腮腺非皮脂腺淋巴腺瘤2例并文献复习

目的：探讨非皮脂腺淋巴腺瘤( nonsebaceous lymphadenoma, NSL)的临床病理学特征、诊断及鉴别诊断。方法分析2例NSL的临床病理学特征、组织学形态及免疫表型并复习相关文献。结果2例NSL均为成年女性。镜检：肿瘤主要由上皮成分及间质增生的淋巴组织混合形成,与周围腮腺组织界限清楚,由纤维结缔组织分隔,间质内可见增生的淋巴滤泡。上皮成分可由囊腔、实性岛状、梁状或腺管样结构组成,其中囊腔及腺管样结构由两种细胞成分构成,腔面细胞及外层细胞,囊腔内含伊红不定形物及偶见的泡沫细胞,上皮细胞无皮脂腺分化,形态温和,无非典型性,未见核分裂象。其中1例见完整的纤维被膜包绕整个肿瘤,被膜下见窦结构。免疫表型：上皮细胞CK(AE1/AE3)和CK7阳性,囊腔、腺管样结构的外层细胞p63、CK34βE12和CK5/6阳性。结论 NSL是一种罕见的涎腺良性肿瘤,位于淋巴结内的病变报道较少,组织学结构的多样性使其易与一些涎腺病变相混淆,与一些恶性肿瘤的鉴别尤为重要。     

急性缺血损伤的心肌细胞对心肌毛细血管形态变化的影响

通过结扎狗的冠状动脉前降支,电镜下观察急性缺血时,损伤的心肌细胞对其偶联的毛细血管形态结构变化的影响。观察的结果发现,与不可逆损伤的心肌细胞相偶联的毛细血管被拉长变细,而过度收缩的心肌细胞所偶联的毛细血管则变为腊肠分节状。同时,肌膜水肿,形成囊泡,挤压毛细血管内皮突入管腔。由于上述这些变化,造成了毛细血管管腔的狭窄或阻塞。     

SARS-CoV功能性受体血管紧张素转换酶2在灵长类动物肾脏上皮细胞的表达(英)

目的：研究血管紧张素转换酶2 (ACE2) 在灵长类动物肾脏上皮细胞上的表达。方法：体外培养非洲绿猴肾细胞Vero E6,利用RT-PCR及免疫细胞化学的方法检测细胞ACE2的表达;利用免疫组织化学方法检测2例恒河猴和2例正常人肾组织ACE2的表达分布。结果：RT-PCR显示,从Vero E6细胞提取的总RNA经逆转录可检测出ACE2的扩增条带;免疫细胞化学方法检测到Vero E6细胞胞浆内反应明显阳性;ACE2主要分布在恒河猴和人肾组织近端肾小管上皮细胞的管腔膜和胞浆。结论：ACE2在灵长类动物肾脏上皮细胞的核酸水平和蛋白水平均有表达,主要位于细胞的管腔膜和胞浆;肾脏上皮细胞表达的ACE2为SARS-CoV的入侵提供了条件,有可能是SARS患者并发肾功能损伤的原因之一。     

TRAF3抑制NF-κB引起的肾囊腔形成作用

目的:研究肿瘤坏死因子受体相关因子3(TRAF3)对多囊肾集合管上皮细胞中核因子κB(NF-κB)信号通路及其下游产物表达的影响;观察TRAF3基因过表达的多囊肾集合管上皮细胞形成管状分支结构的变化,探讨TRAF3在多囊肾囊腔形成的发生发展中可能产生的作用。方法:Western blot检测多囊肾集合管上皮细胞和TRAF3基因过表达多囊肾集合管上皮细胞中NF-κB信号通路的变化,同时检测下游凋亡因子Bax及Bid的表达及caspase-3活性变化;通过Annexin V-FITC/PI双染法检测各组细胞的凋亡情况;应用三维(3D)培养法观察多囊肾集合管上皮细胞形成管状分支结构变化的差异。结果:TRAF3的过表达能显著抑制多囊肾集合管上皮细胞中NF-κB信号通路的活性,使下游的Bax及Bid表达显著下调,细胞凋亡明显减少;TRAF3基因过表达多囊肾集合管上皮细胞管状分支结构较多囊肾集合管上皮细胞组明显增多。结论:TRAF3可能通过调节NF-κB信号通路降低Bax及Bid活性,抑制细胞凋亡,从而抑制多囊肾囊腔形成。     

