Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmit...Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients(BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilatorinduced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients.展开更多
Background Patients with acute brain injury(ABI)are a peculiar population because ABI does not only affect the brain but also other organs such as the lungs,as theorized in brain–lung crosstalk models.ABI patients of...Background Patients with acute brain injury(ABI)are a peculiar population because ABI does not only affect the brain but also other organs such as the lungs,as theorized in brain–lung crosstalk models.ABI patients often require mechanical ventilation(MV)to avoid the complications of impaired respiratory function that can follow ABI;MV should be settled with meticulousness owing to its effects on the intracranial compartment,especially regarding positive end-expiratory pressure(PEEP).This scoping review aimed to(1)describe the physiological basis and mechanisms related to the effects of PEEP in ABI;(2)examine how clinical research is conducted on this topic;(3)identify methods for setting PEEP in ABI;and(4)investigate the impact of the application of PEEP in ABI on the outcome.Methods The five-stage paradigm devised by Peters et al.and expanded by Arksey and O'Malley,Levac et al.,and the Joanna Briggs Institute was used for methodology.We also adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses(PRISMA)extension criteria.Inclusion criteria:we compiled all scientific data from peer-reviewed journals and studies that discussed the application of PEEP and its impact on intracranial pressure,cerebral perfusion pressure,and brain oxygenation in adult patients with ABI.Exclusion criteria:studies that only examined a pediatric patient group(those under the age of 18),experiments conducted solely on animals;studies without intracranial pressure and/or cerebral perfusion pressure determinations,and studies with incomplete information.Two authors searched and screened for inclusion in papers published up to July 2023 using the PubMed-indexed online database.Data were presented in narrative and tubular form.Results The initial search yielded 330 references on the application of PEEP in ABI,of which 36 met our inclusion criteria.PEEP has recognized beneficial effects on gas exchange,but it produces hemodynamic changes that should be predicted to avoid undesired consequences on cerebral blood flo展开更多
The structure and function of brain networks have been altered in patients with end-stage renal disease(ESRD).Manifold regularization(MR)only considers the pairing relationship between two brain regions and cannot rep...The structure and function of brain networks have been altered in patients with end-stage renal disease(ESRD).Manifold regularization(MR)only considers the pairing relationship between two brain regions and cannot represent functional interactions or higher-order relationships between multiple brain regions.To solve this issue,we developed a method to construct a dynamic brain functional network(DBFN)based on dynamic hypergraph MR(DHMR)and applied it to the classification of ESRD associated with mild cognitive impairment(ESRDaMCI).The construction of DBFN with Pearson’s correlation(PC)was transformed into an optimization model.Node convolution and hyperedge convolution superposition were adopted to dynamically modify the hypergraph structure,and then got the dynamic hypergraph to form the manifold regular terms of the dynamic hypergraph.The DHMR and L_(1) norm regularization were introduced into the PC-based optimization model to obtain the final DHMR-based DBFN(DDBFN).Experiment results demonstrated the validity of the DDBFN method by comparing the classification results with several related brain functional network construction methods.Our work not only improves better classification performance but also reveals the discriminative regions of ESRDaMCI,providing a reference for clinical research and auxiliary diagnosis of concomitant cognitive impairments.展开更多
Advanced glycation end products lead to cell apoptosis, and cause cell death by increasing endoplasmic reticulum stress. Advanced glycation end products alone may also directly cause damage to tissues and cells, but t...Advanced glycation end products lead to cell apoptosis, and cause cell death by increasing endoplasmic reticulum stress. Advanced glycation end products alone may also directly cause damage to tissues and cells, but the precise mechanism remains unknown. This study used primary cultures of rat cerebral cortex neurons, and treated cells with different concentrations of glycation end products （50, 100, 200, 400 mg/L）, and with an antibody for the receptor of advanced glycation end products before and after treatment with advanced glycation end products. The results showed that with increasing concentrations of glycation end products, free radical content increased in neurons, and the number of apoptotic cells increased in a dose-dependent manner. Before and after treatment of advanced glycation end products, the addition of the antibody against advanced glycation end-products markedly reduced hydroxyl free radicals, malondialdehyde levels, and inhibited cell apoptosis. This result indicated that the antibody for receptor of advanced glycation end-products in neurons from the rat cerebral cortex can reduce glycation end product-induced oxidative stress damage by suppressing glycation end product receptors. Overall, our study confirms that the advanced glycation end products-advanced glycation end products receptor pathway may be the main signaling pathway leading to neuronal damage.展开更多
