首例成年体细胞克隆山羊夭亡

记者从中国西北农林科技大学生物工程研究所了解到 ,６月１６日降生于该校种养场的世界上第一例成年体细胞克隆山羊“元元”由于肺部发育缺陷 ,造成呼吸困难 ,导致呼吸衰竭于６月１８日凌晨１时０５分死亡。当时研究人员对“元元”的身体状况进行了详细检查 ,发现与普通羊羔相比 ,“元元”的呼吸有点困难 ,判断可能是由于肺部发育不正常所致 ,并对“元元”进行了封闭观察。今天凌晨 ,“元元”终因呼吸衰竭而死亡。“元元”共活了３６小时０３分。专家说 ,“元元”出现这种情况很正常 ,目前 ,克隆技术还有待于完善首例成年体细胞克隆山羊夭亡…     

日本第一头体细胞克隆山羊诞生

日本农林省畜产试验场日前宣布，日本第一头体细胞克隆山羊2000年10月12日在该场诞生。据介绍，这个试验场取出雄山羊脑下垂体的前叶细胞，把它置于除去细胞核的卵细胞内，经过培养使它们相互融合，然后植入母山羊的子宫中。克隆山羊诞生时体重为1．45kg。 迄今为止，日本已经开发成功克隆牛、克隆猪等体格较大哺乳动物的技术，并且通过培育再克隆牛，证明了雄雌克隆牛都有正常的生殖能力，使克隆动物技术不断朝实用化方向前进。世界上第一例成年体细胞山羊是由中国科学家培育成功的，这头名叫“元元”的克隆山羊的诞生时间是2000年6月16日…     

科技动态

日本第一只体细胞克隆山羊诞生　　日本农林省畜产试验场日前宣布 ,日本第一只体细胞克隆山羊 2 0 0 0年 11月 12日在该场诞生。取出雄山羊脑下垂体的前叶细胞 ,把它置于除去核的卵细胞内 ,经过培养使它们相互融合 ,然后植入母山羊子宫中。克隆山羊诞生时体重为 1 4 5ｋｇ。成年体细胞克隆山羊在我国诞生　　由西北农林科技大学张涌教授主持的国家自然科学基金和农业部重点项目“体细胞克隆山羊的研究”取得重大突破。我国又一例成年体细胞克隆山羊 ,2 0 0 0年 6月 16日在西北农林科技大学种羊场顺利诞生。这标志着我国动物体细胞克隆技术已…     

克隆动物重组核再程序化的研究进展

1997年,Wilmut J等人报道了世界首例体细胞克隆动物——Dolly羊的诞生。这一成果突破了高度分化的高等成年动物体细胞不具有基因组全能性,不能支持卵子完成个体发生的禁区。随后体细胞克隆牛、猪、山羊、猫、兔等相继问世。我国的体细胞克隆山羊和牛也分别于2000年和2001年研究     

天津克隆羊生下“龙凤胎”

11月24日，国内首例体细胞克隆波尔山羊“津英”顺利产下一对“龙凤胎”。这标志着渡尔山羊体细胞克隆技术已能应用于生产。     

科技——我国体细胞克隆羊生下“龙凤胎”

国内首例体细胞克隆波尔山羊“津英”11月24日顺利产下一对“龙凤胎”．标志着波尔山羊体细胞克隆技术已能应用于生产。小公羊体重4．4kg,小母羊体重3．7kg。这表明体细胞克隆波尔山羊“津英”与普通波尔山羊一样完全具有正常的繁殖能力。目前两只刚刚产下的小羊．正在天津畜牧兽医研究所试验羊场接受观察．两只小羊发育良好．     

