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Evans syndrome following influenza A presenting with diffuse alveolar hemorrhage managed with extracorporeal membrane oxygenation 认领 引用
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作者 Haotian Lu Anke Shi +3 位作者 Jieqiong Yu Jing Zhao Guoqiang Zhang Shengtao Yan 《World Journal of Emergency Medicine》 SCIE CAS CSCD 2026年第4期382-384,共3页
Diffuse alveolar hemorrhage(DAH)is a lifethreatening clinical condition characterized by bleeding into alveolar spaces,resulting in diffuse pulmonary infiltrates,hemoptysis,and hypoxemic respiratory failure.The etiolo... Diffuse alveolar hemorrhage(DAH)is a lifethreatening clinical condition characterized by bleeding into alveolar spaces,resulting in diffuse pulmonary infiltrates,hemoptysis,and hypoxemic respiratory failure.The etiologies of DAH include,but are not limited to,hematologic abnormalities(e.g.,thrombocytopenia and coagulopathies),autoimmune diseases(e.g.,vasculitis and systemic lupus erythematosus),and toxic or drug-induced lung injury. 展开更多
关键词 Diffuse alveolar hemorrhage diffuse alveolar hemorrhage dah hypoxemic respiratory failurethe systemic lupus erythematosus bleeding alveolar spacesresulting diffuse pulmonary infiltrateshemoptysisand Extracorporeal membrane oxygenation Evans syndrome
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Bromodomain-containing protein 4 knockdown promotes neuronal ferroptosis in a mouse model of subarachnoid hemorrhage 认领 引用 被引量：3
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作者 Peng Lu Fan Zhang +8 位作者 Lei Yang Yijing He Xi Kong Kecheng Guo Yuke Xie Huangfan Xie Bingqing Xie Yong Jiang Jianhua Peng 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第2期715-729,共15页
Neuronal cell death is a common outcome of multiple pathophysiological processes and a key factor in neurological dysfunction after subarachnoid hemorrhage.Neuronal ferroptosis in particular plays an important role in... Neuronal cell death is a common outcome of multiple pathophysiological processes and a key factor in neurological dysfunction after subarachnoid hemorrhage.Neuronal ferroptosis in particular plays an important role in early brain injury.Bromodomain-containing protein 4,a member of the bromo and extraterminal domain family of proteins,participated in multiple cell death pathways,but the mechanisms by which it regulates ferroptosis remain unclear.The primary aim of this study was to investigate how bromodomain-containing protein 4 affects neuronal ferroptosis following subarachnoid hemorrhage in vivo and in vitro.Our findings revealed that endogenous bromodomain-containing protein 4 co-localized with neurons,and its expression was decreased 48 hours after subarachnoid hemorrhage of the cerebral cortex in vivo.In addition,ferroptosis-related pathways were activated in vivo and in vitro after subarachnoid hemorrhage.Targeted inhibition of bromodomain-containing protein 4 in neurons increased lipid peroxidation and intracellular ferrous iron accumulation via ferritinophagy and ultimately led to neuronal ferroptosis.Using cleavage under targets and tagmentation analysis,we found that bromodomain-containing protein 4 enrichment in the Raf-1 promoter region decreased following oxyhemoglobin stimulation in vitro.Furthermore,treating bromodomain-containing protein 4-knockdown HT-22 cell lines with GW5074,a Raf-1 inhibitor,exacerbated neuronal ferroptosis by suppressing the Raf-1/ERK1/2 signaling pathway.Moreover,targeted inhibition of neuronal bromodomain-containing protein 4 exacerbated early and long-term neurological function deficits after subarachnoid hemorrhage.Our findings suggest that bromodomain-containing protein 4 may have neuroprotective effects after subarachnoid hemorrhage,and that inhibiting ferroptosis could help treat subarachnoid hemorrhage. 展开更多
关键词 bromodomain-containing protein 4 cell death early brain injury ferritinophagy ferroptosis neurological deficits neuron oxidative stress RAF proto-oncogene serinehreonine-protein kinase(Raf-1) subarachnoid hemorrhage
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Mitophagy alleviates neuronal damage after subarachnoid hemorrhage:Role of autophagy-targeting chimera 4 认领 引用 被引量：1
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作者 Yongzhi Zhang Jianqiao Li +5 位作者 Qi Sun Peichun Zhou Pei Wu Zhiyong Ji Yuchen Li Huaizhang Shi 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第9期4331-4341,共11页
This study investigated the role of autophagy-targeting chimera 4,a novel activator of autophagy that targets mitochondria,in a subarachnoid hemorrhage model.The data demonstrated that in an in vitro mitochondrial dam... This study investigated the role of autophagy-targeting chimera 4,a novel activator of autophagy that targets mitochondria,in a subarachnoid hemorrhage model.The data demonstrated that in an in vitro mitochondrial damage model,autophagy-targeting chimera 4 reversed carbonyl cyanide 3-chlorophenylhydrazone-induced mitochondrial membrane potential collapse and activated mitophagy.In the in vitro subarachnoid hemorrhage model,autophagy-targeting chimera 4 improved neuronal proliferation and migration during the acute phase and reduced neuronal apoptosis after subarachnoid hemorrhage.In the in vivo subarachnoid hemorrhage model,autophagy-targeting chimera 4 also decreased neuronal apoptosis during the acute phase,improved neurological function,and ultimately reduced long-term neuronal loss.Additionally,increased ring finger protein 144B expression after subarachnoid hemorrhage was associated with poor prognosis,and autophagy-targeting chimera 4 significantly inhibited ring finger protein 144B expression,thereby activating mitophagy and reducing neuronal apoptosis.The results also showed that the mitophagic marker parkin did not exert protective effects during the acute phase after subarachnoid hemorrhage and might be inhibited by ring finger protein 144B.Moreover,parkin inhibition did not interfere with the mitophagic or apoptotic effects of autophagy-targeting chimera 4.These findings not only confirm that autophagy-targeting chimera 4 exerts neuroprotective effects by targeting mitophagy after subarachnoid hemorrhage,but also demonstrate competitive inhibition between ring finger protein 144B and parkin,leading to poor prognosis in the acute phase after subarachnoid hemorrhage. 展开更多