Extracting characteristic brain signals and simultaneous recording animals behaving could help us to understand the complex behavior of neuronal ensembles. Here, a system was established to record local field potentia...Extracting characteristic brain signals and simultaneous recording animals behaving could help us to understand the complex behavior of neuronal ensembles. Here, a system was established to record local field potentials (LFP) and extracellular signal or multiple-unit discharge and behavior synchronously by utilizing electrophysiology and integrated circuit technique. It comprised microelectrodes and micro-driver assembly, analog front end (AFE),while a computer (Pentium III ) was used as the platform for the graphic user interface, which was developed using the LabVIEW programming language. It was designed as a part of ongoing research to develop a portable wireless neural signal recording system. We believe that this information will be useful for the research of brain-computer interface.展开更多
The health safety of methylglyoxal(MGO) has been recognized as a key issue owing to its ultra-high reactivity toward some key biomolecules such as amino acids, proteins, DNA, sulfhydryl-and basic nitrogencontaining co...The health safety of methylglyoxal(MGO) has been recognized as a key issue owing to its ultra-high reactivity toward some key biomolecules such as amino acids, proteins, DNA, sulfhydryl-and basic nitrogencontaining compounds, including amino-bearing neurotransmitters. In this review, we have summarized the endoand exogenous sources of MGO and its accumulation inside the body due to high intake, abnormal glucose metabolism and or malfunctioning glyoxalases, and review the debate concerning the adverse functionality of MGO ingested from foods. Higher than normal concentrations of MGO in the circulatory system and tissues have been found to be closely associated with the production of advanced glycation end products(AGEs), increased oxidative stress, elevated inflammation and RAGE(AGE receptors) activity, which subsequently progresses to a pathological stage of human health, such as diabetes complications, cancer, cardiovascular and degenerative diseases. Having illustrated the mechanisms of MGO trapping in vivo, we advocate the development of efficient and efficacious MGO scavengers, either assisting or enhancing the activity of endogenous glyoxalases to facilitate MGO removal, or providing phytochemicals and functional foods containing them, or pharmaceuticals to irreversibly bind MGO and thus form MGO-complexes that are cleared from the body.展开更多
Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protec...Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway.The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion.Nicotiflorin（10 mg/kg） was administered by tail vein injection.Cell apoptosis in the ischemic cerebral cortex was examined by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase d UTP nick end labeling assay.Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining.Additionally,p-JAK2,p-STAT3,Bcl-2,Bax,and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay.Nicotiflorin altered the shape and structure of injured neurons,decreased the number of apoptotic cells,down-regulates expression of p-JAK2,p-STAT3,caspase-3,and Bax,decreased Bax immunoredactivity,and increased Bcl-2 protein expression and immunoreactivity.These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway.展开更多
BACKGROUND:An updated definition of early allograft dysfunction(EAD) was recently validated in a multicenter study of 300 deceased donor liver transplant recipients.This analysis did not differentiate between donation...BACKGROUND:An updated definition of early allograft dysfunction(EAD) was recently validated in a multicenter study of 300 deceased donor liver transplant recipients.This analysis did not differentiate between donation after brain death(DBD) and donation after cardiac death(DCD) allograft recipients.METHODS:We reviewed our prospectively entered database for all DBD(n=377) and DCD(n=38) liver transplantations between January 1,2006 and October 30,2011.The incidence of EAD as well as its ability to predict graft failure and survival was compared between DBD and DCD groups.RESULTS:EAD was a valid predictor of both graft and patient survival at six months in DBD allograft recipients,but in DCD allograft recipients there was no significant difference in the rate of graft failure in those with EAD(11.5%) compared with those without EAD(16.7%)(P=0.664) or in the rate of death in recipients with EAD(3.8%) compared with those without EAD(8.3%)(P=0.565).The graft failure rate in the first 6 months in those with international normalized ratio ≥1.6 on day 7 who received a DCD allograft was 37.5% compared with 6.7% for those with international normalized ratio <1.6 on day 7(P=0.022).CONCLUSIONS:The recently validated definition of EAD is a valid predictor of patient and graft survival in recipients of DBD allografts.On initial assessment,it does not appear to be a useful predictor of patient and graft survival in recipients of DCD allografts,however a study with a larger sample size of DCD allografts is needed to confirm these findings.The high ALT/AST levels in most recipients of DCD livers as well as the predisposition to biliary complications and early cholestasis make these parameters as poor predictors of graft failure.An alternative definition of EAD that gives greater weight to the INR on day 7 may be more relevant in this population.展开更多
文摘Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients(BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilatorinduced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients.
