155 results about "Platelet activation" patented technology

Biocompatible polymeric materials capable of providing in situ release of nitric oxide (NO) included diazeniumdiolated fumed silica as a filler in a multilayer polymer structure to release NO upon contact with water (blood). The blood-contacting polymer surface is preferably multi-layered so that the NO-releasing layer, containing the diazeniumdiolated fumed silica, is shielded from blood contact by one or more top (or base) coats. When in contact with blood, the NO released at the surface of the polymer prevents platelet activation and adhesion to the surface, thereby reducing platelet consumption, risk of thrombus formation and other clinical complications associated with interactions between blood and foreign materials.

A compound having the general formula (I) wherein R1 represents C1-C6 alkyl, etc., R2 represents hydrogen, C2-C7 alkanoyl, C7-C11 arylcarbonyl, the formula R4—(CH2)1—, etc., R3 represents C6-C10 aryl, etc., X1, X2, X3, X4 and X5 each independently represents hydrogen, halogen, etc., and n represents an integer of 0 to 2, pharmacologically acceptable salts thereof or prodrugs thereof. They have excellent inhibition of platelet activation, etc. and are useful as a prophylactic or therapeutic agents for diseases related to thrombus or embolus formation.

The invention discloses a preparation method of a copper ion mediated anticoagulant coating with function of in situ catalysis of NO release. The method includes steps of preparing an acidic buffer solution, and adding a compound with pyrogallol structure and certain concentration, a compound with amino or thiol, and copper ion soluble salt. The method of the invention has the advantages of simple operation, mild reaction conditions and easiness. The prepared coating has the advantages of controllable content of the units containing multiple amino or thiol compounds, and easily controlled loading amount of copper ion. The modified coating prepared by the method has excellent adhesion with a base material, and through act of the copper ions in the coating with the blood, the coating can conduct in situ catalyze the NO donor molecules in blood to continuously decompose and release NO molecules, thus realizing the inhibition of platelet activation and aggregation, inhibiting smooth muscle cell proliferation and migration, and protecting vascular endothelial layer function.

A method for obtaining a percent aggregation or inhibition of platelets resulting from anti-platelet using a single blood sample is achieved. An assay device is provided. The assay device has multiple channels, each coupled to a common introduction port. A first platelet activator is sensitive to activation pathway targeted by the anti-platelet drug. A second platelet activator is insensitive to the activation pathway targeted by the anti-platelet drug. An anti-coagulated sample is introduced simultaneously to the first and second channels. A level of platelet aggregation is simultaneously made in both channels.

A method and medicament for treating inflammation in a patient with a sulfated polysaccharide without inducing platelet activation or thrombosis in the presence of heparin- and platelet factor 4-complex reactive antibodies using a 2-O desulfated heparin with an average degree of sulfation of 0.6 sulfate groups per monosaccharide or greater and an average molecular weight or 2.4 kD or greater. The medicament preferably is administered intravenously, by aerosolization or orally. Preferably, the 2-O desulfated heparin medicament includes a physiologically acceptable carrier which may be selected from the group consisting of physiologically buffered saline, normal saline, and distilled water. Additionally provided is a method of synthesizing 2-O desulfated heparin.

This invention provides methods for the use of substituted indole compounds of the general formula: and pharmaceutically acceptable salt forms thereof. The invention provides methods for the use of the compounds as inhibitors of the activity of various phospholipase enzymes, particularly phospholipase A2 enzymes, and for the medical treatment, prevention and inhibition diseases and disorders including asthma, stroke, atherosclerosis, multiple sclerosis, Parkinson's disease, arthritic disorders, rheumatic disorders, central nervous system damage resulting from stroke, central nervous system damage resulting from ischemia, central nervous system damage resulting from trauma, inflammation caused or potentiated by prostaglandins, inflammation caused or potentiated by leukotrienes, inflammation caused or potentiated by platelet activation factor, pain caused or potentiated by prostaglandins, pain caused or potentiated by leukotrienes, and pain caused or potentiated by platelet activation factor.

A tubing set for use with a blood handling system is described that decreases the priming volume and surface area of the blood handling circuit, lowering the risk of hemodilution, platelet activation, and hemolysis. The tubing set also reduces the number of manual connections required, and uses quick-disconnect couplings to facilitate connections between the various lines, and between the lines and the arterial and venous cannulae.

