15 results about "Myelin basic protein" patented technology

The invention belongs to the technical field of tolerogen vaccines, and particularly relates to a tolerogen vaccine for treating multiple sclerosis and a preparation method and application of the tolerogen vaccine. The tolerogen vaccine comprises myelin basic protein, protein lipid protein and an antigen peptide fragment composition of myelin oligodendroglia glycoprotein, the preparation method comprises the following steps: S1, preparing a polypeptide mixture solution and an anionic liposome solution; s2, preparing a polypeptide mixture liposome preparation from the polypeptide mixture solution and the anionic liposome solution by adopting an injection method; s3, the polypeptide mixture lipidosome preparation is diluted, filtered and purified, and the lipidosome entrapped tolerogen vaccine is obtained.The multi-antigen tolerogen vaccine can be delivered through lipidosome, the limitation of a single antigen therapy is overcome, the immune tolerance induction effect is enhanced by means of the delivery advantage of lipidosome, and the application prospect is wide. And an efficient and safe novel precise therapy method is provided for MS treatment.

Compositions and methods for treating, preventing, or reversing neuroinflammation-related disorders or autoimmune neurological disorders in a subject in need thereof are disclosed. The methods comprise administering a therapeutically effective amount of a composition comprising a myelin basic protein (MBP) peptide.

Disclosed is a protein comprising no more than three human autoantigenic proteins, wherein a first human autoantigenic protein comprises a truncated myelin oligodendrocyte glycoprotein (MOG) amino acid sequence, a second human autoantigenic protein comprises a myelin basic protein (MBP) amino acid sequence, and a third human autoantigenic protein comprises a truncated proteolipid protein (PLP) amino acid sequence. Also disclosed are related nucleic acids, pharmaceutical compositions, methods of treating a demyelinating disease, and methods of producing the proteins.

This invention provides methods of detecting biomarkers in the biofluid of sepsis-associated encephalopathy (SAE) patients, including but not limited to glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase LI, Tan protein, Neurofilament light chain (NF-L), myelin basic protein (MBP), secretogranin, Copeptin, total all-spectrin, all-spectrin breakdown products (SBDP, including SBDP145, SBDP150, SBDP120 all-spectrin N-terminal fragment or SBDP150N), neuron specific enolase (NSE), mature brain derived neurotrophic factor (BDNF), and full-length Pro-BDNF. These biomarker peptides are markers of axonal and blood brain barrier integrity which can be used to diagnose SAE and to assess and predict cognitive performance and outcomes in acute presentations of sepsis.

The present application provides a kind of nutritional composition in the application of the product for improving learning, memory and cognitive ability.The nutritional composition includes animal bifidobacterium lactis subsp.CP-9 and 3'-sialyllactose.Animal bifidobacterium lactis subsp.CP-9 and 3'-sialyllactose can synergistically enhance the memory retention ability of the body, reduce the degree of learning and memory errors, and up-regulate the expression of oligodendrocyte transcription factor 2 coding gene, myelin basic protein coding gene and brain-derived neurotrophic factor coding gene, realize the double regulation of myelin formation and neurotrophic in hippocampus region of brain, synergistically improve the neural plasticity of central nervous system through gut-brain axis pathway, and then double improve the learning, memory and cognitive function of the body from the behavior and molecular level.

The present invention relates to an engineered regulatory T cell (Treg) comprising a T cell receptor (TCR) which is capable of specifically binding to a myelin basic protein (MBP) peptide or variant or fragment thereof when the peptide is presented by a major histocompatibility complex (MHC) molecule. The present invention further relates to methods for providing an engineered Treg and to methods and uses of said engineered Treg and vectors and kits of vectors encoding said Treg.

The invention discloses a method for researching the action mechanism of saikoside D on paclitaxel-induced peripheral neuropathy, and relates to the technical field of disease mechanism research and drug development. Comprising the following steps: performing continuous administration through intraperitoneal injection of paclitaxel, and establishing a paclitaxel-induced peripheral neuropathy animal model; a von Frey cellosilk experiment and a cold and hot plate experiment are adopted for behavioral detection, and mechanical pain threshold and cold and hot pain sense changes are evaluated; the morphological structure change of the sciatic nerve myelin sheath is observed through Luxol Fast Blue staining; and the expression level of the myelin sheath basic protein in the sciatic nerve is detected by using immunofluorescence staining and Western blotting technologies. According to the invention, a closed-loop research system is formed from animal model construction to molecular mechanism verification; based on behavioral detection, histological analysis and multiple dimensions of a molecular biological technology, the data reliability is ensured, and the curative effect of saikoside D can be comprehensively evaluated.

