细胞因子抗瘢痕的研究进展

瘢痕是创伤修复的必然结果影响,瘢痕的产生,发展的因素很多,虽然国内外学者在病理性瘢痕领域研究取得了一些进展,但其确切的发病机制仍未完全清楚,目前对治疗瘢痕的研究主要集中在生化,细胞水平,对分子机制和基因水平的研究还在不断的深入,人们对细胞因子在瘢痕形成方面起了关键的调节作用这一观点已逐步形成共识,并将细胞因子引入瘢痕的治疗中.常见的细胞因子在抗瘢痕中的应用也将成为可能.本文主要介绍了常见细胞因子的在创面修复中的生物学特征及抗瘢痕的研究情况.     

有氧运动与干细胞动员的缺血心脏血管新生研究进展

有氧运动具有明确的血管新生效应,包括缺血心脏,但其机制尚未完全阐明。心肌梗死(MI)后冠脉微血管新生是心脏修复的前提。新近研究表明,血管新生来源于体内干/祖细胞的动员与参与,并以旁分泌效应影响内皮细胞(EC)功能及微血管分布效果,运动可以动员、激活内源性干细胞因子和血管生成因子的表达与分泌,并能从表观遗传学角度影响心脏血管新生。探索不同运动方式及强度对缺血心脏血管新生的作用及其分子机制,对缺血心脏的预防及术后康复具有重要意义。本文从心脏血管新生及其调控机制、自体干细胞动员参与缺血心脏的血管新生和运动通过干细胞动员促进缺血心脏血管新生等方面综述运动促进缺血心脏血管新生的主要机制、存在问题及相关研究进展。     

天然产物及复方药物抗皮肤瘢痕机制的研究进展

增生性瘢痕和瘢痕疙瘩是皮肤组织损伤后创面过度修复产生的一种常见疑难病。一些天然产物及复方药物中具有较好的抗皮肤瘢痕增生的成分。本文从皮肤瘢痕形成过程中的相关细胞成分、生长因子调节、细胞外基质、胶原代谢、微血管构筑、免疫调节等方面和水平综述天然产物及复方药物的作用机制的研究进展。     

干细胞的旁分泌和自分泌功能——基础与临床研究的新视角

近年发现干细胞具有很强的旁/自分泌功能,本文综述干细胞所分泌的生长因子、细胞因子、调节肽、细胞信号分子等生物活性因子,以及缺血、缺氧、生长因子、性别和其它激素对干细胞分泌功能的调节;并分析干细胞分泌功能在血管生成、心脏、肝脏、肾脏和神经系统保护中的作用,认为干细胞可通过其分泌功能影响靶器官结构、功能状态及其病理状态下的修复,是干细胞治疗改善靶器官功能、抗凋亡、抗炎等作用的机制之一.     

RNA干涉与干细胞

RNA干涉(RNAi)现象普遍存在于生物体细胞中,在理论上已清楚其分子机制,为干细胞研究提供了新的方法。现从RNAi的分子机制、干细胞中的RNAi现象、研究干细胞RNAi效应的方法以及小分子干涉RNA(siRNA)干涉干细胞特异功能基因的检测方法等方面进行了综述。表明应用RNAi技术研究基因功能和干细胞维持及定向分化的调控具有广阔的发展前景。     

肌卫星细胞激活和补给的分子调控与肌肉疾病

肌卫星细胞(muscle satellite cell,SC)作为生肌干细胞,参与司控生后骨骼肌的生长、修复和维持等重要过程.综述了NO-HGF,Myostatin,Notch等重要信号分子及卫星细胞自身的特殊微环境对SC激活和补给的分子调控机制,希冀将来可以从这两方面入手克服目前临床中肌卫星细胞移植治疗各种骨骼肌疾病的瓶颈.     

骨髓间充质干细胞体外趋化神经前体细胞的机制

骨髓间充质干细胞(BMSC)和神经前体细胞(NPC)移植于脑组织损伤动物的实验证明这两类细胞移植后均能在体内迁徙,与周围细胞整合,促进神经功能修复。BMSC促进神经功能修复的机制之一被认为与其分泌一些细胞因子和趋化因子有关,但具体机制不十分明确。为从基质细胞衍生因子-1α(SDF-1α)及其唯一的受体CXCR4这对分子相互作用的机制上探讨BMSC移植的可能治疗作用,实验采用ELISA法检测了体外培养的BMSC上清液中SDF-1α的含量,体外微孔隔离室迁移实验发现NPC能在BMSC分泌的培养上清液中SDF-1α的作用下发生定向迁移,特异性抗CXCR4单抗能有效阻断NPC的定向迁移效应,证实了BMSC分泌的SDF-1α促进表达CXCR4的NPC向病灶处迁移可能是促进神经功能修复的机制之一,从而为干细胞移植治疗神经功能缺损提供了一个新的思路。     

睾丸间质干细胞的研究进展

睾丸间质干细胞(stem leydig cells,SLCs)是位于睾丸组织生精小管外侧壁的一类成体干细胞,具有维持自我更新和分化的特征。其分化形成的成熟间质细胞(adult leydig cells,ALCs)可以大量合成和分泌睾酮,是雄性动物机体睾酮产生的主要来源,广泛参与雄性动物的生殖和生理调控。由于SLCs发现较晚,在特异性标记及潜在调控机制和临床应用等方面的研究还并不深入。该文主要对SLCs的起源、分子标记、自我增殖和分化机制以及临床应用等进行综述,以促进SLCs研究和为雄性激素缺乏所引起疾病的临床应用奠定基础。     