A method and medicament for treating and preventing platelet activation or thrombosis in the presence of heparin-and platelet factor 4-complex reactive antibodies using a 2-O desulfated heparin with an average degree of sulfation of 0.6 sulfate groups per monosaccharide or greater and an average molecular weight or 2.4 kD or greater. The medicament preferably is administered intravenously, by aerosolization or orally. Preferably, the 2-O desulfated heparin medicament includes a physiologically acceptable carrier which may be selected from the group consisting of physiologically buffered saline, normal saline, and distilled water. Additionally provided is a method of synthesizing 2-O desulfated heparin.

The present invention relates to a method and means for diagnosing or risk stratification of co-morbidities, particularly cardiovascular complications in diabetes patients. The invention particularly relates to a method for diagnosing whether a diabetes patient is suffering from a cardiovascular complication or is at risk of suffering from a cardiovascular complication, said method comprising the steps of (a) measuring, preferably in vitro, the level(s) of at least one cardiac hormone or a variant thereof in a sample from the patient, and (b) diagnosing the cardiovascular complication or the risk of suffering from cardiovascular complication by comparing the measured level(s) to known level(s) associated with the cardiovascular complication or risk. The present invention also relates to combining the measurement of markers comprising cardiac hormones, natriuretic peptides, inflammation-associated markers, angiogenesis markers, and markers for platelet activation. Preferred markers are brain natriuretic peptides (particularly NT-proBNP), PIGF, and sCD40L.

The invention discloses a construction method of an anticoagulant artificial blood vessel scaffold material. The method includes: taking a rotating stainless steel pipe as a receiver, employing an electrospinning technology to prepare an organic macromolecular polymer, a mixture of a Cu2<+> complex catalyst and the organic macromolecular polymer, and the organic macromolecular polymer successively into a three-layer structured superfine fiber porous tubular scaffold material; and regulating the types and proportion of the Cu2<+> complex catalyst and the organic macromolecular polymer, as well as the electrospinning time of a three-layer electrospinning solution so as to control the release rate of NO. With a three-layer structure, the blood vessel scaffold material formed by the invention not only realizes loading of the Cu2<+> organic complex catalyst, but also improves the phenomenon of NO burst release catalyzed by an ordinary hybrid electrospun structure scaffold material, improves the loading stability of the Cu2<+> complex catalyst, and can leave the biological signal molecule NO to play a better role in inhibiting platelet adhesion, resisting platelet activation and inhibiting smooth muscle cell proliferation so as to improve its anticoagulant property.

A method for treating acute coronary syndromes (i.e., unstable angina or non-Q-wave MI) or transient ischemic attacks in a human or animal patient by placing a heat exchange apparatus in the patient's vasculature and using that heat exchange apparatus to cool the patient to a temperature (e.g. 30-36° C.) at which platelet inhibition (i.e., inhibition of platelet activation and / or aggregation and / or adhesion) occurs. Anti-shivering drugs or anesthesia may be administered to patients whose body temperature is cooled below that patient's shivering threshold (typically approximately 35.5 C). If it is determined that platelet inhibition is no longer desirable, such as when the patient is about to undergo a surgical or interventional procedure wherein bleeding could be problematic, the hypothermia-induced platelet inhibition may be rapidly reversed by using the intravascular heat exchange apparatus to re-warm the patient's body to normothermia or near normothermia.

The invention features methods for preventing platelet activation and aggregation and for treating individuals suffering from conditions or undergoing procedures that may result in unwanted platelet aggregation. The methods are based on the intravenous, subcutaneous, or transdermal administration of a platelet activation or aggregation inhibitor, e.g., xemilofiban, followed by oral administration of the same or a different platelet activation or aggregation inhibitor. The treatment may commence prior to a medical or surgical procedure or after the outbreak of an adverse medical condition, either of which results in the activation of platelets that may lead to thrombus formation, and may continue thereafter.

A composition comprising a biologically active agent and a permeation enhancing lipid wherein the permeation enhancing lipid is a platelet activating factor antagonist or a biologically inactive a platelet activating factor, and increases permeability of the biologically active agent across a tissue layer. Also disclosed is a process of increasing the permeability of a biological agent across a layer tissue comprising contacting the tissue layer with a composition comprising the biological agent and a permeation enhancing lipid wherein the permeation enhancing lipid is a platelet activating factor antagonist or a biologically inactive platelet activating factor.

An implantable cardiovascular blood pump system is provided, suitable for use as a left ventricular assist device (LVAD) system, having an implantable cardiovascular pump, an extracorporeal battery and a controller coupled to the implantable pump, and a programmer selectively periodically coupled to the controller to configure and adjust operating parameters of the implantable cardiovascular pump. The implantable cardiovascular blood pump includes a coaxial inflow cannula and outflow cannula in fluid communication with one another and with a pumping mechanism. The pumping mechanism may be a vibrating membrane pump which may include a flexible membrane coupled to an electromagnetic actuator assembly that causes wavelike undulations to propagate along the flexible membrane to propel blood through the implantable cardiovascular pump. The implantable cardiovascular pump may be programmed to operate at frequencies and duty cycles that mimic physiologic flow rates and pulsatility while avoiding thrombus formation, hemolysis and / or platelet activation.

