The present invention relates to activating mitochondrial uncoupling as a therapeutic intervention which has many beneficial effects to both healthy and sick subjects. The beneficial effects of activating mitochondrial uncoupling include extended lifespan, decreasing or suppressing harmful or unwanted cellular proliferation, increasing or restoring intestinal homeostasis and slowing or inhibiting tumor growth. The invention includes the administration of activators of mitochondrial uncoupling to subjects in order to extend lifespan, decrease or suppress harmful or unwanted cellular proliferation, increase or restore intestinal homeostasis, prevent and treat cancer, and slow or inhibit tumor growth.

The present invention relates to activating mitochondrial uncoupling as a therapeutic intervention which has many beneficial effects to both healthy and sick subjects. The beneficial effects of activating mitochondrial uncoupling include extended lifespan, decreasing or suppressing harmful or unwanted cellular proliferation, increasing or restoring intestinal homeostasis and slowing or inhibiting tumor growth. The invention includes the administration of activators of mitochondrial uncoupling to subjects in order to extend lifespan, decrease or suppress harmful or unwanted cellular proliferation, increase or restore intestinal homeostasis, prevent and treat cancer, and slow or inhibit tumor growth.

The present invention relates to novel nanomaterial-molecular compositions, methods and devices thereof for efficient and targeted trans-differentiation of cells including fibroblasts and glia into neurons, both in vitro as well as in situ and in-vivo, which is of great importance for cell replacement therapies. Specifically, the invention provides a nanomaterial-molecular composition, device and method for targeted nano-enhanced opto-chemical trans-differentiation of fibroblasts/glia to neurons in the central and peripheral nervous system for restoration of neural functions in patients by delivery of nanomaterial-molecular composition, followed by optical illumination.

The present invention relates to novel nanomaterial-molecular compositions, methods and devices thereof for efficient and targeted trans-differentiation of cells including fibroblasts and glia into neurons, both in vitro as well as in situ and in-vivo, which is of great importance for cell replacement therapies. Specifically, the invention provides a nanomaterial-molecular composition, device and method for targeted nano-enhanced opto-chemical trans-differentiation of fibroblasts/glia to neurons in the central and peripheral nervous system for restoration of neural functions in patients by delivery of nanomaterial-molecular composition, followed by optical illumination.

Described herein are low sodium formulations. In some embodiments, the low sodium formulations can contain an effective concentration of sodium and an effective concentration of calcium. The low sodium formulations can be provided as combination kit that can include, in some embodiments, a low sodium formulation and a defibrillation device. Also described herein are methods of administering the low sodium formulation to a subject in need thereof and performing cardiac resuscitation and/or defibrillation on the subject in need thereof.

A method of treating a host of neuromuscular, neurodegenerative, developmental, autoimmune and metabolic diseases/disorders related to aging, such as traumatic injury, stroke, Huntington's disease, Epilepsy, Multiple Sclerosis (MS), Lupus, Type-1 and Type-2 diabetes, Maturity Onset Diabetes of the Young (MODY), myasthenia gravis (MG), rheumatoid arthritis (RA), Graves' disease, Guillain-Barr syndrome (GBS), metabolic syndrome, Muscular Dystrophy or Duchenne Muscular Dystrophy (DMD), severe burns, aging, Amyotrophic Lateral Sclerosis (ALS), Friedreich's Ataxia, Batten Disease, Alzheimer's disease, optic neuritis, Leber's hereditary optic neuropathy (LHON), autism, Rett syndrome, Batten Disease, Angelman's Syndrome, Leigh disease, Fragile-X Syndrome, depression, Parkinson's disease, mitochondrial diseases, developmental disorders, metabolic disease disorders and/or autoimmune disorders by inducing endogenous BDNF expression with DNP treatment to protect from neuromuscular dysfunction/disorders and/or neurodegeneration and/or muscle wasting. DNP was administered to mice daily over a range of doses, and subsequently BDNF expression in the brain showed a dose dependent and non-linear increase in expression.

A method of treating a host of neuromuscular, neurodegenerative, developmental, autoimmune and metabolic diseases/disorders related to aging, such as traumatic injury, stroke, Huntington's disease, Epilepsy, Multiple Sclerosis (MS), Lupus, Type-1 and Type-2 diabetes, Maturity Onset Diabetes of the Young (MODY), myasthenia gravis (MG), rheumatoid arthritis (RA), Graves' disease, Guillain-Barr syndrome (GBS), metabolic syndrome, Muscular Dystrophy or Duchenne Muscular Dystrophy (DMD), severe burns, aging, Amyotrophic Lateral Sclerosis (ALS), Friedreich's Ataxia, Batten Disease, Alzheimer's disease, optic neuritis, Leber's hereditary optic neuropathy (LHON), autism, Rett syndrome, Batten Disease, Angelman's Syndrome, Leigh disease, Fragile-X Syndrome, depression, Parkinson's disease, mitochondrial diseases, developmental disorders, metabolic disease disorders and/or autoimmune disorders by inducing endogenous BDNF expression with DNP treatment to protect from neuromuscular dysfunction/disorders and/or neurodegeneration and/or muscle wasting. DNP was administered to mice daily over a range of doses, and subsequently BDNF expression in the brain showed a dose dependent and non-linear increase in expression.

Provided are methods of treating a neurological or psychiatric disorder in a subject in need thereof, comprising: administering to the subject a therapeutically effective amount of ketamine or a pharmaceutically acceptable salt thereof in combination with an amount of one or more compounds effective to increase the level of nicotinamide adenine dinucleotide (NAD.sup.+) in the subject.

Provided are methods of treating a neurological or psychiatric disorder in a subject in need thereof, comprising: administering to the subject a therapeutically effective amount of ketamine or a pharmaceutically acceptable salt thereof in combination with an amount of one or more compounds effective to increase the level of nicotinamide adenine dinucleotide (NAD.sup.+) in the subject.

The disclosure provides nicotinamide riboside (NR), the reduced form of NR (NRH), nicotinic acid riboside (NAR), the reduced form of NAR (NARH), derivatives thereof, compositions thereof and uses thereof. The NR and NAR derivatives have improved stability and bioavailability compared to NR and NAR. NR, NRH, NAR, NARH, and derivatives thereof can increase cellular NAD.sup.+ levels and enhance mitochondrial and cellular function and cell viability. Therefore, NR, NRH, NAR, NARH, and derivatives thereof, whether alone or in combination with one or more additional therapeutic agents (e.g., a mitochondrial uncoupler or/and a PARP inhibitor), are useful for treating mitochondrial diseases, mitochondria-related diseases and conditions, metabolic disorders, and other disorders and conditions.