Two hundred years after James Parkinson first described the cardinal motor symptoms of the disorder that would later bear his name,there is still an irrefutable need for a therapy that targets the underlying pathophys...Two hundred years after James Parkinson first described the cardinal motor symptoms of the disorder that would later bear his name,there is still an irrefutable need for a therapy that targets the underlying pathophysiology of the disease and not solely its symptoms.展开更多
Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response pla...Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches.展开更多
The central nervous system has a very high energy requirement. Accord- ingly, despite representing only 2% of the body＇s mass, the brain uses 20% of the total oxygen consumption. Importantly, because most of this ene...The central nervous system has a very high energy requirement. Accord- ingly, despite representing only 2% of the body＇s mass, the brain uses 20% of the total oxygen consumption. Importantly, because most of this energy is used to maintain synaptic activity, even a mild decrease in its supply to the brain has deleterious implications for synaptic function.展开更多
While it is well-known that neuronal activity promotes plasticity and connectivity, the success of activity-based neural rehabilitation programs remains extremely limited in human clinical experience because they cann...While it is well-known that neuronal activity promotes plasticity and connectivity, the success of activity-based neural rehabilitation programs remains extremely limited in human clinical experience because they cannot adequately control neuronal excitability and activity within the injured brain in order to induce repair. However, it is possible to non-invasively modulate brain plasticity using brain stimu- lation techniques such as repetitive transcranial （rTMS） and transcranial direct current stimulation （tDCS） techniques, which show promise for repairing injured neural circuits （Henrich-Noack et al., 2013; Lefaucher et al., 2014）. Yet we are far from having full control of these techniques to repair the brain following neurotrauma and need more fundamen- tal research （Ellaway et al., 2014; Lefaucher et al., 2014）. In this perspective we discuss the mechanisms by which rTMS may facilitate neurorehabilitation and propose experimental techniques with which magnetic stimulation may be investi- gated in order to optimise its treatment potential.展开更多
The irretrievable fate of neurons rhetoric for the first half of this dominated the neuroscience century, a position that was fiercely contested and recently debunked by extensive studies carried out in the field of n...The irretrievable fate of neurons rhetoric for the first half of this dominated the neuroscience century, a position that was fiercely contested and recently debunked by extensive studies carried out in the field of neuroregeneration research. The turning point came in the year 1928, when Ramon Y. Cajal＇s （Lobato, 2008） work suggested that the regenerative capacity of neurons, though limited, could exist beyond their physical be- ing and depended on the environment surrounding them. That the manipulation of the restrictive environment surrounding the neuron could aid the regenerative process was conclusively established by Aguayo and colleagues （Richardson et al., 1980）. Since then, various strategies have been employed to target the different phases of regeneration which include： cell-replacement and augmenting endogenous neurogenesis, the use of trophic factors, reversal of the inhibitory cues, and induction of signal- ing pathways that stimulate axon growth and guidance （Horner and Gage. 2000）.展开更多
Objective To investigate a possibility of repairing damaged brain by intracerebroventricular transplantation of neural stem cells （NSCs） in the adult mice subjected to glutamate-induced excitotoxic injury. Methods M...Objective To investigate a possibility of repairing damaged brain by intracerebroventricular transplantation of neural stem cells （NSCs） in the adult mice subjected to glutamate-induced excitotoxic injury. Methods Mouse NSCs were isolated from the brains of embryos at 15-day postcoitum （dpc）. The expression of nestin, a special antigen for NSC, was detected by immunocytochemistry. Immunofluorescence staining was carried out to observe the survival and location of transplanted NSCs. The animals in the MSG＋NSCs group received intracerebroventricular transplantation of NSCs （approximately 1.0×10^5 cells） separately on day 1 and day 10 after 10-d MSG exposure （4.0 g/kg per day）. The mice in control