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Outdoor Emissions
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
The well-known, acute effects of CO include cardiac effects (angina, ventricular arrhythmia), pulmonary effects (edema), visual effects (decreased light sensitivity, dark adaptation, tunnel vision), auditory effects (central hearing loss), neuropsychiatric effects (seizures, agitation, coma, thermoregulation), dermatologic effects (bullae, alopecia, sweat gland necrosis), and metabolic effects (lactic acidosis, myonecrosis, hyperglycemia, proteinuria). Chronic effects involve the heart (decreased voltage, premature ventricular contractions, conduction block, lower defibrillatory threshold), neuropsychiatric functions (decreased cognitive ability, psychosis, parkinsonism, incontinence), and hematologic function (increased HB and HCT, increased erythroprotein, increased reticulocyte count, and disseminated intravascular coagulation). Such diffuse effects of carbon monoxide on the general population are inevitably intensified in the chemically sensitive, making this population particularly vulnerable to carbon monoxide at any concentration. These effects are due to the adverse responses seen in the enzyme detoxification systems that are already malfunctioning in the chemically sensitive.
Mapping the Injured Brain
Published in Yu Chen, Babak Kateb, Neurophotonics and Brain Mapping, 2017
Chandler Sours, Jiachen Zhuo, Rao P. Gullapalli
The primary injury to the brain is a result of sudden acceleration, deceleration, and/or rotational forces. The acceleration and deceleration of the brain can cause cortical contusions (bruises of the brain tissue) and hemorrhages (bleeding) when the brain hits the skull. The rotational forces may also cause deeper cerebral lesions when white matter (WM) axons are stretched and damaged, as well as shearing injuries at the gray matter (GM) and WM interface (Ommaya et al., 2002). This disperse shearing injury is referred to as diffuse or traumatic axonal injury (DAI or TAI, respectively). Following the initial impact, the injury is propagated throughout the brain through various biomolecular and cellular pathways, which results in widespread degeneration of neurons and glial cells. However, this primary damage can lead to myriad molecular events, referred to as the secondary injury, including cellular edema, inflammation, vascular dysregulation, ischemia, disruption in plasma membrane and neurotransmitter release, mitochondrial dysfunction, production of reactive oxygen species, altered anaerobic metabolism, and lactic acidosis. Together, these secondary injury pathways result in both necrotic and apoptotic cell death (Lye and Shores, 2000; Nemetz et al., 1999). Therefore, secondary injuries likely contribute to long-term cognitive impairment and are ultimately the deciding factors in patient recovery.
Response to the Aids Pandemic
Published in Richard J. Sundberg, The Chemical Century, 2017
Examples of the major classes of the drugs are shown in Scheme 19.1. Each of the classes of HIV drugs has pronounced side effects. The RTI class can result in reduced mitochondria function with resulting changes in pyruvate metabolism that can lead to lactic acidosis. The PIs cause accumulation of fat in the abdomen and are also associated with precipitation of diabetes.
An unexpected world population variation of MCT1 polymorphism 1470T > A involved in lactate transport
Published in European Journal of Sport Science, 2018
Federico Onali, Carla M. Calò, Myosotis Massidda, Miguel M. Álvarez-Álvarez, Maria Esther Esteban
Possible defects in the human gene SLC6A1 that encodes MCT1 protein may be the cause of symptomatic insufficiency in lactate transport (Merezhinskaya, Fishbein, Davis, & Foellmer, 2000). High values of lactate, caused by a reduced transport from liver to muscles, can responsible for lactic acidosis (LA). The effects of LA, increasing lactate concentrations in blood, can be associated with cardiovascular diseases, angiogenesis and tumour progression (Brucculeri, Urso, & Caimi, 2013). Merezhinskaya et al. (2000) first described the common missense mutation 1470T > A (rs1049434) responsible for the substitution of a glutamic acid with an aspartic acid in codon 490. Since then, several studies have been carried in association with lactate transport during and/or after exercise (Cupeiro, Benito, Maffulli, Calderón, & González-Lamuño, 2010; Cupeiro, González Lamuño, Amigo, Peinado, Ruiz, Ortega, & Benito, 2012; Cupeiro, Pérez-Prieto, Amigo, Gortázar, Redondo, & González-Lamuño, 2016), athletic performance (Kikuchi et al., 2017; Sawczuk et al., 2015), muscle injuries (Massidda et al., 2015) and body composition (Massidda et al., 2016).