Ischemic stroke caused by intracranial vascular occlusion has become increasingly prevalent with considerable mortality and disability,which gravely burdens the global economy.Current relatively effective clinical tre...Ischemic stroke caused by intracranial vascular occlusion has become increasingly prevalent with considerable mortality and disability,which gravely burdens the global economy.Current relatively effective clinical treatments are limited to intravenous alteplase and thrombectomy.Even so,patients still benefit little due to the short therapeutic window and the risk of ischemia/reperfusion injury.It is therefore urgent to figure out the neuronal death mechanisms following ischemic stroke in order to develop new neuroprotective strategies.Regarding the pathogenesis,multiple pathological events trigger the activation of cell death pathways.Particular attention should be devoted to excitotoxicity,oxidative stress,and inflammatory responses.Thus,in this article,we first review the principal mechanisms underlying neuronal death mediated by these significant events,such as intrinsic and extrinsic apoptosis,ferroptosis,parthanatos,pyroptosis,necroptosis,and autophagic cell death.Then,we further discuss the possibility of interventions targeting these pathological events and summarize the present pharmacological achievements.展开更多
Transcorneal electrical stimulation （TES） is a novel therapeutic approach to activate the retina and related downstream structures. TES has multiple advantages over traditional treatments, such as being minimally in...Transcorneal electrical stimulation （TES） is a novel therapeutic approach to activate the retina and related downstream structures. TES has multiple advantages over traditional treatments, such as being minimally invasive and readily applicable in a routine manner. Series of animal experiments have shown that TES protects the retinal neuron from traumatic or genetic induced degeneration. These laboratory evidences support its utilization in ophthalmological therapies against various retinal and optical diseases including retinitis pigmentosa （RP）, traumatic optic neuropathy, anterior ischemic optic neuropathy （AION）, and retinal artery occlusions （RAOs）. Several pioneering explorations sought to clarify the functional mechanism underlying the neuroprotective effects of TES. It seems that the neuroprotective effects should not be attributed to a solitary pathway, on the contrary, multiple mechanisms might contribute collectively to maintain cellular homeostasis and promote cell survival in the retina. More precise evaluations y/a functional and morphological techniques would determine the exact mechanism underlying the remarkable neuroprotective effect of TES. Further studies to determine the optimal parameters and the long-term stability of TES are crucial to justify the clinical significance and to establish TES as a popularized therapeutic modality against retinal and optic neuropathy.展开更多
BACKGROUND The coexistence with patent ductus arteriosus(PDA),mitral valve prolapse(MVP),atrial fibrillation(AF)and hyperthyroidism is extremely rare and complex.The optimal therapeutic strategy is difficult to develo...BACKGROUND The coexistence with patent ductus arteriosus(PDA),mitral valve prolapse(MVP),atrial fibrillation(AF)and hyperthyroidism is extremely rare and complex.The optimal therapeutic strategy is difficult to develop.CASE SUMMARY A 27-year-old female with PDA,MVP,AF and hyperthyroidism presented with severe dyspnea.Given that a one-stage operation for PDA,MVP and AF is high risk,we preferred a sequential multidisciplinary minimally invasive therapeutic strategy.First,PDA transcatheter closure was performed.Hyperthyroidism and heart failure were simultaneously controlled via medical treatment.Video-assisted thoracoscopic mitral valve repair and left atrial appendage occlusion were performed when heart failure was controlled.Under this therapeutic strategy,the patient’s sinus rhythm was restored and maintained.Two years after the treatment,the symptoms of heart failure were relieved,and the enlarged heart was reversed.CONCLUSION Sequential multidisciplinary therapeutic strategies,which take advantage of both internal medicine and surgical approaches,might be reasonable for this type of disease.展开更多
Diabetic foot ulcer is a serious complication of diabetes.Excessive accumulation of advanced glycation end products(AGEs)is one of the critical pathogenic factors in postponing diabetic wound healing.The main pathogen...Diabetic foot ulcer is a serious complication of diabetes.Excessive accumulation of advanced glycation end products(AGEs)is one of the critical pathogenic factors in postponing diabetic wound healing.The main pathogenic mechanisms of AGEs include inducing cellular dysfunction,prolonging inflammatory response,increasing oxidative stress and reducing endogenous nitric oxide(NO)production.Combination therapy of blocking the deleterious effects of AGEs and supplementing exogenous NO is hypothesized to promote diabetic wound healing.Here,we presented nanoparticles/hydrogel composite dressings to co-delivery rosiglitazone and S-nitroso glutathione into the wound bed.The designed co-delivery system augmented the survival of fibroblasts,reduced oxidative stress levels,reversed the change of mitochondrial membrane potential and decreased the proinflammatory cytokine expression.Local sustained release of therapeutic agents significantly improved the wound healing of diabetic rats including increasing the wound closure rate,alleviating inflammation,promoting collagen fiber production and angiogenesis.Our finding indicated this local deliver strategy aimed at inhibiting the toxic effects of AGEs has great clinical potential for diabetic wound treatment.展开更多
Cerebral small vessel disease encompasses a group of neurological disorders characterized by injury to small blood vessels,often leading to stroke and dementia.Due to its diverse etiologies and complex pathological me...Cerebral small vessel disease encompasses a group of neurological disorders characterized by injury to small blood vessels,often leading to stroke and dementia.Due to its diverse etiologies and complex pathological mechanisms,preventing and treating cerebral small vessel vasculopathy is challenging.Recent studies have shown that the glymphatic system plays a crucial role in interstitial solute clearance and the maintenance of brain homeostasis.Increasing evidence also suggests that dysfunction in glymphatic clearance is a key factor in the progression of cerebral small vessel disease.This review begins with a comprehensive introduction to the structure,function,and driving factors of the glymphatic system,highlighting its essential role in brain waste clearance.Afterwards,cerebral small vessel disease was reviewed from the perspective of the glymphatic system,after which the mechanisms underlying their correlation were summarized.Glymphatic dysfunction may lead to the accumulation of metabolic waste in the brain,thereby exacerbating the pathological processes associated with cerebral small vessel disease.The review also discussed the direct evidence of glymphatic dysfunction in patients and animal models exhibiting two subtypes of cerebral small vessel disease:arteriolosclerosis-related cerebral small vessel disease and amyloid-related cerebral small vessel disease.Diffusion tensor image analysis along the perivascular space is an important non-invasive tool for assessing the clearance function of the glymphatic system.However,the effectiveness of its parameters needs to be enhanced.Among various nervous system diseases,including cerebral small vessel disease,glymphatic failure may be a common final pathway toward dementia.Overall,this review summarizes prevention and treatment strategies that target glymphatic drainage and will offer valuable insight for developing novel treatments for cerebral small vessel disease.展开更多
