Abstract: Provided is a polynucleotide, including a cis-regulatory element and a nucleotide sequence encoding a vestigial like 4 protein, wherein the cis-regulatory element includes an uncoupling protein 1 enhancer and an uncoupling protein 1 promoter. Also provided is a viral vector including said polynucleotide. Also provided is a method of transfecting a cell or a subject with said polynucleotide or said viral vector.

Abstract: Provided is a polynucleotide, including a cis-regulatory element and a nucleotide sequence encoding a vestigial like 4 protein, wherein the cis-regulatory element includes an uncoupling protein 1 enhancer and an uncoupling protein 1 promoter. Also provided is a viral vector including said polynucleotide. Also provided is a method of transfecting a cell or a subject with said polynucleotide or said viral vector.

Abstract: Previously unknown mutations of the CACNA1C and CACNB2b genes are disclosed which are involved in ion channel disruptions associated with shorter than normal QT interval and ST segment elevation syndrome. These mutations are utilized to diagnose and screen for shorter than normal QT interval and ST segment elevation syndrome, thus providing modalities for diagnosing syncope and/or sudden cardiac death and/or predicting susceptibility to syncope and/or sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant polypeptides described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the CACNA1C and CACNB2b genes are disclosed which are involved in ion channel disruptions associated with shorter than normal QT interval and ST segment elevation syndrome. These mutations are utilized to diagnose and screen for shorter than normal QT interval and ST segment elevation syndrome, thus providing modalities for diagnosing syncope and/or sudden cardiac death and/or predicting susceptibility to syncope and/or sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant polypeptides described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: Previously unknown mutations of the KCNH2, SCN5A and KCNQ1 genes are disclosed which are involved in ion channel disruptions associated with short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease. These mutations are utilized to diagnose and screen for short QT syndrome, long QT syndrome, Brugada syndrome and progressive conduction disease, thus providing modalities for diagnosing sudden cardiac death and/or predicting susceptibility to sudden cardiac death. Nucleic acid probes are provided which selectively hybridize to the mutant nucleic acids described herein. Antibodies are provided which selectively bind to the mutant proteins described herein. The mutations described herein are also utilized to screen for compounds useful in treating the symptoms manifest by such mutations.

Abstract: The invention is directed to a method of treating systematic lupus erythematosus (SLE) in animals, including humans, by the oral administration of kidney extracts to decrease anti-DNA antibody production. The method of the invention includes both prophylactic and therapeutic measures.

Abstract: The reproductive cycle of insects is affected by applying a solution or suspension of a material having the formula:NX.sub.2 (CX.sub.2).sub.m SO.sub.3 Z,where each X is selected from the group consisting of H, OH, C.sub.n H.sub.2n+1, C.sub.n H.sub.2n, Cl, Br, and I; Z is selected from the group consisting of H, K, and Na, and n and m are integral numbers of from 2 to 10. Preferably, the compound applied for control of the insect reproductive cycle is taurine. The material may also be mixed with fruits. The concentration of the material should be at least 0.04M.

Abstract: An acelluar resuscitative fluid, useful as an artificial blood or blood substitute, is prepared from a modified, high molecular weight starch or a tetronic polyol prepared by the interaction of ethylenediamine and ethylene or propylene oxides, which are converted to their aldehyde form. This material is reacted with a stabilized, stroma free hemoglobin, which has been converted to an oxy-acid or diketone. The resulting solution, after purification, can be administered to an animal in the same manner as whole blood. If desired, the solution of the reaction product with the stabilized hemoglobin can be freeze-dried and later reconstituted by the addition of water to provide the administrable fluid.