莪术油注射液致人卵巢癌SKOV3细胞胀亡形态变化研究

目的研究莪术油注射液对人卵巢癌SKOV3细胞形态学改变的影响。方法以不同的药物浓度作用人卵巢癌SKOV3细胞株后,采用光学显微镜和透射电镜观察卵巢癌SKOV3细胞形态学变化。结果光镜下可见莪术油低浓度组部分细胞体积开始变大,细胞胞浆空泡化,胞浆内出现致密颗粒,细胞核开始变形。细胞胞浆出现大面积的空泡,细胞核变形明显,细胞质出现颗粒脱落,出现细胞质空泡,核内染色质分散。高浓度组细胞肿胀,胞浆减少,核浆比例增加,细胞质大量颗粒脱落,细胞质空泡明显,有胞膜崩解、细胞核溶解;电镜下可见卵巢癌SKOV3细胞胀亡,且呈浓度依赖性。结论莪术油注射液诱导SKOV3细胞胀亡是其抑制肿瘤细胞生长的机制之一。     

莪术油注射液致人卵巢癌SKOV_3细胞胀亡形态变化研究

目的研究莪术油注射液对人卵巢癌SKOV3细胞形态学改变的影响。方法以不同的药物浓度作用人卵巢癌SKOV3细胞株后,采用光学显微镜和透射电镜观察卵巢癌SKOV3细胞形态学变化。结果光镜下可见莪术油低浓度组部分细胞体积开始变大,细胞胞浆空泡化,胞浆内出现致密颗粒,细胞核开始变形。细胞胞浆出现大面积的空泡,细胞核变形明显,细胞质出现颗粒脱落,出现细胞质空泡,核内染色质分散。高浓度组细胞肿胀,胞浆减少,核浆比例增加,细胞质大量颗粒脱落,细胞质空泡明显,有胞膜崩解、细胞核溶解;电镜下可见卵巢癌SKOV3细胞胀亡,且呈浓度依赖性。结论莪术油注射液诱导SKOV3细胞胀亡是其抑制肿瘤细胞生长的机制之一。     

微小泰泽球虫大配子发育与受精的超微结构

采用纯种微小泰泽球虫卵囊,人工感染四日龄雏鹅,定时剖杀,取小肠组织进行超薄切片,在透射电镜下观察微小泰泽球虫大配子体的发育与大、小配子的受精过程。大配子体由第二代裂殖子转变而来,在带虫空泡内发育。早期大配子体细胞核的浅层和周围均有多膜空泡分布。在大配子体的表面观察到了正待逸出的电子半透明空泡。成囊颗粒Ⅰ和Ⅱ先后出现,两者在分布、结构、大小及功能上均有明显不同。受精发生在卵囊壁形成之前。小配子的核和鞭毛均进入大配子,随后,小配子的核进入大配子的细胞核。没有观察到小配子鞭毛进入大配子的细胞核。     

锰对大鼠肝细胞,肾小管上皮细胞超微结构的损伤及锌的保护作用

大鼠每日腹腔注射15和30mg/kg硫酸锰及15mg/kg硫酸锰加20mg/kg硫酸锌,连续10天。电镜观察发现,染锰组肾小管上皮细胞内大量线粒体嵴溶解,膜破裂,半个甚至整个线粒体消失成透亮空泡,核内染色质凝聚;肝细胞内细胞器相对减少,局部挤压聚集,较外层的一些内质网和线粒体被损、消失,糖元积聚连接成片,并出现形态异常的细胞核,核内染色质凝聚,边集;染锰加锌组肝细胞和肾小管上皮细胞内的线粒体和内质网损伤均明显减轻,肝细胞内未见形态异常的细胞核及细胞器减少,但仍可见染色质凝聚现象。提示锌对锰引起的膜系统损伤有一定的保护作用。     

