阿苯达唑和甲苯达唑对蛔虫和钩虫作用的超微结构观察

在体个美洲钩虫成虫接触药物后活动性明显下降，体表皱缩，随着作用时间延长，蠕动缓慢，咽收缩无力并且不规律，体态膨胀不均匀，４８小时虫体趋于不动。药行对体内蛔虫和体外钩虫作用的超微结构显示：微绒毛变性且部分消失；肠细胞分泌颗粒积聚并融合，出现自噬空泡，糖原减少，线粒体一。蛔虫卵细胞间出现溶酶体，子宫细胞内质网疏松，分泌颗粒融合，糖原缺乏；精细胞充满蜜小体，线粒体广泛变性。未见钩虫生殖细胞超微结构明显     

三氯苯达唑对卫氏并殖吸虫体壁及卵黄细胞超微结构的影响

目的： 观察三氯苯达唑在体内外杀灭卫氏并殖吸虫后, 虫体体壁及卵黄细胞超微结构的变化。方法：将被药物在体内、外杀死的虫体及对照组正常虫体, 按常规方法制成电镜样品, 用扫描和透射电镜观察。结果： 在药物作用下, 体壁的外质膜及基质层裂解消失, 肌肉层有不同程度的坏死, 皮层细胞膜及卵黄细胞膜破坏消失,核膜部份破坏, 核内异染色质凝固、聚边、直至溶解。胞质内的高尔基体消失, 内质网扩张, 线粒体肿胀变性、直至溶解,但对糖原颗粒无明显影响。对体内虫体的破坏比体外严重。结论： 三氯苯达唑对卫氏并殖吸虫的体壁及卵黄细胞均有明显的破坏作用, 主要破坏细胞核、细胞的膜质结构以及微管系统, 并可使虫体皮层裂解消失。     

伊维菌素和阿苯达唑伍用驱除肠道线虫感染的效果观察

目的 观察伊维菌素和阿苯达唑伍用治疗肠道线虫感染的效果。方法 采用国产伊维菌素伍用阿苯达唑(6mg 200mg)(14岁以下儿童剂量减半)分别治疗蛔虫、钩虫、鞭虫、蛲虫感染者，同时用阿苯达唑400mg治疗钩虫、鞭虫感染者、用伊维菌素12mg治疗钩虫、蛲虫感染者作为对照。结果 伊维菌素伍用阿苯达唑治疗蛔虫、钩虫、鞭虫、蛲虫感染者的虫卵阴转率分别为100．00％(30／30)、86．67％(26／30)、88．24％(30／34)和97．62％(41／42)；阿苯达唑对照组钩虫和鞭虫的虫卵阴转率分别为70．58％(24／34)和47．06％(16／34)，伊维菌素对照治疗组钩虫、蛲虫虫卵阴转率分别为46．15％(12／26)和57．14％(16／28)。伊维菌素伍用阿苯达唑的不良反应发生率低而轻，对血象、肝肾功能和心电图无明显影响。结论 国产伊维菌素伍用阿苯达唑治疗钩虫、鞭虫、蛲虫感染效果显著，对鞭虫疗效明显优于阿苯达唑，对钩虫、蛲虫疗效明显优于伊维菌素，并且有排虫快、不良反应少而轻等优点。     

丙氧达唑治疗钩虫,蛔虫和鞭虫感染的效果

采用双盲法观察丙氧达唑每天15mg/kg×3d治疗钩虫、蛔虫和鞭虫感染者340、196和178例的效果。其钩虫、蛔虫和鞭虫卵阴转率分别为70.3～80.6、92.5～97.8和67.0～71.0％。十二指肠钩虫和美洲钩虫幼虫的阴转率分别为77.7和83.2％。钩虫卵减少率为98.1～98.6％。口服噻嘧啶每天10mg/kg(基质)×3d后,上述三种虫卵的阴转率依次为73.5、90.0和28.8％,钩虫卵减少率为98.8％。口服安慰剂后,上述三种虫卵的阴转率依次为6.5、29.7和7.9％。服药后均未发现严重不良反应。     

阿苯达唑对猪带绦虫损伤作用的超微结构观察

为研究阿苯达唑对猪带绦虫的杀伤机理。用药物驱虫,ＴＥＭ观察。结果表明,阿苯达唑对猪带绦虫有较强的损伤作用,主要表现在两个方面：（１）皮层的损伤：表现为远端胞质区表面的微毛断裂、脱落或隆起呈囊泡样;胞质区内杆状器消失,线粒体、内质网等肿胀,呈空泡样,并出现多个大的坏死区,核周胞质（皮层细胞）变性、肿胀,细胞核异形性变、出现多个切迹;核质浓缩、致密度增高或溶解,胞质内线粒体肿胀、结构不清,或嵴消失呈空泡样,胞质中其它细胞器减少,呈现大量囊泡;（２）实质的损伤：实质浅层的环肌束及纵肌束排列紊乱、扭曲、断裂或溶解;线粒体肿大,嵴消失,代之以较大的空泡;实质深层的实质细胞肿胀、变性、核周隙增宽,细胞器减少。支持细胞内糖原减少或消失,脂滴增多     

