Abstract: The present application provides an amidase mutant and use thereof. The amidase mutant comprises: (a) a protein having an amino acid sequence as shown in SEQ ID NO: 1; or (b) a protein having amidase functions after amino acid mutation at least one of the following sites of the amino acid sequence as shown in (a): L81, E62, M311, N180, P121, R58, E32, T230, N82, N190, D192, D217, H219, K77, M78, P79, F80, F61, D185, D59, L182, T183, P184, 1227, C228, G229, A231 or V232; or (c) a protein having 80% or more identity with the amino acid sequence defined in any one of (a) and (b) and having amidase functions.

Abstract: Provided herein are antibodies that specifically bind to MICA/B having variable heavy chain domains (VH), variable light chain domains (VL), and complementarity determining regions disclosed herein, as well as methods and uses thereof.

Abstract: The present disclosure relates to antibodies that bind the extracellular domain of human TREM2 and the use of anti-TREM2 antibodies in therapy, prophylaxis, diagnosis, screening, and monitoring, including for increasing levels of soluble TREM2 (sTREM2) in serum and brain, increasing phagocytosis by microglia and/or macrophages, and developing treatments to address TREM2-mediated conditions that may benefit from enhanced phagocytosis by microglia and/or macrophages.

Abstract: The present disclosure relates to antibodies that bind the extracellular domain of human TREM2 and the use of anti-TREM2 antibodies in therapy, prophylaxis, diagnosis, screening, and monitoring, including for increasing levels of soluble TREM2 (sTREM2) in serum and brain, increasing phagocytosis by microglia and/or macrophages, and developing treatments to address TREM2-mediated conditions that may benefit from enhanced phagocytosis by microglia and/or macrophages.

Abstract: Provided herein are antibodies that specifically bind to MICA/B having heavy chain, light chain, variable heavy chain domains (VH), variable light chain domains (VL), and complementarity determining regions (CDRs) disclosed herein, as well as methods and uses thereof.

Abstract: The present disclosure relates to antibody peptide conjugates with a means to bind MuSK, such as an anti-MuSK antibody, and a PRAD peptide. The present disclosure also relates to an antibody-drug conjugate including an anti-Musk antibody and a drug, and optionally a PRAD peptide.

Abstract: The invention relates to dibenazine derivatives, pharmaceutical compositions and uses, in particular to a compound shown in formula (I) or a pharmaceutically acceptable salt, stereoisomer, tautomer, precursor drug, amorphous substance, isotope body, polycrystalline substance or solvent compound thereof. Pharmaceutical compositions containing the compound and the use of the compound in improving the bioavailability of desipramine hydrochloride.

Abstract: A connector includes an insulating housing and at least one conductive component. The insulating housing includes an outer casing, at least one first guiding portion and at least one first snapping portion. The outer casing defines an accommodation space and a first opening communicated with the accommodation space. The first guiding portion and the first snapping portion are respectively connected to the outer casing. The conductive component includes a conductive body, a second guiding portion and a second snapping portion. The conductive body is at least partially located in the accommodation space and penetrates through the first opening. The second guiding portion and the second snapping portion are respectively disposed on the conductive body. The second guiding portion is configured to couple with the first guiding portion. The second snapping portion is configured to snap with the first snapping portion.

Abstract: The present disclosure relates to anti-Muscle-Specific Kinase (MuSK) antibodies, in particular agonistic ant-MuSK antibodies, useful to restore or increase the function of the neuromuscular junction (NMJ).

Abstract: The present disclosure relates to antibodies that bind the extracellular domain of human TREM2 and the use of anti-TREM2 antibodies in therapy, prophylaxis, diagnosis, screening, and monitoring, including for increasing levels of soluble TREM2 (sTREM2) in serum and brain, increasing phagocytosis by microglia and/or macrophages, and developing treatments to address TREM2-mediated conditions that may benefit from enhanced phagocytosis by microglia and/or macrophages.

Abstract: The present disclosure relates to antibodies that bind the extracellular domain of human TREM2 and the use of anti-TREM2 antibodies in therapy, prophylaxis, diagnosis, screening, and monitoring, including for increasing levels of soluble TREM2 (sTREM2) in serum and brain, increasing phagocytosis by microglia and/or macrophages, and developing treatments to address TREM2-mediated conditions that may benefit from enhanced phagocytosis by microglia and/or macrophages.

Abstract: A CTC-based train operation adjustment method and apparatus are provided. The adjustment apparatus includes a TDMS system interface server, a TD combined and shared intermediate database, a CTC system, a TD combined interface server and the like. The CTC system further includes a CTC system communication server, a running diagram platform and the like.

Abstract: Provided in the present invention is a pharmaceutical composition comprising hydroxyprogesterone caproate and an additional therapeutic agent for treating tumors, wherein the additional therapeutic agent is preferably a monoclonal antibody against PD-1 or PD-L1. Further provided in the present invention are a method for increasing the number of tumor infiltrating lymphocytes (TIL) as required and a method for treating cancers in a subject in need thereof, which comprises providing the hydroxyprogesterone caproate to the subject.

Abstract: Antibodies and antigen-binding fragments thereof that bind type II transmembrane serine protease 6 (TMPRSS6) on the surface of a cell and increase hepcidin expression, and methods for treating disorders of iron metabolism using anti TMPRSS6 antibodies and fragments, are provided.

Abstract: Using artificial intelligence (AI)-based techniques to detect glitches in audiovisual data can improve the reliability of glitch detection and reduce the cost of system validation and/or maintenance. An AI-based method for detecting glitches in an image can include extracting one or more features from the image; providing the image and the extracted features as inputs to a model; and generating, by the model, a classification output indicating whether the image is glitched. An AI-based method for detecting glitches in an audio data segment can include generating an image including a spectrogram of the audio data segment; providing, the image as input to a model; and generating, by the model, a classification output indicating whether the audio data segment represented by the image is glitched. Records of the glitches can be generated, and the validation status of a system-under-test (SUT) can be determined based on the records.