文摘Background Patients with acute brain injury(ABI)are a peculiar population because ABI does not only affect the brain but also other organs such as the lungs,as theorized in brain–lung crosstalk models.ABI patients often require mechanical ventilation(MV)to avoid the complications of impaired respiratory function that can follow ABI;MV should be settled with meticulousness owing to its effects on the intracranial compartment,especially regarding positive end-expiratory pressure(PEEP).This scoping review aimed to(1)describe the physiological basis and mechanisms related to the effects of PEEP in ABI;(2)examine how clinical research is conducted on this topic;(3)identify methods for setting PEEP in ABI;and(4)investigate the impact of the application of PEEP in ABI on the outcome.Methods The five-stage paradigm devised by Peters et al.and expanded by Arksey and O'Malley,Levac et al.,and the Joanna Briggs Institute was used for methodology.We also adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses(PRISMA)extension criteria.Inclusion criteria:we compiled all scientific data from peer-reviewed journals and studies that discussed the application of PEEP and its impact on intracranial pressure,cerebral perfusion pressure,and brain oxygenation in adult patients with ABI.Exclusion criteria:studies that only examined a pediatric patient group(those under the age of 18),experiments conducted solely on animals;studies without intracranial pressure and/or cerebral perfusion pressure determinations,and studies with incomplete information.Two authors searched and screened for inclusion in papers published up to July 2023 using the PubMed-indexed online database.Data were presented in narrative and tubular form.Results The initial search yielded 330 references on the application of PEEP in ABI,of which 36 met our inclusion criteria.PEEP has recognized beneficial effects on gas exchange,but it produces hemodynamic changes that should be predicted to avoid undesired consequences on cerebral blood flo
基金supported by the National Natural Science Foundation of China (No.51877013),(ZJ),(http://www.nsfc.gov.cn/)the Jiangsu Provincial Key Research and Development Program (No.BE2021636),(ZJ),(http://kxjst.jiangsu.gov.cn/)+1 种基金the Science and Technology Project of Changzhou City (No.CE20205056),(ZJ),(http://kjj.changzhou.gov.cn/)by Qing Lan Project of Jiangsu Province (no specific grant number),(ZJ),(http://jyt.jiangsu.gov.cn/).
文摘The structure and function of brain networks have been altered in patients with end-stage renal disease(ESRD).Manifold regularization(MR)only considers the pairing relationship between two brain regions and cannot represent functional interactions or higher-order relationships between multiple brain regions.To solve this issue,we developed a method to construct a dynamic brain functional network(DBFN)based on dynamic hypergraph MR(DHMR)and applied it to the classification of ESRD associated with mild cognitive impairment(ESRDaMCI).The construction of DBFN with Pearson’s correlation(PC)was transformed into an optimization model.Node convolution and hyperedge convolution superposition were adopted to dynamically modify the hypergraph structure,and then got the dynamic hypergraph to form the manifold regular terms of the dynamic hypergraph.The DHMR and L_(1) norm regularization were introduced into the PC-based optimization model to obtain the final DHMR-based DBFN(DDBFN).Experiment results demonstrated the validity of the DDBFN method by comparing the classification results with several related brain functional network construction methods.Our work not only improves better classification performance but also reveals the discriminative regions of ESRDaMCI,providing a reference for clinical research and auxiliary diagnosis of concomitant cognitive impairments.
文摘Advanced glycation end products lead to cell apoptosis, and cause cell death by increasing endoplasmic reticulum stress. Advanced glycation end products alone may also directly cause damage to tissues and cells, but the precise mechanism remains unknown. This study used primary cultures of rat cerebral cortex neurons, and treated cells with different concentrations of glycation end products （50, 100, 200, 400 mg/L）, and with an antibody for the receptor of advanced glycation end products before and after treatment with advanced glycation end products. The results showed that with increasing concentrations of glycation end products, free radical content increased in neurons, and the number of apoptotic cells increased in a dose-dependent manner. Before and after treatment of advanced glycation end products, the addition of the antibody against advanced glycation end-products markedly reduced hydroxyl free radicals, malondialdehyde levels, and inhibited cell apoptosis. This result indicated that the antibody for receptor of advanced glycation end-products in neurons from the rat cerebral cortex can reduce glycation end product-induced oxidative stress damage by suppressing glycation end product receptors. Overall, our study confirms that the advanced glycation end products-advanced glycation end products receptor pathway may be the main signaling pathway leading to neuronal damage.