and MSG groups received intracerebroventricular injection of Dulbecco＇s minimum essential medium （DMEM） instead of NSCs. On day 11 after the last NSC transplantation, the test of Y-maze discrimination learning was performed, and then the histopathology of the animal brains was studied to analyze the MSG-induced functional and morphological changes of brain and the effects of intracerebroventricular transplantation of NSCs on the brain repair. Results The isolated cells were Nestin-positive. The grafted NSCs in the host brain were region-specifically survived at 10-d post-transplantation. Intracerebroventricular transplantation of NSCs obviously facilitated the brain recovery from glutamate-induced behavioral disturbances and histopathological impairs in adult mice. Conclusion Intracerebroventricular transplantation of NSCs may be feasible in repairing diseased or damaged brain tissue.展开更多
Objective It has been reported that B-cell lymphoma 2 （Bcl-2） enhances neurogenesis as well as supporting axonal growth after injury. In the present study, we investigated whether Bcl-2 overexpression plays a role i...Objective It has been reported that B-cell lymphoma 2 （Bcl-2） enhances neurogenesis as well as supporting axonal growth after injury. In the present study, we investigated whether Bcl-2 overexpression plays a role in the formation of newborn striatonigral projection neurons in the adult rat brain after transient middle cerebral artery occlusion （MCAO）. Methods We infused human Bcl-2-expressing plasmid （pBcl-2） into the lateral ventricle immediately after 30 min of MCAO, injected 5＇-bromodeoxyuridine （BrdU） intraperitoneally to label proliferative cells, and microinjected fluorogold （FG） into the substantia nigra at 11 weeks of reperfusion followed by multiple immunostaining of striatonigral projection neurons at 12 weeks. Results We found that pBcl-2 treatment significantly increased the number of newborn neurons （BrdU＋-NeuN＋） in the striatum ipsilateral to the MCAO. We further detected newborn striatonigral projection neurons （BrdU＋-FG＋-NeuN＋） in the ipsilateral striatum at 12 weeks. More interestingly, the number of newborn striatonigral projection neurons （BrdU＋-FG＋） was significantly increased by pBcl-2 treatment compared to that by pEGFP, a control plasmid. Conclusion Taken together, we found that Bcl-2 overexpression in the brain enhanced the generation of newborn striatonigral projection neurons. This provides a potential strategy for promoting the reestablishment of neural networks and brain repair after ischemic injury.展开更多
Neuro D plays a key regulatory effect on differentiation of neural stem cells into mature neurons in the brain.Thus,we assumed that electroacupuncture at Baihui（DU20） acupoint in newborn rats exposed to in utero fet...Neuro D plays a key regulatory effect on differentiation of neural stem cells into mature neurons in the brain.Thus,we assumed that electroacupuncture at Baihui（DU20） acupoint in newborn rats exposed to in utero fetal distress would influence expression of Neuro D.Electroacupuncture at Baihui was performed for 20 minutes on 3-day-old（Day 3） newborn Sprague-Dawley rats exposed to in utero fetal distress;electroacupuncture parameters consisted of sparse and dense waves at a frequency of 2–10 Hz.Real-time fluorescent quantitative PCR results demonstrated that m RNA expression of Neuro D,a molecule that indicates Neuro D,increased with prolonged time in brains of newborn rats,and peaked on Day 22.The level of m RNA expression was similar between Day 16 and Day 35.These findings suggest that electro acupuncture at Baihui acupoint could effectively increase m RNA expression of molecules involved in Neuro D in the brains of newborn rats exposed to in utero fetal distress.展开更多
Epileptic seizure control and the disappearance of epileptJform discharge are not indicative of the absence of abnormal perfusion foci. Perfusion abnormalities are a major cause of epileptic discharge, and the existen...Epileptic seizure control and the disappearance of epileptJform discharge are not indicative of the absence of abnormal perfusion foci. Perfusion abnormalities are a major cause of epileptic discharge, and the existence of abnormal perfusion loci implies possible relapse. Very little is known about perfusion abnormality repair in epilepsy. The present study selected 43 cases of idiopathic epilepsy under antiepileptic drug control for an average of 24 months. Comparisons between interictal single-photon emission CT （SPECT） images and long-term electroencephalogram （EEG） pre- and post-treatment showed that cases of normal SPECT increased by 