颏下逆行岛状皮瓣血管蒂与面神经分支的应用解剖

目的:研究颏下逆行岛状皮瓣血管蒂与面神经分支的解剖关系,为该皮瓣在临床的推广应用、提高手术成功率、减少面神经损伤提供解剖学依据.方法:利用福尔马林灌注固定的头颈部标本,解剖观测面动、静脉与面神经分支的交叉关系、交叉点至神经人肌点的距离、面神经各分支出腮腺处至入肌处的距离;模拟逆行蒂颏下瓣修复眼部缺损的手术过程.结果:面神经颈支从下颌角后方出腮腺向前下走行于颈阔肌深面而分布于该肌,该神经出腮腺处至面动、静脉与下颌缘交点处的距离为29.4 mm±4.0 mm;面神经下颌缘沿下颌骨下缘走行,与下颌骨之间常有淋巴结分隔,该神经均于面动、静脉浅面与其交叉,交叉点至下颌缘支入肌处的距离为16.9 mm±3.7 mm,下颌缘支出腮腺处至入肌处的距离为44.3 mm±5.1 mm;面神经颊支多以2干出腮腺,行程中各颊支之间及与下颌缘支、颧支之间互相吻合形成多个神经弓,在颊脂体表面常交织成丛,继而发出分支进入颧大肌、颊肌和笑肌,与面静脉形成2～4个交叉点,口角平面通常有一个交叉点,其余交叉点均在口角平面以上.结论:为了提高颏下逆行带蒂岛状皮瓣的转瓣点,须从面神经下颌缘支与下颌骨之间向上牵拉皮瓣,因此需充分分离神经与骨之间的间隙,以免牵拉皮瓣经过该间隙时损伤面神经下颌缘支;血管蒂旋转点不宜高于口角水平,以免损伤面神经颊支、口角诸肌和影响皮瓣的血供.     

下颌支截骨术手术入路的应用解剖学研究

目的:进一步探讨咬肌区浅层的组织结构,为临床行下颌截骨术避免损伤咬肌区的重要结构提供解剖学基础.方法:18例头颈部标本,经双侧颈总动脉插管,加压注入红色乳胶或明胶墨汁,解剖观测咬肌区浅层的组织结构.结果:咬肌区浅层由浅入深的组织层次是:皮肤、皮下组织、SMAS、腮腺咬肌筋膜、咬肌、咬肌下间隙和骨膜.咬肌表面横行结构有面神经颧支、面横动脉、面神经上颊支、腮腺导管、面神经下颊支、下颌缘支和颈支,它们距离下颌角分别为(5.8±0.5)cm、(5.2±0.5)cm、(5.1±0.6)cm、(4.3±0.5)cm、(3.3±0.8)cm、(0.9±0.5)cm和(-0.8±0.4)cm;离角前切迹的距离分别为(6.7±0.6)cm、(5.6±0.6)cm、(5.6±0.7)cm、(4.7±0.5)cm、(3.5±0.7)cm、(1.2±1.0)cm和(-1.0±0.2)cm.该区的动脉供应来源于颞浅动脉、面横动脉、颈外动脉、面动脉和咬肌动脉.结论:行下颌支截骨术时,应熟悉下颌支浅层的组织层次及咬肌浅层横行结构的布局,以免造成误伤.     

面部组织移位入颅底手术的临床解剖学研究

目的：为面部移位颅底手术入路提供解剖学基础。方法：在３６侧成人头面部标本上，对面神经、腮腺管的位置和层次进行了观察与定位。结果：①面动脉在眶下缘水平至鼻旁间距为９．９±５．０ｍｍ，至骨膜的深距为２．１±０．８ｍｍ；②面神经由茎乳孔出颅后，经腮腺、咬肌和颊区三段分布于面肌。在咬肌段，面神经紧贴咬肌表面行走，面神经颧支行于颧骨表面，至骨面的最小深距为１ｍｍ。结论：①旁正中切口不会影响面动脉；②掀翻面肌皮瓣时，颧骨表面和咬肌表面的面神经分支是易损伤区     

三维虚拟穿刺仿真在颈部神经阻滞中的应用

背景：颈部神经阻滞麻醉易引起严重麻醉意外与并发症,目前在建立颈部神经三维可视化模型并对颈部神经节阻滞进行虚拟仿真方面还处在临床探索阶段。 目的：寻求三维虚拟穿刺仿真在颈部神经阻滞中的应用方法。 方法：取健康志愿者颈部连续CT动脉造影/MRI脊髓造影断面图像,Mimics软件对骨骼、肌肉、动静脉、甲状腺、喉软骨、脊髓等组织进行半自动分割和重建,医学计算机辅助设计模块对神经等细小解剖结构进行重建,三维化显示颈部神经及周围相关解剖结构,并进行颈部神经穿刺虚拟仿真,包括模拟颈浅丛阻滞,颈深丛阻滞和星状神经节阻滞。 结果与结论：成功模拟颈浅丛阻滞, 颈深丛阻滞和星状神经节阻滞,显示虚拟穿刺针和骨性结构、动静脉、肌肉、脊髓、颈丛深浅支和星状神经节等解剖结构的三维毗邻关系,并测量穿刺进针的安全角度,深度和最佳穿刺路径。说明三维虚拟穿刺仿真技术可以为颈部神经阻滞术提供直观的形态学参考。     