The present invention provides soluble forms of CD39L3 polypeptides and compositions, and methods useful inhibiting platelet activation and recruitment for the treatment and prevention of thrombotic disorders in mammals administered with soluble forms of CD39L3 polypeptides.

An implantable pump system is provided, suitable for use as a left ventricular assist device (LVAD) system, having an implantable pump, an extracorporeal battery and a controller coupled to the implantable pump, and a programmer selectively periodically coupled to the controller to configure and adjust operating parameters of the implantable pump. The implantable pump includes a flexible membrane coupled to an actuator assembly that is magnetically engagable with electromagnetic coils, so that when the electromagnetic coils are energized, the actuator assembly causes wavelike undulations to propagate along the flexible membrane to propel blood from through the implantable pump. The controller may be programmed by a programmer to operate at frequencies and duty cycles that mimic physiologic flow rates and pulsatility while operating in an efficient manner that avoids thrombus formation, hemolysis and / or platelet activation.

The treatment and prevention of thrombotic events are provided through co-administration of PAR-1 and the P2Y12 ADP receptor antagonists. Combined inhibition of the PAR-1 and the P2Y12 ADP platelet activation pathways had synergistic antithrombotic and antiplatelet effects, as demonstrated in co-administration of SCH 602539 and cangrelor.

The present invention relates to a platelet aggregation function detection kit, and a method using the kit to detect platelet aggregation function. The detection kit mainly includes the following detection reagents: a sodium citrate whole blood activator, a fibrin activator and a platelet activator. The fibrin activator comprises: recombinant batroxobin and activated clotting factor. By using the kit of the invention to detect, blood sample processing requirements are low, repeat testing variability is small, accuracy and stability are high, use and storage are convenient, detection cost is low, and promotion is easy.

The present invention discloses a kind of platelet activation factor resisting compounds in the shown structure and their salts of organic acid or inorganic acid. Structurally, the compounds have various nitrogen-containing radicals connected to the hydroxyl radical in the tenth place of bilobalide B. The compounds of the present invention have the advantages of high water solubility, high bioavailability, full playing of the medicine effect, etc.

The present invention relates to a method and means for diagnosing or risk stratification of co-morbidities, particularly cardiovascular complications in diabetes patients. The invention particularly relates to a method for diagnosing whether a diabetes patient is suffering from a cardiovascular complication or is at risk of suffering from a cardiovascular complication, said method comprising the steps of (a) measuring, preferably in vitro, the level(s) of at least one cardiac hormone or a variant thereof in a sample from the patient, and (b) diagnosing the cardiovascular complication or the risk of suffering from cardiovascular complication by comparing the measured level(s) to known level(s) associated with the cardiovascular complication or risk. The present invention also relates to combining the measurement of markers comprising cardiac hormones, natriuretic peptides, inflammation-associated markers, angiogenesis markers, and markers for platelet activation. Preferred markers are brain natriuretic peptides (particularly NT-proBNP), PIGF, and sCD40L.

An implantable pump system is provided, suitable for use as a left ventricular assist device (LVAD) system, having an implantable pump, an extracorporeal battery and a controller coupled to the implantable pump, and a programmer selectively periodically coupled to the controller to configure and adjust operating parameters of the implantable pump. The implantable pump includes a flexible membrane coupled to an actuator assembly that is magnetically engagable with electromagnetic coils, so that when the electromagnetic coils are energized, the actuator assembly causes wavelike undulations to propagate along the flexible membrane to propel blood from through the implantable pump. The controller may be programmed by a programmer to operate at frequencies and duty cycles that mimic physiologic flow rates and pulsatility while operating in an efficient manner that avoids thrombus formation, hemolysis and / or platelet activation.

An implantable pump system is provided, suitable for use as a left ventricular assist device (LVAD) system, having an implantable pump, a battery, a controller, and a programmer. The implantable pump includes a flexible membrane coupled to an actuator assembly via a skirt that extends toward the inlet of the pump and curves to guide blood toward the outlet. The actuator assembly is magnetically engagable with electromagnetic coils, so that when the electromagnetic coils are energized, the actuator assembly causes wavelike undulations to propagate along the flexible membrane to propel blood from the inlet, across the skirt, and through the outlet of the implantable pump. The controller may be programmed by a programmer to operate at frequencies and duty cycles that mimic physiologic flow rates and pulsatility while operating in an efficient manner that avoids thrombus formation, hemolysis and / or platelet activation.

