High mobility group box 1 (HMGB1) is a nuclear protein that can bind to DNA and act as a co-factor for gene transcription. When released into extracellular fluid, it plays a proinflammatory role by acting as a damage-...High mobility group box 1 (HMGB1) is a nuclear protein that can bind to DNA and act as a co-factor for gene transcription. When released into extracellular fluid, it plays a proinflammatory role by acting as a damage-associated molecular pattern molecule (DAMP) (also known as an alarmin) to initiate innate immune responses by activating multiple cell surface receptors such as the receptor for advanced glycation end-products (RAGE) and toll-like receptors (TLRs), TLR2, TLR4 or TLR9. This proinflammatory role is now considered to be important in the pathogenesis of a wide range of kidney diseases whether they result from hemodynamic changes, renal tubular epithelial cell apoptosis, kidney tissue fibrosis or inflammation. This review summarizes our current understanding of the role of HMGB1 in kidney diseases and how the HMGB1-mediated signaling pathway may constitute a new strategy for the treatment of kidney diseases. (C) 2016 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.展开更多
Bupleurum polysaccharides(BPs)is isolated from Bupleurum smithii var.parvifolium,a key traditional Chinese medicine.The study was to investigate the effects of BPs on diabetic kidney injury.After two intraperitoneal i...Bupleurum polysaccharides(BPs)is isolated from Bupleurum smithii var.parvifolium,a key traditional Chinese medicine.The study was to investigate the effects of BPs on diabetic kidney injury.After two intraperitoneal injections of streptozotozin(STZ)100 mg·kg^–1,renal injury in diabetic mice was induced and BPs was orally administrated at dosages of 30 and 60 mg·kg^–1·d^–1.The STZ injected mice developed renal function damage,renal inflammation and fibrosis known as diabetic kidney disease(DKD).BPs significantly reduced serum creatinine level and urinary albumin excretion rate,with the attenuated swelling of kidneys.BPs treatment obviously alleviated the pathological damage of renal tissue.The progression of renal injury in BPs treated mice was inhibited with less expression of type IV collagen(Col IV),fibronectin(FN)andα-smooth muscle actin(α-SMA).The inhibition of inflammation in kidney was associated with the reduced level of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6).BPs administration suppressed the over-expression of toll like receptor 4(TLR4)and high-mobility group box 1(HMGB1)with lowered activity of nuclear factor kappa B(NF-κB)in renal tissue of diabetic mice.Oral administration of BPs effectively prevented the development of renal injury in diabetic mice.This study suggested that the protection provided by BPs might affect through the interruption of HMGB1-TLR4 pathway,leading to the inhibition of renal inflammation and fibrotic process.展开更多
BACKGROUND Abdominal paracentesis drainage(APD)is a safe and effective strategy for severe acute pancreatitis(SAP)patients.However,the effects of APD treatment on SAPassociated cardiac injury remain unknown.AIM To inv...BACKGROUND Abdominal paracentesis drainage(APD)is a safe and effective strategy for severe acute pancreatitis(SAP)patients.However,the effects of APD treatment on SAPassociated cardiac injury remain unknown.AIM To investigate the protective effects of APD on SAP-associated cardiac injury and the underlying mechanisms.METHODS SAP was induced by 5%sodium taurocholate retrograde injection in Sprague-Dawley rats.APD was performed by inserting a drainage tube with a vacuum ball into the lower right abdomen of the rats immediately after SAP induction.Morphological staining,serum amylase and inflammatory mediators,serum and ascites high mobility group box(HMGB)1,cardiac-related enzymes indexes and cardiac function,oxidative stress markers and apoptosis and associated proteins were assessed in the myocardium in SAP rats.Nicotinamide adenine dinucleotide phosphate oxidase activity and mRNA and protein expression were also examined.RESULTS APD treatment improved cardiac morphological changes,inhibited cardiac dysfunction,decreased cardiac enzymes and reduced cardiomyocyte apoptosis,proapoptotic Bax and cleaved caspase-3 protein