关键词 apoptosis autophagy brain injury mitochondrial membrane potential mitochondrion mitophagy neurons stroke subarachnoid hemorrhage ubiquitin
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MDM2-GPX4-ferroptosis regulatory axis exerts neurotoxic effects in intracerebral hemorrhage 认领 引用 被引量：1
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作者 Yunhu Yu Tao Liu +4 位作者 Yunpeng Cai Yuanmei Song Hang Zhou Fang Cao Rongcai Jiang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3063-3072,共10页
Ferroptosis plays a key role in nerve injury in intracerebral hemorrhage and is associated with the upregulation of murine double minute 2.Investigating the mechanism underlying murine double minute 2-related ferropto... Ferroptosis plays a key role in nerve injury in intracerebral hemorrhage and is associated with the upregulation of murine double minute 2.Investigating the mechanism underlying murine double minute 2-related ferroptosis could help identify new therapies for intracerebral hemorrhage.An in vitro intracerebral hemorrhage model was established by treating BV2 microglial cells with oxygen-glucose deprivation combined with hemin.The role of murine double minute 2 in regulating ferroptosis was investigated via transduction with RNA interference and lentivirus overexpression.Furthermore,intracerebral hemorrhage mouse models were constructed with and without an murine double minute 2 inhibitor(brigimadlin),and behavioral assays were performed to assess the learning ability and cognitive function.Murine double minute 2 dysregulation was associated with oxygen-glucose deprivation combined with hemin-induced BV2 microglial cell ferroptosis and M1/M2 polarization.The results suggested that murine double minute 2 induced glutathione peroxidase 4 ubiquitination and degradation to regulate ferroptosis and inflammatory responses in BV2 microglial cells.Mechanistically,Wilms tumor 1-associated protein induced murine double minute 2 N6-methyladenosine(m6A)modification and regulated ferroptosis and inflammatory responses.In vivo analysis showed that brigimadlin improved neurological deficits and spatial memory in mice with intracerebral hemorrhage.In summary,the results indicate that Wilms tumor 1-associated protein regulates murine double minute 2 m6A modification,and murine double minute 2 induces glutathione peroxidase 4 ubiquitination and degradation.This regulation promotes ferroptosis and inflammatory responses in oxygen-glucose deprivation combined with hemin-induced BV2 microglial cells,suggesting that the murine double minute 2-glutathione peroxidase 4-ferroptosis regulatory axis exerts neurotoxic effects.These findings identify glutathione peroxidase 4 as a potential gene therapy target for intracerebral hemorrhage-related brain injury. 展开更多
关键词 ferroptosis glutathione peroxidase 4 intracerebral hemorrhage m6A murine double minute 2 ubiquitination
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Lactate alleviates early brain damage after subarachnoid hemorrhage:Regulation of lipid metabolism 认领 引用 被引量：1
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作者 Zichen Zhang Xinan Li +9 位作者 Xiaoli Liu Lei Chen Yunzhi Wang Enyan Jiang Jia Zeng Xiaojian Zhang Zhen Fang Zibin Liang Jikai Wang Fei Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3046-3054,共9页
This study investigated the neuroprotective effects of lactate in subarachnoid hemorrhage,a severe cerebrovascular disease that is commonly caused by arterial aneurysm rupture and has limited early treatment options.L... This study investigated the neuroprotective effects of lactate in subarachnoid hemorrhage,a severe cerebrovascular disease that is commonly caused by arterial aneurysm rupture and has limited early treatment options.Lactate,a metabolic byproduct,has been shown to have neuroprotective properties,including enhancing cerebral microcirculation and reducing intracranial pressure in acute brain injury patients.However,the protective mechanisms of lactate in subarachnoid hemorrhage remain unknown.In this study,we showed that lactate alleviates early brain damage in subarachnoid hemorrhage by promoting neuronal lipid synthesis and the formation of lipid droplets in astrocytes.In vivo experiments using a subarachnoid hemorrhage mouse model showed that lactate treatment significantly improved neurological scores,reduced brain inflammation,and promoted lipid droplet formation in astrocytes within 24 hours.Lactate treatment increased free fatty acids levels in the brain.The results suggest that astrocytes absorbed these free fatty acids and converted them into lipid droplets,thus reducing cellular lipotoxicity.Moreover,lactate enhanced the antiapoptotic capacity of astrocytes by upregulating the expression of PLIN5,a protein crucial for lipid droplet formation.The inhibition of lipid synthesis or lipid droplet formation counteracted the neuroprotective effects of lactate,indicating that lactate’s protective role is closely linked to lipid metabolism and lipid droplet formation.In vitro experiments on HT22 neuronal cells exposed to hemin-an agent used to simulate subarachnoid hemorrhage injury-demonstrated that lactate mitigated cellular damage by reducing lipid peroxidation and preserving mitochondrial membrane potential.Lactate treatment in HT22 cells and astrocytes also showed that inhibition of lipid synthesis or lipid droplet formation reversed its protective effects,further emphasizing the importance of lipid metabolism in the neuroprotective action of lactate.This study provides insights into the neuroprotective mechanisms of lactate in subarachnoid hemorrhage.It indicates that lactate plays a role in promoting lipid synthesis in neurons and enhancing lipid droplet formation in astrocytes,thus mitigating brain damage and improving cell survival.These findings suggest that lactate,through its regulation of lipid metabolism,could be a potential therapeutic agent for subarachnoid hemorrhage. 展开更多
