The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model u...The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model using precise strike parameters.In this study,we compare the pathological mechanisms and pathological changes between two rat severe brain injury models to identify the similarities and differences.The severe controlled cortical impact model was produced by an electronic controlled cortical impact device,while the severe free weight drop model was produced by dropping a 500 g free weight from a height of 1.8 m through a plastic tube.Body temperature and mortality were recorded,and neurological deficits were assessed with the modified neurological severity score.Brain edema and bloodbrain barrier damage were evaluated by assessing brain water content and Evans blue extravasation.In addition,a cytokine array kit was used to detect inflammatory cytokines.Neuronal apoptosis in the brain and brainstem was quantified by immunofluorescence staining.Both the severe controlled cortical impact and severe free weight drop models exhibited significant neurological impairments and body temperature fluctuations.More severe motor dysfunction was observed in the severe controlled cortical impact model,while more severe cognitive dysfunction was observed in the severe free weight drop model.Brain edema,inflammatory cytokine changes and cortical neuronal apoptosis were more substantial and blood-brain barrier damage was more focal in the severe controlled cortical impact group compared with the severe free weight drop group.The severe free weight drop model presented with more significant apoptosis in the brainstem and diffused blood-brain barrier damage,with higher mortality and lower repeatability compared with the severe controlled cortical impact group.Severe brainstem damage was not found in the severe controlled cortical impact model.These results indicate that the severe controlled cortical impact model is relat展开更多
BACKGROUND： Studies have reported the combined use of two-dimensional gel electrophoresis and mass spectrometry to detect differentially expressed proteins in the rat brainstem following brain injury. However, the de...BACKGROUND： Studies have reported the combined use of two-dimensional gel electrophoresis and mass spectrometry to detect differentially expressed proteins in the rat brainstem following brain injury. However, the detected differential proteins often exhibit low sensitivity and high relative molecular weight. Although protein chip technology is thought to compensate for these inadequacies, no related studies or results have been reported. OBJECTIVE： To propose the application of weak cation exchange protein chips in combination with mass spectrometry for determining protein expression profiles and characteristics in the brainstem following closed brain injury. DESIGN, TIME AND SETTING： Randomized, controlled, animal experiments utilizing proteomics were performed from June 2007 to December 2008 in the Proteomics Laboratory, Medical College of Chinese People＇s Armed Police Force. MATERIALS： Weak cation exchange 2 protein chip, Ciphergen Proteinchip System （PBS-IIC）. METHODS： A total of 72 rats were randomly assigned to two groups： sham-surgery （n = 12） and injury （n = 60）. A closed traumatic brain injury model caused by falling object was replicated in the injury group, which was then subdivided into five subgroups according to different time points after injury： 4, 8, 12, 24, and 48 hours, with 12 rats in each subgroup. In the sham-surgery group, only the skin was removed and the stainless steel pad was fixed to the skull. MAIN OUTCOME MEASURES： The brain injury rats were sacrificed at 4, 8, 12, 24, and 48 hours after injury, respectively, and the control rats were sacrificed at 24 hours. Pathological changes in the brainstem were determined using hematoxylin-eosin staining, and differential protein expression in the brainstem was detected using a weak cation exchange 2 protein chip and protein chip reader. RESULTS： In the sham-surgery group, cells appeared normal. However, in the brain injury group, some brainstem neurons exhibited pyknosis, with reduced numbers of Nissl bodies in展开更多
The human brain is known to contain a maximum of eight cholinergic nuclei： the basal forebrain region： the medial septal nucleus （Ch 1）, the vertical nucleus of the diagonal band （Ch 2）, the horizontal limb of t...The human brain is known to contain a maximum of eight cholinergic nuclei： the basal forebrain region： the medial septal nucleus （Ch 1）, the vertical nucleus of the diagonal band （Ch 2）, the horizontal limb of the diago- nal band （Ch 3）, and the nucleus basalis of Meynert （Ch 4）; the brainstem： the pedunculopontine nucleus （Ch 5）, the laterodorsal tegmental nucleus （Ch 6）, and the para- bigeminal nucleus （Ch 8）; and the thalamus： the medial habenular nucleus （Ch 7） （Nieuwenhuys et al., 2008; Naidich and Duvernoy, 2009）. The cingulum is the neu- ral tract extending from the orbitofrontal cortex to the medial temporal lobe （Mufson and Pandya, 1984）. The cingulum plays an important role in memory because it is a passage of the medial cholinergic pathway, which pro- vides cholinergic innervations to the cerebral cortex after originating from Ch 1 and Ch 2 as well as Ch 4 （mainly） （Selden et al., 1998; Nieuwenhuys et al., 2008; Hong and lang, 2010）.展开更多