In this article,we make a comment on the recent article by Sun et al,focusing on the advances of neutrophil extracellular traps(NETs)formation in common osteoarticular diseases.Neutrophils are the first line to elimin...In this article,we make a comment on the recent article by Sun et al,focusing on the advances of neutrophil extracellular traps(NETs)formation in common osteoarticular diseases.Neutrophils are the first line to eliminate invading pathogens including fungal and bacterial infections via releasing hydrolytic enzymes and reactive oxygen species.Besides,neutrophils will accumulate at the inflammatory site and release NETs,which are composed of histones,DNA and granular proteins.Traumatic heterotopic ossification(THO)was generally believed to develop through four stages:Inflammation,chondrogenesis,osteogenesis,and bone maturation.Thus,it can be seen that THO was related to inflammation and bone formation.Apart from immune and infectious diseases,recent studies have also shown that NETs play a significant role in the pathogenesis of THO.This article focuses on elaborating the role of NETs in the onset of THO,discussing the existing problems in the current research and outlining future directions.展开更多
Melatonin(N-acetyl-5 methoxytryptamine)is an indolic compound present in almost all fungi,plants,and animals.This neurohormone is synthesized and secreted into the internal environment mainly by the pineal gland,prese...Melatonin(N-acetyl-5 methoxytryptamine)is an indolic compound present in almost all fungi,plants,and animals.This neurohormone is synthesized and secreted into the internal environment mainly by the pineal gland,present in most vertebrates.Non-endocrine extrapineal locations have not been documented.This molecule with pleiotropic bioactions regulates the circadian rhythm,antioxidant,anti-inflammatory,immunostimulant,cardioprotective,antidiabetic,antiobesity,neuroprotective,and antiaging actions.Furthermore,in recent years,many studies have described the key role of melatonin in the prevention and development of cancer.The objective of this narrative review is to describe the different mechanisms through which melatonin exerts its action as an adjuvant in the modulation of carcinogenesis.The general anticarcinogenic mechanisms include epigenetic control,modulation of cell proliferation,regulation of cell cycle,induction of apoptosis,and telomerase inhibition.Melatonin also exerts antiestrogenic activity,which is particularly significant in hormone-dependent tumors,regulating the expression and transactivation of the estrogen receptor,and modulating the enzymes involved in the local synthesis of estrogens.Modulation of metastasis by melatonin includes increased expression of cell adhesion molecules such as E-cadherin andβ1-integrin,inhibition of angiogenesis,and control of fat metabolism by inhibiting the uptake of fatty acids by membrane transporters.Finally,immunomodulatory properties include enhanced production of anti-inflammatory interleukins and other cytokines in lymphocytes and monocytes and modulation of antioxidant activity by neutralizing free radicals.Despite all the mentioned properties,the use of melatonin in daily clinical practice is very limited,and additional studies are needed to better establish the role of this hormone in oncological clinical applications against different types of cancer.展开更多
We are deeply interested in the recent findings onβ-arrestin 2.Liu et al demonstrated thatβ-arrestin 2 knockout provides significant protection in diabetic nephropathy,underscoring its potential as a promising thera...We are deeply interested in the recent findings onβ-arrestin 2.Liu et al demonstrated thatβ-arrestin 2 knockout provides significant protection in diabetic nephropathy,underscoring its potential as a promising therapeutic target for diabetic nephropathy treatment.Furthermore,the role ofβ-arrestin 2 in metabolic regulation is equally critical,particularly in insulin signaling,hepatic glucose production,and adipose tissue function.Althoughβ-arrestin 2 plays a distinct role in metabolism and kidney protection,its tissue-specific regulation opens up valuable avenues for developing targeted therapeutic strategies centered onβ-arrestin 2.展开更多
Precision medicine has become a cornerstone in modern therapeutic strategies, with nucleic acid aptamers emerging aspivotal tools due to their unique properties. These oligonucleotide fragments, selected through the S...Precision medicine has become a cornerstone in modern therapeutic strategies, with nucleic acid aptamers emerging aspivotal tools due to their unique properties. These oligonucleotide fragments, selected through the Systematic Evolution ofLigands by Exponential Enrichment process, exhibit high affinity and specificity toward their targets, such as DNA, RNA,proteins, and other biomolecules. Nucleic acid aptamers offer significant advantages over traditional therapeutic agents,including superior biological stability, minimal immunogenicity, and the capacity for universal chemical modifications thatenhance their in vivo performance and targeting precision. In the realm of osseous tissue repair and regeneration, a complexphysiological process essential for maintaining skeletal integrity, aptamers have shown remarkable potential in influencingmolecular pathways crucial for bone regeneration, promoting osteogenic differentiation and supporting osteoblast survival. Byengineering aptamers to regulate inflammatory responses and facilitate the proliferation and differentiation of fibroblasts,these oligonucleotides can be integrated into advanced drug delivery systems, significantly improving bone repair efficacywhile minimizing adverse effects. Aptamer-mediated strategies, including the use of siRNA and miRNA mimics or inhibitors,have shown efficacy in enhancing bone mass and microstructure. These approaches hold transformative potential for treatinga range of orthopedic conditions like osteoporosis, osteosarcoma, and osteoarthritis. This review synthesizes the molecularmechanisms and biological roles of aptamers in orthopedic diseases, emphasizing their potential to drive innovative andeffective therapeutic interventions.展开更多
This article explores the significant implications of the study by Ovadia et al,which innovatively compares the efficacy of a nutritional intervention(Modulen)to conventional pharmaceutical therapy(budesonide)in promo...This article explores the significant implications of the study by Ovadia et al,which innovatively compares the efficacy of a nutritional intervention(Modulen)to conventional pharmaceutical therapy(budesonide)in promoting mucosal healing in Crohn’s disease.Highlighting the paradox of a well-established yet underutilized nutritional approach,the findings suggest that Modulen may offer comparable therapeutic benefits despite its high withdrawal rate due to adherence challenges.This advancement underscores the evolving paradigm in inflammatory bowel disease treatment,shifting focus toward non-pharmacologic alternatives that target both clinical remission and endoscopic healing.The article advocates for the development of integrative treatment strategies that balance efficacy,patient adherence,and long-term disease management,emphasizing the need for further research to refine and optimize the role of nutritional therapies in clinical practice.展开更多
