Perinatal exposure to infection/inflammation is highly associated with neural injury,and subsequent impaired cortical growth,disturbances in neuronal connectivity,and impaired neurodevelopment.However,our understandin...Perinatal exposure to infection/inflammation is highly associated with neural injury,and subsequent impaired cortical growth,disturbances in neuronal connectivity,and impaired neurodevelopment.However,our understanding of the pathophysiological substrate underpinning these changes in brain structure and function is limited.The objective of this review is to summarize the growing evidence from animal trials and human cohort studies that suggest exposure to infection/inflammation during the perinatal period promotes regional impairments in neuronal maturation and function,including loss of high-frequency electroencephalographic activity,and reduced growth and arborization of cortical dendrites and dendritic spines resulting in reduced cortical volume.These inflammation-induced disturbances to neuronal structure and function are likely to underpin subsequent disturbances to cortical development and connectivity in fetuses and/or newborns exposed to infection/inflammation during the perinatal period,leading,in the long term,to impaired neurodevelopment.The combined use of early electroencephalography monitoring with neuroimaging techniques that enable detailed evaluation of brain microstructure,and the use of therapeutics that successfully target systemic and central nervous system inflammation could provide an effective strategy for early detection and therapeutic intervention.展开更多
This review aims at evaluating the existing evidence regarding post reperfusion syndrome, providing a description of the pathophysiologic mechanisms involved and possible management and preventive strategies. A Pub Me...This review aims at evaluating the existing evidence regarding post reperfusion syndrome, providing a description of the pathophysiologic mechanisms involved and possible management and preventive strategies. A Pub Med search was conducted using the Me SH database, "Reperfusion" AND "liver transplantation" were the combined Me SH headings; EMBASE and the Cochrane library were also searched using the same terms. 52 relevant studies and one ongoing trial were found. The concept of post reperfusion syndrome has evolved through years to a multisystemic disorder. The implications of the main organ, recipient and procedure related factors in the genesis of this complex syndrome are discussed in the text as the novel pharmacologic and technical approaches to reduce its incidence. However the available evidence about risk factors, physiopathology and preventive measures is still confusing, the presence of two main definitions and the numerosity of possible confounding factors greatly complicates the interpretation of the studies.展开更多
Though the pathophysiology of clinical obesity is un-doubtedly multifaceted, several lines of clinical evidence implicate an important functional role for glucagon-like peptide 1(GLP-1) signalling. Clinical studies as...Though the pathophysiology of clinical obesity is un-doubtedly multifaceted, several lines of clinical evidence implicate an important functional role for glucagon-like peptide 1(GLP-1) signalling. Clinical studies assessing GLP-1 responses in normal weight and obese subjects suggest that weight gain may induce functional deficits in GLP-1 signalling that facilitates maintenance of the obesity phenotype. In addition, genetic studies implicate a possible role for altered GLP-1 signalling as a risk factor towards the development of obesity. As reductions in functional GLP-1 signalling seem to play a role in clinical obesity, the pharmacological replenishment seems a promising target for the medical management of obesity in clinical practice. GLP-1 analogue liraglutide at a high dose(3 mg/d) has shown promising results in achieving and maintaining greater weight loss in obese individuals compared to placebo control, and currently licensed antiobesity medications. Generally well tolerated, provided that longer-term data in clinical practice supports the currently available evidence of superior short- and longterm weight loss efficacy, GLP-1 analogues provide promise towards achieving the successful, sustainable medical management of obesity that remains as yet, an unmet clinical need.展开更多
Background: The aim of this study was to elucidate the preoperative clinical and biochemical profile of infants with IHPS to optimize infusion therapy. Patients and Method: We retrospectively analyzed data from 56 inf...Background: The aim of this study was to elucidate the preoperative clinical and biochemical profile of infants with IHPS to optimize infusion therapy. Patients and Method: We retrospectively analyzed data from 56 infants who were operated for IHPS. Our study includes growth and laboratory data prior to the initiation of therapy. Results: Median duration of propulsive vomiting was 4 d;the median age was 37 d (18 - 108), and the median body weight was 3840 g (2760 -5900). Metabolic alkalosis (MAlk) with a pH of 7.45 ± 0.06 and an stHCO3- of 28.7 ± 4.5 mmol/l was found. In a subgroup of the infants, negative base excess (BE) was observed. The sodium concentration was normal or reduced (mean/median of 137 mmol/l). There was a strong negative correlation between stHCO3- and K+. The carbon dioxide partial pressure tended to increase (5.72 ± 0.84 kPa). Calculations of osmolality revealed a normal osmolarity. Hypoglycemia did not occur. The creatinine clearance according to the Schwartz formula remained at a normal level (85.3 ± 24.3 ml/min/1.73 m2). Discussion: The presented case series is characterized by a short duration of preoperative vomiting. MAlk can be classified as a chloride deficiency syndrome. It is accompanied by normo- or hyponatremic dehydration with normal osmolality. Partial respiratory compensation occurred. A normal creatinine clearance indicated good glomerular renal function. Conclusion: The presented study supports the use of an isotonic infusion fluid with a low glucose concentration for preoperative infusion therapy.展开更多
Splenic histiocytic sarcoma(SHS)is a rare,aggressive hematological malignancy with unclear progression and management.Our case illustrates the progression and pathophysiological processes of SHS and provides key data ...Splenic histiocytic sarcoma(SHS)is a rare,aggressive hematological malignancy with unclear progression and management.Our case illustrates the progression and pathophysiological processes of SHS and provides key data for the diagnosis,treatment and management of SHS.A 60-year-old female with incidentally detected splenic mass(6.0 cm×5.7 cm)underwent splenectomy,confirmed as SHS in 2020.Post-op imatinib therapy was given.In 2022,hepatic metastases(2.4 cm×2.9 cm)with pancytopenia led to supportive care.Lesions enlarged to 4.3 cm×2.7 cm,leading to multi-organ failure and death at 33 months.The case was categorized into three distinct stages based on the pathophysiology of SHS:Early-stage splenic tumor growth,mid-stage liver metastasis with hematological abnormalities,and late-stage tumor infiltration leading to multiorgan failure.For SHS,this case highlights the pivotal role of early intervention and the value of personalized treatment strategies.展开更多
