AIM: To compare the short- and long-term outcomes of vascularizing lymph node dissection (VLND) and non-vascularizing lymph node dissection (NVLND) from a single institution.METHODS: Data of 315 patients with advanced...AIM: To compare the short- and long-term outcomes of vascularizing lymph node dissection (VLND) and non-vascularizing lymph node dissection (NVLND) from a single institution.METHODS: Data of 315 patients with advanced gastric cancer who underwent standard D2 lymphadenectomy with curative intent was collected between January 1994 and December 2006. One hundred and fifty-two patients received VLND while 163 patients received NVLND. Short- and long-term clinical outcomes were compared between the two groups.RESULTS: The median followed-up time was 82 mo. The rate of postoperative complications in the VLND group was 13.2%, while that in the NVLND group was 11.7% (P = 0.686). The overall 5-year survival rate was 64% in the VLND group and 59% in the NVLND group (P = 0.047). When subgroup analyses were performed according to Bormann type, type of differentiation and lymph node status, survival benefit was demonstrated in patients with Bormann type III or IV (59% vs 50%, P = 0.032), undifferentiated type (63% vs 49%, P = 0.021) or presence of lymph node metastasis (53% vs 38%, P = 0.010) in the VLND group.CONCLUSION: D2 VLND in advanced gastric cancer treatment allows survival benefit with acceptable morbidity and mortality. VLND for patients with potentially curable advanced gastric cancer is feasible and safe when performed by a well-trained surgical team.展开更多
Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in s...Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury.展开更多
Ischemic stroke,a frequently occurring form of stroke,is caused by obstruction of cerebral blood flow,which leads to ischemia,hypoxia,and necrosis of local brain tissue.After ischemic stroke,both astrocytes and the bl...Ischemic stroke,a frequently occurring form of stroke,is caused by obstruction of cerebral blood flow,which leads to ischemia,hypoxia,and necrosis of local brain tissue.After ischemic stroke,both astrocytes and the blood–brain barrier undergo morphological and functional transformations.However,the interplay between astrocytes and the blood–brain barrier has received less attention.This comprehensive review explores the physiological and pathological morphological and functional changes in astrocytes and the blood–brain barrier in ischemic stroke.Post-stroke,the structure of endothelial cells and peripheral cells undergoes alterations,causing disruption of the blood–brain barrier.This disruption allows various pro-inflammatory factors and chemokines to cross the blood–brain barrier.Simultaneously,astrocytes swell and primarily adopt two phenotypic states:A1 and A2,which exhibit different roles at different stages of ischemic stroke.During the acute phase,A1 reactive astrocytes secrete vascular endothelial growth factor,matrix metalloproteinases,lipid carrier protein-2,and other cytokines,exacerbating damage to endothelial cells and tight junctions.Conversely,A2 reactive astrocytes produce pentraxin 3,Sonic hedgehog,angiopoietin-1,and other protective factors for endothelial cells.Furthermore,astrocytes indirectly influence blood–brain barrier permeability through ferroptosis and exosomes.In the middle and late(recovery)stages of ischemic stroke,A1 and A2 astrocytes show different effects on glial scar formation.A1 astrocytes promote glial scar formation and inhibit axon growth via glial fibrillary acidic protein,chondroitin sulfate proteoglycans,and transforming growth factor-β.In contrast,A2 astrocytes facilitate axon growth through platelet-derived growth factor,playing a crucial role in vascular remodeling.Therefore,enhancing our understanding of the pathological changes and interactions between astrocytes and the blood–brain barrier is a vital therapeutic target for preventing further brain damage in acute stroke.These insights may pave the way for innovative therapeutic strategies for ischemic stroke.展开更多
The central nervous system(CNS)does not function in isolation-it engages in continuous molecular dialogue with the vascular and immune systems.Traditionally,the blood-brain barrier(BBB)was portrayed solely as an imper...The central nervous system(CNS)does not function in isolation-it engages in continuous molecular dialogue with the vascular and immune systems.Traditionally,the blood-brain barrier(BBB)was portrayed solely as an impermeable wall,safeguarding the CNS by excluding blood-derived molecules and circulating cells.However,this view has evolved.The BBB is now recognized as a dynamic interface that selectively regulates the exchange of signals,cells.展开更多
Objective:To characterize placental morphologic features in Moroccan women with adverse outcomes,across different clinical contexts,based on the Amsterdam consensus classification.Methods:A prospective analysis was co...Objective:To characterize placental morphologic features in Moroccan women with adverse outcomes,across different clinical contexts,based on the Amsterdam consensus classification.Methods:A prospective analysis was conducted on placentas with umbilical cords collected fresh between March 1,2024 and July 15,2024 from women with adverse pregnancy outcomes.Clinical data(age,parity,gravidity,complications)were retrieved.Macroscopic parameters(weight,dimensions,cord insertion,membranes,lesions)were assessed,followed by systematic sampling.Tissue was processed by standard histology(formalin fixation,paraffin embedding,hematoxylin and eosin staining),and lesions were classified per Amsterdam criteria.Results:16 placentas from patients with adverse pregnancy outcomes were included.The median maternal age was 30 years.Adverse conditions included placental abruption(50%),intrauterine growth restriction(IUGR,38%),intrauterine fetal death(IUFD,31%),pre-eclampsia/eclampsia(19%),premature rupture of membranes(13%),and oligohydramnios(13%).Several placentas were associated with more than one adverse condition.Histopathology revealed maternal vascular malperfusion lesions in 94%,particularly in pre-eclampsia,IUGR,and IUFD.Fetal vascular malperfusion was found in 88%,mainly in IUGR and IUFD.Inflammatory lesions,dominated by acute maternal and fetal responses stage 3(necrotizing chorioamnionitis and funisitis),were primarily linked to IUFD.Conclusions:Placental examination enhances understanding of the pathophysiology underlying adverse pregnancy outcomes,supports diagnostic confirmation,and guides preventive strategies for recurrence.This study highlights the prevalence of maternal vascular malperfusion in Moroccan women and emphasizes the importance of systematic placental histopathology in obstetric care.展开更多
Recently,Tian et al.published a research paper with significant breakthroughs in Cell[1].The study found that targeting the signalling pathways named Serpine2-lowdensity lipoprotein receptor-related protein 1(Lrp1)and...Recently,Tian et al.published a research paper with significant breakthroughs in Cell[1].The study found that targeting the signalling pathways named Serpine2-lowdensity lipoprotein receptor-related protein 1(Lrp1)and ectonucleoside triphosphate diphosphohydrolase 1(CD39)-adenosine A_(3)receptor(A_(3)AR)is a promising strategy for the treatment of vascular dementia.The Serpine2-Lrp1 signalling pathway primarily exerts its therapeutic effects on myelin regeneration by regulating the differentiation of oligodendrocyte precursor cells.Serpine2 is a secretory serine protease inhibitor regulates proteolytic homeostasis.It may also bind to cell surface receptors such as Lrp1 to directly activate signalling pathways.As a transmembrane glycoprotein receptor,Lrpl mediates the endocytic clearance of ligands.展开更多
Varicocele(VC)is widely recognized as a prevalent and clinically significant cause of male infertility.However,the comprehensive pathogenic mechanisms underlying VC development and progression remain incompletely unde...Varicocele(VC)is widely recognized as a prevalent and clinically significant cause of male infertility.However,the comprehensive pathogenic mechanisms underlying VC development and progression remain incompletely understood,creating an important knowledge gap in the field of andrology.This review establishes that VC pathogenesis centers on abnormal vascular remodeling and integrates multiple contributing elements,including anatomical abnormalities,biochemical disturbances,genetic factors,low body mass index(BMI),age,and specific sports habits,while secondary varicoceles are primarily induced by compressive pathologies.Through a systematic synthesis of current evidence and recent advances,this review aims to elucidate the complex pathogenic network of VC and provide valuable insights to guide future research directions and inform the development of targeted clinical applications.展开更多
