简介:【摘要】目的 :研究 ANCA阳性肺血管炎 临床主要表现。方法:本次研究样本选取时间为 2017年 2月 -2019年 2月,研究对象为我院接受治疗的 50例 ANCA阳性肺血管炎 患者,总结所有患者临床基本资料以及实验室、CI检查结果,分析 ANCA阳性肺血管炎 患者的临床表现。结果:50例 ANCA阳性肺血管炎 患者临床症状表现为咳嗽、咯痰、发热、胸闷气喘、咯血、痰中带血以及肾受累等症状,其中,发热症状最典型,占比78%,其次为咳嗽、咯痰,占比 64%; 44例患者核周型 P-ANCA呈阳性;有 39例患者抗原特异性髓过氧化物酶抗体 MPO呈阳性,其他 5例胞浆型 C-ANCA、 5例均抗原特异性蛋白酶 3抗体 PR3及 11例合并有抗核抗体 ANA,均呈阳性。 结论:ANCA阳性肺血管炎患者的检测缺少无明显特征,因此,还需对其行进一步甄别诊断。
简介:AIDSassociatedmalignancies(ARL)isamajorcomplicationassociatedwithAIDSpatientsuponimmunosuppression.Chronicallyimmunocompromisedpatientshaveamarkedlyincreasedriskofdevelopinglymphoproliferativedisease.Intheeraofpotentantiretroviralstherapy(ARV),themalignantcomplicationsduetoHIV-1infectionhavedecreasedindevelopednationswhereARVisadministered,butstillposesamajorproblemindevelopingcountrieswhereHIV-1incidenceishighandARVisstillnotyetwidelyavailable.EveninARVtreatedindividualsthereisaconcernthattheprolongedsurvivalofmanyHIV-1carriersislikelytoeventuallyresultinanincreasednumberofmalignanciesdiagnosed.MalignanciesthatwerefoundtohavehighincidenceinHIV-infectedindividualsareKaposi'ssarcoma(KS),Hodgkin'sdisease(HD)andnon-Hodgkin'slymphoma(NHL).TheincidenceofNHLhasincreasednearly200foldinHIV-positivepatients,andaccountsforagreaterpercentageofAIDSdefiningillnessintheUSandEuropesincetheadventofHAARTtherapy.TheseAIDSrelatedlymphomasaredistinctfromtheircounterpartsseeninHIV-1seronegativepatients.ForexamplenearlyhalfofallcasesofARLareassociatedwiththepresenceofagammaherpesvirus,EpsteinBarrvirus(EBV)orhumanherpesvirus-8(HHV-8)/Kaposi'ssarcomaassociatedherpesvirus(KSHV).ThepathogenesisofARLsiscomplex.B-cellproliferationdrivenbychronicantigenemiaresultingintheinductionofpolyclonalandultimatelymonoclonallymphoproliferationmayoccurinthesettingofsevereimmunosuppression.
简介:抗中性粒细胞胞浆抗体(ANCA)相关性血管炎(AAV)是一种常见的自身免疫性原发性小血管炎,主要侵犯小血管,如毛细血管、小静脉、小动脉和微动脉,以血管坏死性炎症与破坏为病理特征,肾、肺、皮肤、五官、神经系统等全身多个器官或系统均可受累。AAV的发病率日益增高,中国的流行病学数据仍缺乏。其病因及发病机制至今未明,地域不同,临床表现不同且多样,目前尚无统一的诊断标准。早期诊断及合理治疗可提高患者生存率和生活质量。
简介:MitochondrialtRNAmutationsareoneoftheimportantcausesofbothsyndromicandnon-syndromicdeafness.Ofthose,syndromicdeafness-associatedtRNAmutationssuchastRNALeu(UUR)3243A>Gareoftenpresentinheteroplasmy,whilenon-syndromicdeafness-associatedtRNAmutationsincludingtRNASer(UCN)7445A>Gareofteninhomplasmyorinhighlevelsofheteroplasmy.ThesetRNAmutationsaretheprimarymutationsleadingtohearingloss.However,othertRNAmutationssuchastRNAThr15927G>AandtRNASer(UCN)7444G>AmayactinsynergywiththeprimarymitochondrialDNAmutations,modulatingthephenotypicmanifestationoftheprimarymitochondrialDNAmutations.ThesestRNAmutationscausestructuralandfunctionalalteration.AfailureintRNAmetabolismcausedbythesetRNAmutationsimpairedmitochondrialtranslationandrespiration,therebycausingmitochondrialdysfunctionsresponsiblefordeafness.Thesedataoffervaluableinformationfortheearlydiagnosis,managementandtreatmentofmaternallyinheriteddeafness.
简介:<正>Inthispaper,weinvestigatethegeneralizedSublaplacian.Wegivetheexpressionoftherestrictionoperatorsexplicitly.Byintroducingthegeneralizedλ-twistedconvolutions,weobtaintheestimatesoftherestrictionoperatorsinthemixedL~Pspaces.Finally,wegetarestrictiontheoremassociatedwiththegeneralizedSublaplacian.