48% （12/25） following treatment, with a total number of 15 reduced loci （,36%, 15/41 ）. Perfusion foci, Le., region of interest, were altered following treatment. These changes included： normal to abnormal in 3 cases （7%, 3/43; 2 hyperperfusion and 1 hypoperfusion）; abnormal to normal in 14 cases （32%, 14/43; 10 pre-treatment hypopeffusion and 4 hyperperfusion）; abnormal to abnormal in 7 cases （16%, 7/43; hyperperfusion to hypoperfusion in 5 cases, hypoperfusion to hyperpeffusion in 2 cases）. Long-term EEG revealed in an increase in the number of normal cases by 20 （40%, 20/39）, and there were 25 fewer cases with epileptiform discharges （66%, 25/38）. These findings demonstrate that long-term control of anti-epileptic drugs partially repaired cerebral perfusion abnormalities and reduced epileptiform discharges in idiopathic epilepsy.展开更多
Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of g...Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of great significance in premature infants with hypoxic-ischemic brain damage There is little evidence of direct regulatory effects of hypoxia-inducible factor le on oligodendrocyte lineage gene-l. In this study, brain slices of Sprague-Dawley rats were cultured and subjected to oxygen-glucose deprivation. Then, slices were transfected with hypoxia-inducible factor la or oligodendrocyte lineage gene-1. The expression levels of hypoxia-inducible factor la and oligodendrocyte lineage gene-1 were significantly up-regulated in rat brains prior to transfection, as detected by immunohistochemical staining. Eight hours after transfection of slices with hypoxia-inducible factor la, oligodendrocyte lineage gene-1 expression was upregulated, and reached a peak 24 hours after transfection. Oligodendrocyte lineage gene-1 transfection induced no significant differences in hypoxia-inducible factor la levels in rat brain tissues with oxygen-glucose deprivation. These experimental findings indicate that hypoxia-inducible factor la can regulate oligodendrocyte lineage gene-1 expression in hypoxic brain tissue, thus repairing the neural impairment.展开更多
Hyperglycemia reduces the number of circulating endothelial progenitor cells, accelerates their senescence and impairs their function.However, the relationship between blood glucose levels and endothelial progenitor c...Hyperglycemia reduces the number of circulating endothelial progenitor cells, accelerates their senescence and impairs their function.However, the relationship between blood glucose levels and endothelial progenitor cells in peripheral blood of patients with traumatic brain injury is unclear. In this study, 101 traumatic brain injury patients admitted to the Department of Neurosurgery, Tianjin Medical University General Hospital or the Department of Neurosurgery, Tianjin Huanhu Hospital, China, were enrolled from April 2005 to March 2007. The number of circulating endothelial progenitor cells and blood glucose levels were measured at 1, 4, 7, 14 and 21 days after traumatic brain injury by flow cytometry and automatic biochemical analysis, respectively. The number of circulating endothelial progenitor cells and blood sugar levels in 37 healthy control subjects were also examined. Compared with controls, the number of circulating endothelial progenitor cells in traumatic brain injury patients was decreased at 1 day after injury, and then increased at 4 days after injury,and reached a peak at 7 days after injury. Compared with controls, blood glucose levels in traumatic brain injury patients peaked at 1 day and then decreased until 7 days and then remained stable. At 1, 4, and 7 days after injury, the number of circulating endothelial progenitor cells was negatively correlated with blood sugar levels(r =-0.147, P < 0.05). Our results verify that hyperglycemia in patients with traumatic brain injury is associated with decreased numbers of circulating endothelial progenitor cells. This study was approved by the Ethical Committee of Tianjin Medical University General Hospital, China(approval No. 200501) in January 2015.展开更多
基金supported by the European Union Horizon 2020 Programme(H2020-MSCA-ITN-2015) under the Marie Sklodowska-Curie Innovative Training NetworksGrant Agreement No.676408,Science Foundation Ireland(11/RFP/NES/3183)through a postgraduate scholarship from the Irish Research Council to Niamh Moriarty
文摘Two hundred years after James Parkinson first described the cardinal motor symptoms of the disorder that would later bear his name,there is still an irrefutable need for a therapy that targets the underlying pathophysiology of the disease and not solely its symptoms.