Background:The traditional method of heterotopic abdominal heart transplantation(HTx)involves crossclamping the inferior vena cava,which inevitably leads to bilateral lower limb ischemia(LI).This study first aimed to ...Background:The traditional method of heterotopic abdominal heart transplantation(HTx)involves crossclamping the inferior vena cava,which inevitably leads to bilateral lower limb ischemia(LI).This study first aimed to investigate the impact of LI on renal function in rats subjected to unilateral nephrectomy(UNx).Second,a modified method utilizing renal vessel-assisted anastomosis in rats with left UNx was compared with the traditional method for abdominal HTx.Methods:Male Sprague-Dawley rats were utilized as subjects for both experimental phases.In experiment 1,the animals were divided into four groups:sham operation group;LI group-rats undergoing occlusion of the abdominal aorta and vena cava below the renal vessels;UNx group-rats with left UNx;and LI+UNx group.All operated animals were monitored for up to 7 days for biochemical markers,renal histopathology,and survival rates.In experiment 2,we introduced the renal vessel-assisted method as the experimental group and compared it against the traditional method as the control within rat heterotopic HTx models.We assessed operative characteristics,echocardiography results,histological findings,and graft survival.Results:First,LI resulted in acute kidney dysfunction characterized by a decrease in 7day survival rates and creatinine clearance rates in both the LI and LI+UNx groups compared to the sham operation and UNx groups.Particularly,histopathological damage in the kidney and liver did not exhibit significant effects during this period.Second,the implementation of the renal vessel-assisted method significantly reduced bleeding volume at suture sites and enhanced the 7day survival rate compared to the traditional method.Conclusion:Acute kidney injury was induced by LI postoperation in treated rats.The renal vessel-assisted method demonstrated its effectiveness as a superior alternative that mitigates complications associated with the traditional method.展开更多
The formation of wood is affected by the growing season and the environment.Ring-porous tree species have distinct earlywood-latewood differences.However,it is not clear how early wood and latewood respond to drought ...The formation of wood is affected by the growing season and the environment.Ring-porous tree species have distinct earlywood-latewood differences.However,it is not clear how early wood and latewood respond to drought and the differences in adaptation.Therefore,based on the analyses of phenology,growth,and xylem development over a year,xylem development in Fraxinus mandshurica was divided into earlyw ood,transition,and latewood stages.Variation patterns of 38 wood indices from 31 genotypes indicated that the formation of wood tissues was inhibited,and the proportion of xylem cells was affected by drought at each stage.However,soluble sugar affected osmotic regulation only during drought across early wood and transition stages.To maintain water and nutrient transport during drought and to resist embolism risk,drought in the early wood stage leads to varying degrees of early wood vessel diameter reduction,with pits enlarging to compensate.In contrast,during the late wood stage,drought causes latewood vessel diameter to increase and pits to shrink accordingly.In addition,the results indicate that several wood indices correlate with drought resistance at each stage,but early wood vessel diameter,soluble sugar,and latewood ves sel diameters exhibited the strongest correlations in the early wood,transition,and latewood stages.These findings provide clues to understanding plant survival strategies under drought stress and are of significance for plant ecology research on the growth and adaptation of tree species under climate change.展开更多
Objective:To investigate the effects of health education based on the Transtheoretical Model(TTM)on self-management and vascular crisis in patients undergoing finger replantation surgery.Methods:A total of 106 patient...Objective:To investigate the effects of health education based on the Transtheoretical Model(TTM)on self-management and vascular crisis in patients undergoing finger replantation surgery.Methods:A total of 106 patients who underwent finger replantation surgery between January 2025 and December 2025 were randomly divided into control and intervention groups using a random number table method(control group,n=52;intervention group,n=54).The control group received standard perioperative nursing care,while the intervention group received TTM-based health education in addition to standard care.Self-management levels and incidence of vascular crisis were compared between the two groups.Results:After intervention,the Adult Health Self-Management Skills Rating Scale(AHSMSRS)scores in both groups increased significantly compared with baseline(control:91.26±5.49 to 116.97±8.15;intervention:90.39±6.72 to 136.38±9.36,p<0.001).The intervention group showed significantly higher AHSMSRS scores than the control group(136.38±9.36 vs.116.97±8.15,p<0.001).Similarly,general self-efficacy scores increased significantly in both groups,with the intervention group demonstrating superior improvement(36.73±4.78 vs.28.49±4.11,p<0.001).The incidence of vascular crisis was significantly lower in the intervention group(5.5%)compared with the control group(19.23%,χ2=3.421,p<0.05).Conclusion:Health education based on the Transtheoretical Model effectively enhances self-management abilities and self-efficacy in patients undergoing finger replantation surgery,and significantly reduces the incidence of postoperative vascular crisis.展开更多
Tajikistan represents a core region of the biodiversity hotspot in Central Asian mountains and has exceptional vascular plant diversity.However,the species diversity of the country faces urgent conservation challenges...Tajikistan represents a core region of the biodiversity hotspot in Central Asian mountains and has exceptional vascular plant diversity.However,the species diversity of the country faces urgent conservation challenges.There has been a lack of a comprehensive and multidimensional assessment to inform strategic conservation planning.Therefore,this study integrated 4 key biodiversity indices including species richness(SR),phylogenetic diversity(PD),threatened species richness(TSR),and endemic species richness(ESR)to map species diversity distribution patterns,identify conservation gaps,and elucidate their effects of climatic factors.This study revealed that species diversity shows a clear trend of decreasing from the western region to the eastern region of Tajikistan.The central–western mountains(specifically the Gissar-Darvasian and Zeravshanian regions)emerge as irreplaceable biodiversity hotspots.However,we found a severe spatial mismatch between these priority areas and the existing protected areas(PAs).Protection coverage for all hotspots was alarmingly low,ranging from 31.00%to 38.00%.Consequently,a critical 64.80%of integrated priority areas fall outside of the current PAs,representing a major conservation gap.This study identified precipitation seasonality and isothermality as the principal drivers,collectively explaining over 50.00%of the diversity variation and suggesting high vulnerability to hydrological shifts.Furthermore,we detected significant geographic sampling bias in the public biodiversity databases,with the most critical hotspot being systematically under-sampled.This study provides a robust scientific basis for conservation action,highlighting the urgent need to strategically expand PAs in the under-protected southwestern region and to mitigate critical sampling gaps through targeted data digitization and field surveys.These measures are indispensable for securing Tajikistan’s unique biodiversity and achieving the Kunming-Montreal Global Biodiversity Framework Target 3(“30×30 Protection”).展开更多
