Dopamine-beta-hydroxylase does not appear to provide an index of sympathetic activity in this group of patients who, on the basis of the elevated plasma levels of NE, may demonstrate a chronic state of hyperactivity of the sympathetic nervous system.
Normal alpha-N-acetylglucosaminidase activity was observed in two obligate heterozygotes (the proband's father and her maternal grandmother), suggesting that in addition to the normal and defective alleles, a third, hyperactive allele is also present in this family.
These results support the concept that SLE B cell hyperactivity is promoted by dysregulation of endogenous cytokines and suggest that IL-6, in particular, has an important pathogenic role.
A 32:1 chance for the linkage of this rare IgH haplotype with the hyper-IgG1(A1) syndrome in the family argues for a dominant regulator located at the human IgH locus having a selective influence on the production of IgG1 and IgA1.
The hemostatic system hyperactivity as measured by this assay could be specifically corrected by rising plasma ATIII levels of several persons into the normal range.
Although in mice this cytokine has a well documented role in supporting antibody production, this study provides no evidence that IL-4 is involved in the B cell hyperactivity characteristic of human SLE.
Serum levels of the soluble form of the low-affinity receptor for IgE (FcERII, CD23) (sCD23) are elevated in autoimmune conditions associated with hypergammaglobulinaemia and B cell hyperactivity.
Systemic effects of chronic IL-11 exposure included loss of body fat, thymus atrophy, some alterations in plasma protein levels, frequent inflammation of the eyelids, and often a hyperactive state.
These differences were independent of the line of origin of the mice suggesting a causal relationship between the observed hyperactivity and the presence of multiple copies of the integrated human S100 beta gene.
These differences were independent of the line of origin of the mice suggesting a causal relationship between the observed hyperactivity and the presence of multiple copies of the integrated human S100 beta gene.
This provides a mechanism for their increased response to IL-2 and supports claims that elevated soluble IL-2R alpha serum levels reflect gut T-cell hyperactivity in this disease.
The apoB-100 gene EcoRI polymorphism influences the relationship between features of the insulin resistance syndrome and the hyper-apoB and dense LDL phenotype in men.
Genetically obese rodents also show hyperactivity of the NPY neurones, which is inappropriate to their energy needs and may contribute to their hyperphagia, reduced energy expenditure and excessive weight gain.
Hyperactivity of the FSH axis caused by activating mutations of the FSH receptor gene might parallel the presentation of FSH secreting pituitary adenomas with Sertoli cell hypertrophy in men (Heseltine et al., 1989) or reversible premature ovarian failure in women (Moses et al., 1986; Okuda et al., 1989).
The presence of eosinophilia in most HD patients and the presence of hyper-IgE in a subset of them may suggest that activated lymph node T cells release large amounts of IL5 and IL4, respectively.
The presence of eosinophilia in most HD patients and the presence of hyper-IgE in a subset of them may suggest that activated lymph node T cells release large amounts of IL5 and IL4, respectively.