Alzheimer’s disease(AD)is the most common cause of dementia,characterized by progressive cognitive decline,and affects over 55 million people worldwide.AD is pathological featured by the aberrant accumulation of amyl...Alzheimer’s disease(AD)is the most common cause of dementia,characterized by progressive cognitive decline,and affects over 55 million people worldwide.AD is pathological featured by the aberrant accumulation of amyloid-βplaques,neurofibrillary tangles formed by hyperphosphorylated tau,synaptic loss,and dysfunction of neurotransmitter systems.Evidence from in vivo and autopsy studies has consistently shown that synaptic dysfunction and loss are strongly correlated with cognitive decline in AD,particularly in brain regions such as the hippocampus and cortex,which are critical for memory formation and processing.This perspective highlights recent histopathological findings related to synaptic dysfunction in AD,advancements in the development of imaging and fluid-based biomarkers for synaptic loss,and future studies.展开更多
Cerebral small vessel disease(SVD)represents a range of pathological changes in the small blood vessels of the brain.SVD can be detected on MRI,which includes white matter hyperintensities,lacunes,and cerebral microbl...Cerebral small vessel disease(SVD)represents a range of pathological changes in the small blood vessels of the brain.SVD can be detected on MRI,which includes white matter hyperintensities,lacunes,and cerebral microbleeds(Duering et al.,2023).Patients with SVD exhibit significant clinical heterogeneity,often presenting with cognitive impairment,apathy,gait dysfunction,and lacunar stroke(Wardlaw et al.,2019).展开更多
Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pa...Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pathological factor contributing to the progression of sarcopenia.However,the morphological and functional changes in mitochondria and their interplay in the degeneration of the neuromuscular junction during aging remain poorly understood.A defined systematic search of the Pub Med,Web of Science and Embase databases(last accessed on October 30,2024)was conducted with search terms including'mitochondria','aging'and'NMJ'.Clinical and preclinical studies of mitochondrial dysfunction and neuromuscular junction degeneration during aging.Twentyseven studies were included in this systematic review.This systematic review provides a summary of morphological,functional and biological changes in neuromuscular junction,mitochondrial morphology,biosynthesis,respiratory chain function,and mitophagy during aging.We focus on the interactions and mechanisms underlying the relationship between mitochondria and neuromuscular junctions during aging.Aging is characterized by significant reductions in mitochondrial fusion/fission cycles,biosynthesis,and mitochondrial quality control,which may lead to neuromuscular junction dysfunction,denervation and poor physical performance.Motor nerve terminals that exhibit redox sensitivity are among the first to exhibit abnormalities,ultimately leading to an early decline in muscle strength through impaired neuromuscular junction transmission function.Parg coactivator 1 alpha is a crucial molecule that regulates mitochondrial biogenesis and modulates various pathways,including the mitochondrial respiratory chain,energy deficiency,oxidative stress,and inflammation.Mitochondrial dysfunction is correlated with neuromuscular junction denervation and acetylcholine receptor fragmentation,resulting in muscle atrophy and a decrease in strength during aging.Physical therapy,pharmacotherapy,and gene therapy can alleviate the structural degeneration and functional deterioration of neuromuscular junction by restoring mitochondrial function.Therefore,mitochondria are considered potential targets for preserving neuromuscular junction morphology and function during aging to treat sarcopenia.展开更多
Dengue fever is an acute infectious disease caused by the dengue virus and transmitted by mosquito vectors[1].Its clinical manifestations include high fever,headache,muscle and joint pain,and rash.It holds a significa...Dengue fever is an acute infectious disease caused by the dengue virus and transmitted by mosquito vectors[1].Its clinical manifestations include high fever,headache,muscle and joint pain,and rash.It holds a significant position in global public health.In recent years,its incidence has continued to rise worldwide[2],making it one of the major diseases threatening human health.The disease course of dengue fever is divided into three typical phases:the acute febrile phase,the critical phase,and the recovery phase.While most patients experience mild symptoms,some may progress to severe dengue and potentially fatal outcomes if not promptly and effectively treated during the critical phase.展开更多
Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables th...Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.展开更多
Diabetic cardiomyopathy(DCM)has long been considered as a left ventricular(LV)disease with diastolic dysfunction preceding systolic dysfunction in diabetes.However,it is increasingly recognized that the right ventricl...Diabetic cardiomyopathy(DCM)has long been considered as a left ventricular(LV)disease with diastolic dysfunction preceding systolic dysfunction in diabetes.However,it is increasingly recognized that the right ventricle(RV)is also affected by diabetes and may be independently responsible for adverse outcomes in diabetic patients with or without LV failure.Yu et al conducted a 30-week longitudinal evaluation of biventricular function and pathology in OVE26 diabetic mice and revealed early diastolic dysfunction preceding systolic decline,suggesting that early LV diastolic impairment precedes the later onset of systolic dysfunction.With age,the animals developed fibrosis,hypertrophy,and pulmonary arterial hypertension in the RV.The purpose of this editorial is to contextualize these findings within the existing literature by highlighting the interplay between cardiac chambers and the vasculature.We also seek to reiterate that DCM is a condition extending beyond left ventricular dysfunction.As the authors note,the right side of the heart may remain"the forgotten ventricle"in diabetic patients.We hope that the mechanisms discussed in this paper will help researchers to understand the pathogenesis of cardiovascular disease in this context and encourage clinicians to be more attentive to the associated clinical symptoms.展开更多