Polycystic kidney disease (PKD) is an autosomal dominant genetic disorder that causes the formation of multiple cysts in the kidneys, leading to kidney failure. PKD is a common condition affecting approximately 1 in 5...Polycystic kidney disease (PKD) is an autosomal dominant genetic disorder that causes the formation of multiple cysts in the kidneys, leading to kidney failure. PKD is a common condition affecting approximately 1 in 500 individuals worldwide. The most prevalent type of PKD is autosomal dominant PKD (ADPKD). ADPKD is caused by mutations in either the PKD1 or PKD2 genes, which encode for proteins involved in cell growth and differentiation. These mutations lead to the formation of fluid-filled cysts in the kidneys, which can eventually lead to kidney failure. In addition to affecting the kidneys, PKD can also cause cysts in other organs, such as the liver, pancreas, and spleen. PKD can also lead to various complications, including high blood pressure, heart valve abnormalities, and brain aneurysms. This review focuses on the inheritance, pathophysiology, and treatment of PKD, with a specific emphasis on its effects on the cardiovascular system. Currently, there is no cure for PKD. However, several treatments are available to manage the symptoms and complications of the disease. These treatments include medications to control blood pressure, pain relievers, antibiotics for infections, and dialysis or kidney transplantation for kidney failure. Tolvaptan is the only FDA-approved drug specifically for ADPKD and has been shown to slow disease progression. In addition to summarizing current treatment options, this review will discuss promising future treatments, such as gene therapy and stem cell therapy.展开更多
This editorial discusses Thompson et al's original article,which is published in the most recent edition of the World Journal of Clinical Oncology and sheds critical light on the intertwined issues of health anxie...This editorial discusses Thompson et al's original article,which is published in the most recent edition of the World Journal of Clinical Oncology and sheds critical light on the intertwined issues of health anxiety and work loss in individuals diagnosed with serrated polyposis syndrome(SPS).SPS is rare,characterized by the development of multiple serrated colorectal polyps.This editorial provides an overview of SPS,including its pathophysiology,clinical presentation,diagnostic criteria,management strategies,and the psychosocial impact.SPS is linked to molecular alterations,which drive carcinogenesis.Colonoscopy and histological analysis are used for diagnosis.Genetic testing is also considered where there is a family history.Quality of life can be greatly impacted by the psychosocial effects of SPS,especially health anxiety.Further understanding of the molecular mechanisms and creating individualized surveillance are required.展开更多
This editorial underscores the importance of Maranhão et al’s study,which investigates pleural adenosine deaminase(P-ADA)as a biomarker for inflammatory pleural effusions.Despite advances in imaging,distinguishi...This editorial underscores the importance of Maranhão et al’s study,which investigates pleural adenosine deaminase(P-ADA)as a biomarker for inflammatory pleural effusions.Despite advances in imaging,distinguishing between inflammatory and non-inflammatory causes of pleural effusion remains a diagnostic challenge.The authors conducted a rigorous retrospective cohort analysis of 157 patients(124 with inflammatory exudates and 33 with non-inflammatory transudates),establishing a robust cutoff value of P-ADA≥9.00 U/L for diagnosing inflammatory diseases using receiver operating characteristic curve analysis and internal statistical calibration.This is the first study to define a standardized PADA threshold in a Brazilian cohort,addressing previous inconsistencies in cutoff values.Furthermore,the authors delved into the pathophysiological mechanisms underlying elevated P-ADA,linking it to purinergic signaling pathways and immune cell activation,particularly emphasizing the role of ADA2 isoforms in macrophages and lymphocytes.Their findings support P-ADA as a non-invasive,cost-effective biomarker for early diagnosis,treatment stratification,and minimizing the need for invasive procedures such as thoracentesis.This has particular relevance in resource-limited settings,where streamlined diagnostics can reduce healthcare costs and improve patient outcomes.Future studies must prioritize global validation,explore the integration of adenosine deaminase with additional biomarkers(e.g.,interleukin 6,C-reactive protein),and support the development of point-of-care technologies.展开更多
Diabetic foot ulcers(DFUs)are a serious complication of diabetes mellitus and are associated with high morbidity,risk of amputation,and increasedmortality.AlthoughDFUs typically remain a chronic,non-healing wound,a sm...Diabetic foot ulcers(DFUs)are a serious complication of diabetes mellitus and are associated with high morbidity,risk of amputation,and increasedmortality.AlthoughDFUs typically remain a chronic,non-healing wound,a small portion of DFUsmay undergomalignant transformation.The subsequentmalignancies are skin cancers such as squamous cell carcinoma(SCC),basal cell carcinoma,or melanoma.Understanding the pathophysiology of DFUs and themolecular and clinical determinants that contribute to theirpotentialmalignant transformationif crucial for clinical management.Chronic inflammation,dysregulation of cytokine signaling,faulty immune surveillance,and impaired wound healing all play a role in creating a tumor-permissive environment for the diabetic foot.This review highlights molecularmechanisms driving this transformation,including,vascular endothelial growth factor(VEGF)and plateletderived growth factor(PDGF)pathway dysregulation,hypoxia-inducible factor 1-alpha(HIF-1α)mediated angiogenic signaling,chronic osteomyelitis,and oxidative stress,which can collectively promote progression to malignancies,most notably cutaneous squamous cell carcinoma.Classic examples like Marjolin’s ulcer demonstrate how chronic injury can drive carcinogenesis,reinforcing the importance of vigilant DFU management.Connecting findings across clinical reports and mechanistic studies reveals that understandingDFUcarcinogenesis is essential for earlier detection,informed targeted treatment,and improved patient outcomes.展开更多
Pancreatogenic diabetes,also known as type 3c diabetes,arises from pancreatic dysfunction due to conditions such as chronic pancreatitis and pancreatic cancer.This form of diabetes is characterized by both endocrine a...Pancreatogenic diabetes,also known as type 3c diabetes,arises from pancreatic dysfunction due to conditions such as chronic pancreatitis and pancreatic cancer.This form of diabetes is characterized by both endocrine and exocrine pancreatic insufficiency,leading to insulin deficiency,glycemic variability,and maldigestion.The diagnostic process remains complex,as it shares clinical features with type 2 diabetes,and there are no standardized diagnostic criteria.Current treatment approaches include insulin therapy and pancreatic enzyme replacement therapy,along with nutritional support.However,the efficacy of oral hypoglycemic agents is limited,particularly in the presence of exocrine insufficiency.Epidemiological data indicate a significant overlap between pancreatogenic diabetes and pancreatic cancer,necessitating enhanced screening in high-risk populations.In this minireview,we highlight the pathophysiological mechanisms,diagnostic challenges,and current management strategies,emphasizing the need for improved diagnostic criteria and individualized treatment regimens.展开更多
Blood-brain barrier disruption and the neuroinflammatory response are significant pathological features that critically influence disease progression and treatment outcomes.This review systematically analyzes the curr...Blood-brain barrier disruption and the neuroinflammatory response are significant pathological features that critically influence disease progression and treatment outcomes.This review systematically analyzes the current understanding of the bidirectional relationship between blood-brain barrier disruption and neuroinflammation in traumatic brain injury,along with emerging combination therapeutic strategies.Literature review indicates that blood-brain barrier disruption and neuroinflammatory responses are key pathological features following traumatic brain injury.In the acute phase after traumatic brain injury,the pathological characteristics include primary blood-brain barrier disruption and the activation of inflammatory cascades.In the subacute phase,the pathological features are characterized by repair mechanisms and inflammatory modulation.In the chronic phase,the pathological features show persistent low-grade inflammation and incomplete recovery of the blood-brain barrier.Various physiological changes,such as structural alterations of the blood-brain barrier,inflammatory cascades,and