Subject Index for Volume 32

Subject Index

Subject Index for Volume 32     

Author Index to Volume 32

Myasthenia gravis is a spontaneously occurring autoimmune disease in which antibodies and lymphocytes are specifically reactive with nicotinic ACh receptors of skeletal muscle. Antibodies reactive with junctional receptors of human muscle are found in 90% of patients with myasthenia gravis and not at all in other diseases. Their capacity to cross the placenta suggests their involvement in the pathogenesis of neonatal myasthenia. The role of the thymus in myasthenia gravis remains a mystery, but it has recently been established that the thymus contains nicotinic ACh receptors and that anti-receptor antibodies are present in myasthenic thymuses.

Antibodies of myasthenic patients detect only partial cross reactivity between ACh receptors of different species. However, greater antibody binding is observed with receptors isolated from denervated rat muscle than with receptors from normal rat muscle. This suggests that extrajunctional and junctional ACh receptors might express different antigenic determinants. Although human antibodies bind minimally to ACh receptors of the electric organs of eels and marine rays, lymphocyte reactivity to electric eel receptors is found in high incidence in myasthenic patients. This suggests that electric organ and mammalian muscle ACh receptors may share more lymphocyte-defined than serologically-defined antigenic determinants.

Both cellular and Numeral immune responses to ACh receptors can be induced experimentally. Sufficient antigenic homology exists between receptors of different species that electric organ receptors are capable of inducing in mammals experimental autoimmune myasthenia gravis. Syn-geneic muscle receptor also is immunogenic in rats. Induction of both myasthenia and antibodies to ACh receptor requires participation of thymus-derived lymphocytes. The majority of ACh receptors in myasthenic rat muscle exist complexed with antibody, but antibody is not bound directly to the receptor's ACh-binding site. Anti-receptor antibodies in vitro are capable of impairing the electrophysiological function of ACh receptors with minimal blocking of the ACh-binding site and in the absence of complement. Thus, myasthenia gravis and its experimental model provide unique biological tools for studying the structure, function and pathology of cell membrane receptors.     

Subject Index to Volume 21

ABSTRACT

A novel amperometric immunosensor, based on graphite paste (graphite powder and paraffin oil), has been constructed for the assay of l-T₄. The graphite paste is impregnated with mouse monoclonal anti-(+)-3,3′,5,5′-tetraiodo-l-thyronine (anti-l-T₄). The immunosensor can be reliably used for the assay of l-T₄ in thyroid and in drugs, using chronoamperometry technique, at ppt up to ppb concentration levels. The potential used for l-T₄ assay was +450 mV vs. Ag/AgCl electrode. The surface of the immunosensor can be regenerated by simply polishing, obtaining fresh immunocomposite ready to be used in a new assay.     

Subject Index to Volume 25

Background: Tacrolimus causes post-transplant diabetes mellitus, however the pathogenetic mechanisms remain controversial. In this study we probed into the mechanisms of tacrolimus-induced diabetes mellitus in rats. Methods: Glucose levels were determined on whole blood samples using a glucose oxidase method. Levels of serum insulin and C-peptide were measured with ELISA. Histological damage of ultra-structure and apoptosis of beta cells of the pancreas were assayed with electric microscope and tunnel methods respectively.—Ultra-structure were assayed with electric microscope and apoptosis of beta cells of the pancreas were assayed with tunel methods. Immunohistochemistry was utilized to detect the sum of insulin receptors of hepatic cells. Results: Compared to control group, insulin and C peptide levels in serum decreased in rats of diabetes mellitus models induced with FK506(P<0.05). Compared to the control group, the sum of apoptosis body in pancreatic islets increased in rats of diabetes mellitus models induced with FK506 (P<0.05). Compared to the control group, electron microscopy showed cytoplasm swelling and vacuolization, and marked decrease or absence of dense-core secretory granules in beta cells in rats with diabetes mellitus induced with FK506.Compared to the control group, expression of insulin receptor of hepatic cell decreased in rats of diabetes mellitus models induced with FK506 (P<0.05). Conclusion: Pathogenetic mechanisms of rats of diabetes mellitus models induced with FK506 including reduction of secretion of insulin in beta cells of pancreatic islets, damages of ultra-structure of beta cells of pancreatic islets, increasing of apoptosis of beta cells of pancreatic islets and decreasing of expression of insulin receptors in hepatic cells.