BACKGROUND Global longitudinal strain(GLS)of the left ventricular is a highly sensitive and reliable marker of systolic function and GLS outperforms ejection fraction(EF)in detecting preclinical left ventricular systo...BACKGROUND Global longitudinal strain(GLS)of the left ventricular is a highly sensitive and reliable marker of systolic function and GLS outperforms ejection fraction(EF)in detecting preclinical left ventricular systolic dysfunction(LVSD).In patients with type 2 diabetes(DM2)albuminuria is a predictor of symptomatic heart failure,but data on the relationship between GLS and albuminuria are conflicting.AIM To explore the relationship between GLS and albuminuria in a contemporary cohort of DM2 patients.METHODS The study was performed on DM2 patients consecutively enrolled in the TESEO study.Patients with symptoms/signs of heart failure,EF<50%,coronary artery,other cardiac diseases,or non-adequate acoustic window for GLS assessment were excluded.We collected clinical data,screened for complications,and measured GLS by speckle-tracking echocardiography.Univariate and multiple linear regression analyses were performed to identify independent explanatory variables associated with GLS.Logistic regression analysis was used to assess whether albuminuria was independently associated with GLS-diagnosed(GLS>-18%)LVSD.RESULTS Patients(n=193,age:60.6±8.1,male:57%)had a short DM2 duration(3.8±4.9 years)and good metabolic control(glycated haemoglobin A1c:6.5%±1.0).Preclinical GLS-LVSD was present in 21.8%of the patients.GLS values were significantly higher in patients with albuminuria(-19.88±2.16 vs-18.29±2.99,P<0.001)and in multivariate analysis natural logarithm of albumin-creatinine ratio and uric acid were independent predictors of GLS.In logistic regression analysis,albuminuria was associated with a 6.01(95%confidence interval:1.874-19.286)increased odds ratio of GLS-LVSD,independent of age,sex,diastolic blood pressure,chronic kidney disease,EF,mitral annulus velocity lateral,uric acid,and treatments.CONCLUSION Albuminuria was independently associated with subclinical LVSD in our contemporary cohort of DM2 patients.展开更多
Left ventricular diastolic dysfunction is frequently noticed in patients with chronic kidney disease.Echocardiography is used to determine the presence and severity of diastolic dysfunction.In left ventricular diastol...Left ventricular diastolic dysfunction is frequently noticed in patients with chronic kidney disease.Echocardiography is used to determine the presence and severity of diastolic dysfunction.In left ventricular diastolic dysfunction the ventricular diastolic distensibility,filling or relaxation is abnormal;however,the left ventricular ejection fraction may be normal or decreased.In heart failure with preserved ejection fraction,the patients have symptomatic pulmonary congestion even though the systolic ejection fraction is more than 50%.This condition is commonly associated with ventricular diastolic dysfunction.Increased incidence of major adverse cardiovascular events has been reported in surgical patients having grade III diastolic dysfunction.Peri-operatively haemodynamic instability and fluid overload in this set of patients is known to generate pulmonary oedema.展开更多
The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients wit...The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients with multiple vessel disease and moderately or severely impaired left ventricular function, who underwent coronary surgery with the intention of total arterial revascularization with 2 conduits between March 1995 and August 2002. One hundred and seventy-nine patients were included in the study. Acute coronary insufficiency was present in 3 patients and 43 had unstable angina. Severe left ventricular impairment was present in 29 patients. There were 17 redo operations including 3 redo-redo procedures. Eighty-two percent of patients had a Y graft configuration from the left internal mammary artery （right internal mammary artery 40. 8 %, radial artery 33. 5 %, other 7.8 % ）. The perioperative mortality was 2. 2 %, myocardial infarction 1.7 % and stroke 0. 6 %. Total arterial revascularization in patients with ischaemic left ventricular dysfunction can be safely performed with 2 arterial conduits. The radial artery provides conduit length greater than the right internal mammary artery and allows full revascularization despite left ventricular dilatation.展开更多
BACKGROUND Liver cirrhosis is a chronic hepatic disease which is associated with cardiovascular abnormalities.Hyperdynamic circulation in liver cirrhosis causes functional and structural cardiac alterations.The preval...BACKGROUND Liver cirrhosis is a chronic hepatic disease which is associated with cardiovascular abnormalities.Hyperdynamic circulation in liver cirrhosis causes functional and structural cardiac alterations.The prevalence of left ventricle diastolic dysfunction(LVDD)in cirrhotic patients ranges from 25.7%to as high as 81.4%as reported in different studies.In several studies the severity of diastolic dysfunction(DD)correlated with a degree of liver failure and the rate of dysfunction was higher in patients with decompensated cirrhosis compared with compensated.Future directions of comprehensive assessment of cardiac function in cirrhotic patients might provide a better prognosis for these patients.AIM To clarify the correlation between the severity of liver cirrhosis and left ventricle diastolic dysfunction in the existing literature.METHODS Through January and February of 2019 at Vilnius University we conducted a systematic review of the global existing literature on the prevalence of left ventricle diastolic dysfunction in patients with liver cirrhosis.We searched for articles in PubMed,Medline and Web of science databases.Articles were selected by using adequate inclusion and exclusion criteria.Our interest was the outcome of likely correlation between the severity of cirrhosis[evaluated by Child-Pugh classes,Model For End-Stage Liver Disease(MELD)scores]and left ventricle diastolic dysfunction[classified according to American Society of Echocardiography(ASE)guidelines(2009,2016)],as well as relative risk of dysfunction in cirrhotic patients.Subgroup analyses were performed to evaluate the ratio and grades of left ventricle diastolic dysfunction with respect to cirrhosis severity.RESULTS A total of 1149 articles and abstracts met the initial search criteria.Sixteen articles which met the predefined eligibility criteria were included in the final analysis.Overall,1067 patients(out of them 723 men)with liver cirrhosis were evaluated for left ventricle diastolic dysfunction.In our systemic analysis we have found that 51.2%of cirrhotic patients had left ventricle diastolic dysfunction diagnosed and the grade 1 was the most prevalent(59.2%,P<0.001)among them,the grade 3 had been rarely diagnosed-only 5.1%.The data about the prevalence of diastolic dysfunction in cirrhotic patients depending on Child-Pugh Classes was available from 5 studies(365 patients overall)and only in 1 research diastolic dysfunction was found being associated with severity of liver cirrhosis(P<0.005).We established that diastolic dysfunction was diagnosed in 44.6%of Child-Pugh A class patients,in 62%of Child B class and in 63.3%of Child C patients(P=0.028).The proportion of patients with higher diastolic dysfunction grades increases in more severe cirrhosis presentation(P<0.001).There was no difference between mean MELD scores in patients with and without diastolic dysfunction and in different diastolic dysfunction groups.In all studies diastolic dysfunction was more frequent in patients with ascites.CONCLUSION This systemic analysis suggests that left ventricle diastolic dysfunction is an attribute of liver cirrhosis which has not received sufficient attention from clinicians so far.Future suggestions of a comprehensive assessment of cardiac function in cirrhotic patients might provide a better prognosis for these patients and give hint for better understanding of the left ventricle diastolic dysfunction pathogenesis in liver cirrhosis.展开更多
