动物附红细胞体形态结构的研究

应用光镜和电镜对几种附红细胞体显微和超微结构观察显示：附本属典型原核生物,多数为环表,球形,卵圆形,杆状等多形态生物体,直径为０．２－２．６μｍ大小不等。常在红细胞表面或血浆中单个或成团寄生。该病原无细胞壁,由单层界膜包裹着,无明显细胞器和细胞核,部分附红细胞体尚见有一至数根细长的细丝结构。附红细胞体通过这些细丝在连接到红细胞膜上,使红细胞膜产生小而深的凹陷,导致红细胞结构和功能改变。     

猪附红细胞体病的防治

猪附红细胞体病是由猪附红细胞体又名红细胞孢子虫寄生于红细胞或血浆中而引起猪的一种原虫病,本病主要以高热、贫血、黄疸和全身发红为特征,可引起猪只特别是仔猪的大批死亡。1病原病原附红细胞体,属于立克次体目,无浆体科,附红细胞体属,寄生于红细胞内,也可游离在血浆中。猪附红细胞体呈环形、球形、椭圆形、杆状、月牙状、逗点状和     

猪附红细胞体对红细胞免疫水平的影响

为了探讨附红细胞体对红细胞免疫水平的影响,从河南省新乡市某猪场选取了4头感染附红细胞体阳性猪和4头无附红细胞体感染的健康猪,进行血涂片染色镜检,测定红细胞C3b受体花环率和红细胞免疫复合物花环率.结果显示:红细胞出现凹陷或变形,甚至形成空洞,这就有可能使其结构和功能发生改变,甚至出现破裂溶血现象.感染附红细胞体病猪红细胞C3b受体花环率和红细胞免疫复合物花环率都显著下降,说明附红细胞体侵袭红细胞的同时,破坏了红细胞膜表面的C3b受体,游离状态的C3b受体数量明显减少,导致机体红细胞的免疫黏附活性降低,红细胞免疫功能低下.红细胞免疫功能的破坏将直接或间接地影响到整个免疫系统功能的协调,从而使机体的抵抗力下降,为其他病原菌的侵入打开了门户.     

猪附红细胞体病的诊断和防治

附红细胞体病是由附红细胞体寄生于红细胞表面或血浆中而引起猪、牛、羊等共患的溶血性疾病，其中猪发生该病的报道占绝大多数。附红细胞体病病原体属于立克次体目、无浆体科、附红细胞体属，是一种多形态微生物。多为环形、球形和卵圆形，少数呈顿号形和杆状。病猪以高热、贫血或黄疸为主要特征，常与猪的其它疾病混合感染，给诊断和防治带来很大的困难。为此，必须准确诊断，科学防治。     

猪附红细胞体病的诊断与防制

附红细胞体病(Eperythrozoonosis)是由附红细胞体引起的一种人畜共患病,该病原属立克次氏体(Rickettsia organism)目无形体科附红细胞体(Eperythrozoon suis)属的成员。附红细胞体有14种,无固定形态,多数以单独或呈链状排列形式附着在红细胞表面,少数游离于血浆中。自1928年由Schilling在哺     

猪附红细胞体病的防治

附红细胞体病是由附红细胞体寄生于人和动物红细胞表面、血浆及骨髓内,引起的一种以贫血、黄疸、发热为主要症状的人畜共患病。该病不仅导致畜产品质量、产量降低,动物生育能力下降,而且可导致动物出现严重的临床症状,甚至死亡,阻碍畜牧业的发展,造成经济损失,必须科学防治。一、病原学分类附红细胞体的种类很多,多以寄生的宿主来命名。如牛附红细胞体、兔附红细胞体、犬附红细胞体,尤其猪附红细胞体报道占绝大多数。猪附红细胞体     

浅析猪附红细胞体病的诊疗与防治

<正>猪附红细胞体病又叫红皮病,是由寄生于猪红细胞或血浆中的附红细胞体引起的临床上以贫血、溶血性黄疸、发热、呼吸困难、皮肤发红和虚弱为特征的一种寄生虫病。附红细胞体病主要破坏猪体红细胞造成机体贫血,很容易引起继发感染。近年来本病在我国广泛流行,并继发或伴发其他疾病,如:猪瘟、猪肺疫、猪蓝耳等疫病,发病率和死亡率都很高,对养猪业的危害特别大。1病原附红细胞体病的病原是附红细胞体,一种能引起多种动     