Pancreatic ductal adenocarcinoma(PDAC)is one of the most aggressive and fatal malignancies,with a 5-year survival rate of<15%.Despite significant advancements in targeted therapies and immunotherapy,these approache...Pancreatic ductal adenocarcinoma(PDAC)is one of the most aggressive and fatal malignancies,with a 5-year survival rate of<15%.Despite significant advancements in targeted therapies and immunotherapy,these approaches benefit only a limited subset of patients,leaving chemotherapy as the primary treatment modality for most patients.Chemotherapy is an essential adjunct to surgical resection,the only potentially curative option,playing a crucial role in reducing the tumor burden,delaying disease progression,and alleviating symptoms.However,its long-term efficacy is frequently undermined by the development of chemoresistance,wherein tumor cells adopt diverse strategies to evade or repair chemotherapy-induced damage.Addressing this critical barrier is imperative for improving the clinical outcomes of PDAC.This review comprehensively examines the multifaceted mechanisms of chemoresistance in PDAC and highlights innovative strategies designed to enhance chemosensitivity,thereby offering new hope for overcoming these challenges and improving patient survival.展开更多
Depression is a common comorbidity in gastric cancer(GC)patients,with prevalence rates reaching up to 57%,particularly in advanced stages and during active treatment.While prior studies have explored the bidirectional...Depression is a common comorbidity in gastric cancer(GC)patients,with prevalence rates reaching up to 57%,particularly in advanced stages and during active treatment.While prior studies have explored the bidirectional relationship between GC and depression,this editorial provides a structured synthesis of therapeutic strategies including pharmacological,psychotherapeutic,integrative,and biomarker-driven interventions,within a multidisciplinary care framework.Depression may exacerbate tumor progression through chronic stress and neurotransmitter dysregulation,such asβ2-adrenergic receptor activation,while the cancer burden deepens psychological distress.Antidepressants,especially selective serotonin reuptake inhibitors,have demonstrated efficacy in alleviating depressive symptoms in up to 70%of cases,particularly when used alongside chemotherapy.Psychotherapeutic modalities,including cognitive-behavioral therapy and family-based interventions,help reduce depressive symptoms,improve coping mechanisms,and prevent relapse.Integrative strategies like music therapy,mindfulness,and physical activity further support emotional wellbeing,particularly in mild-to-moderate depression.Multidisciplinary care that combines nutritional support,pain control,and psychosocial interventions is essential.Notably,the integration of interventional therapies with traditional Chinese medicine has shown potential in stabilizing tumor growth and improving mental health,enabling functional“tumor-bearing survival”.Emerging immunotherapies such as cadonilimab may also contribute indirectly to depression alleviation by enhancing treatment efficacy and extending survival.Future research should focus on biomarker-guided approaches,such as targetingβ2-adrenergic signaling,and developing personalized psychosocial care models.A holistic approach that integrates both physical and psychological care is vital to improving outcomes and quality of life in GC patients.展开更多
Background:Pulmonary blastoma(PB)is a rare subtype of lung cancer.Currently,the underlying pathogenesis mechanisms of PB have not been fully illustrated,and the therapeutic approach for this entity is limited.Methods:...Background:Pulmonary blastoma(PB)is a rare subtype of lung cancer.Currently,the underlying pathogenesis mechanisms of PB have not been fully illustrated,and the therapeutic approach for this entity is limited.Methods:Whole-exome sequencing(WES),RNA sequencing,and DNA methylation profiling are applied to seven PB patients.Multi-omics data of pulmonary sarcomatoid carcinoma(PSC)and pituitary blastoma(PitB)from previous studies are invoked to illuminate the associations among PB and these malignacies.Results:We portray the genomic alteration spectrum of PB and find that DICER1 is with the highest alteration rate(86%).We uncover that DICER1 alterations,Wnt signaling pathway dysregulation and IGF2 imprinting dysregulation are the potential pathogenesis mechanisms of PB.Moreover,we reveal that the integrated molecular features of PB are distinct from PSC,and the molecular characteristics of PB are more similar to PitB than to PSC.Pancancer analysis show that the tumor mutation burden(TMB)and leukocyte fraction(LF)of PB are low,while some cases are positive for PD-L1 or have CD8-positive focal areas,implying the potential applicability of immunotherapy in selected PB patients.Conclusion:This study depicts the integrated molecular characteristics of PB and offers novel insights into the pathogenesis and therapeutic strategies of PB.展开更多
The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions,including regulating the inflammatory cascade in various autoimmune and inflammatory diseases,such as multi...The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions,including regulating the inflammatory cascade in various autoimmune and inflammatory diseases,such as multiple sclerosis,neuromyelitis optica spectrum disorder,myasthenia gravis,Guillain–Barre syndrome,acute disseminated encephalomyelitis,diabetes,inflammatory skin diseases,joint inflammation,and cancer.Although the function of the interleukin-17 family has attracted increasing research attention over many years,the expression,function,and regulation mechanisms of different interleukin-17 members are complicated and still only partially understood.Currently,the interleukin-17A pathway is considered a critical therapeutic target for numerous immune and chronic inflammatory diseases,with several monoclonal antibodies against interleukin-17A having been successfully used in clinical practice.Whether other interleukin-17 members have the potential to be targeted in other diseases is still debated.This review first summarizes the recent advancements in understanding the physicochemical properties,physiological functions,cellular origins,and downstream signaling pathways of different members and corresponding receptors of the interleukin-17 family.Subsequently,the function of interleukin-17 in various immune diseases is discussed,and the important role of interleukin-17 in the pathological process of immune diseases is demonstrated from multiple perspectives.Then,the current status of targeted interleukin-17 therapy is summarized,and the effectiveness and safety of targeted interleukin-17 therapy are analyzed.Finally,the clinical application prospects of targeting the interleukin-17 pathway are discussed.展开更多
Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a...Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a stroke.Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes.This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies.Microglia exhibit a dynamic functional state,transitioning between pro-inflammatory(M1)and anti-inflammatory(M2)phenotypes.This duality is crucial in ischemic stroke,as it maintains a balance between neuroinflammation and tissue repair.Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier,while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration.Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B,mitogen-activated protein kinases,Janus kinase/signal transducer and activator of transcription,and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways.These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage.Potential therapeutic agents include natural compounds found in drugs such as minocycline,as well as traditional Chinese medicines.Drugs that target these regulatory mechanisms,such as small molecule inhibitors and components of traditional Chinese medicines,along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics,offer new therapeutic strategies and clinical translational potential for ischemic stroke.展开更多