简介:在性复制,在昆虫和微生物之间的共生关系的不同类型变得例如建立了,一些细菌发展了几乎独占的垂直传播并且甚至定义昆虫交配的相容性合伙许多严格地,性传播疾病也除了如此的相当特定的关系在昆虫被描述了在繁殖过程的机会主义的感染的角色广泛地被忽视了在交配期间消极地播送的机会主义的微生物可能强加一精力充沛的费用,当免疫系统将需要是警戒和愿望,使用资源通过交配创伤和污染繁殖机关与潜在的入侵者作斗争机会主义的微生物可能被转移到交配搭挡并且因为“receiving”性是特别地可能的发展了改编避免或减少机会主义的感染,甚至进入身体洞女性几种的男性显示出高度复杂的精液,它象包含影响males’授精成功的部件一样,也拥有在繁殖过程的抗菌剂的角色不是的物质很好理解的抗菌剂在对微生物的精子的保护的一些证据提示,在由一般来说在复制在性选择和他们的角色强调微生物的潜在的重要性塑造繁殖特点的进化为自然选择显示一个角色我将在性选择为研究做一个案例,特别调查postcopulatory过程的,应该合并环境,象genotypic变化一样,繁殖特点地。
简介:使用每月的风和海面温度(SST)数据,在印度洋与印度洋偶极子模式(IOD)事件联系的南部的南方的大气循环房间第一次被描述并且检验。分叉的风和压力vertical速度为大气循环房间的鉴定被采用。在积极IOD事件的四个不同阶段期间,在西方的印度洋上的异常南方的哈德利发行量证明空气在更低的对流层在热带,在上面的对流层的流动杆病房,在画热带的水池,和回来升起回到热带。在东方印度洋上的塞诺马劳斯·哈德利循环在西方的印度洋上对那相反。在积极IOD事件期间,当它在西方的印度洋上被加强时,在东方IndianOcean上的南方的哈德利发行量被削弱。在IOD索引和哈德利房间的索引之间的相关分析也证明那,大气循环模式在在记录的时期上的每个IOD事件是明显的。
简介:Objective:Toevaluatethetreatmentforpatientswithmajorvascularinjuriesassociatedwithtraumaticorthopedicinjuries.Methods:Atotalof196patients,agedfrom4-67yearswiththemeanageof29.88years,hadmajorvascularinjuriesassociatedwithtraumaticorthopedicinjuriesandweretreatedinourhospitalinaperiodof44years.Themostcommonmechanismoftraumawasblunttrauma(67.3%),openinjuriesaccountedfor32.4%and54.5%oftheinjurieswerelocatedinthelowerextremities.Thevascularinjuryfrequentlyhappenedinthefemoralartery(26.7%)andpoplitealartery(20.3%).Thetreatmentprincipleconsistedofaggressiveresuscitation,Dopplerimagingandstableboneinternalfixationwithsubsequentvascularrepairanddebridement.Thevascularrepairforinjuriesincludedend-to-endanastomosis(80cases,39.6%),interpositionalveingraft(94,46.5%),vasculardecompressionthroughfracturedistraction(18,8.9%),arterialligation(6,3.0%),veinpatch(2,1.0%),bypassgraft(2,1.0%),venousrepairincludingautogenousveingraft(9,24.3%)andligation(28,75.7%)andprophylacticalfasciotomy(15,7.4%).Postoperativeamputationwasperformedin16cases(16.3%).Results:Nointraoperativedeathwasobservedandallfracturesunitedwithin6months.Limbsweresalvagedin180patients(91.8%).Amongthesepatients,earlycomplicationswerefoundin19patients(9.7%)andlatecomplicationswereobservedin8patients(4.1%).Conclusions:Awell-organizedapproach,basedonaspecifictreatmentprinciple,notonlyimprovesclinicaloutcomebutalsodoesgoodtoexcellentfunctionalrecoveryforpatientswithsevereorthopedicinjuriesandconcomitantvascularlesion.
简介:AbstractServing as the interface between the fetal and maternal environments during gestation, the placenta plays critical roles in the protection of the developing fetus and the maintenance of maternal health. The placenta is primarily derived from the embryonic trophectoderm which differentiates into various subtypes of trophoblast cells through villous and extravillous pathways. The interactions among trophoblasts and multiple decidual cells and immune cells at the maternal-fetal interface fundamentally form the functional units of the placenta, which are responsible for blood perfusion and maternal-fetal material exchange, immune tolerance, and the regulation of pregnancy adaptation. Defects in placental development and functional maintenance are in tight association with adverse pregnancy outcomes such as preeclampsia. In this article, we review recent advances on human trophoblast cell differentiation and the construction of placental functional units and discuss the placental and maternal factors that may contribute to the occurrence of preeclampsia.
简介:AbstractFetal growth restriction (FGR) has a prevalence of about 10% worldwide and is associated with an increased risk of perinatal mortality and morbidity. FGR is commonly caused by placental insufficiency and can begin early (<32 weeks) or in late (≥32 weeks) gestational age. A false positive antenatal diagnosis may lead to unnecessary monitoring and interventions, as well as cause maternal anxiety. Whereas a false negative diagnosis exposes the fetus to an increased risk of stillbirth and renders the pregnancy ineligible from the appropriate care and potential treatments. The clinical management of FGR pregnancies faces a complex challenge of deciding on the optimal timing of delivery as currently the main solution is to deliver the baby early, but iatrogenic preterm delivery of infants is associated with adverse short-and long-term outcomes. Early and accurate diagnosis of FGR could aid in better stratification of clinical management, and the development and implementation of treatment options, ultimately benefiting clinical care and potentially improving both short-and long-term health outcomes. The aim of this review is to present the new insights on biomarkers of placenta insufficiency, including their current and potential value of biomarkers in the prediction and prevention for FGR, and highlight the association between biomarkers and adverse outcomes in utero to explore the specific mechanism of impaired fetal growth that establish the basis for disease later in life.
简介:AbstractFetal growth restriction (FGR) is associated with multiple adverse perinatal outcomes, such as increased risk of intrauterine death, neonatal morbidity and mortality, and long-term adverse outcomes. Genetic etiological factors are critical in fetuses with intrauterine growth restriction, including chromosomal abnormalities, copy number variants, single gene disorders, uniparental disomy, epigenetic changes, and confined placental mosaicism. This paper aims to provide an overview of genetic defects related to FGR and to highlight the importance of prenatal genetic counseling and testing for precise diagnosis and management of FGR.