48 results about "Brain damage" patented technology

The application discloses a new use of Leonurine or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating radiation-induced brain injury, specifically, providing a safe and effective therapeutic drug for iron death, neuroinflammation, neuron damage and lipid metabolism disorder accompanying the radiation-induced brain injury, solving the technical problem of lack of specific treatment means in the prior art, and having a wide clinical application prospect. Experiments adopt a C57BL / c mouse 30 Gy whole brain X-ray radiation model, and results show that Leonurine can significantly improve the body weight decrease and survival rate of the model mice, reduce the serum IL-6 and IFN-alpha levels, inhibit the activation of microglial cells in the cerebral cortex and hippocampus, protect and repair damaged neurons, and improve the ultrastructure of mitochondria and synapses; meanwhile, the expression of GPX4 and SLC7A11 proteins in the brain tissue is up-regulated, the GSH content is increased to inhibit iron death, and the levels of GPE, GPS and GPC related to lipid metabolism are restored.

The application discloses a nano guanido drug system and a preparation method and application thereof, and relates to the technical field of medicine, in particular to a GCOF DHM @CAQK platform, can efficiently deliver drugs to a TBI injury site, can accumulate in a TBI brain injury area, can inhibit neuroinflammation, oxidative stress and protect neuron cells after TBI, can precisely intervene in secondary injury of TBI, and provides a new strategy for improving the prognosis of patients.

This invention relates to the field of chemiluminescence detection technology for in vitro diagnostic reagents, specifically to an S100-β chemiluminescence detection kit and its preparation method. It provides a chemiluminescence detection kit for central nervous system-specific proteins using magnetic microparticles. The kit comprises: S100-β calibrator, S100-β monoclonal antibody conjugated with carboxyl magnetic beads, S100-β monoclonal antibody labeled with alkaline phosphatase, AMPPD chemiluminescence substrate solution acted upon by alkaline phosphatase, and concentrated washing buffer. This kit achieves the following: no sample pretreatment required, easy operation, high automation, high sensitivity, automatic result output in 16 minutes, good stability of calibrator and enzyme label, and low cost. It can meet the clinical needs for auxiliary diagnosis and treatment of acute ischemic brain injury.

This invention relates to the use of 5α-androsta-3β,5,6β-triol and its derivatives in the prevention or treatment of radiation-induced brain injury, and to methods for preventing or treating radiation-induced brain injury with 5α-androsta-3β,5,6β-triol and its derivatives.

The present application relates to a kind of cytidine choline dextrohydrotalcid derivatives and its preparation method and application, belong to biological medicine technical field.The present application is aimed at solving the technical problems of low blood-brain barrier penetration rate and limited treatment effect of existing edaravone dextrohydrotalcid compound preparation.The present application prepares a dextrohydrotalcid derivative (C-B) with boronic acid structure, then it is compounded with cytidine choline in specific pH buffer system, and forms cytidine choline dextrohydrotalcid derivative (C-D-B).The present application can effectively improve the efficiency of drug crossing blood-brain barrier by using the dynamic covalent characteristics of boronic ester bond and free radical responsiveness.The experimental results show that, compared with existing combination drug, the derivative of the present application can significantly reduce the infarction area of cerebral ischemia model animal, reduce cell damage and active oxygen level, and promote vascular regeneration, and show better treatment effect on ischemic brain injury.

The invention relates to mammalian mesenchymal stem cells (MSCs) for use in a method of treatment of a hypoxic-ischemic brain injury (HIBI) event in a human neonate. Particular routes of administration are disclosed. The invention also encompasses the MSCs for use in a method of prevention of the consequences and / or treatment of a neurodevelopmental disability in a neonate which has suffered or is suspected of suffering a HIBI event. A ready to use device for the administering of MSCs to human neonates is also disclosed.