SARS-CoV功能性受体血管紧张素转换酶2在灵长类动物肾脏上皮细胞的表达(英文)

目的:研究血管紧张素转换酶2(ACE2)在灵长类动物肾脏上皮细胞上的表达。方法:体外培养非洲绿猴肾细胞VeroE6,利用RT-PCR及免疫细胞化学的方法检测细胞ACE2的表达;利用免疫组织化学方法检测2例恒河猴和2例正常人肾组织ACE2的表达分布。结果:RT-PCR显示,从VeroE6细胞提取的总RNA经逆转录可检测出ACE2的扩增条带;免疫细胞化学方法检测到VeroE6细胞胞浆内反应明显阳性;ACE2主要分布在恒河猴和人肾组织近端肾小管上皮细胞的管腔膜和胞浆。结论:ACE2在灵长类动物肾脏上皮细胞的核酸水平和蛋白水平均有表达,主要位于细胞的管腔膜和胞浆;肾脏上皮细胞表达的ACE2为SARS-CoV的入侵提供了条件,有可能是SARS患者并发肾功能损伤的原因之一。     

大鸨胃的超微结构研究

目的：研究大鸨前胃及肌胃超微结构，为大鸨人工饲养提供理论基础。方法：超薄切片透射电镜观察。结果：在前胃粘膜柱状上皮细胞核上方分布着大量直径约0．2－0．8μm的致密颗粒，核周围可见许多泡状结构。前胃乳头内腔上皮细胞则为柱状粘液细胞，核上方胞质中充满着大量的粘原颗粒。深腺细胞根据核形态及线粒体结构差别可分两种.肌胃粘膜及直管腺上皮细胞的圆形核上方形成许多分泌颗粒，根据其分泌颗粒的结构分为两种细胞，一种分泌颗粒为均质圆形，另一种为纤维状的。两种细胞形成的分泌物参与类角质膜的形成，在腺管底部至粘膜表面 形成的类角质膜的超微结构有所不同。结论：大鸨胃具有较强的消化能力。     

分离的大鼠睾丸曲细精管体外重组的观察

将生后15天和20天大鼠的睾丸,去被膜后以胶原酶反复消化,使Sertoli细胞和生精细胞分离。以HamF-12无血清培养基培养子(35℃)5％CO_2温箱。经过19天的连续培养及光镜和电镜样品观察,发现分离的曲细精管上皮细胞经过贴壁生长期(培养后1～6天),形成单层培养细胞。再经索状生长期(培养后6～14天),由单层细胞变成致密的细胞索,并释放出有头尾结构的蝌蚪形精子样细胞。最后经管状生长期(培养第14天以后),细胞索发育成细胞团和类似曲细精管样的结构。光镜和电镜下见其中有管周细胞、Sertoli细胞和各级生精细胞。本文对分离的曲细精管上皮细胞在体外重组成小管样结构和体外精子发生,进行了讨论。     

肾脏AQP2表达及穿梭调节的分子机制

水通道蛋白是位于细胞膜或细胞内囊泡能够通透水的蛋白质分子 ,其中水通道蛋白 2 (AQP2 )主要分布于肾脏集合管主细胞的管腔侧膜及近管腔侧的胞浆囊泡内 ,是抗利尿激素敏感型水通道。抗利尿激素可调节肾脏集合管AQP2的表达及穿梭 ,在肾脏水平衡调节中起重要作用     

肾小管缺血再灌流损伤的形态学观察

本文用Wistar大鼠30只,随机分为正常对照（CON）组、单纯缺血（ISC）组、缺血再灌流3小时（I／R1）、6小时（I／R2）、12小时（I／R3）、24小时（I／R4）、48／小时（I／R5）、72／小时（I／R6）、1周（I／R7）和2周（I／R8）组。采用暂时夹闭左侧肾动静脉45分钟的方法来诱导肾脏I／R损伤。放血处死动物后,摘取左肾,制备石蜡切片和超薄切片,应用光镜和透射电镜进行观察。结果显示在ISC组肾小管上皮细胞肿胀,近端小管刷状缘和基底纵纹紊乱。I／R1组,肾小管上皮细胞有空泡变性,近端小管刷状缘脱落,细胞之间出现裂隙。I／R2及3组．肾血管内有脱落的细胞碎片和少量上皮细胞出现,并有均质管型和颗粒管型,肾小管管腔扩大。I／R4及5组近端小管和远端小管腔内脱落上皮细胞增多,管腔进一步扩张并有上皮细胞缺失。I／R6组,肾小管内脱落上皮细胞和管型明显减少,近端小管管腔缩小,管壁增厚。互／R7及8组未见肾小管内有脱落上皮细胞和管型,管腔与正常对照相似,但上皮细胞核数量有增加。缺血45分钟再灌流能引起肾小管可逆性损伤。     