Background Heart failure(HF)is a leading cause of hospitalization and mortality for older chronic kidney disease(CKD)patients.However,the epidemiological data is scarce.We aimed to determine the prevalence of left ven...Background Heart failure(HF)is a leading cause of hospitalization and mortality for older chronic kidney disease(CKD)patients.However,the epidemiological data is scarce.We aimed to determine the prevalence of left ventricular(LV)dysfunction and HF,and to explore the risk factors for HF among those patients.Methods This is a cross-sectional analysis of the China Hypertension Survey conducted between October 2012 and December 2015.A total of 5,808 participants aged≥65 years were included in the analysis.Self-reported history of HF and any other cardiovascular diseases was acquired.2-D and Doppler echocardiography were used to assess LV dysfunction.CKD was defined as either estimated glomerular filtration rate(eGFR)<60 mL/min per 1.73 m2 or urinary albumin to creatinine ratio(ACR)≥30 mg/g.Results Among CKD patients aged≥65 years,the weighted prevalence of HF,heart failure with preserved ejection fraction(HFpEF),heart failure with mid-range ejection fraction(HFmrEF),and heart failure with reduced ejection fraction(HFrEF)was 4.8%,2.5%,0.8%,and 1.7%,respectively.The weighted prevalence of HF was 5.0%in patients with eGFR<60 mL/min per 1.73 m2,and was 5.9%in patients with ACR≥30 mg/g.The prevalence of LV systolic dysfunction was 3.1%,and while it was 8.9%for moderate/severe diastolic dysfunction.Multivariate analysis showed that smoking was significantly associated with the risk of HF.Furthermore,age,smoking,and residents in rural areas were significantly associated with a risk of LV diastolic dysfunction.Conclusions The prevalence of HF and LV dysfunction was high in older patients with CKD,suggesting that particular strategies will be required.展开更多
Objective:To investigate the role of natriuretic peptide in the process of left ventricular dysfunction caused by emotional stress.Methods:Adult male SD rats(n=30)and Wistar rats(n=60)were selected in this study.Ather...Objective:To investigate the role of natriuretic peptide in the process of left ventricular dysfunction caused by emotional stress.Methods:Adult male SD rats(n=30)and Wistar rats(n=60)were selected in this study.Atherosclerosis models were induced with high-fat diet and excess VD3 injection(eight consecutive weeks),and anger stress models were prepared by residentintruder stress experiment(two consecutive weeks).Furthermore,left ventricular functions were examined by high-resolution echocardiograph,after which left ventricular myocardium and coronary arteries were prepared for pathological section and observed with electron microscope.At the same time,the hypothalamus,medulla oblongata and left ventricular myocardium were also prepared for pathological sections to detect the localization and expression of AMP,BNP and NPK-A with immunofluorescence and western blot.Results:We found that left ventricular functions of atherosclerosis or emotional stress modeled rats were both inferior to the healthy ones and superior to the combined(atherosclerosis and emotional stress)modeled ones(P<0.05).We also found that atherosclerosis and emotional stress could both cause morphological changes of left ventricular cells and capillary which contribute to apoptosis and hyperblastosis.Further more,there was NPR—A distributed in hypothalamus,medulla oblongata,as well as left ventricular tissues with the same express trend between groups,with atherosclerosis modeled rats the highest and the healthy rats the lowest.Conclusions:The results of our study suggest that anger stress could cause an excess consumption of ANP,BNP and NPR-A in nervous and cardiovascular system which inhibit the compensatory self-repair function of atherosclerosis rats,leading to a promotion of fibrosis and lipid peroxidation,offering insight into the neuroendocrine mechanisms of left heart function obstacle.展开更多
Stroke,as a highly prevalent cerebrovascular disease,often leads to limb dysfunction in patients,severely affecting their quality of life.Seeking effective rehabilitation nursing methods is of great significance for p...Stroke,as a highly prevalent cerebrovascular disease,often leads to limb dysfunction in patients,severely affecting their quality of life.Seeking effective rehabilitation nursing methods is of great significance for patient recovery.This article deeply analyzes various aspects such as intelligent rehabilitation technology,traditional Chinese medical therapies,Western medical therapies,and rehabilitation training methods.It explores the characteristics,effectiveness,and application prospects of various rehabilitation nursing approaches,providing a reference for clinical rehabilitation nursing of limb dysfunction after stroke,and helping to improve the quality of patient recovery and enhance their self-care ability and quality of life.展开更多
The endothelium modulates vascular homeostasis owing to a variety of vasoconstrictors and vasodilators.Endothelial dysfunction(ED),characterized by impaired vasodilation,inflammation,and thrombosis,triggers future car...The endothelium modulates vascular homeostasis owing to a variety of vasoconstrictors and vasodilators.Endothelial dysfunction(ED),characterized by impaired vasodilation,inflammation,and thrombosis,triggers future cardiovascular(CV)diseases.Chronic kidney disease,a state of chronic inflammation caused by oxidative stress,metabolic abnormalities,infection,and uremic toxins damages the endothelium.ED is also associated with a decline in estimated glomerular filtration rate.After kidney transplantation,endothelial functions undergo immediate but partial restoration,promising graft longevity and enhanced CV health.However,the anticipated CV outcomes do not happen due to various transplant-related and unrelated risk factors for ED,culminating in poor CV health and graft survival.ED in kidney transplant recipients is an underrecognized and poorly studied entity.CV diseases are the leading cause of death among kidney transplant candidates with functioning grafts.ED contributes to the pathogenesis of many of the CV diseases.Various biomarkers and vasoreactivity tests are available to study endothelial functions.With an increasing number of transplants happening every year,and improved graft rejection rates due to the availability of effective immunosuppressants,the focus has now shifted to endothelial protection for the prevention,early recognition,and treatment of CV diseases.展开更多
Recent work suggests a link betweenα-synuclein(α-syn)and mitochondrial dysfunction;however,the mechanisms of howα-syn influences mitochondrial function are still unclear.Most notably,whetherα-syn plays a direct ro...Recent work suggests a link betweenα-synuclein(α-syn)and mitochondrial dysfunction;however,the mechanisms of howα-syn influences mitochondrial function are still unclear.Most notably,whetherα-syn plays a direct role during mitochondrial function and/or whether diseasedα-syn-mediated mitochondrial dysfunction is a potential modifiable risk factor in Parkinson’s disease(PD)is unknown.To date,mutations in more than eight genes cause familial PD(fPD)and have functions in diverse pathways including synaptic homeostasis,mitochondria maintenance,autophagy/lysosome,and ubiquitin-proteasome pathways.展开更多
