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Organic Chemicals
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
To the best of our knowledge, this is the first confirmation of a significant association between TCE exposure and PD risk in a population-based study. Two other chlorinated solvents, PERC and CCI4, tended toward significantly increased risk. Results were similar in analyses considering no exposure, exposure duration, or lifetime cumulative exposure. Their findings are consistent with prior case reports115–117 and a rodent model of TCE-induced parkinsonism that recapitulates key pathological and neurochemical features of PD.118 In this model, TCE caused selective dose-dependent loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), and selective accumulation of α-synuclein protein in the dorsal motor nucleus of the vagus nerve and SNpc, a pattern consistent with human pathological staging of PD.119 TCE also reduced mitochondrial complex 1 activity, similar to the neurotoxin 1-methyl-4-phenylpridinium (Mpp+), the insecticide rotenone, and the mitochondrial deficiency seen in typical PD.120,121 Like TCE, PERC122,123 and CCI4124–126 have also been shown to increase markers of oxidative and nitrative stress, activate microglia, and disrupt mitochondrial function.127–131 Due to their lipophilic nature, each of these compounds readily distributes in body tissues and particularly the brain.132–134
The role of low-level vagus nerve stimulation in cardiac therapy
Published in Expert Review of Medical Devices, 2019
Yuhong Wang, Sunny S. Po, Benjamin J. Scherlag, Lilei Yu, Hong Jiang
The control centers of the autonomic nervous system (ANS) in the brain mainly include the paraventricular nucleus of the hypothalamus (PVN), nucleus tractus solitarius (NTS) and dorsal motor nucleus (DMN). The PVN is a key integrative center for sympathetic tone in the brain and contains two different types of neurons, sympathoexcitatory and sympathoinhibitory [8,9]. Other regional nuclei project to these neurons and alter the activity of the PVN pathways, ultimately influencing the sympathetic outflow to the periphery. Vagal afferent fibers carrying sensory information from the periphery converge on the NTS, whereas vagal efferent fibers originate in the DMN, which provides the vagal output from the brain to the periphery. The neuronal interaction between the NTS and DMN is modulated by many inputs from other relevant nuclei.