levels.APD significantly decreased serum levels of HMGB1,inhibited nicotinamide adenine dinucleotide phosphate oxidase expression and ultimately alleviated cardiac oxidative injury.Furthermore,the activation of cardiac nicotinamide adenine dinucleotide phosphate oxidase by pancreatitis-associated ascitic fluid intraperitoneal injection was effectively inhibited by adding anti-HMGB1 neutralizing antibody in rats with mild acute pancreatitis.CONCLUSION APD treatment could exert cardioprotective effects on SAP-associated cardiac injury through suppressing HMGB1-mediated oxidative stress,which may be a novel mechanism behind the effectiveness of APD on SAP.展开更多
Neurotrophins are a family of proteins that support neuronal proliferation, survival, and differentiation in the central and peripheral nervous systems, and are regulators of neuronal plasticity. Nerve growth factor i...Neurotrophins are a family of proteins that support neuronal proliferation, survival, and differentiation in the central and peripheral nervous systems, and are regulators of neuronal plasticity. Nerve growth factor is one of the best-described neurotrophins and has advanced to clinical trials for treatment of ocular and brain diseases due to its trophic and regenerative properties. Prior trials over the past few decades have produced conflicting results, which have principally been ascribed to adverse effects of systemic nerve growth factor administration, together with poor penetrance of the blood-brain barrier that impairs drug delivery. Contrastingly, recent studies have revealed that topical ocular and intranasal nerve growth factor administration are safe and effective, suggesting that topical nerve growth factor delivery is a potential alternative to both systemic and invasive intracerebral delivery. The therapeutic effects of local nerve growth factor delivery have been extensively investigated for different ophthalmic diseases, including neurotrophic keratitis, glaucoma, retinitis pigmentosa, and dry eye disease. Further, promising pharmacologic effects were reported in an optic glioma model, which indicated that topically administered nerve growth factor diffused far beyond where it was topically applied. These findings support the therapeutic potential of delivering topical nerve growth factor preparations intranasally for acquired and degenerative brain disorders. Preliminary clinical findings in both traumatic and non-traumatic acquired brain injuries are encouraging, especially in pediatric patients, and clinical trials are ongoing. The present review will focus on the therapeutic effects of both ocular and intranasal nerve growth factor delivery for diseases of the brain and eye.展开更多
Neuroinflammation and the NACHT,LRR,and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury(TBI).Maraviroc,a ...Neuroinflammation and the NACHT,LRR,and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury(TBI).Maraviroc,a C-C chemokine receptor type 5 antagonist,has been viewed as a new therapeutic strategy for many neuroinflammatory diseases.We studied the effect of maraviroc on TBI-induced neuroinflammation.A moderate-TBI mouse model was subjected to a controlled cortical impact device.Maraviroc or vehicle was injected intraperitoneally 1 hour after TBI and then once per day for 3 consecutive days.Western blot,immunohistochemistry,and TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling)analyses were performed to evaluate the molecular mechanisms of maraviroc at 3 days post-TBI.Our results suggest that maraviroc administration reduced NACHT,LRR,and PYD domains-containing protein 3 inflammasome activation,modulated microglial polarization from M1 to M2,decreased neutrophil and macrophage infiltration,and inhibited the release of inflammatory factors after TBI.Moreover,maraviroc treatment decreased the activation of neurotoxic reactive astrocytes,which,in turn,exacerbated neuronal cell death.Additionally,we confirmed the neuroprotective effect of maraviroc using the modified neurological severity score,rotarod test,Morris water maze test,and lesion volume measurements.In summary,our findings indicate that maraviroc might be a desirable pharmacotherapeutic strategy for TBI,and C-C chemokine receptor type 5 might be a promising pharmacotherapeutic target to improve recovery after TBI.展开更多