Alzheimer’s disease(AD)stands out as the primary manifestation of age-related dementia,portraying a chronic neurodegenerative disorder distinguished by the accumulation of fibrillar amyloid-β(Aβ)plaques and neurofi...Alzheimer’s disease(AD)stands out as the primary manifestation of age-related dementia,portraying a chronic neurodegenerative disorder distinguished by the accumulation of fibrillar amyloid-β(Aβ)plaques and neurofibrillary tangles of hyperphosphorylated tau.However,from a clinical standpoint,AD presents itself as a complex condition with a spectrum of dysfunctions rather than a singular pathological mechanism.An often-overlooked aspect of the disease is the presence of extensive cerebrovascular abnormalities,given that the majority of AD patients experience altered cerebral blood flow,damaged vasculature,increased microinfarcts and microhemorrhages.Animal models of AD further support this observation,showing cerebrovascular dysfunction such as impaired cerebral blood flow and altered cerebrovascular reactivity(Tataryn et al.,2021;Gareau et al.,2023).展开更多
BACKGROUND The development of slow transit constipation(STC)is associated with intestinal barrier damage.Huangqi decoction(HQD)is effective in treating STC,but me-chanisms are unclear.AIM To investigate whether HQD al...BACKGROUND The development of slow transit constipation(STC)is associated with intestinal barrier damage.Huangqi decoction(HQD)is effective in treating STC,but me-chanisms are unclear.AIM To investigate whether HQD alleviates STC by downregulating the nuclear factorκB(NF-κB)signaling pathway and restoring intestinal barrier function.METHODS KM mice were divided into control,model,and HQD treatment groups.Fresh colonic tissues were collected for single-cell RNA sequencing and spatial tra-nscriptome sequencing.The expressions of claudin-1,mucin 2,and NF-κB P65 proteins were detected by immunohistochemistry.In vitro experiments evaluated the effects of HQD on the LS174T cell line.RESULTS HQD improved intestinal motility,restored mucosal epithelium function and morphology.Single-cell RNA sequencing and spatial transcriptome sequencing data showed a reduction in goblet cells,decreased mucin 2 secretion,and activated apoptotic pathways in STC mice.The population of intestinal stem cells was reduced,and proliferation along with Wnt/β-catenin pathways were inhibited.STC also altered the distribution of intestinal cell states,increasing immune-associated Enterocyte_C3.Aberrant NF-κB pathway activation was noted across various cell types.After HQD treatment,NF-κB pathway activity was down-regulated,while cell proliferation pathways were up-regulated,alongside an increase in Enterocyte_C1 related to material transport.Immunocytochemical,Western blot,and immunohistochemistry analyses confirmed NF-κB pathway activation in goblet cells of STC mice,with HQD inhibiting this aberrant activation.CONCLUSION STC involves intestinal mucosal barrier damage.HQD may treat STC by suppressing NF-κB signaling in epithelial cells,restoring intestinal epithelial cell function,and promoting mucosal barrier repair.展开更多
Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not complet...Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.展开更多
BACKGROUND Valvular heart disease affects more than 100 million people worldwide and is associated with significant morbidity and mortality.The prevalence of at least moderate valvular heart disease is 2.5%across all ...BACKGROUND Valvular heart disease affects more than 100 million people worldwide and is associated with significant morbidity and mortality.The prevalence of at least moderate valvular heart disease is 2.5%across all age groups,but its prevalence increases with age.Mitral regurgitation and aortic stenosis are the most frequent types of valvular heart disease in the community and hospital context,res-pectively.Surgical valve replacement(or mitral valve repair)is the standard of care for treating heart valve disease.However,the replacement of a prosthetic heart valve can lead to complications,either in the peri-procedural phase or in the long-term follow-up period.CASE SUMMARY We present a case of a 71-year-old female patient with a history of mitral valve replacement and warfarin anti-coagulation therapy.She was admitted to the intensive care unit due to spontaneously reperfused ischemic stroke of probable cardioembolic etiology.A dysfunctional mitral prosthesis was identified due to malfunction of one of the fixed discs.Furthermore,a possible microthrombotic lesion was suspected.Therefore,systemic thrombolysis was performed with subsequent normalization of mitral disc opening and closing.CONCLUSION This case underscores the critical importance of a multidisciplinary approach for timely decision-making in critically ill patients with prosthetic valve complications.展开更多
BACKGROUND Diabetes has become a widespread metabolic disease affecting multiple organs.Among diabetic complications,cardiovascular complications are the main cause of patient morbidity and mortality.Diabetic cardiomy...BACKGROUND Diabetes has become a widespread metabolic disease affecting multiple organs.Among diabetic complications,cardiovascular complications are the main cause of patient morbidity and mortality.Diabetic cardiomyopathy is a diabetes-specific cardiomyopathy in the absence of other cardiovascular disease and occurs more frequently in type 1 diabetes(T1D)than in type 2 diabetes.Previous studies on diabetic cardiomyopathy have predominantly focused on the effects of diabetes on left ventricular(LV)dysfunction,while studies of right ventricular(RV)dysfunction have been sparse but are gaining attention.Although T1D accounts for only 5%-10%of the total diabetic population,diabetic cardiomyopathy is a major cause of morbidity and mortality in children with life-long,long-term complications.AIM To evaluate longitudinal RV and LV functional changes in female transgenic OVE26,T1D mice and wild-type FVB mice over a 30-week period.METHODS RV and LV structure and function were evaluated by transthoracic echocardiography.RV systolic pressure was measured by a transducer-tipped pressure catheter.Sirius-red staining was used to quantify collagen and fibrosis,wheat germ agglutinin staining was utilized to measure cardiomyocyte size,and quantitative real-time polymerase chain reaction and Western blotting were used to quantify miRNA expression and protein abundance,respectively.RESULTS RV systolic function,measured by tricuspid valve annular plane systolic excursion and RV systolic velocity,was similar between control and T1D mice,but LV systolic function decreased in T1D mice at 30 weeks of age.RV diastolic dysfunction in T1D mice significantly increased by 18 weeks and progressed until 30 weeks,while LV diastolic dysfunction trended towards abnormal at 12 weeks,significantly increased by 18 weeks,and continued to progress by 30 weeks.Furthermore,RV diastolic dysfunction was accompanied by RV cardiac fibrosis and hypertrophy in T1D mice,occurring later than that in the LV.Pulmonary arterial hypertension developed in T1D mice,evidenced by increased pulmonary acceleration time to pulmonary ejection time ratio and increased RV peak systolic pressure at 30 weeks.These results suggest the development of early LV diastolic dysfunction followed by LV systolic dysfunction and RV diastolic dysfunction at 30 weeks in T1D mice.CONCLUSION RV diastolic dysfunction develops later than LV dysfunction in OVE26 T1D mice.Mild pulmonary arterial hypertension appear at later stages of T1D and could contribute to RV systolic impairment and remodeling.展开更多
基金supported by Swiss Center for Applied Human Toxicology(SCAHT AP22-01)(to RN).
