There are various clinical treatments for traumatic brain injury,including surgery,drug therapy,and rehabilitation therapy;howeve r,the therapeutic effects are limited.Scaffolds combined with exosomes represent a prom...There are various clinical treatments for traumatic brain injury,including surgery,drug therapy,and rehabilitation therapy;howeve r,the therapeutic effects are limited.Scaffolds combined with exosomes represent a promising but challenging method for improving the repair of traumatic brain injury.In this study,we determined the ability of a novel 3D-printed collagen/chitosan scaffold loaded with exosomes derived from neural stem cells pretreated with insulin-like growth factor-1(3D-CC-INEXOS) to improve traumatic brain injury repair and functional recove ry after traumatic brain injury in rats.Composite scaffolds comprising collagen,chitosan,and exosomes derived from neural stem cells pretreated with insulin-like growth fa ctor-1(INEXOS) continuously released exosomes for 2weeks.Transplantation of 3D-CC-INExos scaffolds significantly improved motor and cognitive functions in a rat traumatic brain injury model,as assessed by the Morris water maze test and modified neurological seve rity scores.In addition,immunofluorescence staining and transmission electron microscopy showed that3D-CC-INExos implantation significantly improved the recove ry of damaged nerve tissue in the injured area.In conclusion,this study suggests that transplanted3D-CC-INExos scaffolds might provide a potential strategy for the treatment of traumatic brain injury and lay a solid foundation for clinical translation.展开更多
Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family...Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.展开更多
We applied the multiple exp-function scheme to the(2+1)-dimensional Sawada-Kotera(SK) equation and(3+1)-dimensional nonlinear evolution equation and analytic particular solutions have been deduced. The analyti...We applied the multiple exp-function scheme to the(2+1)-dimensional Sawada-Kotera(SK) equation and(3+1)-dimensional nonlinear evolution equation and analytic particular solutions have been deduced. The analytic particular solutions contain one-soliton, two-soliton, and three-soliton type solutions. With the assistance of Maple, we demonstrated the efficiency and advantages of the procedure that generalizes Hirota's perturbation scheme. The obtained solutions can be used as a benchmark for numerical solutions and describe the physical phenomena behind the model.展开更多
In this paper,we mainly focus on proving the existence of lump solutions to a generalized(3+1)-dimensional nonlinear differential equation.Hirota’s bilinear method and a quadratic function method are employed to deri...In this paper,we mainly focus on proving the existence of lump solutions to a generalized(3+1)-dimensional nonlinear differential equation.Hirota’s bilinear method and a quadratic function method are employed to derive the lump solutions localized in the whole plane for a(3+1)-dimensional nonlinear differential equation.Three examples of such a nonlinear equation are presented to investigate the exact expressions of the lump solutions.Moreover,the 3d plots and corresponding density plots of the solutions are given to show the space structures of the lump waves.In addition,the breath-wave solutions and several interaction solutions of the(3+1)-dimensional nonlinear differential equation are obtained and their dynamics are analyzed.展开更多
Instead of the usual Hirota ansatz,i.e.,the functions in bilinear equations being chosen as exponentialtypes,a generalized Hirota ansatz is proposed for a (3+1)-dimensional nonlinear evolution equation.Based on theres...Instead of the usual Hirota ansatz,i.e.,the functions in bilinear equations being chosen as exponentialtypes,a generalized Hirota ansatz is proposed for a (3+1)-dimensional nonlinear evolution equation.Based on theresulting generalized Hirota ansatz,a family of new explicit solutions for the equation are derived.展开更多
We previously found that monocyte locomotion inhibitory factor has a neuroprotective effect on ischemic brain injury during the acute phase of stro ke.Therefore,we modified the structure of an anti-inflammato ry monoc...We previously found that monocyte locomotion inhibitory factor has a neuroprotective effect on ischemic brain injury during the acute phase of stro ke.Therefore,we modified the structure of an anti-inflammato ry monocyte locomotion inhibitory factor peptide to construct an active cyclic peptide—Cyclo(MQCNS)(LZ-3)—and investigated its effects on ischemic stroke.In this study,we established a rat model of ischemic stroke by occluding the middle cerebral artery and then administered LZ-3(2 or 4 mg/kg) via the tail vein for 7 consecutive days.Our res ults showed that LZ-3(2 or 4 mg/kg) substantially decreased infarct volu m e,reduced co rtical ne rve cell death,improved neurological function,reduced cortical and hippocampal injury,and decreased the levels of inflammatory factors in the blood and brain tissues.In a well-diffe rentiated,oxygen-glucose deprivation/reoxygenation-induced BV2 cell model of poststroke,LZ-3(100 μM) inhibited the JAK1-STAT6 signaling pathway.LZ-3 regulated microglia/macrophage polarization from the M1 to the M2 type and inhibited microglia/macrophage phagocytosis and migration via the JAK1/STAT6 signaling pathway.To conclude,LZ-3 regulates microglial activation by inhibiting the JAK1/STAT6 sign aling pathway and improves functional recovery post-stroke.展开更多