猪附红细胞体病发生原因及诊治

附红细胞体病是由附红细胞体寄生于动物和人的红细胞表面或血浆中而引起的一种人畜共患传染病。临床上以发热、黄疸、高热不退为特征。     

犬附红细胞体病诊治体会

正每年的春天开始,又到了附红细胞体病开始高发的季节,但是也有秋冬季节发病的记载。附红细胞体病是指由人、畜红细胞表面或者游离于组织液、脑脊液和血浆中寄生的附红细胞体引起的人畜共患病,由于该病原与柔膜体纲支原体属高度同源,立克次体病也被很多学者认为是附红细胞体病的分支,但笔者认为应该加以区分。     

规模牛场犊牛附红细胞体病的诊治报告

附红细胞体病(Eperythrozoonsis)是由附红细胞体(Eperythrozoon)寄生于人或动物红细胞表面、血浆及骨髓等处引起的人畜共患病,以发热、贫血和黄疽等为主要临床表现[1]。在流行病学特点上,附红细胞体病具有发病动物种类广泛、隐性感染率高的特点。附红细胞体相对宿主有特异性,也有互感性,如猪附红细胞体可以感染小鼠、兔;绵羊附红细胞体可以感染人;牛附红细胞体可以感染小鼠[2]附红细胞体病的传播方式主要有接触性、血源性、垂直性及媒介昆虫4种[3]。     

Cortical constriction during abscission involves helices of ESCRT-III-dependent filaments

After partitioning of cytoplasmic contents by cleavage furrow ingression, animal cells remain connected by an intercellular bridge, which subsequently splits by abscission. Here, we examined intermediate stages of abscission in human cells by using live imaging, three-dimensional structured illumination microscopy, and electron tomography. We identified helices of 17-nanometer-diameter filaments, which narrowed the cortex of the intercellular bridge to a single stalk. The endosomal sorting complex required for transport (ESCRT)-III co-localized with constriction zones and was required for assembly of 17-nanometer-diameter filaments. Simultaneous spastin-mediated removal of underlying microtubules enabled full constriction at the abscission site. The identification of contractile filament helices at the intercellular bridge has broad implications for the understanding of cell division and of ESCRT-III-mediated fission of large membrane structures.     

Helical filaments produced by a Mycoplasma-like organism associated with corn stunt disease

Mycoplasma-like bodies with helical filaments were seen by phase contrast microscopy in juice expressed from tissues of plants infected with corn stunt agent. Each filament is bounded by a "unit membrane" and no cell wall, sheath, envelope, or second membrane has yet been discerned by electron microscopy. The association of these filaments with development of disease, their occurrence in phloem cells as seen by both freeze-etching and thin-section electron microscopy, the diagnosis of infection based on their presence in plants without symptoms, and their absence in noninfected corn are consistent with the hypothesis that these unusual filaments are formed by the mycoplasma-like organism presumed to be the corn stunt agent.     

山羊创伤愈合时组织病理学和超微结构的观察

山羊创伤愈合过程组织病理学和超微结构的动态变化观察结果表明:在几天内伤口中出现许多肌-成纤维细胞,它具有成纤维细胞和平滑肌细胞的共同特征。肌-成纤维细胞的核细长,有深的缺刻,并有发育完善的高尔基体和粗面内质网以及在胞浆中有很多微丝团块等。所以,肌-成纤维细胞在创伤收缩中起重要作用。     

Selective solubilization of a protein component of the red cell membrane

Approximately 20 percent of the membrane-bound protein of erythrocyte ghosts can be solubilized and obtained free of other membrane components by dialysis against adenosine triphosphate and 2-mercaptoethanol. This protein forms one major band on polyacrylamide gels and a single boundary in free-boundary electrophoresis, and it undergoes polymerization in the presence of divalent cations to form coiled filaments visible by electron microscopy. Antibodies to this membrane protein react specifically with red blood cells or their membrane ghosts but do not react with serum, erythrocyte cytoplasm, or other blood cells. The functional role of this protein is unknown, but it appears to be involved in maintaiining the structure of the red cell membrane. We suggest that this protein be called Spectrin since it is obtained from membrane ghosts.     