The present invention pertains to the anti-inflammatory therapeutic effect of xantohumol in spinal cord injury (SCI). The continuous administration of xanthohumol for 1-8 weeks to SCI rats resulted in improved results in 4 clinical tests used and in lowering and faster elimination of macrophages from the SCI lesion. Since the infiltration of the SCI lesion by numerous phagocytic macrophages indicates a severe destructive inflammation of extraordinary longevity, administration of xanthohumol is neuroprotective and resulted in a better and faster recovery of the locomotor function and the strength and sensory function in the hind limbs, in a shorter period of paralysis of the urinary bladder and in the recovery of the body weight lost due to the SCI surgery. Since the traumatic brain injury (TBI) involving the white matter, and stroke involving the white matter initiate the severe destructive inflammation as in the SCI, the administration of xanthohumol is expected to be anti-inflammatory and neuroprotective in both brain diseases. Since neurodegenerative diseases including Alzheimer's disease, frontotemporal dementia and Parkinson's disease, immune mediated neuroinflammation including multiple sclerosis and neuromyelitis optica and cerebrospinal infections have inflammatory pathogenesis involving microgliosis and infiltration by macrophages, the administration of xanthohumol is expected to result in therapeutic inhibition of progression of all above diseases as well as of related neurodegenerative, immune mediated and infectious diseases of the brain and of the spinal cord.

This invention discloses a novel class of monoacylglycerol lipase (MAGL) small molecule inhibitors, as well as their pharmaceutically acceptable compositions, methods of preparation, and uses. The MAGL small molecule inhibitors are represented by formula (I), having the specific substituents and definitions described herein. The disclosed MAGL small molecule inhibitors exhibit excellent MAGL enzyme inhibitory activity. This invention includes these compounds or their pharmaceutically acceptable compositions for the treatment and / or prevention of MAGL-related conditions such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, traumatic brain injury, neurotoxicity, stroke, epilepsy, anxiety, migraine, depression, hepatocellular carcinoma, colorectal cancer lesions, ovarian cancer, neuropathic pain, chemotherapy-induced neuropathy, acute pain, chronic pain, and / or pain-related spasticity.

The application provides application of a reagent for detecting N-acetyl-L-cysteine in preparation of an ischemic brain injury diagnosis product, and relates to the technical field of in-vitro detection.The application provides a biomarker N-acetyl-L-cysteine (NAC) for ischemic brain injury diagnosis.ROC curve analysis shows that NAC has good distinguishing ability for ischemic brain injury, and can be used as a potential marker for ischemic brain injury.

The present invention relates to a pharmaceutical use, of a compound of formula I or a salt thereof, for improving mortality, neurological impairment, and / or daily activity in patients with resuscitated cardiac arrest receiving target temperature management (TTM) for maintaining a temperature between about 32°C and about 36°C, patients with ischemic or hemorrhagic stroke receiving TTM, patients with traumatic brain or spinal cord injury receiving TTM, or patients with hypoxic-ischemic encephalopathy receiving TTM.

Magnetic resonance and ultrasound methods can produce estimates of full rank-4 elasticity tensors (E-tensors) using suitable constraints. E-tensor estimates can be based on E-tensor symmetry conditions and a suitable E-tensor selected from among a set of E-tensors calculated using different symmetry constraints. Displacement fields used in E-tensor calculations can be noise reduced using compatibility conditions. With the selected E-tensor, various stains that are rotation invariant can be computed. In one example, an E-tensor for an in vivo brain is computed using the mechanical disturbance associated with cardiac pulsations. The selected E-tensor and associated stains, physiological disorders such as Alzheimer's disease and traumatic brain injury (TBI) and even neural activation may be more readily detected than with conventional methods that do not use the full E-tensor.