Colon cancer is one of the most prevalent cancers globally,especially in the older age group.A large number of older patients undergoing surgery for colon cancer suffer from postoperative cognitive dysfunction(POCD).T...Colon cancer is one of the most prevalent cancers globally,especially in the older age group.A large number of older patients undergoing surgery for colon cancer suffer from postoperative cognitive dysfunction(POCD).The trial by Bu et al demonstrated that dexmedetomidine(Dex)significantly reduced the incidence of POCD compared to placebo in individuals undergoing colon cancer surgery.Additionally,better cerebral oxygenation and lower cerebral injury markers were reported with the use of Dex.The trial has some limitations,such as a single-center design and a smaller sample size,and further studies with larger patient populations and robust multi-center designs are warranted to establish these findings.展开更多
To compare liver proteolysis and proteasome activation in steatotic liver grafts conserved in University of Wisconsin (UW) and Institut Georges Lopez-1 (IGL-1) solutions.METHODSFatty liver grafts from male obese Z...To compare liver proteolysis and proteasome activation in steatotic liver grafts conserved in University of Wisconsin (UW) and Institut Georges Lopez-1 (IGL-1) solutions.METHODSFatty liver grafts from male obese Zücker rats were conserved in UW and IGL-1 solutions for 24 h at 4 °Cand subjected to “ex vivo” normo-thermic perfusion (2 h; 37 °C). Liver proteolysis in tissue specimens and perfusate was measured by reverse-phase high performance liquid chromatography. Total free amino acid release was correlated with the activation of the ubiquitin proteasome system (UPS: measured as chymotryptic-like activity and 20S and 19S proteasome), the prevention of liver injury (transaminases), mitochondrial injury (confocal microscopy) and inflammation markers (TNF 1 alpha, high mobility group box-1 (HGMB-1) and PPAR gamma), and liver apoptosis (TUNEL assay, cytochrome c and caspase 3).RESULTSProfiles of free AA (alanine, proline, leucine, isoleucine, methionine, lysine, ornithine, and threonine, among others) were similar for tissue and reperfusion effluent. In all cases, the IGL-1 solution showed a significantly higher prevention of proteolysis than UW (P < 0.05) after cold ischemia reperfusion. Livers conserved in IGL-1 presented more effective prevention of ATP-breakdown and more inhibition of UPS activity (measured as chymotryptic-like activity). In addition, the prevention of liver proteolysis and UPS activation correlated with the prevention of liver injury (AST/ALT) and mitochondrial damage (revealed by confocal microscopy findings) as well as with the prevention of inflammatory markers (TNF1alpha and HMGB) after reperfusion. In addition, the liver grafts preserved in IGL-1 showed a significant decrease in liver apoptosis, as shown by TUNEL assay and the reduction of cytochrome c, caspase 3 and P62 levels.CONCLUSIONOur comparison of these two preservation solutions suggests that IGL-1 helps to prevent ATP breakdown more effectively than UW and subsequently achieves a higher UPS inhibition and reduced liver prot展开更多
目的：总结汶川地震中群体伤患者的救治经验。方法：回顾性分析2008年5月12-31日我院收治的1348名地震伤患者临床资料。结果：所有伤员中,气管插管或气管切开61例,胸腔闭式引流101例,清创缝合674例,颅内血肿清除,碎骨清除减压41例,截肢4...目的：总结汶川地震中群体伤患者的救治经验。方法：回顾性分析2008年5月12-31日我院收治的1348名地震伤患者临床资料。结果：所有伤员中,气管插管或气管切开61例,胸腔闭式引流101例,清创缝合674例,颅内血肿清除,碎骨清除减压41例,截肢49例,清创外固定297例,骨筋膜室综合征切开减压13例,肠切除或修补13例,脾切除8例,肝修补10例,剖腹探查1例。脊柱骨折引起完全性或不全性截瘫8人。死亡45例,入院1 h内死亡30例,1-24 h内7例,〉24 h 8例。死亡原因：失血性或/和创伤性休克29例,特重型颅脑伤14例、多器官功能衰竭2例。结论：在地震群体伤的救治中,有三大原则对于提高救治率至关重要：首先,迅速检查、快速诊断和分诊是提高大规模群体伤救治率的关键,早期诊断应以查体、诊断性穿刺和胸部X线、B超检查为主,迅速查明并紧急处理危及生命的伤情,防止漏诊误诊;其次,重视休克复苏和多发伤的处理、防治ARDS、骨筋膜室综合征、继发感染等并发症、防治交叉感染和疫情发生是降低死亡率的关键。第三,按战时前线军队医院管理模式,向周边医院转移患者。展开更多
