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Sensing and Assessment of Brain Injury
Published in Mark A. Mentzer, Mild Traumatic Brain Injury, 2020
According to their company website (Banyon, 2018), Banyan Biomarkers has identified two protein biomarkers, Ubiquitin C-terminal Hydrolase-L1 (UCH-L1) and Glial Fibrillary Acidic Protein (GFAP), that are detectable in the blood shortly after TBI. UCH-L1 is primarily found in neurons and is involved in cellular protein regulation. GFAP is a member of the intermediate filament family of cytoskeletal proteins which form polymeric networks that provide structural support to glia, which support and nourish cells in the brain. Banyan Biomarkers believes that accurate diagnosis of TBI in acute care environments could significantly simplify decisions about patient management and improve medical care.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
In animals treated with 1 × LD50 sarin, both superficial layers (I–III) and deeper layers (IV–V) of the motor cortex and somatosensory cortex showed degeneration of neurons. In the deeper layers of the cortex, neuron degeneration was seen in layer V. Pyramidal neurons in layers III and V of the cortex are the source of the axons of the corticospinal tract, which is the largest descending fiber tract (or motor pathway) from the brain controlling movements of various contralateral muscle groups. Thus, sarin-induced death of layers III and V neurons of the motor cortex could lead to considerable motor and sensory abnormalities, ataxia, weakness, and loss of strength. Furthermore, disruption of the hippocampal circuitry because of the degeneration of neurons in different subfields can lead to learning and memory deficits. Lesions in the cerebellum could result in gait and coordination abnormalities which we often see in the severe chemically sensitive patient as seen in the autistic and other individuals with chemical sensitivity. Since the severely affected areas (e.g., the limbic system, corticofugal system, and central motor system) are associated with mood, judgment, motion, posture, locomotion, and skilled movements, humans exhibiting acute toxicity symptoms following exposure to large doses of OPs may also develop psychiatric and motor deficits. Inasmuch as the severely damaged areas of the brain do not usually regenerate, these symptoms are expected to persist long-term.322–324 However, recent studies with pain in patients suggests that the brain can shrink one-third with pain and then expand where the pain is relieved. These findings are in agreement with a recent study by Kilburn325 who evaluated the neurobehavioral effects of chronic low-level exposure to the organophosphorus insecticide chlorpyrifos in 22 patients. Kilburn demonstrated an association between chlorpyrifos sprayed inside homes and offices and neurophysiological impairments in balance, visual fields, color discrimination, hearing reaction time, and grip strength. These patients also had psychological impairment of verbal recall and cognitive function, and two-thirds of them had been prescribed antidepressant drugs. In addition, the patients exhibited severe respiratory symptoms, accompanied by airway obstruction. Other chlorpyrifos-induced neurotoxicity incidents in humans have been reported.326 These results are consistent with the report that daily dermal application of 0.1 mg/kg chlorpyrifos to adult rats resulted in sensorimotor deficits.327 Also, material exposure to a daily dermal dose of 0.1 mg/kg chlorpyrifos during gestational days 4–20 caused an increased expression of GFAP in the cerebellum and hippocampus of offspring on postnatal day 30.328 A major component of astrocytic intermediate neurofilaments, GFAP is upregulated in response to reactive gliosis resulting from insults such as trauma, neurodegenerative disease, and exposure to neurotoxicants.329
Ameliorative effect of vitamin E and selenium against bisphenol A-induced toxicity in spinal cord and submandibular salivary glands of adult male albino rats
Published in International Journal of Environmental Health Research, 2023
Dina W. Bashir, Yasmine H. Ahmed, Mohamed A. El-Sakhawy
Glial fibrillar acidic protein GFAP is found in many types of CNS cells, including astrocytes and is a protein filament of the intermediate type (Sobaniec-Lotowska 2001). It is an important element in astrocytic processes as it provides structural stability and helps modulate astrocyte motility and shape (Roessmann et al. 1980). In the current work, immunohistochemical evaluation of the SC of Group I rats showed a weakly positive immune reaction in the fibrillar astrocyte body and processes to GFAP in the gray and white matter. Meanwhile, the immune reaction intensity was increased in BPA-exposed rats (Group II). Similar results were reported by Ramadan et al. (2017) who stated that GFAP immune expression was up-regulated in rats sustaining CSCI on day 7. In astrogliosis, rapid synthesis of GFAP takes place. This may occur due to CNS injury, whether because of chemical factors, trauma, genetic disorders, or disease (Li et al. 2009). Bisphenol A caused activation of astrocytes as a compensatory mechanism for the neuronal damage caused by it. These alterations were previously recorded in other forms of neurotoxicity (Borlongan et al. 2000).