改良经眶入路翼腭窝穿刺解剖学观测

目的　为眶入路法行翼腭窝穿刺提供新的进针路径。 方法　对77个（154侧）成人颅的眶和翼腭窝进行相关的观察和测量。 结果　眶外缘点至眶外下缘点、圆孔外口下缘、眶上裂后端、眶下裂前端的距离分别为：左（4.93±1.80）mm,右(4.02±2.05）mm;左（43.74±2.75）mm,右(43.80±2.89）mm;左（47.83±2.47）mm,右(47.74±2.53）mm;左（17.74±2.18）mm,右(17.43±1.97）mm。穿刺针（直针）由眶外缘点进入翼腭窝的成功率为：左侧96.10%;右侧93.51%。对穿刺针（直针）进入翼腭窝失败者改用弯针穿刺,直针和弯针由眶外缘点进入翼腭窝的总成功率为：左、右均达98.70%。 结论　经眶外缘点行眶入路翼腭窝穿刺可明显提高穿刺成功率。     

经鼻腔穿刺行翼管神经封闭的应用解剖

目的：为经鼻腔穿刺行翼管神经封闭提供应用解剖学基础。方法：对８个尸体头部标本及５０个颅骨进行了解剖和观测。结果：①穿刺针经过的途径为鼻孔前内侧缘下端、中鼻道、中鼻甲后端、蝶腭孔、翼管神经（翼管前口）；②穿刺深度为５８．６±３．９ｍｍ；③穿刺针与法兰克福平面的夹角为２２．３°±３．４°；④穿刺针与正中矢状面的夹角为１３．８°±２．７°。结论：经鼻腔穿刺行翼管神经封闭术具有可行性。     

国人咬肌和咬肌神经的应用解剖学

本文观测了31侧面部标本的咬肌和咬肌神经,以可摸到的下颌支和下颌角为标志,测得咬肌神经在 A 线、AB 间线、B 线和 BC 间线上至下颌支后缘的距离分别为2.3cm、2.7cm、3.1cm 和3.3cm;入肌点的位置至下颌角的距离为5.1cm。咬肌神经的体表定位,为临床采用咬肌瓣转位术矫正口颊区面瘫提供解剖学依据.     

面神经颊支和下颌缘支的解剖及临床应用研究进展

临床上吻合血管神经的游离肌肉移植或跨面神经移植整复面瘫时,都需要解剖健侧面神经的分支,其中常解剖的是颊支和下颌缘支。两组分支分别由面神经主干发出,并浅出腮腺缘,在走行过程中,其走行层次以及颊支与腮腺导管、下颌缘支与下颌骨下缘和面动脉关系都有一定的规律性。本文就面神经颊支和下颌缘支的解剖学及临床应用方面的进展作一综述,以指导临床手术,避免损伤神经分支引起继发性的功能障碍。1面神经颊支有学者[1￣3]在腮腺手术中观察到颊支有1￣2支,多数学者[4￣8]观察颊支有1￣4支,以2￣3支为主,占75%￣86.6%,可能与临床手术时术野暴露…     

面神经的应用解剖学研究进展

面神经颅外段由面神经核发出的躯体运动纤维构成,从茎乳孔穿出颅外,分支分布于面部的表情肌.按其与腮腺的毗邻关系,可将面神经颅外段分为腮腺前段、腮腺内段和腮腺后段.本文主要介绍面神经的腮腺后段.腮腺后段指由腮腺丛发出的5组分支,出腮腺以后至表情肌的一段.颞支、颧支和上颊支主要来自颞面干,下颊支、下颌缘支和颈支主要来自颈面干.熟悉面神经的走行方向、分支分布及其与周围组织的毗邻关系,对于保护面神经及其分支免受损伤非常重要.现就面神经各分支的解剖学研究进展综述如下.     

面神经颊支的应用解剖

目的：观测分析面神经颊支的分支类型及其与腮腺管之间的解剖关系，为腮腺区手术提供解剖学基础。方法：60例成人头部标本，观测面神经颊支的分支类型、行程、神经与腮腺管的位置关系。结果：面神经颊支以双干型多见(58．3％)，三干型次之(28．3％)。神经多行于腮腺管浅面(73．3％)。腮腺管走行在颊支之问的占61．7％，导管距上颊支垂直距离约4．86mm；腮腺管走行在神经下方者占11．7％，距下颊支的垂直距离约1．71mm；腮腺管走行在神经上方者占26．7％，距上颊支的垂直距离约2．56mm。结论：面神经颊支多行于腮腺管浅层，与腮腺管关系十分密切，腮腺区手术时循颊支向后追踪面神经是比较安全、有效的方法，容易掌握。     