Stroke is a major cause of death and disability worldwide,and its pathogenesis is complex,involving multiple pathological processes,such as thrombosis,ischemia-repe rfusion injury,inflammato ry response,and blood-brai...Stroke is a major cause of death and disability worldwide,and its pathogenesis is complex,involving multiple pathological processes,such as thrombosis,ischemia-repe rfusion injury,inflammato ry response,and blood-brain barrier disruption.In recent years,neutrophil extracellular traps have been found to be involved in the body's anti-infection defense and to play an important role in stroke.Studies have shown that neutrophil extracellular traps promote thrombus expansion and neuroinflammation in ischemic stroke,and they may be involved in disease progression and recove ry in hemorrhagic stroke by modulating local inflammation and influencing hematoma clearance.This review systematically summarizes the evolution and mechanism of action of neutrophil extracellular traps in stroke pathology.Reactive oxygen species drive the formation of neutrophil extra cellular traps 6-24 hours after cerebral infarction.At 24-48 hours,they exacerbate vascular injury and thrombosis,at 48-72 hours,they aggravate neurological injury,and after 72 hours,neutrophil extra cellular tra ps are involved in the disruption of the blood-brain barrier and the maintenance of the inflammatory response.During stroke development,neutrophil extracellular traps are involved in multiple pathological mechanisms after cerebral infa rction.They induce vascular endothelial damage,exacerbating vascular leakage and edema,injuring neuro ns,inducing apoptosis,promoting thrombosis,participating in reperfusion injury,and damaging the blood-brain barrier.In hemorrhagic stroke,neutrophil extracellular traps are closely associated with hematoma clearance,early brain injury,and delayed cerebral ischemia,and can be used as a biomarker to assess disease progression and efficacy.In the acute phase of stroke,neutrophil extracellular traps mainly promote injury,and in the chronic phase,they mainly promote repair.Neutrophil extracellular traps,as an important biomarker of stro ke,are closely correlated with stroke severity.Additionally,neutrophil extra cellular traps play an important role in atheroscle rosis and intracranial venous thrombosis.Current research has confirmed that deoxyribonuclease is a key drug for degrading neutrophil extracellular traps and has shown significant therapeutic potential.Peptidyl arginine deiminase 4 inhibitors and high mobility group box 1 antagonists effectively inhibit the formation of neutrophil extra cellular traps through their own unique mechanisms.M ulti-targeted inte rvention strategies for neutrophil extracellular traps have shown broad clinical application prospects.Neutrophil extracellular traps exhibit syne rgistic effects with anticoagulants and thrombolytic drugs,and interventions targeting neutrophil extracellular traps can influence the efficacy of anticoagulation and thrombolytic therapy.These findings provide a theoretical basis for developing new anticoagulation and thrombolysis strategies for stroke and im p roving clinical outcomes for patients.展开更多
BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This re...BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This review is to outline the pathomechanism,organ heterogeneity,biomarkers,and therapeutic implications of endothelial dysfunction in sepsis,off ering references and insights for the clinical management of sepsis.METHODS:A systematic search of Web of Science and PubMed from inception to June 10,2025,limited to English publications,was conducted.Two reviewers independently identifi ed studies on EC injury in patients with septic microcirculatory dysfunction.Duplicate articles based on multiple search criteria were excluded.RESULTS:Fifty-nine articles,including cell,animal,and clinical studies,were included.These studies reported the effects of EC injury on the microcirculation in sepsis,including changes in vascular permeability,coagulation dysfunction,vasomotor regulation,and infl ammatory responses.These pathways interact and ultimately lead to septic microcirculation disorders.CONCLUSION:Sepsis-induced endothelial dysfunction involves various interconnected mechanisms,which collectively compromise ECs and impede microcirculatory perfusion.Future research should enhance current understanding of endothelial injury mechanisms,develop synergistic multi-target strategies to disrupt this cycle,and facilitate the clinical application of endothelial markers for early intervention and dynamic assessment.展开更多
Arteriovenous fistula(AVF)calcification is a common complication in hemodialysis patients that leads to AVF dysfunction and decreases the AVF survival,but the mechanisms of AVF calcification,especially the role of hem...Arteriovenous fistula(AVF)calcification is a common complication in hemodialysis patients that leads to AVF dysfunction and decreases the AVF survival,but the mechanisms of AVF calcification,especially the role of hemodynamic changes in AVF calcification have not been fully investigated.In this study,a computational fluid dynamics(CFD)model was carried out based on AVF,at the distal anastomosis of the cephalic vein and radial artery,generated from a patient-specific computed tomography(CT)angiography and Doppler ultrasound image.Hemodynamic factors were considered to explore the mechanisms responsible for the initiation and progression of AVF calcification.Five stages in one cardiac cycle were chosen to be studied for the velocity field,pressure,time-averaged wall shear stress(TAWSS),and oscillatory shear index(OSI).Blood pressure was higher in the arteriovenous anastomosis,and variations of great amplitude of pressure were examined during the cardiac cycle.Blood pressure,transient shear stress,TAWSS,and OSI were higher in the arteriovenous anastomosis and at the bottom of expanded outflow vein,and these sites were highly consistent with the calcified areas shown on CT angiography.On the contrary,no calcification was found in sites where streamline was stable,blood pressure did not change dramatically,as well as TAWSS and OSI were lower.It was shown that AVF calcification was correlated with hemodynamic changes,which may contribute to further understanding the mechanisms of AVF calcification and providing scientific evidence to inform the optimization of surgical strategies and the development of personalized interventional measures in clinical contexts.展开更多
Vascular ageing is increasingly recognised as a key driver of cardiovascular and cerebrovascular disease rather than merely a passive consequence of chronological time.Progressive loss of endothelial regenerative capa...Vascular ageing is increasingly recognised as a key driver of cardiovascular and cerebrovascular disease rather than merely a passive consequence of chronological time.Progressive loss of endothelial regenerative capacity remains central to this process and is characterised by endothelial progenitor cell dysfunction,accumulation of senescent endothelial cells,and aberrant changes in the endothelial secretome.Taken together these alterations contribute to ineffective endothelial repair,chronic(low-grade)vascular inflammation and impaired endothelial barrier integrity and function,ultimately leading to vascular dysfunction.Over the past two decades,accumulating evidence from our group and others has provided mechanistic insight into how oxidative stress,redox imbalance,mitochondrial dysfunction and cellular senescence collectively impair endothelial(barrier)function and compromise overall vascular homeostasis.Age-dependent changes in progenitor cell number and function further limit the capacity of vasculature to respond to damage and stress.More recent work demonstrate that senolytics and senomorphics can preserve endothelial function and delay age-related vascular and cerebral barrier dysfunction in experimental models.This mini review supports an emerging framework that positions defective endothelial renewal as a critical driver of vascular ageing and endothelial dysfunction.We propose that concomitant application of senotherapeutics with progenitor cell-based or secretome-based approaches represents a critical next step in precision vascular medicine.展开更多
Background:The development of materials for cardiovascular surgery that would improve the effectiveness of surgical interventions remains an important task.Surgical intervention during the implantation of vascular pro...Background:The development of materials for cardiovascular surgery that would improve the effectiveness of surgical interventions remains an important task.Surgical intervention during the implantation of vascular prostheses and stents,and the body’s reaction to artificial materials,could lead to chronic inflammation,a local increase in the concentration of proinflammatory factors,and stimulation of unwanted tissue growth.The introduction of nonsteroidal anti-inflammatory drugs into implantable devices could be used to obtain vascular implants that do not induce inflammation and do not induce neointimal tissue outgrowth.Methods:The scaffolds were made by electrospinning from mixtures of polyurethane(PU)with diclofenac(DF).The kinetics of DF release from the scaffolds composed of 3%PU/10%HSA/3%DMSO/DF and 3%PU/DF were studied.The biocompatibility and anti-inflammatory effects of the obtained scaffolds on human gingival fibroblasts and umbilical vein endothelial cells were studied.Results:Both types of scaffolds are characterized by fast DF release.The viability of cells cultured on scaffolds is 2 times worse than that of cells cultured on plastic.The level of the proinflammatory cytokine IL-6 in the culture medium of cells cultured on DF-containing scaffolds was lower than that of cells cultured on scaffolds without DF.Conclusion:The introduction of DF into scaffolds minimizes the inflammation caused by cell reactions to an artificial material.展开更多