Magnetosomes are cell membrane invaginations organized by the actin-like protein MamK

Magnetosomes are membranous bacterial organelles sharing many features of eukaryotic organelles. Using electron cryotomography, we found that magnetosomes are invaginations of the cell membrane flanked by a network of cytoskeletal filaments. The filaments appeared to be composed of MamK, a homolog of the bacterial actin-like protein MreB, which formed filaments in vivo. In a mamK deletion strain, the magnetosome-associated cytoskeleton was absent and individual magnetosomes were no longer organized into chains. Thus, it seems that prokaryotes can use cytoskeletal filaments to position organelles within the cell.     

gCap39, a calcium ion- and polyphosphoinositide-regulated actin capping protein

The polymerization of actin filaments is involved in growth, movement, and cell division. It has been shown that actin polymerization is controlled by gelsolin, whose interactions with actin are activated by calcium ion (Ca2+) and inhibited by membrane polyphosphoinositides (PPI). A smaller Ca2(+)- and PPI-regulated protein, gCap39, which has 49% sequence identity with gelsolin, has been identified by cDNA cloning and protein purification. Like gelsolin, gCap39 binds to the fast-growing (+) end of actin filaments. However, gCap39 does not sever actin filaments and can respond to Ca2+ and PPI transients independently, under conditions in which gelsolin is ineffective. The coexistence of gCap39 with gelsolin should allow precise regulation of actin assembly at the leading edge of the cell.     

小麦生理型雄性不育系微丝骨架和胼胝质的变化与其相关基因的表达分析

【目的】研究生理型雄性不育小麦花粉细胞内微丝和胼胝质的结构及其相关基因的表达,并揭示其与生理型雄性不育的关系,为进一步研究化学杂交剂SQ-1诱导小麦生理型雄性不育的机理提供一定的理论依据。【方法】以化学杂交剂SQ-1诱导的生理型雄性不育系ms(A)-西农1376及对应正常可育系(A)-西农1376为试材,用TRITC-phalloidin标记细胞内微丝,苯胺蓝标记胼胝质,qRT-PCR技术分别对肌动蛋白解聚因子TaADF（Actin depolymerizing factor）、类葡聚糖合成酶TaGSL（Glucan synthase-like）进行差异表达分析。【结果】(1)在减数分裂前期Ⅰ、中期Ⅰ、后期Ⅰ这三个时期,生理型雄性不育系花粉细胞的微丝结构与可育系没有显著差异：前期Ⅰ,微丝分布于整个细胞质中,细胞核区域也可见少量微丝环绕细胞核;中期Ⅰ,微丝分布在细胞质中,在形成纺锤体部位染色更深,形成纺锤体微丝,由细胞两极发出的纺锤体微丝伸向赤道板;后期Ⅰ,在向两极移动的染色体的中间部位染色较深,微丝分布较多。(2)在早末期Ⅰ,与可育系相比,不育系花粉细胞没有形成清晰且明显可见的中国灯笼状成膜体微丝结构,且在细胞中线部位亦没有清晰可见的微丝累积。(3)晚末期Ⅰ,可育系花粉细胞在形成细胞板的部位是线性的、平滑的,成膜体微丝消失,而不育系花粉细胞在形成细胞板的部位形成了很大的缝隙,同时,可育系胼胝质在细胞板处的沉积比较平滑,而不育系胼胝质在细胞板处的沉积较可育系相比缺乏,并且是褶皱的、有裂纹的。(4)四分体时期,可育系花粉可见围绕细胞核的辐射状微丝,不育系花粉细胞中微丝呈模糊状态,并且不育系中胼胝质染色的整体荧光强度较可育系减弱。利用实时荧光定量PCR技术分析肌动蛋白解聚因子TaADF和类葡聚糖合成酶TaGSL在减数分裂期的相对表达量,结果发现,不育系中TaADF的相对表达量是可育系的4.28倍,由于TaADF表达量上调,加剧了细胞内微丝解聚,微丝结构受到破坏,同时不育系中TaGSL表达量下降,只有可育系的0.83倍,胼胝质的沉积也受到影响。【结论】TaADF在不育系中上调表达,破坏了细胞内微丝的正常结构,使微丝不能正常行使其功能,进而可能导致花药发育中与育性相关的某些代谢通路等受到影响。与此同时,微丝结构的破坏导致细胞板形成出现异常也可能是引起胼胝质在细胞板处沉积受到影响的一个重要原因。因此,微丝和胼胝质的异常变化与化学杂交剂SQ-1诱导的生理型雄性不育密切相关。     