日本第一只体细胞

日本第一只体细胞克隆山羊诞生 　　日本农林省畜产试验场日前宣布，日本第一只体细胞克隆山羊2000年11月12日在该场诞生。取出雄山羊脑下垂体的前叶细胞，把它置于除去核的卵细胞内，经过培养使它们相互融合，然后植入母山羊子宫中。克隆山羊诞生时体重为1.45 kg。 成年体细胞克隆山羊在我国诞生 　　由西北农林科技大学张涌教授主持的国家自然科学基金和农业部重点项目“体细胞克隆山羊的研究”取得重大突破。我国又一例成年体细胞克隆山羊，2000年6月16日在西北农林科技大学种羊场顺利诞生。这标志着我国动物体细胞克隆技术已跻身于世界先进行列，将对我国体细胞克隆技术的发展与完善产生重大影响。 世界上首次克隆出抗病牛 　　美国得克萨斯农机大学研究人员2000年12月18日宣布，他们克隆出了一头可自然抵抗三种疾病的公牛。这是科学家第一次克隆出抗病牛。 　　近30年来，他们在检测的数百头牛中，发现一头公牛具有自然抵抗布鲁氏菌病、结核病和沙门氏杆菌病的能力。3年前，这头抗病公牛自然死亡，但来自该公牛的DNA物质被保存下来并克隆出了小牛，这头小牛现已有一个月大。 第一只克隆野牛将诞生 　　近日，美国将诞生世界上第一只克隆野牛。 　　据介绍，科学家成功地将奶牛卵子中的细胞核剔除，植入印度野牛皮肤细胞的细胞核。细胞核包含了所有野牛成长所需的基因资料。专家称，2001年1月内就会诞生的这只牛肯定会是一只野牛，而非奶牛和野牛的杂交种。这个试验一旦成功，将为挽救世界上大量的濒危野生动物带来希望。 东北农业大学培育出体细胞克隆猪囊胚 　　东北农业大学通过培育获得了中国第一个体细胞克隆猪囊胚。组织这项研究的东北农大动物组织胚胎教研室谭景和教授说，这项试验的成功，意味着可以获得足够多的囊胚，保证其在猪这种多胚胎动物体内顺利着床发育，成功产下克隆猪活体。同时也意味着用转入人体基因的猪细胞克隆猪不久也可能问世，届时，人体移植猪器官就不必担心排异的危险了。 墨西哥培育出矮种牛 　　墨西哥经过数10年的研究，终于培育出数十头矮种牛。矮种牛体重135 kg，身高90 cm。矮种牛具有许多优点，既节省饲料，又可增加产肉产奶量，而它们的奶和肉与正常牛的肉、奶没有任何区别。矮种牛还有一个特点，就是1头矮种母牛每年可产4头牛犊。专家们认为，矮种牛可能引起世界畜牧业革命，成为世界上牛奶和牛肉的主要来源。 (木子辑)     

我国首例体细胞克隆波尔山羊降生

我国首例、世界第二例体细胞克隆波尔山羊于2007年4月9日在天津市畜牧兽医研究所顺利降生,这标志着我国的动物体细胞克隆技术达到国际先进水平。     

世界首批亚种间体细胞克隆羊试验在上海获成功

<正>从波尔山羊耳朵上提取细胞核,由莎能奶山羊代孕产仔,世界首批亚种间体细胞克隆羊试验获得成功。羊体呈蕉叶耳、酒桶身,颈上“围”褐色“巾”,前额有块俏皮的白斑。上海转基因研究中心6只品相上乘的羊娃娃仿佛从一个模子里刻出来。它们是世界首批由亚种间体细胞克隆获得的波尔山羊,通过了权威鉴定。     

我国体细胞克隆羊生下“龙凤胎”

国内首例体细胞克隆波尔山羊"津英"11月24日顺利产下一对"龙凤胎",标志着波尔山羊体细胞克隆技术已能应用于生产。小公羊体重4.4kg,小母羊体重3.7kg。这表明体细胞克隆波尔山羊"津英"与普通波尔     

Light and electron-microscopic localization of CD9 and surfactant protein A and D in normal lungs of the horse

The lung is a complex organ, and its physiology and immunology are regulated by various immune molecules and cells. Lung surfactant, a mixture of phospholipids and proteins produced by the bronchiolar and type II alveolar epithelial cells, is one such important player in lung physiology. Compared to knowledge about the biology of the surfactant in rodents and humans, only limited data are available on the surfactant in the horse. Although there are data linking levels of surfactant proteins with respiratory disease in the horse, there are no data on the cellular localization of surfactant protein A (SP-A) and surfactant protein D (SP-D). A member of the tetraspanin family of proteins, CD9 is a cell-signaling and adhesion protein and its expression has been detected in both normal and cancer cells, including those in the lung. Because there are no immunolocalization data on SP-A, SP-D, and CD9 in the normal lungs of the horse, our objective was to conduct a light and electron microscopic immunocytochemical study on normal lungs of the horse. The data showed SP-A and SP-D in bronchiolar epithelial and type II alveolar epithelial cells. These proteins were also localized in type I alveolar epithelial cells, pulmonary intravascular macrophages, and neutrophils, which is likely an outcome of endocytosis of the proteins by these cells. CD9 was present in the airway and vascular smooth muscle cells, endothelium, and blood cells, but not in the airway epithelium. These new data provide a baseline to further examine the expression and functions of SP-A, SP-D, and CD9 proteins in inflammation associated with respiratory diseases in the horse.     

