Abstract: A method and system for automatic analysis of a testing substrate for an analyte in a liquid sample. The sample is applied to a testing substrate having an immobilized thereon, in a limited region of the testing substrate, a receptor capable of binding to the analyte. A labeled reagent, capable of binding to the analyte, is added to the testing substrate. If the analyte is present, a color is generated at the area of the testing substrate where the receptor is immobilized. The testing substrate is then illuminated and, using electronic equipment a digital image of the testing substrate is acquired and automatically scanned to locate an area of the testing substrate having the highest color density and generating a first measurement of color density. Next, an area peripheral to the area of highest color density is located and a second measurement of color density is generated.

Abstract: The present invention involves the use of Tripterygium Wilfordii Hook F extracts in the treatment of rheumatoid arthritis. An alcohol extract of this plant (T2) inhibited antigen- and mitogen-stimulated proliferation of T cells and B cells, cell cycle progression, interleukin-2 (IL-2) production by T cells, immunoglobulin production by B cells and interleukin-2 mRNA production. T2 did not affect IL-2 receptor expression by T cells, IL-1 production by monocytes, the capacity of monocytes to present antigen, or signaling pathways. Inhibition could not be accounted for by nonspecific toxicity. These results support the conclusion that T2 exerts a powerful suppressive effect on human immune responses. Suppressing autoimmune disease is a most preferred embodiment of this invention.

Abstract: The present invention provides for the use of Tripterygium wilfordii Hook F extracts and purified components thereof in the treatment of inflammation or an immune disorder with concomitant lack of steroidal effect. Extracts of this plant (T2) bound to the glucocorticoid receptor and competitively inhibited glucocorticoid mediated cellular processes, such as dexamethasone binding to the glucocorticoid receptor, glucocorticoid mediated activation of target genes, dexamethasone dependent cellular growth, with concomitant inhibition of cyclooxygenase-2 induction and inflammatory processes such as the production of prostaglandin E.sub.2. The T2 extract components triptolide and tripdiolide were effective inhibitors. The particular advantage provided by the methods herein is the treatment or prevention of inflammation and the concomitant lack of steroidal agonist effects and NSAID side effects. Conditions treatable by the present methods include inflammation and immune disorders including autoimmune disease.

Abstract: A method and system for automatically analyzing the presence of an analyte in a liquid specimen of biological origin are described. The liquid specimen is added to a testing substrate that has a receptor immobilized on a portion of its surface. If analyte is present in the specimen, it will specifically bind to the receptor. A labeled reagent is added to the testing substrate which will bind to the analyte, if present, and generate a color on the testing substrate. The testing substrate is then illuminated and, using electronic equipment, a digital image of its surface is acquired and automatically scanned to locate an area that has the highest color density, which corresponds to the presence of labeled reagent. A measurement of color density, corresponding to pixels per unit area, is generated. An area peripheral to the area of highest color density, which represents background density, is also located and a measured.

Abstract: The present invention provides for the use of Tripterygium wilfordii Hook F extracts and purified components thereof in the treatment of inflammation or an immune disorder with concomitant lack of steroidal effect. Extracts of this plant (T2) bound to the glucocorticoid receptor and competitively inhibited glucocorticoid mediated cellular processes, such as dexamethasone binding to the glucocorticoid receptor, glucocorticoid mediated activation of target genes, dexamethasone dependent cellular growth, with concomitant inhibition of cyclooxygenase-2 induction and inflammatory processes such as the production of prostaglandin E.sub.2. The T2 extract components triptolide and tripdiolide were effective inhibitors. The particular advantage provided by the methods herein is the treatment or prevention of inflammation and the concomitant lack of steroidal agonist effects and NSAID side effects. Conditions treatable by the present methods include inflammation and immune disorders including autoimmune disease.

Abstract: The present invention involves the use of Tripterygium Wilfordii Hook F extracts in the treatment of rheumatoid arthritis. An alcohol extract of this plant (T2) inhibited antigen- and mitogen-stimulated proliferation of T cells and B cells, cell cycle progression, interleukin-2 (IL-2) production by T cells, immunoglobulin production by B cells and interleukin-2 mRNA production. T2 did not affect IL-2 receptor expression by T cells, IL-1 production by monocytes, the capacity of monocytes to present antigen, or signaling pathways. Inhibition could not be accounted for by nonspecific toxicity. These results support the conclusion that T2 exerts a powerful suppressive effect on human immune responses. Suppressing autoimmune disease is a most preferred embodiment of this invention.

Abstract: The present invention involves the use of Tripterygium Wilfordii Hook F extracts in the treatment of rheumatoid arthritis. An alcohol extract of this plant (T2) inhibited antigen- and mitogen-stimulated proliferation of T cells and B cells, cell cycle progression, interleukin-2 (IL-2) production by T cells, immunoglobulin production by B cells and interleukin-2 mRNA production. T2 did not affect IL-2 receptor expression by T cells, IL-1 production by monocytes, the capacity of monocytes to present antigen, or signaling pathways. Inhibition could not be accounted for by nonspecific toxicity. These results support the conclusion that T2 exerts a powerful suppressive effect on human immune responses. Suppressing autoinnune disease is a most preferred embodiment of this invention.