Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice

Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction.

Alpha-synuclein in mitochondrial dysfunction:opportunities or obstacles

Recent work suggests a link betweenα-synuclein(α-syn)and mitochondrial dysfunction;however,the mechanisms of howα-syn influences mitochondrial function are still unclear.Most notably,whetherα-syn plays a direct role during mitochondrial function and/or whether diseasedα-syn-mediated mitochondrial dysfunction is a potential modifiable risk factor in Parkinson’s disease(PD)is unknown.To date,mutations in more than eight genes cause familial PD(fPD)and have functions in diverse pathways including synaptic homeostasis,mitochondria maintenance,autophagy/lysosome,and ubiquitin-proteasome pathways.

Fibrinogen’s potential role in connecting cerebrovascular abnormalities with glymphatic dysfunction in Alzheimer’s disease

Alzheimer’s disease(AD)stands out as the primary manifestation of age-related dementia,portraying a chronic neurodegenerative disorder distinguished by the accumulation of fibrillar amyloid-β(Aβ)plaques and neurofibrillary tangles of hyperphosphorylated tau.However,from a clinical standpoint,AD presents itself as a complex condition with a spectrum of dysfunctions rather than a singular pathological mechanism.An often-overlooked aspect of the disease is the presence of extensive cerebrovascular abnormalities,given that the majority of AD patients experience altered cerebral blood flow,damaged vasculature,increased microinfarcts and microhemorrhages.Animal models of AD further support this observation,showing cerebrovascular dysfunction such as impaired cerebral blood flow and altered cerebrovascular reactivity(Tataryn et al.,2021;Gareau et al.,2023).

Interleukin 1βreceptor and synaptic dysfunction in recurrent brain infection with Herpes simplex virus type-1

Several experimental evidence suggests a link between brain Herpes simplex virus type-1 infection and the occurrence of Alzheimer’s disease.However,the molecular mechanisms underlying this association are not completely understood.Among the molecular mediators of synaptic and cognitive dysfunction occurring after Herpes simplex virus type-1 infection and reactivation in the brain neuroinflammatory cytokines seem to occupy a central role.Here,we specifically reviewed literature reports dealing with the impact of neuroinflammation on synaptic dysfunction observed after recurrent Herpes simplex virus type-1 reactivation in the brain,highlighting the role of interleukins and,in particular,interleukin 1βas a possible target against Herpes simplex virus type-1-induced neuronal dysfunctions.

The emerging role of nitric oxide in the synaptic dysfunction of vascular dementia

With an increase in global aging,the number of people affected by cerebrovascular diseases is also increasing,and the incidence of vascular dementia-closely related to cerebrovascular risk-is increasing at an epidemic rate.However,few therapeutic options exist that can markedly improve the cognitive impairment and prognosis of vascular dementia patients.Similarly in Alzheimer’s disease and other neurological disorders,synaptic dysfunction is recognized as the main reason for cognitive decline.Nitric oxide is one of the ubiquitous gaseous cellular messengers involved in multiple physiological and pathological processes of the central nervous system.Recently,nitric oxide has been implicated in regulating synaptic plasticity and plays an important role in the pathogenesis of vascular dementia.This review introduces in detail the emerging role of nitric oxide in physiological and pathological states of vascular dementia and summarizes the diverse effects of nitric oxide on different aspects of synaptic dysfunction,neuroinflammation,oxidative stress,and blood-brain barrier dysfunction that underlie the progress of vascular dementia.Additionally,we propose that targeting the nitric oxide-sGC-cGMP pathway using certain specific approaches may provide a novel therapeutic strategy for vascular dementia.

Endothelial dysfunction in the kidney transplant population:Current evidence and management strategies

The endothelium modulates vascular homeostasis owing to a variety of vasoconstrictors and vasodilators.Endothelial dysfunction(ED),characterized by impaired vasodilation,inflammation,and thrombosis,triggers future cardiovascular(CV)diseases.Chronic kidney disease,a state of chronic inflammation caused by oxidative stress,metabolic abnormalities,infection,and uremic toxins damages the endothelium.ED is also associated with a decline in estimated glomerular filtration rate.After kidney transplantation,endothelial functions undergo immediate but partial restoration,promising graft longevity and enhanced CV health.However,the anticipated CV outcomes do not happen due to various transplant-related and unrelated risk factors for ED,culminating in poor CV health and graft survival.ED in kidney transplant recipients is an underrecognized and poorly studied entity.CV diseases are the leading cause of death among kidney transplant candidates with functioning grafts.ED contributes to the pathogenesis of many of the CV diseases.Various biomarkers and vasoreactivity tests are available to study endothelial functions.With an increasing number of transplants happening every year,and improved graft rejection rates due to the availability of effective immunosuppressants,the focus has now shifted to endothelial protection for the prevention,early recognition,and treatment of CV diseases.