Experimentally induced parainfluenza type 3 virus infection in young lambs: pathologic response

Pulmonary changes in five 1-week-old, colostrum-deprived lambs transtracheally inoculated with parainfluenza type 3 virus were studied by immunofluorescent, microscopic, and ultrastructural techniques. The lambs were killed at postinoculation days (PID) 3, 5, and 7. Immunofluorescence specific for parainfluenza type 3 virus was first seen in small airways and alveolar epithelium and later in the lumens of airways and alveoli and, to a lesser extent, in the interstitium of the lungs. Grossly, there were multifocal areas of consolidation in all lobes of the lungs. These areas were characterized microscopically by bronchiolitis and interstitial pneumonitis. The bronchiolitis involved the terminal airways and consisted of necrosis and sloughing of epithelial cells followed by hyperplasia of the epithelium. The interstitial lesion comprised extensive infiltration of alveolar septa and alveoli with macrophages and the necrosis of alveolar epithelium. This was followed by hyperplasia of the epithelium. Degenerated bronchiolar and alveolar epithelium contained numerous intracytoplasmic inclusions early in the infection, but such inclusions were not seen in the lambs killed at PID 7. The degenerated changes were also seen with the electron microscope, as were numerous inclusions of viral nucleoprotein and a few viral buds at PID 3 and 5. Viral inclusions and buds were seen in ciliated and nonciliated bronchial epithelial cells and type I and type II alveolar epithelial cells.     

Expression of cytokeratin 18 during pre- and post-natal porcine lung development

The expression pattern of the intermediate filament protein cytokeratin 18 (CK 18) is described during pre- and post-natal development of the porcine lung using a monoclonal antibody against human CK 18. Lungs from 16 foetuses in pseudoglandular, canalicular, saccular and alveolar stages of lung development and lungs from 12 pigs ranging in age from birth to 49 days after birth were studied by immunohistochemistry.In the early pseudoglandular stage of development (day 70 of gestation) all the columnar epithelial cells lining the tubular endbuds strongly expressed CK 18 predominantly in the apical cell compartment. A modest staining was found in the more cuboidal cells of the canalicular stage (day 80 of gestation) where the labelling occurred as a distinct positive rim at the apical cell membrane in most of the cells lining the canaliculi. In 96- and 100-day-old foetuses, parts of the gas exchanging area were formed as terminal sacs by extreme attenuation of the epithelium. In this stage, CK 18 was clearly detectable in the flat type I as well as in the cuboidal type II alveolar epithelial cells. A marked change of the CK 18 expression pattern occurred during formation of the alveoli by septal outgrowth and maturation of the epithelium in 105- and 111-day-old foetuses. Differentiated type I cells no longer expressed CK 18, whereas type II cells were still labelled. Moreover, a specific change in the subcellular distribution pattern from the luminal periphery in immature porcine type II cells to a cytoplasmic localization in differentiated type II cells could be observed. Our investigation additionally demonstrated that the epithelium of bronchi, bronchioli and terminal bronchioli expressed CK 18 in all pre- and post-natal developmental stages. From the 96 days of gestation onwards the epithelial cells of developing bronchial glands were also labelled. Our results clearly show that during porcine lung development profound changes in the cellular expression pattern of CK 18 occur and that CK 18 can be regarded as a selective marker for differentiated porcine alveolar type II cells from the 105th day of gestation onwards. We also assume that the intermediate filament CK 18 could be of significance in the maturation process of the type II alveolar cells.     

Ultrastructural Observation of Nasal and Pulmonary Intracellular Pasteurella multocida A:3 in Rabbits

