简介：AbstractPurpose:Malnutrition is a common problem among hospitalized patients, especially among traumatic brain injury (TBI) patients. It is developed from hypermetabolism and the condition may worsen under the circumstance of underfeeding or incompatible dietary management. However, the data of nutrient intake especially calorie and protein among TBI patients were scarce. Hence, this study aimed to determine the calorie and protein intake among acute and sub-acute TBI patients receiving medical nutrition therapy in hospital Sultanah Nur Zahirah, Terengganu.Methods:This observational study involved 50 patients recruited from the neurosurgical ward. Method of 24 h dietary recall was utilized and combined with self-administered food diaries for 2-8 days. Food consumptions including calorie intake and protein intake were analyzed using Nutritionist PRO™ (Woodinville, USA) and manual calculation based on the Malaysian food composition database (2015).Results:Patients consisted of 56% males and 44% females with the median age of 28.0 (IQR = 22.8-36.5) years, of which 92% were diagnosed as mild TBI and the remaining (8%) as moderate TBI. The Glasgow coma scale (GCS) was adopted to classify TBI severity with the score 13-15 being mild and 9-12 being moderate. The median length of hospital stay was 2 (IQR = 2.0-3.3) days. Calorie and protein intake improved significantly from day 1 to discharge day. However, the intake during discharge day was still considered as suboptimal, i.e. 75% of calorie requirement, whilst the median protein intake was only 61.3% relative to protein requirement. Moreover, the average percentages of calorie and protein intakes throughout hospitalization were remarkably lower, i.e. 52.2% and 41.0%, respectively.Conclusion:Although the calorie and protein intakes had increased from baseline, hospitalized TBI patients were still at a risk to develop malnutrition as the average intakes were considerably low as compared to their requirements. Optimum nutrient intakes especially calorie and protein are crucial to ensure optimum recovery process as well as to minimize risks of infection and complications.

简介：AbstractBackground:Arteriosclerosis obliterans (ASO) is a major cause of adult limb loss worldwide. Autophagy of vascular endothelial cell (VEC) contributes to the ASO progression. However, the molecular mechanism that controls VEC autophagy remains unclear. In this study, we aimed to explore the role of the GRB2 associated binding protein 1 (GAB1) in regulating VEC autophagy.Methods:In vivo and in vitro studies were applied to determine the loss of adapt protein GAB1 in association with ASO progression. Histological GAB1 expression was measured in sclerotic vascular intima and normal vascular intima. Gain- and loss-of-function of GAB1 were applied in VEC to determine the effect and potential downstream signaling of GAB1.Results:The autophagy repressor p62 was significantly downregulated in ASO intima as compared to that in healthy donor (0.80 vs. 0.20, t= 6.43, P < 0.05). The expression level of GAB1 mRNA (1.00 vs. 0.24, t= 7.41, P < 0.05) and protein (0.72 vs. 0.21, t = 5.97, P < 0.05) was significantly decreased in ASO group as compared with the control group. Loss of GAB1 led to a remarkable decrease in LC3II (1.19 vs. 0.68, t = 5.99, P < 0.05), whereas overexpression of GAB1 significantly led to a decrease in LC3II level (0.41 vs. 0.93, t= 7.12, P < 0.05). Phosphorylation levels of JNK and p38 were significantly associated with gain- and loss-of-function of GAB1 protein.Conclusion:Loss of GAB1 promotes VEC autophagy which is associated with ASO. GAB1 and its downstream signaling might be potential therapeutic targets for ASO treatment.

