100results about How to "Reduced infarct volume" patented technology

Methods and pharmaceutical compositions for preconditioning and / or providing neuroprotection to the animal central nervous system against the effects of ischemia, trauma, metal poisoning and neurodegeneration, including the associated cognitive, behavioral and physical impairments. In one embodiment, the method is accomplished by stimulating and stabilizing hypoxia-inducible factor-1α (HIF-1α). HIF-1α is known to provide a neuroprotective benefit under ischemic conditions. Patients at risk for certain diseases or disorders that are associated with risk for cerebral ischemia may benefit, e.g., those at risk for Alzheimer's disease, Parkinson's disease, Wilson's disease or stroke or those patients having head or spinal cord injury. Patients undergoing certain medical procedures that may result in ischemia may also benefit. Initially, the possibility of ischemia or neurodegeneration is recognized. Intranasal therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and / or copper such as iron chelators, copper chelators, and antioxidants. A particular example of such therapeutic agents is the iron chelator deferoxamine (DFO). Intranasal administration of DFO is known to stimulate and / or stabilize HIF-1α and provides an efficient and safe method for pre-conditioning the brain to protect against cerebral ischemia. Moreover, DFO is shown to decrease weight loss in subjects when administered pre and / or post stroke.

A method of screening peptides which bind to at least one PDZ domain and comprise a cell-membrane transduction domain for use in treating traumatic injury to the brain or spinal cord by deforming neurons on a flexible substrate with sublethal stretch, then inflicting a secondary injury, and determining survival of the stretched neurons in the absence or presence of the peptide which is being screened.

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron the method comprising administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor neuronal protein. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity and ischemic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95 / NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults and dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia. The treatment was effective when applied either before, or one hour after, the onset of excitotoxicity in vitro and cerebral ischemia in vivo. This approach prevents negative consequences associated with blocking NMDAR activity and constitutes practical therapy for stroke.

Methods and pharmaceutical compositions for providing neuroprotection to the animal central nervous system against the effects of ischemia, and neurodegeneration. Patients at risk for certain diseases or disorders that are associated with cerebral ischemia may benefit, e.g., those at risk for Alzheimer's disease, Parkinson's disease, Wilson's disease or stroke or those patients having head or spinal cord injury. Patients undergoing certain medical procedures that may result in ischemia may also benefit. Initially, the possibility of ischemia or neurodegeneration is recognized. Intranasal therapeutic agents are administered to the upper third of the nasal cavity to bypass the blood-brain barrier and access the central nervous system directly to avoid unwanted and potentially lethal side effects. Therapeutic agents include those substances that interact with iron and / or copper such as iron chelators and copper chelators. A particular example of such therapeutic agents is the iron chelator deferoxamine (DFO). Intranasal administration of DFO provides an effective method for pre-conditioning the brain to protect against cerebral ischemia.

The invention discloses application of curcumin to preparation of drugs for treating cerebral ischemia / reperfusion injuries, belonging to the technical field of drug preparation. A cerebral ischemia / reperfusion injury model is prepared and curcumin-PVP (polyvinylpyrrolidone) solid dispersions are used for treating the disease model after being dissolved with the saline for injection. Results show that curcumin can obviously improve the injuries of vital organs such as distant livers and kidneys caused by cerebral tissue injuries and cerebral ischemia / reperfusion injuries and can control the expression levels of several factors related to apoptosis, inflammations and oxidation, control further aggravation of the injuries and protect the vital organs such as cerebral tissues and livers and kidneys.

The present disclosure relates generally to methods for treating neurodegenerative diseases, including their progressive forms. In particular, the present disclosure pertains to methods of treating or preventing neurodegenerative diseases, including their progressive forms and their associated symptoms by administering a combination of ibudilast (3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine) and riluzole, or pharmaceutically acceptable salts of one or both thereof.

This invention discloses the uses of IL-22 in the treatment and prevention of a nerve damage disease or a neurodegenerative disease. In particular, the invention discloses the uses of IL-22 or IL-22 dimers as follows: (i) can protect neurons to recover the functions of injured neurons after ischemic nerve damage in animals in vivo, thus enabling effective treatment of nerve damage diseases, (ii) can significantly inhibit the loss of dopaminergic neurons in substantia nigra in PD model animal, enhance the functions of dopaminergic neurons, significantly reduce neuronal apoptosis in hippocampus, improve learning and memory capacity of AD model rats, and effectively prevent neuronal loss, thereby enabling more effective treatment of neurodegenerative diseases.

The invention discloses an application of oxymatrine in medicines for treating neonatal hypoxic ischemic brain damages. An experiment result shows that oxymatrine has a certain dose-effect correlation when used in a safe dose range; when the dose is 120mg / kg of body weight, the volume of ischemia area cerebral infarction and neuron apoptosis rate can be reduced; pathological damages to brain tissues can be relieved; the activity of antioxidase in the brain tissues can be improved; and the content of malondialdehyde is lowered. The oxymatrine has the effects of preventing injuries and deaths caused by neonatal hypoxic ischemic brain damages and promoting neural functional recovery.

The invention provides an edaravone composition for injection, and relates to the technical field of medicine manufacturing. The main medicine of the composition comprises edaravone and melatonin, wherein the melatonin comprises a quick release part and a cyclodextrin-included slow release part. According to the edaravone composition for injection provided by the invention, the therapeutic effect of edaravone is improved, instability caused by oral administration of MT (Melatonin) is avoided and MT is quick to distribute and eliminate and the like, and the first pass effect of MT is reduced. The dosage of edaravone is reduced, and the side effect of edaravone is reduced. The design of dosage combining quick release and slow release is in accordance with secretion characteristic of MT, so that the problem of half-life period of MT is solved and the bioavailability of a product is improved. The melatonin combined with edaravone acted on nerve cells has the synergistic effect of preventing encephaledema, reducing the infarct volume and improving the neurological function.

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor-neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARS) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95 / NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

The invention relates to methods of treatment of medical conditions (e.g., diseases and injuries) in a mammal (e.g., a human), such as hypoxia / ischemia, burns, and viral infections (e.g., influenza, West Nile virus, and Dengue fever), in adults and in children (e.g., neonates) by administering a composition that includes an IAIP.