This invention relates to the pharmaceutical field, specifically to the application of tissue inhibitor metalloproteinases-2 (TIMP2) in the preparation of drugs for the prevention or treatment of traumatic brain injury. TIMP2 protein can increase the fall latency in rotarod experiments in mice with traumatic brain injury; improve the motor balance ability of mice with traumatic brain injury on a balance beam; improve neurological function impairment in mice with traumatic brain injury; and reduce Evans blue permeability in brain tissue. In brain microvascular endothelial cells (HBMECs), TIMP2 protein can participate in maintaining the integrity of the endothelial barrier, reversing the loss of expression and altered localization of the connectome complex induced in an in vitro traumatic brain injury model, and reducing luciferase leakage. This invention also provides the application of TIMP2 protein as an Integrin α3β1 ligand in the preparation of drugs for the treatment of central nervous system diseases caused by blood-brain barrier dysfunction. TIMP2 protein exerts its function by binding to the cell membrane receptor Integrin α3β1, regulating VE-Cadherin phosphorylation. TIMP2 protein shows promising application prospects in the treatment of blood-brain barrier dysfunction caused by traumatic brain injury.

Provided are: a therapeutic and / or prophylactic agent for at least one type of epilepsy selected from the group consisting of epilepsy after brain injury and epilepsy after the formation of compensatory brain areas; and a pharmaceutical composition containing the same.　This therapeutic and / or prophylactic agent for epilepsy after brain injury comprises a compound represented by general formula (1) or a salt thereof. (R1 and R2 are the same or different and represent one or more groups selected from a hydrogen atom, a halogen atom, an optionally substituted C1-6 alkyl group, an optionally substituted aryl group, an optionally substituted C1-6 alkoxy group, an optionally substituted aryloxy group, an optionally substituted C1-6 alkylthio group, an optionally substituted arylthio group, an optionally substituted C2-6 alkenyl group, an optionally substituted C2-6 alkenyloxy group, an optionally substituted C1-6 alkylamino group, an optionally substituted C1-6 alkylsulfonyl group, an optionally substituted arylsulfonyl group, an optionally substituted carbamoyl group, an optionally substituted heterocyclic group, an optionally protected amino group, an optionally protected hydroxyl group, an optionally protected carboxyl group, a nitro group, and an oxo group; R3 represents an optionally substituted C1-6 alkylamino group, an optionally protected amino group, or an optionally protected hydroxyl group; and m and n are the same or different and each represent an integer of 1-6.)

The present disclosure relates to methods diagnosing or aiding in the diagnosis of a traumatic brain injury (TBI) or adjudicating a TBI diagnosis of a subject that has sustained, may have sustained, or is suspected of sustaining an injury to the head. The methods involve (a) receiving diagnostic criteria of a subject that has sustained, may have sustained, or is suspected of sustaining an injury to the head; (b) executing a TBI adjudication algorithm by compiling the diagnostic criteria; and (c) adjudicating a TBI diagnosis based on the diagnostic criteria compiled in step (b). The diagnostic criteria includes, inter alia, the presence or absence of (i) a trauma mechanism; (ii) a neuroimaging intracranial abnormality; (iii) one or more clinical signs indicative of TBI; (iv) one or more confounding factors; and (v) a level of glial fibrillary acidic protein (GFAP) and / or a level of ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) measured in a sample obtained from the subject. The present disclosure also relates to systems and kits for implementing the methods.

Disclosed are novel compounds of structural formula (I) and pharmaceutically acceptable salts, hydrates, and solvates thereof, which are inhibitors of NLRP3 and can be used to treat, prevent, manage, ameliorate, control, and suppress diseases mediated by NLPR3. The compounds of structural formula I can be used to treat, prevent, or manage diseases, disorders, and conditions mediated by NLRP3, such as, but not limited to, gout, pseudogout, CAPS, NASH fibrosis, heart failure, idiopathic pericarditis, atopic dermatitis, inflammatory bowel disease, Alzheimer's disease, Parkinson's disease, and traumatic brain injury.