卡氏住白虫裂殖子和配子体的超微结构

卡氏住白虫(Leueocytozoon caulleryi的裂殖子和配子体是从天然感染鸡的外周血液、肝、脾及其他内脏组织采取。通过透视电镜观察其超微结构,裂殖子呈圆形或卵圆形,外包有两层膜,外膜较薄,内膜比较厚,内含有一个圆形或卵圆形的核,在核中央有一核仁、核酸糖小体、食物空泡,具有一个管状嵴的线粒体和1～2个脂类包含体。 卡氏住白虫雄性和雌性配子体都具有三层明显的膜,但成熟的配子体仅见到两层膜。雌雄配子体含有细胞核、核仁、核酸糖小体、食物空泡、管状嵴的线粒体、内质网、雄配子体较小而细胞核较大。雌配子体染色较雄配子体深,并含有较发达的内质网。     

髓核化学溶解术治疗腰痛和坐骨神经痛

髓核化学溶解术是将一种酶——木瓜凝乳蛋白酶注入到椎间盘内。自1963年开始用于临床以来。本法已治疗了12,000多名患者。椎间盘是由三个部分组成:(1)椎体的软骨内壁(透明软骨)。(2)纤维环,它是包绕髓核并附着于上下椎体缘的非常致密的成胶原纤维组成的一种网状物。(3)髓核,居于椎间盘的中央,它由薄层的成胶原纤维网和其空隙内充满富有水分的粘蛋白质凝胶组成。成年后,粘蛋白质发生解聚作用,髓核所含的水分逐渐减少。随着年龄的增长,椎间盘作为“减震器”的效用也逐渐降低。由于椎间盘间隙变狭,身高也随之有轻微的下降,椎体间的活动度有所增加。这一过程,称为“变性的椎间盘病变”。木瓜凝乳蛋白酶是从番木瓜乳液中分离出来的一种酶。此酶与髓核接触后,能使粘蛋白质发生     

成年人先天性巨结肠同源病的诊治

先天性巨结肠是在病变肠段内,肌间神经丛和粘膜下神经丛中的神经节细胞完全缺如,因此又称为无神经节细胞病。先天性巨结肠同源病是神经节细胞减少,未成熟、发育不全等。成年人出现腹胀便秘等临床症状的时间较晚,程度轻。现将我们遇到的五例报告如下:     

肝硬化胶原纤维分布特征及其形成机制探讨

本文采用免疫组化等方法,对150例肝硬化标本胶原纤维形成机制进行了探讨,结果表明,胶原纤维增生明显者呈带状分布,且向肝实质扩展形成假小叶结构,常伴有活动性病变,肝细胞坏死较明显,无活动性病变者,则胶原纤维束较细,肝细胞变性坏死较轻微。纤维连接蛋白免疫酶标提示在肝组织内沉积与肝内胶原纤维增生程度成平行关系。电镜观察发现,在活动性肝硬化纤维化区发现贮脂细胞形态异常,并向成纤维细胞转化而形成胶原纤维,说明肝内胶原纤维形成与其有关。     

热休克蛋白72在兔视网膜缺血再灌注损伤中的表达及重组人碱性成纤维细胞生长因子对其表达的影响

目的研究兔视网膜缺血再灌注损伤(RIRI)后重组人碱性成纤维细胞生长因子(rh-bFGF)对其组织中热休克蛋白(HSP)72活化程度的影响。方法选取66只大耳白兔,随机分为3组:缺血再灌注模型组(RIRI组30只)、rh-bFGF治疗组(RIRI+rh-bFGF组30只)、正常假手术组(6只),RIRI组、RIRI+rh-bFGF组又平均分为5个亚组(缺血再灌注后6、12、24、48、72h),每组6只大耳白兔。造模初期,RIRI组和rh-bFGF治疗组实验动物分别往玻璃体腔内注入相同剂量的0.9%氯化钠注射液和rh-bFGF溶液,并分别于制模后5个时间点处死动物摘取眼球,组织标本行苏木精-伊红(HE)染色及原位杂交。正常假手术组实验动物给予前房穿刺,无其他操作。常规HE染色后观察各组兔视网膜组织病理学变化,免疫组织化学法检测HSP72表达情况。结果正常假手术组兔视网膜各层次清晰、细胞平行排列且形态规则,视网膜神经节细胞呈单层排列、规则,无空泡变性。RIRI组兔视网膜出现高度水肿,层次紊乱、细胞结构疏松,视网膜神经节细胞出现空泡样变性,神经节细胞数目减少。RIRI+rh-bFGF组兔视网膜结构层次和细胞组织变化与RIRI组变化大致相同,但损害程度较其明显减轻。正常假手术组兔视网膜中没有发现HSP72;与RIRI组比较,RIRI+rh-bFGF组RIRI后5个时间点视网膜组织中HSP72的表达水平增高(P均<0.05)。结论 rh-bFGF对兔视网膜损伤有保护作用,其机制可能与上调HSP72的活化水平有关     

