TRANSFORM THE MECHANISM OF RENMINBI’S EXCHANGE RATE SYSTEM IN CONFORMITY WITH THE DEMAND OF MARKET ECONOMY——The academic report delivered at the Annual Meeting of NNCIFS on October 1993

Exchange rate functions under systems of centrallyplanned economy and market economy are quite different,and the mechanism to determine such exchange rate is alsodifferent. To adopt a socialist market economic system inChina, the exchange rate mechanism of Renminbi must bethoroughly transformed. To accomplish this goal, I believethere are three problems that must be solved: first,

2021年老挝M_(S)6.0地震序列研究

云南地震活动与周边强震存在“构造相连,动力同源”的特征,研究周边强震的序列演化特征及发震构造,对云南地区地震研究具有重要意义。2021年12月24日老挝M_(S)6.0地震发生在滇西南地区的NW向整董断裂附近,震源机制解显示,此次地震是一次走滑型破裂事件,破裂方向与区域构造特征一致。老挝M_(S)6.0地震序列属于前震-主震-余震型序列,主震前震中附近出现3~4级地震非常活跃的现象,前震序列参数计算显示b值波动相对幅度较大,h值出现“上翘”形态,而余震序列b值和h值变化均相对平稳,主震的同震库伦应力结果表明老挝地震可能对云南地区有应力加载作用。

遗传性蛋白S缺乏症致兄弟二人患肺栓塞报告

肺栓塞(pulmonary embolism, PE)是临床上常见的急危重症之一,具有致死性,由于症状及体征均不典型,常常导致漏诊、误诊。青少年肺栓塞性相对少见,更容易被临床医师忽视。但该类患者可能发病年龄早,应注重其求因的检查尤其遗传缺陷。本文通过报道兄弟患肺栓塞病例,最终确诊为遗传性蛋白S缺乏症,且为少见的复杂杂合变异病例,而提高临床医师对于青少年PE的诊治水平。

基于“微生物-肠-脑轴”探讨补肾通腑方对APP/PS1小鼠肠道菌群及LPS/TLR4/NF-κB通路的影响

目的探讨补肾通腑方调控肠道菌群,改善阿尔茨海默病(Alzheimer’s disease,AD)模型小鼠学习记忆能力的作用机制。方法以APP/PS1小鼠为研究对象,给予补肾通腑方治疗8周,采用Morris水迷宫法观察小鼠空间学习记忆能力变化;16S rDNA检测小鼠肠道菌群丰度、多样性变化;HE染色观察海马病理形态学变化;免疫荧光检测海马区小胶质细胞活化情况;Western blot检测TLR4、NF-κB、IL-6等炎症因子表达。结果与模型组相比,补肾通腑方可以缩短AD模型小鼠逃避潜伏期、游泳路径,增加跨越平台次数(P<0.05),提升肠道菌群多样性,调节肠道菌群丰度,促进海马神经元细胞损伤修复,降低iNOS/Iba1共表达,提高Arg1/Iba1共表达(P<0.01),促进小胶质细胞从M1型向M2型转化,下调TLR4、NF-κB、IL-6等促炎因子的表达。结论补肾通腑方改善AD模型小鼠学习记忆能力的作用机制可能与调节肠道菌群介导的LPS/TLR4/NF-κB通路,从而抑制促炎型小胶质细胞活化、减轻中枢神经系统炎症、改善海马区神经元细胞损伤有关。

2021年漾濞M_(S)6.4地震前重力段差指标量分析及场源特征反演

基于2016-2021年云南地区流动重力重复观测资料,利用流动重力段差变化可视化方法及重力场变化显著性程度指标量G和C值研究了2021年漾濞M_(S)6.4地震前的重力变化,并反演了其与地震孕育相关的场源分布特征,开展了对研究区重力变化及场源特征的定性和定量研究。结果表明:①段差表示法的大小和方向对地下物质的运移方向有一定的指示意义,震前重力指标量呈显著上升,震后又迅速回落,重力变化指标量G和C值可作为评价测网区域重力变化显著性程度的定量依据;②反演得到的重力变化场源位置主要集中在红河断裂带北段至滇西北一带,且表现出与维西-乔后断裂及红河断裂带走向较为一致的分布特征,这可能与地震前中上地壳的深部物质运移相关。