Microfilaments in cellular and developmental processes

In our opinion, all of the phenomena that are inhibited by cytochalasin can be thought of as resulting from contractile activity of cellular organelles. Smooth muscle contraction, clot retraction, beat of heart cells, and shortening of the tadpole tail are all cases in which no argument of substance for alternative causes can be offered. The morphogenetic processes in epithelia, contractile ring function during cytokinesis, migration of cells on a substratum, and streaming in plant cells can be explained most simply on the basis of contractility being the causal event in each process. The many similarities between the latter cases and the former ones in which contraction is certain argue for that conclusion. For instance, platelets probably contract, possess a microfilament network, and behave like undulating membrane organelles. Migrating cells possess undulating membranes and contain a similar network. It is very likely, therefore, that their network is also contractile. In all of the cases that have been examined so far, microfilaments of some type are observed in the cells; furthermore, those filaments are at points where contractility could cause the respective phenomenon. The correlations from the cytochalasin experiments greatly strengthen the case; microfilaments are present in control and "recovered" cells and respective biological phenomena take place in such cells; microfilaments are absent or altered in treated cells and the phenomena do not occur. The evidence seems overwhelming that microfilaments are the contractile machinery of nonmuscle cells. The argument is further strengthened if we reconsider the list of processes insensitive to cytochalasin (Table 2). Microtubules and their sidearms, plasma membrane, or synthetic machinery of cells are presumed to be responsible for such processes, and colchicine, membrane-active drugs, or inhibitors of protein synthesis are effective at inhibiting the respective phenomena. These chemical agents would not necessarily be expected to affect contractile apparatuses over short periods of time, they either do not or only secondarily interfere with the processes sensitive to cytochalasin (Table 1). It is particularly noteworthy in this context that microtubules are classed as being insensitive to cytochalasin and so are not considered as members of the "contractile microfilament" family. The overall conclusion is that a broad spectrum of cellular and developmental processes are caused by contractile apparatuses that have at least the common feature of being sensitive to cytochalasin. Schroeder's important insight (3) has, then, led to the use of cytochalasin as a diagnostic tool for such contracile activity: the prediction is that sensitivity to the drug implies presence of some type of contractile microfilament system. Only further work will define the limits of confidence to be placed upon such diagnoses. The basis of contraction in microfilament systems is still hypothetical. Contraction of glycerol-extracted cells in response to adenosine triphosphate (53), extraction of actin-like or actomyosin-like proteins from cells other than muscle cells (54), and identification of activity resembling that of the actomyosin-adenosine triphosphatase system in a variety of nonmuscle tissues (40, 54) are consistent with the idea that portions of the complex, striated muscle contractile system may be present in more primitive contractile machinery. In the case of the egg cortex, calcium-activated contractions can be inhibited by cytochalasin. If, as seems likely, microfilaments are the agents activated by calcium, then it will be clear that they have the same calcium requirement as muscle. Biochemical analyses of primitive contractile systems are difficult to interpret. Ishikawa's important observation (31), that heavy meromyosin complexes with fine filaments oriented parallel to the surface of chondrocytes and perpendicular to the surface of intestinal epithelial cells, implies that both types of filaments are "actin-like" in this one respect. Yet, it is very likely that these actin-like filaments correspond respectively to the cytochalasin-insensitive sheath of glial and heart fibroblasts and the core filaments of oviduct microvilli. No evidence from our studies links contractility directly to these meromyosin-binding filaments. Apart from this problem, activity resembling that of the myosin-adenosine triphosphatase has been associated with the microtubule systems of sperm tails and cilia (55), but those organelles are insensitive to cytochalasin in structure and function. Clearly, a means must be found to distinguish between enzymatic activities associated with microfilament networks, microfilament bundles, microtubules, and the sheath filaments of migratory cells. Until such distinctions are possible, little of substance can be said about the molecular bases of primitive contractile systems. Three variables are important for the control of cellular processes dependent upon microfilaments: (i) which cells of a population shall manufacture and assemble the filaments; (ii) where filaments shall be assembled in cells; and (iii) when contractility shall occur. With respect to distribution among cells, the networks involved in cell locomotion are presumed to be present in all cells that have the potential to move in cell culture. In this respect, the networks can be regarded as a common cellular organelle in the sense that cytoplasmic microtubules are so regarded. In some developing systems, all cells of an epithelium possess microfilament bundles (7, 13), whereas, in others, only discrete subpopulations possess the bundles (5, 6). In these cases the filaments can be regarded as being differentiation products associated only with certain cell types. These considerations may be related to the fact that microfilament networks are associated with behavior of individual cells (such as migration, wound healing, and cytokinesis), whereas the bundles are present in cells that participate in coordinated changes in shape of cell populations. With respect to placement in cells, two alternatives are apparent, namely, localized or ubiquitous association with the plasma membrane. Microfilament bundles of epithelial cells are only found extending across the luminal and basal ends of cells. In this respect they contrast with desmosomal tonofilaments and with microtubules, each of which can curve in a variety of directions through the cell. The strict localization of microfilament bundles probably rests upon their association with special junctional complex insertion regions that are only located near the ends of cells. In the case of mitotically active cells, the orientation of the spindle apparatus may determine the site at which the contractile ring of microfilaments will form (4, 56); this raises the question of what sorts of cytoplasmic factors can influence the process of association between filament systems and plasma membranes. In contrast to such cases of localized distribution, contractile networks responsible for cell locomotion are probably found beneath all of the plasma membrane, just as the network of thrombosthenin may extend to all portions of the periphery of a blood platelet. This ubiquitous distribution probably accounts for the ability of a fibroblast or glial cell to establish an undulating membrane at any point on its edge, or of an axon to form lateral microspikes along its length. The third crucial aspect of control of these contractile apparatuses involves the choice of when contraction shall occur (and as a corollary the degree or strength of contraction that will occur). In the simplest situation, contraction would follow automatically upon assembly of the microfilament bundles or networks. In cleavage furrows of marine embryos (4), for instance, microfilaments are seen beneath the central cleavage furrow and at its ends, but not beyond, under the portion of plasma membrane that will subsequently become part of the furrow. This implies that the furrow forms very soon after the contractile filaments are assembled in the egg cortex. In other cases, microfilaments are apparently assembled but not in a state of (maximal?) contraction. Thus, networks are seen along the sides of migratory cells, although such regions are not then active as undulating membrane organelles. Similarly, microfilament bundles occur in all epithelial cells of the salivary gland (13), or pancreatic anlage (7), although only the ones at discrete points are thought to generate morphogenetic tissue movements. Likewise, bundles begin to appear as early as 12 hours after estrogen administration to oviduct, although visible tubular gland formation does not start until 24 to 30 hours. Finally, streaming in plant cells can wax and wane, depending upon external factors such as auxin (57). All of these cases imply a control mechanism other than mere assembly of the microfilament systems and even raise the possibility that within one cell some filaments may be contracting while others are not. In discussing this problem, it must be emphasized that different degrees of contraction or relaxation cannot as yet be recognized with the electron microscope. In fact, every one of the cases cited above could be explained by contraction following immediately upon some subtle sort of "assembly." Inclusive in the latter term are relations between individual filaments, relations of the filaments and their insertion points on plasma membrane, and quantitative alterations in filament systems. Furthermore, the critical role of calcium and high-energy compounds in muscle contraction suggest that equivalent factors may be part of primitive, cytochalasinsensitive systems. The finding that calcium-induced contraction in the cortex of eggs is sensitive to cytochalasin strengthens that supposition and emphasizes the importance of compartmentalization of cofactors as a means of controlling microfilaments in cells.     