假腺性神经鞘瘤

目的：探讨假腺性神经鞘瘤的临床和病理学特征,诊断与鉴别诊断及其发生原因。方法：对2例假腺性神经鞘瘤的组织形态和免疫组化表现进行观察与分析。结果：肿瘤组织具有通常型神经鞘瘤结构外,尚有类似上皮细胞衬覆的腺样或囊样腔隙特征,但衬覆腔隙的细胞下面无基膜存在,而与邻近的梭形瘤细胞移行;黏液和免疫组化CK、EMA、CEA染色均阴性,而S-100蛋白和MBP阳性,结论：衬覆腺样或囊样腔隙的细胞仍系神经鞘细胞,肿瘤内的腺样或囊样腔隙及其内衬覆有似上皮细胞的改变可能与肿瘤的变性有关。     

The sequential contractions of the rumen associated with eructation in sheep

1. The orderly sequential movements of the reticulum and the rumen were studied in conscious sheep by electromyography using enamelled stainless-steel wires implanted in various regions of the stomach wall and by recording mechanical changes within the various parts of the organ. Electrical activity of the rumen and/or pressure changes were related to eructation when the animals were at rest, feeding or ruminating.2. Secondary contractions of the rumen were found to originate in the ventral blind sac immediately following a primary contraction or independently. The wave of contraction originating in the ventral blind sac was seen to pass in a circular manner to the dorsal blind sac, the dorsal sac, the ventral sac and finally once more to the ventral blind sac. Eructation occurs at the end of the contraction of the dorsal sac. In each case, the time required to initiate the secondary cycle depended on the strength of contraction of the ventral blind sac.3. Sustained gaseous distension elicited numerous secondary contractions of the rumen concurrent with a lower frequency of reticular contractions. Although some secondary contractions were incomplete, all began with contraction of the ventral blind sac and were associated with eructation.4. Chemical stimulation of the rumen by fatty acids at pH 5.5-5.9 increased the ratio of secondary to primary contractions of the rumen to a varying extent depending on their initial rate.5. It was concluded that the seemingly random occurrence of a secondary cycle of the rumen was dependent on the activity of the ventral blind sac and its pattern could be altered by both mechanical and chemical stimulation.     

维生素E对慢性染镉肾小体滤过屏障超微结构损伤的保护作用

目的探讨维生素E(Vitamin E,VE)对慢性染镉小鼠肾小体滤过屏障超微结构损伤的保护作用。方法健康昆明种小鼠75只,体重28～32g,随机分3组:染镉组(CdCl 22mg/kg,皮下注射,每周2次,共3个月)、VE+镉组(染镉同时给VE 10mg/kg/天,灌胃)、正常对照组(注射等量生理盐水)。用透射电镜观察结合形态计量分析,研究经VE同时处理的慢性染镉小鼠肾小体滤过屏障的超微结构改变。结果染镉组肾小体滤过屏障的三层结构受损,与正常对照组相比,表现为毛细血管内皮增厚,血管系膜增生,血管球基膜增厚,基膜和内皮间有电子致密物沉积,足细胞次级突起间裂孔缩小和裂孔膜变薄等(P<0.001)。而VE+镉组滤过屏障的三层结构的上述变化明显减轻,形态接近正常(P>0.05)。结论VE可防止慢性染镉对肾小体滤过屏障的损害。     

The presence of a local immune system in the upper blind and lower part of the human nasolacrimal duct

The nasolacrimal duct is exposed to exogenous agents, including potentially harmful microorganisms, coming from the eye surface by the lacrimal sac, and from the nasal cavity by the inferior meatus of the nose. The upper blind and lower part of the human nasolacrimal duct were examined immunohistochemically to ascertain the presence and localization of immunoglobulin-producing cells and the epithelial expression of IgA, IgM, and IgG in order to verify the possible antimicrobial properties of this duct. IgA-, IgM-, and IgG-positive immunocompetent cells were recognizable in the lamina propria of the upper blind and lower part of the human nasolacrimal duct, while an evident immunoreactivity for sIgA, IgM, and IgG was demonstrated in the cytoplasm of the apical epithelial cells. The results suggest that all the effector components of the mucosal immune system are present in that area of the human nasal mucosa next to the opening of the nasolacrimal duct as well as in the human lacrimal sac.     