骨髓间充质干细胞促进皮肤创伤愈合的作用机制及临床应用

皮肤是人体面积最大的器官,不同来源的损伤可使皮肤正常结构遭到破坏,皮肤创面修复过程失衡,从而导致皮肤愈合缓慢或畸形愈合,损害皮肤正常功能。骨髓间充质干细胞因其易获取、体外培养技术简单、低免疫原性、旁分泌、高度自我复制能力及多向分化潜能等特点而使其具有独特的优越性。已有研究表明骨髓间充质干细胞(BMSC)可通过多种复杂机制实现其促进皮肤创面愈合的作用,其趋化性可使BMSC向损伤部位迁移,并在局部分化为多种皮肤细胞、皮肤附属器细胞以及血管内皮细胞,促进皮肤的再生,通过抑制免疫细胞的生物学活性来发挥免疫调节作用。此外,BMSC可以分泌多种重要的生物活性因子,起到抗炎、促进新血管形成、抗纤维化及瘢痕形成、加快伤口愈合等作用。目前,BMSC已运用于多种类型皮肤损伤的临床治疗以及组织工程和再生医学中,且已取得了一定成果。本文主要就骨髓间充质干细胞的生物学特性、促进皮肤创伤愈合的作用机制及其临床应用进行了综述。     

Entwicklungsgeschichte und Ultrastruktur von Pollenkitt und Exine bei nahe verwandten entomophilen und anemophilen Angiospermensippen derAlismataceae,Liliaceae, Juncaceae,Cyperaceae, Poaceae undAraceae

Some closely related members of the monocotyledonous familiesAlismataceae, Liliaceae, Juncaceae, Cyperaceae, Poaceae andAraceae with variable modes of pollination (insect- and wind-pollination) were studied in relation to the ultrastructure of pollenkitt and exine (amount, consistency and distribution of pollenkitt on the surface of pollen grains). The character syndromes of pollen cementing in entomophilous, anemophilous and intermediate (ambophilous or amphiphilous) monocotyledons are the same in principal as in dicotyledons. Comparing present with former results one can summarize: 1) The pollenkitt is always produced in the same manner by the anther tapetum in all angiosperm sub-classes. 2) The variable stickiness of entomophilous and anemophilous pollen always depends on the particular distribution and consistency of the pollenkitt, but not its amount on the pollen surface. 3) The mostly dry and powdery pollen of anemophilous plants always contains a variable amount of inactive pollenkitt in its exine cavities. 4) A step-by step change of the pollen cementing syndrome can be observed from entomophily towards anemophily. 5) From the omnipresence of pollenkitt in all wind-pollinated angiosperms studied one can conclude that the ancestors of anemophilous angiosperms probably have been zoophilous (i.e. entomophilous) throughout.

     

Identification and Characterization of the First Equine Parainfluenza Virus 5

正Dear Editor,Parainfluenza virus 5 (PIV5), known as canine parainfluenza virus in the veterinary field, is a negative-sense,nonsegmented, single-stranded RNA virus belonging to the Paramyxoviridae family (Chen 2018). The virus was first reported in primary monkey kidney cells in 1954 (Hsiung1972), then it has been frequently discovered in various     

Pathogenic Characterization and Full Length Genome Sequence of a Reassortant Infectious Bursal Disease Virus Newly Isolated in Pakistan

<正>Dear Editor,Infectious bursal disease (IBD) is one of the most important diseases of the poultry. The IBD virus (IBDV), a nonenveloped virus belonging to the Birnaviridae family with a genome consisting of two segments of double-stranded RNA (segments A and B), targets B lymphocytes of bursa of Fabricious leading to immunosuppression. In Pakistan,poultry farming is the second biggest industry and IBD is the second biggest disease threating the poultry sector.However, there is limited genome information of IBDV     

Mink Circovirus Can Infect Minks,Foxes and Raccoon Dogs

正Dear Editor,Mink circovirus (MiCV), which is clustered in the genus Circovirus of the family Circoviridae, was first described in minks from farms in Dalian, China in 2013 (Lian et al.2014). The complete single-stranded circular genome of the virus is 1,753 nucleotides long and contains two major open reading frames (ORFs), designated ORF1 (Rep gene)and ORF2 (Cap gene)(Lian et al. 2014; Ge et al. 2018).Sequence analysis has shown that MiCV is most closely     

CypA Regulates AIP4-Mediated M1 Ubiquitination of Influenza A Virus

Cyclophilin A (CypA) is a peptidyl-prolyl cis/trans isomerase that interacts with the matrix protein (M1) of influenza A virus (IAV) and restricts virus replication by regulating the ubiquitin–proteasome-mediated degradation of M1. However,the mechanism by which CypA regulates M1 ubiquitination remains unknown. In this study, we reported that E3 ubiquitin ligase AIP4 promoted K48-linked ubiquitination of M1 at K102 and K104, and accelerated ubiquitin–proteasome-mediated degradation of M1. The recombinant IAV with mutant M1 (K102 R/K104 R) could not be rescued, suggesting that the ubiquitination of M1 at K102/K104 was essential for IAV replication. Furthermore, CypA inhibited AIP4-mediated M1 ubiquitination by impairing the interaction between AIP4 and M1. More importantly, both the mutations of M1 (K102 R/K104 R) and CypA inhibited the nuclear export of M1, indicating that CypA regulates the cellular localization of M1 via inhibition of AIP4-mediated M1 ubiquitination at K102 and K104, which results in the reduced replication of IAV.Collectively, our findings reveal a novel ubiquitination-based mechanism by which CypA regulates the replication of IAV.