AIM:To investigate the changes of retinal vascular parameters and retinal layer thickness in patients with multiple sclerosis(MS).METHODS:This single-centered case-control study was performed on a MS group of 42 patie...AIM:To investigate the changes of retinal vascular parameters and retinal layer thickness in patients with multiple sclerosis(MS).METHODS:This single-centered case-control study was performed on a MS group of 42 patients diagnosed with MS and a control group of 43 healthy hospital staff matched in terms of age and sex at Iran University,department of neurology and ophthalmology from March 2020 to March 2021.The ophthalmic parameters of each patient were recorded,and optical coherence tomography was used to evaluate the retinal thickness in the layers.RESULTS:This study enrolled a total of 85 participants,with a mean age of 40.44±11.52 years,including 61 females(72%).The control group consisted of 43 individuals with a mean age of 39.49±11.07 years,while the MS group comprised 42 participants with a mean age of 41.40±12.01 years.The mean disease duration in the MS group was 8.45±6.04 a.The thickness of the ganglion cell layer in the right eye was significantly lower in the MS group compared to the control group(P=0.034).In addition,except for the left nasal sector(P=0.106),the mean peripapillary neurofibrillation in all examined sectors were significantly lower in the MS group than in the control group(P<0.05).The average vessel density in both the deep and superficial capillary plexuses across all regions of both eyes was lower in the MS group than in the control group,with all comparisons for the superficial capillary plexus showing statistical significance(P<0.05 for all except the left nasal sector).CONCLUSION:The thickness of the retina of patients with MS is significantly reduced.Therefore,optical coherence tomography results can be used as a reliable tool to evaluate disease progression and prognosis in MS patients.展开更多
AIM:To investigate the association between anti-DFS70 antibody positivity and ocular parameters,specifically,the choroidal vascularity index(CVI)and other optical coherence tomography(OCT)metrics,in a healthy populati...AIM:To investigate the association between anti-DFS70 antibody positivity and ocular parameters,specifically,the choroidal vascularity index(CVI)and other optical coherence tomography(OCT)metrics,in a healthy population.METHODS:This age-and sex-matched case-control study enrolled 84 healthy individuals with positive anti-DFS70 antibody findings and 84 healthy negative controls.All participants underwent detailed ophthalmological examinations,including biometry and OCT imaging.Anti-DFS70 positivity was determined by indirect immunofluorescence and scored semi-quantitatively(1+to 3+).CVI was calculated from OCT images using a standardized protocol with Image J software.Statistical analyses,including Student’s t-test,Mann-Whitney U test,Spearman correlation,and logistic regression,were used to compare groups and identify predictive factors.RESULTS:The individuals who tested positive and negative for anti-DFS70 included in the study were matched for age(median age=47y)and sex(F:M=7:1).CVI was significantly lower in the anti-DFS70-positive group compared to the negative group.A higher anti-DFS70 antibody titer was significantly associated with decreased subfoveal and nasal choroidal thickness(P=0.016 and P=0.014,respectively).In univariate regression analysis,CVI was the only significant predictor of anti-DFS70 positivity[odds ratio(OR)=0.02,P=0.025].Multivariate analysis revealed a positive correlation between macular thinning outside the subfoveal area and anti-DFS70 status(P<0.05).CONCLUSION:Our study demonstrates a novel association between anti-DFS70 antibody positivity and reduced choroidal vascularity in healthy individuals.These findings suggest that anti-DFS70 antibodies may be associated with subtle choroidal vascular changes detectable by OCT,even in asymptomatic individuals.Further longitudinal research is warranted to clarify the underlying mechanisms and long-term clinical significance of these ocular changes.展开更多
Nail changes following upper extremity transplantation(UET)cannot be overlooked as they possess diagnostic and prognostic relevance in allotransplantation of upper limbs.This comprehensive review explores nail and nai...Nail changes following upper extremity transplantation(UET)cannot be overlooked as they possess diagnostic and prognostic relevance in allotransplantation of upper limbs.This comprehensive review explores nail and nail bed related changes encountered in UET recipients in the literature.The differential diagnosis of nail abnormalities in UET includes a wide range of systemic,local and iatrogenic conditions other than immune responses to the allograft.It requires interdisciplinary evaluation by primary transplant surgeons,pathologists,dermatologists and immunologists.The possible underlying mechanisms of nail pathology in UET and the management are discussed.It also underscores the importance of onychodystrophy and need for timely intervention and to improve outcomes in UET recipients.展开更多
Alzheimer’s disease(AD)is the most common form of dementia,affecting over 50 million people worldwide.This figure is projected to nearly double every 20 years,reaching 82 million by 2030 and 152 million by 2050(Alzhe...Alzheimer’s disease(AD)is the most common form of dementia,affecting over 50 million people worldwide.This figure is projected to nearly double every 20 years,reaching 82 million by 2030 and 152 million by 2050(Alzheimer’s Disease International).The apolipoproteinε4(APOE4)allele is the strongest genetic risk factor for late-onset AD(after age 65 years).Apolipoprotein E,a lipid transporter,exists in three variants:ε2,ε3,andε4.APOEε2(APOE2)is protective against AD,APOEε3(APOE3)is neutral,while APOE4 significantly increases the risk.Individuals with one copy of APOE4 have a 4-fold greater risk of developing AD,and those with two copies face an 8-fold risk compared to non-carriers.Even in cognitively normal individuals,APOE4 carriers exhibit brain metabolic and vascular deficits decades before amyloid-beta(Aβ)plaques and neurofibrillary tau tangles emerge-the hallmark pathologies of AD(Reiman et al.,2001,2005;Thambisetty et al.,2010).Notably,studies have demonstrated reduced glucose uptake,or hypometabolism,in brain regions vulnerable to AD in asymptomatic middle-aged APOE4 carriers,long before clinical symptoms arise(Reiman et al.,2001,2005).展开更多
文摘AIM: To compare the short- and long-term outcomes of vascularizing lymph node dissection (VLND) and non-vascularizing lymph node dissection (NVLND) from a single institution.METHODS: Data of 315 patients with advanced gastric cancer who underwent standard D2 lymphadenectomy with curative intent was collected between January 1994 and December 2006. One hundred and fifty-two patients received VLND while 163 patients received NVLND. Short- and long-term clinical outcomes were compared between the two groups.RESULTS: The median followed-up time was 82 mo. The rate of postoperative complications in the VLND group was 13.2%, while that in the NVLND group was 11.7% (P = 0.686). The overall 5-year survival rate was 64% in the VLND group and 59% in the NVLND group (P = 0.047). When subgroup analyses were performed according to Bormann type, type of differentiation and lymph node status, survival benefit was demonstrated in patients with Bormann type III or IV (59% vs 50%, P = 0.032), undifferentiated type (63% vs 49%, P = 0.021) or presence of lymph node metastasis (53% vs 38%, P = 0.010) in the VLND group.CONCLUSION: D2 VLND in advanced gastric cancer treatment allows survival benefit with acceptable morbidity and mortality. VLND for patients with potentially curable advanced gastric cancer is feasible and safe when performed by a well-trained surgical team.
