Inflammatory cell recruitment to local sites of tissue injury and/or infection is controlled by many signaling processes influencing cell-to-cell interactions between vascular endothelial cells (EC) in post-capillary venules and circulating leukocytes. Here we report that the ATP-release channel Pannexin1 (Panx1) opens downstream of EC activation by tumor necrosis factor α (TNFα). This process involves activation of Type 1 TNF receptors, recruitment of Src Family Kinases (SFK), and SFK-dependent phosphorylation of Panx1. We report a previously unidentified role for Panx1 channels in promoting leukocyte adhesion and emigration through the venous wall during acute systemic inflammation. The present application further discloses that Panx IL2 peptide consisting of amino acid sequence KYPIVEQYLKYGRKKQRR (SEQ ID NO:3) or .sup.10Panx1 peptide consisting of amino acid sequence WRQAAFVDSY (SEQ ID NO:8) are inhibitors of leukocyte adhesion.

The present disclosure provides monoclonal antibodies that target intracytoplasmic inclusion bodies and/or hepacivirus C NS4A and methods for their use.

Among the various aspects of the present disclosure is the provision of a method of detection, treatment, and monitoring of cardiovascular disease or a foot wound by detection of a novel biomarker, Fatty Acid Synthase (FAS). Briefly, therefore, the present disclosure is directed to methods that allow for improved, noninvasive, and reliable diagnosis of these conditions, particularly in subjects suffering from Type 2 Diabetes (T2D).

Compositions and methods are provided for diagnosis, prognosis, and/or monitoring of Kawasaki disease or MIS-C (e.g., associated with SARS-CoV-2 infection) in a subject. In some embodiments, the method includes measuring, comparing and weighting the level of particular proteins to other proteins. In other embodiments, the method includes comparison with clinical variable information.

A biomarker for determining Kawasaki disease is identified by lipidomic analysis and mass spectrometry. With the use of the biomarker, we develop and provide a kit and a method capable of directly and objectively determining whether the subject suspected of having Kawasaki disease suffers from Kawasaki disease. A kit for determining Kawasaki disease, the kit including LOX-1 protein and/or part thereof having LAB-binding ability, the protein or part thereof being immobilized on a surface of a base material, is provided.

The present disclosure provides pharmaceutical formulations of compounds designed for improving the condition of the glycocalyx and/or reducing inflammation and/or oxidative damage, as well as related methods.

The present invention relates to the determination of levels or expression of particular biomarkers in biological samples which can be utilized to diagnose, prognose, and treat Kawasaki disease in subjects, and further to select subjects who would benefit from a Kawasaki disease therapy other than, or in addition to, IVIG treatment. Accordingly, the present invention encompasses methods and compositions that utilize these biomarkers for the diagnosis, prognosis, and treatment of Kawasaki disease.

Some embodiments of the methods and compositions provided herein relate to the detection of biomarkers for Kawasaki disease (KD), the diagnosis of KD in a subject, and/or the amelioration or treatment of KD in a subject. In some embodiments, a biomarker can include a long intergenic non-coding RNA (lincRNA). In some embodiments, the biomarker can be present in an exosome-enriched serum sample from a subject.

Means and methods for determining whether an individual that does not have rheumatoid arthritis, AAV or Sjgren syndrome at the moment of sampling is at risk of developing the disease, the method comprising determining whether an antibody-containing sample of the individual comprises an autoantibody associated with the disease that comprises an N-linked glycosylation at one or more positions in a Fab-portion of the antibody, the method further comprising determining the risk of the individual for developing the disease. The disease is preferably rheumatoid arthritis.

Two patients diagnosed with KLS were treated. One patient had severe KLS that progressed to the equivalent of pediatric Kawasaki Disease Shock Syndrome (KDSS). The second patient had a typical KLS presentation and clinical course. Cytokines and chemokines provide inflammatory signatures in the serum that reflect the polarity of the immune response and the affected cell types. Multiplex ELISA technology was used to define the cytokine milieu in the serum of the two adult HIV patients with KLS during the acute and convalescent phases. Those sera were compared with sera from asymptomatic HIV subjects and a normal serum control. Those comparisons suggest that HIV KLS is a dysfunctional Th2 response to an unknown inciting agent in the vascular wall, and that a multiplex ELISA or similar technology based a limited combination of KLS/KD pathogenesis-related cytokines (IL-6, IL-13, sTNFRII) and endothelial/smooth muscle chemokines (CCL1, CCL2, CxCL11) may provide an objective tool for diagnosing KLS and Kawasaki Disease. Because KD and HIV KLS are the only known Th2 vasculitidies that spare the lungs (unique clinical presentation) and include plasma cell infiltration of the vascular wall as a prominent histopathologic feature (unique pathophysiology), a diagnostic test based on combinations of the above analytes will be highly specific and therefore clinically useful.