老年CPB下心脏手术患者的rSO_(2)监测及其与术后早期POCD的相关性

目的监测老年心肺转流术(CPB)下心脏手术患者的局部脑氧饱和度(rSO_(2))的变化,并分析其与术后认知功能障碍(POCD)发生的相关性。方法回顾性分析2022年9月至2023年12月于河南省胸科医院接受CPB下心脏手术的100例老年患者的临床资料,根据患者术后7 d内是否发生POCD分为POCD组39例和非POCD组61例。比较两组患者吸氧前rSO_(2)、CPB前期rSO_(2)平均值(rSO_(2mean))、CPB中期rSO_(2mean)、CPB后期rSO_(2mean)、术中最低rSO_(2),并采用Pearson法分析rSO_(2)与术后早期POCD发生的相关性。结果两组患者吸氧前的rSO_(2)、CPB前期rSO_(2mean)比较差异均无统计学意义(P>0.05);POCD组患者CPB中期rSO_(2mean)、CPB后期rSO_(2mean)、术中最低rSO_(2)分别为(64.00±5.37)%、(67.19±5.25)%、(60.07±5.99)%,明显低于非POCD组的(70.44±6.75)%、(72.38±5.70)%、(69.48±6.17)%,差异均有统计学意义(P<0.05);Pearson相关性分析结果显示,CPB中期rSO_(2mean)、CPB后期rSO_(2mean)、术中最低rSO_(2)与术后早期POCD均呈负相关(r=-0.453、-0.420、-0.605,P<0.05)。结论老年CPB下心脏手术患者术中rSO_(2)可出现降低,且CPB中期rSO_(2mean)、CPB后期rSO_(2mean)、术中最低rSO_(2)与术后早期POCD的发生均具有相关性,应受到临床关注。

Evaluation of Efficacy and Safety of Electro-acupuncture Precondition on Postoperative Cognitive Dysfunction (POCD) Following Knee Replacement in Elderly: A Randomized Controlled Trial

OBJECTIVE: To investigate that whether electro-acupuncture(EA) precondition can reduce the incidence of postoperative cognitive dysfunction(POCD) following knee replacement and its safety in elderly. METHODS: A total of 60 participants met the inclusion criteria were enrolled in a randomized controlled trial with the ratio of 1:1, with 30 cases in the treatment group and 30 cases in the control group. The participants in the treatment group were provided with realEA therapy whereas participants in control group were provided with placebo-EA therapy. Interventions were offered 5 days prior to the surgery, once daily, and for a total of 5 days. The scores of Mini-Mental State Examination(MMSE), and contents of serumal inflammatory cytokines including interleukin 1β(IL-1β) and tumor necrosis factor-α(TNF-α) were observed at 24 hours prior-and posterior-to the surgery respectively for assessing the incidence of POCD among patients. Meanwhile, adverse effects were monitored and recorded. RESULTS:(1) After surgery, both treatment group and control group showed a significant decrease in MMSE global scores(P < 0.001, < 0.001, respectively), and the score in control group decreased more significantly than that in treatment group(P < 0.05);(2) Contents of serumal IL-1β and TNF-α were significantly increased in both groups after 24 hours posterior to the surgery(P < 0.001), and the contents in control group increased more significantly than that in treatment group(P < 0.001);(3) After surgery, the incidence of POCD was 20% in treatment group versus 36.67% in control group. There was no statistical difference between 2 groups(P > 0.05);(4) No serious adverse events were reported in this trial, except 1 patient from treatment group had a slight hematoma after receiving acupuncture. CONCLUSION: EA precondition might reduce cognitive impairments after 24 hours posterior to knee replacement surgery in elderly through inhibiting expression of inflammatory cytokines, including both IL-1β and TNF-α. However, there is insufficient evidence to support that EA precondition could reduce incidence of POCD.

