Abstract: The compounds of the current disclosure include propynyl substituted indoles, where one or more hydrido radicals is substituted with a deuterium atom, wherein the compound binds a mutant p53 protein and increases wild-type p53 activity of the mutant p53 protein.

Abstract: The present disclosure relates to the use of substituted heterocycles for the inhibition of the activity of WIP1. Suitably, the present disclosure relates to the use of substituted heterocycles for the treatment of cancer.

Abstract: Provided herein are methods and compositions of treating a condition by intratumorally administering MDM2 inhibitors. In some embodiments, the pharmaceutical compositions for intratumoral administration are formulated for controlled release and can comprise a biodegradable polymer.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: An implantable device includes a substrate and protective cover that cooperate to define an enclosed sensor volume. A sealed enclosure is provided within the sensor volume, with an electronic component assembly (ECA) being located within the sealed enclosure. A flexible circuit board assembly (FCBA) is electrically coupled with the ECA through a wall of the sealed enclosure. At least one transducer is provided on the FCBA in contact with the substrate, and the FCBA is held apart from the enclosure via a polymeric spacer provided therebetween. An inert polymer fill is provided within the sensor volume external to the enclosure.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: The compounds of the current disclosure include propynyl substituted indoles, where one or more hydrido radicals is substituted with a deuterium atom, wherein the compound binds a mutant p53 protein and increases wild-type p53 activity of the mutant p53 protein.

Abstract: A cerclage system used to affix a bone includes a tension plate, a cable lock, and a cerclage cable configured to encircle the bone. The tension plate, which is engageable with the cerclage cable, is moveable between a natural shape and an insertion shape where the tension plate stores energy. The cable lock locks the cerclage cable about the bone in engagement with the tension plate. The tension plate is configured for positioning atop the bone while residing in the insertion shape. The tension plate, through an engagement thereof with the cerclage cable and upon attempted movement thereof from the insertion shape toward the natural shape, delivers the energy stored therein to the cerclage cable thereby tensioning the cerclage cable such that the cerclage system continuously compresses the bone.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods that restore DNA binding affinity of p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. Disclosed herein are compounds and methods to recover wild-type function of p53 mutants using x-ray co-crystal structures of mutant p53 and compounds of the disclosure. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: A patient monitoring system, including: a bone plate configured to be secured to a bone; a plurality of sensors on the bone plate configured to: measure a parameter; transmit a data signal communicating the measured parameter value; and wherein the transmitted data signals from the plurality of sensors are time division multiplexed; and an external wireless reader including an antenna, a processor, and wireless communication radio, wherein the external wireless reader is configured to: transmit an modulated RF signal; and receive the time division multiplexed transmitted data signals from the plurality of sensors.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present disclosure can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

Abstract: Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.