RESUMEN
Objective:To investigate the changes of cognitive function in non-fatal drowning rats after blast-induced traumatic brain injury (bTBI).Methods:Eighty SD rats were divided into normal group, bTBI group, drowning group and bTBI plus drowning group according to the random number table, with 20 rats per group. Rats in normal group were not injured. In bTBI group, bTBI was established in a BST-I biological shock tube with a pressure of 4.0 MPa in the driving section. In drowning group, rats were subjected to non-fatal drowning by falling into the water with temperature of 18 ℃ and depth of 30 cm from the height of 1 m and were taken out quickly after swimming to exhaustion. After being injured in a biological shock tube, rats in bTBI plus drowning group were immediately forced to drowning using the same method. On day 3 post-injury, the neurocognitive function was evaluated by elevated plus maze and Morris water maze tests. Morphological changes of neurons in CA1 and CA3 regions of hippocampus were observed by Nissl staining, and the number of surviving neurons were counted. The concentrations of hippocampal neurotransmitters glutamate, γ-aminobutyric acid (GABA), glycine and endoplasmic reticulum stress (ERS) related glucose-regulated protein 78 (GRP78) and caspase-12 were examined by ELISA analysis. Levels of B-cell lymphoma-2 (Bcl-2), Bcl-2 associated protein (Bax) and caspase-3 were detected by Western blotting. The ratio of Bcl-2 to Bax was calculated as well.Results:In elevated plus maze test, the percentage of open arm entry and number of head-dipping behaviour were decreased in bTBI plus drowning group compared with normal and bTBI groups at 3 days after injury ( P<0.05 or 0.01), with no statistical difference from those in drowning group ( P>0.05). The number of head-dipping behaviour in drowning group was lower than that in bTBI group ( P<0.05). In Morris water maze test, bTBI plus drowning group showed increased target latency on the third and fourth days of spatial acquisition training and decreased number of crossing the target area and percentage of swimming time in the target quadrant during probe trials as compared with normal group ( P<0.05 or 0.01), but there was no statistical difference among bTBI, drowning and normal groups (all P>0.05). Nissl staining showed that the neurons in the CA1 and CA3 regions of hippocampus in normal group were arranged neatly with clear Nissl bodies at 3 days after injury, while the other groups showed different degrees of injury. In contrast with normal group, the neurons in the CA1 and CA3 regions of hippocampus in all other groups were decreased with the lowest number in bTBI plus drowning groups ( P<0.05 or 0.01). In ELISA analysis, the level of hippocampal glutamate in bTBI plus drowning group was higher than that in all other groups at 3 days after injury and the level in bTBI injury and drowning groups was higher than that in normal group ( P<0.05 or 0.01); the level of hippocampal glycine in bTBI plus drowning group was lower than that in normal group ( P<0.05), but there was no statistical difference among bTBI, drowning or normal groups (all P>0.05); the concentration of hippocampal GABA had no statistical difference among all groups (all P>0.05). In addition, the concentration of GRP78 in bTBI injury, drowning and bTBI injury plus drowning groups were increased compared with normal group ( P<0.05 or 0.01), but did not statistically differ from each other (all P>0.05). The concentration of caspase-12 in drowning and bTBI plus drowning groups were increased compared with normal group ( P<0.05 or 0.01), but was not statistically different from each other ( P>0.05), and its concentration in bTBI plus drowning group was increased compared with bTBI group ( P<0.05). In Western blotting, the level of Bcl-2 in bTBI plus drowning group was decreased compared with all other groups at 3 days after injury, and the level in bTBI and drowning groups were decreased compared with normal group, but a much lower level was observed in drowning group than that in bTBI group ( P<0.05 or 0.01); the level of Bax in bTBI plus drowning group was increased compared with all other groups at 3 days after injury, and the level in drowning group was increased compared with normal group ( P<0.05 or 0.01), with no statistical difference between bTBI and drowning groups ( P>0.05). The ratio of Bcl-2 to Bax in bTBI plus drowning group was decreased compared with all other groups, while the ratio in bTBI and drowning groups were decreased compared with normal group, showing a much lower level in drowning group than that in bTBI group ( P<0.05 or 0.01). Also, the level of caspase-3 in drowning and bTBI plus drowning groups were increased compared with normal and bTBI groups ( P<0.05 or 0.01), but there was no statistical difference between drowning and bTBI plus drowning groups ( P>0.05). Conclusions:Non-fatal drowning can aggravate hippocampal neuron damage in bTBI rats and cause memory, emotion and other cognitive dysfunction. The mechanism may involve the imbalance of hippocampal neurotransmitters glutamate and glycine, which activates the downstream pro-apoptotic pathway through ERS in the early stage of injury to induce hippocampal neuron apoptosis.
