多发性硬化和视神经脊髓炎患者血尿酸水平分析

类风湿关节炎(Rheumatoid Arthritis)是一种以慢性关节滑膜炎为主要特征的自身免疫性疾病,以形成侵袭性滑膜血管翳,破坏软骨、骨与周围组织为基本病理改变,发病2年内即可能出现全身性骨量减少及小关节的破坏,Wnt信号通路在在类风湿关节炎慢性炎症和骨质破坏的病理生理过程中起重要作用,研究Wnt信号通路作用,能为我们理解类风湿关节炎临床分型和预后提供理论依据,同时也能为类风湿关节炎的治疗提供新的研究方向。     

Comprehensive Wnt-related gene expression during cochlear duct development in chicken

The avian cochlear duct houses both a vestibular and auditory sensory organ (the lagena macula and basilar papilla, respectively), which each have a distinct structure and function. Comparative mRNA in situ hybridization mapping conducted over the time course of chicken cochlear duct development reveals that Wnt-related gene expression is concomitant with various developmental processes such as regionalization, convergent extension of the cochlear duct, cell fate specification, synaptogenesis, and the establishment of planar cell polarity. Wnts mostly originate from nonsensory tissue domains, whereas the sensory primordia preferentially transcribe Frizzled receptors, suggesting that paracrine Wnt signaling predominates in the cochlear duct. Superimposed over this is the strong expression of two secreted Frizzled-related Wnt inhibitors that tend to show complementary expression patterns. Frzb (SFRP3) is confined to the nonsensory cochlear duct and the lagena macula, whereas SFRP2 is maintained in the basilar papilla along with Fzd10 and Wnt7b. Flanking the basilar papilla are Wnt7a, Wnt9a, Wnt11, and SFRP2 on the neural side and Wnt5a, Wnt5b, and Wnt7a on the abneural side. The lateral nonsensory cochlear duct continuously expresses Frzb and temporarily expresses Wnt6 and SFRP1. Characteristic for the entire lagena is the expression of Frzb; in the lagena macula are Fzd1, Fzd7, and Wnt7b, and in the nonsensory tissues are Wnt4 and Wnt5a. Auditory hair cells preferentially express Fzd2 and Fzd9, whereas the main receptors expressed in vestibular hair cells are Fzd1 and Fzd7, in addition to Fzd2 and Fzd9.     

Bone morphogenetic proteins and their antagonists

Skeletal homeostasis is determined by systemic hormones and local factors. Bone morphogenetic proteins (BMPs) are unique because they induce the commitment of mesenchymal cells toward cells of the osteoblastic lineage and also enhance the differentiated function of the osteoblast. BMP activities in bone are mediated through binding to specific cell surface receptors and through interactions with other growth factors. BMPs are required for skeletal development and maintenance of adult bone homeostasis, and play a role in fracture healing. BMPs signal by activating the mothers against decapentaplegic (Smad) and mitogen activated protein kinase (MAPK) pathways, and their actions are tempered by intracellular and extracellular proteins. The BMP antagonists block BMP signal transduction at multiple levels including pseudoreceptor, inhibitory intracellular binding proteins, and factors that induce BMP ubiquitination. A large number of extracellular proteins that bind BMPs and prevent their binding to signaling receptors have emerged. The extracellular antagonists are differentially expressed in cartilage and bone tissue and exhibit BMP antagonistic as well as additional activities. Both intracellular and extracellular antagonists are regulated by BMPs, indicating the existence of local feedback mechanisms to modulate BMP cellular activities. This work was supported by Grant AR21707 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases.     

桡骨远端不稳定型骨折的远期疗效分析

小儿脑性瘫痪(Cerebral Palsy)是以慢性、非进行性运动功能障碍为特征的一组症候群,患儿常伴有不同程度的认知障碍.我国的小儿脑性瘫痪定义为:以妊娠到新生儿之间的各种原因所致的脑的非进行性病变为基础,形成永存的,但可以变化的运动和姿势异常,其症状在2岁之前出现.随着早产儿存活率的升高,脑瘫的发病率也上升至人口总数的0.06%~0.59%.我国此类患儿不少于250万,且每年新增患儿约20万左右.脑性瘫痪是目前小儿时期最主要的运动功能伤残疾病,而且多数伴发有智力低下及语言功能障碍.     

Expression of Wnt3a,Wnt10b, β-catenin and DKK1 in periodontium during orthodontic tooth movement in rats

Objective: To investigate the expression of Wnt3a, Wnt10b, β-catenin and DKK1 in the periodontal ligament (PDL) during orthodontic tooth movement (OTM) in rats. Materials and methods: Nickel-titanium closed-coil springs were used to deliver an initial 50 g mesial force to the left maxillary first molars in 30 rats. The force was kept constant for 1, 3, 5, 7, 10 and 14 days until the animals were sacrificed. The right maxillary molars without force application served as control. Paraffin-embedded sections of the upper jaws were prepared for histological and immunohistochemical analyses to detect Wnt3a, Wnt10b, β-catenin and DKK1 expression in PDL. Results: Wnt3a, Wnt10b, β-catenin and DKK1 were expressed on both the ipsilateral and contralateral sides of PDL in each group. After the application of orthodontic force, the expression of β-catenin and DKK1 was initially increased and then decreased on both sides, with maximal levels of expression at day 7 and day 10, respectively. On the compression side, Wnt3a and Wnt10b levels started to increase at day 5, while on the tension side, these two molecules began to increase at day 1. Furthermore, the expression levels of Wnt3a, Wnt10b, and β-catenin were much stronger on the tension side than on the compression side at any of the observation points, while DKK1 level was much higher on the compression side. Conclusion: Wnt3a, Wnt10b, β-catenin and DKK1 expression may be related to the periodontal tissue remodeling following the application of an orthodontic force in rats. These observations suggest that the Wnt/β-catenin signaling pathway may play a crucial role in periodontal tissue remodeling during OTM.     

Wnts and the neural crest

The neural crest is a multipotent tissue that originates between the neural epithelium and non-neural ectoderm, which can develop into numerous cell types, including neurons, glia, pigment cells, smooth muscle, cartilage and bone. Work in a variety of animal models has shown that a number of signalling factors are necessary for the induction, delamination and differentiation of neural crest cells. However one family of proteins, the Wnts, shows an overriding influence on this tissue. Here we review recent studies that pinpoint specific roles that Wnts play in the development of the neural crest.     

Targeting axon guidance cues for neural circuit repair after spinal cord injury

At least two-thirds of spinal cord injury cases are anatomically incomplete, without complete spinal cord transection, although the initial injuries cause complete loss of sensory and motor functions. The malleability of neural circuits and networks allows varied extend of functional restoration in some individuals after successful rehabilitative training. However, in most cases, the efficiency and extent are both limited and uncertain, largely due to the many obstacles of repair. The restoration of function after anatomically incomplete injury is in part made possible by the growth of new axons or new axon branches through the spared spinal cord tissue and the new synaptic connections they make, either along the areas they grow through or in the areas they terminate. This review will discuss new progress on the understanding of the role of axon guidance molecules, particularly the Wnt family proteins, in spinal cord injury and how the knowledge and tools of axon guidance can be applied to increase the potential of recovery. These strategies, combined with others, such as neuroprotection and rehabilitation, may bring new promises. The recovery strategies for anatomically incomplete spinal cord injuries are relevant and may be applicable to traumatic brain injury and stroke.