泸定M_(S)4.5地震不对称高陡谷坡地震动响应

基于2023年四川泸定M_(S)4.5地震实测地震动数据,开展不对称斜坡时频域数据分析。结果表明:1)位于右岸1^(#)监测点的PGA放大系数最大,水平向和竖直向分别为3.16~15.08、4.37;2)Arias强度右岸最大值为2.24 cm/s,左岸最大值为0.79 cm/s,说明右岸地震动响应能量更强;3)斜坡右岸监测点的卓越频率为2~9 Hz,左岸卓越频率为2~17 Hz,地震幅值所呈现出来的能量在水平向比竖直向更为集中。地震动响应在不对称高陡谷坡右岸凸出半岛状斜坡地形比直线形斜坡更为强烈,高位覆盖层的存在会增强地震动响应。

SphK1/S1P/S1PR2信号通路促进肌生成:运动改善骨骼肌健康的新视角

背景:近年来,运动改善骨骼肌的健康已成为学者们关注的一个重要研究内容,适宜的运动对骨骼肌具有积极的作用,其中在运动激活鞘氨醇激酶1(sphingosine kinase1,SphK1)/鞘氨醇-1-磷酸(sphingosine-1-phosphate,S1P)/鞘氨醇-1-磷酸受体2(sphingosine-1-phosphate receptor2,S1PR2)信号通路如何改善骨骼肌的健康,正受到科研人员的重视。目的:研究运动经SphK1/S1P/S1PR2信号通路如何改善骨骼肌的健康,探索治疗相关肌肉疾病的新方法,以改善人的骨骼肌健康。方法:检索Web of Science、PubMed、中国知网、万方和维普数据库从建库至今与文章主题相关的文献,以“signaling pathway,SphK1,S1P,S1PR2,skeletal muscle,satellite cell,myogenesis,exercise”为英文检索词,以“信号通路,SphK1,S1P,S1PR2,骨骼肌,卫星细胞,肌生成,运动”为中文检索词,最终纳入69篇文献进行分析。结果与结论:①SphK1/S1P/S1PR2信号通路是一个复杂的调控网络,通过SphK1催化产生的S1P,与S1PR2等受体的相互作用,触发下游信号转导过程,进而调控细胞、组织、器官和系统的多种生物学功能。②SphK1/S1P/S1PR2信号通路能调控卫星细胞增殖和成肌细胞分化,改善肌生成。③文章通过文献资料调研法分析了SphK1/S1P/S1PR2信号通路的生理基础以及运动对其影响的可能性。急性有氧运动可提高骨骼肌中SphK1的表达,人体和动物研究中已证实急性和长期运动均可提高骨骼肌中S1P水平,另外研究表明长期抗阻运动可提高S1PR2在骨骼肌中的表达,部分实验结果表明急性和长期运动对肌肉或者血液中S1P水平无显著影响,出现不同结果的原因可能是选择的研究对象、方式、强度及频率不同,而具体机制尚不明确。④研究认为,运动能够促进SphK1/S1P/S1PR2信号通路在骨骼肌中的表达,调控下游相关信号通路,并且针对这一信号通路的研究可能为骨骼肌疾病的治疗提供新的策略和方法,从而改善骨骼肌健康。⑤未来应深化对SphK1/S1P/S1PR2信号通路与骨骼肌健康关联的研究,进一步揭示其与卫星细胞、成肌细胞的调控关系及与上下游通路的相互作用,挖掘其临床应用价值,制定康复方案时考虑该通路变化,探索不同运动对该通路的影响机制,并将其作为潜在治疗靶点,结合人体肌肉模型提升研究深度和准确性。

Bo’s abdominal acupuncture treatment for adult-onset Still's disease:A case report