extracellular matrix remodeling,interact with each other and are influenced by genetic,age,sex,and environmental factors.The dynamic balance between blood-brain barrier permeability and neuroinflammation is regulated by hormones,particularly sex hormones and stress-related hormones.Additionally,the role of gastrointestinal hormones is receiving increasing attention.Current treatment strategies for traumatic brain injury include various methods such as conventional drug combinations,multimodality neuromonitoring,hyperbaric oxygen therapy,and non-invasive brain stimulation.Artificial intelligence also shows potential in treatment decision-making and personalized therapy.Emerging sequential combination strategies and precision medicine approaches can help improve treatment outcomes;however,challenges remain,such as inadequate research on the mechanisms of the chronic phase traumatic brain injury and difficulties with technology integration.Future research on traumatic brain injury should focus on personalized treatment strategies,the standardization of techniques,costeffectiveness evaluations,and addressing the needs of patients with comorbidities.A multidisciplinary approach should be used to enhance treatment and improve patient outcomes.展开更多
Cirrhosis represents the end stage of chronic liver disease,significantly reducing life expectancy as it progresses from a compensated to a decompensated state,leading to serious complications.Recent improvements in m...Cirrhosis represents the end stage of chronic liver disease,significantly reducing life expectancy as it progresses from a compensated to a decompensated state,leading to serious complications.Recent improvements in medical treatment have created a shift in cirrhosis management.Various causes,including hepatitis viruses,alcohol consumption,and fatty liver disease,contribute to cirrhosis and are closely linked to liver cancer.The disease develops through hepatocyte necrosis and regeneration,resulting in fibrosis and sinusoidal capillarization,leading to portal hypertension and complications such as ascites,hepatic encephalopathy,and organ dysfunction.Cirrhosis also holds an increased risk of hepatocellular carcinoma.Diagnosing cirrhosis involves assessing fibrosis scores through blood tests and measuring liver stiffness through elastography.Liver transplantation is the definitive treatment for endstage liver disease and acute liver failure.展开更多
BACKGROUND Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy,limiting treatment efficacy and worsening patient outcomes.Recent studies have implicated the gut microbiome and its key m...BACKGROUND Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy,limiting treatment efficacy and worsening patient outcomes.Recent studies have implicated the gut microbiome and its key metabolites,such as shortchain fatty acids(SCFAs)and trimethylamine-N-oxide(TMAO),in mediating inflammation,oxidative stress,and cardiac damage.The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction.AIM To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients.METHODS A systematic literature search was conducted in PubMed,Scopus,and Web of Science for studies published between January 2013 and December 2024.Studies were included if they examined chemotherapy-induced cardiotoxicity in relation to gut microbiota composition,microbial metabolites(e.g.,SCFAs,TMAO),or microbiome-targeted interventions.Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.Data extraction focused on microbiota alterations,mechanistic pathways,cardiac outcomes,and quality assessments using standardized risk-of-bias tools.RESULTS Eighteen studies met the inclusion criteria.Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains.This imbalance contributed to gut barrier disruption,systemic inflammation,and oxidative stress,all of which promote myocardial damage.SCFA depletion weakened anti-inflammatory responses,while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction.Preclinical studies showed promising cardioprotective effects from probiotics,prebiotics,dietary interventions,and fecal microbiota transplantation,though human data remain limited.CONCLUSION Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity.Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury.Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology,warranting further clinical validation through well-designed trials.展开更多
Focal segmental glomerulosclerosis(FSGS)is a histological pattern of glomerular damage that significantly contributes to chronic kidney disease and end-stage renal disease.Its incidence is rising globally,necessitatin...Focal segmental glomerulosclerosis(FSGS)is a histological pattern of glomerular damage that significantly contributes to chronic kidney disease and end-stage renal disease.Its incidence is rising globally,necessitating timely and personalized management strategies.This paper aims to provide an updated overview of the pathophysiology,diagnosis,and therapeutic strategies for FSGS,emphasizing the importance of early interventions and tailored treatments.This editorial synthesizes key findings from recent literature to highlight advancements in understanding and managing FSGS.Emerging evidence supports the role of targeted therapies and personalized approaches in improving outcomes for FSGS patients.Advances include novel biomarkers,genetic testing,and innovative therapeutics such as transient receptor potential ion channel blockers and antisense oligonucleotides for apolipoprotein 1-related FSGS.Effective mana-gement of FSGS requires a combination of timely diagnosis,evidence-based therapeutic strategies,and ongoing research to optimize patient outcomes and address gaps in the current understanding of the disease.展开更多
Cardiovascular disease remains the leading global cause of mortality,projected to increase by 73.4%from 2025 to 2050 despite declining age-standardized rates.Contemporary interventions,such as percutaneous coronary in...Cardiovascular disease remains the leading global cause of mortality,projected to increase by 73.4%from 2025 to 2050 despite declining age-standardized rates.Contemporary interventions,such as percutaneous coronary intervention and statins,reduce major adverse cardiovascular events(MACE)by 25%-30%,yet a 20%five-year MACE risk persists in high-risk cohorts.These approaches,histor-ically focused on luminal stenosis,fail to address systemic atherogenesis drivers like endothelial dysfunction and inflammation.Specifically,dietary linoleic acid restriction(<5 g/day)reduces oxidized low-density lipoprotein by approximately 15%by limiting peroxidation-prone bisallylic bonds,mitigating arterial inflam-mation,a key atherogenic trigger.Enhanced external counterpulsation,through pulsatile shear stress,enhances nitric oxide-mediated coronary perfusion,alle-viating angina in approximately 70%of refractory cases unresponsive to revascu-larization.Nanoparticle-facilitated chelation targets atherosclerotic plaques with precision,reducing calcium content by up to 30%in preclinical models,offering a novel avenue for lesion reversal.These innovations collectively address residual risk by tackling root causes,oxidative stress,endothelial dysfunction,and plaque instability,potentially halving MACE rates with widespread adoption.Despite promising preliminary data,gaps remain in long-term safety and scalability.Robust clinical trials are needed to validate these approaches,which collectively aim to transform cardiovascular disease management by prioritizing prevention and vascular restoration,potentially reducing coronary events to a public health rarity.展开更多