Objective: To study the correlation of serum HMGB1 and sTLT-1 contents with oxidative stress response and endothelial injury in patients with ischemic stroke. Methods: The patients who were diagnosed with ischemic str...Objective: To study the correlation of serum HMGB1 and sTLT-1 contents with oxidative stress response and endothelial injury in patients with ischemic stroke. Methods: The patients who were diagnosed with ischemic stroke in Zhouzhi County People's Hospital between February 2015 and March 2017 were selected as the stroke group of the study, and healthy subjects who received physical examination during the same period were selected as the control group of the study. Serum was collected to determine the contents of HMGB1, sTLT-1, oxidative stress reaction molecules and endothelial injury molecules. Results: Serum HMGB1, sTLT-1, vWF, vWF-cp, sTM, ET-1, D-D, 8-OHdG, LPO and NOS contents of stroke group were significantly higher than those of control group while T-SOD and GSH-Px contents were significantly lower than those of control group;serum T-SOD and GSH-Px contents of stroke patients with high HMBG-1 content were significantly lower than those of stroke patients with low HMBG-1 content while 8-OHdG, LPO and NOS contents were significantly higher than those of stroke patients with low HMBG-1 content;serum vWF, vWF-cp, sTM, ET-1 and D-D contents of stroke patients with high sTLT-1 content were significantly higher than those of stroke patients with low sTLT-1 content. Conclusion: The abnormally elevated HMGB1 and sTLT-1 in serum of patients with ischemic stroke can induce oxidative stress response and aggravate endothelial injury.展开更多
基金funded by the New Xiangya Talent Project of the Third Xiangya Hospital of Central South University(No.20150218)Program for New Century Excellent Talents in University(NCET-13-0605)+1 种基金the National Natural Science Foundation of China(No.81102512)Hunan Provincial Natural Science Foundation of China(No.14JJ7001)
文摘High mobility group box 1 (HMGB1) is a nuclear protein that can bind to DNA and act as a co-factor for gene transcription. When released into extracellular fluid, it plays a proinflammatory role by acting as a damage-associated molecular pattern molecule (DAMP) (also known as an alarmin) to initiate innate immune responses by activating multiple cell surface receptors such as the receptor for advanced glycation end-products (RAGE) and toll-like receptors (TLRs), TLR2, TLR4 or TLR9. This proinflammatory role is now considered to be important in the pathogenesis of a wide range of kidney diseases whether they result from hemodynamic changes, renal tubular epithelial cell apoptosis, kidney tissue fibrosis or inflammation. This review summarizes our current understanding of the role of HMGB1 in kidney diseases and how the HMGB1-mediated signaling pathway may constitute a new strategy for the treatment of kidney diseases. (C) 2016 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
基金funded by the National Natural Science Foundation of China(Nos.81673658,81274165 and 30925042)Ministry of Science and Technology of China(No.2018ZX09735003-002)the Science and Technology Commission of Shanghai Municipality(No.12JC1400800)
文摘Bupleurum polysaccharides(BPs)is isolated from Bupleurum smithii var.parvifolium,a key traditional Chinese medicine.The study was to investigate the effects of BPs on diabetic kidney injury.After two intraperitoneal injections of streptozotozin(STZ)100 mg·kg^–1,renal injury in diabetic mice was induced and BPs was orally administrated at dosages of 30 and 60 mg·kg^–1·d^–1.The STZ injected mice developed renal function damage,renal inflammation and fibrosis known as diabetic kidney disease(DKD).BPs significantly reduced serum creatinine level and urinary albumin excretion rate,with the attenuated swelling of kidneys.BPs treatment obviously alleviated the pathological damage of renal tissue.The progression of renal injury in BPs treated mice was inhibited with less expression of type IV collagen(Col IV),fibronectin(FN)andα-smooth muscle actin(α-SMA).The inhibition of inflammation in kidney was associated with the reduced level of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6).BPs administration suppressed the over-expression of toll like receptor 4(TLR4)and high-mobility group box 1(HMGB1)with lowered activity of nuclear factor kappa B(NF-κB)in renal tissue of diabetic mice.Oral administration of BPs effectively prevented the development of renal injury in diabetic mice.This study suggested that the protection provided by BPs might affect through the interruption of HMGB1-TLR4 pathway,leading to the inhibition of renal inflammation and fibrotic process.
