2150 results about "Normal cell" patented technology

The identification of mutations that are present in a small fraction of DNA templates is essential for progress in several areas of biomedical research. Though massively parallel sequencing instruments are in principle well-suited to this task, the error rates in such instruments are generally too high to allow confident identification of rare variants. We here describe an approach that can substantially increase the sensitivity of massively parallel sequencing instruments for this purpose. One example of this approach, called “Safe-SeqS” for (Safe-Sequencing System) includes (i) assignment of a unique identifier (UID) to each template molecule; (ii) amplification of each uniquely tagged template molecule to create UID-families; and (iii) redundant sequencing of the amplification products. PCR fragments with the same UID are truly mutant (“super-mutants”) if ≧95% of them contain the identical mutation. We illustrate the utility of this approach for determining the fidelity of a polymerase, the accuracy of oligonucleotides synthesized in vitro, and the prevalence of mutations in the nuclear and mitochondrial genomes of normal cells.

The present invention provides assay systems and related methods for determining genetic abnormalities in mixed samples comprising cell free DNA from both normal and putative genetically atypical cells. Exemplary mixed samples for analysis using the assay systems of the invention include samples comprising both maternal and fetal cell free DNA and samples that contain DNA from normal cells and circulating cancerous cells.

A spinal disc annulus repair stent for repair and reconstruction of the spinal disc wall (annulus) after surgical invasion or pathologic rupture, which may incorporate suture closure or other means of stent insertion and fixation, designed to reduce the failure rate of conventional surgical procedures on the spinal discs. In an illustrative embodiment, the design of the spinal disc annulus stent advantageously allows ingrowth of normal cells of healing in an enhanced fashion strengthening the normal reparative process.

The present invention relates to prioritizing special cells in cell selection in a cellular radio network. In a cellular radio network one or more cells provide a subscriber with special services or tariffs not offered to all subscribers. These cells are called subscriber's special cells. The mobile station measures an average reception level and calculates by means of them cell selection parameters on the basis of which the best cell is selected. In accordance with the invention, when the mobile station detects that the cell is one of cells of a special cell list stored in a memory, it checks first if the cell fulfils a minimum requirement of cell selection on the basis of the measured signal level. If the minimum requirement is fulfilled, the mobile station manipulates the calculation of the cell selection parameter of a special cell to the effect that the selection probability of a special cell is improved with respect to a normal cell. In a preferred embodiment of the invention, the manipulation of the calculation comprises a step of adding a predetermined margin to the measured signal level of a special cell before the cell selection parameter is calculated. This will minimize the possibility that the mobile station would accidentally be camped on a normal cell when it is within the area of a special cell.

The present invention provides assay systems and related methods for determining genetic abnormalities in mixed samples comprising cell free DNA from both normal and putative genetically atypical cells. Exemplary mixed samples for analysis using the assay systems of the invention include samples comprising both maternal and fetal cell free DNA and samples that contain DNA from normal cells and circulating cancerous cells.

A semiconductor memory device having an error check and correction (ECC) type error recovery circuit in which disposition of ECC cells is improved. The memory device comprises: a memory cell array including a plurality of normal cell array portions and an ECC cell array portion; an X decoder for selecting one of word lines in the memory cell array, the word lines extending from the X decoder to the memory cell array; an ECC operation circuit for performing error check and correction based on cell data read out from a selected word line, the cell data including data from normal cells and ECC cells of the selected word line. The ECC memory cell array portion is disposed at a location other than the far end of the word lines from the X decoder, that is, the ECC cell array portion is disposed at a location in which read out speed of data from ECC cell or cells does not become the worst speed in the memory device. Therefore, the worst data read out speed can be measured from outside.

The present invention provides a method to enhance apoptosis in a cell by the administration of p53 in combination with a calpain inhibitor. The present invention provides a method of increasing the infectivity of a cell to a viral vector by treatment of the cell with a calpain inhibitor. the present invention further provides a method of enhancing transciption of a therapeutic transgene from the CMV promoter. The present invention also provides a method of suppress the in vivo CTL response to viral vectors by the use of calpain inhibitors. The present invention further provides a pharmaceutical formulations of p53 and a calpain inhibitor in a pharmaceutically acceptable carrier. The present invention provides a method of ablating neoplastic cells in a mammalian organism in vivo by the co-administration of a calpain inhibitor and p53. The present invention also provides a method of ablating neoplastic cells in a population of normal cells contaminated by said neoplastic cells ex vivo by the administration of a recombinant adenovirus in combination with a calpain inhibitor to said population.