Sixteen 8- to 9-week-old Pasteurella multocida-free rabbits were divided into two equal groups. Eight rabbits in one group were inoculated intranasally with P. multocida type A:3. The other eight were inoculated intranasally with phosphate-buffered saline and used as controls. Nasal swabs taken before and after inoculation were cultured for bacterial isolation. Post-mortem nasal swabs and lung samples were cultured for bacteriological isolation. Nasal mucosa and lung samples were collected and processed for transmission electron microscopy. Pasteurella multocida was isolated from the nasal cavity of all infected rabbits and from the lungs of four infected rabbits. Degenerative ultrastructural changes in epithelial cells and endothelial cells were seen in the infected rabbits. Deciliation of the cilated epithelium and hyperplasia of the goblet cells in the nasal mucosa were noted. Thickening of the alveolar septa due to hyperplasia of type II pneumocytes, swelling of the endothelial lining of capillaries and infiltration of inflammatory cells were also observed. Intracellular invasion of the nasal epithelial cells and of type II pneumocytes by the organism was observed. Coccobacilli were observed in membrane-bound vacuoles in the cytoplasm of these cells. The vacuoles were adjacent to the host-cell mitochondria and some of these vacuoles appeared to be fused to the mitochondrial membrane. Some type I pneumocytes with intracellular membrane-bound vacuoles containing bacterial cells showed protrusions, which appeared to detach into the alveolar lumina. These results indicated that P. multocida serotype A:3 in rabbits can invade the epithelial cell and cause structural changes in the interstitium, epithelium and endothelium. Heterophils and macrophages appear to play important roles in tissue injury.     

Ultrastructural features of alveolar lesions in induced respiratory syncytial virus pneumonia of calves

Ultrastructural changes occurred in alveolar epithelium in the acute and repair stages of induced respiratory syncytial virus pneumonia induced in eight calves (calf Nos. 1-7, 3 to 6 days old and calf No. 8, 2 weeks old), using a bovine strain of respiratory syncytial virus. Five of the calves were Friesians, three were Hereford x Friesians, and all were male. Tissues from three mock-infected control calves (two Friesian, one Hereford x Friesian) were also examined. Evidence of respiratory syncytial virus infection was observed in both type I and type II pneumocytes from day 4 to day 8 after infection. Infection of type I pneumocytes frequently resulted in necrosis. The response of type II pneumocytes to respiratory syncytial virus infection varied and included hypertrophy, hyperplasia, and syncytial formation. In some infected type II pneumocytes, there were numerous irregular projections of the cell surface, associated with viral budding. Hypertrophy and hyperplasia of type II pneumocytes, epithelial syncytium formation, and irregular cytoplasmic projections from epithelial cells caused considerable thickening of respiratory membrane and occlusion of alveolar lumina. Neutrophils were frequently observed in close association with virus-infected epithelial cells, but evidence of respiratory syncytial virus infection and replication was not observed in alveolar macrophages or neutrophils. Proliferation of type II pneumocytes appeared to play a major role in maintaining the integrity of the alveolar epithelium during the acute stage of the experimental pneumonia. Increased numbers of type II pneumocytes were present on alveolar walls, particularly from 4 to 8 days after infection, and some alveoli were lined entirely by this cell type. In some areas, however, squamous epithelial cells were also involved in covering exposed alveolar basement membrane.     

不同发育阶段高原牦牛肺泡超微结构的研究

利用透射电镜和计算机图像分析系统对1日龄、30日龄、180日龄和成年4个年龄组的高原牦牛肺泡超微结构进行观测,并与同日龄平原黄牛进行比较。结果表明:不同发育阶段高原牦牛和平原黄牛肺泡壁均由扁平的肺泡I型上皮细胞和立方的肺泡II型上皮细胞组成,气-血屏障均由肺泡I型上皮、基膜和肺泡隔毛细血管内皮3层结构组成,但高原牦牛肺泡I型上皮处可见一些凹陷和空泡状结构。此外,1日龄高原牦牛肺泡II型细胞明显多于同日龄黄牛;除1日龄外,其余年龄段高原牦牛的气-血屏障算术平均厚度和调和平均厚度均显著小于同日龄平原黄牛(P<0.05)。高原牦牛气-血屏障的算术平均厚度和调和平均厚度随年龄增加不断减小,这不同于平原黄牛随年龄增加不断增大的特点。结论:高原牦牛出生后肺泡迅速发育,在超微结构方面表现出较多适应高原低氧环境的组织学结构特点。     

Pneumonia in lambs inoculated with Bordetella parapertussis: bronchoalveolar lavage and ultrastructural studies

Eight colostrum-deprived lambs were inoculated intratracheally with ovine isolates of Bordetella parapertussis. Fluids obtained by bronchoalveolar lavage had a large increase in total cell counts 24 hours after inoculation; up to 93% of cells were neutrophils. From 3 days after inoculation, the number of alveolar macrophages in lavage samples was markedly increased. From 5 days onwards, many alveolar macrophages had moderate to severe cytoplasmic vacuolation. Topographically, tracheal and bronchial epithelium was covered by a large amount of inflammatory exudate 24 hours after inoculation. Later, the tracheobronchial epithelium showed focal extrusions from ciliated cells, which were occasionally associated with B. parapertussis organisms. Ultrastructurally, cytopathological changes associated with B. parapertussis infection were mild focal degeneration of airway epithelium with slight loss of cilia, moderate to severe degeneration of type I and type II alveolar epithelial cells, and focal inflammation in the lungs. These results suggest that the primary targets of B. parapertussis infection are alveolar macrophages and the epithelial cells of bronchioles and alveoli.     