关键词 apoptosis astrocytes free fatty acids lactate lipid droplets lipid metabolism neuronal lipid synthesis neuroprotection PLIN5 subarachnoid hemorrhage
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Intranasal pterostilbene nanoparticles delivery alleviates neuroinflammation and brain injury after intracerebral hemorrhage 认领 引用
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作者 Zhongxin Duan Yue Wang +8 位作者 Yunchu Zhang Xia Liu Wanyu Wang Hua Li Qingyang Lu Chao You Yongzhong Cheng Cong Wu Xiang Gao 《Chinese Chemical Letters》 SCIE CAS CSCD 2026年第5期433-437,共5页
Intracerebral hemorrhage(ICH)is a devastating subtype of stroke with high mortality and poor prognosis among survivors.Neuroinflammation after ICH plays a critical role in both secondary brain injury and repair.In the... Intracerebral hemorrhage(ICH)is a devastating subtype of stroke with high mortality and poor prognosis among survivors.Neuroinflammation after ICH plays a critical role in both secondary brain injury and repair.In the early stages of ICH,excessive activation of microglia triggers pro-inflammation,leading to the release of various pro-inflammatory cytokines that exacerbate neuronal damage and worsen neurological deficits.Pterostilbene(PTE),a natural polyphenol with potent anti-inflammatory and antioxidant properties,is an ideal neuroprotective agent.However,its clinical application is limited by poor bioavailability and low blood-brain barrier(BBB)penetrability following oral administration.Here,we developed PTE-loaded methoxy poly(ethylene glycol)-poly(ε-caprolactone)(m PEG-PCL)nanoparticles(PTE-NPs)to enhance the bioavailability of PTE and performed an intranasal delivery strategy for non-invasive and efficient transport to the ICH lesion.PTE-NPs significantly suppressed pro-inflammatory microglia activation and cytokine release,thereby reducing inflammation-mediated neuronal damage in the peri–hematomal region.In the two ICH mouse models,PTE-NPs demonstrated significant therapeutic efficacy in improving neurological function with good biosafety.This study provides a potential therapeutic strategy for the treatment of ICH and its future clinical translation. 展开更多
关键词 Nanoparticles Blood-brain barriers penetrability Intranasal delivery Intracerebral hemorrhage Neuroinflammation
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Severe hemorrhage of the colorectum after heart transplantation:a case report 认领 引用
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作者 Zhiyuan Zhu Jie Huang +5 位作者 Zhongkai Liao Xiaofeng Zhuang Jianfen Li Xuejing Duan Ru Liu Sheng Liu 《World Journal of Emergency Medicine》 SCIE CAS CSCD 2026年第3期284-287,共4页
Approximately 6,000 heart transplantations were performed worldwide in 2023.[1]However,posttransplant graft rejection and infections remain major factors limiting long-term survival.Immunosuppressed recipients are par... Approximately 6,000 heart transplantations were performed worldwide in 2023.[1]However,posttransplant graft rejection and infections remain major factors limiting long-term survival.Immunosuppressed recipients are particularly vulnerable to cytomegalovirus(CMV)infection,either from primary infection or reactivation. 展开更多
关键词 heart transplantations colorectum cytomegalovirus infection immunosuppressed recipients severe hemorrhage
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Subsequent Pregnancy Outcomes After Conservative Treatment of Postpartum Hemorrhage Following Cesarean Delivery 认领 引用
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作者 Xiao-xian Qu Wen-ting Zhou +2 位作者 Mark Landon Kara Rood Xiao-hua Liu 《Current Medical Science》 SCIE CAS CSCD 2026年第2期417-423,共7页
Objective This study aimed to investigate pregnancy outcomes after conservative treatment for severe postpartum hemorrhage(PPH)following cesarean delivery(CD).Methods A total of 9,366 women who underwent CD for two co... Objective This study aimed to investigate pregnancy outcomes after conservative treatment for severe postpartum hemorrhage(PPH)following cesarean delivery(CD).Methods A total of 9,366 women who underwent CD for two consecutive pregnancies were included.Bakri balloon tamponade was employed in 87 women,and compression sutures were used in 87 women to control PPH during the first CD.The subsequent pregnancy outcomes and operative findings during the second CD were compared among the groups.Results The preterm delivery rate was 3.2%in the control group,12.6%in the Bakri group,and 11.5%in the compression suture group(P<0.001).The rates of placenta accreta(1.4%vs.1.3%vs.5.3%,P=0.017),PPH(0.9%vs.3.9%vs.8.0%,P<0.001),and pelvic adhesions(5.2%vs.6.5%vs.13.3%,P=0.004)were significantly greater in the compression suture group.After adjustment,conservative treatment increased the rate of preterm birth in subsequent pregnancies threefold.A compression suture increased the risk of placenta accreta by four fold and the incidence of pelvic adhesions by more than two fold in subsequent CD.Conclusions Conservative treatment for PPH following CD is associated with an increased risk of subsequent preterm birth.Women receiving compression sutures have an increased risk of placenta accreta and pelvic adhesions in subsequent pregnancies. 展开更多
关键词 Postpartum hemorrhage Cesarean section Bakri balloon tamponade Uterine compression suture Placenta accreta Pregnancy outcome Subsequent pregnancy
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Tumor necrosis factor-α-stimulated gene 6 promotes hematoma clearance after intracerebral hemorrhage in a mouse model 认领 引用