基金Supported by National Natural Science Foundation of China,No.81772001National Clinical Key Subject of China,No.41792113Technology Plan Program of Sichuan Provence,No.2015SZ0229,No.2016HH0067,No.2018JY0041and No.2019YJ0277
文摘BACKGROUND Abdominal paracentesis drainage(APD)is a safe and effective strategy for severe acute pancreatitis(SAP)patients.However,the effects of APD treatment on SAPassociated cardiac injury remain unknown.AIM To investigate the protective effects of APD on SAP-associated cardiac injury and the underlying mechanisms.METHODS SAP was induced by 5%sodium taurocholate retrograde injection in Sprague-Dawley rats.APD was performed by inserting a drainage tube with a vacuum ball into the lower right abdomen of the rats immediately after SAP induction.Morphological staining,serum amylase and inflammatory mediators,serum and ascites high mobility group box(HMGB)1,cardiac-related enzymes indexes and cardiac function,oxidative stress markers and apoptosis and associated proteins were assessed in the myocardium in SAP rats.Nicotinamide adenine dinucleotide phosphate oxidase activity and mRNA and protein expression were also examined.RESULTS APD treatment improved cardiac morphological changes,inhibited cardiac dysfunction,decreased cardiac enzymes and reduced cardiomyocyte apoptosis,proapoptotic Bax and cleaved caspase-3 protein levels.APD significantly decreased serum levels of HMGB1,inhibited nicotinamide adenine dinucleotide phosphate oxidase expression and ultimately alleviated cardiac oxidative injury.Furthermore,the activation of cardiac nicotinamide adenine dinucleotide phosphate oxidase by pancreatitis-associated ascitic fluid intraperitoneal injection was effectively inhibited by adding anti-HMGB1 neutralizing antibody in rats with mild acute pancreatitis.CONCLUSION APD treatment could exert cardioprotective effects on SAP-associated cardiac injury through suppressing HMGB1-mediated oxidative stress,which may be a novel mechanism behind the effectiveness of APD on SAP.
文摘Neurotrophins are a family of proteins that support neuronal proliferation, survival, and differentiation in the central and peripheral nervous systems, and are regulators of neuronal plasticity. Nerve growth factor is one of the best-described neurotrophins and has advanced to clinical trials for treatment of ocular and brain diseases due to its trophic and regenerative properties. Prior trials over the past few decades have produced conflicting results, which have principally been ascribed to adverse effects of systemic nerve growth factor administration, together with poor penetrance of the blood-brain barrier that impairs drug delivery. Contrastingly, recent studies have revealed that topical ocular and intranasal nerve growth factor administration are safe and effective, suggesting that topical nerve growth factor delivery is a potential alternative to both systemic and invasive intracerebral delivery. The therapeutic effects of local nerve growth factor delivery have been extensively investigated for different ophthalmic diseases, including neurotrophic keratitis, glaucoma, retinitis pigmentosa, and dry eye disease. Further, promising pharmacologic effects were reported in an optic glioma model, which indicated that topically administered nerve growth factor diffused far beyond where it was topically applied. These findings support the therapeutic potential of delivering topical nerve growth factor preparations intranasally for acquired and degenerative brain disorders. Preliminary clinical findings in both traumatic and non-traumatic acquired brain injuries are encouraging, especially in pediatric patients, and clinical trials are ongoing. The present review will focus on the therapeutic effects of both ocular and intranasal nerve growth factor delivery for diseases of the brain and eye.
