The term neurodegeneration emphasizes the destruction of neuronal cells as the primary explanation of many major neurological illnesses, including Alzheimer’s disease. Specialized functioning of cells requires more c...The term neurodegeneration emphasizes the destruction of neuronal cells as the primary explanation of many major neurological illnesses, including Alzheimer’s disease. Specialized functioning of cells requires more cellular energy than is needed for basic cell survival. Cells can acquire energy both from the metabolism of food and from the alternative cellular energy (ACE) pathway. The ACE pathway is an added dynamic (kinetic) quality of the body’s fluids occurring from the absorption of an external force termed KELEA (Kinetic Energy Limiting Electrostatic Attraction). KELEA is attracted to separated electrical charges and is seemingly partially released as the charges become more closely linked. As suggested elsewhere, the fluctuating electrical activity in the brain may attract KELEA from the environment and, thereby, contribute to the body’s ACE pathway. Certain illnesses affecting the brain may impede this proposed antenna function of the brain, leading to a systemic insufficiency of cellular energy (ICE). Furthermore, individual neurons may derive some of the energy for their own activities from the repetitive depolarization of the cell. This may explain why hyper-excitability of neurons can occur in response to cell damage. This adaptive mechanism is unlikely to be sustainable, however, especially if there is a continuing need to synthesize neurotransmitters and membrane ion channels. The energy deficient neurons would then become quiescent and, although remaining viable, would not perform their intended specialized functions. Actual cell death would not necessarily occur till much later in the disease process. The distinction between quiescent and degenerated cells is important since the ACE pathway can be enhanced by several means, including the regular consumption of KELEA activated water. This, in turn, may improve the proposed antenna function of individual neurons, leading to a sustained restoration of specialized function via the ACE pathway. This paper explores this novel concept and provides 展开更多
Effects of inhibitors and glucose on cytochrome and alternative respiration and on adenylate energy charge (AEC) in glucose starved Chlorella protothecoides were investigated. 1 mmol/L azide (NaN 3), which immediate...Effects of inhibitors and glucose on cytochrome and alternative respiration and on adenylate energy charge (AEC) in glucose starved Chlorella protothecoides were investigated. 1 mmol/L azide (NaN 3), which immediately caused an increase of O 2 uptake by inhibiting the cytochrome pathway and stimulating alternative respiration, resulted in a decrease of AEC value from 0.83 to 0.34 within 3 minutes. When 1 mmol/L salicylhydroxamic acid (SHAM) was added into the cell suspension, there was no apparent variation in AEC. Adding NaN 3 and SHAM together into cell suspension to inhibit both cytochrome and alternative pathways showed a same change of AEC as that of adding NaN 3 alone. When 2.0 mmol/L of glucose was added to a suspension of glucose starved cells, the O 2 uptake rate was immediately stimulated from 0.81 up to 1.34 [μmol/L O 2[DK]·min -1 ·(mL PCV) -1 ]. The respiration stimulated by glucose could be inhibited about 20% by adding 1 mmol/L SHAM. It was found by titration with SHAM in the absence and presence of NaN 3 that 53% of O 2 uptake went through the cytochrome pathway and 45% of the alternate pathway was operational in enhanced respiration. It implied that induced operation of the alternative respiratory pathway probably resulted from the burst of the electron flux into the electron transport chain by glucose stimulation. . The respiration stimulated by glucose could be inhibited about 20% by adding 1 mmol/L SHAM. It was found by titration with SHAM in the absence and presence of NaN 3 that 53% of O 2 uptake went through the cytochrome pathway and 45% of the alternate pathway was operational in enhanced respiration. It implied that induced operation of the alternative respiratory pathway probably resulted from the burst of the electron flux into the electron transport chain by glucose stimulation. 展开更多
文摘The term neurodegeneration emphasizes the destruction of neuronal cells as the primary explanation of many major neurological illnesses, including Alzheimer’s disease. Specialized functioning of cells requires more cellular energy than is needed for basic cell survival. Cells can acquire energy both from the metabolism of food and from the alternative cellular energy (ACE) pathway. The ACE pathway is an added dynamic (kinetic) quality of the body’s fluids occurring from the absorption of an external force termed KELEA (Kinetic Energy Limiting Electrostatic Attraction). KELEA is attracted to separated electrical charges and is seemingly partially released as the charges become more closely linked. As suggested elsewhere, the fluctuating electrical activity in the brain may attract KELEA from the environment and, thereby, contribute to the body’s ACE pathway. Certain illnesses affecting the brain may impede this proposed antenna function of the brain, leading to a systemic insufficiency of cellular energy (ICE). Furthermore, individual neurons may derive some of the energy for their own activities from the repetitive depolarization of the cell. This may explain why hyper-excitability of neurons can occur in response to cell damage. This adaptive mechanism is unlikely to be sustainable, however, especially if there is a continuing need to synthesize neurotransmitters and membrane ion channels. The energy deficient neurons would then become quiescent and, although remaining viable, would not perform their intended specialized functions. Actual cell death would not necessarily occur till much later in the disease process. The distinction between quiescent and degenerated cells is important since the ACE pathway can be enhanced by several means, including the regular consumption of KELEA activated water. This, in turn, may improve the proposed antenna function of individual neurons, leading to a sustained restoration of specialized function via the ACE pathway. This paper explores this novel concept and provides
基金the National Natural Science Foundationof China(No. 39870 0 6 4and30 0 70 0 6 5 ) partly bythe State Key Basic Research and Developm entProgram s of China(No.G19980 10 10 0 and G19990 433)
文摘Effects of inhibitors and glucose on cytochrome and alternative respiration and on adenylate energy charge (AEC) in glucose starved Chlorella protothecoides were investigated. 1 mmol/L azide (NaN 3), which immediately caused an increase of O 2 uptake by inhibiting the cytochrome pathway and stimulating alternative respiration, resulted in a decrease of AEC value from 0.83 to 0.34 within 3 minutes. When 1 mmol/L salicylhydroxamic acid (SHAM) was added into the cell suspension, there was no apparent variation in AEC. Adding NaN 3 and SHAM together into cell suspension to inhibit both cytochrome and alternative pathways showed a same change of AEC as that of adding NaN 3 alone. When 2.0 mmol/L of glucose was added to a suspension of glucose starved cells, the O 2 uptake rate was immediately stimulated from 0.81 up to 1.34 [μmol/L O 2[DK]·min -1 ·(mL PCV) -1 ]. The respiration stimulated by glucose could be inhibited about 20% by adding 1 mmol/L SHAM. It was found by titration with SHAM in the absence and presence of NaN 3 that 53% of O 2 uptake went through the cytochrome pathway and 45% of the alternate pathway was operational in enhanced respiration. It implied that induced operation of the alternative respiratory pathway probably resulted from the burst of the electron flux into the electron transport chain by glucose stimulation. . The respiration stimulated by glucose could be inhibited about 20% by adding 1 mmol/L SHAM. It was found by titration with SHAM in the absence and presence of NaN 3 that 53% of O 2 uptake went through the cytochrome pathway and 45% of the alternate pathway was operational in enhanced respiration. It implied that induced operation of the alternative respiratory pathway probably resulted from the burst of the electron flux into the electron transport chain by glucose stimulation.