Olfactory dysfunction and its related molecular mechanisms in Parkinson’s disease

Changes in olfactory function are considered to be early biomarkers of Parkinson’s disease.Olfactory dysfunction is one of the earliest non-motor features of Parkinson’s disease,appearing in about 90%of patients with early-stage Parkinson’s disease,and can often predate the diagnosis by years.Therefore,olfactory dysfunction should be considered a reliable marker of the disease.However,the mechanisms responsible for olfactory dysfunction are currently unknown.In this article,we clearly explain the pathology and medical definition of olfactory function as a biomarker for early-stage Parkinson’s disease.On the basis of the findings of clinical olfactory function tests and animal model experiments as well as neurotransmitter expression levels,we further characterize the relationship between olfactory dysfunction and neurodegenerative diseases as well as the molecular mechanisms underlying olfactory dysfunction in the pathology of early-stage Parkinson’s disease.The findings highlighted in this review suggest that olfactory dysfunction is an important biomarker for preclinical-stage Parkinson’s disease.Therefore,therapeutic drugs targeting non-motor symptoms such as olfactory dysfunction in the early stage of Parkinson’s disease may prevent or delay dopaminergic neurodegeneration and reduce motor symptoms,highlighting the potential of identifying effective targets for treating Parkinson’s disease by inhibiting the deterioration of olfactory dysfunction.

Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage

The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow.Mitochondria are directly affected by direct factors such as ischemia,hypoxia,excitotoxicity,and toxicity of free hemoglobin and its degradation products,which trigger mitochondrial dysfunction.Dysfunctional mitochondria release large amounts of reactive oxygen species,inflammatory mediators,and apoptotic proteins that activate apoptotic pathways,further damaging cells.In response to this array of damage,cells have adopted multiple mitochondrial quality control mechanisms through evolution,including mitochondrial protein quality control,mitochondrial dynamics,mitophagy,mitochondrial biogenesis,and intercellular mitochondrial transfer,to maintain mitochondrial homeostasis under pathological conditions.Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage.This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage,particularly mitochondrial quality control mechanisms.It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage.

Elaidic acid leads to mitochondrial dysfunction via mitochondria-associated membranes triggers disruption of mitochondrial calcium fluxes

Elaidic acid(EA)stimulation can lead to endoplasmic reticulum stress(ERS),accompanied by a large release of Ca^(2+),and ultimately the activation of NLRP3 inflammasome in Kupffer cells(KCs).Mitochondrial instability or dysfunction may be the key stimulating factors to activate NLRP3 inflammasome,and sustained Ca^(2+)transfer can result in mitochondrial dysfunction.We focused on KCs to explore the damage to mitochondria by EA.After EA stimulation,cells produced an oxidative stress(OS)response with a significant increase in ROS release.Immunoprecipitation experiments and the addition of inhibitors revealed that the increase in the level of intracellular Ca^(2+)led to Ca^(2+)accumulation in the mitochondrial matrix via mitochondria-associated membranes(MAMs).This was accompanied by a significant release of m ROS,loss of MMP and ATP,and a significant increase in mitochondrial permeability transition pore opening,ultimately leading to mitochondrial instability.These findings confirmed the mechanism that EA induced mitochondrial Ca^(2+)imbalance in KCs via MAM,ultimately leading to mitochondrial dysfunction.Meanwhile,EA induced OS and the decrease of MMP and ATP in rat liver,and significant lesions were found in liver mitochondria.Swelling of the inner mitochondrial cristae and mitochondrial vacuolization occurred,with a marked increase in lipid droplets.

Dysfunctional attitudes,social support,negative life events,and depressive symptoms in Chinese adolescents:A moderated mediation model

BACKGROUND Depression is a prevalent psychological issue in adolescents that is significantly related to negative life events(NLEs)and dysfunctional attitudes.High levels of social support can significantly buffer NLEs’effect on depression.Currently,there is limited research on how social support moderates the relationship between NLEs,dysfunctional attitudes,and depression in adolescents in China.It is imperative to investigate this moderating effect to mitigate dysfunctional attitudes in adolescent undergoing depressive mood,ultimately enhancing their overall mental health.AIM To investigate the relationship and underlying mechanisms between specific dysfunctional attitudes,social support,and depression among Chinese adolescents.METHODS This is a cross-sectional study which selected five middle schools in Shandong Province for investigation in March 2022.Participants included 795 adolescents(49.87%male,mage=15.15,SD=1.84,age range=11-18 years old).All participants completed the Dysfunctional Attitude Scale,Adolescent Life Event Scale,Beck Depression Inventory,and Social Support Rating Scale.A moderated mediation model was conducted to examine the relationship between specific dysfunctional attitudes,social support,and depression.RESULTS Results indicated that NLEs affected depression through the mediating role of specific dysfunctional attitudes(autonomy attitudesβ=0.21;perfectionismβ=0.25).Moreover,social support was found to moderate the mediating effect between NLEs,specific dysfunctional attitudes,and depressive symptoms(autonomy attitudes b2=-0.08;perfectionism b2=-0.09).CONCLUSION Dysfunctional attitudes mediated and social support moderated the relationship between NLEs and depression.Social support can buffer depression symptoms among adolescents with autonomy attitudes and perfectionism.

