PORCINE FOCAL SYMMETRICAL POLIOMYELOMALACIA

猪局灶性对称性脊髓灰质炎软化症（PFSP）的多次爆发， 已经描述了未知的病因。 这种综合征的特点是 神经病理学上通过双侧神经元坏死和支持 颈椎和腰椎/骶椎前角结构 膨大核和各种脑干核团。 澳大利亚工人，引发了由 6例广泛分离的神经病变的相似性 在他们的国家暴发PFSP引起的神经病理学病变， 6-氨基烟酰胺（6-AN）的实验动物，实验 用6-AN注射猪产生PFSP。 他们的结论是， 以前的现场病例是由急性烟酸缺乏症引起的。 宾夕法尼亚州立大学的工作人员报告说， PFSP，与澳大利亚人相同。 膳食中高水平的 硒（Se）被认为是致病因子。 宾夕法尼亚 州立大学的工作人员复制了具有神经病理学病变的PFSP 与澳大利亚人相同， 添加50 ppm硒。 神经损伤的相同性质向我们暗示了 硒在烟酸代谢中可能具有拮抗作用。 高硒膳食 用于产生PFSP的给药水平将作为烟酸 拮抗剂通过测量特定的烟酸尿代谢产物。 刺激 硒解毒途径可能会破坏烟酸 代谢物，其以类似的方式进行生物化学处理。 的 高硒水平的猪的管理选择性地损害前 颈和腰/骶膨大的角细胞。 我们建议获得神经病理学病变的深入信息 是硒中毒造成的 此外，我们还将获得重要的生化 关于硒和烟酸在PFSP生产中的相互作用的数据， 尤其是烟酸代谢物。 目前，Se是一种积极研究的 微量营养素，在比较医学中具有广泛的意义， 尤其是其抗癌潜力。 最近已经 在美国，硒的毒性与 增加使用维生素和矿物质补充剂。 目前小电流 关于硒毒性信息可用。 我们的数据应该能为 有关硒毒性的信息。

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.