BACKGROUND Adult-onset Still's disease(AOSD)is a rare autoinflammatory disease charac-terized by nonspecific symptoms such as fever,rash,sore throat and arthralgia.This paper reports a clinical case of AOSD successfully treated with Bo’s abdo-minal acupuncture(BAA).CASE SUMMARY We report a 20-year-old man who suffered from cold exposure,presenting with high fever,rash,sore throat,arthralgia,and elevated erythrocyte sedimentation rate,leukocytosis with neutrophilic predominance,elevated ferritin,elevated C-reactive protein,and negative rheumatoid factors.He was diagnosed with AOSD based on the Yamaguchi criteria.After treatment with traditional Chinese medi-cine(TCM)decoction and prednisone acetate tablets,there was some alleviation of sore throat,joint and muscle pain,and fever,but he still had persistent low-grade fever,rash,sore throat and arthralgia.He went to the TCM acupuncture outpatient department to receive BAA.Abdominal acupoints Zhongwan(CV12),Xiawan(CV10),0.5 cm below Xiawan(CV10),Qihai(CV6),Guanyuan(CV4),bilateral Qixue(KI13),bilateral Huaroumen(ST24),bilateral Shangfengshidian(AB1)and bilateral Daheng(SP15)were selected.After 3 months treatment,all symptoms disappeared,and the laboratory examination returned to normal levels.He did not take glucocorticoids or nonsteroidal anti-inflammatory drugs afterwards,and no relapse was observed during the 3-year follow-up period.CONCLUSION BAA can be used as a complementary medical approach for treatment of AOSD.

Gut microbiota-astrocyte axis: new insights into age-related cognitive decline

With the rapidly aging human population,age-related cognitive decline and dementia are becoming increasingly prevalent worldwide.Aging is considered the main risk factor for cognitive decline and acts through alterations in the composition of the gut microbiota,microbial metabolites,and the functions of astrocytes.The microbiota–gut–brain axis has been the focus of multiple studies and is closely associated with cognitive function.This article provides a comprehensive review of the specific changes that occur in the composition of the gut microbiota and microbial metabolites in older individuals and discusses how the aging of astrocytes and reactive astrocytosis are closely related to age-related cognitive decline and neurodegenerative diseases.This article also summarizes the gut microbiota components that affect astrocyte function,mainly through the vagus nerve,immune responses,circadian rhythms,and microbial metabolites.Finally,this article summarizes the mechanism by which the gut microbiota–astrocyte axis plays a role in Alzheimer’s and Parkinson’s diseases.Our findings have revealed the critical role of the microbiota–astrocyte axis in age-related cognitive decline,aiding in a deeper understanding of potential gut microbiome-based adjuvant therapy strategies for this condition.

Role of metabolic dysfunction and inflammation along the liver-brain axis in animal models with obesity-induced neurodegeneration

The interaction between metabolic dysfunction and inflammation is central to the development of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.Obesity-related conditions like type 2 diabetes and non-alcoholic fatty liver disease exacerbate this relationship.Peripheral lipid accumulation,particularly in the liver,initiates a cascade of inflammatory processes that extend to the brain,influencing critical metabolic regulatory regions.Ceramide and palmitate,key lipid components,along with lipid transporters lipocalin-2 and apolipoprotein E,contribute to neuroinflammation by disrupting blood–brain barrier integrity and promoting gliosis.Peripheral insulin resistance further exacerbates brain insulin resistance and neuroinflammation.Preclinical interventions targeting peripheral lipid metabolism and insulin signaling pathways have shown promise in reducing neuroinflammation in animal models.However,translating these findings to clinical practice requires further investigation into human subjects.In conclusion,metabolic dysfunction,peripheral inflammation,and insulin resistance are integral to neuroinflammation and neurodegeneration.Understanding these complex mechanisms holds potential for identifying novel therapeutic targets and improving outcomes for neurodegenerative diseases.

