共查询到20条相似文献,搜索用时 156 毫秒
1.
2.
3.
4.
5.
6.
7.
猪传染性胸膜肺炎病原的分离鉴定及防治 总被引:1,自引:0,他引:1
胸膜肺炎放线杆菌是猪传染性胸膜肺炎的致病菌,该病是一种呼吸道疾病,影响着全球养猪业的发展.本研究采用多种培养基进行接种培养,从某猪场典型传染性胸膜肺炎症状猪的肺脏和扁桃体中分离到了革兰氏阴性杆菌.通过该病原菌的培养特性、生物学特性和生化鉴定结果显示,该细菌为猪胸膜肺炎放线杆菌.同时本研究也为今后对该病的预防控制与诊断治疗奠定了有效的基础. 相似文献
8.
猪传染性胸膜肺炎的流行情况调查 总被引:1,自引:0,他引:1
猪传染性胸膜肺炎是由胸膜肺炎放线杆菌引起的一种严重呼吸系统传染病。随着近年来养猪业的发展,该病在全国各地均有发生,并对养猪业造成巨大的经济损失。为了解该病在永安地区的流行情况,笔者就猪传染性胸膜肺炎在农村的流行情况进行了调查,并就本病的控制方法进行了初步研究并报告。 相似文献
9.
10.
11.
Protease nexin-II (amyloid beta-protein precursor): a platelet alpha-granule protein 总被引:8,自引:0,他引:8
W E Van Nostrand A H Schmaier J S Farrow D D Cunningham 《Science (New York, N.Y.)》1990,248(4956):745-748
Protease nexin-II (PN-II) [amyloid beta-protein precursor (APP)] and the amyloid beta-protein are major constituents of neuritic plaques and cerebrovascular deposits in individuals with Alzheimer's disease and Down syndrome. Both the brain and the circulation have been implicated as sources of these molecules, although they have not been detected in blood. Human platelets have now been found to contain relatively large amounts of PN-II/APP. Platelet PN-II/APP was localized in platelet alpha-granules and was secreted upon platelet activation. Because PN-II/APP is a potent protease inhibitor and possesses growth factor activity, these results implicate PN-II/APP in wound repair. In certain disease states, alterations in platelet release and processing and clearance of PN-II/APP and its derived fragments could lead to pathological accumulation of these proteins. 相似文献
12.
Amyloid protein precursor messenger RNAs: differential expression in Alzheimer's disease 总被引:25,自引:0,他引:25
M R Palmert T E Golde M L Cohen D M Kovacs R E Tanzi J F Gusella M F Usiak L H Younkin S G Younkin 《Science (New York, N.Y.)》1988,241(4869):1080-1084
In situ hybridization was used to assess total amyloid protein precursor (APP) messenger RNA and the subset of APP mRNA containing the Kunitz protease inhibitor (KPI) insert in 11 Alzheimer's disease (AD) and 7 control brains. In AD, a significant twofold increase was observed in total APP mRNA in nucleus basalis and locus ceruleus neurons but not in hippocampal subicular neurons, neurons of the basis pontis, or occipital cortical neurons. The increase in total APP mRNA in locus ceruleus and nucleus basalis neurons was due exclusively to an increase in APP mRNA lacking the KPI domain. These findings suggest that increased production of APP lacking the KPI domain in nucleus basalis and locus ceruleus neurons may play an important role in the deposition of cerebral amyloid that occurs in AD. 相似文献
13.
F S Esch P S Keim E C Beattie R W Blacher A R Culwell T Oltersdorf D McClure P J Ward 《Science (New York, N.Y.)》1990,248(4959):1122-1124
The amyloid beta peptide (A beta P) is a small fragment of the much larger, broadly distributed amyloid precursor protein (APP). Abundant A beta P deposition in the brains of patients with Alzheimer's disease suggests that altered APP processing may represent a key pathogenic event. Direct protein structural analyses showed that constitutive processing in human embryonic kidney 293 cells cleaves APP in the interior of the A beta P, thus preventing A beta P deposition. A deficiency of this processing event may ultimately prove to be the etiological event in Alzheimer's disease that gives rise to senile plaque formation. 相似文献
14.
[目的]研究APP家族胞内段对神经细胞定向分化的影响。[方法]通过分离体外培养神经干细胞,转染导入APP蛋白家族胞内段以过表达后,研究其对神经干细胞向神经元定向分化的影响。[结果]APP家族蛋白胞内段的过表达可以抑制神经干细胞向神经元细胞的分化,其中APP和APLP2胞内段的影响尤为显著。突变试验表明,通过Capase水解释放末端31氨基酸片断是这个过程必需的。APP家族胞内段是通过释放APP-ICD31来抑制神经干细胞向神经元细胞的定向分化。[结论]该研究进一步证实了APP蛋白和老年痴呆病发生的联系,也为老年痴呆症的治疗提供新的靶点。 相似文献
15.