In vitro endothelial differentiation of long-term cultured murine embryonic yolk sac cells induced by matrigel

The yolk sac of an early mammalian embryo contains progenitors of hematopoietic cells and vascular endothelial cells. We established a cell line, YS4, from murine embryonic yolk sac 10 years ago. The line has been successfully cultured since then. To determine whether these long-term cultured yolk sac cells still have the potential to differentiate into endothelial cells, an in vitro model of yolk sac cell differentiation into tubeforming endothelial cells was established in the present study by culturing the yolk sac cells on basement membrane proteins (Matrigel). The results indicate that upon plating onto Matrigel, YS4 cells attach quickly, align in tandem, and form a complete network of capillary structures within 12 h. By using antibodies against the known components of Matrigel in a tube formation inhibition assay, we found that extracellular matrix proteins such as laminin, collagen IV, vitronectin, and fibronectin are the most important components in the Matrigel which induce the yolk sac cells to undergo endothelial differentiation. New basement membrane proteins are also required for the endothelial differentiation process, as indicated by the fact that base membrane protein synthesis inhibitor, D609, can block the differentiation process. Furthermore, our experiments revealed the involvement of several signal transduction pathways, such as protein kinase A, C and protein tyrosine kinase in this differentiation process.     

The ultrastructure of megakaryopoietic cells of the yolk sac and liver in mouse embryo

Megakaryopoietic cells in the yolk sac and liver of mouse embryos were examined by electron microscopy. At 10 days' gestation, yolk sac vitelline vessels contained a few free megakaryopoietic cells. On the basis of the development of demarcation membranes and granules, yolk sac megakaryopoietic cells were classified into three types: YM1, YM2, and YM3. The YM1 cells, which comprised 75% of the yolk sac megakaryopoietic cells, had poorly developed demarcation membranes and few granules in the cytoplasm. The YM2 cells had a developed demarcation membrane system around the nucleus and comprised 24% of the yolk sac megakaryopoietic cells. The YM3 cells, the rarest type, had an eccentrically located nucleus and a cluster of demarcation membrane structures. In the liver of 11-day embryos, immature megakaryopoietic cells were present in both the sinusoidal lumen and the hepatic cords. Most of the hepatic megakaryopoietic cells of 11-day embryos had ultrastructural features similar to those of YM1 cells or intermediate between YM1 and YM2 cells.     

Southern society of anatomists prgram and abstracts presented at the. XIX annual meeting

The permeabilities of the parietal yolk sac placenta and the preplacental region of the hamster conceptus during early postimplantation (day 8) were compared by means of electron microscopy and a macromolecular protein tracer, horseradish peroxidase (HRP). HRP was administered by injection into the maternal venous system; samples of the two placental tissues were obtained for examination at intervals between 4 minutes and 1 hour later. The three layers of the parietal yolk sac wall (from outer to inner: capsular trophoblast, Reichert's membrane, parietal endoderm) appeared to provide little impediment to the passage of HRP from perivitelline maternal blood spaces to the yolk sac cavity. HRP passed through the outer trophoblast layer, both by way of intracellular fenestrae (60-200 nm diameter) and narrower intercellular channels, and completely permeated the meshwork of Reichert's membrane within minutes after injection. The inner parietal endoderm cell layer was widely discontinuous and clearly presented no barrier to HRP movement. HRP reaching the yolk sac cavity was avidly endocytosed by the visceral yolk sac epithelium. In contrast to the parietal yolk sac, the preplacental region of the conceptus was impermeable to HRP. Zonular occluding junctions located between contiguous cells of the chorionic ectoderm layer of the preplacenta were the obvious barrier to the HRP molecules. These results suggest that in this rodent species, during the early postimplantation period of gestation, the parietal yolk sac placenta potentially plays a more important role in the maternal-embryonic transfer of macromolecular substances than does the preplacenta.     