Differential distribution of PINK1 and Parkin in the primate brain implies distinct roles

The vast majority of in vitro studies have demonstrated that PINK1 phosphorylates Parkin to work together in mitophagy to protect against neuronal degeneration.However,it remains largely unclear how PINK1 and Parkin are expressed in mammalian brains.This has been difficult to address because of the intrinsically low levels of PINK1 and undetectable levels of phosphorylated Parkin in small animals.Understanding this issue is critical for elucidating the in vivo roles of PINK1 and Parkin.Recently,we showed that the PINK1 kinase is selectively expressed as a truncated form(PINK1–55)in the primate brain.In the present study,we used multiple antibodies,including our recently developed monoclonal anti-PINK1,to validate the selective expression of PINK1 in the primate brain.We found that PINK1 was stably expressed in the monkey brain at postnatal and adulthood stages,which is consistent with the findings that depleting PINK1 can cause neuronal loss in developing and adult monkey brains.PINK1 was enriched in the membrane-bound fractionations,whereas Parkin was soluble with a distinguishable distribution.Immunofluorescent double staining experiments showed that PINK1 and Parkin did not colocalize under physiological conditions in cultured monkey astrocytes,though they did colocalize on mitochondria when the cells were exposed to mitochondrial stress.These findings suggest that PINK1 and Parkin may have distinct roles beyond their well-known function in mitophagy during mitochondrial damage.

Comparative proteomic analysis of plasma exosomes reveals the functional contribution of N-acetyl-alpha-glucosaminidase to Parkinson’s disease

Parkinson’s disease is the second most common progressive neurodegenerative disorder,and few reliable biomarkers are available to track disease progression.The proteins,DNA,mRNA,and lipids carried by exosomes reflect intracellular changes,and thus can serve as biomarkers for a variety of conditions.In this study,we investigated alterations in the protein content of plasma exosomes derived from patients with Parkinson’s disease and the potential therapeutic roles of these proteins in Parkinson’s disease.Using a tandem mass tag-based quantitative proteomics approach,we characterized the proteomes of plasma exosomes derived from individual patients,identified exosomal protein signatures specific to patients with Parkinson’s disease,and identified N-acetyl-alpha-glucosaminidase as a differentially expressed protein.N-acetyl-alpha-glucosaminidase expression levels in exosomes from the plasma of patients and healthy controls were validated by enzyme-linked immunosorbent assay and western blot.The results demonstrated that the exosomal N-acetyl-alpha-glucosaminidase concentration was not only lower in Parkinson’s disease,but also decreased with increasing Hoehn-Yahr stage,suggesting that N-acetyl-alpha-glucosaminidase could be used to rapidly evaluate Parkinson’s disease severity.Furthermore,western blot and immunohistochemistry analysis showed that N-acetyl-alpha-glucosaminidase levels were markedly reduced both in cells treated with 1-methyl-4-phenylpyridinium and cells overexpressingα-synuclein compared with control cells.Additionally,N-acetyl-alpha-glucosaminidase overexpression significantly increased cell viability and inhibitedα-synuclein expression in 1-methyl-4-phenylpyridinium-treated cells.Taken together,our findings demonstrate for the first time that exosomal N-acetyl-alpha-glucosaminidase may serve as a biomarker for Parkinson’s disease diagnosis,and that N-acetyl-alpha-glucosaminidase may reduceα-synuclein expression and 1-methyl-4-phenylpyridinium-induced neurotoxicity,thus providing a new therapeutic target for Parkinson’s disease.

Netrin-1 signaling pathway mechanisms in neurodegenerative diseases

Netrin-1 and its receptors play crucial roles in inducing axonal growth and neuronal migration during neuronal development.Their profound impacts then extend into adulthood to encompass the maintenance of neuronal survival and synaptic function.Increasing amounts of evidence highlight several key points:(1)Diminished Netrin-1 levels exacerbate pathological progression in animal models of Alzheimer’s disease and Parkinson’s disease,and potentially,similar alterations occur in humans.(2)Genetic mutations of Netrin-1 receptors increase an individuals’susceptibility to neurodegenerative disorders.(3)Therapeutic approaches targeting Netrin-1 and its receptors offer the benefits of enhancing memory and motor function.(4)Netrin-1 and its receptors show genetic and epigenetic alterations in a variety of cancers.These findings provide compelling evidence that Netrin-1 and its receptors are crucial targets in neurodegenerative diseases.Through a comprehensive review of Netrin-1 signaling pathways,our objective is to uncover potential therapeutic avenues for neurodegenerative disorders.