简介：Epstein-Barr病毒(EBV)编码了潜伏的膜蛋白质1(LMP1)被知道了在鼻咽的癌(NPC)在潜伏的感染期间有oncogenic性质。我们的研究在NPC集中了于LMP1的角色，并且证明LMP1触发表明小径的NF-B，AP-1和STAT。惊人地，LMP1被发现调停在c6月和JunB之间的新heterodimer的形成。另外，我们鉴别了JAK/STAT和PI-PLC-PKC激活通过upregulating由LMP1被触发JAK3的表示并且提高STAT的phosphorylation。这些发信号的串联的组成的激活解释LMP1的能力导致如此的一个多样的数组词法并且phenotypic在房间完成并且提供LMP1怎么可以导致房间转变，multihit在下游的戏在指向了基因的卓见一个必要角色。LMP1触发的所有发信号的串联最终导致房间周期的混乱：G1/S阶段的加速和G2/M阶段的拘捕。我们也发现LMP1导致了hTERT的表示并且支持了房间不减。重要地，由干涉物理细胞内部的信号transduction小径并且扰乱房间周期的前进，LMP1，重要oncoprotein由EBV编码了，被认为是在NPC的致病的一个关键调节的人。介入的LMP1发信号能是有希望的策略指向NPC的恶意的显型。

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简介：BackgroundAldosteroneblockerscouldreducetheincidenceofventriculararrhythmiasinmyocardialinfarction(MI)patientsbyregulatinghyperpolarization-activatedcyclicnucleotide-gatedchannel(HCN)expression.ButthemechanismunderlingHCNexpressionisunclear.MethodsEighteenratssurviving24hourspostMIwererandomlydividedinto3groups:MI,spironolactone,andspironolactone+antagomir-133(miRNA-133suppression).Shamgroupratshadasuturelooselytiedaroundtheleftcoronaryartery,withoutligation.HCN2andHCN4proteinandmRNAlevel,andmiRNA-133levelintheborderzoneofpost-MI1weekmyocardiumweremeasured.ResultsSpironolactonesignificantlyincreasedmiRNA-133levelsanddown-regulatedHCN2andHCN4atbothmRNAandproteinlevelsinpost-MIborderzonemyocardium.Antagomir-133reducedtheeffectsofspironolactoneonHCN2andHCN4proteinlevels.ConclusionsTheresultssuggestthatmiRNA-133isinvolvedinspironolactoneinducedHCNexpression,andpartiallycontributedtopost-MIventriculararrhythmias.

简介：Objective:Toexploretheeffectofdexamethasonebylocaltreatmentofcerebraledemaandbraindamageafterbraininjury.Methods:Twenty-tworabbitswereclassifiedinto2groups,GroupA(thecontrolgroup,n=11)andGroupB(thetreatedgroup,n=11).Anrabbitbraincontusionmodelwasmadebybonewindowplastybyextraduralhitting.Groupbwastreatedbylocalinfiltratingandsprayingofdexamethasoneatequidistancetolesions.GroupAwasgivennormalsalineinthesamewayasGroupB.Thechangesofmoistureinbraintissuesandserummyelinbasicprotein(MBP)wereobserved.Results:ThepercentageofwatercontentindamagedhemisphereinGroupAandGroupbwas81.7%±0.56%and79.45%±0.52%respectively.Therewasasignificantdifferencebetweenthe2groups(P<0.05).ThenormallevelofMBPwas1.66μg/L±0.71μg/L,whilethevalueofMBPinGroupAandGroupbwere5.98μg/L±2.08μg/Land3.15μg/L±1.09μg/Lseparately.ThelevelofMBPinGroupAandGroupBwerehigherthannormallevelandtherewasalsoasignificantdifferencebetweenGroupAandGroupB(P<0.05).Conclusions:TheresultsofourstudyshowedthatthebrainmoistureandMBPinserumwereincreasedafterbraininjurywhilereducedaftertreatmentwithdexamethasone.ItisdemonstratedthatlocaltreatmentofbraininjurywithdexamethasonehasanobvioustherapeuticeffectoncerebraledemaandserumMBP.

简介：Animprovedmethod,calledAlternativeSpectralRotation(ASR)measure,forpredictingproteincodingregionsinriceDNAhasbeendeveloped.ThemethodisbasedontheSpectralRotation(SR)measureproposedbyKotlarandLavner,anditsaccuracyishigherthanthatoftheSRmeasureandtheSpectralContent(SC)measureproposedbyTiwarietal.Inordertoincreasetheidentifyingaccuracy,wechosethreedifferentcodingcharacters,namelytheasymmetric,purine,andstop-codonvariablesasparameters,andanapprovingresultwaspresentedbythemethodofLinearDiscriminantAnalysis(LDA).

