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A novel active power filter based on linear transformer harmonic current compensation is proposed for high voltage power distribution systems application. In the active power filter, the primary of the transformer is in parallel with the harmonic-producing loads, the secondary of the transformer is connected with PWM voltage source inverters that produce harmonic compensation current. The harmonic current of the primary is detected and tracked by the inverters with a fixed compensation coefficient. When satisfied the harmonic current compensation condition, the linear transformer can really exhibit nearly zero impedance to harmonic current and excitation impedance to fundamental current, thus lead harmonic current flow into the linear transformer circuit. The principle of operation of the proposed active power filter is discussed in detail. Simulated waveforms and experimental results obtained from a prototype are presented to verify the effectiveness of the active power filter

Lactate has long been considered a cellular waste product. However, we found that as extracellular lactate accumulates, it also enters the mitochondrial matrix and stimulates mitochondrial electron transport chain (ETC) activity. The resulting increase in mitochondrial ATP synthesis suppresses glycolysis and increases the utilization of pyruvate and/or alternative respiratory substrates. The ability of lactate to increase oxidative phosphorylation does not depend on its metabolism. Both L- and D-lactate are effective at enhancing ETC activity and suppressing glycolysis. Furthermore, the selective induction of mitochondrial oxidative phosphorylation by unmetabolized D-lactate reversibly suppressed aerobic glycolysis in both cancer cell lines and proliferating primary cells in an ATP-dependent manner and enabled cell growth on respiratory-dependent bioenergetic substrates. In primary T cells, D-lactate enhanced cell proliferation and effector function. Together, these findings demonstrate that lactate is a critical regulator of the ability of mitochondrial oxidative phosphorylation to suppress glucose fermentation.