RESUMEN
Objective:To explore the establishment of the interconvertible injury parameters of same severe blast injury in mice at plain and plateau.Methods:A total of 157 C57BL/6 male mice were randomly divided into plain control group (8 mice), plain injury group (77 mice), plateau control group (8 mice) and plateau injury group (64 mice) according to random number table method. The mice in plateau control group and plateau blast injury group had been placed in animal experimental low-pressure oxygen chamber to simulate 4 000 meters plateau environment for 5 days in advance. Then the mice in plain blast injury group and plateau blast injury group were put into biological shock tube, respectively. Different pressures of the driving section were selected to establish the severe blast injury models in mice at plain and 4 000 meters plateau to reach approximately 70% mortality within 72 hours. The equivalent traumatic condition at 24 hours after blast injury in different groups was verified by the series of experiments including gross autopsy, lung wet/dry weight ratio (W/D), hematoxylin-eosin (HE) staining and histological scoring.Results:The mice mortality were basically consistent between the plain injury group (65%) and plateau injury group (75%) when 5.4 MPa and 4.0 MPa of the driving section pressures were chosen, respectively. Compared with the corresponding control groups, the lungs showed massive hemorrhage (patchy and diffuse) with significant pulmonary edema in both plain 5.4 MPa-injured group and the plateau 4.0 MPa-injured group at 24 hours after blast injury. Compared with the plateau control group, the pulmonary W/D ratio were significantly increased in the plateau injury group (5.579±0.646 vs. 4.476±0.076, P < 0.05), while the difference between plateau injury group and the plain control group was not statistically significant (5.303±1.020 vs. 4.015±0.144, P > 0.05). Also, compared with the corresponding control groups, the analysis of lung histopathological sections showed that there were several pathological changes including large alveolar rupture and fusion, thickened alveolar walls, and a small amount of inflammatory cell infiltration in the alveolar lumen in the groups of plain 5.4 MPa and plateau 4.0 MPa. In addition, the histopathological scores of lung in the groups of plain 5.4 MPa and plateau 4.0 MPa were significantly higher than that in corresponding control group (8.67±0.82 vs. 1.67±0.52, 9.00±1.10 vs. 2.17±0.41, both P < 0.05), however, there was no statistical difference for the above score between plain blast injury group and plateau blast injury group. Conclusions:The pressures of driving section 5.4 MPa and 4.0 MPa are injury parameters to establish equivalent severe blast injury in mice at plain and plateau, respectively, which can be converted to each other. This study provides support for the application and evaluation of prevention and treatment technology for severe blast injury in special environment.
RESUMEN
Road traffic accidents (RTA) can cause a large number of casualties and property losses. Driving fatigue is one of the important factors leading to RTA. Electrophysiological signals, as a kind of information feedback for the nervous system to regulate body functions, can reflect drivers’ fatigue state. However, there is a lack of systematic reviews on the current research on electrophysiological signals as information input of machine learning methods for driving fatigue recognition. By investigating fatigue-related literature, the current paper summarized the neural regulation mechanism of fatigue, clarified that driving fatigue is caused by both psychological and physiological loads, recognized inducing factors related to driving fatigue, and summed up electrophysiological signals now in use of driving fatigue recognition, as well as their physiological mechanisms and related indicators. Machine learning algorithms are widely used in identifying driving fatigue. Based on existing studies that used electrophysiological signals as information input source and applied various machine learning algorithms to build driving fatigue identification models, this paper compared the effectiveness of various machine learning algorithms, and described the advantages and disadvantages of supervised machine learning. It is pointed out that suitable classification algorithms should be selected according to sample conditions and model eigenvalues when applied to driving fatigue recognition. In addition, a variety of electrophysiological signals as information sources can help improve the accuracy of a fatigue recognition model, but the increase of model input eigenvalues cannot. Finally, the research progress of identification methods based on electrophysiological signals provided new opportunities for identifying driving fatigue.