眼球破裂伤相关因素分析

目的 观察眼球破裂伤的致伤原因、常见部位、视力预后。方法 眼科住院眼球破裂伤51例的回顾性总结分析。结果 眼球破裂伤的首要致伤因素是打架斗殴(占43％)、其次工伤(占20％)、家庭休闲和旅游误伤(占17％)，交通事故(10％)，其他(10％)。眼球破裂伤的常见部位是上方角膜缘(占45％)，颞侧、鼻侧角膜缘和肌止点后巩膜(各占15％)。经过治疗，Ⅰ度破裂伤7／13获得0．02以上视力，Ⅱ度破裂伤9／20保留光感以上视力，Ⅲ度破裂伤1／18保留光感视力。结论 打架斗殴是眼球破裂伤首要致伤因素，常见伤口位置是上方角膜缘，眼球破裂伤的预后和损伤程度密切相关。     

Horner syndrome

Horner syndrome is an uncommon but important clinical entity, representing interruption of the sympathetic pathway to the eye and face. Horner syndrome is almost always diagnosed clinically, though pharmacological testing can be used to confirm the diagnosis. Imaging modalities such as PET, CT and MRI are important components of work‐up for patients presenting with acquired Horner syndrome. Our patient’s presentation with Horner syndrome unmasked the causative superior sulcus squamous cell carcinoma and a coincidental lower lobe adenocarcinoma. Successful radical treatment of these cancers resulted in complete resolution of the syndrome and disease‐free survival at 18 months. We review the anatomy and pathophysiology underlying this and other causes of Horner syndrome.     

668颗后牙镍铬合金PFM边缘适合性的临床观察

目的：观察采用2种边缘形式的后牙烤瓷熔附金属全冠边缘适合性和对牙龈健康的影响.方法：对668颗后牙,分别采用2种边缘形式的后牙烤瓷熔附金属全冠（单冠或桥的基牙）在修复2年后进行复查,检测其边缘适合性及牙龈指数（GI）和牙周探诊深度（PD）,用统计学方法分析修复体边缘形式与牙龈病变间的关系.结果：采用羽状边缘360°金属脚边的PFM边缘适合性明显优于凹面肩台型边缘PFM,凹面肩台型边缘的PFM的牙龈病变发生率,明显高于羽状边缘360°金属脚边的PFM,而边缘适合性差者较适合性好者牙龈病变发生率显著增高.结论：后牙PFM的边缘采用羽状边缘360°金属脚边是一种好的选择.     

聚氯乙烯增塑糊流变行为的研究——Ⅳ.表面活性剂的影响

本文研究了各类表面活性剂对聚氯乙烯增塑糊流变行为的影响。阴离子表面活性剂使其增塑糊有较高致流值,呈明显假塑性流动;阳离子和非离子表面活性剂使其增塑糊有低的表观粘度,接近牛顿型流动。测定了聚氯乙烯粒子表面的Zeta电位和接触角,并讨论了表面活性剂影响增塑糊流变性能的机理。     

An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immuno-reactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.