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Microalgae biofuel is believed to be a powerful potential solver to this issue [ 3- 7] and biofuels from metabolic modified microalgae is regarded as the 4th generation of biofuels [ 8].
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For simplicity they were assumed to exhibit the same metabolic rates like metabolically modified cells (r met,2 ).
Fig. 8 Schematic representation of the Horowitz hypothesis on the origin and evolution of metabolic pathways (modified from Fondi et al. 2009a) Fig. 9 The patchwork hypothesis on the origin and evolution of metabolic pathways.
Fig. 4 Schematic representation of an ancestral cell community with a selective pressure allowing for the acquisition and spreading of a new metabolic trait (modified from Fondi et al. 2009a).
We examined whether the status of metabolic abnormalities modified the effects of bone lead on HRV (Table 4).
Metabolic syndrome (modified American Heart Association AHAA) standard [ 45]) was identified by the presence of three or more of these components: (1) BMI > 30; (2) fasting blood triglycerides ≥ 150 mg/dl; (3) blood high-density lipoprotein (HDL) cholesterol (men: < 40 mg/dl (1.03 mmol/l), women: < 50 mg/dl (1.3mmol/l)); (4) blood pressure ≥ 130/85 mmHg; and (5) fasting glucose ≥ 100 mg/dl.
Metabolic engineering modifies cellular function to address various biochemical applications.
This action could be due to increased bioavailability or stability of the anticancer drugs, activation or inhibition of metabolic pathways modifying levels of pro- and anti-apoptotic proteins.
In this dynamical situation, both metabolic subsystems modify uninterruptedly their activity so that it never repeats itself for arbitrarily long periods of time.
In this situation, each metabolic subsystem modifies uninterruptedly its enzymatic activity in such a way that it changes between different periodic and/or stationary regimes that never repeat its activity along arbitrarily long periods of time.
Therefore, fructose may indirectly influence appetite and reward through changes in the levels of peripheral neural input or metabolic intermediaries modifying the activation of brain regions implicated in appetite and reward.
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