文摘Alzheimer’s disease(AD)is the most common cause of dementia,characterized by progressive cognitive decline,and affects over 55 million people worldwide.AD is pathological featured by the aberrant accumulation of amyloid-βplaques,neurofibrillary tangles formed by hyperphosphorylated tau,synaptic loss,and dysfunction of neurotransmitter systems.Evidence from in vivo and autopsy studies has consistently shown that synaptic dysfunction and loss are strongly correlated with cognitive decline in AD,particularly in brain regions such as the hippocampus and cortex,which are critical for memory formation and processing.This perspective highlights recent histopathological findings related to synaptic dysfunction in AD,advancements in the development of imaging and fluid-based biomarkers for synaptic loss,and future studies.
基金supported by China Scholarship Council(No.202106380078 to HL)the Netherlands Cardiovascular Research Initiative:The Dutch Heart Foundation(CVON 2018-28 and 2012-06 Heart Brain Connection to AMT)。
文摘Cerebral small vessel disease(SVD)represents a range of pathological changes in the small blood vessels of the brain.SVD can be detected on MRI,which includes white matter hyperintensities,lacunes,and cerebral microbleeds(Duering et al.,2023).Patients with SVD exhibit significant clinical heterogeneity,often presenting with cognitive impairment,apathy,gait dysfunction,and lacunar stroke(Wardlaw et al.,2019).
基金supported by grants from Collaborative Research Fund(Ref:C4032-21GF)General Research Grant(Ref:14114822)+1 种基金Group Research Scheme(Ref:3110146)Area of Excellence(Ref:Ao E/M-402/20)。
文摘Mitochondrial dysfunction and oxidative stress are widely regarded as primary drivers of aging and are associated with several neurodegenerative diseases.The degeneration of motor neurons during aging is a critical pathological factor contributing to the progression of sarcopenia.However,the morphological and functional changes in mitochondria and their interplay in the degeneration of the neuromuscular junction during aging remain poorly understood.A defined systematic search of the Pub Med,Web of Science and Embase databases(last accessed on October 30,2024)was conducted with search terms including'mitochondria','aging'and'NMJ'.Clinical and preclinical studies of mitochondrial dysfunction and neuromuscular junction degeneration during aging.Twentyseven studies were included in this systematic review.This systematic review provides a summary of morphological,functional and biological changes in neuromuscular junction,mitochondrial morphology,biosynthesis,respiratory chain function,and mitophagy during aging.We focus on the interactions and mechanisms underlying the relationship between mitochondria and neuromuscular junctions during aging.Aging is characterized by significant reductions in mitochondrial fusion/fission cycles,biosynthesis,and mitochondrial quality control,which may lead to neuromuscular junction dysfunction,denervation and poor physical performance.Motor nerve terminals that exhibit redox sensitivity are among the first to exhibit abnormalities,ultimately leading to an early decline in muscle strength through impaired neuromuscular junction transmission function.Parg coactivator 1 alpha is a crucial molecule that regulates mitochondrial biogenesis and modulates various pathways,including the mitochondrial respiratory chain,energy deficiency,oxidative stress,and inflammation.Mitochondrial dysfunction is correlated with neuromuscular junction denervation and acetylcholine receptor fragmentation,resulting in muscle atrophy and a decrease in strength during aging.Physical therapy,pharmacotherapy,and gene therapy can alleviate the structural degeneration and functional deterioration of neuromuscular junction by restoring mitochondrial function.Therefore,mitochondria are considered potential targets for preserving neuromuscular junction morphology and function during aging to treat sarcopenia.
文摘Dengue fever is an acute infectious disease caused by the dengue virus and transmitted by mosquito vectors[1].Its clinical manifestations include high fever,headache,muscle and joint pain,and rash.It holds a significant position in global public health.In recent years,its incidence has continued to rise worldwide[2],making it one of the major diseases threatening human health.The disease course of dengue fever is divided into three typical phases:the acute febrile phase,the critical phase,and the recovery phase.While most patients experience mild symptoms,some may progress to severe dengue and potentially fatal outcomes if not promptly and effectively treated during the critical phase.
文摘Neurodevelopmental processes represent a finely tuned interplay between genetic and environmental factors,shaping the dynamic landscape of the developing brain.A major component of the developing brain that enables this dynamic is the white matter(WM),known to be affected in neurodevelopmental disorders(NDDs)(Rokach et al.,2024).WM formation is mediated by myelination,a multifactorial process driven by neuro-glia interactions dependent on proper neuronal functionality(Simons and Trajkovic,2006).Another key aspect of neurodevelopmental abnormalities involves neuronal dynamics and function,with recent advances significantly enhancing our understanding of both neuronal and glial mitochondrial function(Devine and Kittler,2018;Rojas-Charry et al.,2021).Energy homeostasis in neurons,attributed largely to mitochondrial function,is critical for proper functionality and interactions with oligodendrocytes(OLs),the cells forming myelin in the brain’s WM.We herein discuss the interplay between these processes and speculate on potential dysfunction in NDDs.
文摘Diabetic cardiomyopathy(DCM)has long been considered as a left ventricular(LV)disease with diastolic dysfunction preceding systolic dysfunction in diabetes.However,it is increasingly recognized that the right ventricle(RV)is also affected by diabetes and may be independently responsible for adverse outcomes in diabetic patients with or without LV failure.Yu et al conducted a 30-week longitudinal evaluation of biventricular function and pathology in OVE26 diabetic mice and revealed early diastolic dysfunction preceding systolic decline,suggesting that early LV diastolic impairment precedes the later onset of systolic dysfunction.With age,the animals developed fibrosis,hypertrophy,and pulmonary arterial hypertension in the RV.The purpose of this editorial is to contextualize these findings within the existing literature by highlighting the interplay between cardiac chambers and the vasculature.We also seek to reiterate that DCM is a condition extending beyond left ventricular dysfunction.As the authors note,the right side of the heart may remain"the forgotten ventricle"in diabetic patients.We hope that the mechanisms discussed in this paper will help researchers to understand the pathogenesis of cardiovascular disease in this context and encourage clinicians to be more attentive to the associated clinical symptoms.
基金Supported by the Italian Ministry for Education,University and Research under the Programme“Dipartimenti di Eccellenza 2018-2022”Project,No.D15D18000410001Novo Nordisk“Gestione delle complicanze croniche del diabete:From bedside to bench?”,No.n1/2021.