基金supported by the National Natural Science Foundation of China,Nos.82072165 and 82272256(both to XM)the Key Project of Xiangyang Central Hospital,No.2023YZ03(to RM)。
文摘Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited.Microglia is the resident immune cells of the central nervous system,play a critical role in spinal cord injury.Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors.However,excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars,which hinder axonal regeneration.Despite this,the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood.To elucidate the role of microglia in spinal cord injury,we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia.We observed that sustained depletion of microglia resulted in an expansion of the lesion area,downregulation of brain-derived neurotrophic factor,and impaired functional recovery after spinal cord injury.Next,we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia.We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function.Additionally,brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury.Furthermore,through using specific transgenic mouse lines,TMEM119,and the colony-stimulating factor 1 receptor inhibitor PLX73086,we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages.In conclusion,our findings suggest the critical role of microglia in the formation of protective glial scars.Depleting microglia is detrimental to recovery of spinal cord injury,whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury.
基金supported by the National Natural Science Foundation of China,No.U21A20400(to QW)the National Natural Science Foundation of China,No.82104560(to CL)+1 种基金the Natural Science Foundation of Beijing,No.7232279(to XW)the Project of Beijing University of Chinese Medicine,Nos.2024-JYB-JBZD-043(to CL),2022-JYB-JBZR-004(to XW)。
文摘Ischemic stroke,a frequently occurring form of stroke,is caused by obstruction of cerebral blood flow,which leads to ischemia,hypoxia,and necrosis of local brain tissue.After ischemic stroke,both astrocytes and the blood–brain barrier undergo morphological and functional transformations.However,the interplay between astrocytes and the blood–brain barrier has received less attention.This comprehensive review explores the physiological and pathological morphological and functional changes in astrocytes and the blood–brain barrier in ischemic stroke.Post-stroke,the structure of endothelial cells and peripheral cells undergoes alterations,causing disruption of the blood–brain barrier.This disruption allows various pro-inflammatory factors and chemokines to cross the blood–brain barrier.Simultaneously,astrocytes swell and primarily adopt two phenotypic states:A1 and A2,which exhibit different roles at different stages of ischemic stroke.During the acute phase,A1 reactive astrocytes secrete vascular endothelial growth factor,matrix metalloproteinases,lipid carrier protein-2,and other cytokines,exacerbating damage to endothelial cells and tight junctions.Conversely,A2 reactive astrocytes produce pentraxin 3,Sonic hedgehog,angiopoietin-1,and other protective factors for endothelial cells.Furthermore,astrocytes indirectly influence blood–brain barrier permeability through ferroptosis and exosomes.In the middle and late(recovery)stages of ischemic stroke,A1 and A2 astrocytes show different effects on glial scar formation.A1 astrocytes promote glial scar formation and inhibit axon growth via glial fibrillary acidic protein,chondroitin sulfate proteoglycans,and transforming growth factor-β.In contrast,A2 astrocytes facilitate axon growth through platelet-derived growth factor,playing a crucial role in vascular remodeling.Therefore,enhancing our understanding of the pathological changes and interactions between astrocytes and the blood–brain barrier is a vital therapeutic target for preventing further brain damage in acute stroke.These insights may pave the way for innovative therapeutic strategies for ischemic stroke.
基金supported by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health under Award Number K02NS110973 and R01NS126498(to MAP).
文摘The central nervous system(CNS)does not function in isolation-it engages in continuous molecular dialogue with the vascular and immune systems.Traditionally,the blood-brain barrier(BBB)was portrayed solely as an impermeable wall,safeguarding the CNS by excluding blood-derived molecules and circulating cells.However,this view has evolved.The BBB is now recognized as a dynamic interface that selectively regulates the exchange of signals,cells.
文摘Objective:To characterize placental morphologic features in Moroccan women with adverse outcomes,across different clinical contexts,based on the Amsterdam consensus classification.Methods:A prospective analysis was conducted on placentas with umbilical cords collected fresh between March 1,2024 and July 15,2024 from women with adverse pregnancy outcomes.Clinical data(age,parity,gravidity,complications)were retrieved.Macroscopic parameters(weight,dimensions,cord insertion,membranes,lesions)were assessed,followed by systematic sampling.Tissue was processed by standard histology(formalin fixation,paraffin embedding,hematoxylin and eosin staining),and lesions were classified per Amsterdam criteria.Results:16 placentas from patients with adverse pregnancy outcomes were included.The median maternal age was 30 years.Adverse conditions included placental abruption(50%),intrauterine growth restriction(IUGR,38%),intrauterine fetal death(IUFD,31%),pre-eclampsia/eclampsia(19%),premature rupture of membranes(13%),and oligohydramnios(13%).Several placentas were associated with more than one adverse condition.Histopathology revealed maternal vascular malperfusion lesions in 94%,particularly in pre-eclampsia,IUGR,and IUFD.Fetal vascular malperfusion was found in 88%,mainly in IUGR and IUFD.Inflammatory lesions,dominated by acute maternal and fetal responses stage 3(necrotizing chorioamnionitis and funisitis),were primarily linked to IUFD.Conclusions:Placental examination enhances understanding of the pathophysiology underlying adverse pregnancy outcomes,supports diagnostic confirmation,and guides preventive strategies for recurrence.This study highlights the prevalence of maternal vascular malperfusion in Moroccan women and emphasizes the importance of systematic placental histopathology in obstetric care.
基金support from the Sichuan Science and Technology Program(2024JDHJ0043 and 2025YFHZ0121).