简介：AbstractThe coronavirus disease 2019 (COVID-19) is still causing a wide range of infections and deaths due to the high variability of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Therefore, it is necessary to establish a reliable and convenient pseudovirus-based neutralization assay to develop drug targeted variants of SARS-CoV-2. Based on the HIV-1 backbone, we generated a high titer luciferase (Luc)-expressing pseudovirus packaging system. Three dominant S mutant substitution pseudovirus were also established and identified compared to wide type in hACE2-overexpressing HEK-293T cells (293T-ACE2 cells). Compared to serine protease inhibitor camostat mesylate, the cysteine protease inhibitor E-64d could significantly block all SARS-CoV-2 mutant S pseudovirus infection in 293T-ACE2 cells. Furthermore, the neutralization ability of two antibodies targeted receptor-binding domain (RBD) of SARS-CoV-2 spike protein (S) was evaluated, which showed different inhibition dose-effect curves among four types of S pseudovirus. Overall, we developed a pseudovirus-based neutralization assay for SARS-CoV-2, which would be readily adapted to SARS-CoV-2 variants for evaluating antibodies.

简介：AbstractObjective:This study aimed to screen for novel mutations in ACTL7A and expand the spectrum of known mutations responsible for recurrent fertilization failure.Methods:Whole-exome sequencing was performed on samples from couples who experienced recurrent assisted reproductive technology failure and visited the General Hospital of Ningxia Medical University. Western blotting and quantitative Real-time PCR were used to investigate the effects of the mutation on HEK293T cells.Results:Samples from 12 couples with total fertilization failure or poor fertilization (fertilization rate <20%) were subjected to whole-exome sequencing, and a novel homozygous protein-truncating mutation (c. 1101dupC, p. S368Qfs*5) in ACTL7A was identified in a patient with recurrent poor fertilization. The mutant resulted in a truncated protein as well as decreased protein expression level in HEK293T cells.Conclusions:Our findings expand the mutational and phenotypic spectrum of ACTL7A, thus providing a potential diagnostic marker for fertilization failure due to male factors.

简介：AbstractBackground:The screening of periprosthetic joint infection (PJI) in patients with inflammatory diseases before revision arthroplasty remains uncertain. Serum C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), plasma fibrinogen (FIB), monocyte/lymphocyte ratio, and neutrophil/lymphocyte ratio (NLR) can help screening PJI, but their values in patients with inflammatory diseases have not been determined.Methods:Patients with inflammatory diseases who underwent revision hip or knee arthroplasty at West China Hospital, Sichuan University, from January 2008 to September 2020 were divided into infected and non-infected groups based on the 2013 International Consensus Meeting criteria. Sensitivity and specificity of the tested biomarkers for diagnosing infection were determined based on receiver operating characteristic (ROC) curves, and optimal cutoffs were determined based on the Youden index. The diagnostic ability of these biomarkers was re-assessed after combining them with each other.Results:A total of 62 patients with inflammatory diseases were studied; of them 30 were infected. The area under the ROC curve was 0.813 for CRP, 0.638 for ESR, 0.795 for FIB, and 0.656 for NLR. The optimal predictive cutoff of CRP was 14.04 mg/L with a sensitivity of 86.2% and a specificity of 68.7%, while FIB had a sensitivity of 72.4% and a specificity of 81.2% with the optimal predictive cutoff of 4.04 g/L. The combinations of CRP with FIB produced a sensitivity of 86.2% and specificity of 78.1%.Conclusion:CRP with a slightly higher predictive cutoff and FIB are useful for screening PJI in patients with inflammatory diseases, and the combination of CRP and FIB may further improve the diagnostic values.Trial Registration:ChiCTR.org.cn, ChiCTR2000039989