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作者 Xia Liu Dabao Yao +11 位作者 Yunjie Li Shiling Chen Yingxin Tang Jingyi Wang Jingfei Yang Jie Jing Jiahui Wang Ge Zhang Luwei Nie Yangyang Feng Gaigai Li Zhouping Tang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3629-3640,共12页
The prognosis for patients who experience intracerebral hemorrhage is poor because of a lack of effective treatments.Tumor necrosis factor-α-stimulated gene 6(TSG6)is a secreted glycoprotein that exerts anti-inflamma... The prognosis for patients who experience intracerebral hemorrhage is poor because of a lack of effective treatments.Tumor necrosis factor-α-stimulated gene 6(TSG6)is a secreted glycoprotein that exerts anti-inflammatory effects in various inflammatory diseases.We previously showed that adipose-derived stem cells can inhibit inflammation by upregulating TSG6 secretion in an in vitro model of intracerebral hemorrhage.However,the direct effects of TSG6 on hematoma clearance in vivo remain largely unknown.The aim of this study was to determine how TSG6 affects hematoma absorption in mice subjected to intracerebral hemorrhage and to explore the potential underlying mechanisms.We first analyzed the gene profiles of patients with intracerebral hemorrhage from the GEO database and examined changes in TSG6 expression in the brain tissues of mice subjected to intracerebral hemorrhage.We found that TSG6 expression exhibited a transient increase following intracerebral hemorrhage,and that there was a negative correlation between the initial hematoma volume and TSG6 levels.Immunofluorescence analysis showed that TSG6 was primarily expressed in microglia and macrophages.Furthermore,we found that TSG6 promoted functional recovery in mice subjected to intracerebral hemorrhage by accelerating hematoma clearance,reducing the number of apoptotic cells and degenerated neurons,increasing the proportion of phagocytic microglia/macrophages,and decreasing iron deposition.Western blotting and immunofluorescence analysis indicated that TSG6 promoted M2 polarization of microglia/macrophages.In vitro phagocytosis experiments confirmed that TSG6 enhanced the ability of microglia to phagocytize red blood cells.Finally,we identified the signal transducer and activator of transcription 6/growth arrest-specific protein 6 signaling pathway as playing a critical role in TSG6-mediated hematoma absorption.In summary,our results demonstrate an essential role for TSG6 in promoting hematoma absorption in a mouse model of intracerebral hemorrhage.These findings suggest that TSG6 accelerates hematoma clearance and improves neurological function by promoting microglia/macrophage polarization to the M2 phenotype,activating the STAT6/GAS6 signaling pathway,and increasing phagocytic receptor expression on the surface of phagocytes,thereby enhancing their ability to phagocytize red blood cells. 展开更多
关键词 apoptosis growth arrest-specific protein 6 hematoma absorption inflammation intracerebral hemorrhage iron deposition microglia/macrophages polarization signal transducer and activator of transcription 6 tumor necrosis factor-α-stimulated gene 6
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Phosphodiesterase 4 regulates pyroptosis in subarachnoid hemorrhage 认领 引用
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作者 Jiahe Tan Yinrui Ma +3 位作者 Rui Song Hongjiang Ye Jun Su Zhaohui He 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2609-2620,共12页
Phosphodiesterase 4 is a key enzyme involved in the regulation of cell signal transduction,but its role in subarachnoid hemorrhage remains unclear.Neuronal pyroptosis has been reported to be involved in early brain in... Phosphodiesterase 4 is a key enzyme involved in the regulation of cell signal transduction,but its role in subarachnoid hemorrhage remains unclear.Neuronal pyroptosis has been reported to be involved in early brain injury after subarachnoid hemorrhage.This study aimed to investigate whether phosphodiesterase 4 contributes to early brain injury after subarachnoid hemorrhage by mediating neuronal pyroptosis and its related mechanisms.Endovascular perforation of male C57BL/6J mice was performed to model subarachnoid hemorrhage in vivo,and oxyhemoglobin was added to the culture medium of primary neurons to model subarachnoid hemorrhage in vitro.A phosphodiesterase 4-specific inhibitor,etazolate,was intraperitoneally injected 30 minutes after subarachnoid hemorrhage induction.Small interfering RNA(siRNA)was administered intracerebroventricularly 72 hours before subarachnoid hemorrhage to achieve genetic knockdown of phosphodiesterase 4.To investigate the mechanism,a nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3(NLRP3)-specific agonist,nigericin,was intracerebroventricularly injected 60 minutes before subarachnoid hemorrhage.Neuronal phosphodiesterase 4 expression increased after subarachnoid hemorrhage and reached the highest point at 24 hours.Etazolate treatment reduced neurological deficits and brain edema in mice,alleviated neuronal pyroptosis and inflammatory response,and improved neuronal injury.Treatment with phosphodiesterase 4 siRNA had the same neuroprotective effects as etazolate.Mechanistically,phosphodiesterase 4 triggered the nuclear factor kappa-B pathway,and simultaneously caused lysosomal and mitochondrial dysfunction after subarachnoid hemorrhage,which promoted NLRP3 inflammasome activation and induced neuronal pyroptosis.Blocking of phosphodiesterase 4 inhibited the nuclear factor kappa-B pathway,and improved lysosome and mitochondrial function.Activation of NLRP3 reversed the neuroprotective effects of etazolate without affecting phosphodiesterase 4 expression.Together,the results indicate that phosphodiesterase 4 regulates NLRP3-mediated neuronal pyroptosis in early brain injury after subarachnoid hemorrhage.Phosphodiesterase 4 may be a potential therapeutic molecular target for subarachnoid hemorrhage. 展开更多
