PORCINE FOCAL SYMMETRICAL POLIOMYELOMALACIA

年猪局灶性对称性脊髓灰质炎(PFSP)多次暴发 未知的病因已被描述。这种综合征的特点是 由双侧神经元和支撑性神经元坏死引起的神经病理学 颈椎和腰椎/骶骨前角的结构 膨大和各种脑干核团。澳大利亚工人，由 6例相距较远的神经病理损害的相似性 在他们国家暴发的PFSP引起的神经病理损害 6-氨基吲哚青胺(6-AN)实验动物 给猪注射6-AN，产生PFSP。他们的结论是，他们的 以前的现场病例是由急性烟酸缺乏引起的。 宾夕法尼亚州立大学的工作人员报告了一次大规模的疫情 PFSP，与澳大利亚的相同。饮食中的高水平 硒(Se)被认为是病因。宾夕法尼亚州 州立大学的工作人员复制了带有神经病理损害的PFSP 和澳大利亚人一样，有标准的猪种植口粮 添加50ppm的Se。 神经损伤的相同性质向我们表明 硒在烟酸代谢中可能的拮抗作用。高膳食硒 生产全氟辛烷磺酸的剂量将作为烟酸进行评估。 通过测量特定的烟酸尿代谢物来拮抗烟酸。刺激 Se解毒途径的改变可能会破坏烟酸 以类似方式进行生化处理的代谢物。这个 给猪注射高水平的硒会选择性地损害前额叶 颈椎和腰椎/骶部膨大的角细胞。 我们建议获得关于神经病理损害的深入信息。 由硒中毒产生。此外，我们还将获得重要的生化指标 全氟辛烷磺酸生产中硒和烟酸相互作用的数据， 尤其是烟酸代谢物。目前，Se是一个正在积极研究的 微量营养素，在比较医学中有广泛的含义， 尤其是它的抗癌作用。它是最近发生的 已证实美国的硒中毒与 增加维生素和矿物质补充剂的使用。目前，电流很小 关于硒毒性的信息是可用的。我们的数据应该会增加无价的 与硒毒性相关的信息。

Numerous outbreaks of porcine focal symmetrical poliomyelomalacia (PFSP) of unknown etiology have been described. This syndrome is characterized neuropathologically by bilateral necrosis of the neurons and supporting structure in the anterior horns of the cervical and lumbar/sacral intumescens and various brain stem nuclei. Australian workers, sparked by the similarity of the neuropathological lesion in 6 widely separated outbreaks of PFSP in their country to neuropathological lesions induced in experimental animals with 6-aminonicontinamide (6-AN), experimentally injected swine with 6-AN and produced PFSP. They concluded that their previous field cases were caused by acute niacin deficiency. The Pennsylvania State University workers reported one large outbreak of PFSP, identical to those of the Australians. High dietary levels of selenium (Se) were incriminated as the etiologic agent. The Pennsylvania State University workers reproduced PFSP with neuropathological lesions identical to those of the Australians, with standard swine growing rations supplemented with 50 ppm Se. The identical nature of the neurological lesions has suggested to us a possible antagonist role for Se in niacin metabolism. High dietary Se levels administered to produce PFSP will be evaluated as a niacin antagonist by measuring specific niacin urinary metabolites. Stimulation of the Se detoxification pathway might be expected to disrupt niacin metabolites which are biochemically processed a similar manner. The administration of high Se levels in pigs selectively damages the anterior horn cells of the cervical and lumber/sacral intumescens. We propose to obtain in-depth information on the neuropathological lesions produced by Se toxicity. In addition, we will obtain important biochemical data on the interraction of Se and niacin in the production of PFSP, especially niacin metabolites. Se, at present, is an aggressively studied micronutrient and has wide ranging implications in comparative medicine, especially its anticarcinogenic potential. It has been recently established that Se toxicity in the U.S. has been associated with the increased use of vitamin and mineral supplements. Presently little current information is available on Se toxicity. Our data should add invaluable information relevant to Se toxicity.