143 results about "Myelin sheaths" patented technology

The invention discloses an IL7R gene-deleted zebra fish mutant and a preparation method thereof. The construction of the IL7R gene-deleted zebra fish mutant is realized through a CRISPR / Cas9 technology. Moreover, the invention also discloses application of the IL7R gene-deleted zebra fish mutant; a mutant model provided by the invention can be used for studying an effect of IL7R in the nervous system development and myelination.

A pharmaceutical for prevention and treatment of demyelination-associated neural function impairing diseases contains erythropoietin as an active ingredient, and protectively act on the survival of oligodendrocytes, which form a myelin sheath, in cerebrovascular dementia typified by multiple sclerosis and Binswanger disease, diseases involving demyelination. The pharmaceutical and method also promote maturation of undifferentiated oligodendrocytes present in the brain, activating remyelination. Through these mechanisms, the pharmaceutical and method can prevent and treat demyelination-associated neural function impairing diseases.

The invention discloses transgenic zebrafish with specific myelin sheath removal capacity as well as a preparation method and an application thereof. The preparation method comprises the following steps: recombinant plasmid mbp-nfsB-EGFP and a Tol 2 transposase mRNA (messenger ribonucleic acid) are jointly introduced into wild zebrafish; and a zebrafish strain with stable inheritance is cultured and obtained, and the zebrafish strain with stable inheritance is the transgenic zebrafish with specific myelin sheath removal capacity, wherein the nucleotide sequence of an mbp gene promoter carried in the recombinant plasmid mbp-nfsB-EGFP is represented as SEQ ID NO.1. With adoption of the method, the transgenic zebrafish which can specifically remove myelin sheath, cause myelinoclasis and has stable inheritance capacity can be prepared and obtained effectively, under the action of metronidazole, oligodendrocyte of juvenile transgenic zebrafish can be removed specifically and the juvenile transgenic zebrafish has pathologic change of myelinoclasis together with decreased motor function, therefore, the transgenic zebrafish can provide a forceful animal model for a regulatory mechanism for viviperception of myelin sheath damage and regeneration and related drug screening.

The present invention relates to methods and formulations for GAD- vaccination to evoke a systemic effect rather that a GAD-specific effect. The present invention may therefore be used in the treatment of disease in humans not bearing on a GAD-specific effect. The invention includes a method to treat an autoimmune disease or disorder by administering at least one sequestered autoantigen in a primeand boost regimen for sensitization purposes followed by a boost for treatment purposes. This may be done upon diagnosis. Examples of sequestered autoantigens include: GAD65, GAD67, Pro-Insulin, Basic Myelin Protein, MOG and Chondrotoin II. The present invention relates to medications and methods for treatment of autoimmune disease within six months from diagnosis.

The present invention relates to pharmaceutical compositions comprising glandular kallikrein in combination with myelin basic protein or copaxone for use in the treatment of multiple sclerosis. The present invention further relates to a method of suppressing autoimmune responses in a patient afflicted with or suffering at least one clinical sign of multiple sclerosis, comprising administering to said patient a therapeutically effective amount of glandular kallikrein in combination with a therapeutically effective amount of myelin basic protein or copaxone.

The invention relates to a composite stem cell bionic nerve conduit. The composite stem cell bionic nerve conduit comprises a braided hose side wall; a round hose is formed via coiling of the braided hose side wall; and gel and stem cells are arranged in the round hose formed via coiling of the braided hose side wall. The materials of the composite stem cell bionic nerve conduit are high-molecular degradable materials, are easily available, and possesses certain strength and excellent biocompatibility; the nerve conduit side wall formed via braiding possesses a lot of pores with the same directivity; the compactness of the nerve conduit side wall can be adjusted via different braiding methods, so that it is beneficial for nutrient delivery and exchanging; atmospheric pressure plasma jet processing is capable of increasing nerve conduit braided fiber surface area, and improving conduit hydrophilic performance and cellular affinity; the gel in the nerve conduit is semi-solidified, a support interface and a material exchange interface are formed by the semi-solidified gel, so that it is beneficial for uniform distribution of stem cell in the nerve conduit, and cell fixing and differentiation, and it is also beneficial for growth of regenerated nerve axon and formation of myelin sheath, and repairing of long nerve.

The invention discloses application of shikimic acid in preparing a drug for preventing or treating demyelinating diseases. In studying the effect of the shikimic acid in preventing or treating the demyelinating diseases, it is found that the shikimic acid can alleviate the severity of an inflammatory mouse demyelinating disease model induced by myelin sheath oligodendrocyte glycoprotein, improvethe demyelination lesion conditions of a focal mouse spinal cord demyelinating model induced by lysoph-osphatidylcholine, and accelerate remyelination and reduce the demyelination size by promoting oligodendrocyte progenitor cells to be differentiated into mature oligodendrocytes. As is shown by all above, the shikimic acid has a great application prospect in clinical treatment of the demyelinating diseases.

Methods and devices are provided for activating brown adipose tissue (BAT) using electrical energy. In general, the methods and devices can facilitate activation of BAT to increase thermogenesis. The BAT can be activated by applying an electrical signal thereto that can be configured to target sympathetic nerves that can directly innervate the BAT. The electrical signal can be configured to target the sympathetic nerves using fiber diameter selectivity. In other words, the electrical signal can be configured to activate nerve fibers having a first diameter without activating nerve fibers having diameters different than the first diameter. Sympathetic nerves include postganglionic unmyelinated, small diameter fibers, while parasympathetic nerves that can directly innervate BAT include preganglionic myelinated, larger diameter fibers. The electrical signal can be configured to target and activate the postganglionic unmyelinated, small diameter fibers without activating the preganglionic myelinated, larger diameter fibers.

The invention discloses an acellular nerve graft which is an acellular heterogeneous nerve scaffold and contains a well-preserved three-dimensional orientation structure, which can guide nerve regeneration, of a nerve fiber nerve basilar membrane vessel. The structure has the components of cells, myelin sheaths, axons and fat that cause immunoreaction removed. The invention also discloses a preparation method of the acellular nerve graft, wherein the preparation method includes the steps: obtaining mammalian peripheral nerves under an aseptic condition, and stripping and removing fat and connective tissues around nerves under the aseptic condition; freezing and thawing the treated nerves repeatedly, carrying out decellularization by a chemical extraction and ultrasound combined method, cleaning with normal saline and adding deoxyribonuclease and ribonuclease solutions, and thus obtaining an initial acellular nerve graft; and freezing and drying the initial acellular nerve graft, then carrying out fat extraction treatment with supercritical carbon dioxide, and carrying out sterilization treatment to obtain the acellular nerve graft.

The present invention disclosed methods of inducing maturation of oligodendrocyte cells. A method of inducing myelination in a patient suffering from demyelination is also disclosed