栅极偏压对纳米金刚石薄膜沉积过程的影响

在HFCVD系统中施加栅极偏压和衬底偏压,采用双偏压成核和栅极偏压生长的方法成功制备了高质量的纳米金刚石薄膜.采用显微Raman高分辨率SEM和AFM等现代理化分析手段分析纳米金刚石膜的微结构,结果表明双偏压显著促进了金刚石的成核密度,平均晶粒尺寸在20 nm以内.试验观察和理论分析表明栅极偏压促进了热丝附近的等离子体浓度,提高了衬底附近的碳氢基团和氢原子浓度,提高了金刚石的成核密度、在保持晶粒的纳米尺寸的同时保持了较高的成膜质量和较低的生长缺陷.     

光对美洲蛙肌肉纤维衍射强度的分布研究

肌原纤维是由粗丝和细丝重迭而成的Ａ带和只含细丝的Ⅰ带组成，形成了天然光栅，因此可用光学方法探讨肌原纤维分子结构及其动力学问题。试验表明，单色光通过美洲蛙肌原纤维后，衍射光左右两端为非对称性，且左右条纹锋值间隔随肌原纤维节长度增大而减小。肌肉运动有张有弛，于是肌原纤维长度有变异，共变异与非对称有关。当肌原纤维长度增加时，左右两端强度差异变大，而相对应条纹的锋值间隔距离变小。这一现象与布拉格方程和折射