Methods and compositions for modulating the FGF effect on the sensitivity of malignant and normal cells to anticancer agents are provided. In particular, methods and compositions for inhibiting FGF-induced resistance to a broad spectrum of anticancer agents in solid and soft-tissue tumors, metastatic lesions, leukemia and lymphoma are provided. Preferably, the compositions include at least one FGF inhibitor in combination with a cytotoxic agents, e.g., antimicrotubule agents, topoisomerase I inhibitors, topoisomerase II inhibitors, antimetabolites, mitotic inhibitors, alkylating agents, intercalating agents, agents capable of interfering with a signal transduction pathway (e.g., g., a protein kinase C inhibitor, e.g., an anti-hormone, e.g., an antibody against growth factor receptors), an agent that promotes apoptosis and/or necrosis, and interferon, an interleukin, a tumor necrosis factor, and radiation. In other embodiments, methods and composition for protecting a cell in a subject, from one or more of killing, inhibition of growth or division or other damage caused, e.g., by a cytotoxic agent, are provided. Preferably, the method includes: administering, to the subject, an effective amount of at least one FGF agonist, thereby treating the cell, e.g., protecting or reducing the damage to the dividing cell from said cytotoxic agent.

This invention is directed to methods and compositions for diagnosis, prognosis and for determining methods of treatment. The physiological status of cells present in a sample (e.g. clinical sample) can be used in diagnosis or prognosis of a condition (e.g. Chronic Lymphocytic Leukemia), in patient selection for therapy, to monitor treatment and to modify or optimize therapeutic regimens. The physiological status of a cell can be determined by comparing the intracellular status of one or more activation elements (e.g. the phosphorylation status of a signaling molecule) in a cell (e.g. a cancer cell) to that of another cell (e.g. a normal cell). The physiological status of a cell can be further classified by adding one or more modulators (e.g. an inhibitor or activator) to the cell in question. In some embodiments, the invention is directed to methods of determining a phenotypic profile of a population of cells.

A semiconductor device includes memory blocks MB1 and MB2 and redundancy determination circuit 25 that can enter a normal operation mode that accesses either memory block MB1 or memory block MB2 and a refresh mode that simultaneously accesses both memory block MB1 and memory block MB2. In response to normal memory cell NMC that belongs to at least one of memory blocks MB1 and MB2 being replaced by redundant memory cell RMC in the refresh mode, redundancy determination circuit 25 deactivates normal cell area NCA to which normal memory cell NMC that is a source of replacement belongs, and activates redundant cell area RCA to which redundant memory cell RMC that is to be replaced belongs and normal cell area NCA to which normal memory cell NMC that is not being replaced belongs.

Methods are provided for cancer and pre-cancer detection by increased uptake of fluorophore glucose or deoxyglucose conjugates in cancerous and pre-cancerous cells relative to normal cells.

The invention relates to the field of pharmaceutical chemistry and specifically discloses an aryl ruthenium-beta-carboline complex and its preparation method and application. The aryl ruthenium-beta-carboline complex is [Ru(Eta6-arene)(N-N)Cl](PF6), wherein Eta6-arene is aryl ligand p-cymene(p-cymene, CYM) or benzene(benzene, Ben), N-N is beta-carboline alkaloid derivative1-(2-pyridine)-9H-pyridine[3,4-b]indole(L1), 1-(2-quinoline)-9H-pyridine[3,4-b]indole(L2) or 1-(2-imidazole)-9H-pyridine[3,4-b]indole(L3). The complex provided by the invention has very outstanding activity in in-vitro antitumor screening. In addition, in comparison with cancer cell lines, toxicity of the complex to normal cells is greatly reduced, and the complex has a good potential for development of antitumor drugs.

The invention discloses an automatic screening system and an automatic screening method using a thin-prep cytology test. The system comprises an image acquisition module, an image segmentation module, a target recognition module and a comprehensive analysis module. The method provided by the invention respectively adopts a three-point evolutionary uniform sampling method to guarantee the reliability of automatic focusing, the coarse-to-fine segmentation algorithm to improve the segmentation accuracy of pathological cell nucleuses, a series of filters to rapidly filter various impurities, and a cascade classifier training method to greatly reduce the false positive rate, and uses relative features to conduct comprehensive analysis. The method disclosed by the invention has the advantages of high sensitivity over pathological cells, high specificity over normal cells, high recognition speed and high automation degree, so that the diagnostic accuracy can be improved and the workload of a cytopathologist is reduced at the same time.