Frequency and associated factors of accommodation and non-strabismic binocular vision dysfunction among medical university students

AIM:To investigate the frequency and associated factors of accommodation and non-strabismic binocular vision dysfunction among medical university students.METHODS:Totally 158 student volunteers underwent routine vision examination in the optometry clinic of Guangxi Medical University.Their data were used to identify the different types of accommodation and nonstrabismic binocular vision dysfunction and to determine their frequency.Correlation analysis and logistic regression were used to examine the factors associated with these abnormalities.RESULTS:The results showed that 36.71%of the subjects had accommodation and non-strabismic binocular vision issues,with 8.86%being attributed to accommodation dysfunction and 27.85%to binocular abnormalities.Convergence insufficiency(CI)was the most common abnormality,accounting for 13.29%.Those with these abnormalities experienced higher levels of eyestrain(χ2=69.518,P<0.001).The linear correlations were observed between the difference of binocular spherical equivalent(SE)and the index of horizontal esotropia at a distance(r=0.231,P=0.004)and the asthenopia survey scale(ASS)score(r=0.346,P<0.001).Furthermore,the right eye's SE was inversely correlated with the convergence of positive and negative fusion images at close range(r=-0.321,P<0.001),the convergence of negative fusion images at close range(r=-0.294,P<0.001),the vergence facility(VF;r=-0.234,P=0.003),and the set of negative fusion images at far range(r=-0.237,P=0.003).Logistic regression analysis indicated that gender,age,and the difference in right and binocular SE did not influence the emergence of these abnormalities.CONCLUSION:Binocular vision abnormalities are more prevalent than accommodation dysfunction,with CI being the most frequent type.Greater binocular refractive disparity leads to more severe eyestrain symptoms.

Metabolic dysfunction-associated steatotic liver disease:A silent pandemic

The worldwide epidemiology of non-alcoholic fatty liver disease(NAFLD)is showing an upward trend,parallel to the rising trend of metabolic syndrome,owing to lifestyle changes.The pathogenesis of NAFLD has not been fully understood yet.Therefore,NAFLD has emerged as a public health concern in the field of hepatology and metabolisms worldwide.Recent changes in the nomenclature from NAFLD to metabolic dysfunction-associated steatotic liver disease have brought a positive outlook changes in the understanding of the disease process and doctor-patient communication.Lifestyle changes are the main treatment modality.Recently,clinical trial using drugs that target‘insulin resistance’which is the driving force behind NAFLD,have shown promising results.Further translational research is needed to better understand the underlying pathophysiological mechanism of NAFLD which may open newer avenues of therapeutic targets.The role of gut dysbiosis in etiopathogenesis and use of fecal microbiota modification in the treatment should be studied extensively.Prevention of this silent epidemic by spreading awareness and early intervention should be our priority.

