Electromagnetic field therapy delays cellular senescence and death by enhancement of the heat shock response
First Claim
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1. A method comprising:
- applying repetitive radio frequency electromagnetic field shock to at least one living cell, wherein the repetitive radio frequency electromagnetic field shock is configured to precondition improvement in either heat shock factor 1 (HSF1) or heat shock response (HSR) function, or HSF1 and HSR function, and increasing expression of heat shock proteins (HSPs) without increasing temperature or causing external heat damage, wherein the precondition improvement is characterized in an increase in HSF1-heat shock element (HSE) binding.
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Abstract
Disclosed herein is a method comprising repetitive electromagnetic field shock to at least one living cell, wherein the repetitive electromagnetic field shock improves HSF1 and/or HSR function, and producing delaying and reversal of aging and age related diseases. Also disclosed herein is an apparatus adapted to deliver repetitive electromagnetic field shock to at least one living cell, wherein the repetitive electromagnetic field shock improves HSF1 and HSR function.
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23 Claims
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1. A method comprising:
applying repetitive radio frequency electromagnetic field shock to at least one living cell, wherein the repetitive radio frequency electromagnetic field shock is configured to precondition improvement in either heat shock factor 1 (HSF1) or heat shock response (HSR) function, or HSF1 and HSR function, and increasing expression of heat shock proteins (HSPs) without increasing temperature or causing external heat damage, wherein the precondition improvement is characterized in an increase in HSF1-heat shock element (HSE) binding. - View Dependent Claims (2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20)
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21. A method comprising:
applying repetitive radio frequency electromagnetic field shock to at least one living cell, wherein the repetitive radio frequency electromagnetic field shock is configured to precondition enhancement of the heat shock response (HSR)/heat shock factor 1 (HSF1) pathway and augment chaperone induction during stress, and increasing expression of heat shock proteins (HSPs) without increasing temperature or causing external heat damage wherein the precondition enhancement is characterized in an increase of HSF1-heat shock element (HSE) binding. - View Dependent Claims (22, 23)
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