逆转录病毒载体介导的反义c-myc抗白血病作用的研究

目的：研究c-myc基因在L6565小鼠白血病发生中的作用以及抑制其表达所起的治疗作用。方法：用逆转录病毒载体pGNC构建一个含有小鼠反义c-myc基因的逆转录病毒表达系统pGNCas。用磷酸钙沉淀法将pGNCas导入包装细胞PA317,筛选获得病毒生产细胞。用pGNCas病毒感染L6565白血病克隆细胞,筛选后,获得抗G418阳性克隆细胞L6565as。PCR方法检测反义c-myc序列是否稳定整合入L6565as细胞中。最后从细胞生长、形态、周期、软琼脂集落形成能力以及c-myc基因表达方面观察其恶性和表型的改变。结果：L6565as细胞形态变圆,大小较一致。生长曲线显示:L6565as细胞生长被抑制;流式细胞仪检测细胞周期：L6565as阻滞于G₀/G₁期,S期细胞减少;软琼脂集落形成试验发现L6565as细胞形成克隆数明显减少。免疫组化检测：L6565as细胞c-myc蛋白表达呈弱阳性,而对照组细胞呈强阳性。结论：c-myc基因在L6565小鼠白血病的发生中起着重要的作用;抑制c-myc的表达,可部分逆转L6565白血病的恶性表型和恶性行为。     

Regulation by protein kinase of phagocytosis of Mycobacterium leprae by macrophages

Mycobacterium leprae multiplies within host macrophages. The mechanism of internalisation of the bacteria by the phagocytic cells is unknown. In this study, M. leprae was purified from the foot pads of experimentally infected nu/nu mice. Peritoneal macrophages were harvested from BALB/c mice or C57 beige (bg/bg) mice. The effect of protein kinase inhibitors (erbstatin, genistein or staurosporine for BALB/c and bg/bg mice, plus herbimycin for bg/bg mice) on phagocytosis of the mycobacteria by the macrophage monolayers was tested. The untreated (control) macrophages phagocytosed M. leprae. Phagocytosis by BALB/c macrophages was inhibited by erbstatin and staurosporine but not by genistein; all the protein kinase inhibitors prevented uptake of M. leprae by bg/bg cells. The results demonstrate that protein kinase regulates phagocytosis of M. leprae by macrophages. The mechanism might prove to be a rational drug target for mycobacteria that multiply intracellularly.     

Modification by environmental conditions of retrograde amnesia produced by ECS

A single ECS following one trial appetitive learning produced retrograde amnesia after 24–72 hr in rats housed individually in a colony during the ECS-retention trial interval. In animals given the same treatment procedures and housed individually in a dark chamber with a constant level of background noise, no retrograde amnesia following ECS was noted. These results suggest that varying environmental conditions during the ECS-retention interval may eliminate or enhance retrograde amnesia. Further, these deficits in retention appear to be retrieval deficits which are associated with events producing brain dysfunction and loss of retention.     

Induction of immunodeficiency by benzene and its correction by anabol

All-Union Research Institute of Biotechnology, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 105, No. 4, pp. 457–459, April, 1988.     

Prevention by curantil of damage to the myocardium by isoproterenol

Experiments on sexually mature albino rats showed that a single subcutaneous injection of isoproterenol caused electrocardiographic and ultrastructural changes in the myocardium characteristic of ischemia and necrosis of the heart muscle and disturbances of its contractile function. Preliminary administration of curantil for 3 days to sexually mature rats in a dose of 10 mg/kg had a marked protective action on the myocardium against damage produced by isoproterenol.Department of Human Anatomy and Department of Pharmacology, Ivano-Frankovsk Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR S. V. Anichkov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 11, pp. 546–548, November, 1978.     

Attraction of phagocytes by apoptotic cells is mediated by lysophosphatidylcholine

Apoptotic cells promote the phagocytosis of themselves via the exposure of "eat me" signals. Furthermore, a second, "find me" signal is required to attract phagocytes. In this review the double function of lysophosphatidylcholine for the clearance of apoptotic material as factor leading to attraction of phagocytes as a soluble "find me" signal and opsonisation of apoptotic cells as a membrane bound "eat me" signal is outlined. Lysophosphatidylcholine, exerting this bivalent function, leads to a sufficient clearance of apoptotic cell as a "keep calm" mechanism to prevent activation of the immune system by secondary necrosis.     

Attraction of phagocytes by apoptotic cells is mediated by lysophosphatidylcholine

Apoptotic cells promote the phagocytosis of themselves via the exposure of “eat me” signals. Furthermore, a second, “find me” signal is required to attract phagocytes. In this review the double function of lysophosphatidylcholine for the clearence of apoptotic material as factor leading to attraction of phagocytes as a soluble “find me” signal and opsonisation of apoptotic cells as a membrane bound “eat me” signal is outlined. Lysophosphatidylcholine, exerting this bivalent function, leads to a sufficient clearance of apoptotic cell as a “keep calm” mechanism to prevent activation of the immune system by secondary necrosis.