The mode of action of ochratoxin A in acute enteritis in rats

The mode of action of ochratoxin A(OCT A) was studied in male Wistar rats in connection with the development of acute enteritis. Acute enteritis in the duodenum and jejunum identical with that induced by oral administration was also induced by parenteral application at the dose level of 15 mg/kg OCT A and was completely inhibited by ligation of the choledochus. Direct application of OCT A into the jejunal blind sac lumen constructed by two ligations induced severe inflammation in situ and also revealed remote action to the duodenum and jejunum where separated from the blind sac by ligation. This remote action was inhibited by ligation of the choledochus. These results clearly demonstrated the enterohepatic circulation of OCT A. The ileal injection also revealed remote action of OCT A, although no pathologic change was caused in the ileal mucosa. The results obtained suggest that the enteritis may be induced by direct exposure of OCT A to the intestinal mucosa without metabolic activation, although certain participation of ochratoxin alpha to accelerate the inflammation was suspected.     

The permeability of the guinea pig parietal yolk sac placenta to peroxidase and ferritin

The permeability of the guinea pig parietal yolk sac placenta late in gestation was investigated by means of electron microscopy using the tracer proteins ferritin and peroxidase. The parietal yolk sac consists of a layer of trophoblast, a thick extracellular lamina (Reichert's membrane) and a layer of endoderm. After injection into the maternal vascular system, the proteins crossed the trophoblast by means of small pinocytotic vesicles. Both proteins readily permeated Reichert's membrane and then moved by an intercellular pathway between endoderm cells to reach the uterine lumen. After injection of ferritin into the uterine lumen, the protein was observed between endoderm cells and throughout Reichert's membrane. Presumably the marked permeability of the endodermal epithelium to the tracer molecules is due to the absence of zonulae occludentes around the endoderm cells. Parietal endoderm cells exhibited limited pinocytotic activity regardless of the site of injection. The results indicate that the parietal yolk sac placenta of the guinea pig is permeable to relatively large molecules and therefore it may be an important pathway in overall maternal-fetal exchange in this species.     

Functional morphology of blind and other processes in the lymph capillary system

"Blind" lymph capillaries of the diaphragmatic tendon center were studied in normal rabbits and after injections of India ink, yellow cadmium, chicken erythrocyte suspensions, and whole chicken blood into the abdominal cavity. Three groups of blind capillaries differing by morphological and functional signs were distinguished. Some blind capillaries can deposit foreign particles. The process of intracapillary endothelial growth is described.     

Is the capacity of lead acetate and cadmium chloride to induce genotoxic damage due to direct DNA-metal interaction?

Even though the toxic effects of lead and cadmium compounds have been studied over many years, inconsistent results have been obtained about their mutagenic, clastogenic and carcinogenic properties. However, these metals are considered to be potential human carcinogens. The mechanism of metal-induced carcinogenesis is still unknown, but one possible pathway may involve the interaction of metals with DNA, either directly or indirectly. In this work we explore the capacity of lead, cadmium or a mixture of both metals to interact with acellular DNA, by employing a variant of the comet assay. Our results, using low non-cytotoxic metal concentrations (0.01, 0.1 and 1.0 microM) with the standard protocol for the acellular assay, showed an induction of DNA damage in cells of all organs studied; however, basal DNA damage was different in each organ. To confirm that we were working with pure DNA, proteinase K was added to the lysis solution. With this enriched-lysis solution we found a negative response in the induction of DNA damage in cells derived from the liver, kidney and lung of CD-1 male mice. To support the results obtained by the enriched-acellular assay, we studied the capacity of lead and cadmium (0.1 microM) to induce breaks in pooled genomic DNA in cells of the same organs, with negative results. Consistent with these findings, these metals do not induce DNA breaks in the plasmid pUSE amp+. On the whole, we did not detect direct induction of DNA strand breaks by lead acetate, cadmium chloride or a mixture of both metals, all at low non-cytotoxic concentrations. However, we found an induction of lipid peroxidation and an increase in free radical levels in the different organs of CD-1 male mice after inhalation of lead acetate (0.0068 microg/cc) or cadmium chloride (0.08 microg/cc) for 1 h, suggesting the induction of genotoxicity and carcinogenicity by indirect interactions, such as oxidative stress.