MALAT1调控自噬参与异氟烷诱导老年大鼠POCD的机制研究

探究MALAT1调控自噬参与异氟烷诱导老年大鼠POCD的机制。 方法 40只SD大鼠分为4组,A组作为对照,B组作为模型,C组给予MALAT1 过表达干预:D组给予MALAT1 siRNA,比较各组血气分析、Morris水迷宫实验、BCL-2、LC3、ATG-5 mRNA和蛋白表达水平及清淀粉样前体蛋白(APP)、β-淀粉样蛋白(Aβ)、IL-1、IL-6和TNF-α水平。结果 四组大鼠血糖、pH、PaO2、PaCO2、SaO2 比较,差异均无统计学意义(P>0.05),与A组相比,B组大鼠大鼠逃避潜伏期时间延长,目标象限停留时间占比降低,穿越平台次数减少,与B组相比,C组逃避潜伏期时间缩短,目标象限停留时间占比增加,穿越平台次数增加,D组大鼠逃避潜伏期时间增加,目标象限停留时间占比减少,穿越平台次数减少,差异具有统计学意义(P<0.05)。与A组相比,B组大鼠海马组织BCL-2、LC3、ATG-5 mRNA和蛋白表达水平、血清APP、Aβ、IL-1、IL-6和TNF-α水平增加,差异具有统计学意义(P<0.05)。与B组相比,C组海马组织BCL-2、LC3、ATG-5 mRNA和蛋白表达水平及血清APP、Aβ、IL-1、IL-6和TNF-α水平均明显增加,D组海马组织BCL-2、LC3、ATG-5 mRNA和蛋白、血清APP、Aβ、IL-1、IL-6和TNF-α水平均明显减少,差异具有统计学意(P<0.05)。结论 降低MALAT1表达可通过减轻自噬缓解异氟烷诱导老年大鼠POCD。

Lower synaptic density and its association with cognitive dysfunction in patients with obsessive-compulsive disorder

Background Understanding synaptic alteration in obsessive-compulsive disorder(OCD)is crucial for elucidating its pathological mechanisms,but in vivo research on this topic remains limited.Aims This study aimed to identify the synaptic density indicators in OCD and explore the relationship between cognitive dysfunction and synaptic density changes in OCD.Methods This study enrolled 28 drug-naive adults with OCD aged 18-40 years and 16 healthy controls(HCs).Three-dimensional T1-weighted structural magnetic resonance imaging and 18F-SynVesT-1 positron emission tomography were conducted.Cognitive function was assessed using the Wisconsin Cart Sorting Test(WCST)in patients with OCD and HCs.Correlative analysis was performed to examine the association between synaptic density reduction and cognitive dysfunction.Results Compared with HCs,patients with OCD showed reduced synaptic density in regions of the cortico-striatothalamo-cortical circuit such as the bilateral putamen,left caudate,left parahippocampal gyrus,left insula,left parahippocampal gyrus and left middle occipital lobe(voxel p<0.001,uncorrected,with cluster level above 50 contiguous voxels).The per cent conceptual-level responses of WCST were positively associated with the synaptic density reduction in the left middle occipital gyrus(R^(2)=0.1690,p=0.030),left parahippocampal gyrus(R^(2)=0.1464,p=0.045)and left putamen(R^(2)=0.1967,p=0.018)in patients with OCD.Conclusions Adults with OCD demonstrated lower 18Flabelled difluoro analogue of 18F-SynVesT-1 compared with HCs,indicating potentially lower synaptic density.This is the first study to explore the synaptic density in patients with OCD and provides insights into potential biological targets for cognitive dysfunctions in OCD.

Circadian rhythm dysfunction and psychopathology in the offspring of parents with bipolar disorder:a highrisk study in the Chinese population

Background Understanding the evolution of circadian rhythm dysfunction and psychopathology in the high-risk population has important implications for the prevention of bipolar disorder.Nevertheless,some of the previous studies on the emergence of psychopathologies and circadian dysfunction among high-risk populations were inconsistent and limited.Aims To examine the prevalence rates of sleep and circadian dysfunctions,mental disorders and their symptoms in the offspring of parents with(O-BD)and without bipolar disorder(O-control).Methods The study included 191 O-BD and 202 O-control subjects aged 6-21 years from the Greater Bay Area,China.The diagnoses and symptoms of sleep/circadian rhythm and mental disorders were assessed by the Diagnostic Interview for Sleep Patterns and Disorders,and the Schedule for Affective Disorders and Schizophrenia for School-Age Children-Present and Lifetime Version,respectively.Generalised estimating equations and shared frailty proportional hazards models of survival analysis were applied to compare the outcomes in the offspring.Results Adjusting for age,sex and region of recruitment,there was a significantly higher risk of delayed sleep phase symptoms(9.55%vs 2.58%,adjusted OR:4.04)in O-BD than in O-control.O-BD had a nearly fivefold higher risk of mood disorders(11.70%vs 3.47%,adjusted OR:4.68)and social anxiety(6.28%vs 1.49%,adjusted OR:4.70),a fourfold higher risk of depressive disorders(11.17%vs 3.47%,adjusted OR:3.99)and a threefold higher risk of mood symptoms(20.74%vs 10.40%,adjusted OR:2.59)than O-control.Subgroup analysis revealed that O-BD children(aged under 12 years)had a nearly 2-fold higher risk of any mental and behavioural symptoms than O-control,while there was a nearly 4-fold higher risk of delayed sleep phase symptoms,a 7.5-fold higher risk of social anxiety and a 3-fold higher risk of mood symptoms in O-BD adolescents(aged 12 years and over).Conclusions There was an increase in delayed sleep phase symptoms in O-BD adolescents compared with their control counterparts,confirming the central role of circadian rhythm dysfunction in bipolar disorder.The findings of the specific age-related and stage-related developmental patterns of psychopathologies and circadian dysfunction in children and adolescent offspring of parents with bipolar disorder paved the way to develop specific and early clinical intervention and prevention strategies.

