555 results about "Cell damage" patented technology

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.

Peptides able to inhibit or activate the translocation or function of δPKC are identified. Administration of the peptides for protection or enhancement of cell damage due to ischemia is described. Therapeutic methods to reduce damage to cells or to enhance damage to cells due to ischemia are also described, as well as methods for screening test compounds for δPKC-selective agonists and antagonists.

An NVM controller measures cell damage for wear leveling in an NVM, thus improving performance, reliability, lifetime, and/or cost of a storage sub-system, such as an SSD. In a first aspect, the controller determines that an error reading a page of NVM was caused by cell damage and/or cell leakage. The controller reprograms and immediately reads back the page, detecting that the error was caused by cell damage if an error is detected during the immediate read. In a second aspect, the cell damage is tracked by updating cell damage counters for pages and/or blocks of NVM. In a third aspect, wear leveling is performed based at least in part upon measured cell damage for pages and/or blocks of NVM.

The present invention provides a masking system for selectively applying cells to predetermined regions of a surface. A mask is positioned adjacent to a surface to cover some portions of the surface while allowing other portions of the surface to remain uncovered. Cells then are applied to uncovered portions of the surface and the mask removed. Alternatively, a cell-adhesion promoter is applied to uncovered portions of the surface, and then cells are applied to the surface before or after removal of the mask from the surface. The masking system can be pre-coated, at least on those surfaces which will come into contact with cells, with a cell-adhesion inhibitor to resist absorption of cells and thereby avoid cell damage when the mask is removed (if cells are deposited prior to removal of the mask). A polymeric elastomeric mask that comes into cohesive-conformal contact with a surface to be patterned can be used.

Methods that involve detection of a DSG3 protein for diagnosing cancer are disclosed. In lung cancer, the expression of DSG3 was found to be enhanced at very high frequency at the gene level and protein level. Methods of the present invention can be carried out using an antibody that recognizes a DSG3 protein. Pharmaceutical compositions, cell growth inhibitors, and anticancer agents containing a DSG3-binding antibody as an active ingredient are also disclosed. Methods of inducing cell damage in DSG3-expressing cells and methods of suppressing proliferation of DSG3-expressing cells by contacting the DSG3-expressing cells with DSG3-binding antibodies are also disclosed.

Administering water-soluble or dispersible synthetic analogs or derivatives of astaxanthin, lutein, zeaxanthin, or lycophyll and/or other carotenoids to a subject may reduce some of the adverse effects of inflammation in a body organ or tissue. The analogs or derivatives may be incorporated into pharmaceutical, over-the-counter, or nutraceutical preparations. Administration of the analogs or derivatives described herein may reduce deposition of inflammatory mediators such as C-reactive protein, complement system proteins or the membrane attack complex (MAC) in tissues. Reduced deposition of these molecules in tissues may reduce cell damage and/or lysis in the tissues.

The present invention relates to a testing system for assessing hypoxia induced cellular damage in a mammal including human, comprising a disposable device having a sample inlet and a collection chamber separated by a separation device wherein the collection chamber is connected to at least two, a first and a second, visible detection compartments, whereof at least one is arranged with chemical means for direct visual detection, said first detection compartment being arranged to determine whether level of hemoglobin (Hb) in a sample of body fluid taken from said mammal exceeds a predetermined threshold value, and said second detection compartment being arranged to evaluate level of total amount of lactate dehydrogenase (LDH) in said sample.

The invention discloses a construction method of an umbilical cord mesenchyma stem cell bank utilizing newborn umbilical cords as resources, aiming at causing the steps to be less and the operation to be simpler and easier when constructing the umbilical cord mesenchyma stem cell bank. The invention comprises the following steps: (1), taking a human umbilical cord for detection, using a buffer solution to wash and remove residual blood, shearing to pieces, thus obtaining human umbilical cord tissue; (2), adding collagenase for digestion; (3), adding the buffer solution for diluting the digested tissue followed by organizing, mixing evenly and centrifuging; (4), abandoning the supernatant, adding the buffer solution for heavy suspension precipitation, screening, collecting filtrate and centrifuging, and repeating twice to obtain the human umbilical cord mesenchyma stem cell; (5), saving the obtained human umbilical cord mesenchyma stem cell in liquid nitrogen according to ABO/Rh parting and HLA parting thereof, establishing a cell information archive for retrieval, thus constructing the human umbilical cord mesenchyma stem cell bank. Compared with the existing method, the invention is more fast and convenient, and has less damage to the cell.

A method for alleviating a symptom of chemotherapy in a subject comprises identifying a subject undergoing chemotherapy and then administering a therapeutically effective amount of a GH/IGF-1 Axis inhibitory composition to the subject. Typically, the levels of IGF-1 and/or GH in the subject are monitored as well as chemotherapy related symptoms. A method of alleviating oxidative damage, cellular damage including mutations, and insulin resistance in a subject is also provided.

Methods for the prevention or treatment of disorders and complications of disorders resulting from cell damage caused by an aging-related isoform of NADH oxidase (arNOX) are described. The agent for such inhibition comprises processed various Narcissus tazzeta extracts, preferably IBR-DORMIN®, both alone and in combination with other inhibition agents, including ubiquinones like coenzyme Q. These agents bind arNOX and inhibit the ability of arNOX to generate reactive oxygen species, thereby decreasing the ability of arNOX to generate reactive oxygen species. Such agents, and their methods of administration, as extremely effective as part of anti-aging treatments.

