INCREASED NERVE-GROWTH FACTOR BETA-CHAIN CROSS-REACTING MATERIAL IN FAMILIAL DYSAUTONOMIA

被引：43

作者：

SIGGERS, DC

ROGERS, JG

BOYER, SH

MARGOLET, L

DORKIN, H

BANERJEE, SP

SHOOTER, EM

机构：

[1] JOHNS HOPKINS UNIV, SCH MED, DEPT MED, DIV MED GENET, BALTIMORE, MD 21218 USA

[2] JOHNS HOPKINS UNIV, SCH MED, DEPT PHARMACOL & EXPTL THERAPEUTICS, CLAYTON LABS, BALTIMORE, MD 21218 USA

[3] JOHNS HOPKINS UNIV HOSP, BALTIMORE, MD 21205 USA

[4] STANFORD UNIV, SCH MED, DEPT GENET, STANFORD, CA 94305 USA

[5] STANFORD UNIV, SCH MED, LT JOSEPH P KENNEDY JR LABS, STANFORD, CA 94305 USA

来源：

NEW ENGLAND JOURNAL OF MEDICINE | 1976年 / 295卷 / 12期

关键词：

D O I：

10.1056/NEJM197609162951201

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

To determine whether human dysautonomia arises from an alteration in nerve-growth factor (NGF), serum levels of NGF subunits in normal and dysautonomic subjects were measured using a biologic assay based on neurite outgrowth from chick ganglions, a binding assay based on displacement of radiolabeled .beta.NGF from rabbit-ganglion microsomes, and radioimmunoassays of .alpha., .gamma. and .beta.NGF subunits via antiserum to mouse NGF polypeptides. A 3-fold increase (P < 0.001) in serum antigen levels of the biologically active subunit (.beta.NGF) was found for dysautonomic as compared with normal subjects. By all other assays the groups were alike. The marked discrepancy in .beta.NGF levels between antigenic and functional (biologic and binding) measurements suggests a qualitative abnormality of .beta.NGF in dysautonomia. Alternatively, elevation of .beta.NGF antigen can be regarded as secondary to disease. This alternative seems likely since it must then be suppossed that the normalcy of functional assays is spurious.

引用

页码：629 / 634

页数：6

共 29 条

[21] CURRENT CONCEPTS OF DYSAUTONOMIA - NEUROPATHOLOGICAL DEFECTS [J].