Percutaneous coronary intervention(PCI),as an essential treatment for coronary artery disease,has significantly improved the prognosis of patients with large coronary artery lesions.However,some patients continue to e...Percutaneous coronary intervention(PCI),as an essential treatment for coronary artery disease,has significantly improved the prognosis of patients with large coronary artery lesions.However,some patients continue to experience myocar-dial ischemic symptoms post-procedure,largely due to coronary microvascular dysfunction(CMD).The pathophysiological mechanisms of CMD are complex and involve endothelial dysfunction,microvascular remodeling,reperfusion in-jury,and metabolic abnormalities.Moreover,components of metabolic syndrome,including obesity,hyperglycemia,hypertension,and dyslipidemia,exacerbate the occurrence and progression of CMD through multiple pathways.This review systematically summarizes the latest research advan-cements in CMD after PCI,including its pathogenesis,diagnostic techniques,management strategies,and future research directions.For diagnosis,invasive techniques such as coronary flow reserve and the index of microcirculatory resistance,as well as non-invasive imaging modalities(positron emission tomography and cardiac magnetic reso-nance),provide tools for early CMD detection.In terms of management,a multi-level intervention strategy is emphasized,incorporating lifestyle modifications(diet,exercise,and weight control),pharmacotherapy(vasodilators,hypoglycemic agents,statins,and metabolic modulators),traditional Chinese medicine,and specialized treatments(enhanced external counterpulsation,metabolic surgery,and lipoprotein apheresis).However,challenges remain in CMD treatment,including limitations in diagnostic tools and the lack of personalized treatment strategies.Future research should focus on the complex interactions between CMD and metabolic risks,aiming to optimize diagnostic and therapeutic strate-gies to improve the long-term prognosis of patients post-PCI.展开更多
The mechanisms underlying the pathophysiology of ischemic stroke are complex and multifactorial and include excitotoxicity,oxidative stress,inflammatory responses,and blood–brain barrier disruption.While vascular rec...The mechanisms underlying the pathophysiology of ischemic stroke are complex and multifactorial and include excitotoxicity,oxidative stress,inflammatory responses,and blood–brain barrier disruption.While vascular recanalization treatments such as thrombolysis and mechanical thrombectomy have achieved some success,reperfusion injury remains a significant contributor to the exacerbation of brain injury.This emphasizes the need for developing neuroprotective strategies to mitigate this type of injury.The purpose of this review was to examine the application of nanotechnology in the treatment of ischemic stroke,covering research progress in nanoparticlebased drug delivery,targeted therapy,and antioxidant and anti-inflammatory applications.Nanobased drug delivery systems offer several advantages compared to traditional therapies,including enhanced blood–brain barrier penetration,prolonged drug circulation time,improved drug stability,and targeted delivery.For example,inorganic nanoparticles,such as those based on CeO_(2),have been widely studied for their strong antioxidant capabilities.Biomimetic nanoparticles,such as those coated with cell membranes,have garnered significant attention owing to their excellent biocompatibility and targeting abilities.Nanoparticles can be used to deliver a wide range of neuroprotective agents,such as antioxidants(e.g.,edaravone),anti-inflammatory drugs(e.g.,curcumin),and neurotrophic factors.Nanotechnology significantly enhances the efficacy of these drugs while minimizing adverse reactions.Although nanotechnology has demonstrated great potential in animal studies,its clinical application still faces several challenges,including the long-term safety of nanoparticles,the feasibility of large-scale production,quality control,and the ability to predict therapeutic effects in humans.In summary,nanotechnology holds significant promise for the treatment of ischemic stroke.Future research should focus on further exploring the mechanisms of action of nanoparticles,developing multifunctional nanoparticles,and validating their safety and efficacy through rigorous clinical trials.Moreover,interdisciplinary collaboration is essential for advancing the use of nanotechnology in stroke treatment.展开更多
Tumor microenvironmentresponsive nanocatalysts enhance reactive oxygen species(ROS)accumulation by compromising tumor antioxidant defenses,offering a promising cancer treatment strategy.Leveraging the catalytic potent...Tumor microenvironmentresponsive nanocatalysts enhance reactive oxygen species(ROS)accumulation by compromising tumor antioxidant defenses,offering a promising cancer treatment strategy.Leveraging the catalytic potential of metalphenolic networks(MPNs),this study constructed GA-Cu MPNs as multifunctional carriers.Since endogenous catalase(CAT)limits hydrogen peroxide(H_(2)O_(2))accumulation,the CAT inhibitor 3-amino-1,2,4-triazole was encapsulated within the MPNs to form GA-Cu-AT,which was further modified with hyaluronic acid to produce GA-Cu-AT@HA.GA-Cu-AT@HA converts superoxide anions to H_(2)O_(2),which is further transformed into toxic hydroxyl radicals through peroxidase-like activity,while inhibits endogenous CAT to amplify oxidative stress.Under 808 nm near-infrared light,it exhibits photothermal activity,enabling synergistic photothermal-catalytic effects.In vitro,it induces ROS accumulation,mitochondrial damage,apoptosis,and immunogenic cell death(ICD).In in situ hepatocellular carcinoma,GA-Cu-AT@HA effectively suppresses tumor growth,induces apoptosis,and enhances damage-associated molecular patterns release via targeted accumulation.In 4T1 breast cancer xenografts,photothermal therapy enhances the infiltration of CD8^(+)T cells into tumors,promotes dendritic cell maturation,and elicits systemic CD8^(+)T cell responses,and reduces regulatory T cells.This tripartite strategy,encompassing oxidative cytotoxicity,ICD activation,and immune microenvironment remodeling,offers a novel approach for tumor redox regulation therapy.展开更多
BACKGROUND Postpartum depression(PPD)is a prevalent and debilitating psychiatric disorder affecting maternal mental health,infant development,and family well-being.Despite increasing global awareness,significant dispa...BACKGROUND Postpartum depression(PPD)is a prevalent and debilitating psychiatric disorder affecting maternal mental health,infant development,and family well-being.Despite increasing global awareness,significant disparities remain in screening,diagnosis,and treatment,particularly in low-resource and culturally diverse settings.The complex interplay of biological and psychosocial determinants complicates conventional intervention models.Integrating epidemiological patterns,pathophysiological mechanisms,and sociocultural factors will inform more effective and equitable strategies for PPD screening,prevention,and treatment.METHODS A narrative review was conducted following PRISMA 2020 guidelines.Peer-reviewed studies published from January 2010 to May 2025 were systematically searched in PubMed,Web of Science,EMBASE,and PsycINFO.Inclusion criteria comprised studies addressing PPD epidemiology,risk stratification,biological mechanisms,and intervention strategies.After screening and full-text review,84 studies were included.Study designs primarily involved cohort studies,randomized controlled trials,and meta-analyses.Extracted data were categorized thematically and assessed for methodological quality and generalizability.RESULTS PPD arises from multifactorial interactions involving hormonal dysregulation,neurochemical changes,psychosocial stressors,and cultural influences.Primary risk factors include personal or family history of depression,antenatal anxiety,low maternal self-efficacy,and inadequate social support.Evidence-based interventions encompass Edinburgh Postnatal Depression Scale-based screening,cognitive behavioral therapy,interpersonal psychotherapy,psychoeducation,and pharmacological treatments such as brexanolone and zuranolone.Culturally adapted,community-integrated models—including stepped-care approaches and task-shifting—improve feasibility and scalability,particularly in underserved populations.Emerging evidence highlights inflammatory biomarkers(e.g.,interleukin-6 and C-reactive protein),AI-assisted screening tools,and family-inclusive strategies as promising for enhanced detection and outcomes.CONCLUSION Effective PPD management requires integrative,culturally sensitive approaches,prioritizing scalable,personalized non-pharmacological interventions to reduce disparities and enhance maternal mental health equity across diverse populations.展开更多
