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Biomarkers of neuronal damage in saturation diving-a controlled observational study.
Rosén, A, Gennser, M, Oscarsson, N, Kvarnström, A, Sandström, G, Blennow, K, Seeman-Lodding, H, Zetterberg, H
European journal of applied physiology. 2020;(12):2773-2784
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Abstract
PURPOSE A prospective and controlled observational study was performed to determine if the central nervous system injury markers glial fibrillary acidic protein (GFAp), neurofilament light (NfL) and tau concentrations changed in response to a saturation dive. METHODS The intervention group consisted of 14 submariners compressed to 401 kPa in a dry hyperbaric chamber. They remained pressurized for 36 h and were then decompressed over 70 h. A control group of 12 individuals was used. Blood samples were obtained from both groups before, during and after hyperbaric exposure, and from the intervention group after a further 25-26 h. RESULTS There were no statistically significant changes in the concentrations of GFAp, NfL and tau in the intervention group. During hyperbaric exposure, GFAp decreased in the control group (mean/median - 15.1/ - 8.9 pg·mL-1, p < 0.01) and there was a significant difference in absolute change of GFAp and NfL between the groups (17.7 pg·mL-1, p = 0.02 and 2.34 pg·mL-1, p = 0.02, respectively). Albumin decreased in the control group (mean/median - 2.74 g/L/ - 0.95 g/L, p = 0.02), but there was no statistically significant difference in albumin levels between the groups. In the intervention group, haematocrit and mean haemoglobin values were slightly increased after hyperbaric exposure (mean/median 2.3%/1.5%, p = 0.02 and 4.9 g/L, p = 0.06, respectively). CONCLUSION Hyperbaric exposure to 401 kPa for 36 h was not associated with significant increases in GFAp, NfL or tau concentrations. Albumin levels, changes in hydration or diurnal variation were unlikely to have confounded the results. Saturation exposure to 401 kPa seems to be a procedure not harmful to the central nervous system. TRIAL REGISTRATION ClinicalTrials.gov NCT03192930.
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Evaluation of Cerebral Blood Flow Alterations and Acute Neuronal Damage due to Water-Pipe Smoking.
Karakayalı, O, Utku, U, Yılmaz, S
Balkan medical journal. 2019;(2):106-112
Abstract
BACKGROUND Although water-pipe smoking is a great public health problem, data regarding the acute and chronic effects and the degree of toxin exposure are limited. While water pipe-related malignancy, pulmonary, infectious, cardiac effects, infertility, and biological effects have been described in a meta-analysis, there are no studies in the literature about its neurologic effects. AIMS To evaluate water pipe-related acute neurological effects and cerebral blood flow through transcranial Doppler ultrasonography and serum S100 calcium binding protein calcium binding protein level measurements. STUDY DESIGN Prospective observational study. METHODS Vital signs and baseline carboxyhemoglobin and S100 calcium binding protein levels, cerebral flood changes with transcranial Doppler ultrasound were evaluated and recorded before and after water-pipe smoking. RESULTS The mean age of the 31 volunteers was 30.61 (±5.67) years, and 24 of them (77.42%) were male. A statistically significant difference was determined in heart rate, oxygen saturation, systolic and diastolic arterial pressure values before and after water-pipe smoking (p<0.001, p=0.035, p=0.009, p=0.021, respectively). Mean carboxyhemoglobin level was 2.68% (±1.68) before, 14.97% (±4.83) after water-pipe smoking (p<0.001). The S100 calcium binding protein level was 25.05 μ/mL (±8.34) at the beginning, 40.71 μ/mL (±14.06) after water-pipe smoking (p<0.001). An increase was determined in peak, and median middle, anterior and posterior cerebral artery blood flow rates, and a decrease was determined in both the pulsatility index and resistivity index values after water-pipe smoking using transcranial Doppler ultrasound. CONCLUSION Cerebral vasodilation develops due to the increase in cerebral blood flow rate and the decrease in pulsatility index, resistivity index values, and the elevation in carboxyhemoglobin, S100 calcium binding protein level indicates that water-pipe smoking leads to neuronal damage in the acute period.
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Neuroimaging identifies increased manganese deposition in infants receiving parenteral nutrition.
Aschner, JL, Anderson, A, Slaughter, JC, Aschner, M, Steele, S, Beller, A, Mouvery, A, Furlong, HM, Maitre, NL
The American journal of clinical nutrition. 2015;(6):1482-9
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Abstract
BACKGROUND Manganese, an essential metal for normal growth and development, is neurotoxic on excessive exposure. Standard trace element-supplemented neonatal parenteral nutrition (PN) has a high manganese content and bypasses normal gastrointestinal absorptive control mechanisms, which places infants at risk of manganese neurotoxicity. Magnetic resonance (MR) relaxometry demonstrating short T1 relaxation time (T1R) in the basal ganglia reflects excessive brain manganese accumulation. OBJECTIVE This study tested the hypothesis that infants with greater parenteral manganese exposure have higher brain manganese accumulation, as measured by MR imaging, than do infants with lower parenteral manganese exposure. DESIGN Infants exposed to parenteral manganese were enrolled in a prospective cohort study. Infants classified as having high manganese exposure received >75% of their nutrition in the preceding 4 wk as PN. All others were classified as having low exposure. Daily parenteral and enteral manganese intakes were calculated. Whole-blood manganese was measured by high-resolution inductively coupled plasma mass spectrometry. Brain MR relaxometry was interpreted by a masked reviewer. Linear regression models, adjusted for gestational age (GA) at birth, estimated the association of relaxometry indexes with total and parenteral manganese exposures. RESULTS Seventy-three infants were enrolled. High-quality MR images were available for 58 infants, 39 with high and 19 with low manganese exposure. Four infants with a high exposure had blood manganese concentrations >30 μg/L. After controlling for GA, higher parenteral and total manganese intakes were associated with a lower T1R (P = 0.01) in the globus pallidus and putamen but were not associated with whole-blood manganese (range: 3.6-56.6 μg/L). Elevated conjugated bilirubin magnified the association between parenteral manganese and decreasing T1R. CONCLUSION A short T1R for GA identifies infants at risk of increased brain manganese deposition associated with PN solutions commonly used to nourish critically ill infants. These trials were registered at clinicaltrials.gov as NCT00392977 and NCT00392730.