The autophagy-lysosome pathway:a potential target in the chemical and gene therapeutic strategies for Parkinson’s disease

Parkinson’s disease is a common neurodegenerative disease with movement disorders associated with the intracytoplasmic deposition of aggregate proteins such asα-synuclein in neurons.As one of the major intracellular degradation pathways,the autophagy-lysosome pathway plays an important role in eliminating these proteins.Accumulating evidence has shown that upregulation of the autophagy-lysosome pathway may contribute to the clearance ofα-synuclein aggregates and protect against degeneration of dopaminergic neurons in Parkinson’s disease.Moreover,multiple genes associated with the pathogenesis of Parkinson’s disease are intimately linked to alterations in the autophagy-lysosome pathway.Thus,this pathway appears to be a promising therapeutic target for treatment of Parkinson’s disease.In this review,we briefly introduce the machinery of autophagy.Then,we provide a description of the effects of Parkinson’s disease–related genes on the autophagy-lysosome pathway.Finally,we highlight the potential chemical and genetic therapeutic strategies targeting the autophagy–lysosome pathway and their applications in Parkinson’s disease.

Computed tomography enterography-based radiomics for assessing mucosal healing in patients with small bowel Crohn's disease

BACKGROUND Mucosal healing(MH)is the major therapeutic target for Crohn's disease(CD).As the most commonly involved intestinal segment,small bowel(SB)assessment is crucial for CD patients.Yet,it poses a significant challenge due to its limited accessibility through conventional endoscopic methods.AIM To establish a noninvasive radiomic model based on computed tomography enterography(CTE)for MH assessment in SBCD patients.METHODS Seventy-three patients diagnosed with SBCD were included and divided into a training cohort(n=55)and a test cohort(n=18).Radiomic features were obtained from CTE images to establish a radiomic model.Patient demographics were analysed to establish a clinical model.A radiomic-clinical nomogram was constructed by combining significant clinical and radiomic features.The diagnostic efficacy and clinical benefit were evaluated via receiver operating characteristic(ROC)curve analysis and decision curve analysis(DCA),respectively.RESULTS Of the 73 patients enrolled,25 patients achieved MH.The radiomic-clinical nomogram had an area under the ROC curve of 0.961(95%confidence interval:0.886-1.000)in the training cohort and 0.958(0.877-1.000)in the test cohort and provided superior clinical benefit to either the clinical or radiomic models alone,as demonstrated by DCA.CONCLUSION These results indicate that the CTE-based radiomic-clinical nomogram is a promising imaging biomarker for MH and serves as a potential noninvasive alternative to enteroscopy for MH assessment in SBCD patients.

Nanomaterials-mediated lysosomal regulation:a robust protein-clearance approach for the treatment of Alzheimer’s disease

Alzheimer’s disease is a debilitating,progressive neurodegenerative disorder characterized by the progressive accumulation of abnormal proteins,including amyloid plaques and intracellular tau tangles,primarily within the brain.Lysosomes,crucial intracellular organelles responsible for protein degradation,play a key role in maintaining cellular homeostasis.Some studies have suggested a link between the dysregulation of the lysosomal system and pathogenesis of neurodegenerative diseases,including Alzheimer’s disease.Restoring the normal physiological function of lysosomes hold the potential to reduce the pathological burden and improve the symptoms of Alzheimer’s disease.Currently,the efficacy of drugs in treating Alzheimer’s disease is limited,with major challenges in drug delivery efficiency and targeting.Recently,nanomaterials have gained widespread use in Alzheimer’s disease drug research owing to their favorable physical and chemical properties.This review aims to provide a comprehensive overview of recent advances in using nanomaterials(polymeric nanomaterials,nanoemulsions,and carbon-based nanomaterials)to enhance lysosomal function in treating Alzheimer’s disease.This review also explores new concepts and potential therapeutic strategies for Alzheimer’s disease through the integration of nanomaterials and modulation of lysosomal function.In conclusion,this review emphasizes the potential of nanomaterials in modulating lysosomal function to improve the pathological features of Alzheimer’s disease.The application of nanotechnology to the development of Alzheimer’s disease drugs brings new ideas and approaches for future treatment of this disease.