基金supported by European Union-NextGeneration EU under the Italian University and Research(MUR)National Innovation Ecosystem grant ECS00000041-VITALITY-CUP E13C22001060006(to MdA)。
文摘Stroke is a major cause of death and disability worldwide.It is characterized by a highly interconnected and multiphasic neuropathological cascade of events,in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury.Neuroinflammation,a key player in the pathophysiology of stroke,has a dual role.In the acute phase of stroke,neuroinflammation exacerbates brain injury,contributing to neuronal damage and blood–brain barrier disruption.This aspect of neuroinflammation is associated with poor neurological outcomes.Conversely,in the recovery phase following stroke,neuroinflammation facilitates brain repair processes,including neurogenesis,angiogenesis,and synaptic plasticity.The transition of neuroinflammation from a harmful to a reparative role is not well understood.Therefore,this review seeks to explore the mechanisms underlying this transition,with the goal of informing the development of therapeutic interventions that are both time-and context-specific.This review aims to elucidate the complex and dual role of neuroinflammation in stroke,highlighting the main actors,biomarkers of the disease,and potential therapeutic approaches.
基金supported in part by National Institutes of Health Grants NS-091201(to MY)and NS-079331(to MY)VA MERIT Award IO1BX003441(to MY)
文摘The central nervous system has a very high energy requirement. Accord- ingly, despite representing only 2% of the body＇s mass, the brain uses 20% of the total oxygen consumption. Importantly, because most of this energy is used to maintain synaptic activity, even a mild decrease in its supply to the brain has deleterious implications for synaptic function.
文摘While it is well-known that neuronal activity promotes plasticity and connectivity, the success of activity-based neural rehabilitation programs remains extremely limited in human clinical experience because they cannot adequately control neuronal excitability and activity within the injured brain in order to induce repair. However, it is possible to non-invasively modulate brain plasticity using brain stimu- lation techniques such as repetitive transcranial （rTMS） and transcranial direct current stimulation （tDCS） techniques, which show promise for repairing injured neural circuits （Henrich-Noack et al., 2013; Lefaucher et al., 2014）. Yet we are far from having full control of these techniques to repair the brain following neurotrauma and need more fundamen- tal research （Ellaway et al., 2014; Lefaucher et al., 2014）. In this perspective we discuss the mechanisms by which rTMS may facilitate neurorehabilitation and propose experimental techniques with which magnetic stimulation may be investi- gated in order to optimise its treatment potential.
基金supported by a grant from the National Institutes of Health-National Center for Complementary and Alternative Medicine (R00AT004197)Start-up Funds from The University of Toledo to Shah ZA
文摘The irretrievable fate of neurons rhetoric for the first half of this dominated the neuroscience century, a position that was fiercely contested and recently debunked by extensive studies carried out in the field of neuroregeneration research. The turning point came in the year 1928, when Ramon Y. Cajal＇s （Lobato, 2008） work suggested that the regenerative capacity of neurons, though limited, could exist beyond their physical be- ing and depended on the environment surrounding them. That the manipulation of the restrictive environment surrounding the neuron could aid the regenerative process was conclusively established by Aguayo and colleagues （Richardson et al., 1980）. Since then, various strategies have been employed to target the different phases of regeneration which include： cell-replacement and augmenting endogenous neurogenesis, the use of trophic factors, reversal of the inhibitory cues, and induction of signal- ing pathways that stimulate axon growth and guidance （Horner and Gage. 2000）.
