32 results about "Cellular mechanism" patented technology

A method for detecting compounds of interest in bodily fluids, including exhaled breath and blood. The present invention uses biosensors that mimic naturally occurring cellular mechanisms, including RNA oligonucleotide chains or “aptamers,” in combination with signaling agents or nanotechnology to provide an effective and efficient method for diagnosing a condition and/or disease within a patient. The subject invention also provides a method for screening those analytes/biomarkers likely to be present in exhaled breath.

A method for detecting compounds of interest in bodily fluids, including exhaled breath and blood. The present invention uses biosensors that mimic naturally occurring cellular mechanisms, including RNA oligonucleotide chains or “aptamers,” in combination with molecular beacons or nanotechnology to provide an effective and efficient method for diagnosing a condition and/or disease within a patient. The subject invention also provides a method for screening those analytes/biomarkers likely to be present in exhaled breath.

The activity of multiple proteins in a single living cell, portion of a cell or in a group of cells is simultaneously measured by introducing reporter molecules. The reporter(s) is chemically modified by the enzyme of interest. In some cases the enzyme(s) is affected by the addition of a stimulus or a pharmaceutical compound to the cell. The reactions between the enzymes and the reporters are diminished or terminated, and the reporter and modified reporter are removed. The activity of the enzyme(s) is determined by measuring the amount of reporter remaining, the amount of altered reporter produced, or by comparing the amount of reporter to the amount of altered reporter. A database is compiled of the activities of the different proteins. By performing a series of experiments at different time points, conditions, and varieties of cell types, a database is developed for molecular cellular mechanisms in health and disease states. By exposing cells to a variety of compounds data for drug development and screening is provided.

Disclosed herein is a three-dimensional culture containing human articular chondrocytes with induced terminal differentiation changes, as well as a process for preparing the same. The three-dimensional culture, which was found to mimic the biological characteristics of articular chondrocytes that undergo terminal differentiation in vivo, can be used as a tool in the studies of the molecular and cellular mechanisms of osteoarthritis, and in the screening of candidate drugs for use in treatment of a disorder associated with articular chondrocytes.

Disclosed are biological reagents which comprise compounds that inhibit beta-amyloid peptide release and/or its synthesis, and, accordingly, have utility in determining the cellular mechanism involved in the generation of beta-amyloid peptide.

A treatment solution used to prevent posterior capsular opacification is applied or introduced into the lens capsular bag before, during, or after cataract surgery. The treatment solution may also be applied to an intraocular lens prior to surgery. The treatment solution comprises an ion transport mechanism interference agent, which either alone or in combination with other treatment agents such as an osmotic stress agent and an agent to establish a suitable pH, selectively induces detachment and/or death of lens epithelial cells such that posterior capsular opacification is prevented. While the ion transport mechanism interference agent is capable of interfering with the cellular mechanisms and cell ion distribution of a broad range of cells, a concentration of agent is selected such that the treatment solution interferes selectively with the cellular mechanisms of lens epithelial cells while leaving other ocular cells substantially unharmed. The treatment solution selectively induces cellular death and/or detachment of lens epithelial cells while other ocular cells and tissue remain substantially unharmed and without lengthy preoperative pre-treatment.

The present invention relates to a culture support for cultivating hematopoietic stem cells (HSCs) and/or hematopoietic progenitors (HPs), comprising a calcium biomaterial, osteoclasts, endothelial cells and mesenchymatous stem cells (MSCs) and/or osteoblasts and/or adipocytes. The present invention also relates to a method for preparing such a culture support, and an in vitro HSC and/or HP cultivation method. The use of such a culture support for studying cellular mechanisms involved in hematopoiesis and/or differentiation of HSC/HPs and/or for studying the efficacy and/or the toxicity of a medicament candidate is also described.

The present disclosure relates to diets, compounds, e.g., GCN2 agonists and methods that selectively reduce adipose tissue mass relative to the mass of other tissue types and increase insulin sensitivity. Another aspect of the disclosure relates to methods for identifying GCN2 agonists that will decrease the activity and/or expression of one or more of adipogenic genes thereby selectively inhibiting the cellular mechanisms that lead to fat production. Such agonists have the effect of reducing adipose tissue mass in an individual.