基金supported by the National Major Scientific and Technological Special Project for Significant New Drugs Development,No.2019ZX09301-147 (to LXZ)。
文摘There are various clinical treatments for traumatic brain injury,including surgery,drug therapy,and rehabilitation therapy;howeve r,the therapeutic effects are limited.Scaffolds combined with exosomes represent a promising but challenging method for improving the repair of traumatic brain injury.In this study,we determined the ability of a novel 3D-printed collagen/chitosan scaffold loaded with exosomes derived from neural stem cells pretreated with insulin-like growth factor-1(3D-CC-INEXOS) to improve traumatic brain injury repair and functional recove ry after traumatic brain injury in rats.Composite scaffolds comprising collagen,chitosan,and exosomes derived from neural stem cells pretreated with insulin-like growth fa ctor-1(INEXOS) continuously released exosomes for 2weeks.Transplantation of 3D-CC-INExos scaffolds significantly improved motor and cognitive functions in a rat traumatic brain injury model,as assessed by the Morris water maze test and modified neurological seve rity scores.In addition,immunofluorescence staining and transmission electron microscopy showed that3D-CC-INExos implantation significantly improved the recove ry of damaged nerve tissue in the injured area.In conclusion,this study suggests that transplanted3D-CC-INExos scaffolds might provide a potential strategy for the treatment of traumatic brain injury and lay a solid foundation for clinical translation.
文摘Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.
基金The National Natural Science Foundation of China(11701134)The National Natural Science Foundation of Shandong Province,China(ZR2017JL008)The Science and Technology Plan Project of the Educational Department of Shandong Province,China(J16LI12,J15LI54)
文摘We applied the multiple exp-function scheme to the(2+1)-dimensional Sawada-Kotera(SK) equation and(3+1)-dimensional nonlinear evolution equation and analytic particular solutions have been deduced. The analytic particular solutions contain one-soliton, two-soliton, and three-soliton type solutions. With the assistance of Maple, we demonstrated the efficiency and advantages of the procedure that generalizes Hirota's perturbation scheme. The obtained solutions can be used as a benchmark for numerical solutions and describe the physical phenomena behind the model.
基金supported by the National Natural Science Foundation of China(Nos.12101572,12371256)2023 Shanxi Province Graduate Innovation Project(No.2023KY614)the 19th Graduate Science and Technology Project of North University of China(No.20231943)。
文摘In this paper,we mainly focus on proving the existence of lump solutions to a generalized(3+1)-dimensional nonlinear differential equation.Hirota’s bilinear method and a quadratic function method are employed to derive the lump solutions localized in the whole plane for a(3+1)-dimensional nonlinear differential equation.Three examples of such a nonlinear equation are presented to investigate the exact expressions of the lump solutions.Moreover,the 3d plots and corresponding density plots of the solutions are given to show the space structures of the lump waves.In addition,the breath-wave solutions and several interaction solutions of the(3+1)-dimensional nonlinear differential equation are obtained and their dynamics are analyzed.
文摘Instead of the usual Hirota ansatz,i.e.,the functions in bilinear equations being chosen as exponentialtypes,a generalized Hirota ansatz is proposed for a (3+1)-dimensional nonlinear evolution equation.Based on theresulting generalized Hirota ansatz,a family of new explicit solutions for the equation are derived.
文摘We previously found that monocyte locomotion inhibitory factor has a neuroprotective effect on ischemic brain injury during the acute phase of stro ke.Therefore,we modified the structure of an anti-inflammato ry monocyte locomotion inhibitory factor peptide to construct an active cyclic peptide—Cyclo(MQCNS)(LZ-3)—and investigated its effects on ischemic stroke.In this study,we established a rat model of ischemic stroke by occluding the middle cerebral artery and then administered LZ-3(2 or 4 mg/kg) via the tail vein for 7 consecutive days.Our res ults showed that LZ-3(2 or 4 mg/kg) substantially decreased infarct volu m e,reduced co rtical ne rve cell death,improved neurological function,reduced cortical and hippocampal injury,and decreased the levels of inflammatory factors in the blood and brain tissues.In a well-diffe rentiated,oxygen-glucose deprivation/reoxygenation-induced BV2 cell model of poststroke,LZ-3(100 μM) inhibited the JAK1-STAT6 signaling pathway.LZ-3 regulated microglia/macrophage polarization from the M1 to the M2 type and inhibited microglia/macrophage phagocytosis and migration via the JAK1/STAT6 signaling pathway.To conclude,LZ-3 regulates microglial activation by inhibiting the JAK1/STAT6 sign aling pathway and improves functional recovery post-stroke.