文摘Recently,Tian et al.published a research paper with significant breakthroughs in Cell[1].The study found that targeting the signalling pathways named Serpine2-lowdensity lipoprotein receptor-related protein 1(Lrp1)and ectonucleoside triphosphate diphosphohydrolase 1(CD39)-adenosine A_(3)receptor(A_(3)AR)is a promising strategy for the treatment of vascular dementia.The Serpine2-Lrp1 signalling pathway primarily exerts its therapeutic effects on myelin regeneration by regulating the differentiation of oligodendrocyte precursor cells.Serpine2 is a secretory serine protease inhibitor regulates proteolytic homeostasis.It may also bind to cell surface receptors such as Lrp1 to directly activate signalling pathways.As a transmembrane glycoprotein receptor,Lrpl mediates the endocytic clearance of ligands.
基金funded by China Postdoctoral Science Foundation(Grant Number:2025M773939)NationalNatural Science Foundation of China(Grant Number:82205131)Sichuan Science and Technology Program(Grant Number:2025ZNSFSC1798).
文摘Varicocele(VC)is widely recognized as a prevalent and clinically significant cause of male infertility.However,the comprehensive pathogenic mechanisms underlying VC development and progression remain incompletely understood,creating an important knowledge gap in the field of andrology.This review establishes that VC pathogenesis centers on abnormal vascular remodeling and integrates multiple contributing elements,including anatomical abnormalities,biochemical disturbances,genetic factors,low body mass index(BMI),age,and specific sports habits,while secondary varicoceles are primarily induced by compressive pathologies.Through a systematic synthesis of current evidence and recent advances,this review aims to elucidate the complex pathogenic network of VC and provide valuable insights to guide future research directions and inform the development of targeted clinical applications.
基金The Youth Project of Tianjin Natural Science Foundation,Grant/Award Number:23JCQNJC01380。
文摘Background:The traditional method of heterotopic abdominal heart transplantation(HTx)involves crossclamping the inferior vena cava,which inevitably leads to bilateral lower limb ischemia(LI).This study first aimed to investigate the impact of LI on renal function in rats subjected to unilateral nephrectomy(UNx).Second,a modified method utilizing renal vessel-assisted anastomosis in rats with left UNx was compared with the traditional method for abdominal HTx.Methods:Male Sprague-Dawley rats were utilized as subjects for both experimental phases.In experiment 1,the animals were divided into four groups:sham operation group;LI group-rats undergoing occlusion of the abdominal aorta and vena cava below the renal vessels;UNx group-rats with left UNx;and LI+UNx group.All operated animals were monitored for up to 7 days for biochemical markers,renal histopathology,and survival rates.In experiment 2,we introduced the renal vessel-assisted method as the experimental group and compared it against the traditional method as the control within rat heterotopic HTx models.We assessed operative characteristics,echocardiography results,histological findings,and graft survival.Results:First,LI resulted in acute kidney dysfunction characterized by a decrease in 7day survival rates and creatinine clearance rates in both the LI and LI+UNx groups compared to the sham operation and UNx groups.Particularly,histopathological damage in the kidney and liver did not exhibit significant effects during this period.Second,the implementation of the renal vessel-assisted method significantly reduced bleeding volume at suture sites and enhanced the 7day survival rate compared to the traditional method.Conclusion:Acute kidney injury was induced by LI postoperation in treated rats.The renal vessel-assisted method demonstrated its effectiveness as a superior alternative that mitigates complications associated with the traditional method.
基金supported by the National Key R&D Program of China(2021YFD2200303)the National Natural Science Foundation of China(32271903,U24A20428)。
文摘The formation of wood is affected by the growing season and the environment.Ring-porous tree species have distinct earlywood-latewood differences.However,it is not clear how early wood and latewood respond to drought and the differences in adaptation.Therefore,based on the analyses of phenology,growth,and xylem development over a year,xylem development in Fraxinus mandshurica was divided into earlyw ood,transition,and latewood stages.Variation patterns of 38 wood indices from 31 genotypes indicated that the formation of wood tissues was inhibited,and the proportion of xylem cells was affected by drought at each stage.However,soluble sugar affected osmotic regulation only during drought across early wood and transition stages.To maintain water and nutrient transport during drought and to resist embolism risk,drought in the early wood stage leads to varying degrees of early wood vessel diameter reduction,with pits enlarging to compensate.In contrast,during the late wood stage,drought causes latewood vessel diameter to increase and pits to shrink accordingly.In addition,the results indicate that several wood indices correlate with drought resistance at each stage,but early wood vessel diameter,soluble sugar,and latewood ves sel diameters exhibited the strongest correlations in the early wood,transition,and latewood stages.These findings provide clues to understanding plant survival strategies under drought stress and are of significance for plant ecology research on the growth and adaptation of tree species under climate change.
文摘Objective:To investigate the effects of health education based on the Transtheoretical Model(TTM)on self-management and vascular crisis in patients undergoing finger replantation surgery.Methods:A total of 106 patients who underwent finger replantation surgery between January 2025 and December 2025 were randomly divided into control and intervention groups using a random number table method(control group,n=52;intervention group,n=54).The control group received standard perioperative nursing care,while the intervention group received TTM-based health education in addition to standard care.Self-management levels and incidence of vascular crisis were compared between the two groups.Results:After intervention,the Adult Health Self-Management Skills Rating Scale(AHSMSRS)scores in both groups increased significantly compared with baseline(control:91.26±5.49 to 116.97±8.15;intervention:90.39±6.72 to 136.38±9.36,p<0.001).The intervention group showed significantly higher AHSMSRS scores than the control group(136.38±9.36 vs.116.97±8.15,p<0.001).Similarly,general self-efficacy scores increased significantly in both groups,with the intervention group demonstrating superior improvement(36.73±4.78 vs.28.49±4.11,p<0.001).The incidence of vascular crisis was significantly lower in the intervention group(5.5%)compared with the control group(19.23%,χ2=3.421,p<0.05).Conclusion:Health education based on the Transtheoretical Model effectively enhances self-management abilities and self-efficacy in patients undergoing finger replantation surgery,and significantly reduces the incidence of postoperative vascular crisis.
基金the Chinese Academy of Sciences Research Center for Ecology and Environment of Central Asia(RCEECA),the construction and joint research for the China-Tajikistan“Belt and Road”Joint Laboratory on Biodiversity Conservation and Sustainable Use(2024YFE0214200)the Shanghai Cooperation Organization Partnership and International Technology Cooperation Plan of Science and Technology Projects(2023E01018,2025E01056)the Chinese Academy of Sciences President’s International Fellowship Initiative(PIFI)(2024VBC0006).
文摘Tajikistan represents a core region of the biodiversity hotspot in Central Asian mountains and has exceptional vascular plant diversity.However,the species diversity of the country faces urgent conservation challenges.There has been a lack of a comprehensive and multidimensional assessment to inform strategic conservation planning.Therefore,this study integrated 4 key biodiversity indices including species richness(SR),phylogenetic diversity(PD),threatened species richness(TSR),and endemic species richness(ESR)to map species diversity distribution patterns,identify conservation gaps,and elucidate their effects of climatic factors.This study revealed that species diversity shows a clear trend of decreasing from the western region to the eastern region of Tajikistan.The central–western mountains(specifically the Gissar-Darvasian and Zeravshanian regions)emerge as irreplaceable biodiversity hotspots.However,we found a severe spatial mismatch between these priority areas and the existing protected areas(PAs).Protection coverage for all hotspots was alarmingly low,ranging from 31.00%to 38.00%.Consequently,a critical 64.80%of integrated priority areas fall outside of the current PAs,representing a major conservation gap.This study identified precipitation seasonality and isothermality as the principal drivers,collectively explaining over 50.00%of the diversity variation and suggesting high vulnerability to hydrological shifts.Furthermore,we detected significant geographic sampling bias in the public biodiversity databases,with the most critical hotspot being systematically under-sampled.This study provides a robust scientific basis for conservation action,highlighting the urgent need to strategically expand PAs in the under-protected southwestern region and to mitigate critical sampling gaps through targeted data digitization and field surveys.These measures are indispensable for securing Tajikistan’s unique biodiversity and achieving the Kunming-Montreal Global Biodiversity Framework Target 3(“30×30 Protection”).