关键词 early brain injury etazolate lysosome function mitochondrial function neuron nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3(NLRP3) nuclear factor kappa-B phosphodiesterase 4 pyroptosis subarachnoid hemorrhage
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NLRP3 inflammasome and gut microbiota–brain axis:A new perspective on white matter injury after intracerebral hemorrhage 认领 引用 被引量：4
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作者 Xiaoxi Cai Xinhong Cai +4 位作者 Quanhua Xie Xueqi Xiao Tong Li Tian Zhou Haitao Sun 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第1期62-80,共19页
Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have rev... Intracerebral hemorrhage is the most dangerous subtype of stroke,characterized by high mortality and morbidity rates,and frequently leads to significant secondary white matter injury.In recent decades,studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis.This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury.The NACHT,LRR,and pyrin domain-containing protein 3(NLRP3)inflammasome plays a crucial role in this context.This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome.These mechanisms include metabolic pathways(involving short-chain fatty acids,lipopolysaccharides,lactic acid,bile acids,trimethylamine-N-oxide,and tryptophan),neural pathways(such as the vagus nerve and sympathetic nerve),and immune pathways(involving microglia and T cells).We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage.The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier,inducing neuroinflammation,and interfering with nerve regeneration.Finally,we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury.Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage,paving the way for exploring potential therapeutic approaches. 展开更多
关键词 gut microbiota gut microbiota–brain axis immune intracerebral hemorrhage neuroinflammation NLRP3 protein stroke therapeutics white matter injury
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Intracranial pressure management in severe intraventricular hemorrhage:A minireview 认领 引用
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作者 Wu-Si Qiu Hao-Dong Chen +1 位作者 Wen-Jie Yang Ming-Min Chen 《World Journal of Critical Care Medicine》 2026年第1期82-90,共9页
Severe intraventricular hemorrhage(IVH)is a life-threatening neurological emergency that poses significant risks of morbidity and mortality,particularly due to the associated elevated intracranial pressure(ICP).Studie... Severe intraventricular hemorrhage(IVH)is a life-threatening neurological emergency that poses significant risks of morbidity and mortality,particularly due to the associated elevated intracranial pressure(ICP).Studies have shown that the incidence of IVH in very preterm infants is high,with management strategies playing a significant role in its development.Moreover,predictive models have been developed to forecast early mortality and severe IVH in very-low birth weight preterm infants,indicating the complexity and multifactorial nature of this condition.This mini-review synthesizes recent advances in the understanding of intracranial dynamics,monitoring technologies,and therapeutic strategies for managing ICP in IVH.The Monro-Kellie 4.0 framework integrates cerebrovascular autoregulation,intracranial compliance,and glymphatic clearance as core determinants of ICP.Pathophysiological mechanisms include obstructive hydrocephalus,hemoglobin-mediated neurotoxicity,and cortical spreading depolarizations.Advancements in non-invasive monitoring techniques,such as ICP monitoring and genetic testing,coupled with the integration of artificial intelligence,are significantly improving early detection capabilities and enabling more personalized management strategies.Therapeutic advances in-clude algorithmic cerebrospinal fluid drainage,glymphaticenhanced therapies,and precision hyperosmolar therapy.This review highlights the need for standardized protocols,large-scale trials,and artificial intelligence-driven approaches to improve outcomes in severe IVH. 展开更多
关键词 Intraventricular hemorrhage Intracranial pressure External ventricular drainage Multimodal monitoring Artificial intelligence Glymphatic system
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Recombinant tissue plasminogen activator protects neurons after intracerebral hemorrhage through activating the PI3K/AKT/mTOR pathway 认领 引用 被引量：1
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作者 Jie Jing Shiling Chen +7 位作者 Xuan Wu Jingfei Yang Xia Liu Jiahui Wang Jingyi Wang Yunjie Li Ping Zhang Zhouping Tang 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第4期1574-1585,共12页
Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage.However,during minimally invasive surgery,recombinant tissue plasminog... Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage.However,during minimally invasive surgery,recombinant tissue plasminogen activator may come into contact with brain tissue.Therefore,a thorough assessment of its safety is required.In this study,we established a mouse model of intracerebral hemorrhage induced by type VII collagenase.We observed that the administration of recombinant tissue plasminogen activator without hematoma aspiration significantly improved the neurological function of mice with intracerebral hemorrhage,reduced pathological damage,and lowered the levels of apoptosis and autophagy in the tissue surrounding the hematoma.In an in vitro model of intracerebral hemorrhage using primary cortical neurons induced by hemin,the administration of recombinant tissue plasminogen activator suppressed neuronal apoptosis,autophagy,and endoplasmic reticulum stress.Transcriptome sequencing analysis revealed that recombinant tissue plasminogen activator upregulated the phosphoinositide 3-kinase/RAC-alpha serinehreonine-protein kinase/mammalian