The present disclosure provides a microbead and a method for preparing the same. Also provided is a method for detecting and analyzing biomolecules in sample by using element analysis.

Disclosed are methods of isolating a TCR having antigenic specificity for a mutated amino acid sequence encoded by a cancer-specific mutation, the method comprising: identifying one or more genes in the nucleic acid of a cancer cell of a patient, each gene containing a cancer-specific mutation that encodes a mutated amino acid sequence; inducing autologous APCs of the patient to present the mutated amino acid sequence; co-culturing autologous T cells of the patient with the autologous APCs that present the mutated amino acid sequence; selecting the autologous T cells; and isolating a nucleotide sequence that encodes the TCR from the selected autologous T cells, wherein the TCR has antigenic specificity for the mutated amino acid sequence encoded by the cancer-specific mutation. Also disclosed are related methods of preparing a population of cells, populations of cells, TCRs, pharmaceutical compositions, and methods of treating or preventing cancer.

A method for predicting sepsis or diagnosing systemic inflammatory response syndrome (SIRS) and/or sepsis in a subject comprises determining levels of at least three markers selected from CCL23, A1AT, CRP, sICAM, PLA2, IL-6, procalcitonin, MMP8, TNFalpha, AcPGP, enzymatic MMP activity, TIMP1, sRAGE and desmosine in a sample taken from the subject. The combined levels of the at least three markers are used to predict or diagnose SIRS and/or sepsis. The methods may be performed on a subject with SIRS and which is used to identify an infection in the subject. A preferred panel of markers includes CCL23, A1AT, sICAM, sICAM/VCAM-1 and CRP. Corresponding products, methods of treatment and medical uses are provided.

Disclosed herein is a method for detecting liver disease in a patient. Also, disclosed are methods of isolating EVs derived from hepatocytes. Methods of assessing effectiveness of liver therapies are also disclosed. Methods involve isolating or otherwise obtaining EVs derived from hepatocytes and analyzing the content of the EVs.

Peptide with high binding affinity for tumor necrosis factor alpha (TNF-α). The peptide has an amino acid sequence of SEQ.ID.NO.1, or the peptide is a tandem or branched peptide with a single repeat or multiple repeats of SEQ.ID.NO.1 and SEQ.ID.NO.3 and has an amino acid sequence of SEQ.ID.NO.4. The peptide can bind to TNF-α with high affinity and can antagonize TNF-α function. When being directly injected to an animal, the peptide can significantly reduce the degree of inflammation of an animal body and improve the resistance of the animal body on an inflammatory damage. The peptide can be used for developing TNF-α antagonist drugs for treating various acute and chronic inflammatory damage, such as inflammatory, autoimmune and stress damage caused by physical, chemical and biological factors. Thus, the peptide has an extremely wide application prospect. Moreover, the peptide has a small molecular weight and low immunogenicity, and is easy to synthesize, thereby avoiding the side effects and disadvantages of traditional monoclonal antibody drug antagonists.

The present invention relates to predictors of a cancer patient's responsiveness to immunotherapy for cancer.

The present inventors have identified specific oncogenic pathways preferentially activated in BRAF-mutated-melanoma cells and a pathway pattern that predicts resistance of BRAF-mutated melanoma to BRAF/MEK inhibitors, providing novel clinical implications for melanoma therapy. In one embodiment, a method comprises (a) testing a sample oiBRAF-mutated melanoma cells isolated from a patient and measuring the expression levels of genes expressed in the following oncogenic pathways: TNFa, EGFR, IFNa, hypoxia, IFNy, STAT3 and Myc; (b) calculating a 7-pathway activation pattern based on the measured expression levels of step (a); and (c) identifying the patient's resistance level to BRAF/MEK inhibitor treatment based on comparison of the calculated 7-pathway activation pattern to a reference.

Presented herein are systems and methods for developing classifiers useful for predicting response to particular treatments. For example, in some embodiments, the present disclosure provides a method of treating subjects suffering from an autoimmune disorder, the method comprising administering an alternative to anti-TNF therapy to subjects who have been determined to be non-responsive via a classifier established to distinguish between responsive and non-responsive prior subjects in a cohort who have received the anti-TNF therapy.

A new, stable trimeric TNFα structure is disclosed with distorted symmetry which can bind to the TNFR1 receptor to attenuate signalling therefrom, which can be used in the treatment and/or prevention of diseases associated with the soluble TNFα/TNFR1 interaction. Membrane-bound TNFα is not affected in its ability to signal through TNFR2, and thus the new structure of TNFα may be used in therapies which do not significantly raise the risk of infection or malignancy.

The application relates to methods of treating chronic viral infection by modulating Tim-3 activity. In addition, the present application relates to methods of diagnosing or monitoring immune system activity or function, chronic viral infection and inflammatory disease using Tim-3 expression.