Regenerative medicine is a promising therapeutic avenue for previously incurable diseases.As the risk of chronic and degenerative diseases significantly increases with age,the elderly population represents a major coh...Regenerative medicine is a promising therapeutic avenue for previously incurable diseases.As the risk of chronic and degenerative diseases significantly increases with age,the elderly population represents a major cohort for stem cell-based therapies.However,the regenerative potential of stem cells significantly decreases with advanced age and deteriorating health status of the donor.Therefore,the efficacy of autologous stem cell therapy is significantly compromised in older patients.To overcome these limitations,alternative strategies have been used to restore the age-and disease-depleted function of stem cells.These methods aim to restore the therapeutic efficacy of aged stem cells for autologous use.This article explores the effect of donor age and health status on the regenerative potential of stem cells.It further highlights the limitations of stem cell-based therapy for autologous treatment in the elderly.A comprehensive insight into the potential strategies to address the“age”and“disease”compromised regenerative potential of autologous stem cells is also presented.The information provided here serves as a valuable resource for physicians and patients for optimization of stem cellbased autologous therapy for aged patients.展开更多
基金supported by National Health and Medical Research Council of Australia(APP1090890 and APP1164954)Cerebral Palsy Alliance(ERG02123)the Victorian Government’s Operational Infrastructure Support Program。
文摘Perinatal exposure to infection/inflammation is highly associated with neural injury,and subsequent impaired cortical growth,disturbances in neuronal connectivity,and impaired neurodevelopment.However,our understanding of the pathophysiological substrate underpinning these changes in brain structure and function is limited.The objective of this review is to summarize the growing evidence from animal trials and human cohort studies that suggest exposure to infection/inflammation during the perinatal period promotes regional impairments in neuronal maturation and function,including loss of high-frequency electroencephalographic activity,and reduced growth and arborization of cortical dendrites and dendritic spines resulting in reduced cortical volume.These inflammation-induced disturbances to neuronal structure and function are likely to underpin subsequent disturbances to cortical development and connectivity in fetuses and/or newborns exposed to infection/inflammation during the perinatal period,leading,in the long term,to impaired neurodevelopment.The combined use of early electroencephalography monitoring with neuroimaging techniques that enable detailed evaluation of brain microstructure,and the use of therapeutics that successfully target systemic and central nervous system inflammation could provide an effective strategy for early detection and therapeutic intervention.
基金Supported by The Department of Anesthesiology of the University of Bologna
文摘This review aims at evaluating the existing evidence regarding post reperfusion syndrome, providing a description of the pathophysiologic mechanisms involved and possible management and preventive strategies. A Pub Med search was conducted using the Me SH database, "Reperfusion" AND "liver transplantation" were the combined Me SH headings; EMBASE and the Cochrane library were also searched using the same terms. 52 relevant studies and one ongoing trial were found. The concept of post reperfusion syndrome has evolved through years to a multisystemic disorder. The implications of the main organ, recipient and procedure related factors in the genesis of this complex syndrome are discussed in the text as the novel pharmacologic and technical approaches to reduce its incidence. However the available evidence about risk factors, physiopathology and preventive measures is still confusing, the presence of two main definitions and the numerosity of possible confounding factors greatly complicates the interpretation of the studies.
文摘Though the pathophysiology of clinical obesity is un-doubtedly multifaceted, several lines of clinical evidence implicate an important functional role for glucagon-like peptide 1(GLP-1) signalling. Clinical studies assessing GLP-1 responses in normal weight and obese subjects suggest that weight gain may induce functional deficits in GLP-1 signalling that facilitates maintenance of the obesity phenotype. In addition, genetic studies implicate a possible role for altered GLP-1 signalling as a risk factor towards the development of obesity. As reductions in functional GLP-1 signalling seem to play a role in clinical obesity, the pharmacological replenishment seems a promising target for the medical management of obesity in clinical practice. GLP-1 analogue liraglutide at a high dose(3 mg/d) has shown promising results in achieving and maintaining greater weight loss in obese individuals compared to placebo control, and currently licensed antiobesity medications. Generally well tolerated, provided that longer-term data in clinical practice supports the currently available evidence of superior short- and longterm weight loss efficacy, GLP-1 analogues provide promise towards achieving the successful, sustainable medical management of obesity that remains as yet, an unmet clinical need.
文摘Background: The aim of this study was to elucidate the preoperative clinical and biochemical profile of infants with IHPS to optimize infusion therapy. Patients and Method: We retrospectively analyzed data from 56 infants who were operated for IHPS. Our study includes growth and laboratory data prior to the initiation of therapy. Results: Median duration of propulsive vomiting was 4 d;the median age was 37 d (18 - 108), and the median body weight was 3840 g (2760 -5900). Metabolic alkalosis (MAlk) with a pH of 7.45 ± 0.06 and an stHCO3- of 28.7 ± 4.5 mmol/l was found. In a subgroup of the infants, negative base excess (BE) was observed. The sodium concentration was normal or reduced (mean/median of 137 mmol/l). There was a strong negative correlation between stHCO3- and K+. The carbon dioxide partial pressure tended to increase (5.72 ± 0.84 kPa). Calculations of osmolality revealed a normal osmolarity. Hypoglycemia did not occur. The creatinine clearance according to the Schwartz formula remained at a normal level (85.3 ± 24.3 ml/min/1.73 m2). Discussion: The presented case series is characterized by a short duration of preoperative vomiting. MAlk can be classified as a chloride deficiency syndrome. It is accompanied by normo- or hyponatremic dehydration with normal osmolality. Partial respiratory compensation occurred. A normal creatinine clearance indicated good glomerular renal function. Conclusion: The presented study supports the use of an isotonic infusion fluid with a low glucose concentration for preoperative infusion therapy.
基金Supported by the Program of General Hospital of Western Theater,No.2021-XZYG-C33.
文摘Splenic histiocytic sarcoma(SHS)is a rare,aggressive hematological malignancy with unclear progression and management.Our case illustrates the progression and pathophysiological processes of SHS and provides key data for the diagnosis,treatment and management of SHS.A 60-year-old female with incidentally detected splenic mass(6.0 cm×5.7 cm)underwent splenectomy,confirmed as SHS in 2020.Post-op imatinib therapy was given.In 2022,hepatic metastases(2.4 cm×2.9 cm)with pancytopenia led to supportive care.Lesions enlarged to 4.3 cm×2.7 cm,leading to multi-organ failure and death at 33 months.The case was categorized into three distinct stages based on the pathophysiology of SHS:Early-stage splenic tumor growth,mid-stage liver metastasis with hematological abnormalities,and late-stage tumor infiltration leading to multiorgan failure.For SHS,this case highlights the pivotal role of early intervention and the value of personalized treatment strategies.