文摘BACKGROUND Global longitudinal strain(GLS)of the left ventricular is a highly sensitive and reliable marker of systolic function and GLS outperforms ejection fraction(EF)in detecting preclinical left ventricular systolic dysfunction(LVSD).In patients with type 2 diabetes(DM2)albuminuria is a predictor of symptomatic heart failure,but data on the relationship between GLS and albuminuria are conflicting.AIM To explore the relationship between GLS and albuminuria in a contemporary cohort of DM2 patients.METHODS The study was performed on DM2 patients consecutively enrolled in the TESEO study.Patients with symptoms/signs of heart failure,EF<50%,coronary artery,other cardiac diseases,or non-adequate acoustic window for GLS assessment were excluded.We collected clinical data,screened for complications,and measured GLS by speckle-tracking echocardiography.Univariate and multiple linear regression analyses were performed to identify independent explanatory variables associated with GLS.Logistic regression analysis was used to assess whether albuminuria was independently associated with GLS-diagnosed(GLS>-18%)LVSD.RESULTS Patients(n=193,age:60.6±8.1,male:57%)had a short DM2 duration(3.8±4.9 years)and good metabolic control(glycated haemoglobin A1c:6.5%±1.0).Preclinical GLS-LVSD was present in 21.8%of the patients.GLS values were significantly higher in patients with albuminuria(-19.88±2.16 vs-18.29±2.99,P<0.001)and in multivariate analysis natural logarithm of albumin-creatinine ratio and uric acid were independent predictors of GLS.In logistic regression analysis,albuminuria was associated with a 6.01(95%confidence interval:1.874-19.286)increased odds ratio of GLS-LVSD,independent of age,sex,diastolic blood pressure,chronic kidney disease,EF,mitral annulus velocity lateral,uric acid,and treatments.CONCLUSION Albuminuria was independently associated with subclinical LVSD in our contemporary cohort of DM2 patients.
文摘Left ventricular diastolic dysfunction is frequently noticed in patients with chronic kidney disease.Echocardiography is used to determine the presence and severity of diastolic dysfunction.In left ventricular diastolic dysfunction the ventricular diastolic distensibility,filling or relaxation is abnormal;however,the left ventricular ejection fraction may be normal or decreased.In heart failure with preserved ejection fraction,the patients have symptomatic pulmonary congestion even though the systolic ejection fraction is more than 50%.This condition is commonly associated with ventricular diastolic dysfunction.Increased incidence of major adverse cardiovascular events has been reported in surgical patients having grade III diastolic dysfunction.Peri-operatively haemodynamic instability and fluid overload in this set of patients is known to generate pulmonary oedema.
文摘The feasibility and safety of total arterial coronary revascularization with 2 arterial conduits in patients with impaired left ventricular function was evaluated. Data were prospectively collected on all patients with multiple vessel disease and moderately or severely impaired left ventricular function, who underwent coronary surgery with the intention of total arterial revascularization with 2 conduits between March 1995 and August 2002. One hundred and seventy-nine patients were included in the study. Acute coronary insufficiency was present in 3 patients and 43 had unstable angina. Severe left ventricular impairment was present in 29 patients. There were 17 redo operations including 3 redo-redo procedures. Eighty-two percent of patients had a Y graft configuration from the left internal mammary artery （right internal mammary artery 40. 8 %, radial artery 33. 5 %, other 7.8 % ）. The perioperative mortality was 2. 2 %, myocardial infarction 1.7 % and stroke 0. 6 %. Total arterial revascularization in patients with ischaemic left ventricular dysfunction can be safely performed with 2 arterial conduits. The radial artery provides conduit length greater than the right internal mammary artery and allows full revascularization despite left ventricular dilatation.
文摘BACKGROUND Liver cirrhosis is a chronic hepatic disease which is associated with cardiovascular abnormalities.Hyperdynamic circulation in liver cirrhosis causes functional and structural cardiac alterations.The prevalence of left ventricle diastolic dysfunction(LVDD)in cirrhotic patients ranges from 25.7%to as high as 81.4%as reported in different studies.In several studies the severity of diastolic dysfunction(DD)correlated with a degree of liver failure and the rate of dysfunction was higher in patients with decompensated cirrhosis compared with compensated.Future directions of comprehensive assessment of cardiac function in cirrhotic patients might provide a better prognosis for these patients.AIM To clarify the correlation between the severity of liver cirrhosis and left ventricle diastolic dysfunction in the existing literature.METHODS Through January and February of 2019 at Vilnius University we conducted a systematic review of the global existing literature on the prevalence of left ventricle diastolic dysfunction in patients with liver cirrhosis.We searched for articles in PubMed,Medline and Web of science databases.Articles were selected by using adequate inclusion and exclusion criteria.Our interest was the outcome of likely correlation between the severity of cirrhosis[evaluated by Child-Pugh classes,Model For End-Stage Liver Disease(MELD)scores]and left ventricle diastolic dysfunction[classified according to American Society of Echocardiography(ASE)guidelines(2009,2016)],as well as relative risk of dysfunction in cirrhotic patients.Subgroup analyses were performed to evaluate the ratio and grades of left ventricle diastolic dysfunction with respect to cirrhosis severity.RESULTS A total of 1149 articles and abstracts met the initial search criteria.Sixteen articles which met the predefined eligibility criteria were included in the final analysis.Overall,1067 patients(out of them 723 men)with liver cirrhosis were evaluated for left ventricle diastolic dysfunction.In our systemic analysis we have found that 51.2%of cirrhotic patients had left ventricle diastolic dysfunction diagnosed and the grade 1 was the most prevalent(59.2%,P<0.001)among them,the grade 3 had been rarely diagnosed-only 5.1%.The data about the prevalence of diastolic dysfunction in cirrhotic patients depending on Child-Pugh Classes was available from 5 studies(365 patients overall)and only in 1 research diastolic dysfunction was found being associated with severity of liver cirrhosis(P<0.005).We established that diastolic dysfunction was diagnosed in 44.6%of Child-Pugh A class patients,in 62%of Child B class and in 63.3%of Child C patients(P=0.028).The proportion of patients with higher diastolic dysfunction grades increases in more severe cirrhosis presentation(P<0.001).There was no difference between mean MELD scores in patients with and without diastolic dysfunction and in different diastolic dysfunction groups.In all studies diastolic dysfunction was more frequent in patients with ascites.CONCLUSION This systemic analysis suggests that left ventricle diastolic dysfunction is an attribute of liver cirrhosis which has not received sufficient attention from clinicians so far.Future suggestions of a comprehensive assessment of cardiac function in cirrhotic patients might provide a better prognosis for these patients and give hint for better understanding of the left ventricle diastolic dysfunction pathogenesis in liver cirrhosis.