Novel compounds of Formula (I), and the pharmaceutically acceptable salts thereof, are inhibitors of NLRP3 and may be useful in the treatment, prevention, management, amelioration, control, and suppression of diseases mediated by NLPR3. The compounds of the present invention may be useful in the treatment, prevention or management of diseases, disorders and conditions mediated by NLRP3 such as, but not limited to, obesity, gout, pseudogout, CAPS, NASH, MASH, fibrosis, osteoarthritis, atherosclerosis, heart failure, idiopathic pericarditis, myocarditis, atopic dermatitis, hidradenitis suppurativa, inflammatory bowel disease, cancer, Alzheimer's Disease, Parkinson's Disease, dementia with Lewy bodies (DLB), and traumatic brain injury.

This invention provides a neurodevelopmental drug screening system and its applications based on a set of microglia markers. Specifically, this invention provides a neurodevelopmental supportive microglia subset that expresses markers of neurogenesis and development, as well as energy metabolism. This invention also provides a neurodevelopmental drug screening system and method using changes in the state of this cell subset as the core evaluation indicator. The system of this invention can sensitively and quantitatively reflect the regulatory effect of candidate drugs on the pro-neural maturation function of microglia in developmental brain injury, filling the technical gap in existing drug screening systems that lack "developmental immune-metabolic-synaptic linkage indicators."

This invention belongs to the field of pharmaceutical technology and relates to an iron-tea polyphenol coordination polymer nanoparticle, its preparation method, and its application. The application of nanotechnology in the medical field is rapidly developing. Nanomaterials, as potential "smart" drugs, can enhance therapeutic effects through targeted drug release. Although research on nanomaterials is promising, the challenge of ineffective drug treatment in the brain, especially in the treatment of radiation-induced brain injury, still needs to be overcome. Therefore, developing novel nanomaterials, particularly those with neuroprotective effects, and further elucidating their neuroprotective effects, will provide new possibilities for the treatment of radiation-induced brain injury. This invention provides a novel iron-tea polyphenol (Fe-TP) coordinated nanomaterial that utilizes the coordination properties of Fe-TP to mitigate adverse reactions caused by radiation damage, thereby addressing the serious health problems caused by radiation-induced brain injury.

Novel compounds of Formula (I), and the pharmaceutically acceptable salts thereof, are inhibitors of NLRP3 and may be useful in the treatment, prevention, management, amelioration, control and suppression of diseases mediated by NLPR3. The compounds of the present invention may be useful in the treatment, prevention or management of diseases, disorders and conditions mediated by NLRP3 such as, but not limited to, obesity, gout, pseudogout, CAPS, NASH, MASH, fibrosis, heart failure, idiopathic pericarditis, atopic dermatitis, inflammatory bowel disease, Alzheimer's Disease, Parkinson's Disease, dementia with Lewy bodies (DLB), and traumatic brain injury.

The present disclosure relates to methods and compositions comprising cannabidiol (CBD) and a volatile anaesthetic, particularly isoflurane, useful for treating or preventing traumatic brain injury (TBI).

Embodiments of the disclosure include treatments of subconcussive and / or concussive brain damage by administering fibroblasts and / or fibroblasts cultured with one or more types of immunocytes. In one specific embodiment fibroblasts are cultured with monocytes in the presence of patient-specific T cells, and subsequently the T cells are re-administered into the patient. In one particular embodiment, products derived from fibroblast-immunocyte mixtures are comprised of cellular lysate, apoptotic bodies, exosomes, and / or other microvesicles. In one embodiment, the fibroblast cells and / or products derived from the fibroblast cells are administered subsequent to one or multiple head injuries. In other embodiments, products are administered in combination with neurorestorative and / or neuroprotective interventions.

The present application provides a central nervous system targeting pharmaceutical composition which can be used to treat various brain injury patterns, by genetically engineering an integrin antibody to bind to a transmembrane protein of an exosome, and coating the exosome as a carrier with a therapeutic drug.

