Siggers D C, Rogers J G, Boyer S H, Margolet L, Dorkin H, Banerjee S P, Shooter E M
N Engl J Med. 1976 Sep 16;295(12):629-34. doi: 10.1056/NEJM197609162951201.
To determine whether dysautonomia arises from alteration in nerve-growth factor (NGF), we measured serum levels of NGF subunits in normal and dysautonomic subjects using a biologic assay based on neurite outgrowth from chick ganglions, a binding assay based on displacement of radiolabeled betaNGF from rabbit-ganglion microsomes, and radioimmunoassays of chi, gamma and betaNGF subunits via antiserum to mouse NGF polypeptides. A threefold increase (P less than 0.001) in serum antigen levels of the biologically active subunit (betaNGF) was found for dysautonomic as compared with normal subjects. By all other assays, the groups were alike. The marked discrepancy in betaNGF levels between antigenic and functional (biologic and binding) measurements suggests a qualitative abnormaltiy of betaNGF in dysautonomia. Alternatively, elevation of betaNGF antigen can be regarded as secondary to disease. This alternative seems less likely since we must then suppose that the normalcy of functional assays in spurious.
为了确定自主神经功能障碍是否由神经生长因子（NGF）的改变引起，我们使用基于鸡神经节神经突生长的生物学检测法、基于从兔神经节微粒体中置换放射性标记βNGF的结合检测法以及通过针对小鼠NGF多肽的抗血清对α、γ和βNGF亚基进行放射免疫测定，来测量正常和自主神经功能障碍受试者血清中NGF亚基的水平。与正常受试者相比，自主神经功能障碍受试者血清中生物活性亚基（βNGF）的抗原水平增加了三倍（P<0.001）。通过所有其他检测，两组情况相似。βNGF水平在抗原性和功能性（生物学和结合）测量之间的明显差异表明自主神经功能障碍中βNGF存在质量异常。或者，βNGF抗原的升高可被视为疾病的继发结果。这种可能性似乎较小，因为那样我们就必须假定功能性检测的正常性是虚假的。