The invention disclosed herein comprises methods for analyzing a biological sample, such as undiluted or diluted whole blood, as well as fractions thereof, for the presence or absence and / or the concentration of disease-specific and / or other medical condition-specific markers. Such markers may include platelet activation and coagulation activation markers. The methods may comprise combining the biological sample with a coated solid phase and analyzing for the presence or absence and / or the concentration of the markers. The analysis may be performed either before or after separation of the solid phase from the biological sample. The analysis may be performed on the combined components or on any of the separated components. A preferred solid phase may be paramagnetic microparticles coated with antibodies or proteins specific for platelet activation and / or coagulation activation markers.

The invention relates to a rich-blood-platelet plasma preparation method without exogenous additives. The rich-blood-platelet plasma preparation method comprises the following steps of sample preparation: adding venous blood whole blood into a precooled centrifugal tube; primary centrifugation: performing primary centrifugation on 180g of venous blood whole blood for 10 minutes; secondary centrifugation: transferring 1550g of plasma layers into a novel centrifugal tube and performing trimming and secondary centrifugation for 10 minutes; abandoning the plasma supernate after the centrifugation; remaining the plasma supernate accounting for 1 / 10 of the venous blood whole blood volume; performing resuspension and thrombocyte precipitation; preparing and obtaining the rich-blood-platelet plasma, wherein all operations are performed at low temperature. The blood anticoagulation and blood platelet activation are regulated through physical temperature control; the addition of anticoagulants and coagulants is avoided; the clinic untoward effect caused by the addition of exogenous materials is avoided; the clinic use safety of the rich-blood-platelet plasma is ensured.

The present invention relates to high purity cangrelor, pharmaceutical formulations comprising high purity cangrelor as an active ingredient, methods for preparing such compounds and formulations, and methods for using the pharmaceutical formulations in the inhibition of platelet activation and aggregation.

The invention relates to a compound with effects of resisting inflammation and platelet activation and aggregation as well as a preparation method and application thereof. The compound has the structure of (25R)-26-oxy-beta-D-glucopyranose-5alpha-furostanol-3beta,12beta,22,26-tetraalcohol-3-oxy-beta-D-glucopyranose(1->2)[beta-D-glucopyranose(1->3)]-beta-D-glucopyranose(1->4)-beta-D-galapyranoside. The effects of the compound in the field of cardial vessels are comprehensively researched from platelet aggregation, platelet activation, platelet calcium ion variation, platelet activation signal transduction pathway and expression of platelet activation relevant inflammatory factors in the invention for the first time. Results show that the compound is a substance found to be with a strong effect on resisting platelet aggregation so far in the allium macrostemon saponin compounds, which has the stronger effect than that of aspirin with the same concentration; and the compound simultaneously has an obvious effect on resisting relevant platelet inflammations. The compound provided by the invention can be applied to medicines for treating thrombus and atherosclerosis.

A method and medicament for treating and preventing platelet activation or thrombosis in the presence of heparin- and platelet factor 4-complex reactive antibodies using a 2-O desulfated heparin with an average degree of sulfation of 0.6 sulfate groups per monosaccharide or greater and an average molecular weight or 2.4 kD or greater. The medicament preferably is administered intravenously, by aerosolization or orally. Preferably, the 2-O desulfated heparin medicament includes a physiologically acceptable carrier which may be selected from the group consisting of physiologically buffered saline, normal saline, and distilled water. Additionally provided is a method of synthesizing 2-O desulfated heparin.

This invention provides methods for the use of substituted indole compounds of the general formula:and pharmaceutically acceptable salt forms thereof. The invention provides methods for the use of the compounds as inhibitors of the activity of various phospholipase enzymes, particularly phospholipase A2 enzymes, and for the medical treatment, prevention and inhibition diseases and disorders including asthma, stroke, atherosclerosis, multiple sclerosis, Parkinson's disease, arthritic disorders, rheumatic disorders, central nervous system damage resulting from stroke, central nervous system damage resulting from ischemia, central nervous system damage resulting from trauma, inflammation caused or potentiated by prostaglandins, inflammation caused or potentiated by leukotrienes, inflammation caused or potentiated by platelet activation factor, pain caused or potentiated by prostaglandins, pain caused or potentiated by leukotrienes, and pain caused or potentiated by platelet activation factor.