文摘Polycystic kidney disease (PKD) is an autosomal dominant genetic disorder that causes the formation of multiple cysts in the kidneys, leading to kidney failure. PKD is a common condition affecting approximately 1 in 500 individuals worldwide. The most prevalent type of PKD is autosomal dominant PKD (ADPKD). ADPKD is caused by mutations in either the PKD1 or PKD2 genes, which encode for proteins involved in cell growth and differentiation. These mutations lead to the formation of fluid-filled cysts in the kidneys, which can eventually lead to kidney failure. In addition to affecting the kidneys, PKD can also cause cysts in other organs, such as the liver, pancreas, and spleen. PKD can also lead to various complications, including high blood pressure, heart valve abnormalities, and brain aneurysms. This review focuses on the inheritance, pathophysiology, and treatment of PKD, with a specific emphasis on its effects on the cardiovascular system. Currently, there is no cure for PKD. However, several treatments are available to manage the symptoms and complications of the disease. These treatments include medications to control blood pressure, pain relievers, antibiotics for infections, and dialysis or kidney transplantation for kidney failure. Tolvaptan is the only FDA-approved drug specifically for ADPKD and has been shown to slow disease progression. In addition to summarizing current treatment options, this review will discuss promising future treatments, such as gene therapy and stem cell therapy.
文摘This editorial discusses Thompson et al's original article,which is published in the most recent edition of the World Journal of Clinical Oncology and sheds critical light on the intertwined issues of health anxiety and work loss in individuals diagnosed with serrated polyposis syndrome(SPS).SPS is rare,characterized by the development of multiple serrated colorectal polyps.This editorial provides an overview of SPS,including its pathophysiology,clinical presentation,diagnostic criteria,management strategies,and the psychosocial impact.SPS is linked to molecular alterations,which drive carcinogenesis.Colonoscopy and histological analysis are used for diagnosis.Genetic testing is also considered where there is a family history.Quality of life can be greatly impacted by the psychosocial effects of SPS,especially health anxiety.Further understanding of the molecular mechanisms and creating individualized surveillance are required.
文摘This editorial underscores the importance of Maranhão et al’s study,which investigates pleural adenosine deaminase(P-ADA)as a biomarker for inflammatory pleural effusions.Despite advances in imaging,distinguishing between inflammatory and non-inflammatory causes of pleural effusion remains a diagnostic challenge.The authors conducted a rigorous retrospective cohort analysis of 157 patients(124 with inflammatory exudates and 33 with non-inflammatory transudates),establishing a robust cutoff value of P-ADA≥9.00 U/L for diagnosing inflammatory diseases using receiver operating characteristic curve analysis and internal statistical calibration.This is the first study to define a standardized PADA threshold in a Brazilian cohort,addressing previous inconsistencies in cutoff values.Furthermore,the authors delved into the pathophysiological mechanisms underlying elevated P-ADA,linking it to purinergic signaling pathways and immune cell activation,particularly emphasizing the role of ADA2 isoforms in macrophages and lymphocytes.Their findings support P-ADA as a non-invasive,cost-effective biomarker for early diagnosis,treatment stratification,and minimizing the need for invasive procedures such as thoracentesis.This has particular relevance in resource-limited settings,where streamlined diagnostics can reduce healthcare costs and improve patient outcomes.Future studies must prioritize global validation,explore the integration of adenosine deaminase with additional biomarkers(e.g.,interleukin 6,C-reactive protein),and support the development of point-of-care technologies.
文摘Diabetic foot ulcers(DFUs)are a serious complication of diabetes mellitus and are associated with high morbidity,risk of amputation,and increasedmortality.AlthoughDFUs typically remain a chronic,non-healing wound,a small portion of DFUsmay undergomalignant transformation.The subsequentmalignancies are skin cancers such as squamous cell carcinoma(SCC),basal cell carcinoma,or melanoma.Understanding the pathophysiology of DFUs and themolecular and clinical determinants that contribute to theirpotentialmalignant transformationif crucial for clinical management.Chronic inflammation,dysregulation of cytokine signaling,faulty immune surveillance,and impaired wound healing all play a role in creating a tumor-permissive environment for the diabetic foot.This review highlights molecularmechanisms driving this transformation,including,vascular endothelial growth factor(VEGF)and plateletderived growth factor(PDGF)pathway dysregulation,hypoxia-inducible factor 1-alpha(HIF-1α)mediated angiogenic signaling,chronic osteomyelitis,and oxidative stress,which can collectively promote progression to malignancies,most notably cutaneous squamous cell carcinoma.Classic examples like Marjolin’s ulcer demonstrate how chronic injury can drive carcinogenesis,reinforcing the importance of vigilant DFU management.Connecting findings across clinical reports and mechanistic studies reveals that understandingDFUcarcinogenesis is essential for earlier detection,informed targeted treatment,and improved patient outcomes.
文摘Pancreatogenic diabetes,also known as type 3c diabetes,arises from pancreatic dysfunction due to conditions such as chronic pancreatitis and pancreatic cancer.This form of diabetes is characterized by both endocrine and exocrine pancreatic insufficiency,leading to insulin deficiency,glycemic variability,and maldigestion.The diagnostic process remains complex,as it shares clinical features with type 2 diabetes,and there are no standardized diagnostic criteria.Current treatment approaches include insulin therapy and pancreatic enzyme replacement therapy,along with nutritional support.However,the efficacy of oral hypoglycemic agents is limited,particularly in the presence of exocrine insufficiency.Epidemiological data indicate a significant overlap between pancreatogenic diabetes and pancreatic cancer,necessitating enhanced screening in high-risk populations.In this minireview,we highlight the pathophysiological mechanisms,diagnostic challenges,and current management strategies,emphasizing the need for improved diagnostic criteria and individualized treatment regimens.
基金supported by Open Scientific Research Program of Military Logistics,No.BLB20J009(to YZhao).
文摘Blood-brain barrier disruption and the neuroinflammatory response are significant pathological features that critically influence disease progression and treatment outcomes.This review systematically analyzes the current understanding of the bidirectional relationship between blood-brain barrier disruption and neuroinflammation in traumatic brain injury,along with emerging combination therapeutic strategies.Literature review indicates that blood-brain barrier disruption and neuroinflammatory responses are key pathological features following traumatic brain injury.In the acute phase after traumatic brain injury,the pathological characteristics include primary blood-brain barrier disruption and the activation of inflammatory cascades.In the subacute phase,the pathological features are characterized by repair mechanisms and inflammatory modulation.In the chronic phase,the pathological features show persistent low-grade inflammation and incomplete recovery of the blood-brain barrier.Various physiological changes,such as structural alterations of the blood-brain barrier,inflammatory cascades,and extracellular matrix remodeling,interact with each other and are influenced by genetic,age,sex,and environmental factors.The dynamic balance between blood-brain barrier permeability and neuroinflammation is regulated by hormones,particularly sex hormones and stress-related hormones.Additionally,the role of gastrointestinal hormones is receiving increasing attention.Current treatment strategies for traumatic brain injury include various methods such as conventional drug combinations,multimodality neuromonitoring,hyperbaric oxygen therapy,and non-invasive brain stimulation.Artificial intelligence also shows potential in treatment decision-making and personalized therapy.Emerging sequential combination strategies and precision medicine approaches can help improve treatment outcomes;however,challenges remain,such as inadequate research on the mechanisms of the chronic phase traumatic brain injury and difficulties with technology integration.Future research on traumatic brain injury should focus on personalized treatment strategies,the standardization of techniques,costeffectiveness evaluations,and addressing the needs of patients with comorbidities.A multidisciplinary approach should be used to enhance treatment and improve patient outcomes.
