Stevenson et al., 2016 - Google Patents
Mechanisms of blood–brain barrier disintegration in the pathophysiology of multiple sclerosisStevenson et al., 2016
- Document ID
- 9352143079837217757
- Author
- Stevenson E
- Alexander J
- Yun J
- Becker F
- Gonzalez-Toledo E
- Minagar A
- Publication year
- Publication venue
- Multiple sclerosis
External Links
Snippet
Multiple sclerosis (MS) is a demyelinating and neurodegenerative disease of the human brain, optic nerves, and spinal cord, which commonly leads to irreversible neurological disability. The etiology and cure of MS remain far from our reach. However, we are making …
- 201000006417 multiple sclerosis 0 title abstract description 138
Classifications
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
- A61K38/00—Medicinal preparations containing peptides
- A61K38/16—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof
- A61K38/17—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans
- A61K38/1703—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans from vertebrates
- A61K38/1709—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans from vertebrates from mammals
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
- A61K38/00—Medicinal preparations containing peptides
- A61K38/16—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof
- A61K38/17—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans
- A61K38/19—Cytokines; Lymphokines; Interferons
- A61K38/21—Interferons [IFN]
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
- A61K38/00—Medicinal preparations containing peptides
- A61K38/16—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof
- A61K38/17—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof from animals; from humans
- A61K38/177—Receptors; Cell surface antigens; Cell surface determinants
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
- A61K38/00—Medicinal preparations containing peptides
- A61K38/16—Peptides having more than 20 amino acids; Gastrins; Somatostatins; Melanotropins; Derivatives thereof
- A61K38/43—Enzymes; Proenzymes; Derivatives thereof
- A61K38/46—Hydrolases (3)
- A61K38/48—Hydrolases (3) acting on peptide bonds (3.4)
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
- A61K35/00—Medicinal preparations containing materials or reaction products thereof with undetermined constitution
- A61K35/12—Materials from mammals; Compositions comprising non-specified tissues or cells; Compositions comprising non-embryonic stem cells; Genetically modified cells
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N33/00—Investigating or analysing materials by specific methods not covered by the preceding groups
- G01N33/48—Investigating or analysing materials by specific methods not covered by the preceding groups biological material, e.g. blood, urine; Haemocytometers
- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
- G01N33/5005—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells
- G01N33/5008—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics
- G01N33/5044—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells for testing or evaluating the effect of chemical or biological compounds, e.g. drugs, cosmetics involving specific cell types
Similar Documents
Publication | Publication Date | Title |
---|---|---|
Liu et al. | IL-17A exacerbates neuroinflammation and neurodegeneration by activating microglia in rodent models of Parkinson's disease | |
Kocur et al. | IFNβ secreted by microglia mediates clearance of myelin debris in CNS autoimmunity | |
Sait et al. | Viral involvement in Alzheimer’s disease | |
Hauptmann et al. | Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood–brain barrier | |
Lehmann et al. | Social defeat induces depressive-like states and microglial activation without involvement of peripheral macrophages | |
Shi et al. | Rapid endothelial cytoskeletal reorganization enables early blood–brain barrier disruption and long-term ischaemic reperfusion brain injury | |
Ryu et al. | Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation | |
Mishra et al. | Expression and distribution of Toll-like receptors 11–13 in the brain during murine neurocysticercosis | |
Chaudhary et al. | Lipoic acid inhibits expression of ICAM-1 and VCAM-1 by CNS endothelial cells and T cell migration into the spinal cord in experimental autoimmune encephalomyelitis | |
Arima et al. | A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model | |
Fisher et al. | Th1 polarization of T cells injected into the cerebrospinal fluid induces brain immunosurveillance | |
US20220054554A1 (en) | Scalable Production of Standardized Extracellular Vesicles, Extracellular Vesicle Preparations and Uses Thereof | |
Hawkins et al. | Neurovascular protection by post‐ischemic intravenous injections of the lipoxin A4 receptor agonist, BML‐111, in a rat model of ischemic stroke | |
Yang et al. | Meningitic Escherichia coli-induced upregulation of PDGF-B and ICAM-1 aggravates blood-brain barrier disruption and neuroinflammatory response | |
Salimi et al. | Disruption of the blood-brain barrier during neuroinflammatory and neuroinfectious diseases | |
Malamud et al. | Tryptase activates peripheral blood mononuclear cells causing the synthesis and release of TNF-α, IL-6 and IL-1β: possible relevance to multiple sclerosis | |
Li et al. | Shuxuening injection facilitates neurofunctional recovery via down-regulation of G-CSF-mediated granulocyte adhesion and diapedesis pathway in a subacute stroke mouse model | |
Lotfi et al. | The role of immune semaphorins in the pathogenesis of multiple sclerosis: Potential therapeutic targets | |
Xie et al. | Single-cell RNA sequencing of peripheral blood reveals that monocytes with high cathepsin S expression aggravate cerebral ischemia–reperfusion injury | |
Reinhold et al. | Tissue plasminogen activator and neuropathy open the blood-nerve barrier with upregulation of microRNA-155-5p in male rats | |
Fan et al. | Time-dependent dual effect of microglia in ischemic stroke | |
Stevenson et al. | Mechanisms of blood–brain barrier disintegration in the pathophysiology of multiple sclerosis | |
Wang et al. | Endothelial genetic deletion of CD147 induces changes in the dual function of the blood‐brain barrier and is implicated in Alzheimer’s disease | |
Wu et al. | Astrocyte‐Derived Extracellular Vesicular miR‐143‐3p Dampens Autophagic Degradation of Endothelial Adhesion Molecules and Promotes Neutrophil Transendothelial Migration after Acute Brain Injury | |
Zamboni et al. | Extracellular vesicles as contributors in the pathogenesis of multiple sclerosis |