A charger for ultracapacitors that allows many ultracapacitors, that may be connected in several different configurations, to be charged from a very low voltage to their rated voltage very rapidly without cell damage. The charger also allows for the detection of failed cells.

The present invention includes delivery of isolated and purified nucleic acids that encode GTPCH proteins in nanoparticles for the treatment of endothelial cells damaged by diabetes, smoking, dyslipidemia, hypertension, and cardiovascular disease. The nanoparticles contain a nucleic acid sequence, polymer and a targeting ligand. The targeting ligand facilitates the selective delivery of the nucleic acid sequence to damaged endothelial cells. Examples involving a nucleic acid sequence encoding GTP-cyclohydrolase I (GTPCH), PEG/PEI polymers, and a monoclonal antibody or other molecule that binds to the lectin-like oxidized low density lipoprotein (LDL) receptor-1 (Lox-1) or associated molecules are presented.

The invention relates to a synergistic heat radiation solar cell assembly and a preparation method thereof. The synergistic heat radiation solar cell assembly comprises a frame body good for air flow and an assembly structure mounted in the frame body, wherein the assembly structure consists of a transmission front board, a transparent EVA (Ethylene-Vinyl Acetate copolymer) layer, a solar cell chip and a circuit which are sealed by a packaging glue film, a heat conduction composite EVA back seal glue film and a heat radiation back board in sequence. With the adoption of the synergistic heat radiation solar cell assembly, heat generated by absorbing and coupling when a cell works can be more efficiently transmitted and emitted, so as to effectively reduce the temperature of the cell assembly, improve the light-electric converting efficiency of the cell assembly and be good for delaying the aging damage of the cell damage. According to the invention, the heat transmission effect of the cell assembly is improved through a compound modification method without changing a basic structure and the appearance of the typical solar cell assembly and increasing volume and weight, and is low in cost and convenient for installation, use and maintenance.

The invention discloses a new type immersion ore bioreactor to proceed biological oxidation of sulfide mineral in biological metallurgical technical domain, which is characterized by the following: adopting internal ring gas-flow elevating type reactor; using compressed air as liquid hoisting power to accelerate the macrography mixing of material and mass transfer course; and providing oxygen for growth of microbe and biological oxidation of mineral; lightening the attrition and damage of microbiological thallus caused by ore sand greatly; comparing to traditional stirring type immersion ore bioreactor; composing by cylindrical tank and bottom of tank; assembling three built-in type guild shell to decrease the height of reactor; making the high diameter ratio (H/D) reach 1-1.5 range of the reactor. This invention possesses merits of soft stirring, small hurt for cell, good mass transfer effect and simple structure, which compared to traditional method.

Described herein are methods for treating and/or preventing bone tissue and cell damage caused by reactive oxygen species in mammals. More specifically, embodiments of the invention relate to the prevention and/or reduction of bone tissue and cell damage through the administration of histamine, histamine agonists, and related compounds.

A method is disclosed for cryopreserving living animal cells in immunoisolation membranes, including: (1) cutting out a living organ from an animal, (2) digesting the cutout organ into the discrete living animal cells and separating the discrete cells, (3) suspending the separated cells in a solution of sodium chloride containing sodium alginate and collagen, (4) forming microcapsules of the living animal cells by using the resulting suspension, (5) forming immunoisolation membranes around outer surfaces of the microcapsules of the living animal cells by covering the outer surfaces with alginate-(poly-L-lysine) and thereby obtaining the living animal cells enclosed in the immunoisolation membranes, (6) suspending the resulting living animal cells enclosed in the immunocapsules in a cell damage-preventing solution, and (7) immediately with liquid nitrogen.

The invention describes methods for predicting outcome for patients suffering from traumatic brain injury (TBI) by evaluating levels of markers commonly associated with cellular damage in bodily fluids. Utilization of such methods improves diagnosis and treatment of patients suffering from traumatic brain injury, thus potentially minimizing and/or eliminating long-term adverse effects in these patients.

The invention discloses a micro blood cell separation device and a method for using the same. The separation device comprises a signal generator, a sample-adding pump, a separation chip and separated cell collectors; a separating cavity is arranged on the separation chip; the front end of the separation cavity is provided with an infusion opening; the rear end of the separation cavity is provided with two outlets; an electrode plate is arranged in the separation cavity; interdigital electrode groups are arranged on the electrode plate; the signal generator is connected with the interdigital electrode groups through conducting wires; the sample-adding pump is communicated with the infusion opening through a sample infusion pipe; and the outlets are connected onto the separated cell collectors. According to the invention, the separation is carried out by using the dielectrophoresis characteristic differences of blood cells in an electric field; and the continuous separation manner has the advantages of high efficiency, low cost, little cell damage, capability of large-flux separation and the like compared with the traditional cell separation method.

A method of reducing the occurrence of brain cell damage or death caused by transient cerebral hypoxia/ischemia condition or a traumatic brain injury (TBI) event. The method typically comprises identifying a subject with a transient cerebral hypoxic and/or ischemic condition, or a TBI, and within 24 hours of onset of the condition, administering to the subject a continuous intravenous infusion dose of methamphetamine in an amount sufficient to reduce the occurrence of brain cell damage or death caused by the condition. Preferably, in addition to the continuous intravenous infusion dose, a bolus dose of methamphetamine is administered to the subject as soon as possible after onset of the condition or occurrence of the TBI event.