基金Natural Science Foundation of Shandong Province,No.ZR2022MH124Taian Science and Technology Development Fund,Nos.2023NS155,2023NS164。
文摘Stroke is a major cause of death and disability worldwide,and its pathogenesis is complex,involving multiple pathological processes,such as thrombosis,ischemia-repe rfusion injury,inflammato ry response,and blood-brain barrier disruption.In recent years,neutrophil extracellular traps have been found to be involved in the body's anti-infection defense and to play an important role in stroke.Studies have shown that neutrophil extracellular traps promote thrombus expansion and neuroinflammation in ischemic stroke,and they may be involved in disease progression and recove ry in hemorrhagic stroke by modulating local inflammation and influencing hematoma clearance.This review systematically summarizes the evolution and mechanism of action of neutrophil extracellular traps in stroke pathology.Reactive oxygen species drive the formation of neutrophil extra cellular traps 6-24 hours after cerebral infarction.At 24-48 hours,they exacerbate vascular injury and thrombosis,at 48-72 hours,they aggravate neurological injury,and after 72 hours,neutrophil extra cellular tra ps are involved in the disruption of the blood-brain barrier and the maintenance of the inflammatory response.During stroke development,neutrophil extracellular traps are involved in multiple pathological mechanisms after cerebral infa rction.They induce vascular endothelial damage,exacerbating vascular leakage and edema,injuring neuro ns,inducing apoptosis,promoting thrombosis,participating in reperfusion injury,and damaging the blood-brain barrier.In hemorrhagic stroke,neutrophil extracellular traps are closely associated with hematoma clearance,early brain injury,and delayed cerebral ischemia,and can be used as a biomarker to assess disease progression and efficacy.In the acute phase of stroke,neutrophil extracellular traps mainly promote injury,and in the chronic phase,they mainly promote repair.Neutrophil extracellular traps,as an important biomarker of stro ke,are closely correlated with stroke severity.Additionally,neutrophil extra cellular traps play an important role in atheroscle rosis and intracranial venous thrombosis.Current research has confirmed that deoxyribonuclease is a key drug for degrading neutrophil extracellular traps and has shown significant therapeutic potential.Peptidyl arginine deiminase 4 inhibitors and high mobility group box 1 antagonists effectively inhibit the formation of neutrophil extra cellular traps through their own unique mechanisms.M ulti-targeted inte rvention strategies for neutrophil extracellular traps have shown broad clinical application prospects.Neutrophil extracellular traps exhibit syne rgistic effects with anticoagulants and thrombolytic drugs,and interventions targeting neutrophil extracellular traps can influence the efficacy of anticoagulation and thrombolytic therapy.These findings provide a theoretical basis for developing new anticoagulation and thrombolysis strategies for stroke and im p roving clinical outcomes for patients.
文摘BACKGROUND:Sepsis is a prevalent and severe condition,with microcirculation disruptions playing a crucial role in its progression.Endothelial cell(EC)injury is the primary factor behind microcirculatory issues.This review is to outline the pathomechanism,organ heterogeneity,biomarkers,and therapeutic implications of endothelial dysfunction in sepsis,off ering references and insights for the clinical management of sepsis.METHODS:A systematic search of Web of Science and PubMed from inception to June 10,2025,limited to English publications,was conducted.Two reviewers independently identifi ed studies on EC injury in patients with septic microcirculatory dysfunction.Duplicate articles based on multiple search criteria were excluded.RESULTS:Fifty-nine articles,including cell,animal,and clinical studies,were included.These studies reported the effects of EC injury on the microcirculation in sepsis,including changes in vascular permeability,coagulation dysfunction,vasomotor regulation,and infl ammatory responses.These pathways interact and ultimately lead to septic microcirculation disorders.CONCLUSION:Sepsis-induced endothelial dysfunction involves various interconnected mechanisms,which collectively compromise ECs and impede microcirculatory perfusion.Future research should enhance current understanding of endothelial injury mechanisms,develop synergistic multi-target strategies to disrupt this cycle,and facilitate the clinical application of endothelial markers for early intervention and dynamic assessment.
基金supported by the Scientific Program of Tianjin Municipal Education Commission(Natural Science,Grant No.2022KJ254)Science Foundation of the Second Hospital of Tianjin Medical University(Grant No.2021ydey05)Tianjin Municipal Health Commission Integrated Traditional Chinese and Western Medicine Project(Grant No.2021173).
文摘Arteriovenous fistula(AVF)calcification is a common complication in hemodialysis patients that leads to AVF dysfunction and decreases the AVF survival,but the mechanisms of AVF calcification,especially the role of hemodynamic changes in AVF calcification have not been fully investigated.In this study,a computational fluid dynamics(CFD)model was carried out based on AVF,at the distal anastomosis of the cephalic vein and radial artery,generated from a patient-specific computed tomography(CT)angiography and Doppler ultrasound image.Hemodynamic factors were considered to explore the mechanisms responsible for the initiation and progression of AVF calcification.Five stages in one cardiac cycle were chosen to be studied for the velocity field,pressure,time-averaged wall shear stress(TAWSS),and oscillatory shear index(OSI).Blood pressure was higher in the arteriovenous anastomosis,and variations of great amplitude of pressure were examined during the cardiac cycle.Blood pressure,transient shear stress,TAWSS,and OSI were higher in the arteriovenous anastomosis and at the bottom of expanded outflow vein,and these sites were highly consistent with the calcified areas shown on CT angiography.On the contrary,no calcification was found in sites where streamline was stable,blood pressure did not change dramatically,as well as TAWSS and OSI were lower.It was shown that AVF calcification was correlated with hemodynamic changes,which may contribute to further understanding the mechanisms of AVF calcification and providing scientific evidence to inform the optimization of surgical strategies and the development of personalized interventional measures in clinical contexts.