NMDA receptor losses in putamen from patients with Huntington's disease 总被引:19,自引:0,他引:19
A B Young J T Greenamyre Z Hollingsworth R Albin C D'Amato I Shoulson J B Penney 《Science (New York, N.Y.)》1988,241(4868):981-983
N-Methyl-D-aspartate (NMDA), phencyclidine (PCP), and quisqualate receptor binding were compared to benzodiazepine, gamma-aminobutyric acid (GABA), and muscarinic cholinergic receptor binding in the putamen and cerebral cortex of individuals with Huntington's disease (HD). NMDA receptor binding was reduced by 93 percent in putamen from HD brains compared to binding in normal brains. Quisqualate and PCP receptor binding were reduced by 67 percent, and the binding to other receptors was reduced by 55 percent or less. Binding to these receptors in the cerebral cortex was unchanged in HD brains. The results support the hypothesis that NMDA receptor-mediated neurotoxicity plays a role in the pathophysiology of Huntington's disease. 相似文献
16.
Amyloid beta protein precursor gene and hereditary cerebral hemorrhage with amyloidosis (Dutch) 总被引:22,自引:0,他引:22
C Van Broeckhoven J Haan E Bakker J A Hardy W Van Hul A Wehnert M Vegter-Van der Vlis R A Roos 《Science (New York, N.Y.)》1990,248(4959):1120-1122
Human hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), an autosomal dominant form of cerebral amyloid angiopathy (CAA), is characterized by extensive amyloid deposition in the small leptomeningeal arteries and cortical arterioles, which lead to an early death of those afflicted in their fifth or sixth decade. Immunohistochemical and biochemical studies have indicated that the amyloid subunit in HCHWA-D is antigenically related to and homologous in sequence with the amyloid beta protein isolated from brains of patients with Alzheimer's disease and Down syndrome. The amyloid beta protein is encoded by the amyloid beta protein precursor (APP) gene located on chromosome 21. Restriction fragment length polymorphisms detected by the APP gene were used to examine whether this gene is a candidate for the genetic defect in HCHWA-D. The data indicate that the APP gene is tightly linked to HCHWA-D and therefore, in contrast to familial Alzheimer's disease, cannot be excluded as the site of mutation in HCHWA-D. 相似文献
17.
Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP 总被引:2,自引:0,他引:2
Lewis J Dickson DW Lin WL Chisholm L Corral A Jones G Yen SH Sahara N Skipper L Yager D Eckman C Hardy J Hutton M McGowan E 《Science (New York, N.Y.)》2001,293(5534):1487-1491
JNPL3 transgenic mice expressing a mutant tau protein, which develop neurofibrillary tangles and progressive motor disturbance, were crossed with Tg2576 transgenic mice expressing mutant beta-amyloid precursor protein (APP), thus modulating the APP-Abeta (beta-amyloid peptide) environment. The resulting double mutant (tau/APP) progeny and the Tg2576 parental strain developed Abeta deposits at the same age; however, relative to JNPL3 mice, the double mutants exhibited neurofibrillary tangle pathology that was substantially enhanced in the limbic system and olfactory cortex. These results indicate that either APP or Abeta influences the formation of neurofibrillary tangles. The interaction between Abeta and tau pathologies in these mice supports the hypothesis that a similar interaction occurs in Alzheimer's disease. 相似文献
18.
19.
通过全灭菌环境下的土壤五氯酚(PCP)污染模拟实验,分别测定水提取态、乙醇提取态、腐殖质固定态以及蚯蚓生物累积态PCP的变化,研究添加两种不同蚯蚓品种(赤子爱胜蚓和壮尾环毛蚓)和堆肥对土壤PCP老化过程的影响。结果显示,在42d的培养期内,水提取态PCP在全灭菌土壤对照和添加灭菌堆肥的处理中随时间推移逐渐下降,存在明显的老化效应。在蚯蚓处理中,水提取态PCP呈现先下降后上升的趋势,说明蚯蚓促进土壤PCP的解吸附,这主要与蚯蚓的生物扰动作用以及调节土壤pH趋向中性的作用直接相关。培养结束时,蚯蚓能够有效促进土壤PCP向腐殖质固定态转化,并进一步促进PCP的去除,这与蚯蚓提高土壤腐殖质的含量,促进PCP的化学还原转化作用以及蚯蚓自身对PCP的消解作用有关。壮尾环毛蚓比赤子爱胜蚓更能有效促进PCP的转化与去除,这与两者的生活习性不同有关。灭菌堆肥对全灭菌土壤PCP向其他形态转化的影响不显著。 相似文献
20.
Meyer-Luehmann M Coomaraswamy J Bolmont T Kaeser S Schaefer C Kilger E Neuenschwander A Abramowski D Frey P Jaton AL Vigouret JM Paganetti P Walsh DM Mathews PM Ghiso J Staufenbiel M Walker LC Jucker M 《Science (New York, N.Y.)》2006,313(5794):1781-1784
Protein aggregation is an established pathogenic mechanism in Alzheimer's disease, but little is known about the initiation of this process in vivo. Intracerebral injection of dilute, amyloid-beta (Abeta)-containing brain extracts from humans with Alzheimer's disease or beta-amyloid precursor protein (APP) transgenic mice induced cerebral beta-amyloidosis and associated pathology in APP transgenic mice in a time- and concentration-dependent manner. The seeding activity of brain extracts was reduced or abolished by Abeta immunodepletion, protein denaturation, or by Abeta immunization of the host. The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains. 相似文献