Neuronal function is necessary but not sufficient for consciousness: consciousness is necessary for will.

Behavioral neuroscience has presented philosophers with the task of clarifying the relationship between neural determinism and free will. If neural functions encode information and govern decision-making, are the constructs of will, agency and indeed morality illusions of pre-scientific ignorance? This article will argue that neuronal function is necessary for representing distinct sensory-perceptual, cognitive, motivational, emotional states, and motor functions. However, neural transmission and action potentials are simply chemical-physical representations of these informational states but are not the embodiment of consciousness itself.

Genetic polymorphisms of GSTT1, GSTM1, GSTP1, MnSOD, and catalase in nonhereditary chronic pancreatitis: evidence of xenobiotic stress and impaired antioxidant capacity.

Epidemiological studies have demonstrated a variety of potential environmental factors that may alter susceptibility to chronic pancreatitis (CP) through oxidative/xenobiotic stress; however, a direct causal and mechanistic role has not been established. We aimed (1) to determine the prevalence of functional genetic polymorphisms in the antioxidant enzymes, glutathione S-transferase GSTM-1, GSTP-1, and GSTT-1, manganese superoxide dismutase, and catalase in CP and (2) to reveal evidence of oxidative stress in patients with CP by measuring whole-blood glutathione redox status. In total, 122 patients with CP (75 alcohol-induced [A1CP], 33 idiopathic [ICP], and 13 hereditary) and 245 age- and sex-matched controls were recruited.

Association of antioxidant enzyme gene polymorphisms and glutathione status with severe acute pancreatitis.

Background & Aims: Genetic variations in antioxidant metabolism may explain varying biological responses to acute pancreatitis (AP). We studied the contribution of oxidative stress to the pathogenesis of severe pancreatitis by examining the prevalence of functional gene polymorphisms of antioxidant enzymes and evidence of heightened oxidative stress.

Methods: DNA from 320 patients with AP (90 severe) and 263 controls was genotyped for glutathione S-transferase (Mu-1 [M-1], theta-1 [T-1], and pi-1 [P-1: Ile-105Val]), manganese superoxide dismutase (Ala-9Val), and catalase (C-260T) polymorphisms.