文摘Vascular ageing is increasingly recognised as a key driver of cardiovascular and cerebrovascular disease rather than merely a passive consequence of chronological time.Progressive loss of endothelial regenerative capacity remains central to this process and is characterised by endothelial progenitor cell dysfunction,accumulation of senescent endothelial cells,and aberrant changes in the endothelial secretome.Taken together these alterations contribute to ineffective endothelial repair,chronic(low-grade)vascular inflammation and impaired endothelial barrier integrity and function,ultimately leading to vascular dysfunction.Over the past two decades,accumulating evidence from our group and others has provided mechanistic insight into how oxidative stress,redox imbalance,mitochondrial dysfunction and cellular senescence collectively impair endothelial(barrier)function and compromise overall vascular homeostasis.Age-dependent changes in progenitor cell number and function further limit the capacity of vasculature to respond to damage and stress.More recent work demonstrate that senolytics and senomorphics can preserve endothelial function and delay age-related vascular and cerebral barrier dysfunction in experimental models.This mini review supports an emerging framework that positions defective endothelial renewal as a critical driver of vascular ageing and endothelial dysfunction.We propose that concomitant application of senotherapeutics with progenitor cell-based or secretome-based approaches represents a critical next step in precision vascular medicine.
基金supported by the Russian state-funded project for ICBFM SB RAS(grant number 125012300656-5)。
文摘Background:The development of materials for cardiovascular surgery that would improve the effectiveness of surgical interventions remains an important task.Surgical intervention during the implantation of vascular prostheses and stents,and the body’s reaction to artificial materials,could lead to chronic inflammation,a local increase in the concentration of proinflammatory factors,and stimulation of unwanted tissue growth.The introduction of nonsteroidal anti-inflammatory drugs into implantable devices could be used to obtain vascular implants that do not induce inflammation and do not induce neointimal tissue outgrowth.Methods:The scaffolds were made by electrospinning from mixtures of polyurethane(PU)with diclofenac(DF).The kinetics of DF release from the scaffolds composed of 3%PU/10%HSA/3%DMSO/DF and 3%PU/DF were studied.The biocompatibility and anti-inflammatory effects of the obtained scaffolds on human gingival fibroblasts and umbilical vein endothelial cells were studied.Results:Both types of scaffolds are characterized by fast DF release.The viability of cells cultured on scaffolds is 2 times worse than that of cells cultured on plastic.The level of the proinflammatory cytokine IL-6 in the culture medium of cells cultured on DF-containing scaffolds was lower than that of cells cultured on scaffolds without DF.Conclusion:The introduction of DF into scaffolds minimizes the inflammation caused by cell reactions to an artificial material.
文摘AIM:To investigate the changes of retinal vascular parameters and retinal layer thickness in patients with multiple sclerosis(MS).METHODS:This single-centered case-control study was performed on a MS group of 42 patients diagnosed with MS and a control group of 43 healthy hospital staff matched in terms of age and sex at Iran University,department of neurology and ophthalmology from March 2020 to March 2021.The ophthalmic parameters of each patient were recorded,and optical coherence tomography was used to evaluate the retinal thickness in the layers.RESULTS:This study enrolled a total of 85 participants,with a mean age of 40.44±11.52 years,including 61 females(72%).The control group consisted of 43 individuals with a mean age of 39.49±11.07 years,while the MS group comprised 42 participants with a mean age of 41.40±12.01 years.The mean disease duration in the MS group was 8.45±6.04 a.The thickness of the ganglion cell layer in the right eye was significantly lower in the MS group compared to the control group(P=0.034).In addition,except for the left nasal sector(P=0.106),the mean peripapillary neurofibrillation in all examined sectors were significantly lower in the MS group than in the control group(P<0.05).The average vessel density in both the deep and superficial capillary plexuses across all regions of both eyes was lower in the MS group than in the control group,with all comparisons for the superficial capillary plexus showing statistical significance(P<0.05 for all except the left nasal sector).CONCLUSION:The thickness of the retina of patients with MS is significantly reduced.Therefore,optical coherence tomography results can be used as a reliable tool to evaluate disease progression and prognosis in MS patients.
文摘AIM:To investigate the association between anti-DFS70 antibody positivity and ocular parameters,specifically,the choroidal vascularity index(CVI)and other optical coherence tomography(OCT)metrics,in a healthy population.METHODS:This age-and sex-matched case-control study enrolled 84 healthy individuals with positive anti-DFS70 antibody findings and 84 healthy negative controls.All participants underwent detailed ophthalmological examinations,including biometry and OCT imaging.Anti-DFS70 positivity was determined by indirect immunofluorescence and scored semi-quantitatively(1+to 3+).CVI was calculated from OCT images using a standardized protocol with Image J software.Statistical analyses,including Student’s t-test,Mann-Whitney U test,Spearman correlation,and logistic regression,were used to compare groups and identify predictive factors.RESULTS:The individuals who tested positive and negative for anti-DFS70 included in the study were matched for age(median age=47y)and sex(F:M=7:1).CVI was significantly lower in the anti-DFS70-positive group compared to the negative group.A higher anti-DFS70 antibody titer was significantly associated with decreased subfoveal and nasal choroidal thickness(P=0.016 and P=0.014,respectively).In univariate regression analysis,CVI was the only significant predictor of anti-DFS70 positivity[odds ratio(OR)=0.02,P=0.025].Multivariate analysis revealed a positive correlation between macular thinning outside the subfoveal area and anti-DFS70 status(P<0.05).CONCLUSION:Our study demonstrates a novel association between anti-DFS70 antibody positivity and reduced choroidal vascularity in healthy individuals.These findings suggest that anti-DFS70 antibodies may be associated with subtle choroidal vascular changes detectable by OCT,even in asymptomatic individuals.Further longitudinal research is warranted to clarify the underlying mechanisms and long-term clinical significance of these ocular changes.
文摘Nail changes following upper extremity transplantation(UET)cannot be overlooked as they possess diagnostic and prognostic relevance in allotransplantation of upper limbs.This comprehensive review explores nail and nail bed related changes encountered in UET recipients in the literature.The differential diagnosis of nail abnormalities in UET includes a wide range of systemic,local and iatrogenic conditions other than immune responses to the allograft.It requires interdisciplinary evaluation by primary transplant surgeons,pathologists,dermatologists and immunologists.The possible underlying mechanisms of nail pathology in UET and the management are discussed.It also underscores the importance of onychodystrophy and need for timely intervention and to improve outcomes in UET recipients.
基金supported by National Institute on Aging(NIH-NIA)R01AG054459(to ALL).
文摘Alzheimer’s disease(AD)is the most common form of dementia,affecting over 50 million people worldwide.This figure is projected to nearly double every 20 years,reaching 82 million by 2030 and 152 million by 2050(Alzheimer’s Disease International).The apolipoproteinε4(APOE4)allele is the strongest genetic risk factor for late-onset AD(after age 65 years).Apolipoprotein E,a lipid transporter,exists in three variants:ε2,ε3,andε4.APOEε2(APOE2)is protective against AD,APOEε3(APOE3)is neutral,while APOE4 significantly increases the risk.Individuals with one copy of APOE4 have a 4-fold greater risk of developing AD,and those with two copies face an 8-fold risk compared to non-carriers.Even in cognitively normal individuals,APOE4 carriers exhibit brain metabolic and vascular deficits decades before amyloid-beta(Aβ)plaques and neurofibrillary tau tangles emerge-the hallmark pathologies of AD(Reiman et al.,2001,2005;Thambisetty et al.,2010).Notably,studies have demonstrated reduced glucose uptake,or hypometabolism,in brain regions vulnerable to AD in asymptomatic middle-aged APOE4 carriers,long before clinical symptoms arise(Reiman et al.,2001,2005).