BackgroundFew studies have compared change in the health-related quality of life （HRQL） following treatment of non-ST-elevation acute coronary syndrome （NSTE-ACS） with either percutaneous coronary intervention （...BackgroundFew studies have compared change in the health-related quality of life （HRQL） following treatment of non-ST-elevation acute coronary syndrome （NSTE-ACS） with either percutaneous coronary intervention （PCI） or coronary artery bypass grafting （CABG）. This study is tocompare changes in HRQL six months after hospital discharge between NSTE-ACS pa-tients who underwent either PCI or CABG.Methods HRQL was assessed using the Seattle angina questionnaire at admission and six months after discharge in 1012 consecutive patients with NSTE-ACS. To assess associations of PCI and CABG with HRQL changes, logistic regression models were constructed treating changes in the score of each dimension of the Seattle angina question-naire as dependent variables.Results Although both the PCI and CABG groups experienced angina relief and other improvements at 6-month follow-up （P〈0.001）, the CABG relative to PCI group showed more significant improvements in angina frequency （P= 0.044） and quality of life （P= 0.028）. In multivariable logistic analysis, CABG also was an independent predictor for both im-provement of angina frequency （OR： 1.62, 95%CI： 1.09-4.63,P= 0.042） and quality of life （OR： 2.04, 95%CI： 1.26-6.92,P= 0.038） relative to PCI.Conclusions In patients with NSTE-ACS, both PCI and CABG provide great improvement in disease-specific health status at six months, with that of CABG being more prominent in terms of angina frequency and quality of life.展开更多
The intrinsic heterogeneity of metabolic dysfunction-associated fatty liver disease(MASLD)and the intricate pathogenesis have impeded the advancement and clinical implementation of therapeutic interventions,underscori...The intrinsic heterogeneity of metabolic dysfunction-associated fatty liver disease(MASLD)and the intricate pathogenesis have impeded the advancement and clinical implementation of therapeutic interventions,underscoring the critical demand for novel treatments.A recent publication by Li et al proposes mesenchymal stem cells as promising effectors for the treatment of MASLD.This editorial is a continuum of the article published by Jiang et al which focuses on the significance of strategies to enhance the functionality of mesenchymal stem cells to improve efficacy in curing MASLD,including physical pretreatment,drug or chemical pretreatment,pretreatment with bioactive substances,and genetic engineering.展开更多
Complications in the healing process are challenging, especially in clinical situations of caloric restriction （CR）. The lasertherapy becomes an important strategy that aids the repair, especially in CR. Thus, it i...Complications in the healing process are challenging, especially in clinical situations of caloric restriction （CR）. The lasertherapy becomes an important strategy that aids the repair, especially in CR. Thus, it is important to investigate the InGaAlP-660 nm laser as an strategy to repair cutaneous wounds in rats submitted to 30% of CR and to understand the tissue repair in clinical situations of CR. Thirty-six male Wistar rats were used, of which half were fed with 30% less ration, and half with ad libitum diet, for 21 days. Then, punch lesions of 1.5 cm in diameter were made on the animals backs, which were divided into： NR （no-restricted）, R （restricted）-both before lesion; C （control）, RC （restricted-control）, L （laser）, RL （restricted-laser）-after lesion. Samples of the skin/lesion/scar were collected on the 2nd, 7th and 14th days post-injury for histological, biochemical and molecular analyses. The R group showed reduction of body mass, epidermal/dermal thickness, inflammation, angiogenesis, fibroplasia and collagenesis. The RL group showed control of inflammation, oxidative damage and increase of antioxidants than RC, which probably favored angiogenesis, collagenesis and reepithelialization, similar to C and L. Thus, 30% of CR impaired the skin （before lesion）. In the lesion, lasertherapy has shown to be effective in tissue repair mainly in CR status, being thus, the laser clinically important strategy to tissue repair in critical situations of caloric restriction.展开更多
Objective: the purpose of this project is to explore the strategies and effects of clinical treatment for patients suffering from acute cerebrovascular diseases accompanied by conscious disturbance. Methods: 30 patien...Objective: the purpose of this project is to explore the strategies and effects of clinical treatment for patients suffering from acute cerebrovascular diseases accompanied by conscious disturbance. Methods: 30 patients suffering from acute cerebrovascular diseases accompanied by conscious disturbance in our hospital were randomly divided into control group (15 cases) and observation group (15 cases) during the period from March 2019 to March 2021. The therapeutic effects of the two treatments were evaluated and compared. Results: the total effective rate observed in the observation group was 93.33%, and the total effective rate observed in the control group was 60.00% (P<0.05). Before treatment, there was no significant difference in GCS and GOS scores between the two groups (P > 0.05). After treatment, the GCS and GOS scores of both groups were improved, but the observation group was higher than the control group (P<0.05). Before treatment, the total average value of quality of life in the two groups was not statistically significant (P > 0.05). After treatment, the total average value of the two groups increased to varying degrees, but the total average value of the observation group was higher than that of the control group (P<0.05). The incidence of complications in the observation group was 6.67%(1/15) and the incidence of complications in the control group was 40.00%(6/15), with a comparison between the two groups (P<0.05). The levels of TNF-a, IL-6, IFN-y, HMGB-1 and other inflammatory factors in the observation group after treatment were lower than those in the control group (P<0.05). It can not only improve the treatment effect, promote the recovery of patients' consciousness and nerve function, but also improve the quality of life of patients. At the same time, the naloxone drug effect is more stable and takes effect faster, reducing the level of inflammatory factors, with fewer complications and higher safety. It can be actively promoted in clinical practice.展开更多
In recent years, multiple disciplines have focused on mitochondrial biology and contributed to understanding its relevance towards adult-onset neurodegenerative disorders. These are complex dynamic organelles that hav...In recent years, multiple disciplines have focused on mitochondrial biology and contributed to understanding its relevance towards adult-onset neurodegenerative disorders. These are complex dynamic organelles that have a variety of functions in ensuring cellular health and homeostasis. The plethora of mitochondrial functionalities confers them an intrinsic susceptibility to internal and external stressors(such as mutation accumulation or environmental toxins), particularly so in long-lived postmitotic cells such as neurons. Thus, it is reasonable to postulate an involvement of mitochondria in aging-associated neurological disorders, notably neurodegenerative pathologies including Alzheimer’s disease and Parkinson’s disease. On the other hand, biological effects resulting from neurodegeneration can in turn affect mitochondrial health and function, promoting a feedback loop further contributing to the progression of neuronal dysfunction and cellular death. This review examines state-of-the-art knowledge, focus on current research exploring mitochondrial health as a contributing factor to neuroregeneration, and the development of therapeutic approaches aimed at restoring mitochondrial homeostasis in a pathological setting.展开更多
基金This review was supported by the National Natural Science Foundation of China(81920108017,82130036,and 81630028)the Key Research and Development Program of Jiangsu Province of China(BE2020620)Jiangsu Province Key Medical Discipline(ZDXKA2016020).
