1144 results about "Cerebral infarction" patented technology

A compound represented by general formula (I):a salt thereof, a solvate thereof, or a prodrug thereof wherein all symbols are as defined in the specification has an antagonistic activity against CXCR4 and is therefore useful as a preventive and / or therapeutic agent for CXCR4-mediated diseases, for example, inflammatory and immune diseases (for example, rheumatoid arthritis, arthritis, systemic erythematosus, retinopathy, macular degeneration, pulmonary fibrosis, transplanted organ rejection, etc.), allergic diseases, infections (for example, human immunodeficiency virus infection, acquired immunodeficiency syndrome, etc.), psychoneurotic diseases, cerebral diseases, cardiac / vascular disease (for example, arteriosclerosis, myocardial infarction, stenocardia, cerebral infarction, chronic arterial occlusive disease, etc.), metabolic diseases, and cancerous diseases (for example, cancer, cancer metastasis, etc.), a preventive and / or therapeutic agent for cancerous diseases or infections, or an agent for regeneration therapy.

An ultrasonic cerebral infarction therapeutic apparatus that does not produce side effects of destruction of brain cells, occurrence of intracerebral hemorrhage, destruction of nerve cells, etc. by avoiding formation of a standing wave by interference between an irradiated beam of an ultrasonic wave irradiated to the inside of the cranium and its reflected beam. An ultrasonic probe cap is constructed by arranging a plurality of laminated small transducers each made up of a PVDF film, a PZT ceramic, or the like in a mosaic-like pattern or in other form on the inside of the cap and one or more transducers are selected and activated according to a thrombus position. As a high frequency for actuating a transducer, a continuous sinusoidal wave, a burst wave, or a pulse wave shall be used so that no standing wave may be produced inside the cranium.

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.