简介：在脂肪和肌肉房间，刺激胰岛素的葡萄糖举起被葡萄糖transporter主要调停4(GLUT4)，哪个到响应胰岛素刺激的房间表面的从细胞内部的分隔空间的translocates。AS160是Akt的底层之一并且在调整胰岛素的GLUT4translocation起重要作用。在这研究，(RUVBL2)象RuvB一样蛋白质2用与集体spectrometry相结合的哺乳动物的双人脚踏车亲密关系纯化(龙头)作为新AS160有约束力的蛋白质被识别。在3T3-L1adipocytes，RUVBL2高度被表示并且在cytosol主要是分布式的。在adipocytes的RUVBL2的弄空通过减少刺激胰岛素的AS160phosphorylation禁止刺激胰岛素的GLUT4translocation和葡萄糖举起。然而，人的RUVBL2的介绍能颠倒这禁止的效果。这些数据建议RUVBL2通过它和AS160的相互作用在刺激胰岛素的GLUT4translocation起一个重要作用。

简介：HIV-1p24察觉提供一个工具帮助HIV-1感染的早诊断，追踪疾病的前进并且估计antiretroviral治疗的功效。在对HIV-1的现在的学习，三monoclonal抗体(mAbs)p3JB9，p5F1和p6F4，p24被产生。所有mAbs能检测HIV-1B，HIV-1Ada-M，HIV-174vmAbsp5F1和p6F4的p24能检测HIV-1KM018，当p3JB9不能时。三mAbs没与HIV-2ROD，HIV-2CBL-20和SIVagmTyo-1反应。p5F1的公认的epitope位于Gag氨基酸区域DCKTILKALGPAATLEEMMTAC。p5F1被用来与兔子anti-p24浆液建立修改三明治ELISA并且显示出好特性和高敏感，它被用来在研究测量HIV-1p24抗原层次。

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简介：一综合(dimethylsiloxane)(PDMS)poly，有二的微芯片削尖为方便样品注射，跑的缓冲区更新和清洗的隧道拉长建议被介绍了。没有交换供应和注射十字隧道的复杂电源，样品直接通过拉长的入口尖端被介绍进分离隧道。运用缓冲区更新或隧道清洗的操作被vacuuming简化尖端的结束并且把另外的尖端放进答案小瓶。因此，没有软平版印刷术和血浆结合设备，这个制造方法罐头容易经济地被用于很分析的实验室。新奇PDMS微芯片的吸引人的表演被为蛋白质的分离使用导致激光的荧光察觉表明了。在0.04mol/L磷酸盐缓冲区的0.04%Brij35的增加(pH7.0)能在multienzyme药片减少蛋白质的粘附并且更容易做分离。electroosmotic流动(文件结束)在动态修改microchannel在311的范围展出pH独立。

简介：G-proteincoupledreceptors(GPCRs)representoneofthemostimportantclassesofdrugtargetsforpharmaceuticalindustryandplayimportantrolesincellularsignaltransduction.PredictingthecouplingspecificityofGPCRstoG-proteinsisvitalforfurtherunderstandingthemechanismofsignaltransductionandthefunctionofthereceptorswithinacell,whichcanprovidenewcluesforpharmaceuticalresearchanddevelopment.Inthisstudy,thefeaturesofaminoacidcompositionsandphysiochemicalpropertiesofthefull-lengthGPCRsequenceshavebeenanalyzedandextracted.Basedonthesefeatures,classifiershavebeendevelopedtopredictthecouplingspecificityofGPCRstoG-proteinsusingsupportvectormachines.Thetestingresultsshowthatthismethodcouldobtainbetterpredictionaccuracy.