Methods and compositions are provided for the protection of normal cells from cytoreductive therapy that target proliferating cells, by administering an inhibitor of Wnt signaling pathways. Wnt signaling is critically important for homeostasis of the epithelial lining of the adult intestine and other proliferating normal adult tissues.

A novel modified matrix system, mimicking a metastatic environment, that can be used to capture and detect viable cancer and normal cells from tissue fluid samples derived from cancer subjects and which provides effective cell separation for diagnostic and therapeutic applications in treating patients with metastatic diseases.

A method and apparatus are provided for at least partially disinfecting biological fluid of a mammal, which comprises pathogens in addition to normal cellular fractions. The method includes placing the biological fluid in a reaction volume and contacting a non-thermal plasma with the biological fluid to thereby kill at least a portion of the pathogens within the biological fluid.

The invention provides a tumor chemotherapeutic medicinal preparation and a preparation method thereof. The tumor chemotherapeutic medicinal preparation comprises a cell vesicle derived from apoptotic tumor cells and a chemotherapeutic medicine which is wrapped in the cell vesicle and serves as an active ingredient. The chemotherapeutic medicine in the medicinal preparation comprises an active ingredient for treating tumor which provides the cell vesicle. The invention also provides a preparation method for the tumor chemotherapeutic medicinal preparation. By the technical scheme provided by the invention, the chemotherapeutic medicine can be selectively released at the tumor site, so that the chemotherapeutic medicine can exert medicine effect continuously, the killing effect of the chemotherapeutic medicine on the tumor cells can be improved, and the toxic or side effect of the chemotherapeutic medicine on the normal cells can be reduced.

The invention discloses a method for rapidly cleaning and shielding a junk notice. The method comprises the following steps of: 1, when a user carries out normal cell phone operation or bides, displaying a new notice on a notice board by an operation interface; 2, downwards dragging the notice board, showing a pull-down notice board; 3, displaying a notice message in the pull-down notice board and pressing the notice for a long time by the user to have an information message popping frame; 4, judging the notice message by the system and judging the message to a system notice or the junk notice; 5, displaying a message source by the popping frame and clicking to conform to quit the popping frame; and 6, displaying a message source and whether the notice is shielded or not by the popping frame; cleaning the junk notice by pressing a OK key by the user and shielding second-time receiving of the notice; prompting the user that the notice is shielded by the operation interface and opening the notice in a notice center; and pressing a cancel key to prompt the user to finish the shielding operation in the notice center. The method disclosed by the invention can conveniently and effectively shield the junk notice, can rapidly obtain the message source and brings good experience to the user.

Normal cells, such as fibroblasts or other tissue or organ cell types, are genetically engineered to express biologically active, therapeutic agents, such as proteins that are normally produced in small amounts, for example, MIS, or other members of the TGF-beta family Herceptin(TM), interferons, andanti-angiogenic factors. These cells are seeded into a matrix for implantation into the patient to be treated. Cells may also be engineered to include a lethal gene, so that implanted cells can be destroyed once treatment is completed. Cells can be implanted in a variety of different matrices. In a preferred embodiment, these matrices are implantable and biodegradable over a period of time equal to or less than the expected period of treatment, when cells engraft to form a functional tissue producing the desired biologically active agent. Implantation may be ectopic or in some cases orthotopic. Representative cell types include tissue specific cells, progenitor cells, and stem cells. Matrices can be formed of synthetic or natural materials, by chemical coupling at the time of implantation, using standard techniques for formation of fibrous matrices from polymeric fibers, and using micromachining or microfabrication techniques. These devices and strategies are used as delivery systems via standard or minimally invasive implantation techniques for any number of parenterally deliverable recombinant proteins, particularly those that are difficult to produce in large amounts and/or active forms using conventional methods of purification, for the treatment of a variety of conditions that produce abnormal growth, including treatment of malignant and benign neoplasias, vascular malformations (hemangiomas), inflammatory conditions, keloid formation, abdominal or plural adhesions, endometriosis, congenital or endocrine abnormalities, and other conditions that can produce abnormal growth such as infection. Efficacy of treatment with the therapeutic biologicals is detected by determining specific criteria, for example, cessation of cell proliferation, regression of abnormal tissue, or cell death, or expression of genes or proteins reflecting the above.