文摘Ischemic stroke caused by intracranial vascular occlusion has become increasingly prevalent with considerable mortality and disability,which gravely burdens the global economy.Current relatively effective clinical treatments are limited to intravenous alteplase and thrombectomy.Even so,patients still benefit little due to the short therapeutic window and the risk of ischemia/reperfusion injury.It is therefore urgent to figure out the neuronal death mechanisms following ischemic stroke in order to develop new neuroprotective strategies.Regarding the pathogenesis,multiple pathological events trigger the activation of cell death pathways.Particular attention should be devoted to excitotoxicity,oxidative stress,and inflammatory responses.Thus,in this article,we first review the principal mechanisms underlying neuronal death mediated by these significant events,such as intrinsic and extrinsic apoptosis,ferroptosis,parthanatos,pyroptosis,necroptosis,and autophagic cell death.Then,we further discuss the possibility of interventions targeting these pathological events and summarize the present pharmacological achievements.
基金Supported by the National Key Basic Research Program of China (973 Program, No. 2013CB967001)
文摘Transcorneal electrical stimulation （TES） is a novel therapeutic approach to activate the retina and related downstream structures. TES has multiple advantages over traditional treatments, such as being minimally invasive and readily applicable in a routine manner. Series of animal experiments have shown that TES protects the retinal neuron from traumatic or genetic induced degeneration. These laboratory evidences support its utilization in ophthalmological therapies against various retinal and optical diseases including retinitis pigmentosa （RP）, traumatic optic neuropathy, anterior ischemic optic neuropathy （AION）, and retinal artery occlusions （RAOs）. Several pioneering explorations sought to clarify the functional mechanism underlying the neuroprotective effects of TES. It seems that the neuroprotective effects should not be attributed to a solitary pathway, on the contrary, multiple mechanisms might contribute collectively to maintain cellular homeostasis and promote cell survival in the retina. More precise evaluations y/a functional and morphological techniques would determine the exact mechanism underlying the remarkable neuroprotective effect of TES. Further studies to determine the optimal parameters and the long-term stability of TES are crucial to justify the clinical significance and to establish TES as a popularized therapeutic modality against retinal and optic neuropathy.
基金Supported by National Natural Science Foundation of China,No.81800342 and 81800138Zhejiang Provincial Natural Science Foundation of China,No.LQ20H020012.
文摘BACKGROUND The coexistence with patent ductus arteriosus(PDA),mitral valve prolapse(MVP),atrial fibrillation(AF)and hyperthyroidism is extremely rare and complex.The optimal therapeutic strategy is difficult to develop.CASE SUMMARY A 27-year-old female with PDA,MVP,AF and hyperthyroidism presented with severe dyspnea.Given that a one-stage operation for PDA,MVP and AF is high risk,we preferred a sequential multidisciplinary minimally invasive therapeutic strategy.First,PDA transcatheter closure was performed.Hyperthyroidism and heart failure were simultaneously controlled via medical treatment.Video-assisted thoracoscopic mitral valve repair and left atrial appendage occlusion were performed when heart failure was controlled.Under this therapeutic strategy,the patient’s sinus rhythm was restored and maintained.Two years after the treatment,the symptoms of heart failure were relieved,and the enlarged heart was reversed.CONCLUSION Sequential multidisciplinary therapeutic strategies,which take advantage of both internal medicine and surgical approaches,might be reasonable for this type of disease.
基金financially supported by the National Natural Science Foundation of China(no.82273878).
文摘Diabetic foot ulcer is a serious complication of diabetes.Excessive accumulation of advanced glycation end products(AGEs)is one of the critical pathogenic factors in postponing diabetic wound healing.The main pathogenic mechanisms of AGEs include inducing cellular dysfunction,prolonging inflammatory response,increasing oxidative stress and reducing endogenous nitric oxide(NO)production.Combination therapy of blocking the deleterious effects of AGEs and supplementing exogenous NO is hypothesized to promote diabetic wound healing.Here,we presented nanoparticles/hydrogel composite dressings to co-delivery rosiglitazone and S-nitroso glutathione into the wound bed.The designed co-delivery system augmented the survival of fibroblasts,reduced oxidative stress levels,reversed the change of mitochondrial membrane potential and decreased the proinflammatory cytokine expression.Local sustained release of therapeutic agents significantly improved the wound healing of diabetic rats including increasing the wound closure rate,alleviating inflammation,promoting collagen fiber production and angiogenesis.Our finding indicated this local deliver strategy aimed at inhibiting the toxic effects of AGEs has great clinical potential for diabetic wound treatment.
基金supported by the National Natural Science Foundation of China,No.82274304(to YH)the Major Clinical Study Projects of Shanghai Shenkang Hospital Development Center,No.SHDC2020CR2046B(to YH)Shanghai Municipal Health Commission Talent Plan,No.2022LJ010(to YH).
文摘Cerebral small vessel disease encompasses a group of neurological disorders characterized by injury to small blood vessels,often leading to stroke and dementia.Due to its diverse etiologies and complex pathological mechanisms,preventing and treating cerebral small vessel vasculopathy is challenging.Recent studies have shown that the glymphatic system plays a crucial role in interstitial solute clearance and the maintenance of brain homeostasis.Increasing evidence also suggests that dysfunction in glymphatic clearance is a key factor in the progression of cerebral small vessel disease.This review begins with a comprehensive introduction to the structure,function,and driving factors of the glymphatic system,highlighting its essential role in brain waste clearance.Afterwards,cerebral small vessel disease was reviewed from the perspective of the glymphatic system,after which the mechanisms underlying their correlation were summarized.Glymphatic dysfunction may lead to the accumulation of metabolic waste in the brain,thereby exacerbating the pathological processes associated with cerebral small vessel disease.The review also discussed the direct evidence of glymphatic dysfunction in patients and animal models exhibiting two subtypes of cerebral small vessel disease:arteriolosclerosis-related cerebral small vessel disease and amyloid-related cerebral small vessel disease.Diffusion tensor image analysis along the perivascular space is an important non-invasive tool for assessing the clearance function of the glymphatic system.However,the effectiveness of its parameters needs to be enhanced.Among various nervous system diseases,including cerebral small vessel disease,glymphatic failure may be a common final pathway toward dementia.Overall,this review summarizes prevention and treatment strategies that target glymphatic drainage and will offer valuable insight for developing novel treatments for cerebral small vessel disease.
文摘In this article,we make a comment on the recent article by Sun et al,focusing on the advances of neutrophil extracellular traps(NETs)formation in common osteoarticular diseases.Neutrophils are the first line to eliminate invading pathogens including fungal and bacterial infections via releasing hydrolytic enzymes and reactive oxygen species.Besides,neutrophils will accumulate at the inflammatory site and release NETs,which are composed of histones,DNA and granular proteins.Traumatic heterotopic ossification(THO)was generally believed to develop through four stages:Inflammation,chondrogenesis,osteogenesis,and bone maturation.Thus,it can be seen that THO was related to inflammation and bone formation.Apart from immune and infectious diseases,recent studies have also shown that NETs play a significant role in the pathogenesis of THO.This article focuses on elaborating the role of NETs in the onset of THO,discussing the existing problems in the current research and outlining future directions.
