282 results about "Ischemic injury" patented technology

Methods and pharmaceutical compositions of matter are disclosed and claimed relating to cardioprotective effect mediated by delta ( delta ) opioid receptor agonists or more specifically delta-1 ( delta 1)-opioid receptor agonists. Further, methods drawn to reducing ischemic damage to organs and tissues having delta ( delta ) opioid receptor agonists or more specifically delta-1 ( delta 1)-opioid receptors are disclosed and claimed. Specifically, methods and pharmaceutical compositions of matter are taught as a means of providing cardioprotective treatment through the administration of delta ( delta ) opioid receptor agonists or more specifically delta-1 ( delta 1)-opioid receptor agonists, such as TAN67(-). Said methods and pharmaceutical compositions are envisioned as a means of reducing myocardial infarction arising from the onset and sequelae of myocardial ischemia.

Methods and devices are provided for the local delivery of anti-ischemic agents which reduce myocardial tissue damage due to ischemia or reperfusion, in combination with compounds that sensitize the response of the tissue to the anti-ischemic agent. The therapeutic agents are delivered to the myocardial tissue over an administration period sufficient to achieve reduction in ischemic or reperfusion injury of the tissue.

The invention relates to various substituted isoquinoline-1,3,4-trione, the synthetic method thereof and the use for treating neurodegenerative diseases, especially as the medicine for Alzheimer's disease, apoplexy and brain ischemic injuries.

An exsanguinous metabolic support system for maintaining an organ or tissue at a near normal metabolic rate is disclosed. The system employs a warm perfusion solution capable of supporting the metabolism of the organ or tissue thereby preserving its functional integrity. The system also monitors parameters of the circulating perfusion solution, such as pH, temperature, osmolarity, flow rate, vascular pressure and partial pressure of respiratory gases, and regulates them to insure that the organ is maintained under near-physiologic conditions. Use of the system for long-term maintenance of organs for transplantation, for resuscitation and repair of organs having sustained warm ischemic damage, as a pharmaceutical delivery system and prognosticator of posttransplantation organ function is also disclosed.

Disclosed is an apparatus and method for preventing secondary ischemic injury in the brain. The apparatus includes an interstitial brain probe and an introducer sheath, which are placed into an ischemic region of the brain by stereotaxic surgical technique. The interstitial brain probe and introducer sheath provide for thermal coagulation to provide hemostasis, aspiration of blood clots, infusion of therapeutic agents, and localized hypothermia within an ischemic region of the brain. The interstitial brain probe cools an ischemic region of the brain from within the ischemic region, and cooling is substantially limited to the ischemic region. Cooling is provided for a period of time greater than one hour.

A therapeutic method for treating ischemic or vascular disorders by administering an agent capable of inhibiting human delta-like ligand 4 (Dll4) activity to a subject in need thereof. In one embodiment, the agent is an anti-Dll4 antibody or antibody fragment capable of inhibiting the binding of Dll4 to a Notch receptor. The method of the invention is useful for treating eye disorders such as ischemic retinopathy, diabetic retinopathy, age related macular degeneration, corneal neovascularization, neovascular glaucoma, or retinopathy of prematurity. The method is also useful or treating ischemic or vascular disorders such as ischemic injury, cerebral ischemia, cardiac ischemia, ischemic conditions affecting the limbs and other organs or tissues, arteriovenous malformations, wound healing, organ or tissue transplantation, placental insufficiency, arterial narrowing and occlusion, atherosclerosis, and systemic or pulmonary hypertension.

Methods of regulating angiogenesis, ischemic injury and/or wound healing by modulating the activity of leptin, particularly as mediated by the leptin receptor, and/or the interaction between leptin and the leptin receptor. Correspondingly, these methods can also be used to treat diseases mediated by angiogenesis, including wound healing, tumors and tumor metastasis, diabetic microangiopathy, retinal neovascularization, neovascularization of adipose tissue and fat metabolism, revascularization of necrotic tissue, enhancement or vascularization in microvascular transplants, and ovarian follicle maturation. Assays for identifying agents that modulate leptin and/or leptin receptor-mediated angiogenesis and/or wound healing and their use in treating angiogenesis-mediated diseases or conditions involving wound healing are also disclosed.

A method of ameliorating tissue damage resulting from hypoxia or ischemia by administering systemically a synthetic oxygen carrier to an individual having or suspected of having blood vessel obstruction is disclosed. A synthetic oxygen carrier in a physiologically acceptable vehicle, wherein the synthetic oxygen carrier comprises submicron sized particles capable of passing through emboli-obstructed blood vessels is also disclosed.