阿苯达唑糖片驱除肠道线虫的现场观察

蛲虫感染者顿服阿苯达唑糖片１００ｍｇ１３５例、２００ｍｇ，２ｄ分服３２１例，治后３ｗｋ复查肛周虫卵全部阴转。蛔虫、钩虫和鞭虫感染者分别服用该药３００ｍｇ和４００ｍｇ两个剂量组的虫卵阴转率依次为蛔虫９９．４％（４６６／４６９）和９９．８％（４８７／４８８）、钩虫９６．８％（９１／９４）和９４．３％（９９／１０５）及鞭虫５３．４％（２２８／４２７）和７６．３％（３７０／４８６）。排出蛲虫、蛔虫和钩虫成虫最多的依次为１９４条、８８条和５８８条。其排虫高峰时间依次为ｄ２－３、ｄ３－５和ｄ２－４，而鞭虫排虫较少，平均排出虫体仅４．３条。表明该药对蛲虫、蛔虫和钩虫的疗效均佳，而对鞭虫的效果较差。本品副反应轻微，不需特殊处理，味道甜，服用方便，易被患者接受。     

阿苯达唑和氟苯达唑对旋毛虫作用的形态学,组织学及组织…

应用形态学、组织学及组织化学方法，观察比较阿苯达唑、氟苯达唑对旋毛虫幼虫的杀虫作用机制。实验结果表明两种药物作用机制同，均使旋毛虫囊包破坏，虫体破损，囊包炎性细胞浸润，终至虫体被完全机化；对糖代谢有明显干扰作用，对酸性磷酸酶、碱性磷酸酶活性无变化。     

复方阿苯达唑驱除肠道线虫的现场观察

目的：观察复方阿苯达唑（每片含阿苯达唑６７ｍｇ和噻嘧啶８３．３ｍｇ基质）的驱虫效果。方法：对成人钩虫感染者１８６４例、蛔虫感染者１５６８例和鞭虫感染者１７８５例及儿童蛲虫感染者３７３例，随机分组，比较服用单剂复方阿苯达唑３片或２片与单剂阿苯达唑４００ｍｇ或噻嘧啶３０ｍｇ（含基质１０ｍｇ）／ｋｇ的驱虫效果和副作用。结果：成人复方阿苯达唑３片和２片的虫卵阴转率，钩虫分别为６５．０％和５２．７％（Ｐ＜０．０１），蛔虫均为１００％，鞭虫分别为２６．５％和１９．２％（Ｐ＜０．０１）。３片的驱钩虫效果显著优于阿苯达唑和噻嘧啶组（Ｐ均＜０．０１）。２片的驱钩虫效果亦优于噻嘧啶（Ｐ＜０．０１），与阿苯达唑无显著性差异，但驱鞭虫效果低于阿苯达唑。２－６岁儿童服复方阿苯达唑１．５片的，蛲虫卵阴转率为１００％，显著优于噻嘧啶（Ｐ＜０．０１）。复方阿苯达唑的驱虫作用快速，副作用轻，对血象、肝肾功能和心电图无显著影响。结论：复方阿苯达唑具有阿苯达唑和噻嘧啶两药的协同作用。     

吡喹酮、阿苯达唑和甲苯达唑对小鼠细粒棘球蚴生发膜超微结构的影响

小鼠感染的细粒棘球蚴囊经吡喹酮、阿苯达唑和甲苯达唑治疗后,其生发膜的超微结构均示有广泛的变化,主要是皮层基质变性、溶解和空泡变化;皮层细胞核周胞质的溶解、空泡形成,线粒体密集、变性、肿大,间质及肌束的广泛或局灶性溶解,以及囊腔面的溶解和脱落。甲苯达唑和阿苯达唑尚可引起角质层的损害及核染色质减少等。     