Disclosed is a protein comprising no more than three human autoantigenic proteins, wherein a first human autoantigenic protein comprises a truncated myelin oligodendrocyte glycoprotein (MOG) amino acid sequence, a second human autoantigenic protein comprises a myelin basic protein (MBP) amino acid sequence, and a third human autoantigenic protein comprises a truncated proteolipid protein (PLP) amino acid sequence. Also disclosed are related nucleic acids, pharmaceutical compositions, methods of treating a demyelinating disease, and methods of producing the proteins.

A method of differentiating nonhuman primate induced pluripotent stem cells (iPSCs) to oligodendrocytes is provided. The method may include providing a modified vector comprising a piggyBac vector backbone that expresses one or more differentiation factor genes, including SOX10, OLIG2, and NKX6-2. The piggyBac vector backbone may comprise one or more terminal inverted repeats and one or more transposase recognition sites configured to interact with a piggyBac transposase to mediate genomic integration at TTAA or noncanonical target sequences. The vector may further include a selectable marker and a promoter for regulated expression. The modified vector may be introduced into nonhuman primate iPSCs, for example from Macaca fascicularis, by electroporation and used in a feeder-free differentiation workflow. The resulting differentiated cells may be identified by expression of oligodendrocyte-associated markers including O4, O1, PDGFRA, MOG, GALC, CNPase, and myelin basic protein (MBP).

The invention belongs to the technical field of fusion proteins, and particularly relates to a fusion protein and application thereof in treatment of multiple sclerosis, the fusion protein is prepared by fusing myelin basic protein, myelin oligodendroglia glycoprotein and proteolipid protein, key epitopes of three main myelin sheath antigens, namely MBP, MOG and PLP, are fused by using an escherichia coli recombinant expression technology to prepare a tolerogen, a multivalent tolerogen is formed, immune tolerance is more comprehensively induced, the risk of immune escape is reduced, an escherichia coli expression system has a mature industrial production basis, fusion protein can be efficiently produced in a large scale at low cost, and the application prospect is wide. In the antigen-specific treatment of multiple sclerosis, the tolerogen of the fusion protein can be directly injected, does not need individual preparation, is safer, more conforms to a clinical conventional administration mode, and is convenient for wide application.

The present invention relates to a composition comprising a peptide derived from myelin basic protein (MBP) peptide for use in treating or preventing uveitis in a subject

A method for non-invasive nerve imaging using ultrasound imaging in conjunction with administration of a myelin basic protein (MBP) nerve imaging contrast agent. A pharmaceutical formulation for the administration (e.g., intravenous administration) of the contrast agents for nerve identification in ultrasound imaging is also provided.

A method for non-invasive nerve imaging using ultrasound imaging in conjunction with administration of a myelin basic protein (MBP) nerve imaging contrast agent. A pharmaceutical formulation for the administration (e.g., intravenous administration) of the contrast agents for nerve identification in ultrasound imaging is also provided.

The disclosure relates to methods of administering to a subject a regulatory T cell comprising an engineered T cell receptor (TCR) that binds to and is activated by a myelin basic protein (MBP) peptide complexed with an MHC Class II comprising HLA-DRB1*11:04, HLA-DRB1*04:02, HLA-DRB1*04:04, HLA-DRB1*15:01, HLA-DRB1*15:02, or HLA-DRB1*15:03 wherein the subject has been diagnosed with multiple sclerosis and has been identified as having an HLA-DRB1*11:04 allele, an HLA-DRB1*04:02 allele, an HLA-DRB1*04:04 allele, HLA-DRB1*15:01 allele, or an HLA-DRB1*15:03 allele.

The present invention disclosed herein relates to the novel in-situ process for preparation of conjugate of magnesium with acetylated aminosulfonic acid with high purity and high yield. The process comprising steps of in-situ catalytic acetylation of aminosulfonic acid followed by conjugation of magnesium in presence of base. Particularly, the invention provides the conjugate of magnesium with acetylated aminosulfonic acid which regulates the myelin basic protein (MBP) expression, thereby facilitating myelin sheath formation and maintenance. Furthermore, the present magnesium conjugate is useful in the treatment of disorders related to dysregulation of myelin basic protein (MBP) expression.