基金financed by the Department of Education of the Junta de Castilla-León and the European Regional Development Fund(FEDER)by TCUE Plan 2021-2023,134/2021,within the research project“Application of Genomics through the Study of Genetic polymorphisms in the treatment and prevention of chronic diseases in older adult patients”,(grant nos.SO002P23).
文摘Melatonin(N-acetyl-5 methoxytryptamine)is an indolic compound present in almost all fungi,plants,and animals.This neurohormone is synthesized and secreted into the internal environment mainly by the pineal gland,present in most vertebrates.Non-endocrine extrapineal locations have not been documented.This molecule with pleiotropic bioactions regulates the circadian rhythm,antioxidant,anti-inflammatory,immunostimulant,cardioprotective,antidiabetic,antiobesity,neuroprotective,and antiaging actions.Furthermore,in recent years,many studies have described the key role of melatonin in the prevention and development of cancer.The objective of this narrative review is to describe the different mechanisms through which melatonin exerts its action as an adjuvant in the modulation of carcinogenesis.The general anticarcinogenic mechanisms include epigenetic control,modulation of cell proliferation,regulation of cell cycle,induction of apoptosis,and telomerase inhibition.Melatonin also exerts antiestrogenic activity,which is particularly significant in hormone-dependent tumors,regulating the expression and transactivation of the estrogen receptor,and modulating the enzymes involved in the local synthesis of estrogens.Modulation of metastasis by melatonin includes increased expression of cell adhesion molecules such as E-cadherin andβ1-integrin,inhibition of angiogenesis,and control of fat metabolism by inhibiting the uptake of fatty acids by membrane transporters.Finally,immunomodulatory properties include enhanced production of anti-inflammatory interleukins and other cytokines in lymphocytes and monocytes and modulation of antioxidant activity by neutralizing free radicals.Despite all the mentioned properties,the use of melatonin in daily clinical practice is very limited,and additional studies are needed to better establish the role of this hormone in oncological clinical applications against different types of cancer.
基金Supported by National Natural Science Foundation of China,No.82471616,No.82170418,and No.82271618Natural Science Foundation of Hubei Province,No.2022CFA015+2 种基金Central Guiding Local Science and Technology Development Project,No.2022BGE237Key Research and Development Program of Hubei Province,No.2022BCE001,and No.2023BCB139Hubei Provincial Health Commission Project,No.WJ2023M151。
文摘We are deeply interested in the recent findings onβ-arrestin 2.Liu et al demonstrated thatβ-arrestin 2 knockout provides significant protection in diabetic nephropathy,underscoring its potential as a promising therapeutic target for diabetic nephropathy treatment.Furthermore,the role ofβ-arrestin 2 in metabolic regulation is equally critical,particularly in insulin signaling,hepatic glucose production,and adipose tissue function.Althoughβ-arrestin 2 plays a distinct role in metabolism and kidney protection,its tissue-specific regulation opens up valuable avenues for developing targeted therapeutic strategies centered onβ-arrestin 2.
基金Key research and development projects of Sichuan Science and Technology Plan Project(2024YFFK0135)Fujian Provincial Natural Science Foundation of China(2024J011450).
文摘Precision medicine has become a cornerstone in modern therapeutic strategies, with nucleic acid aptamers emerging aspivotal tools due to their unique properties. These oligonucleotide fragments, selected through the Systematic Evolution ofLigands by Exponential Enrichment process, exhibit high affinity and specificity toward their targets, such as DNA, RNA,proteins, and other biomolecules. Nucleic acid aptamers offer significant advantages over traditional therapeutic agents,including superior biological stability, minimal immunogenicity, and the capacity for universal chemical modifications thatenhance their in vivo performance and targeting precision. In the realm of osseous tissue repair and regeneration, a complexphysiological process essential for maintaining skeletal integrity, aptamers have shown remarkable potential in influencingmolecular pathways crucial for bone regeneration, promoting osteogenic differentiation and supporting osteoblast survival. Byengineering aptamers to regulate inflammatory responses and facilitate the proliferation and differentiation of fibroblasts,these oligonucleotides can be integrated into advanced drug delivery systems, significantly improving bone repair efficacywhile minimizing adverse effects. Aptamer-mediated strategies, including the use of siRNA and miRNA mimics or inhibitors,have shown efficacy in enhancing bone mass and microstructure. These approaches hold transformative potential for treatinga range of orthopedic conditions like osteoporosis, osteosarcoma, and osteoarthritis. This review synthesizes the molecularmechanisms and biological roles of aptamers in orthopedic diseases, emphasizing their potential to drive innovative andeffective therapeutic interventions.
文摘This article explores the significant implications of the study by Ovadia et al,which innovatively compares the efficacy of a nutritional intervention(Modulen)to conventional pharmaceutical therapy(budesonide)in promoting mucosal healing in Crohn’s disease.Highlighting the paradox of a well-established yet underutilized nutritional approach,the findings suggest that Modulen may offer comparable therapeutic benefits despite its high withdrawal rate due to adherence challenges.This advancement underscores the evolving paradigm in inflammatory bowel disease treatment,shifting focus toward non-pharmacologic alternatives that target both clinical remission and endoscopic healing.The article advocates for the development of integrative treatment strategies that balance efficacy,patient adherence,and long-term disease management,emphasizing the need for further research to refine and optimize the role of nutritional therapies in clinical practice.
基金supported by grants from the CAMS Innovation Fund for Medical Sciences(No.2024-I2M-ZD-001)National Key R&D Program of China(No.2023YFC2413400)+5 种基金National Natural Science Foundation of China(No.82272917,No.62133006,No.82203158,No.82473086,No.82473096,and No.82403006)Beijing Natural Science Foundation(No.7242104,No.7244385,and No.L248053)Research and Translational Application of Clinical Characteristic Diagnosis and Treatment Techniques in the Capital(No.Z221100007422070)Beijing Science and Technology Plan(No.Z231100007223006)National High Level Hospital Clinical Research Funding(No.2022-PUMCH-B-004)the Postdoctoral Fellowship Program of CPSF(No.GZB20240074).