文摘Cirrhosis represents the end stage of chronic liver disease,significantly reducing life expectancy as it progresses from a compensated to a decompensated state,leading to serious complications.Recent improvements in medical treatment have created a shift in cirrhosis management.Various causes,including hepatitis viruses,alcohol consumption,and fatty liver disease,contribute to cirrhosis and are closely linked to liver cancer.The disease develops through hepatocyte necrosis and regeneration,resulting in fibrosis and sinusoidal capillarization,leading to portal hypertension and complications such as ascites,hepatic encephalopathy,and organ dysfunction.Cirrhosis also holds an increased risk of hepatocellular carcinoma.Diagnosing cirrhosis involves assessing fibrosis scores through blood tests and measuring liver stiffness through elastography.Liver transplantation is the definitive treatment for endstage liver disease and acute liver failure.
文摘BACKGROUND Chemotherapy-induced cardiotoxicity is a significant complication in cancer therapy,limiting treatment efficacy and worsening patient outcomes.Recent studies have implicated the gut microbiome and its key metabolites,such as shortchain fatty acids(SCFAs)and trimethylamine-N-oxide(TMAO),in mediating inflammation,oxidative stress,and cardiac damage.The gut-heart axis is increasingly recognized as a pivotal pathway linking microbiota dysregulation to chemotherapy-related cardiac dysfunction.AIM To systematically review existing evidence on the role of gut microbiome alterations in chemotherapy-induced cardiotoxicity and evaluate emerging microbiome-based therapeutic strategies aimed at mitigating cardiovascular risk in cancer patients.METHODS A systematic literature search was conducted in PubMed,Scopus,and Web of Science for studies published between January 2013 and December 2024.Studies were included if they examined chemotherapy-induced cardiotoxicity in relation to gut microbiota composition,microbial metabolites(e.g.,SCFAs,TMAO),or microbiome-targeted interventions.Selection followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.Data extraction focused on microbiota alterations,mechanistic pathways,cardiac outcomes,and quality assessments using standardized risk-of-bias tools.RESULTS Eighteen studies met the inclusion criteria.Chemotherapy was consistently associated with gut dysbiosis characterized by reduced SCFA-producing bacteria and increased TMAO-producing strains.This imbalance contributed to gut barrier disruption,systemic inflammation,and oxidative stress,all of which promote myocardial damage.SCFA depletion weakened anti-inflammatory responses,while elevated TMAO levels exacerbated cardiac fibrosis and dysfunction.Preclinical studies showed promising cardioprotective effects from probiotics,prebiotics,dietary interventions,and fecal microbiota transplantation,though human data remain limited.CONCLUSION Gut microbiome dysregulation plays a crucial role in the development of chemotherapy-induced cardiotoxicity.Altered microbial composition and metabolite production trigger systemic inflammation and cardiac injury.Microbiome-targeted therapies represent a promising preventive and therapeutic approach in cardio-oncology,warranting further clinical validation through well-designed trials.
文摘Focal segmental glomerulosclerosis(FSGS)is a histological pattern of glomerular damage that significantly contributes to chronic kidney disease and end-stage renal disease.Its incidence is rising globally,necessitating timely and personalized management strategies.This paper aims to provide an updated overview of the pathophysiology,diagnosis,and therapeutic strategies for FSGS,emphasizing the importance of early interventions and tailored treatments.This editorial synthesizes key findings from recent literature to highlight advancements in understanding and managing FSGS.Emerging evidence supports the role of targeted therapies and personalized approaches in improving outcomes for FSGS patients.Advances include novel biomarkers,genetic testing,and innovative therapeutics such as transient receptor potential ion channel blockers and antisense oligonucleotides for apolipoprotein 1-related FSGS.Effective mana-gement of FSGS requires a combination of timely diagnosis,evidence-based therapeutic strategies,and ongoing research to optimize patient outcomes and address gaps in the current understanding of the disease.
文摘Cardiovascular disease remains the leading global cause of mortality,projected to increase by 73.4%from 2025 to 2050 despite declining age-standardized rates.Contemporary interventions,such as percutaneous coronary intervention and statins,reduce major adverse cardiovascular events(MACE)by 25%-30%,yet a 20%five-year MACE risk persists in high-risk cohorts.These approaches,histor-ically focused on luminal stenosis,fail to address systemic atherogenesis drivers like endothelial dysfunction and inflammation.Specifically,dietary linoleic acid restriction(<5 g/day)reduces oxidized low-density lipoprotein by approximately 15%by limiting peroxidation-prone bisallylic bonds,mitigating arterial inflam-mation,a key atherogenic trigger.Enhanced external counterpulsation,through pulsatile shear stress,enhances nitric oxide-mediated coronary perfusion,alle-viating angina in approximately 70%of refractory cases unresponsive to revascu-larization.Nanoparticle-facilitated chelation targets atherosclerotic plaques with precision,reducing calcium content by up to 30%in preclinical models,offering a novel avenue for lesion reversal.These innovations collectively address residual risk by tackling root causes,oxidative stress,endothelial dysfunction,and plaque instability,potentially halving MACE rates with widespread adoption.Despite promising preliminary data,gaps remain in long-term safety and scalability.Robust clinical trials are needed to validate these approaches,which collectively aim to transform cardiovascular disease management by prioritizing prevention and vascular restoration,potentially reducing coronary events to a public health rarity.
文摘Percutaneous coronary intervention(PCI),as an essential treatment for coronary artery disease,has significantly improved the prognosis of patients with large coronary artery lesions.However,some patients continue to experience myocar-dial ischemic symptoms post-procedure,largely due to coronary microvascular dysfunction(CMD).The pathophysiological mechanisms of CMD are complex and involve endothelial dysfunction,microvascular remodeling,reperfusion in-jury,and metabolic abnormalities.Moreover,components of metabolic syndrome,including obesity,hyperglycemia,hypertension,and dyslipidemia,exacerbate the occurrence and progression of CMD through multiple pathways.This review systematically summarizes the latest research advan-cements in CMD after PCI,including its pathogenesis,diagnostic techniques,management strategies,and future research directions.For diagnosis,invasive techniques such as coronary flow reserve and the index of microcirculatory resistance,as well as non-invasive imaging modalities(positron emission tomography and cardiac magnetic reso-nance),provide tools for early CMD detection.In terms of management,a multi-level intervention strategy is emphasized,incorporating lifestyle modifications(diet,exercise,and weight control),pharmacotherapy(vasodilators,hypoglycemic agents,statins,and metabolic modulators),traditional Chinese medicine,and specialized treatments(enhanced external counterpulsation,metabolic surgery,and lipoprotein apheresis).However,challenges remain in CMD treatment,including limitations in diagnostic tools and the lack of personalized treatment strategies.Future research should focus on the complex interactions between CMD and metabolic risks,aiming to optimize diagnostic and therapeutic strate-gies to improve the long-term prognosis of patients post-PCI.