基金supported by the National Natural Science Foundation of China,No.81671221(to RCJ)
文摘The rat high-impact free weight drop model mimics the diffuse axonal injury caused by severe traumatic brain injury in humans,while severe controlled cortical impact can produce a severe traumatic brain injury model using precise strike parameters.In this study,we compare the pathological mechanisms and pathological changes between two rat severe brain injury models to identify the similarities and differences.The severe controlled cortical impact model was produced by an electronic controlled cortical impact device,while the severe free weight drop model was produced by dropping a 500 g free weight from a height of 1.8 m through a plastic tube.Body temperature and mortality were recorded,and neurological deficits were assessed with the modified neurological severity score.Brain edema and bloodbrain barrier damage were evaluated by assessing brain water content and Evans blue extravasation.In addition,a cytokine array kit was used to detect inflammatory cytokines.Neuronal apoptosis in the brain and brainstem was quantified by immunofluorescence staining.Both the severe controlled cortical impact and severe free weight drop models exhibited significant neurological impairments and body temperature fluctuations.More severe motor dysfunction was observed in the severe controlled cortical impact model,while more severe cognitive dysfunction was observed in the severe free weight drop model.Brain edema,inflammatory cytokine changes and cortical neuronal apoptosis were more substantial and blood-brain barrier damage was more focal in the severe controlled cortical impact group compared with the severe free weight drop group.The severe free weight drop model presented with more significant apoptosis in the brainstem and diffused blood-brain barrier damage,with higher mortality and lower repeatability compared with the severe controlled cortical impact group.Severe brainstem damage was not found in the severe controlled cortical impact model.These results indicate that the severe controlled cortical impact model is relat
基金the National Natural Science Foundation of China, No.30471934
文摘BACKGROUND： Studies have reported the combined use of two-dimensional gel electrophoresis and mass spectrometry to detect differentially expressed proteins in the rat brainstem following brain injury. However, the detected differential proteins often exhibit low sensitivity and high relative molecular weight. Although protein chip technology is thought to compensate for these inadequacies, no related studies or results have been reported. OBJECTIVE： To propose the application of weak cation exchange protein chips in combination with mass spectrometry for determining protein expression profiles and characteristics in the brainstem following closed brain injury. DESIGN, TIME AND SETTING： Randomized, controlled, animal experiments utilizing proteomics were performed from June 2007 to December 2008 in the Proteomics Laboratory, Medical College of Chinese People＇s Armed Police Force. MATERIALS： Weak cation exchange 2 protein chip, Ciphergen Proteinchip System （PBS-IIC）. METHODS： A total of 72 rats were randomly assigned to two groups： sham-surgery （n = 12） and injury （n = 60）. A closed traumatic brain injury model caused by falling object was replicated in the injury group, which was then subdivided into five subgroups according to different time points after injury： 4, 8, 12, 24, and 48 hours, with 12 rats in each subgroup. In the sham-surgery group, only the skin was removed and the stainless steel pad was fixed to the skull. MAIN OUTCOME MEASURES： The brain injury rats were sacrificed at 4, 8, 12, 24, and 48 hours after injury, respectively, and the control rats were sacrificed at 24 hours. Pathological changes in the brainstem were determined using hematoxylin-eosin staining, and differential protein expression in the brainstem was detected using a weak cation exchange 2 protein chip and protein chip reader. RESULTS： In the sham-surgery group, cells appeared normal. However, in the brain injury group, some brainstem neurons exhibited pyknosis, with reduced numbers of Nissl bodies in
基金supported by Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education,Science and Technology,No.2012R1A1A4A01001873
文摘The human brain is known to contain a maximum of eight cholinergic nuclei： the basal forebrain region： the medial septal nucleus （Ch 1）, the vertical nucleus of the diagonal band （Ch 2）, the horizontal limb of the diago- nal band （Ch 3）, and the nucleus basalis of Meynert （Ch 4）; the brainstem： the pedunculopontine nucleus （Ch 5）, the laterodorsal tegmental nucleus （Ch 6）, and the para- bigeminal nucleus （Ch 8）; and the thalamus： the medial habenular nucleus （Ch 7） （Nieuwenhuys et al., 2008; Naidich and Duvernoy, 2009）. The cingulum is the neu- ral tract extending from the orbitofrontal cortex to the medial temporal lobe （Mufson and Pandya, 1984）. The cingulum plays an important role in memory because it is a passage of the medial cholinergic pathway, which pro- vides cholinergic innervations to the cerebral cortex after originating from Ch 1 and Ch 2 as well as Ch 4 （mainly） （Selden et al., 1998; Nieuwenhuys et al., 2008; Hong and lang, 2010）.
