咽旁间隙原发性肿块流行病学分析

目的：对咽旁间隙原发性肿块进行流行病学分析。方法：对咽旁间隙原发性239例肿块进行统计分析。结果：原发良性肿瘤患病比为61．09％，其中上皮源性肿瘤患病比最高，占19.25％；神经源性肿瘤第二位，占17．57％。原发性恶性肿瘤的患病比为35．15％，其中上皮源性恶性肿瘤的患病比最高，占21.76％；恶性淋巴瘤第2位，占7．95％。炎症的患病比为3．77％，其中淋巴结反应性增生最高。结论：咽旁间隙原发性肿块良性肿瘤的患病比最高，恶性肿瘤次之，炎症居第3位，比例约为17：9：1。     

Synergistic effects of Nell-1 and BMP-2 on the osteogenic differentiation of myoblasts.

Osteogenesis is synergistically enhanced by the combined effect of complimentary factors. This study showed that Nell-1 and BMP-2 synergistically enhanced osteogenic differentiation of myoblasts and phosphorylated the JNK MAPK pathway. The findings are important because of the osteochondral specificity of Nell-1 signaling and the potential therapeutic effects of coordinated BMP-2 and Nell-1 delivery. INTRODUCTION: BMPs play an important role in the migration and proliferation of mesenchymal cells and have a unique ability to alter the differentiation of mesenchymal cells toward chondrogenic and osteogenic lineages. Signaling upstream of Cbfa1/Runx2, BMPs effects are not limited to cells of the osteoblast lineage. Thus, additional osteoblast-specific factors that could synergize with BMP-2 would be advantageous for bone regeneration procedures. NELL-1 (NEL-like molecule-1; NEL [a protein strongly expressed in neural tissue encoding epidermal growth factor like domain]) is a novel growth factor believed to preferentially target cells committed to the osteochondral lineage. MATERIALS AND METHODS: C2C12 myoblasts were transduced with AdLacZ, AdNell-1, AdBMP-2, or AdNell-1+AdBMP-2 overexpression viruses. Effects were studied by cell morphology, alkaline phosphatase activity, osteopontin production, and MAPK signaling. Additionally, in a nude mouse model, viruses were injected into leg muscles, and new bone formation was examined after 2 and 8 wk. RESULTS: C2C12 myoblasts co-transduced with AdNell-1+AdBMP-2 showed a synergistic effect on osteogenic differentiation as detected by alkaline phosphatase activity and osteopontin production. Nell-1 stimulation on AdNell-1 + AdBMP-2 preconditioned C2C12 cells revealed significant activation of the non-BMP-2 associated c-Jun N-terminal kinase (JNK) MAPK signaling pathway, but not the p38 or extracellular signal-regulated kinase (ERK1/2) MAPK pathways. Importantly Nell-1 alone did not induce osteogenic differentiation of myoblasts. In a nude mouse model, injection of AdNell-1 alone stimulated no bone formation within muscle; however, injection of AdNell-1+AdBMP-2 stimulated a synergistic increase in bone formation compared with AdBMP-2 alone. CONCLUSIONS: These findings are important because of the confirmed osteochondral specificity of Nell-1 signaling and the potential therapeutic effects of enhanced BMP-2 action with coordinated Nell-1 delivery.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.     

唇腭裂患者上颌骨牵引成骨术后发音方式的变化

目的:通过对行颅外支架式上颌骨牵引成骨术(rigidexternaldistraction,RED)唇腭裂患者治疗前后的错误发音数量变化、不同发音部位、不同发音方法以及不同类型错误发音发生特点及其变化评价,分析上颌骨RED对患者发音方式的影响。方法:1999年至2001年行上颌骨RED的唇腭裂术后上颌发育不足患者21例,其中男性13例,女性8例,平均年龄15.05岁。所有患者RED前后进行语音测听并分类。治疗前后错误发音的差异性用非参数检验。结果:RED术后42.9%患者错误发音数较RED前增加,19.0%减少,38.1%无变化。从发音部位,舌尖前音错误发音发生率最高,其次为舌面音。从发音方法,错误发音多发于塞擦音。错误发音类型以咽喉摩擦/爆破音为主,其次为腭化构音和声门爆破音。上颌骨RED后腭化构音累及音节数减少,但咽喉摩擦/爆破音和声门爆破音反而增加,尤其是咽喉摩擦/爆破音。结论:唇腭裂患者经RED前移上颌骨后,会对患者发音方式产生影响,在行语音治疗前需考虑全面。     

BKV in Simultaneous Pancreas-Kidney Transplant Recipients: A Leading Cause of Renal Graft Loss in First 2 Years Post-Transplant

With the introduction of more potent immunosuppressive agents, rejection has decreased in simultaneous pancreas/kidney transplant (SPK) recipients. However, as a consequence, opportunistic infections have increased. The purpose of this report is to outline the course of SPK patients who developed polyomavirus-associated nephropathy (PVAN). A retrospective review of 146 consecutive SPK recipients from January 1, 1996 to December 31, 2002 was performed. Immunosuppression, rejection and development of PVAN were reviewed. Nine patients were identified. All received induction with either OKT3 or thymoglobulin. Immunosuppression included tacrolimus/cyclosporine, MMF/azathioprine and sirolimus/prednisone. Two patients were treated for kidney rejection prior to the diagnosis of PVAN. Time to diagnosis was an average of 359.3 days post-transplantation. Immunosuppression was decreased but five ultimately lost function. However, none developed pancreatic abnormalities as demonstrated by normal glucose and amylase. Two underwent renal retransplantation after PVAN diagnosis and both have normal kidney function. PVAN was the leading cause of renal loss in SPK patients in the first 2 years after transplantation and is a serious concern for SPK recipients. The pancreas, however, is spared from evidence of infection, and no pancreatic rejection occurred when immunosuppression was decreased.     

胫骨平台骨折合并内侧副韧带损伤的诊治体会

[目的]探讨胫骨平台骨折伴膝内侧副韧带损伤的诊断及治疗方法。[方法]回顾性分析本院1996年1月~2005年12月期间收治的52例胫骨平台骨折合并重度内侧副韧带损伤病例,并对有随访的49例(保守治疗21例,手术治疗28例)进行分析。[结果]随访10个月~9年(平均1.7年),按照Schatzker分型:Ⅱ型39例,Ⅲ型6例,Ⅵ型4例。骨折均切开复位内固定,对韧带损伤的治疗分为2组,保守治疗组21例,膝关节功能:优11例,良9例,差1例。手术治疗组28例,Ⅰ期修复19例:优17例,良2例。Ⅱ期修复9例:优5例,良3例,差1例。[结论]胫骨平台骨折合并内侧副韧带损伤Ⅰ期修复效果理想。     

搭建基础平台实现高职医学订单教学

搭建基础平台是改传统三年制医学教学“1＋1＋1”模式为“1＋1”模式，为以“市场为导向，就业为中心”的高职教学进行多向培养提供条件，既拓宽教学渠道，适应市场需求，解决学生就业问题，同时又有利于学校发展，符合教学新模式量展要求。     

鹿鞭的药理研究与临床应用展望

综述了近年来传统中药鹿鞭的药理作用以及临床应用，资料表明鹿鞭具有抗衰老、抗疲劳、增强机体免疫、促进伤口愈合等药理作用，且临床疗效突出，是具有开发前景的中药材。