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281 results about "Ischemic injury" patented technology

An ischemic brain injury is damage to brain tissue that results from decreased oxygen supply. Examples include stroke or transient ischemic attack (TIA), which is when arteries supplying blood/oxygen get clogged by clots, any problem that affects breathing (breathing failure, choking, drowning), or poisonous gas exposure.

Methods and Devices for Reducing Tissue Damage After Ischemic Injury

Methods and devices are provided for the delivery of therapeutic agents which reduce myocardial tissue damage due to ischemia and anti-restenotic agents which inhibit restenosis following a cardiac procedure such as stent implantation. The anti-ischemia agents are delivered to the myocardial tissue over an administration period sufficient to achieve reduction in ischemic or reperfusion injury of the myocardial tissue. The anti-restenotic agents are delivered over an administration period sufficient to reduce the re-narrowing of a blood vessel following a cardiac procedure such as implantation of a device. Preferred anti-restenotic drugs are those that do not reduce the beneficial effects provided by the anti-ischemic drug, such as drugs that do not act on the mammalian target of rapamycin (mTOR).
Owner:INNOVATIONAL HLDG LLC

Compounds for treatment of ischemic injury

The present invention relates to microRNA (miRNA) compounds for use in the treatment of consequences of acute ischemia / reperfusion, a method for preparing miRNA compounds by using test ischemia-reperfusion, test preconditioning and test postconditioning of biological samples, use of the miRNA compounds in the preparation of pharmaceutical compositions having cytoprotective and / or anti-ischemic effect in ischemic cardiac diseases.
Owner:PHARMAHUNGARY 2000

Treatment with Sigma Receptor Agonists Post-Stroke

A method of post-stroke treatment at delayed timepoints with sigma receptor agonists. Sigma receptors are promising targets for neuroprotection following ischemia. One of the key components in the demise of neurons following ischemic injury is the disruption of intracellular calcium homeostasis. The sigma receptor agonist, DTG, was shown to depress [Ca2+]i elevations observed in response to ischemia induced by sodium azide and glucose deprivation. Two sigma receptor antagonists, metaphit and BD-1047, were shown to blunt the ability of DTG to inhibit ischemia-evoked increases in [Ca2+]i. DTG inhibition of ischemia-induced increases in [Ca2+]i was mimicked by the sigma-1 receptor-selective agonists, carbetapentane, (+)-pentazocine and PRE-084, but not by the sigma-2 selective agonist, ibogaine, showing that activation of sigma-1 receptors is responsible for the effects. Activation of sigma receptors can ameliorate [Ca2+]i dysregulation associated with ischemia in cortical neurons, providing neuroprotective properties. The effects of 1,3-di-o-tolyguanidine (DTG), a high affinity sigma receptor agonist, as a potential treatment for decreasing infarct area at delayed time points was further examined in rats. DTG treatment significantly reduced infarct area in both cortical/striatal and cortical/hippocampal regions by >80%, relative to control rats. These findings were confirmed by immunohistochemical experiments using the neuronal marker, mouse anti-neuronal nuclei monoclonal antibody (NeuN), which showed that application of DTG significantly increased the number of viable neurons in these regions. Furthermore, DTG blocked the inflammatory response evoked by MCAO, as indicated by decreases in the number of reactive astrocytes and activated microglia/macrophages detected by immunostaining for glial fibrillary acidic protein (GFAP) and binding of isolectin IB4, respectively. Thus, the sigma receptor-selective agonist, DTG, can enhance neuronal survival when administered 24 hr after an ischemic stroke. In addition, the efficacy of sigma receptors for stroke treatment at delayed time points is likely the result of combined neuroprotective and anti-inflammatory properties of these receptors.
Owner:UNIV OF SOUTH FLORIDA
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