in a lack of uncoupling ... thus making the product ineffectiveresultedin a lack of uncoupling ... thus making the product ineffective

a reduction in mTOR signalling and thus protein synthesis[76,90causesa reduction in mTOR signalling and thus protein synthesis[76,90

phosphorylation of FPR1 and thus preserves the unphosphorylated FPR1 C - terminuspreventsphosphorylation of FPR1 and thus preserves the unphosphorylated FPR1 C - terminus

to reduced calcium ATPase activity and thus a failure to repair any injury caused by reactive metabolites , such as an increase in intracellular calciumcould leadto reduced calcium ATPase activity and thus a failure to repair any injury caused by reactive metabolites , such as an increase in intracellular calcium

this seems(passive) to be caused bythis seems

in ATP / ADP ratio disturbance - activated AMPK and the following PGC-1a / NRF-1/2 pathwayresultedin ATP / ADP ratio disturbance - activated AMPK and the following PGC-1a / NRF-1/2 pathway

the resting KATP channel tone in DA neurons(passive) was caused bythe resting KATP channel tone in DA neurons

to a low ratio of ATP/[ADP+AMPleadingto a low ratio of ATP/[ADP+AMP

activation of Ira2 activity to reduce GTP - Ras1 levelscausesactivation of Ira2 activity to reduce GTP - Ras1 levels

to increased anaerobic metabolism ( which generates ATP from glycogen during hypoxialeadsto increased anaerobic metabolism ( which generates ATP from glycogen during hypoxia

to cellular organelle dysfunction and cellular death in high - metabolic end organs such as the heart , brain , and kidneyleadsto cellular organelle dysfunction and cellular death in high - metabolic end organs such as the heart , brain , and kidney

a metabolic disease(passive) caused bya metabolic disease

extreme fatigue ... both physically and mentallymay causeextreme fatigue ... both physically and mentally

T3 workingcan preventT3 working

cells to be sick and decrease their ability to heal , regenerate or function properlycausescells to be sick and decrease their ability to heal , regenerate or function properly

SLC17A9 channelopathymay causeSLC17A9 channelopathy

to low Glutathione level in the bodyleadsto low Glutathione level in the body

in low energy levelswill resultin low energy levels

to AMPK stimulation ( 1 ) and presumably autophagy inductionleadsto AMPK stimulation ( 1 ) and presumably autophagy induction

in the same increase in cell volumewill resultin the same increase in cell volume

low energy bulletscreateslow energy bullets

in mitochondrial dysfunctionresultedin mitochondrial dysfunction

numerous bodily dysfunctions ... because organs do n't have the energy they need to work rightcan causenumerous bodily dysfunctions ... because organs do n't have the energy they need to work right

to 3 things protein + hemeleadsto 3 things protein + heme

problems(passive) caused byproblems

from brain traumaresultingfrom brain trauma

opening of ATP - sensitive K+ ( K+ATP ) channels , which would counteract the depolarization ... ultimately reducing the time for Ca2 + influxmay ... triggeropening of ATP - sensitive K+ ( K+ATP ) channels , which would counteract the depolarization ... ultimately reducing the time for Ca2 + influx

elevated BUN / Creatinine ratios(passive) possibly caused byelevated BUN / Creatinine ratios

in low cellular energyresultingin low cellular energy

calcium increase and there is a self - sustaining cycle Ca2+→ — Pores — |causescalcium increase and there is a self - sustaining cycle Ca2+→ — Pores — |

HIF-1 DNA bindingcan preventHIF-1 DNA binding

to increased membrane tension by strengthening the spectrin - membrane connection , which can result in membrane blebs ( Sens and Gov , 2007 ; Betz et al . , 2009leadsto increased membrane tension by strengthening the spectrin - membrane connection , which can result in membrane blebs ( Sens and Gov , 2007 ; Betz et al . , 2009

in a characteristic fatigue syndromeresultingin a characteristic fatigue syndrome