肱骨近端记忆接骨器的设计与临床应用

目的 探索肱骨头解剖颈至外科颈及肱骨近端干段骨折、骨不连的内固定新技术。方法 根据生物记忆材料镍钛合金性能与肱骨近端解剖生理特征，研制肱骨近端记忆接骨器（proximal humerus memory connector，PHMC），并临床治疗肱骨近端粉碎性骨折、畸形愈合、骨不连共22例。患者平均年龄41．7岁，平均随访18．5个月。结果 骨折骨性愈合时间平均3．6个月；骨不连骨性愈合时间平均4．5个月。骨愈合形式均呈骨板样骨替代，未见无序骨痂出现。PHMC术后弃用外固定，创伤反应期（7～12d）后，进行主动渐进性功能锻炼。肩关节功能按Michael Reese评分，平均88．5分。结论 PHMC能有效治疗肱骨解剖颈始至肱骨近端的各类型骨折与骨不连，亦为减少该部的假体关节置换探索出了新路。     

利浦松软膏防治烧伤创面瘢痕120例疗效观察

目的 :观察利浦松软膏防治烧伤创面瘢痕的疗效。方法 :将利浦松软膏涂擦于烧伤愈合创面 ,观察瘢痕生长情况。结果 :12 0例烧伤病人创面显效 32例 ,有效 72例 ,无效 16例。结论 :利浦松软膏用于防治烧伤创面瘢痕疗效显著 ,方法简单 ,便于推广应用     

MR扩散加权成像鉴别脑结核瘤及高级星形细胞瘤和脑转移瘤的价值

目的探讨MR扩散加权成像（DWI）在脑结核瘤、高级星形细胞瘤和脑转移瘤鉴别诊断中的价值。方法14例脑结核瘤、15例脑高级星形细胞瘤和21例脑转移瘤患者，在术前或接受治疗前行常规MRI和DWI。测量并计算3种疾病瘤体、瘤周围水肿带的平均表观扩散系数（ADC）值和病灶与对侧相应部位正常脑白质区ADC值的比值（rADC值）。结果脑结核瘤瘤体平均ADC值和rADC值分别为（1．2±0．2）×10^-3mm^2·s^-1和1．6±0．3，高级星形细胞瘤瘤体平均ADC值和rADC值分别为（0．8±0．1）×10^-3mm^2·s^-1和1．1±0．1，转移瘤瘤体平均ADC值和rADC值分别为（0．8±0．1）×10^-3mm^2·s^-1和1．0±0．2。3种疾病瘤体平均ADC值（F=33．57，P〈0．01）之间和rADC值（F=33．27，P〈0．01）之间差异均有统计学意义。脑结核瘤瘤周水肿带平均ADC值和rADC值分别为（1．8±0．1）×10^-3mm^2·s^-1和2．5±0．2，脑高级星形细胞瘤瘤周水肿带平均ADC值和rADC值分别为（1．4±0．2）×10^-3mm^2·s^-1和1．8±0．3，脑转移瘤瘤周水肿带平均ADC值和rADC值分别为（1．9±0．2）×10^-3mm^2·s^-1和2．3±0．5。3种疾病瘤周围水肿带平均ADC值（F=23．17，P〈0．01）之间和rADC值（F=5．94，P〈0．01）之间差异均有统计学意义。结论结合MRI、DWI检测方法，根据病灶瘤体和瘤周水肿带的ADC和rADC值可帮助鉴别脑结核瘤、脑高级星形细胞瘤和脑转移瘤。     

Oddi括约肌功能异常与胆管胆色素结石病

1887年,意大利一位名为Ruggero Oddi的大学四年级医学生在其毕业论文中首次提出了十二指肠乳头括约肌的概念,被后人证实并命名为Oddi括约肌以示纪念。120年来随着医学科学的不断发     

Model of reentrant ventricular tachycardia based on infarct border zone geometry predicts reentrant circuit features as determined by activation mapping

BACKGROUND: Infarct border zone (IBZ) geometry likely affects inducibility and characteristics of postinfarction reentrant ventricular tachycardia, but the connection has not been established. OBJECTIVE: The purpose of this study was to determine characteristics of postinfarction ventricular tachycardia in the IBZ. METHODS: A geometric model describing the relationship between IBZ geometry and wavefront propagation in reentrant circuits was developed. Based on the formulation, slow conduction and block were expected to coincide with areas where IBZ thickness (T) is minimal and the local spatial gradient in thickness (DeltaT) is maximal, so that the degree of wavefront curvature rho proportional, variant DeltaT/T is maximal. Regions of fastest conduction velocity were predicted to coincide with areas of minimum DeltaT. In seven arrhythmogenic postinfarction canine heart experiments, tachycardia was induced by programmed stimulation, and activation maps were constructed from multichannel recordings. IBZ thickness was measured in excised hearts from histologic analysis or magnetic resonance imaging. Reentrant circuit properties were predicted from IBZ geometry and compared with ventricular activation maps after tachycardia induction. RESULTS: Mean IBZ thickness was 231 +/- 140 microm at the reentry isthmus and 1440 +/- 770 microm in the outer pathway (P <0.001). Mean curvature rho was 1.63 +/- 0.45 mm(-1) at functional block line locations, 0.71 +/- 0.18 mm(-1) at isthmus entrance-exit points, and 0.33 +/- 0.13 mm(-1) in the outer reentrant circuit pathway. The mean conduction velocity about the circuit during reentrant tachycardia was 0.32 +/- 0.04 mm/ms at entrance-exit points, 0.42 +/- 0.13 mm/ms for the entire outer pathway, and 0.64 +/- 0.16 mm/ms at outer pathway regions with minimum DeltaT. Model sensitivity and specificity to detect isthmus location was 75.0% and 97.2%. CONCLUSIONS: Reentrant circuit features as determined by activation mapping can be predicted on the basis of IBZ geometrical relationships.     

Prostaglandin E2 inhibition of keloid fibroblast migration, contraction, and transforming growth factor (TGF)-β1–induced collagen synthesis

Keloid formation has been linked to aberrant fibroblast activity, exacerbated by growth factors and inflammatory mediators. Prostaglandin E2 (PGE2), synthesized from arachidonic acid by cyclooxygenases (COX) and synthases (PGES), acts as both an inflammatory mediator and fibroblast modulator. Although PGE2 has known antifibrotic effects in the lower airway, its role in dermal fibrosis in general, and keloid formation in particular, remains unclear. This study focused on: (1) the effects of PGE2 on keloid fibroblast migration, contraction, and collagen synthesis and (2) endogenous PGE2 synthesis in response interleukin-1beta. PGE2 decreased keloid fibroblast migration and contraction via an EP2/EP4-cAMP mechanism that disrupted actin cytoskeletal dynamics and reversed transforming growth factor-beta1-induced collagen I and III synthesis. Impaired fibroblast PGE2 production has been linked to lower airway fibrosis and recently to keloid formation. Here, we showed that interleukin-1beta stimulation leads to nuclear factor-kappaB translocation to the nucleus, resulting in up-regulation of COX-2 and microsomal PGE2 synthase 1. Up-regulation of COX-2 in, and secretion of PGE2 by keloid fibroblasts are diminished compared with their normal fibroblast counterparts. We suggest that the antifibrotic effects of PGE2 during keloid formation are potentially diminished due to aberrant paracrine fibroblast signaling. Exogenous PGE2 may supplement decreased endogenous levels and inhibit keloid formation or progression.