基于YOLOv5s的自动驾驶车辆行人检测方法

提出一种改进的YOLOv5s模型,旨在提高自动驾驶车辆行人检测的准确性。通过增加一个小目标检测层,将原有的三尺度检测层扩展为四尺度,提高小目标的检测能力;在颈部网络中将坐标注意力(CA)机制引入C3模块,构建C3-CA模块,以强化特征间的空间关系,从而更精确地定位行人;将原有的CIoU损失函数替换为EIoU,改善模型收敛性。在BDD100K数据集进行试验验证,结果显示:与YOLOv5s模型相比,改进后的模型检测精度提高了1.7%,召回率提高了4.8%,平均精度提高了2.2%,降低了漏检和误检概率。

Glycolytic dysregulation in Alzheimer's disease:unveiling new avenues for understanding pathogenesis and improving therapy

Alzheimer's disease poses a significant global health challenge owing to the progressive cognitive decline of patients and absence of curative treatments.The current therapeutic strategies,primarily based on cholinesterase inhibitors and N-methyl-Daspartate receptor antagonists,offer limited symptomatic relief without halting disease progression,highlighting an urgent need for novel research directions that address the key mechanisms underlying Alzheimer's disease.Recent studies have provided insights into the critical role of glycolysis,a fundamental energy metabolism pathway in the brain,in the pathogenesis of Alzheimer's disease.Alterations in glycolytic processes within neurons and glial cells,including microglia,astrocytes,and oligodendrocytes,have been identified as significant contributors to the pathological landscape of Alzheimer's disease.Glycolytic changes impact neuronal health and function,thus offering promising targets for therapeutic intervention.The purpose of this review is to consolidate current knowledge on the modifications in glycolysis associated with Alzheimer's disease and explore the mechanisms by which these abnormalities contribute to disease onset and progression.Comprehensive focus on the pathways through which glycolytic dysfunction influences Alzheimer's disease pathology should provide insights into potential therapeutic targets and strategies that pave the way for groundbreaking treatments,emphasizing the importance of understanding metabolic processes in the quest for clarification and management of Alzheimer's disease.

Exploring gut microbiota as a novel therapeutic target in Crohn’s disease: Insights and emerging strategies

Extensive research has investigated the etiology of Crohn’s disease(CD),encompassing genetic predisposition,lifestyle factors,and environmental triggers.Recently,the gut microbiome,recognized as the human body’s second-largest gene pool,has garnered significant attention for its crucial role in the patho-genesis of CD.This paper investigates the mechanisms underlying CD,focusing on the role of‘creeping fat’in disease progression and exploring emerging therapeutic strategies,including fecal microbiota transplantation,enteral nutri-tion,and therapeutic diets.Creeping fat has been identified as a unique patho-logical feature of CD and has recently been found to be associated with dysbiosis of the gut microbiome.We characterize this dysbiotic state by identi-fying key microbiome-bacteria,fungi,viruses,and archaea,and their contributions to CD pathogenesis.Additionally,this paper reviews contemporary therapies,empha-sizing the potential of biological therapies like fecal microbiota transplantation and dietary interventions.By elucidating the complex interactions between host-microbiome dynamics and CD pathology,this article aims to advance our under-standing of the disease and guide the development of more effective therapeutic strategies for managing CD.

Decoding molecular mechanisms:brain aging and Alzheimer's disease

The complex morphological,anatomical,physiological,and chemical mechanisms within the aging brain have been the hot topic of research for centuries.The aging process alters the brain structure that affects functions and cognitions,but the worsening of such processes contributes to the pathogenesis of neurodegenerative disorders,such as Alzheimer's disease.Beyond these observable,mild morphological shifts,significant functional modifications in neurotransmission and neuronal activity critically influence the aging brain.Understanding these changes is important for maintaining cognitive health,especially given the increasing prevalence of age-related conditions that affect cognition.This review aims to explore the age-induced changes in brain plasticity and molecular processes,differentiating normal aging from the pathogenesis of Alzheimer's disease,thereby providing insights into predicting the risk of dementia,particularly Alzheimer's disease.