文摘Pancreatic ductal adenocarcinoma(PDAC)is one of the most aggressive and fatal malignancies,with a 5-year survival rate of<15%.Despite significant advancements in targeted therapies and immunotherapy,these approaches benefit only a limited subset of patients,leaving chemotherapy as the primary treatment modality for most patients.Chemotherapy is an essential adjunct to surgical resection,the only potentially curative option,playing a crucial role in reducing the tumor burden,delaying disease progression,and alleviating symptoms.However,its long-term efficacy is frequently undermined by the development of chemoresistance,wherein tumor cells adopt diverse strategies to evade or repair chemotherapy-induced damage.Addressing this critical barrier is imperative for improving the clinical outcomes of PDAC.This review comprehensively examines the multifaceted mechanisms of chemoresistance in PDAC and highlights innovative strategies designed to enhance chemosensitivity,thereby offering new hope for overcoming these challenges and improving patient survival.
文摘Depression is a common comorbidity in gastric cancer(GC)patients,with prevalence rates reaching up to 57%,particularly in advanced stages and during active treatment.While prior studies have explored the bidirectional relationship between GC and depression,this editorial provides a structured synthesis of therapeutic strategies including pharmacological,psychotherapeutic,integrative,and biomarker-driven interventions,within a multidisciplinary care framework.Depression may exacerbate tumor progression through chronic stress and neurotransmitter dysregulation,such asβ2-adrenergic receptor activation,while the cancer burden deepens psychological distress.Antidepressants,especially selective serotonin reuptake inhibitors,have demonstrated efficacy in alleviating depressive symptoms in up to 70%of cases,particularly when used alongside chemotherapy.Psychotherapeutic modalities,including cognitive-behavioral therapy and family-based interventions,help reduce depressive symptoms,improve coping mechanisms,and prevent relapse.Integrative strategies like music therapy,mindfulness,and physical activity further support emotional wellbeing,particularly in mild-to-moderate depression.Multidisciplinary care that combines nutritional support,pain control,and psychosocial interventions is essential.Notably,the integration of interventional therapies with traditional Chinese medicine has shown potential in stabilizing tumor growth and improving mental health,enabling functional“tumor-bearing survival”.Emerging immunotherapies such as cadonilimab may also contribute indirectly to depression alleviation by enhancing treatment efficacy and extending survival.Future research should focus on biomarker-guided approaches,such as targetingβ2-adrenergic signaling,and developing personalized psychosocial care models.A holistic approach that integrates both physical and psychological care is vital to improving outcomes and quality of life in GC patients.
基金supported by National Natural Sciences Foundation(grant number:82203827).
文摘Background:Pulmonary blastoma(PB)is a rare subtype of lung cancer.Currently,the underlying pathogenesis mechanisms of PB have not been fully illustrated,and the therapeutic approach for this entity is limited.Methods:Whole-exome sequencing(WES),RNA sequencing,and DNA methylation profiling are applied to seven PB patients.Multi-omics data of pulmonary sarcomatoid carcinoma(PSC)and pituitary blastoma(PitB)from previous studies are invoked to illuminate the associations among PB and these malignacies.Results:We portray the genomic alteration spectrum of PB and find that DICER1 is with the highest alteration rate(86%).We uncover that DICER1 alterations,Wnt signaling pathway dysregulation and IGF2 imprinting dysregulation are the potential pathogenesis mechanisms of PB.Moreover,we reveal that the integrated molecular features of PB are distinct from PSC,and the molecular characteristics of PB are more similar to PitB than to PSC.Pancancer analysis show that the tumor mutation burden(TMB)and leukocyte fraction(LF)of PB are low,while some cases are positive for PD-L1 or have CD8-positive focal areas,implying the potential applicability of immunotherapy in selected PB patients.Conclusion:This study depicts the integrated molecular characteristics of PB and offers novel insights into the pathogenesis and therapeutic strategies of PB.
基金supported by the National Natural Science Foundational of China(Key Program),No.U24A20692(to CJZ)the National Natural Science Foundational of China,Nos.82101414(to MLJ),82371355(to CJZ)+4 种基金the National Natural Science Foundational of China for Excellent Young Scholars,No.82022019(to CJZ)Sichuan Special Fund for Distinguished Young Scholars,No.24NSFJQ0052(to CJZ)The Innovation and Entrepreneurial Team of Sichuan Tianfu Emei Program,No.CZ2024018(to CJZ)Funding for Distinguished Young Scholars of Sichuan Provincial People’s Hospital,No.30420230005(to CJZ)Funding for Distinguished Young Scholars of University of Electronic Science and Technology of China,No.A1098531023601381(to CJZ)。
文摘The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions,including regulating the inflammatory cascade in various autoimmune and inflammatory diseases,such as multiple sclerosis,neuromyelitis optica spectrum disorder,myasthenia gravis,Guillain–Barre syndrome,acute disseminated encephalomyelitis,diabetes,inflammatory skin diseases,joint inflammation,and cancer.Although the function of the interleukin-17 family has attracted increasing research attention over many years,the expression,function,and regulation mechanisms of different interleukin-17 members are complicated and still only partially understood.Currently,the interleukin-17A pathway is considered a critical therapeutic target for numerous immune and chronic inflammatory diseases,with several monoclonal antibodies against interleukin-17A having been successfully used in clinical practice.Whether other interleukin-17 members have the potential to be targeted in other diseases is still debated.This review first summarizes the recent advancements in understanding the physicochemical properties,physiological functions,cellular origins,and downstream signaling pathways of different members and corresponding receptors of the interleukin-17 family.Subsequently,the function of interleukin-17 in various immune diseases is discussed,and the important role of interleukin-17 in the pathological process of immune diseases is demonstrated from multiple perspectives.Then,the current status of targeted interleukin-17 therapy is summarized,and the effectiveness and safety of targeted interleukin-17 therapy are analyzed.Finally,the clinical application prospects of targeting the interleukin-17 pathway are discussed.
基金supported by the National Natural Science Foundation of China,82471345(to LC)the Key Research and Development Program for Social Development by the Jiangsu Provincial Department of Science and Technology.No.BE2022668(to LC).
文摘Ischemic stroke is a major cause of neurological deficits and high disability rate.As the primary immune cells of the central nervous system,microglia play dual roles in neuroinflammation and tissue repair following a stroke.Their dynamic activation and polarization states are key factors that influence the disease process and treatment outcomes.This review article investigates the role of microglia in ischemic stroke and explores potential intervention strategies.Microglia exhibit a dynamic functional state,transitioning between pro-inflammatory(M1)and anti-inflammatory(M2)phenotypes.This duality is crucial in ischemic stroke,as it maintains a balance between neuroinflammation and tissue repair.Activated microglia contribute to neuroinflammation through cytokine release and disruption of the blood-brain barrier,while simultaneously promoting tissue repair through anti-inflammatory responses and regeneration.Key pathways influencing microglial activation include Toll-like receptor 4/nuclear factor kappa B,mitogen-activated protein kinases,Janus kinase/signal transducer and activator of transcription,and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathways.These pathways are targets for various experimental therapies aimed at promoting M2 polarization and mitigating damage.Potential therapeutic agents include natural compounds found in drugs such as minocycline,as well as traditional Chinese medicines.Drugs that target these regulatory mechanisms,such as small molecule inhibitors and components of traditional Chinese medicines,along with emerging technologies such as single-cell RNA sequencing and spatial transcriptomics,offer new therapeutic strategies and clinical translational potential for ischemic stroke.