伊维菌素和阿苯达唑伍用驱除肠道线虫感染的效果观察

目的 观察伊维菌素和阿苯达唑伍用治疗肠道线虫感染的效果。方法 采用国产伊维菌素伍用阿苯达唑(6mg+200mg)(14岁以下儿童剂量减半)分别治疗蛔虫、钩虫、鞭虫、蛲虫感染者,同时用阿苯达唑400mg治疗钩虫、鞭虫感染者、用伊维菌素12mg治疗钩虫、蛲虫感染者作为对照。结果 伊维菌素伍用阿苯达唑治疗蛔虫、钩虫、鞭虫、蛲虫感染者的虫卵阴转率分别为100.00％(30/30)、86.67％(26/30)、88.24％(30/34)和97.62％(41/42);阿苯达唑对照组钩虫和鞭虫的虫卵阴转率分别为70.58％(24/34)和47.06％(16/34),伊维菌素对照治疗组钩虫、蛲虫虫卵阴转率分别为46.15％(12/26)和57.14％(16/28)。伊维菌素伍用阿苯达唑的不良反应发生率低而轻,对血象、肝肾功能和心电图无明显影响。结论 国产伊维菌素伍用阿苯达唑治疗钩虫、鞭虫、蛲虫感染效果显著,对鞭虫疗效明显优于阿苯达唑,对钩虫、蛲虫疗效明显优于伊维菌素,并且有排虫快、不良反应少而轻等优点。     

日本血吸虫病与肠线虫病联合化疗的效果

血吸虫病人合并感染肠线虫者(A组)采取;吡喹酮40mg/kg加阿苯达唑200mg和复方甲苯咪唑400mg(尚含左旋咪唑100mg)分2d顿服,1个半月后血吸虫阴转率88.0％,蛔虫、鞭虫和钩虫阴转率分别为77.4％、23.6％及100.0％。对不合并血吸虫病的肠线虫病患者采取两种联合化疗方案:B组—阿苯达唑200mg和复方甲苯咪唑200mg(尚含左旋咪唑50mg)顿服,蛔虫、鞭虫和钩虫的阴转率分别为66.7％、18.8％和62.5％,较A组结果稍低;C组—阿苯达唑100mg和噻嘧啶900mg顿服的驱虫效果差,蛔虫和鞭虫的阴转率分别为50.0％及11.1％。3种驱虫方案对血吸虫和蛔虫的减卵率可达97.0％～99.9％;对钩虫的减卵率达68.9％～100％;对鞭虫的效果差。相应增加药物的剂量及改进服法,当可提高疗效。     

Histology of islets of langerhans of the obese-hyperglycemic (ob/ob) mouse and changes with alloxan and streptozotocin

Summary The islets of Langerhans in the obese homozygous mutant (ob/ob) saline-control mice were markedly increased in the size and total cell numbers over those of lean controls. There was marked degranulation of B-cells, but with still present β-granules in some cells, enlarged swollen mitochondria, vesicular endoplasmic reticulum, dilated Golgi, and the presence of many tightly-bound secretory granules. There were many lysosomes and much osmiophilic material (probably lipid) in many B-cells. A-cells showed slight degranulation and dilated endoplasmic reticulum. Six weeks after a single dose ofalloxan, there was degranulation and increased numbers of tightly-bound granules, swollen mitochondria, minimal dilatation of endoplasmic reticulum, and many lipid bodies and lysosomes in B-cells. Six weeks after administration ofstreptozotocin, there was marked degranulation of many cells, with some persisting β-granules, markedly vesiculated and dilated rough endoplasmic reticulum, swollen degenerating mitochondria, and many tightly-bound granules in B-cells. Degenerative changes were present in occasional A-cells, characterized by empty vacuoles and dilated endoplasmic reticulum. The presence of numerous membrane-bound vesicles, many immature β-granules and proliferations of Golgi and endoplasmic reticulum indicate attempt at recovery of function in the streptozotocin-treated obese mouse. However, the association of numerous empty endoplasmic cysts and vesicles and the persisting significantly fewer B-cells, as compared with saline- or alloxan-treated obese mice (p⩽0.05), points to lack of recovery from the toxic insult after six weeks. Islet hyperplasia and degranulation, accompanied by evidence of accelerated formation of secretion products of B-cells, as well as enlarged bizarre mitochondria, are anatomic support for accelerated insulin turnover as a response of the islets of Langerhans of the obese mouse to an insulin stimulatory factor. A-cell changes were probably secondary to hyperglycemia. Traduzione a cura degli AA.     