文摘Objective To investigate a possibility of repairing damaged brain by intracerebroventricular transplantation of neural stem cells （NSCs） in the adult mice subjected to glutamate-induced excitotoxic injury. Methods Mouse NSCs were isolated from the brains of embryos at 15-day postcoitum （dpc）. The expression of nestin, a special antigen for NSC, was detected by immunocytochemistry. Immunofluorescence staining was carried out to observe the survival and location of transplanted NSCs. The animals in the MSG＋NSCs group received intracerebroventricular transplantation of NSCs （approximately 1.0×10^5 cells） separately on day 1 and day 10 after 10-d MSG exposure （4.0 g/kg per day）. The mice in control and MSG groups received intracerebroventricular injection of Dulbecco＇s minimum essential medium （DMEM） instead of NSCs. On day 11 after the last NSC transplantation, the test of Y-maze discrimination learning was performed, and then the histopathology of the animal brains was studied to analyze the MSG-induced functional and morphological changes of brain and the effects of intracerebroventricular transplantation of NSCs on the brain repair. Results The isolated cells were Nestin-positive. The grafted NSCs in the host brain were region-specifically survived at 10-d post-transplantation. Intracerebroventricular transplantation of NSCs obviously facilitated the brain recovery from glutamate-induced behavioral disturbances and histopathological impairs in adult mice. Conclusion Intracerebroventricular transplantation of NSCs may be feasible in repairing diseased or damaged brain tissue.
基金supported by grants from the National Basic Research Development Program of China (2006CB504100 and 2006CB943702)the National Natural Science Foundation of China(81030020 and J0730860)
文摘Objective It has been reported that B-cell lymphoma 2 （Bcl-2） enhances neurogenesis as well as supporting axonal growth after injury. In the present study, we investigated whether Bcl-2 overexpression plays a role in the formation of newborn striatonigral projection neurons in the adult rat brain after transient middle cerebral artery occlusion （MCAO）. Methods We infused human Bcl-2-expressing plasmid （pBcl-2） into the lateral ventricle immediately after 30 min of MCAO, injected 5＇-bromodeoxyuridine （BrdU） intraperitoneally to label proliferative cells, and microinjected fluorogold （FG） into the substantia nigra at 11 weeks of reperfusion followed by multiple immunostaining of striatonigral projection neurons at 12 weeks. Results We found that pBcl-2 treatment significantly increased the number of newborn neurons （BrdU＋-NeuN＋） in the striatum ipsilateral to the MCAO. We further detected newborn striatonigral projection neurons （BrdU＋-FG＋-NeuN＋） in the ipsilateral striatum at 12 weeks. More interestingly, the number of newborn striatonigral projection neurons （BrdU＋-FG＋） was significantly increased by pBcl-2 treatment compared to that by pEGFP, a control plasmid. Conclusion Taken together, we found that Bcl-2 overexpression in the brain enhanced the generation of newborn striatonigral projection neurons. This provides a potential strategy for promoting the reestablishment of neural networks and brain repair after ischemic injury.
基金supported by the Natural Science Foundation of Fujian Province of China,No.2015J01133the Professor Academic Development Foundation of Fujian Medical University of China,No.JS11003
文摘Neuro D plays a key regulatory effect on differentiation of neural stem cells into mature neurons in the brain.Thus,we assumed that electroacupuncture at Baihui（DU20） acupoint in newborn rats exposed to in utero fetal distress would influence expression of Neuro D.Electroacupuncture at Baihui was performed for 20 minutes on 3-day-old（Day 3） newborn Sprague-Dawley rats exposed to in utero fetal distress;electroacupuncture parameters consisted of sparse and dense waves at a frequency of 2–10 Hz.Real-time fluorescent quantitative PCR results demonstrated that m RNA expression of Neuro D,a molecule that indicates Neuro D,increased with prolonged time in brains of newborn rats,and peaked on Day 22.The level of m RNA expression was similar between Day 16 and Day 35.These findings suggest that electro acupuncture at Baihui acupoint could effectively increase m RNA expression of molecules involved in Neuro D in the brains of newborn rats exposed to in utero fetal distress.