This invention discloses a polypeptide drug for treating septic encephalopathy. The invention's research discovered a direct interaction between ATF2 and c-JUN protein in SAE mice, forming an ATF2-c-JUN complex. Based on this discovery, a cell-penetrating peptide that competitively inhibits this direct interaction was designed and synthesized. Experiments have demonstrated that this cell-penetrating peptide can effectively improve brain damage in SAE mice.

The novel compounds of Formula (I), and the pharmaceutically acceptable salts thereof, are NLRP3 inhibitors and may be useful in the treatment, prevention, management, improvement, control, and suppression of NLRP3-mediated diseases. The compounds of the present invention may be useful in the treatment, prevention, or management of NLRP3-mediated diseases, disorders, and conditions such as, but not limited to, obesity, gout, pseudogout, CAPS, NASH, MASH, fibrosis, heart failure, idiopathic pericarditis, atopic dermatitis, inflammatory bowel disease, Alzheimer's disease, Parkinson's disease, Lewy body dementia (LBD), and traumatic brain injury. (I)

Novel compounds of the structural Formula (I), and the pharmaceutically acceptable salts thereof are inhibitors of NLRP3 and may be useful in the treatment, prevention, management, amelioration, control and suppression of diseases mediated by NLPR3. The compounds of structural formula I may be useful in the treatment, prevention or management of diseases, disorders and conditions mediated by NLRP3 such as, but not limited to, gout, pseudogout, CAPS, NASH fibrosis, heart failure, idiophathic pericarditis, atopic dermatitis, inflammatory bowel disease, Alzheimer's Disease. Parkinson's Disease and traumatic brain injury.

An injectable, self-healing hydrogel, its preparation method, and its applications. This invention belongs to the field of biomedical engineering and neural regeneration, specifically relating to a hydrogel, its preparation method, and its applications. This invention provides an injectable, self-healing hydrogel for carrying neural stem cells based on Schiff base crosslinking. This hydrogel achieves self-healing and injectability through dynamic Schiff base bonds. A reversible imine bond crosslinking structure is formed through the Schiff base reaction between amino and aldehyde groups, exhibiting good biocompatibility and structural stability. The surface of biological tissue is rich in amino and hydroxyl groups, which can react again with the aldehyde groups in the OHA to form a dynamic covalent crosslinking network. Through interfacial Schiff base bonding, electrostatic attraction, and hydrogen bonding, this hydrogel can achieve strong wet adhesion to biological tissue and form a stable scaffold at the site of brain injury. Simultaneously, the nanospheres in the system can achieve sustained release of growth factors, effectively promoting the survival, proliferation, and differentiation of neural stem cells, ultimately achieving precise repair and functional recovery of neural tissue.

The application provides a preparation method of fat stem cells and the use thereof in nerve repair, and further, a specific differentiation-promoting peptide CF-8 for promoting differentiation of fat mesenchymal stem cells into nerve-like cells is screened from a deer antler polypeptide, wherein the nerve-like cells differentiated after the action of the differentiation-promoting peptide have a good therapeutic effect on treating traumatic brain injury, and have a good application prospect.

The novel compounds of formula (I) and their pharmaceutically acceptable salts are inhibitors of NLPR3 and can be used to treat, prevent, manage, improve, control, and inhibit NLPR3-mediated diseases. The compounds of this invention can be used to treat, prevent, or manage NLPR3-mediated diseases, symptoms, and conditions, such as, but not limited to, obesity, gout, pseudogout, CAPS, NASH, MASH, fibrosis, heart failure, idiopathic pericarditis, atopic dermatitis, inflammatory bowel disease, Alzheimer's disease, Parkinson's disease, Lewy body dementia (DLB), and traumatic brain injury. (I).

The present invention provides detection reagents and method for determining risk of traumatic brain injury (TBI) and / or susceptibility to neurodegenerative disease in a subject.