简介：Objective:Mucoepidermoidcarcinoma(MEC)isthemostcommonprimarymalignancyofthesalivaryglands.Insulin-likegrowthfactor-IImRNA-bindingprotein-3(IMP3)isanimportantprognosticfactorinsomecancersandatoolthatdifferentiatesbetweenbenignandmalignantpancreaticlesions.ThisstudyaimedtoidentifyarelationshipbetweentheexpressionofIMP3andtheoutcomeofsalivaryglandMEC,aswellastodifferentiateMECfrompleomorphicadenoma(PA).Methods:Tissuespecimensfrom70casesofsalivaryglandMEC,40casesofPA,and10caseswithnormalsalivaryglandwereexaminedimmunohistochemicallyforIMP3.TheassociationamongtheexpressionofIMP3,clinicopathologicalcharacteristicsandpatient'ssurvivalwasassessed.Results:IMP3waspresentin51.4%ofMECbutabsentinPAandnormalsalivaryglandtissues.IMP3expressionwasassociatedwithage>60years,submandibularglandtumors,tumorsize>4cm,high-gradetumors,lymphnodemetastasis,involvementofsurgicalmargins,perineuralinvasion,distantmetastasis,advancedTNMstage,tumorrelapse,anddeath(P<0.05).IncreasedexpressionofIMP3,tumorsofthesubmandibulargland,andlymphnodemetastasiswereindependentprognosticfactorsofdisease-freesurvival(DFS).Inaddition,IMP3wasastrongpredictorofoverallsurvival(OS)togetherwithdistantmetastasisandintermediateandhigh-gradetumors.Conclusions:IMP3expressionishighlyimportantinevaluatingtheoutcomeofMEC.IMP3canbeusedtodifferentiateMECfromPAofsalivaryglands.

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简介：ObjectivesToinvestigatetheeffectofGαq/11signalingpathwayandATP-sensitivepotassiumchannel(KATPchannel)onischemicpreconditioning(IPC)protectioninrathearts.MethodsTwoseriesofexperimentswereperformedinWistarrathearts.Inthefirstseriesofexperiment,ischemicpreconditioningwasinducedbyleftanteriordescendingocclusion(three,5minepisodesseparatedby5minofreperfusion),ischemia-reperfusioninjurywasinducedby30mincoronaryarteryocclusionfollowedby90minreperfusion.Hemodynamics,infarctsizeandscoresofventriculararrhythmiasweremeasured.TheexpressionofGαq/11proteinintheheartwasmeasuredbyWesternblotanalysisinthesecondseries.ResultsIschemicpreconditioningratsshoweddecreasedinfarctsizeandscoresofventriculararrhythmiavsnon-IPcontrolrats.TheeffectofIPCwassignificantlyattenuatedbyglibenclamide(1mg/kg,ip),anonselectiveKATPchannelinhibitor.IPCcausedasignificantincreaseintheexpressionofGαq/11protein.ConclusionsActivationsofGαq/11signalpathwayandKATPchannelplayedsignificantrolesintheclassicalcardioprotectionofischemicprecon-ditioningratheartandmightbeanimportantmechanismofsignaltransductionpathwayduringtheischemicpreconditioning.

简介：(QS)治安法官察觉到是细菌用称为autoinducers的细胞外的信号由交流的细菌的房间房间通讯进程。二个QS系统在EscherichiacoliK-12被识别了，包括一个未经触动的QS系统2那被周期的安培(营地)营地受体蛋白质(CRP)刺激建筑群和一个部分QS系统1那由对另外的微生物引起的种类产生的信号作出回应的SdiA(房间部门禁止者的suppressor)组成。在QS之间的关系在E的系统1和系统2。然而，coli仍然保持阴暗。这里，我们显示出那EAL域蛋白质，由ydiV，和营地编码了在E涉及在二个QS系统之间的相互作用。coli。sdiA和ydiV的表示被葡萄糖禁止。SdiA在一个剂量依赖者，而是nonspecific绑在ydiV倡导者区域，举止；细胞外的autoinducer1以一种sdiA依赖的方式从另外的种类刺激ydiV表示。而且，我们发现双sdiA-ydiV变化，然而并非单个变化，在导致QS系统2的抑制的细胞内部的营地集中引起2褶层减少。这些结果显示对重要环境暗示作出回应的发信号的小径例如autoinducers和葡萄糖，在E为他们的控制一起被连接。coli。

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