用尾核给药法研究γ-氨基丁酸选择性地抑制电刺激产生转头反应

γ-氨基丁酸(GABA)是中枢神经系统的抑制性递质,在脑的黑质、苍白球、基底神经节区含量最高,尾核和壳脑含量也较高。最近 Perry 等对 Huntington 舞蹈综合症尸检发现,基底神经节区 GABA 量不足。     

Localization of venom antigens in the venom gland of Vipera palaestinae using a fluorescent-antibody technique

Venom glands of the black widow spider were examined in the electron microscope. The venom-producing epithelial cells were found to be innervated by small axons from larger nerve trunks, penetrating the collagenous sheath surrounding the gland. The axons, which possess no glial sheath, are inserted between the epithelial cells, or occasionally invaginated into the cells in mesaxon-like folds. Axoplasmic contents showed a variety of neurosecretory products and electron-lucent vesicles. Regions of axoplasm with the structural characteristics of synapses were noted adjoining the epithelial cell membrane. The possible function of this nerve supply is discussed.     

Lectin binding pattern of schwann cells and macrophages in 2,5-hexanedione-induced axonal degeneration in rats

The lectin binding pattern of both Schwann cells and macrophages has been studied during axonal degeneration induced in the rat sciatic nerve by chronic administration of 2,5-hexanedione (0.8 ml/kg per day i.p. for 20 days). In particular, the present study aimed to establish a possible relationship between macrophage activation and expression of lectin binding sites. To identify and distinguish between Schwann cells and macrophages, electron microscopy was combined with the lectin staining method. On 2,5-hexanedione injury, a drastic disorganization of both axon and myelin sheath occurred and nerve fibers were replaced by a chain of ovoids. Besides the well-established concept that Schwann cells and macrophages cooperate in the removal of the myelin debris during axonal degeneration, evidence is presented that expression of binding sites to lectins is closely related to macrophage activation. Monocytes occasionally present in control nerves were labelled only by con A and sialidase-peanut sequence; in 2,5-hexanedione degeneration monocytes, prephagocytes (macrophages with minute bubbles) and phagocytes (macrophages with large bubbles) were labelled also by peanut, wheat germ and BSA I-B₄; moreover, phagocytes were labelled by soybean as well, thus showing a clearly differentiation-dependent binding pattern. Since changes in lectin binding pattern may reflect changes in complex carbohydrate structures, the results show that the expression of certain glycoproteins may be closely related to activation of macrophages in response to toxic injuries.     

人类外周神经在化学萃取前后的组织形态变化研究

目的研究人类外周神经在化学萃取前后的组织形态变化，探讨化学萃取法制备人类长段粗大去细胞神经的可行性。方法用TritonX-100和脱氧胆酸钠对人体长段胫神经作不同次数的萃取处理，经常规HE染色、砂罗铬花青、网状纤维组织化学染色和S-100免疫组织化学染色后，在光镜下观察神经萃取前后的组织形态变化，并比较不同萃取次数对神经结构的影响。结果人体长段胫神经经2次萃取后，其轴突、髓鞘、许旺细胞及其他结缔组织中的细胞均已消失，仅见网格纤维，而神经基底膜管、神经柬膜等纤维性支架保存完整，与未经萃取的神经相仿。萃取1次者仍残留少量细胞碎屑，而萃取3次者，细胞清除更彻底，但纤维性支架结构明显破坏。结论人类长段粗大神经干经化学萃取后不含细胞，而保留有完整的纤维性支架结构。化学萃取法制备人类长段粗大去细胞神经可行。     