The invention provides an acquisition method for exosomes derived from human urinary cells. The acquisition method includes the steps that firstly, human urine source cells are separately cultured, a culture medium is collected, the culture medium of the human urine source cells is filtered through a 0.22-micrometer filter membrane, and then large cell fragments and other impurities are removed; then an organelle is centrifugally removed, and supernatant is reserved; a membrane capable of intercepting 100KD molecular weight is used, the exosomes in the supernatant are centrifugally intercepted, after interception, PBS is used for eluting the membrane, and an exosome concentrated solution is obtained. The exosomes can be used for preparing medicine with the effects of resisting apoptosis, promoting angiogenesis, restoring ischemia damage and promoting cell growth and used for treating skin defects, skin ulcers, pressure sores, bone defects, bone ununion, femoral head necrosis, renal injury, ischemic injury, spinal cord injury, islet damage, diabetes, complications of diabetes, Alzheimer's diseases and the like.

The present invention relates to novel heterocyclic amide compounds of Formula I: as disclosed herein or a pharmaceutically acceptable salt, solvate, ester, prodrug or stereoisomer thereof. Also disclosed are compositions comprising said compounds, and methods for using said compounds for treating or preventing a proliferative disease, an anti-proliferative disorder, inflammation, arthritis, a neurological or neurodegenerative disease, a cardiovascular disease, alopecia, a neuronal disease, an ischemic injury, a viral disease or a fungal disease.

The invention provides a remote end ischemia preadaptation therapeutic apparatus with a function of measuring blood pressure. The remote end ischemia preadaptation therapeutic apparatus comprises a power supply unit, at least one inflatable arm band, at least one inflatable tube, at least one air pressure sensor and release valve, an inflator pump and a circuit module, wherein the at least one inflatable tube is correspondingly connected and communicated with the inflatable arm band; the inflatable tube is provided with the at least one air pressure sensor and the release valve; the inflator pump is communicated with the inflatable tube and is used for inflating the inflatable arm band; the circuit module is connected with the inflator pump and comprises an air pressure acquisition unit, a blood pressure measuring unit, a microprocessor unit and a driving control unit. Due to the implementation of the remote end ischemia preadaptation therapeutic apparatus with the function of measuring the blood pressure, the health status of the human body blood pressure can be monitored in the treatment and training process, and effects of preventing and treating thrombosis of brain tissues and heart tissues and ischemic injury are achieved.

The present disclosure relates to a composition for treating and preventing an ischemic injury. More particularly, it relates to a composition containing a peptide derived from a telomerase, which is effective in treating and preventing an ischemic injury. The peptide according to the present disclosure, a peptide having 80% or more sequence identity with the amino acid sequence of the peptide or a peptide which is a fragment thereof, has a superior effect of treating and preventing an ischemic injury. Accordingly, a composition containing the peptide may be effectively used for an ischemic injury, particularly for an ischemic-reperfusion injury.

A method for protection of tissues subject to ischemic and/or reperfusion damage is provided. The method includes administering to the tissue a composition comprising nanodevices. The nanodevices can take the form of, for example, polymeric nanoparticles or lipidic nanoparticles. The nanodevices also find use in methods for reducing ischemic injury in tissue at risk of such injury, such as heart and brain tissue.

This invention is directed to novel oxamyl depeptide ICE/ced-3 family inhibitor compounds. The invention is also directed to pharmaceutical compositions containing these compounds, as well as to the use of such compositions in the treatment of patients suffering inflammatory, autoimmune and neurodegenerative diseases, for the prevention of ischemic injury, and for the preservation of organs that are to undergo a transplantation procedure.

The present invention provides peptide-based peroxidase inhibitors having the formula AA₁-AA₂-AA₃, wherein AA₁ is a positively charged, negatively charged or neutral amino acid, AA₂ is a redox active amino acid, and AA₃ is an amino acid possessing a reducing potential such that AA₃ is capable of undergoing a redox reaction with a radical of amino acid AA₂ or a retro or retro-inverso analog thereof. The result of such a combination is a highly effective inhibitor of peroxidase activity that has potent anti-inflammatory properties in widely diverse models of vascular disease and injury. Exemplary tripeptides effectively inhibit peroxidase mediated LDL oxidation, increase vasodilation in SCD mice, inhibit eosinophil infiltration and collagen deposition in asthma mice, inhibit acute lung injury, and decrease ischemic injury of the heart.

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.

Disclosed are compositions and methods for inducing therapeutic hypothermia in a subject.