target of rapamycin pathway in neurons.Moreover,the phosphoinositide 3-kinase inhibitor LY294002 abrogated the neuroprotective effects of recombinant tissue plasminogen activator in inhibiting excessive apoptosis,autophagy,and endoplasmic reticulum stress.Furthermore,to specify the domain of recombinant tissue plasminogen activator responsible for its neuroprotective effects,various inhibitors were used to target distinct domains.It has been revealed that the epidermal growth factor receptor inhibitor AG-1478 reversed the effect of recombinant tissue plasminogen activator on the phosphoinositide 3-kinase/RAC-alpha serinehreonineprotein kinase/mammalian target of rapamycin pathway.These findings suggest that recombinant tissue plasminogen activator exerts a direct neuroprotective effect on neurons following intracerebral hemorrhage,possibly through activation of the phosphoinositide 3-kinase/RAC-alpha serinehreonine-protein kinase/mammalian target of rapamycin pathway. 展开更多
关键词 apoptosis autophagy endoplasmic reticulum stress epidermal growth factor intracerebral hemorrhage mammalian target of rapamycin minimally invasive surgery phosphoinositide 3-kinase RAC-alpha serinehreonine-protein kinase recombinant tissue plasminogen activator
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Colonic diverticular hemorrhage:Etiology,diagnostic challenges,and evolving therapeutic strategies 认领 引用 被引量：1
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作者 Yi-Qing Hui Zhi-Xuan Wang +1 位作者 Chun-Xi Wang Chuan Tong 《World Journal of Gastroenterology》 SCIE CAS 2026年第4期8-17,共10页
Colonic diverticular hemorrhage is a major cause of acute lower gastrointestinal bleeding,particularly in aging populations with increasing prevalence of diverticulosis.Its pathogenesis is multifactorial,involving vas... Colonic diverticular hemorrhage is a major cause of acute lower gastrointestinal bleeding,particularly in aging populations with increasing prevalence of diverticulosis.Its pathogenesis is multifactorial,involving vascular fragility of the vasa recta,mechanical stress,and patient-related factors such as comorbidities and use of antithrombotic agents.Diagnosis remains challenging due to the intermittent nature of bleeding,with colonoscopy serving as the primary tool and computed tomography angiography providing complementary value for source localization.Endoscopic therapy,especially band ligation,has demonstrated superiority over clipping in reducing rebleeding,while transcatheter arterial embolization has emerged as an effective salvage approach when endoscopic treatment fails.Surgical intervention is reserved for refractory or complicated cases.Recent advances include risk stratification models to guide management and early feeding strategies to accelerate recovery.Despite these improvements,challenges remain in recurrence prevention and individualized treatment selection.This editorial synthesizes current evidence on the etiology,diagnostic modalities,and evolving therapeutic strategies of colonic diverticular hemorrhage,aiming to support clinical decision-making and optimize patient outcomes. 展开更多
关键词 Colonic diverticular hemorrhage Etiology Diagnostic techniques Endoscopic therapy Interventional embolization Surgical treatment
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Deep learning-based imaging model to predict early hematoma enlargement and hospital mortality in spontaneous intracerebral hemorrhage 认领 引用 被引量：3
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作者 Yu-Han Yang Yuan Li 《World Journal of Radiology》 2026年第1期30-45,共16页
BACKGROUND Spontaneous intracerebral hemorrhage(ICH)is a severe form of stroke with high early mortality,and hematoma enlargement(HE)occurs in roughly one-third of patients and strongly predicts poor outcomes.Quantita... BACKGROUND Spontaneous intracerebral hemorrhage(ICH)is a severe form of stroke with high early mortality,and hematoma enlargement(HE)occurs in roughly one-third of patients and strongly predicts poor outcomes.Quantitative image analysis using handcrafted radiomics and deep learning-derived features can capture hematoma and perihematomal edema(PHE)heterogeneity objectively that the combination of these approaches with clinical data may improve early prediction of HE and in-hospital mortality.AIM To evaluate and validate the predictive performance of hematoma-and PHE-derived features on non-contrast computed tomography via handcrafted radiomics and automatic deep learning analysis for prediction of early HE and hospital mortality in spontaneous ICH.METHODS Of 322 patients with basal ganglia ICHs were included retrospectively between June 2018 and June 2020,and assigned into the training cohort(n=225)and the testing cohort(n=97).We extracted features on hematoma and PHE subregions via handcrafted radiomics analysis manually and deep learning analysis of pretrained convolutional neural networks via transfer learning automatically.Support vector machine was adopted as the classifier for prediction of HE and hospital mortality.The clinical-radiological integrated models for HE and hospital mortality were constructed on clinical data and radiological signatures generated from the radiological models with the optimal area under the receiver operating characteristics curve in the testing cohort.RESULTS The clinical-radiological model combining clinical information and hematoma-and PHE-derived computed tomography features for prediction of HE implied an area under the receiver operating characteristics curve of 0.828 with 95%confidence interval of 0.714 to 0.942 with accuracy of 72.89%,sensitivity of 70.00%,and specificity of 74.52%in the testing cohort.The model integrating clinical and radiological features showed great identification performance for predicting hospital mortality,demonstrating significant classification and discrimination abilities after validation.CONCLUSION Quantitative radiomics features from hematoma and PHE regions on non-contrast computed tomography images showed good performance for predicting HE and hospital mortality in patients with ICH. 展开更多