Neuronal glia interactions at the vertebrate neuromuscular junction

Emerging studies demonstrate that perisynaptic Schwann cells (PSCs), which are the glia cells juxtaposed to the motor nerve terminal, actively participate in multiple aspects of the neuromuscular junction. During development, PSCs guide and promote synaptic growth. In adult muscles, PSCs can sense nerve stimulation by increasing intracellular calcium and are also capable of modulating transmitter release. Although adult PSCs are not required for acute synaptic maintenance and function, they are indispensable for long-term synaptic maintenance. Furthermore, PSC sprouts lead nerve terminal extension during synaptic remodeling. After nerve injury, PSCs sprout profusely and PSC processes guide regenerating nerve terminals. Future challenges will be to identify the molecular mechanisms by which PSCs interact with the nerve terminal and the muscle fiber.     

Structure and behaviour of hydrophilic matrix sustained release dosage forms: 1. The origin and mechanism of formation of gas bubbles in the hydrated surface layer

Gas bubbles are an important feature of the surface hydrated layer of hydrophilic matrix tablets in that they may significantly influence the performance of these dosage forms. Cryogenic SEM studies on the hydrated layer provide direct visual evidence for the origin and mechanism of formation of these bubbles. Air within the voids of the dry tablet core is observed to be progressively entrapped by swelling polymer particles within a partially hydrated region at the core/pseudogel interface, giving rise to discrete air pockets within the pseudogel layer.     

bFGF对断层皮片组织学变化影响的实验研究

目的:探讨应用外源性bFGF对实验断层皮片组织变化的影响。方法:建立豚鼠断层皮片自体移植模型。A组为对照组,B、C、D组为实验组,分别给予bFGF300Au/ml、600Au/ml、900Au/ml,术后第1、2、4周切取皮片,行常规组织学、电镜观察并计数真皮毛细血管数量与成纤维细胞密度值。结果:术后第1周,除A组外,各组均见毛细血管、成纤维细胞及胶原纤维增生,D组更显。术后第2周,B、C、D组毛细血管、成纤维细胞及胶原纤维增生。仍以D组更显,术后第4周,B、C、D组轻度毛细血管、成纤维细胞及胶原纤维增生,各组差别不明显。结论:外源性bFGF具有促进实验断层皮片毛细血管、成纤维细胞及胶原纤维增生的作用,并呈剂量依赖性。bFGF有利于皮片的念合及创面修复。     

牛磺酸对肾血管性高血压大鼠左室肥厚的保护作用

目的　观察牛磺酸 (Tau)对肾血管性高血压大鼠左室肥厚的影响 ,并探讨其机制。方法　建立二肾一夹 (2K1C)肾动脉狭窄性高血压模型。羟脯氨酸法测定大鼠心肌胶原含量 (MCC) ;放免法测定心肌AngⅡ (MAC)及Ald(MDC) ;原位杂交方法检测c fosmRNA表达 ;显微镜观察心肌组织结构改变并测量心肌纤维直径 (MFD) ,并进行线性相关分析。结果　 2K1C组大鼠MCC、MAC、MDC含量及MFD较Sham组增加 (P <0 0 1) ,c fosmRNA表达高于Sham组 (P<0 0 1) ;心肌冠状动脉周围胶原纤维大量增生并向周围间质延伸 ;相关分析显示MCC及MFD皆与MAC、MDC正相关 (P <0 0 1)。牛磺酸 (5 0mg·kg-1·d-1)治疗 8wk降低2K1C大鼠尾动脉收缩压 (SBP)、MAC、MDF及MCC(P <0 0 1) ,左心室 /体重比 (LVWI)、MDC及心室肌c fosmRNA表达量亦明显下降 (P <0 0 1) ,并抑制心肌冠脉周围胶原纤维增生。结论　牛磺酸可通过降低心肌局部RAAS活性及c fosmRNA表达 ,从而抑制心肌细胞肥大及胶原纤维增生 ,有效防治肾血管性高血压左室肥厚。     