甲苯达唑、阿苯达唑和吡喹酮对继发性细粒棘球蚴囊液游离氨基酸含量的影响

对感染了继发性细粒棘球蚴的小鼠，于吡喹酮（Ｐｒａ）５００ｍｇ／ｋｇ／ｄ、甲苯达唑（Ｍｅｂ）２５ｍｇ／ｋｇ／ｄ或阿苯达唑（Ａｌｂ）３００ｍｙｋｇ／ｄ治疗１４天后，取包囊液测定了其中１８种游离氨基酸的含量，发现吡喹酮组小鼠囊液中有２种氨基酸的浓度高于对照组，有３种氨基酸的浓度低于对照组。而甲苯达唑组和阿苯达唑组囊液中的氨基酸浓度均低于对照组，其中各有１４种和１３种氨基酸含量明显低于对照组，表明甲苯达唑和阿苯达唑可干扰细粒棘球蚴囊的氨基酸代谢。     

Pituitary physiological and ultrastructural changes during aging

Although it is known that both aged human beings and animals exhibit a decrease in pituitary hormone production and release, there is controversy about the true nature of these changes. Whereas some authors postulate an extra pituitary cause, i.e., a dopaminergic failure, others consider that the problem is at the level of the gland itself. CFW mice 2, 6, 12 and 18 months old, were i.p. inoculated withL: -Dopa. The pituitary gland was removed and sectioned, then observed and photographed in an electron microscope. Photomicrographs were scanned into a computer and digital image analysis made to determine secretory granules and organelle kinetics. Normal GH and TSH cells of elder mice responded to stimulation withL: -Dopa in a similar way as did cells of juveniles. The responsiveness rate of those cells to the amine precursor during the first hour of treatment was 38±3.5% and 26±0.3% of the studied cells in young and aged animals, respectively. Fully functional cells, i.e., GH and TSH cells showing 5 to 90% of their cytoplasm occupied by secretory granules (some of them immature), with a developed RER, and with absence of cell damage, were seen to be reduced from 98% in younger to 65.7% in aged animals. In successive steps, cells showed cell desquamation, darkened cytoplasm, differential swollen endoplasmic reticulum without secretory granules, increased number of secondary lysosomes (more than two per cell in a cross-section), differential swollen mitochondria, cytoplasm only containing two to five giant secondary lysosomes and finally, a complete loss of cell architecture. Therefore, GH and TSH cells at the end of their life-span were seen to derive into apoptotic images. In the whole gland, an increasing number of those pathologic images were seen as aging proceeded, thus reducing the number of normal and productive cells. From the results presented here it is proposed that an extrapituitary failure is insufficient to explain the reduced production of GH and TSH, and that the problem evolves also at the level of the gland itself.     

伯氏疟原虫氯喹敏感株和抗性株在疟色素形成和致病性上的差异

目的：研究伯氏疟原虫氯喹敏感株（Ｎ）和抗性株（ＲＣ）在疟色素形成和致病性上的差异。方法：用伯氏疟原虫氯喹敏感株和抗性株分别感染ＩＲＣ小鼠。实验分为５组：正常对照组（ＮＣ）,氯喹治疗对照组（ＣＣ）,Ｎ株感染组（Ｎ）,ＲＣ株感染组（ＲＣ）和ＲＣ株感染加氯喹治疗组（ＲＣＣ）,比较各组间末梢血中疟原虫的形态、原虫血症、肝脏组织学及超微结构的改变。结果：Ｎ组肝细胞损害较严重,细胞内线粒体肿胀融合,溶酶体增多,肝血窦内疟原虫少见。ＲＣ组炎症反应较突出,主要为单核细胞浸润以及枯否细胞活跃,大滋养体和裂殖体在肝血窦滞留;肝细胞损害较轻,表现为线粒体增生、肿胀及空泡化。Ｎ株疟原虫富含内食物泡,其内有疟色素颗粒,被寄生红细胞结构较完整;而ＲＣ株疟原虫外食物泡较多,位于疟原虫外围的红细胞胞质内,被寄生的红细胞呈蜂窝样改变,食物泡内无疟色素。结论：ＲＣ株疟原虫可能改变了原敏感株（Ｎ株）对血红蛋白的摄取和消化方式,从而阻碍了疟色素形成;Ｎ株和ＲＣ株疟原虫可能因诱导宿主免疫反应的明显差异,导致ＲＣ株较Ｎ株致病力为弱     

The cellular response of saurian pancreatic islets to chronic insulin administration

