A composition for reducing microbial activity in an environment susceptible to microbial activity, comprising: metallic nanoparticles; and an oxygenation agent.

A composition for reducing microbial activity in an environment susceptible to microbial activity, comprising: metallic nanoparticles; and an oxygenation agent.

The present invention relates to a hypoxia-inducible factor (HIF) activator, or a pharmaceutically acceptable salt or solvate thereof, for use in promoting tissue repair. The HIF activator, or the pharmaceutically acceptable salt or solvate thereof, is for use with a prototypical tissue-protective cytokine, or a pharmaceutically acceptable salt or solvate thereof, which is administered exogenously to the body being treated.

The present invention relates to a hypoxia-inducible factor (HIF) activator, or a pharmaceutically acceptable salt or solvate thereof, for use in promoting tissue repair. The HIF activator, or the pharmaceutically acceptable salt or solvate thereof, is for use with a prototypical tissue-protective cytokine, or a pharmaceutically acceptable salt or solvate thereof, which is administered exogenously to the body being treated.

The present invention relates to a hypoxia-inducible factor (HIF) activator, or a pharmaceutically acceptable salt or solvate thereof, for use in promoting tissue repair. The HIF activator, or the pharmaceutically acceptable salt or solvate thereof, is for use with a prototypical tissue-protective cytokine, or a pharmaceutically acceptable salt or solvate thereof, which is administered exogenously to the body being treated.

This present invention discloses compositions comprising Dead Sea extract in combination with one or more plant extracts, uses thereof and methods of preventing and/or reducing and/or inhibiting the glycation of one or more biomolecules and/or preventing and/or reducing and/or inhibiting the formation of Advanced Glycation End Products.

This present invention discloses compositions comprising Dead Sea extract in combination with one or more plant extracts, uses thereof and methods of preventing and/or reducing and/or inhibiting the glycation of one or more biomolecules and/or preventing and/or reducing and/or inhibiting the formation of Advanced Glycation End Products.

Compositions and methods for combination therapy are provided. The compositions comprise a multiple unit dosage form having both a therapeutic agent and a nutritional supplement. The combination therapy is useful for restoring a nutrient depletion associated with a particular disease state. Additionally, the combination therapy can prevent or attenuate the depletion of a nutrient caused, in whole or in part, by the co-administrated therapeutic drug. Methods of manufacturing the formulations are likewise described.

Disclosed is a method for enhancing tumor response to chemotherapy, the method comprising administering a short-acting anti-angiogenic agent (AAA) capable of activating ASMase to a subject afflicted with a solid tumor, and thereby creating a time interval of increased susceptibility of said tumor to one or more chemotherapeutic agents, followed by administration of at least one chemotherapeutic agent within the interval. The interval can be defined in terms of a short-duration activation of ASMase signaling by the AAA. Disclosed are also methods for predicting the tumor response in a patient afflicted with a solid tumor to a chemotherapeutic agent, using as an indicator of the response ASMase level or activity (or ceramide level) in the patient following the administration of the chemotherapeutic agent to the patient, or dynamic IVIM based DW-MRI to measure perfusion alterations following administration of the chemotherapeutic agent.

Disclosed is a method for enhancing tumor response to chemotherapy, the method comprising administering a short-acting anti-angiogenic agent (AAA) capable of activating ASMase to a subject afflicted with a solid tumor, and thereby creating a time interval of increased susceptibility of said tumor to one or more chemotherapeutic agents, followed by administration of at least one chemotherapeutic agent within the interval. The interval can be defined in terms of a short-duration activation of ASMase signaling by the AAA. Disclosed are also methods for predicting the tumor response in a patient afflicted with a solid tumor to a chemotherapeutic agent, using as an indicator of the response ASMase level or activity (or ceramide level) in the patient following the administration of the chemotherapeutic agent to the patient, or dynamic IVIM based DW-MRI to measure perfusion alterations following administration of the chemotherapeutic agent.