文摘BackgroundFew studies have compared change in the health-related quality of life （HRQL） following treatment of non-ST-elevation acute coronary syndrome （NSTE-ACS） with either percutaneous coronary intervention （PCI） or coronary artery bypass grafting （CABG）. This study is tocompare changes in HRQL six months after hospital discharge between NSTE-ACS pa-tients who underwent either PCI or CABG.Methods HRQL was assessed using the Seattle angina questionnaire at admission and six months after discharge in 1012 consecutive patients with NSTE-ACS. To assess associations of PCI and CABG with HRQL changes, logistic regression models were constructed treating changes in the score of each dimension of the Seattle angina question-naire as dependent variables.Results Although both the PCI and CABG groups experienced angina relief and other improvements at 6-month follow-up （P〈0.001）, the CABG relative to PCI group showed more significant improvements in angina frequency （P= 0.044） and quality of life （P= 0.028）. In multivariable logistic analysis, CABG also was an independent predictor for both im-provement of angina frequency （OR： 1.62, 95%CI： 1.09-4.63,P= 0.042） and quality of life （OR： 2.04, 95%CI： 1.26-6.92,P= 0.038） relative to PCI.Conclusions In patients with NSTE-ACS, both PCI and CABG provide great improvement in disease-specific health status at six months, with that of CABG being more prominent in terms of angina frequency and quality of life.
文摘The intrinsic heterogeneity of metabolic dysfunction-associated fatty liver disease(MASLD)and the intricate pathogenesis have impeded the advancement and clinical implementation of therapeutic interventions,underscoring the critical demand for novel treatments.A recent publication by Li et al proposes mesenchymal stem cells as promising effectors for the treatment of MASLD.This editorial is a continuum of the article published by Jiang et al which focuses on the significance of strategies to enhance the functionality of mesenchymal stem cells to improve efficacy in curing MASLD,including physical pretreatment,drug or chemical pretreatment,pretreatment with bioactive substances,and genetic engineering.
文摘Complications in the healing process are challenging, especially in clinical situations of caloric restriction （CR）. The lasertherapy becomes an important strategy that aids the repair, especially in CR. Thus, it is important to investigate the InGaAlP-660 nm laser as an strategy to repair cutaneous wounds in rats submitted to 30% of CR and to understand the tissue repair in clinical situations of CR. Thirty-six male Wistar rats were used, of which half were fed with 30% less ration, and half with ad libitum diet, for 21 days. Then, punch lesions of 1.5 cm in diameter were made on the animals backs, which were divided into： NR （no-restricted）, R （restricted）-both before lesion; C （control）, RC （restricted-control）, L （laser）, RL （restricted-laser）-after lesion. Samples of the skin/lesion/scar were collected on the 2nd, 7th and 14th days post-injury for histological, biochemical and molecular analyses. The R group showed reduction of body mass, epidermal/dermal thickness, inflammation, angiogenesis, fibroplasia and collagenesis. The RL group showed control of inflammation, oxidative damage and increase of antioxidants than RC, which probably favored angiogenesis, collagenesis and reepithelialization, similar to C and L. Thus, 30% of CR impaired the skin （before lesion）. In the lesion, lasertherapy has shown to be effective in tissue repair mainly in CR status, being thus, the laser clinically important strategy to tissue repair in critical situations of caloric restriction.
文摘Objective: the purpose of this project is to explore the strategies and effects of clinical treatment for patients suffering from acute cerebrovascular diseases accompanied by conscious disturbance. Methods: 30 patients suffering from acute cerebrovascular diseases accompanied by conscious disturbance in our hospital were randomly divided into control group (15 cases) and observation group (15 cases) during the period from March 2019 to March 2021. The therapeutic effects of the two treatments were evaluated and compared. Results: the total effective rate observed in the observation group was 93.33%, and the total effective rate observed in the control group was 60.00% (P<0.05). Before treatment, there was no significant difference in GCS and GOS scores between the two groups (P > 0.05). After treatment, the GCS and GOS scores of both groups were improved, but the observation group was higher than the control group (P<0.05). Before treatment, the total average value of quality of life in the two groups was not statistically significant (P > 0.05). After treatment, the total average value of the two groups increased to varying degrees, but the total average value of the observation group was higher than that of the control group (P<0.05). The incidence of complications in the observation group was 6.67%(1/15) and the incidence of complications in the control group was 40.00%(6/15), with a comparison between the two groups (P<0.05). The levels of TNF-a, IL-6, IFN-y, HMGB-1 and other inflammatory factors in the observation group after treatment were lower than those in the control group (P<0.05). It can not only improve the treatment effect, promote the recovery of patients' consciousness and nerve function, but also improve the quality of life of patients. At the same time, the naloxone drug effect is more stable and takes effect faster, reducing the level of inflammatory factors, with fewer complications and higher safety. It can be actively promoted in clinical practice.
基金supported by a grant from the Fundacao para a Ciencia e Tecnologia of the Ministerio da Educacao e Ciencia (2020.02006.CEECIND)iBiMED,University of Aveiro and the Fundacao para a Ciência e Tecnologia of the Ministerio da Educacao e Ciencia (to DT)。
文摘In recent years, multiple disciplines have focused on mitochondrial biology and contributed to understanding its relevance towards adult-onset neurodegenerative disorders. These are complex dynamic organelles that have a variety of functions in ensuring cellular health and homeostasis. The plethora of mitochondrial functionalities confers them an intrinsic susceptibility to internal and external stressors(such as mutation accumulation or environmental toxins), particularly so in long-lived postmitotic cells such as neurons. Thus, it is reasonable to postulate an involvement of mitochondria in aging-associated neurological disorders, notably neurodegenerative pathologies including Alzheimer’s disease and Parkinson’s disease. On the other hand, biological effects resulting from neurodegeneration can in turn affect mitochondrial health and function, promoting a feedback loop further contributing to the progression of neuronal dysfunction and cellular death. This review examines state-of-the-art knowledge, focus on current research exploring mitochondrial health as a contributing factor to neuroregeneration, and the development of therapeutic approaches aimed at restoring mitochondrial homeostasis in a pathological setting.
