B-cell immune dysregulation with low soluble CD22 levels in refractory seronegative myasthenia gravis.

Myasthenia gravis (MG), primarily caused by acetylcholine receptor (AChR) autoantibodies, is a chronic autoimmune disorder causing severe muscle weakness and fatigability. In particular, seronegative MG constitutes 10%-15% of MG cases and presents diagnostic challenges especially in early-onset female patients who often show severe disease and resistance to immunosuppressive therapy. Furthermore, the immunopathology of seronegative MG remains unclear.

Photonic digital-to-analog conversion using a blue frequency chirp in a semiconductor optical amplifier.

In this Letter, we present a photonic digital-to-analog conversion (DAC) technique based on blue-chirp spectral slicing using a semiconductor optical amplifier (SOA). Because the gain change in an SOA leads to a refractive-index change based on the change in intensity of the input data signal, the probe signals experience a dynamic frequency shift to a shorter-wavelength side called a blue-chirp. After passing through the SOA, the probe signals corresponding to the logic level of the input digital signal are extracted by filtering only the blue-chirp component of the probe signals using rectangular-shape filters.

Gene Signature-Based Approach Identified MEK1/2 as a Potential Target Associated With Relapse After Anti-TNFα Treatment for Crohn's Disease.

Background: Anti-tumor necrosis factor alpha (anti-TNFα) therapy has become the mainstay of therapy for Crohn's disease (CD). However, post-therapy, the recurrence rate is still high. The aim of this study was to dissect the molecular mechanism for recurrence of CD treated with anti-TNFα therapy and investigate novel therapeutic options that could induce complete remission.

Pharmacological inhibitory profile of TAK-828F, a potent and selective orally available RORγt inverse agonist.

Retinoic acid-related orphan receptor γt (RORγt) is a key master regulator of the differentiation and activation of IL-17 producing CD4 Th17, CD8 Tc17 and IL-17/IFN-γ co-producing cells (Th1/17 cells). These cells play critical roles in the pathogenesis of autoimmune diseases such as inflammatory bowel disease and multiple sclerosis. Thus, RORγt is an attractive target for the treatment of these diseases.

The adenomatous polyposis coli-associated guanine nucleotide exchange factor Asef is involved in angiogenesis.

Mutation of the tumor suppressor adenomatous polyposis coli (APC) is a key early event in the development of most colorectal tumors. APC promotes degradation of beta-catenin and thereby negatively regulates Wnt signaling, whereas mutated APCs present in colorectal tumor cells are defective in this activity. APC also stimulates the activity of the guanine nucleotide exchange factor Asef and regulates cell morphology and migration.

Adenomatous polyposis coli and Asef function downstream of hepatocyte growth factor and phosphatidylinositol 3-kinase.

Mutations of the tumor suppressor adenomatous polyposis coli (APC) are responsible for sporadic and familial colorectal tumors. APC negatively regulates Wnt signaling by inducing beta-catenin degradation. It has also been shown that APC plays a role in the organization of cytoskeletal networks.