基金the China National Science&Technology Pillar Program(2011BAI11B01)the National Health and Family Planning Commission,China(No.201402002)the CAMS Innovation Fund for Medical Sciences(2017-I2M-1-004)。
文摘Background Heart failure(HF)is a leading cause of hospitalization and mortality for older chronic kidney disease(CKD)patients.However,the epidemiological data is scarce.We aimed to determine the prevalence of left ventricular(LV)dysfunction and HF,and to explore the risk factors for HF among those patients.Methods This is a cross-sectional analysis of the China Hypertension Survey conducted between October 2012 and December 2015.A total of 5,808 participants aged≥65 years were included in the analysis.Self-reported history of HF and any other cardiovascular diseases was acquired.2-D and Doppler echocardiography were used to assess LV dysfunction.CKD was defined as either estimated glomerular filtration rate(eGFR)<60 mL/min per 1.73 m2 or urinary albumin to creatinine ratio(ACR)≥30 mg/g.Results Among CKD patients aged≥65 years,the weighted prevalence of HF,heart failure with preserved ejection fraction(HFpEF),heart failure with mid-range ejection fraction(HFmrEF),and heart failure with reduced ejection fraction(HFrEF)was 4.8%,2.5%,0.8%,and 1.7%,respectively.The weighted prevalence of HF was 5.0%in patients with eGFR<60 mL/min per 1.73 m2,and was 5.9%in patients with ACR≥30 mg/g.The prevalence of LV systolic dysfunction was 3.1%,and while it was 8.9%for moderate/severe diastolic dysfunction.Multivariate analysis showed that smoking was significantly associated with the risk of HF.Furthermore,age,smoking,and residents in rural areas were significantly associated with a risk of LV diastolic dysfunction.Conclusions The prevalence of HF and LV dysfunction was high in older patients with CKD,suggesting that particular strategies will be required.
基金suppprted by Nature Science Fund of Hunan Province (No 20122345)
文摘Objective:To investigate the role of natriuretic peptide in the process of left ventricular dysfunction caused by emotional stress.Methods:Adult male SD rats(n=30)and Wistar rats(n=60)were selected in this study.Atherosclerosis models were induced with high-fat diet and excess VD3 injection(eight consecutive weeks),and anger stress models were prepared by residentintruder stress experiment(two consecutive weeks).Furthermore,left ventricular functions were examined by high-resolution echocardiograph,after which left ventricular myocardium and coronary arteries were prepared for pathological section and observed with electron microscope.At the same time,the hypothalamus,medulla oblongata and left ventricular myocardium were also prepared for pathological sections to detect the localization and expression of AMP,BNP and NPK-A with immunofluorescence and western blot.Results:We found that left ventricular functions of atherosclerosis or emotional stress modeled rats were both inferior to the healthy ones and superior to the combined(atherosclerosis and emotional stress)modeled ones(P<0.05).We also found that atherosclerosis and emotional stress could both cause morphological changes of left ventricular cells and capillary which contribute to apoptosis and hyperblastosis.Further more,there was NPR—A distributed in hypothalamus,medulla oblongata,as well as left ventricular tissues with the same express trend between groups,with atherosclerosis modeled rats the highest and the healthy rats the lowest.Conclusions:The results of our study suggest that anger stress could cause an excess consumption of ANP,BNP and NPR-A in nervous and cardiovascular system which inhibit the compensatory self-repair function of atherosclerosis rats,leading to a promotion of fibrosis and lipid peroxidation,offering insight into the neuroendocrine mechanisms of left heart function obstacle.
文摘Stroke,as a highly prevalent cerebrovascular disease,often leads to limb dysfunction in patients,severely affecting their quality of life.Seeking effective rehabilitation nursing methods is of great significance for patient recovery.This article deeply analyzes various aspects such as intelligent rehabilitation technology,traditional Chinese medical therapies,Western medical therapies,and rehabilitation training methods.It explores the characteristics,effectiveness,and application prospects of various rehabilitation nursing approaches,providing a reference for clinical rehabilitation nursing of limb dysfunction after stroke,and helping to improve the quality of patient recovery and enhance their self-care ability and quality of life.
文摘The endothelium modulates vascular homeostasis owing to a variety of vasoconstrictors and vasodilators.Endothelial dysfunction(ED),characterized by impaired vasodilation,inflammation,and thrombosis,triggers future cardiovascular(CV)diseases.Chronic kidney disease,a state of chronic inflammation caused by oxidative stress,metabolic abnormalities,infection,and uremic toxins damages the endothelium.ED is also associated with a decline in estimated glomerular filtration rate.After kidney transplantation,endothelial functions undergo immediate but partial restoration,promising graft longevity and enhanced CV health.However,the anticipated CV outcomes do not happen due to various transplant-related and unrelated risk factors for ED,culminating in poor CV health and graft survival.ED in kidney transplant recipients is an underrecognized and poorly studied entity.CV diseases are the leading cause of death among kidney transplant candidates with functioning grafts.ED contributes to the pathogenesis of many of the CV diseases.Various biomarkers and vasoreactivity tests are available to study endothelial functions.With an increasing number of transplants happening every year,and improved graft rejection rates due to the availability of effective immunosuppressants,the focus has now shifted to endothelial protection for the prevention,early recognition,and treatment of CV diseases.
文摘Recent work suggests a link betweenα-synuclein(α-syn)and mitochondrial dysfunction;however,the mechanisms of howα-syn influences mitochondrial function are still unclear.Most notably,whetherα-syn plays a direct role during mitochondrial function and/or whether diseasedα-syn-mediated mitochondrial dysfunction is a potential modifiable risk factor in Parkinson’s disease(PD)is unknown.To date,mutations in more than eight genes cause familial PD(fPD)and have functions in diverse pathways including synaptic homeostasis,mitochondria maintenance,autophagy/lysosome,and ubiquitin-proteasome pathways.
基金supported by the National Institute of Health NS104386(to HJA)and AG078245(to HJA).
文摘Alzheimer’s disease(AD)stands out as the primary manifestation of age-related dementia,portraying a chronic neurodegenerative disorder distinguished by the accumulation of fibrillar amyloid-β(Aβ)plaques and neurofibrillary tangles of hyperphosphorylated tau.However,from a clinical standpoint,AD presents itself as a complex condition with a spectrum of dysfunctions rather than a singular pathological mechanism.An often-overlooked aspect of the disease is the presence of extensive cerebrovascular abnormalities,given that the majority of AD patients experience altered cerebral blood flow,damaged vasculature,increased microinfarcts and microhemorrhages.Animal models of AD further support this observation,showing cerebrovascular dysfunction such as impaired cerebral blood flow and altered cerebrovascular reactivity(Tataryn et al.,2021;Gareau et al.,2023).