关键词 Intracerebral hemorrhage Enlargement Computed tomography Radiomics Deep learning Hospital mortality
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Telomere length as a predictive marker for long-term cognitive function in a mouse model of subarachnoid hemorrhage 认领 引用
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作者 Qia Zhang Chaoran Xu +4 位作者 Jiayong Fan Chengjian Lou Jiarui Chen Jianmin Zhang Jun Mo 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3055-3062,共8页
Subarachnoid hemorrhage is a subtype of stroke that causes severe neurological damage and is associated with poor long-term prognosis.Cognitive impairment is a major manifestation of long-term neurological dysfunction... Subarachnoid hemorrhage is a subtype of stroke that causes severe neurological damage and is associated with poor long-term prognosis.Cognitive impairment is a major manifestation of long-term neurological dysfunction in patients with subarachnoid hemorrhage.However,there is notable absence of biological markers to predict long-term prognosis in this patient population.Given the aging-like neurocognitive phenomena associated with subarachnoid hemorrhage,this study postulates that telomere length,a recognized biomarker for aging,could be used as a prognostic indicator for subarachnoid hemorrhage.A left internal carotid artery intravascular puncture mouse model was used to simulate subarachnoid hemorrhage.Comprehensive neurological test scores were obtained through neurobehavioral assessments conducted at one-month intervals.Concurrently,the relative telomere length was analyzed by quantitative polymerase chain reaction,which was performed using DNA extracted from ear notch and brain tissue after each assessment.Furthermore,proteomic analysis was employed to investigate differential protein expression in hippocampal tissue.Subarachnoid hemorrhage mice exhibited persistent neurocognitive impairment over a prolonged period of time.There was a significant positive correlation between telomere length and neurological test scores,confirming the usefulness of telomere length as a prognostic indicator in subarachnoid hemorrhage.Hippocampal tissue from subarachnoid hemorrhage mice showed reduced expression of acetyl-coenzyme A synthetase-2 and abnormalities in the expression of proteins related to ribosomes,energy metabolism,and cellular signal transduction.This study confirmed telomere shortening in the brain and metabolic disturbances in the hippocampi of subarachnoid hemorrhage mice.Thus,telomere length is a predictive marker for long-term impairment of cognitive function in mice following experimental subarachnoid hemorrhage. 展开更多
关键词 acetyl-coenzyme A synthetase-2 brain aging DNA damage response long-term prognosis subarachnoid hemorrhage telomere length
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Delayed microglial depletion protects against white matter injury following neonatal cerebral hemorrhage in mice 认领 引用
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作者 Xiaoxiao Jing Xiaoli Zhang +13 位作者 Hongwei Li Yu Yang Zuhang Zhao Yuandan Li Jinjin Zhu Yiran Xu Jing Yuan Tiantian He Chen Zhang Juan Song Xin Zhao Xiaoyang Wang Changlian Zhu Falin Xu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第6期2621-2631,共11页
Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury respons... Germinal matrix hemorrhage in preterm neonates often leads to white matter injury,contributing to long-term neurodevelopmental impairments.As resident brain immune cells,microglia play a complex role in injury response,including inflammation and repair.Although colony-stimulating factor 1 receptor inhibitors such as PLX5622 enable the selective depletion of microglia,their therapeutic potential in neonatal germinal matrix hemorrhage remains underexplored.Here,we used a collagenase-induced germinal matrix hemorrhage model in postnatal day 5 mice,and intraperitoneally administered PLX562272 hours post-germinal matrix hemorrhage to achieve targeted,temporary microglial depletion during the peak injury response.We then assessed the effects of this delayed intervention on oligodendrocyte lineage cell maturation,white matter integrity,and neurobehavioral outcomes.Additionally,RNA sequencing data from a germinal matrix hemorrhage rat model were analyzed using weighted gene co-expression network analysis to identify the critical phases for interventions.RNA sequencing data revealed a critical period in which key synaptic functions declined while immune responses intensified post-germinal matrix hemorrhage,thus pinpointing the critical response phases for potential interventions.Delayed PLX5622 treatment effectively depleted activated microglia,protecting against white matter injury and enhancing oligodendrocyte lineage cell maturation and myelination in subcortical white matter regions.Moreover,magnetic resonance imaging analysis revealed reduced brain lesion volumes in treated mice.Behaviorally,PLX5622-treated mice exhibited significant improvements in motor coordination and reduced hyperactivity compared with vehicle-treated germinal matrix hemorrhage model mice.These findings suggest that,when timed to avoid interference with initial oligodendrocyte lineage cell proliferation,targeted microglial depletion with PLX5622 significantly mitigates white matter damage and improves neurobehavioral outcomes in neonatal germinal matrix hemorrhage.The present study highlights the therapeutic potential of selectively modulating microglial reactivity to support neurodevelopment in preterm infants with brain injury. 展开更多
关键词 colony-stimulating factor 1 receptor germinal matrix hemorrhage microglia myelination neonatal brain oligodendrocyte lineage cell PLX5622 white matter injury