Compositions and methods for targeted gene therapy are disclosed. Compositions containing double duplex-forming pseudocomplementary oligonucleotides are administered in combination with a donor oligonucleotide that is homologous to a target sequence on a double-stranded DNA molecule in need of repair or replacement. By activating cellular mechanisms involved in DNA synthesis, repair and recombination, the double duplex-forming pseudocomplementary oligonucleotides can introduce one or more mutations at a site of interest by increasing the efficiency of targeted recombination of the donor oligonucleotide. The pseudocomplementary oligonucleotides/donor oligonucleotide compositions may be administered in combination with a second therapeutic agent that enhances access of the pseudocomplementary oligonucleotides and/or the donor oligonucleotide to the target site, an agent that enhances or increases DNA repair or recombination, or an agent that enhances uptake or delivery of the oligonucleotides.

As described herein, a method of inhibiting metastasis in cancer includes administering to a human subject diagnosed with a cancer of an organ of the peritoneal cavity a therapeutically effective amount of an inhibitor of CCR5 or P-selectin. Preferably the subject has a tumor positive for a ligand of P-selectin such as a CD24+ or PSGL-1+ tumor. Analysis of samples from HGSOC patients confirmed increased MIP-1β and P-selectin, suggesting that this novel multi-cellular mechanism can be targeted to slow or stop metastasis in cancers such as high-grade serous ovarian cancer, for example by using anti-CCR5 and P-selectin therapies developed for other indications.

The invention discloses an NTDs (neural tube defects) rat embryo animal model and a constructing method thereof. Normal pregnant rats which have been pregnant for 6 to 10 days are injected with 19-23 mg/kg of retinoic acid at one time for intragastric administration intervention, then construction of the stable and efficient NTDs rat embryo animal mode can be induced rapidly after pregnant 10.5 days, and further, rat embryo brain vesicle tissue is separated out for cell culture while an NTDs cell model can be built. The animal model and the cell model constructed by the method can provide good platforms for research on NTDs molecular mechanism and cellular mechanism in vivo and vitro.

The role of the JAK/STAT signal transduction pathway cellular mechanisms that lead to the onset and progression of degenerative joint diseases or disorders such as osteoarthritis (OA) is disclosed. Certain known effective OA therapeutics such as hymenialdisine, debromohymenialdisine, and its variants and derivatives are shown to function as JAK3-specific inhibitors, which downregulate steady state mRNA levels of key cellular components involved in cartilage degradation. Another JAK3-specific inhibitor, not previously known as an OA therapeutic, is shown to downregulate steady state mRNA levels of various cellular components involved in cartilage degradation in a manner identical to that of the known OA therapeutics.

The present invention relates to DNA signatures that are characteristic of DNA that has been repaired in a cell by double strand break repair (DSBR) and that furthermore are characteristic of the specific cellular mechanism used to repair the DNA—such as homologous recombination (“HR”), non-homologous end joining (“NHEJ”), or microhomology-mediated end-joining (“MMEJ”). The present invention provides methods for identifying such DNA signatures, and also provides certain identified DNA signatures that are characteristic of DNA repair by HR, NHEJ, or MMEJ. The present invention also provides various methods and compositions that can be used to determine the presence of such DNA signatures in the genomes of living cells.

A novel neuroprotectant was identified by microarray analysis that is differentially expressed between the ventricular zone and the cortex of human adult and fetal brain. The secreted protein antagonizes Wnt action in Xenopus embryos. Methods are described for modulating free radical neurotoxicity by contacting cells with the protein, treating neuronal diseases associated with free radical-mediated cell death by administering the protein, determining neuroprotective genomic targets associated with select free radical toxicity pathways by screening with the protein and using the protein to identify other compounds that modulate the biological activity of the secreted protein and the cell machinery that reacts to the secreted protein.