Anesthesia,Anesthetics,and Postoperative Cognitive Dysfunction in Elderly Patients

Postoperative cognitive dysfunction(POCD)remains a major issue that worsens the prognosis of elderly surgery patients.This article reviews the current research on the effect of different anesthesia methods and commonly utilized anesthetics on the incidence of POCD in elderly patients,aiming to provide an understanding of the underlying mechanisms contributing to this condition and facilitate the development of more reasonable anesthesia protocols,ultimately reducing the incidence of POCD in elderly surgery patients.

Efficacy and safety of platelet-rich plasma intracavernous injection for patients with erectile dysfunction:A systematic review,meta-analysis,and meta-regression

ObjectiveIntracavernous injection might be offered to patients with erectile dysfunction (ED) who did not respond to the first-line oral treatment. Platelet-rich plasma (PRP) might offer improvement in erectile function since it contains numerous growth factors. This study aimed to evaluate the efficacy and safety of PRP intracavernous injection for patients with ED.MethodsWe conducted relevant literature searches on Cochrane Library, Medline, Scopus, and ClinicalTrials.gov databases using specific keywords. The results of continuous variables were pooled into the mean difference (MD) and dichotomous variables into the odds ratio along with 95% confidence interval (95% CI).ResultsA total of six studies were included. Our pooled analysis revealed that PRP intracavernous injection was associated with a significant increase in the erectile function domain of the International Index of Erectile Function at 1 month (MD 3.47 [95% CI 2.62–4.32], p<0.00001, I^(2)=7%), 3 months (MD 3.19 [95% CI 2.25–4.12], p<0.00001, I^(2)=0%), and 6 months (MD 3.21 [95% CI 2.30–4.13], p<0.00001, I^(2)=0%) after the intervention when compared with baseline values. PRP was also superior to a placebo in terms of improvement in erectile function domain of the International Index of Erectile Function score at 1 month (MD 2.83, p<0.00001), 3 months (MD 2.87, p<0.00001), and 6 months (MD 3.20, p<0.00001) post-intervention. The adverse events from PRP injection were only mild without any serious adverse events.ConclusionPRP intracavernous injection may offer benefits in improving erectile function in patients with ED with a relatively good safety profile.

Efficacy of tadalafil on improvement of men with erectile dysfunction caused by COVID-19:A randomized placebo-controlled trial

Objective: According to the high prevalence of COVID-19 and the subsequent risk of men's sexual health, we decided to investigate the efficacy of tadalafil on improvement of men with erectile dysfunction caused by COVID-19.Methods: In this study, 70 outpatients who were recovered from COVID-19 without acute respiratory distress syndrome with negative polymerase chain reaction test and a complaint of erectile dysfunction were divided into two groups: 35 patients who received tadalafil 5 mg daily and 35 who received placebo. For each patient, basic assessment of sexual function was performed using the 5-item version of the International Index of Erectile Function (IIEF-5) questionnaire. Then, treatment was started from 2 months after complete recovery of COVID-19 with negative polymerase chain reaction test for 3 months. At the end of the treatments, the patients were re-evaluated for sexual function using the complete version of IIEF questionnaire. Finally, the results before and after treatment in the intervention group were compared with those of the control group.Results: Treatment with both tadalafil and placebo improved the patients' sexual function criteria compared to the baseline. However, this improvement was significantly higher in the intervention group with tadalafil than the control group with placebo (p<0.05).Conclusion: Daily administration of tadalafil 5 mg seems to be effective and safe for improvement of erectile dysfunction caused by COVID-19.