基金supported by the National Natural Science Foundation of China,Nos.82301093(to QC)and 22334004(to HY)the Fuzhou University Fund for Testing Precious Equipment,No.2025T038(to QC)。
文摘The mechanisms underlying the pathophysiology of ischemic stroke are complex and multifactorial and include excitotoxicity,oxidative stress,inflammatory responses,and blood–brain barrier disruption.While vascular recanalization treatments such as thrombolysis and mechanical thrombectomy have achieved some success,reperfusion injury remains a significant contributor to the exacerbation of brain injury.This emphasizes the need for developing neuroprotective strategies to mitigate this type of injury.The purpose of this review was to examine the application of nanotechnology in the treatment of ischemic stroke,covering research progress in nanoparticlebased drug delivery,targeted therapy,and antioxidant and anti-inflammatory applications.Nanobased drug delivery systems offer several advantages compared to traditional therapies,including enhanced blood–brain barrier penetration,prolonged drug circulation time,improved drug stability,and targeted delivery.For example,inorganic nanoparticles,such as those based on CeO_(2),have been widely studied for their strong antioxidant capabilities.Biomimetic nanoparticles,such as those coated with cell membranes,have garnered significant attention owing to their excellent biocompatibility and targeting abilities.Nanoparticles can be used to deliver a wide range of neuroprotective agents,such as antioxidants(e.g.,edaravone),anti-inflammatory drugs(e.g.,curcumin),and neurotrophic factors.Nanotechnology significantly enhances the efficacy of these drugs while minimizing adverse reactions.Although nanotechnology has demonstrated great potential in animal studies,its clinical application still faces several challenges,including the long-term safety of nanoparticles,the feasibility of large-scale production,quality control,and the ability to predict therapeutic effects in humans.In summary,nanotechnology holds significant promise for the treatment of ischemic stroke.Future research should focus on further exploring the mechanisms of action of nanoparticles,developing multifunctional nanoparticles,and validating their safety and efficacy through rigorous clinical trials.Moreover,interdisciplinary collaboration is essential for advancing the use of nanotechnology in stroke treatment.
基金supported by the National Natural Science Foundation of China(Nos.82474130,22073025,and 82074077)the Natural Science Foundation of Hubei Province(Nos.2025AFD479,and 2025AFD544)+1 种基金the Open Project of Hubei Key Laboratory of Resources and Chemistry of Chinese Medicine(No.KLRCCM2404)the Central Government-Guided Local Science and Technology Development Fund Project(No.2024EIA064).
文摘Tumor microenvironmentresponsive nanocatalysts enhance reactive oxygen species(ROS)accumulation by compromising tumor antioxidant defenses,offering a promising cancer treatment strategy.Leveraging the catalytic potential of metalphenolic networks(MPNs),this study constructed GA-Cu MPNs as multifunctional carriers.Since endogenous catalase(CAT)limits hydrogen peroxide(H_(2)O_(2))accumulation,the CAT inhibitor 3-amino-1,2,4-triazole was encapsulated within the MPNs to form GA-Cu-AT,which was further modified with hyaluronic acid to produce GA-Cu-AT@HA.GA-Cu-AT@HA converts superoxide anions to H_(2)O_(2),which is further transformed into toxic hydroxyl radicals through peroxidase-like activity,while inhibits endogenous CAT to amplify oxidative stress.Under 808 nm near-infrared light,it exhibits photothermal activity,enabling synergistic photothermal-catalytic effects.In vitro,it induces ROS accumulation,mitochondrial damage,apoptosis,and immunogenic cell death(ICD).In in situ hepatocellular carcinoma,GA-Cu-AT@HA effectively suppresses tumor growth,induces apoptosis,and enhances damage-associated molecular patterns release via targeted accumulation.In 4T1 breast cancer xenografts,photothermal therapy enhances the infiltration of CD8^(+)T cells into tumors,promotes dendritic cell maturation,and elicits systemic CD8^(+)T cell responses,and reduces regulatory T cells.This tripartite strategy,encompassing oxidative cytotoxicity,ICD activation,and immune microenvironment remodeling,offers a novel approach for tumor redox regulation therapy.
文摘BACKGROUND Postpartum depression(PPD)is a prevalent and debilitating psychiatric disorder affecting maternal mental health,infant development,and family well-being.Despite increasing global awareness,significant disparities remain in screening,diagnosis,and treatment,particularly in low-resource and culturally diverse settings.The complex interplay of biological and psychosocial determinants complicates conventional intervention models.Integrating epidemiological patterns,pathophysiological mechanisms,and sociocultural factors will inform more effective and equitable strategies for PPD screening,prevention,and treatment.METHODS A narrative review was conducted following PRISMA 2020 guidelines.Peer-reviewed studies published from January 2010 to May 2025 were systematically searched in PubMed,Web of Science,EMBASE,and PsycINFO.Inclusion criteria comprised studies addressing PPD epidemiology,risk stratification,biological mechanisms,and intervention strategies.After screening and full-text review,84 studies were included.Study designs primarily involved cohort studies,randomized controlled trials,and meta-analyses.Extracted data were categorized thematically and assessed for methodological quality and generalizability.RESULTS PPD arises from multifactorial interactions involving hormonal dysregulation,neurochemical changes,psychosocial stressors,and cultural influences.Primary risk factors include personal or family history of depression,antenatal anxiety,low maternal self-efficacy,and inadequate social support.Evidence-based interventions encompass Edinburgh Postnatal Depression Scale-based screening,cognitive behavioral therapy,interpersonal psychotherapy,psychoeducation,and pharmacological treatments such as brexanolone and zuranolone.Culturally adapted,community-integrated models—including stepped-care approaches and task-shifting—improve feasibility and scalability,particularly in underserved populations.Emerging evidence highlights inflammatory biomarkers(e.g.,interleukin-6 and C-reactive protein),AI-assisted screening tools,and family-inclusive strategies as promising for enhanced detection and outcomes.CONCLUSION Effective PPD management requires integrative,culturally sensitive approaches,prioritizing scalable,personalized non-pharmacological interventions to reduce disparities and enhance maternal mental health equity across diverse populations.
文摘Regenerative medicine is a promising therapeutic avenue for previously incurable diseases.As the risk of chronic and degenerative diseases significantly increases with age,the elderly population represents a major cohort for stem cell-based therapies.However,the regenerative potential of stem cells significantly decreases with advanced age and deteriorating health status of the donor.Therefore,the efficacy of autologous stem cell therapy is significantly compromised in older patients.To overcome these limitations,alternative strategies have been used to restore the age-and disease-depleted function of stem cells.These methods aim to restore the therapeutic efficacy of aged stem cells for autologous use.This article explores the effect of donor age and health status on the regenerative potential of stem cells.It further highlights the limitations of stem cell-based therapy for autologous treatment in the elderly.A comprehensive insight into the potential strategies to address the“age”and“disease”compromised regenerative potential of autologous stem cells is also presented.The information provided here serves as a valuable resource for physicians and patients for optimization of stem cellbased autologous therapy for aged patients.