基金supported by grants from the National Natural Science Foundation of China, Nos. 81930031 (to JNZ), 81720108015 (to JNZ), 81901525 (to SZ), 82101440 (to DDS), 81801234 (to YZ) and 82071389 (to GLY)the Natural Science Foundation of Tianjin, Nos. 20JCQNJC01270 (to JWW), 20JCQNJC00460 (to GLY), 18JCQNJC81000 (to HTR)+4 种基金Scientific Research Project of Tianjin Education Commission (Natural Science), No. 2018KJ052 (to ZWZ)Tianjin Health and Health Committee Science and Technology Project, No. QN20015 (to JWW)the Science & Technology Development Fund of Tianjin Education Commission for Higher Education, No. 2016YD02 (to YW)Tianjin Key Science and Technology Projects of Innovative Drugs and Medical Devices, No. 19ZXYXSY00070 (to YW)the Clinical Research Fundation of Tianjin Medical University, No. 2018kylc002 (to YW)
文摘Neuroinflammation and the NACHT,LRR,and PYD domains-containing protein 3 inflammasome play crucial roles in secondary tissue damage following an initial insult in patients with traumatic brain injury(TBI).Maraviroc,a C-C chemokine receptor type 5 antagonist,has been viewed as a new therapeutic strategy for many neuroinflammatory diseases.We studied the effect of maraviroc on TBI-induced neuroinflammation.A moderate-TBI mouse model was subjected to a controlled cortical impact device.Maraviroc or vehicle was injected intraperitoneally 1 hour after TBI and then once per day for 3 consecutive days.Western blot,immunohistochemistry,and TUNEL(terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling)analyses were performed to evaluate the molecular mechanisms of maraviroc at 3 days post-TBI.Our results suggest that maraviroc administration reduced NACHT,LRR,and PYD domains-containing protein 3 inflammasome activation,modulated microglial polarization from M1 to M2,decreased neutrophil and macrophage infiltration,and inhibited the release of inflammatory factors after TBI.Moreover,maraviroc treatment decreased the activation of neurotoxic reactive astrocytes,which,in turn,exacerbated neuronal cell death.Additionally,we confirmed the neuroprotective effect of maraviroc using the modified neurological severity score,rotarod test,Morris water maze test,and lesion volume measurements.In summary,our findings indicate that maraviroc might be a desirable pharmacotherapeutic strategy for TBI,and C-C chemokine receptor type 5 might be a promising pharmacotherapeutic target to improve recovery after TBI.
文摘Colon cancer is one of the most prevalent cancers globally,especially in the older age group.A large number of older patients undergoing surgery for colon cancer suffer from postoperative cognitive dysfunction(POCD).The trial by Bu et al demonstrated that dexmedetomidine(Dex)significantly reduced the incidence of POCD compared to placebo in individuals undergoing colon cancer surgery.Additionally,better cerebral oxygenation and lower cerebral injury markers were reported with the use of Dex.The trial has some limitations,such as a single-center design and a smaller sample size,and further studies with larger patient populations and robust multi-center designs are warranted to establish these findings.
