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Our finding that M1 dopaminergic signaling is important for motor skill learning and synaptic plasticity could explain accelerated movement recovery after brain injury when motor training is combined with systemic levodopa administration [1]; plasticity in M1 is a candidate mechanism to support movement recovery after brain injury [2], [47] and this plasticity my be facilitated by levodopa.
This proposed mechanism could explain accelerated CD8 T-cell immunosenescence in cytomegalovirus-seropositive patients with MI, as well as progression of atherosclerosis.
Mechanisms to explain accelerated liver disease in co-infected patients are not well understood but may include direct viral effects and immunologic alterations such as immune activation, apoptosis, and diminished HCV-specific T-cell responses (Table 1) [ 16– 16].
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We illustrate how it differs from other evolutionary processes that may occur during invasions, and how it can help explain accelerating rates of invasions.
Bribes, he explained, accelerated growth.
A broadly accepted theory explains accelerated telomere shortening by oxidative stress (ROS), with men having the greater load [ 23- 28].
Our data indicate that loss of casp2 accelerates age-dependent alterations in mROS production and metabolism, likely through complex III and may in part explain the accelerated aging phenotype that we observe in casp2 null mice (Zhang et al. 2007).
Two approaches have been adopted to explain this accelerated expansion.
Deforestation and agriculture can explain the accelerated physical erosion in the two developed catchments.
In order to explain the accelerated expansion of the universe, three main classes of model exist [3]: (1) a cosmological constant Λ, (2) dark energy, and (3) modified gravity.
Dark energy was proposed to explain the accelerated expansion of the universe with an equation of state (EoS) parameter γ = p/ρ < − 1/3.
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