基金Supported by the Natural Science Foundation of Guangdong Province for Distinguished Young Scholars,No.2022B1515020003the National Natural Science Foundation of China,No.82174369,No.82405397,No.82374442,and No.81973847+2 种基金Postdoctoral Fellowship Program of CPSF No.GZC20233247National Key Clinical Disciplineand the Program of Guangdong Provincial Clinical Research Center for Digestive Diseases,No.2020B1111170004.
文摘BACKGROUND The development of slow transit constipation(STC)is associated with intestinal barrier damage.Huangqi decoction(HQD)is effective in treating STC,but me-chanisms are unclear.AIM To investigate whether HQD alleviates STC by downregulating the nuclear factorκB(NF-κB)signaling pathway and restoring intestinal barrier function.METHODS KM mice were divided into control,model,and HQD treatment groups.Fresh colonic tissues were collected for single-cell RNA sequencing and spatial tra-nscriptome sequencing.The expressions of claudin-1,mucin 2,and NF-κB P65 proteins were detected by immunohistochemistry.In vitro experiments evaluated the effects of HQD on the LS174T cell line.RESULTS HQD improved intestinal motility,restored mucosal epithelium function and morphology.Single-cell RNA sequencing and spatial transcriptome sequencing data showed a reduction in goblet cells,decreased mucin 2 secretion,and activated apoptotic pathways in STC mice.The population of intestinal stem cells was reduced,and proliferation along with Wnt/β-catenin pathways were inhibited.STC also altered the distribution of intestinal cell states,increasing immune-associated Enterocyte_C3.Aberrant NF-κB pathway activation was noted across various cell types.After HQD treatment,NF-κB pathway activity was down-regulated,while cell proliferation pathways were up-regulated,alongside an increase in Enterocyte_C1 related to material transport.Immunocytochemical,Western blot,and immunohistochemistry analyses confirmed NF-κB pathway activation in goblet cells of STC mice,with HQD inhibiting this aberrant activation.CONCLUSION STC involves intestinal mucosal barrier damage.HQD may treat STC by suppressing NF-κB signaling in epithelial cells,restoring intestinal epithelial cell function,and promoting mucosal barrier repair.
基金supported by UniversitàCattolica(D1 intramural funds to RP)Italian Ministry of University and Research(PRIN 2022ZYLB7B,P2022YW7BP funds to CG).
文摘Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.
文摘BACKGROUND Valvular heart disease affects more than 100 million people worldwide and is associated with significant morbidity and mortality.The prevalence of at least moderate valvular heart disease is 2.5%across all age groups,but its prevalence increases with age.Mitral regurgitation and aortic stenosis are the most frequent types of valvular heart disease in the community and hospital context,res-pectively.Surgical valve replacement(or mitral valve repair)is the standard of care for treating heart valve disease.However,the replacement of a prosthetic heart valve can lead to complications,either in the peri-procedural phase or in the long-term follow-up period.CASE SUMMARY We present a case of a 71-year-old female patient with a history of mitral valve replacement and warfarin anti-coagulation therapy.She was admitted to the intensive care unit due to spontaneously reperfused ischemic stroke of probable cardioembolic etiology.A dysfunctional mitral prosthesis was identified due to malfunction of one of the fixed discs.Furthermore,a possible microthrombotic lesion was suspected.Therefore,systemic thrombolysis was performed with subsequent normalization of mitral disc opening and closing.CONCLUSION This case underscores the critical importance of a multidisciplinary approach for timely decision-making in critically ill patients with prosthetic valve complications.
基金Supported by the University of Louisville-China Pediatric Research Exchange Program(Cai L,Tan Y,Huang J,and Keller B,no salary support)University of Louisville Executive Vice President for Research and Innovation Internal Grant(Huang J and Cai L)University of Louisville School of Medicine Basic Grant(Huang J and Cai L).
文摘BACKGROUND Diabetes has become a widespread metabolic disease affecting multiple organs.Among diabetic complications,cardiovascular complications are the main cause of patient morbidity and mortality.Diabetic cardiomyopathy is a diabetes-specific cardiomyopathy in the absence of other cardiovascular disease and occurs more frequently in type 1 diabetes(T1D)than in type 2 diabetes.Previous studies on diabetic cardiomyopathy have predominantly focused on the effects of diabetes on left ventricular(LV)dysfunction,while studies of right ventricular(RV)dysfunction have been sparse but are gaining attention.Although T1D accounts for only 5%-10%of the total diabetic population,diabetic cardiomyopathy is a major cause of morbidity and mortality in children with life-long,long-term complications.AIM To evaluate longitudinal RV and LV functional changes in female transgenic OVE26,T1D mice and wild-type FVB mice over a 30-week period.METHODS RV and LV structure and function were evaluated by transthoracic echocardiography.RV systolic pressure was measured by a transducer-tipped pressure catheter.Sirius-red staining was used to quantify collagen and fibrosis,wheat germ agglutinin staining was utilized to measure cardiomyocyte size,and quantitative real-time polymerase chain reaction and Western blotting were used to quantify miRNA expression and protein abundance,respectively.RESULTS RV systolic function,measured by tricuspid valve annular plane systolic excursion and RV systolic velocity,was similar between control and T1D mice,but LV systolic function decreased in T1D mice at 30 weeks of age.RV diastolic dysfunction in T1D mice significantly increased by 18 weeks and progressed until 30 weeks,while LV diastolic dysfunction trended towards abnormal at 12 weeks,significantly increased by 18 weeks,and continued to progress by 30 weeks.Furthermore,RV diastolic dysfunction was accompanied by RV cardiac fibrosis and hypertrophy in T1D mice,occurring later than that in the LV.Pulmonary arterial hypertension developed in T1D mice,evidenced by increased pulmonary acceleration time to pulmonary ejection time ratio and increased RV peak systolic pressure at 30 weeks.These results suggest the development of early LV diastolic dysfunction followed by LV systolic dysfunction and RV diastolic dysfunction at 30 weeks in T1D mice.CONCLUSION RV diastolic dysfunction develops later than LV dysfunction in OVE26 T1D mice.Mild pulmonary arterial hypertension appear at later stages of T1D and could contribute to RV systolic impairment and remodeling.