基金Shandong Science Development FundGrant number:041120101
文摘Extracting characteristic brain signals and simultaneous recording animals behaving could help us to understand the complex behavior of neuronal ensembles. Here, a system was established to record local field potentials (LFP) and extracellular signal or multiple-unit discharge and behavior synchronously by utilizing electrophysiology and integrated circuit technique. It comprised microelectrodes and micro-driver assembly, analog front end (AFE),while a computer (Pentium III ) was used as the platform for the graphic user interface, which was developed using the LabVIEW programming language. It was designed as a part of ongoing research to develop a portable wireless neural signal recording system. We believe that this information will be useful for the research of brain-computer interface.
基金supported by the USDA National Institute of Food and Agriculture, Hatch project 1007898
文摘The health safety of methylglyoxal(MGO) has been recognized as a key issue owing to its ultra-high reactivity toward some key biomolecules such as amino acids, proteins, DNA, sulfhydryl-and basic nitrogencontaining compounds, including amino-bearing neurotransmitters. In this review, we have summarized the endoand exogenous sources of MGO and its accumulation inside the body due to high intake, abnormal glucose metabolism and or malfunctioning glyoxalases, and review the debate concerning the adverse functionality of MGO ingested from foods. Higher than normal concentrations of MGO in the circulatory system and tissues have been found to be closely associated with the production of advanced glycation end products(AGEs), increased oxidative stress, elevated inflammation and RAGE(AGE receptors) activity, which subsequently progresses to a pathological stage of human health, such as diabetes complications, cancer, cardiovascular and degenerative diseases. Having illustrated the mechanisms of MGO trapping in vivo, we advocate the development of efficient and efficacious MGO scavengers, either assisting or enhancing the activity of endogenous glyoxalases to facilitate MGO removal, or providing phytochemicals and functional foods containing them, or pharmaceuticals to irreversibly bind MGO and thus form MGO-complexes that are cleared from the body.
基金financially supported by the Natural Science Foundation of Education Department of Sichuan Province of China,No.14ZB0152the Joint Research Program of Luzhou and Southwest Medical University,in China,No.14JC0120
文摘Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway.The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion.Nicotiflorin（10 mg/kg） was administered by tail vein injection.Cell apoptosis in the ischemic cerebral cortex was examined by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase d UTP nick end labeling assay.Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining.Additionally,p-JAK2,p-STAT3,Bcl-2,Bax,and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay.Nicotiflorin altered the shape and structure of injured neurons,decreased the number of apoptotic cells,down-regulates expression of p-JAK2,p-STAT3,caspase-3,and Bax,decreased Bax immunoredactivity,and increased Bcl-2 protein expression and immunoreactivity.These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway.
文摘BACKGROUND:An updated definition of early allograft dysfunction(EAD) was recently validated in a multicenter study of 300 deceased donor liver transplant recipients.This analysis did not differentiate between donation after brain death(DBD) and donation after cardiac death(DCD) allograft recipients.METHODS:We reviewed our prospectively entered database for all DBD(n=377) and DCD(n=38) liver transplantations between January 1,2006 and October 30,2011.The incidence of EAD as well as its ability to predict graft failure and survival was compared between DBD and DCD groups.RESULTS:EAD was a valid predictor of both graft and patient survival at six months in DBD allograft recipients,but in DCD allograft recipients there was no significant difference in the rate of graft failure in those with EAD(11.5%) compared with those without EAD(16.7%)(P=0.664) or in the rate of death in recipients with EAD(3.8%) compared with those without EAD(8.3%)(P=0.565).The graft failure rate in the first 6 months in those with international normalized ratio ≥1.6 on day 7 who received a DCD allograft was 37.5% compared with 6.7% for those with international normalized ratio <1.6 on day 7(P=0.022).CONCLUSIONS:The recently validated definition of EAD is a valid predictor of patient and graft survival in recipients of DBD allografts.On initial assessment,it does not appear to be a useful predictor of patient and graft survival in recipients of DCD allografts,however a study with a larger sample size of DCD allografts is needed to confirm these findings.The high ALT/AST levels in most recipients of DCD livers as well as the predisposition to biliary complications and early cholestasis make these parameters as poor predictors of graft failure.An alternative definition of EAD that gives greater weight to the INR on day 7 may be more relevant in this population.
