摘要:
The invention relates to the treatment of various injuries, disorders, dysfunctions, diseases, and the like of the brain with MAPCs, particularly in some aspects, to the treatment of the same resulting from hypoxia, including that caused by systemic hypoxia and that caused by insufficient blood supply. In some further particulars the invention relates, for example, to the treatment of hypoxic ischemic brain injury with MAPCs, in children for example, and to the treatment of cortical infarcts and stroke with MAPCs in adults, for example.
摘要:
The present invention provides the identfication and characterization of a novel transmembrane transporter, a Na'-coupled citrate transporter ("NaCT"). Isolated polynucleotides encoding the transmembrane transporter, the transmembrane transporter polypeptide itself, antibodies thereto, and methods of use, are provided.
摘要:
The examples demonstrate that GIP receptor mRNA and protein are present in normal bone and osteoblastic-like cell lines, and that high-affinity receptors for GIP can be demonstrated by 125 I GIP binding studies. When applied to osteoblast-like cells (SaOS2), GIP stimulated an increase in cellular cAMP content and in intracellular calcium, with both responses being dose dependent. Moreover, administration of GIP results in elevated expression of collagen type I mRNA as well as an increase in alkaline phosphatase activity. Both of these effects reflect anabolic actions of presumptive osteoblasts. These results provide the first evidence that GIP receptors are present in bone and osteoblastic-like cells and that GIP modulates the function of these cells. GIP has anabolic actions on remodeling bone, increasing vertebral bone density in a rat model of osteoporosis. GIP at 10nM inhibits PTH-induced bone resorption in a fetal long bone assay and stimulates the synthesis of type 1 collagen mRNA. Transgenic mice overexpressing GIP have increased bone density compared to same age controls. GIP or analogs thereof can therefore be used as a therapeutic to inhibit bone resorption and to maintain or increase bone density. GIP antagonists, compounds which block binding to the GIP receptor, can be used to decrease bone density.
摘要:
A number of cDNA clones whose products may interact with D1 receptors in vivo were identified. One of the clones, P24, was characterized further. P24 is localized in dendtrites and spines of pyramidal cells in PFC. The extent of overlap between P24 expressing and D1 receptor expressing pyramidal cells appeared to be 100 %. In contrast, only a limited number D1 receptor antibody labeled neurons in caudate expressed P24. P24 lowers the threshold of D1 receptor response to dopamine (DA) by an order of magnitude. Sequence similarity suggests P24 is a diverged member of the RAMP family. The P24 protein is therefore referred to as a D1 DA RAMP, calcyon. The isolated protein and nucleotide molecule encoding the protein, as well as primers for the nucleotide, are described. The protein and compounds modifying DA binding to the receptor or calcium release which is mediated by the Calcyon, are useful in research studies, drug screening, and therapeutically.
摘要:
The present invention related to the α7-selective ligand (2S,3R)-N-(2-((3-pyridinyl)methyl)-l-azabicyclo[2.2.2]oct-3-yl)-5-methylthiophene-2-carboxamide or a pharmaceutical acceptable salt thereof and (2S,3R)-N-(2-((3-pyridinyl)methyl)-1-azabicyclo[2.2.2]oct-3-yl)-5-methylthiophene-2-carboxamide or a pharmaceutical acceptable salt thereof, substantially free of (2R,3R)-N-(2-((3-pyridinyl)methyl)-1-azabicyclo[2.2.2]oct-3-yl)-5-methylthiophene-2-carboxamide or a pharmaceutical acceptable salt thereof, (2S,3S)-N-(2-((3-pyridinyl)methyl)-1-azabicyclo[2.2.2]oct-3-yl)-5-methylthiophene-2-carboxamide or a pharmaceutical acceptable salt thereof and (2R,3S)-N-(2-((3-pyridinyl)methyl)-1-azabicyclo[2.2.2]oct-3-yl)-5-methylthiophene -2-carboxamide or a pharmaceutical acceptable salt thereof.
摘要:
It has been discovered that the human GT198 gene (gene symbol PSMC3IP) at chromosome 17q21 acts as a tumor suppressor. The mutation of the GT198 gene causes the increased dominant negative splice variant activity and leads to the loss of wild type GT198 function, and in turn, induces breast and ovarian cancers. One embodiment provides compositions and methods for treating or alleviating one or more symptoms associated with cancer due to the GT198 gene mutations. Another embodiment provides methods and compositions for detecting cancer due to the mutation of the GT198 gene. Still another embodiment provides methods for identifying compounds, antibodies and natural product molecules that are useful for treating cancer due to the mutations of the GT198 gene. Preferably the disclosed compositions antagonize or interfere with the biological activity of splice variants of GT198.
摘要:
The present invention provides the identification and characterization of a novel transmembrane transporter, a Na+-coupled citrate transporter ('NaCT'). Isolated polynucleotides encoding the transmembrane transporter, the transmembrane transporter polypeptide itself, antibodies thereto, and methods of use, are provided.