Ultrastructural morphogenesis of 4-ipomeanol-induced bronchiolitis and interstitial pneumonia in calves

The two objectives of this research were 1) to describe the ultrastructural morphogenesis of pulmonary damage and repair induced in calves after treatment with 4-ipomeanol and 2) to characterize infiltrating pulmonary inflammatory cells by bronchoalveolar lavage. Interstitial edema was observed as early as 4 hours after intravenous injection of 4-ipomeanol (5 mg/kg body weight) and progressed to severe alveolar edema by 72 hours. Damage to type I alveolar epithelial cells and terminal bronchiolar nonciliated cells included dilation of endoplasmic reticulum and perinuclear envelopes and was present at 4 hours after treatment. Necrosis and sloughing of these cells from basement membranes occurred at times from 12 to 96 hours after treatment. Alveolar capillary endothelial cells had mild dilation of endoplasmic reticulum at times from 12 to 72 hours after treatment. Necrosis of endothelial cells was not observed. Inflammatory cell infiltrates in bronchioles and alveoli were dominated by macrophages and neutrophils. Significant elevations (P less than 0.05) in numbers of neutrophils and macrophages were recovered by bronchoalveolar lavage at times from 24 to 96 hours after 4-ipomeanol-treatment. Hyperplasia of nonciliated bronchiolar epithelial cells and of type II alveolar epithelial cells were observed at 72 and 96 hours after treatment. The results indicate that type I alveolar epithelial cells and nonciliated bronchiolar epithelial cells are most susceptible to 4-ipomeanol-induced damage and necrosis in calves. 4-ipomeanol-induced pulmonary edema in calves occurs prior to ultrastructurally-demonstrable, mild, alveolar capillary endothelial cell damage.     

Detection of annexins I and IV in bronchoalveolar lavage fluids from calves inoculated with bovine herpes virus-1

Annexins are phospholipid-binding proteins and are abundant in the lung. Annexins I and IV, but not II and VI, have been detected in bronchoalveolar lavage (BAL) fluids from calves inoculated with Pasteurella haemolytica, the pathogen for calf pneumonia. In this study, BAL fluids from calves with experimental pneumonia induced by inoculation to right lung lobes of bovine herpes virus-1 (BHV-1), the major viral pathogen for pneumonia, were examined for detection of annexins I and IV. Of 6 calves inoculated with BHV-1, annexins I and IV were coincidentally detected in BAL fluids from right lung lobes of 4 calves, but not in BAL fluids from left lung lobes of 6 inoculated calves or those from left and right lung lobes of 3 control calves. Annexin II and VI were not found in any BAL fluids examined. These results, together with previous findings on calves inoculated with Pasteurella haemolytica, suggest that the release of annexins I and IV onto the alveolar surface is an essential event occurring in response to pulmonary infections of BHIV-1 and Pasteurella haemolytica.     

Immunohistochemical and histopathological findings of ovine pulmonary adenocarcinoma (Jaagsiekte) in Egyptian sheep

Ovine pulmonary adenocarcinoma (OPA) is a naturally occurring retrovirus-induced transmissible lung cancer in sheep. Lungs and associated (bronchial and mediastinal) lymph nodes of seven sheep with OPA were examined. Lungs had few multifocal consolidated slightly elevated gray to white masses ranging from 0.5 to 3 cm in diameter. Histopathologically, these masses appeared as well-differentiated acinar adenocarcinoma with little evidence of anaplasia. The acini composed of well-differentiated cuboidal to low columnar epithelium with clear or vacuolated cytoplasm and low mitotic index. No metastases were observed in the bronchial and mediastinal lymph nodes of any animal. The presence of Jaagsiekte sheep retrovirus (JSRV) was demonstrated in the lungs by immunohistochemistry. JSRV protein was detected in all tumor epithelial cells, histologically normal alveolar type II cells, and few bronchiolar epithelial cells, alveolar macrophages, lymphocytes, and plasma cells. This study is the first to confirm the presence of natural OPA in Egypt.