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Detecting altered spontaneous activities of different brain areas in diabetic vitreous hemorrhage patients:a magnetic resonance imaging study 认领 引用
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作者 Kai Yan Jing Yu +9 位作者 Yan-Mei Zeng Cheng Chen Lei Zhong Jin-Yu Hu Liang-Qi He Xiao-Yu Wang Qian Ling Xu Chen Yi Shao Yao Yu 《International Journal of Ophthalmology(English edition)》 SCIE CAS 2026年第2期273-280,共8页
AIM:To compare spontaneous brain regional activities between diabetic vitreous hemorrhage patients(DVHs)and healthy controls(HCs).METHODS:Thirty-two DVHs and 32 HCs were enrolled in this study.Baseline demographic and... AIM:To compare spontaneous brain regional activities between diabetic vitreous hemorrhage patients(DVHs)and healthy controls(HCs).METHODS:Thirty-two DVHs and 32 HCs were enrolled in this study.Baseline demographic and vision data were compared between groups using an independent sample t-test.Resting-state functional magnetic resonance imaging(rs-fMRI)was used in all participants.fMRI data was obtained and analyzed using MRIcro and SPM8 software.Fractional amplitude of low-frequency fluctuation(fALFF)technology was used to measure regional spontaneous brain activity,and sensitivity was tested using receiver operating characteristic curves(ROCs).The fALFF values were analyzed using REST software and two-sample t-tests were used to compare values between groups.Hospital anxiety and depression scale(HADS)score was assessed in DVHs and Pearson’s correlation was used to test relationships between mean fALFF value and both HADS score and duration of DVH.RESULTS:Except for the best-corrected visual acuity(BCVA)in both eyes,which showed a statistically significant difference(P0.05)between the HCs and DVHs group.Compared with controls,fALFF value was higher in DVH in cerebellum posterior lobe(CPL)and lower in right anterior cingulate cortex(ACC)and right medial orbitofrontal cortex(OFC).In DVH patients,mean fALFF value of CPL was positively correlated with HADS score and duration of diabetes.However,no such correlation was found,for right ACC or right medial OFC.DVH may lead to abnormal activities in certain brain regions related to visual control and mood.CONCLUSION:Visual impairment caused by DVH may lead to adjustment in regional visual brain activities and may be related to depression or reward system processing in some brain regions. 展开更多
关键词 diabetic vitreous hemorrhage functional magnetic resonance fractional amplitude of low-frequency fluctuation cerebellum posterior lobe right anterior cingulate cortex right medial orbitofrontal cortex clinical trials
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Microglia and macrophages in brain injury and repair after subarachnoid hemorrhage 认领 引用
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作者 David C.Lauzier Harry V.Vinters Shino D.Magaki 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第1期308-309,共2页
Subarachnoid hemorrhage(SAH) is a devastating condition that affects a total of 8 million people worldwide each year(Lauzier and Athiraman, 2024). Etiologies of SAH can be traumatic or nontraumatic, with the majority ... Subarachnoid hemorrhage(SAH) is a devastating condition that affects a total of 8 million people worldwide each year(Lauzier and Athiraman, 2024). Etiologies of SAH can be traumatic or nontraumatic, with the majority of non-traumatic SAH occurring due to intracranial aneurysm rupture(Rutledge et al., 2014). 展开更多
关键词 traumatic hemorrhage
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Letter to the Editor:Evaluation of the pathological cascade of postsubarachnoid hemorrhage anxiety and depression 认领 引用
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作者 Teng-Fei Zeng Jing-Yuan Zhang Xue-Jian Wang 《World Journal of Psychiatry》 SCIE 2026年第8期444-450,共7页
Anxiety and depression disorders following subarachnoid hemorrhage(SAH)are common neuropsychological complications,which will definitely affect the longterm functional recovery and quality of life of patients.So far,t... Anxiety and depression disorders following subarachnoid hemorrhage(SAH)are common neuropsychological complications,which will definitely affect the longterm functional recovery and quality of life of patients.So far,the pathophysiological mechanisms of such complications have not been fully elucidated,and effective treatment strategies are lacking.This letter to the editor is a comment on a preclinical study published in World Journal of Psychiatry by Qin et al.The research team established the SAH rat model,combined with multi-dimensional behavior detection,diffusion tensor imaging(DTI)scanning,inflammatory factor expression level detection and other methods to clarify the specific mechanism of emotional dysfunction after SAH.The study not only identified the temporal dynamic characteristics of emotional disorders,discovered a new pathological cascade of“cytotoxic edema-NOD-like receptor pyrin domain-containing 3 inflammasome activation-limbic-prefrontal circuit injury”,and verified the feasibility of diffusion tensor imaging parameters(fractional anisotropy/apparent diffusion coefficient values)and cerebrospinal fluid interleukin-1βas objective indicators for disease progression assessment.This article summarizes the core academic value of this study,and combined with the existing research progress in this field,further analyzes the reference value of this achievement for defining the intervention time window,the practical difficulties in the process of clinical transformation,and the possible breakthrough direction of follow-up research,in order to provide new ideas for the precise prevention and treatment of neuropsy chiatric complications after SAH. 展开更多
关键词 Subarachnoid hemorrhage Anxiety Depression NOD-like receptor pyrin domain-containing 3 inflammasome Diffusion tensor imaging Limbic-prefrontal circuit
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