The clinical need for clustered AChR cell-based assay testing of seronegative MG.

Trial eligibility in myasthenia gravis (MG) remains largely dependent on a positive autoantibody serostatus. This significantly hinders seronegative MG (SNMG) patients from receiving potentially beneficial new treatments. In a subset of SNMG patients, acetylcholine receptor (AChR) autoantibodies are detectable by a clustered AChR cell-based assay (CBA).

Elevated N-Linked Glycosylation of IgG V Regions in Myasthenia Gravis Disease Subtypes.

Elevated N-linked glycosylation of IgG V regions (IgG-V) is an emerging molecular phenotype associated with autoimmune disorders. To test the broader specificity of elevated IgG-V, we studied patients with distinct subtypes of myasthenia gravis (MG), a B cell-mediated autoimmune disease. Our experimental design focused on examining the B cell repertoire and total IgG.

Aberrant expression of USF2 in refractory rheumatoid arthritis and its regulation of proinflammatory cytokines in Th17 cells.

IL-17-producing Th17 cells are implicated in the pathogenesis of rheumatoid arthritis (RA) and TNF-α, a proinflammatory cytokine in the rheumatoid joint, facilitates Th17 differentiation. Anti-TNF therapy ameliorates disease in many patients with rheumatoid arthritis (RA). However, a significant proportion of patients do not respond to this therapy.

Thymus-derived B cell clones persist in the circulation after thymectomy in myasthenia gravis.

Myasthenia gravis (MG) is a neuromuscular, autoimmune disease caused by autoantibodies that target postsynaptic proteins, primarily the acetylcholine receptor (AChR) and inhibit signaling at the neuromuscular junction. The majority of patients under 50 y with AChR autoantibody MG have thymic lymphofollicular hyperplasia. The MG thymus is a reservoir of plasma cells that secrete disease-causing AChR autoantibodies and although thymectomy improves clinical scores, many patients fail to achieve complete stable remission without additional immunosuppressive treatments.

Single-cell repertoire tracing identifies rituximab-resistant B cells during myasthenia gravis relapses.

Rituximab, a B cell-depleting therapy, is indicated for treating a growing number of autoantibody-mediated autoimmune disorders. However, relapses can occur after treatment, and autoantibody-producing B cell subsets may be found during relapses. It is not understood whether these autoantibody-producing B cell subsets emerge from the failed depletion of preexisting B cells or are generated de novo.

Molecular determinants of permeation in a fluoride-specific ion channel.

Fluoride ion channels of the Fluc family combat toxicity arising from accumulation of environmental F. Although crystal structures are known, the densely packed pore region has precluded delineation of the ion pathway. Here we chart out the Fluc pore and characterize its chemical requirements for transport.

Tuning the threshold voltage in electrolyte-gated organic field-effect transistors.

Low-voltage organic field-effect transistors (OFETs) promise for low power consumption logic circuits. To enhance the efficiency of the logic circuits, the control of the threshold voltage of the transistors are based on is crucial. We report the systematic control of the threshold voltage of electrolyte-gated OFETs by using various gate metals.

Selectivity and sensitivity of a reagentless electrochemical DNA sensor studied by square wave voltammetry and fluorescence.

Poly(5-hydroxy-1,4-naphthoquinone-co-5-hydroxy-3-thioacetic acid-1,4-naphthoquinone)-modified electrode is used for the direct electrochemical detection of oligonucleotide hybridization. The polymer film presents well-defined electroactivity in the cathodic potential domain (between 0 and -0.8 V/SCE), due to the quinone group embedded into the polymer structure.