Moderately degranulated pancreatic A cells were observed by light, phase, and electron microscopy after chronic insulin administration in the lizard Anolis carolinensis. The reduced granularity of A cells is presumably due to glucagon release in response to insulin-induced hypoglycemia. Secretion of glucagon is compatible with the observed reduction in glycogen content of the hepatocytes. The ultrastructural observations made during the periods of maximal A cell degranulation suggest a new interpretation of glucagon secretion. The salient feature of the proposed secretory mechanism is intracytoplasmic release of glucagon. Other ultrastructural changes appear to be associated with the secretory process. The two most prominent changes were: pleomorphic A granule profiles often exhibiting knoblike protuberances, and short, basal infoldings of the A cell plasma membrane abutting the capillary space. The role these changes might have in the release of glucagon is discussed.A, B, and D cells were identified by light, phase, and electron microscopy. With the light microscope, A cells were stained by phosphotungstic acid-hematoxylin, and Ponceau-acid fuchsin. B cells were aldehyde fuchsin positive. D cells were argyrophilic. With the phase microscope, A cells contained large, dense secretory granules; B cells had the smallest secretory granules of the three major cell types; and D cells had large granules which were less dense than A granules. With the electron microscope, A granules tended to be oval in profile, were electron opaque with a predominantly homogeneous matrix, and had a long axis of 700 to 800 nm. B granules were round to oval in profile, had a moderately electron opaque matrix with a central dense core, and were approximately 450 nm in diameter. D granules were large, approximately 650 nm in diameter, round in profile and moderately electron opaque. The matrix of D granules was separated from the limiting membrane of the granule by a narrow, electron lucent space. Using the above criteria, the islet cell population contained approximately 50% A cells, about 40% B cells, and 10–15% D cells.     

阿苯达唑、噻嘧啶治疗肠道线虫及控制钩虫感染回升的效果

采用阿苯达唑400mg/d×3d、400mg/d×5d和噻嘧啶1500mg/d×3d、1500mg/d×5d治疗肠道线虫感染者720例。治后半月检查,钩虫卵阴转率分别为98.6、98.6、86.2和93.5％;蛔虫卵阴转率分别为96.5、98.2、92.9和96.3％;鞭虫卵阴转率分别为86.4、89.0、68.9和67.0％。钩虫卵减少率均在98.0％以上。治后半年复查,各组钩虫阳性率均有不同程度回升,虫种由治前美洲钩虫为主,转为十二指肠钩虫为主。结果显示,回升的原因主要是十二指肠钩虫引起,而阿苯达唑400mg/d×3d和400ms/d×5d控制钩虫感染回升有明显作用。     

Edaravone Suppresses Reperfusion Injury following Leg Ischemia in Rats: A Transmission Electron Microscopic Study

It is well known that free radicals cause reperfusion injury following leg ischemia. We showed that the free radical scavenger, edaravone (Radicut, Mitsubishi Tanabe Pharma Co., Osaka, Japan), might suppress reperfusion injury in rat. In this study, we used transmission electron microscope (TEM) to investigate how edaravone suppresses reperfusion injury by focusing on glycogen granules in the lower extremity muscles. Male Lewis rats (582 ± 35 g) were intraperitoneally injected with edaravone (3.0 mg/kg, edaravone group, n = 5) or the same dose of saline (control group, n = 5). The rat reperfusion injury models were induced by clamping the bilateral common femoral arteries for 5 hours and then declamping. The muscles were harvested at 5 hours after the start of reperfusion. Under a TEM (JEM-1220, Nippon Denshi Co., Tokyo, Japan), we counted the number of glycogen granules at ×50,000 magnification on each five different fields. The TEM sections from the control group showed a marked loss of glycogen granules and swollen mitochondria. In contrast, the TEM sections from the edaravone group showed numerous glycogen granules and normal mitochondria. The mean density of glycogen granules in the edaravone group was significantly higher than that in the control group (88.5 ± 5.3 vs. 16.4 ± 3.1 particles/µm², p < 0.001). Our TEM results confirmed that edaravone suppresses reperfusion injury following leg ischemia by maintaining the glycogen granules in muscles.     

Morphological studies of the canine pituitary luteinizing hormone (LH) cells after long-term treatment with the LH-releasing hormone (LHRH) agonist [D-Trp6]LHRH ethylamide

Since treatment with LHRH agonists (LHRH-A) cause changes in LH secretion which are similar in both man and dog, we have studied cytological changes occurring in canine LH cells after chronic administration of an LHRH-A, [D-Trp6] LHRH ethylamide. At the light microscopic level, LH cells were distributed evenly in the gland, but showed a decrease in cell surface area of 10% after 1 month and 23% after 4 months of daily injection of 50 micrograms LHRH-A. At the electron microscopic level, the gonadotrophs from control animals were characterized by the presence of two types of secretory granules and a dilatation of the rough endoplasmic reticulum. Immunostaining for LH was localized only to secretory granules. LHRH-A administration caused the appearance of glycogen in the cytoplasm. Four months after cessation of the treatment, the gonadotrophs showed a normal cytological appearance, thus indicating full reversibility of the morphological changes induced by long-term treatment with an LHRH-A.