黄体酮对视神经损伤大鼠视网膜神经节细胞微管相关蛋白-1B的影响

目的：观察并探讨黄体酮对视神经损伤早期视网膜神经节细胞微管相关蛋白-1B的影响,以期为黄体酮在视神经保护方面的作用提供实验依据。方法60只大鼠随机分为3组,每组20只。正常对照组不做任何处理,损伤1组制作右眼视神经夹伤模型,给予0)．9％氯化钠溶液腹腔注射,损伤2组制作右眼视神经夹伤模型,给予黄体酮腹腔注射。分别于损伤后1、3、7、14、28 d将3组大鼠右眼球摘除,取视网膜组织, HE染色光学显微镜观察视网膜形态学变化,并计数视网膜神经节细胞存活数量,免疫组织化学染色观察视网膜组织中MAP-1B在视网膜神经节细胞的表达情况。结果视神经损伤后损伤1组视网膜神经纤维层明显水肿,视网膜神经节细胞数目迅速减少,经黄体酮治疗的损伤2组视网膜形态改变轻微,视网膜神经纤维层轻度水肿,视网膜神经节细胞数目减少缓慢。损伤2组各时间段视网膜MAP-1B平均光密度值较损伤1组高,差异有统计学意义（ P ＜0．05）。结论黄体酮可以通过增加细胞骨架蛋白MAP-1B减轻视神经损伤早期视网膜神经节细胞的损害,对视神经及视网膜有保护作用。     

The effects of simvastatin on ischemia-reperfusion injury of sciatic nerve in adult rats

Severe ischemia to nerve results in fiber degeneration and reperfusion results in oxidative injury to endothelial cells and augments fiber degeneration. Statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, the most widely used lipid-lowering drugs, have been demonstrated to play a neuroprotective role. So we evaluated the effectiveness of simvastatin in protecting sciatic nerve from ischemia-reperfusion injury using the model of experimental nerve ischemia. Sixty adult male Sprague-Dawley rats weighing 250-300 g were used. They were divided into ten groups (N=6 per group). We used ischemia model in these groups by occluding the femoral artery and vein with a silk suture 6-0 using slipknot technique. All ischemia groups were rendered in ischemic for 3 h reperfused for various times of zero (0 h), 3 h (3 hour reperfusion), 7 days (7 day reperfusion), 14 days (14 day reperfusion). Half of the groups had experimental simvastatin (1 mg/kg) i.v. injection treatment via tail vein 1 h before ischemia. The other half experienced only ischemia-reperfusion as control groups. After euthanasia, histological samples were taken from distal part of the sciatic nerve. Sections were cut at 5 microm and then were stained with H and E and modified trichrome. We used H and E stain for edema and trichrome gomori for ischemic fiber degeneration. Samples were observed to assess their fiber degeneration and edema changes. By observation the level of fiber degeneration and endoneurial edema were also decreased in these recent groups (in both ischemia and reperfusion duration). In conclusion, pre-ischemic administration of simvastatin exhibits neuroprotective properties in ischemia-reperfusion nerve injury.     

浅表膀胱肿瘤汽化切除术中膀胱穿孔分析

目的探讨经尿道膀胱肿瘤汽化切除术（TVB t）中膀胱穿孔的原因及预防措施。方法总结分析158例经尿道膀胱肿瘤汽化切除术中11例膀胱穿孔病历。结果11例中,7例因闭孔神经反射发生腹膜外穿孔,其中6例未行闭孔神经阻滞;4例腹膜内穿孔,其中3例在处理膀胱顶部及前壁肿瘤时,汽化过深而出现,1例切除膀胱前壁肿瘤时,气泡爆炸引起。结论穿孔是TVB t手术的严重并发症,患侧闭孔神经阻滞,术中保持低压冲洗或保持回流水通畅,均能有效地避免或减少穿孔的发生;术中应及时排出汽化中产生的气体,或改变体位避开气泡,预防气泡爆炸的发生。