文摘Epileptic seizure control and the disappearance of epileptJform discharge are not indicative of the absence of abnormal perfusion foci. Perfusion abnormalities are a major cause of epileptic discharge, and the existence of abnormal perfusion loci implies possible relapse. Very little is known about perfusion abnormality repair in epilepsy. The present study selected 43 cases of idiopathic epilepsy under antiepileptic drug control for an average of 24 months. Comparisons between interictal single-photon emission CT （SPECT） images and long-term electroencephalogram （EEG） pre- and post-treatment showed that cases of normal SPECT increased by 48% （12/25） following treatment, with a total number of 15 reduced loci （,36%, 15/41 ）. Perfusion foci, Le., region of interest, were altered following treatment. These changes included： normal to abnormal in 3 cases （7%, 3/43; 2 hyperperfusion and 1 hypoperfusion）; abnormal to normal in 14 cases （32%, 14/43; 10 pre-treatment hypopeffusion and 4 hyperperfusion）; abnormal to abnormal in 7 cases （16%, 7/43; hyperperfusion to hypoperfusion in 5 cases, hypoperfusion to hyperpeffusion in 2 cases）. Long-term EEG revealed in an increase in the number of normal cases by 20 （40%, 20/39）, and there were 25 fewer cases with epileptiform discharges （66%, 25/38）. These findings demonstrate that long-term control of anti-epileptic drugs partially repaired cerebral perfusion abnormalities and reduced epileptiform discharges in idiopathic epilepsy.
基金supported by the National Natural Science Foundation of China,No. 81241022the Natural Science Foundation of Beijing,No. 7072023,7122045
文摘Oligodendrocyte lineage gene-1 expressed in oligodendrocytes may trigger the repair of neuronal myelin impairment, and play a crucial role in myelin repair. Hypoxia-inducible factor la, a transcription factor, is of great significance in premature infants with hypoxic-ischemic brain damage There is little evidence of direct regulatory effects of hypoxia-inducible factor le on oligodendrocyte lineage gene-l. In this study, brain slices of Sprague-Dawley rats were cultured and subjected to oxygen-glucose deprivation. Then, slices were transfected with hypoxia-inducible factor la or oligodendrocyte lineage gene-1. The expression levels of hypoxia-inducible factor la and oligodendrocyte lineage gene-1 were significantly up-regulated in rat brains prior to transfection, as detected by immunohistochemical staining. Eight hours after transfection of slices with hypoxia-inducible factor la, oligodendrocyte lineage gene-1 expression was upregulated, and reached a peak 24 hours after transfection. Oligodendrocyte lineage gene-1 transfection induced no significant differences in hypoxia-inducible factor la levels in rat brain tissues with oxygen-glucose deprivation. These experimental findings indicate that hypoxia-inducible factor la can regulate oligodendrocyte lineage gene-1 expression in hypoxic brain tissue, thus repairing the neural impairment.
基金supported by the National Natural Science Foundation of China,No.30772229(to JNZ),No.81200907(to HJW)the Natural Science Foundation of Tianjin of China,No.12JCQNJC06800(to HJW)+1 种基金the Science and Technology Projects in Key Areas of Traditional Chinese Medicine of Tianjin of China,No.2018001(to ZGW)the Scientific Research Program Project of Tianjin Education Commission of China,No.2018ZD03(to ZGW)
文摘Hyperglycemia reduces the number of circulating endothelial progenitor cells, accelerates their senescence and impairs their function.However, the relationship between blood glucose levels and endothelial progenitor cells in peripheral blood of patients with traumatic brain injury is unclear. In this study, 101 traumatic brain injury patients admitted to the Department of Neurosurgery, Tianjin Medical University General Hospital or the Department of Neurosurgery, Tianjin Huanhu Hospital, China, were enrolled from April 2005 to March 2007. The number of circulating endothelial progenitor cells and blood glucose levels were measured at 1, 4, 7, 14 and 21 days after traumatic brain injury by flow cytometry and automatic biochemical analysis, respectively. The number of circulating endothelial progenitor cells and blood sugar levels in 37 healthy control subjects were also examined. Compared with controls, the number of circulating endothelial progenitor cells in traumatic brain injury patients was decreased at 1 day after injury, and then increased at 4 days after injury,and reached a peak at 7 days after injury. Compared with controls, blood glucose levels in traumatic brain injury patients peaked at 1 day and then decreased until 7 days and then remained stable. At 1, 4, and 7 days after injury, the number of circulating endothelial progenitor cells was negatively correlated with blood sugar levels(r =-0.147, P < 0.05). Our results verify that hyperglycemia in patients with traumatic brain injury is associated with decreased numbers of circulating endothelial progenitor cells. This study was approved by the Ethical Committee of Tianjin Medical University General Hospital, China(approval No. 200501) in January 2015.