基金Supported by Instituto de Salud Carlos III(ISCIII)through the FIS project PI12/0056,co-funded by FEDER from Regional Development European Funds(European Union)
文摘To compare liver proteolysis and proteasome activation in steatotic liver grafts conserved in University of Wisconsin (UW) and Institut Georges Lopez-1 (IGL-1) solutions.METHODSFatty liver grafts from male obese Zücker rats were conserved in UW and IGL-1 solutions for 24 h at 4 °Cand subjected to “ex vivo” normo-thermic perfusion (2 h; 37 °C). Liver proteolysis in tissue specimens and perfusate was measured by reverse-phase high performance liquid chromatography. Total free amino acid release was correlated with the activation of the ubiquitin proteasome system (UPS: measured as chymotryptic-like activity and 20S and 19S proteasome), the prevention of liver injury (transaminases), mitochondrial injury (confocal microscopy) and inflammation markers (TNF 1 alpha, high mobility group box-1 (HGMB-1) and PPAR gamma), and liver apoptosis (TUNEL assay, cytochrome c and caspase 3).RESULTSProfiles of free AA (alanine, proline, leucine, isoleucine, methionine, lysine, ornithine, and threonine, among others) were similar for tissue and reperfusion effluent. In all cases, the IGL-1 solution showed a significantly higher prevention of proteolysis than UW (P < 0.05) after cold ischemia reperfusion. Livers conserved in IGL-1 presented more effective prevention of ATP-breakdown and more inhibition of UPS activity (measured as chymotryptic-like activity). In addition, the prevention of liver proteolysis and UPS activation correlated with the prevention of liver injury (AST/ALT) and mitochondrial damage (revealed by confocal microscopy findings) as well as with the prevention of inflammatory markers (TNF1alpha and HMGB) after reperfusion. In addition, the liver grafts preserved in IGL-1 showed a significant decrease in liver apoptosis, as shown by TUNEL assay and the reduction of cytochrome c, caspase 3 and P62 levels.CONCLUSIONOur comparison of these two preservation solutions suggests that IGL-1 helps to prevent ATP breakdown more effectively than UW and subsequently achieves a higher UPS inhibition and reduced liver prot
文摘目的：总结汶川地震中群体伤患者的救治经验。方法：回顾性分析2008年5月12-31日我院收治的1348名地震伤患者临床资料。结果：所有伤员中,气管插管或气管切开61例,胸腔闭式引流101例,清创缝合674例,颅内血肿清除,碎骨清除减压41例,截肢49例,清创外固定297例,骨筋膜室综合征切开减压13例,肠切除或修补13例,脾切除8例,肝修补10例,剖腹探查1例。脊柱骨折引起完全性或不全性截瘫8人。死亡45例,入院1 h内死亡30例,1-24 h内7例,〉24 h 8例。死亡原因：失血性或/和创伤性休克29例,特重型颅脑伤14例、多器官功能衰竭2例。结论：在地震群体伤的救治中,有三大原则对于提高救治率至关重要：首先,迅速检查、快速诊断和分诊是提高大规模群体伤救治率的关键,早期诊断应以查体、诊断性穿刺和胸部X线、B超检查为主,迅速查明并紧急处理危及生命的伤情,防止漏诊误诊;其次,重视休克复苏和多发伤的处理、防治ARDS、骨筋膜室综合征、继发感染等并发症、防治交叉感染和疫情发生是降低死亡率的关键。第三,按战时前线军队医院管理模式,向周边医院转移患者。
文摘Objective: To study the correlation of serum HMGB1 and sTLT-1 contents with oxidative stress response and endothelial injury in patients with ischemic stroke. Methods: The patients who were diagnosed with ischemic stroke in Zhouzhi County People's Hospital between February 2015 and March 2017 were selected as the stroke group of the study, and healthy subjects who received physical examination during the same period were selected as the control group of the study. Serum was collected to determine the contents of HMGB1, sTLT-1, oxidative stress reaction molecules and endothelial injury molecules. Results: Serum HMGB1, sTLT-1, vWF, vWF-cp, sTM, ET-1, D-D, 8-OHdG, LPO and NOS contents of stroke group were significantly higher than those of control group while T-SOD and GSH-Px contents were significantly lower than those of control group;serum T-SOD and GSH-Px contents of stroke patients with high HMBG-1 content were significantly lower than those of stroke patients with low HMBG-1 content while 8-OHdG, LPO and NOS contents were significantly higher than those of stroke patients with low HMBG-1 content;serum vWF, vWF-cp, sTM, ET-1 and D-D contents of stroke patients with high sTLT-1 content were significantly higher than those of stroke patients with low sTLT-1 content. Conclusion: The abnormally elevated HMGB1 and sTLT-1 in serum of patients with ischemic stroke can induce oxidative stress response and aggravate endothelial injury.
