生的煽动性的反应是批评的因为病原体的消除和织物动态平衡，dysregulated或持续发炎的维护导致象长期的感染那样的病理学的条件，煽动性的自体免疫的疾病。在这评论，我们为天生的免疫和煽动性的回答的建立和规定在我们细胞、分子的机制的理解讨论一些最近的进展。

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