SOM and the lateral interaction

4 结论以某型号的自升式平台坠物风险较大的作业甲板为对象，根据实际工况建立有限元模型，结果显示立管坠落后不仅会穿透甲板，还依旧以较大的动能继续向下坠落，对下部结构和设备造成很大威胁。

通过将纵骨由角钢替换为T型材和增加纵骨的数量都可以有效防止甲板被击穿，且增加纵骨数量的改良方案效果较为明显。

本研究可以为工程设计实践提供一定的指导。

参考文献：[1]郝灜. 物体坠落对平台甲板冲击破坏的判据研究[D].哈尔滨: 哈尔滨工程大学, 2009.[2]HSE UK. An Examination of the Number andFrequency of Serious Dropped Object and Swinging Load Involving Cranes and Lifting Devices on Offshore Installations for the Period 1981 to 1995[R]. 1996. [3]DNV. Accident Statistics for Mobile Offshore Units onthe UK Continental Shelf 1980—1998[S]. 1996.[4]张海, 刘蕊, 王秀存, 等. 坠落物体产生的冲击载荷对海底管线的损伤分析[J]. 海洋技术, 2008 (1):77-80.[5]ALSOS H S, AMADH J. On the Resistance toPenetration of Stiffened Plates, Part II, Experiments[J].International Journal of Impact Engineering, 2009, 36 (6): 799-807.[6]CHO S R, LEE H S. Experimental and AnalyticalInvestigations on the Response of Stiffened Plates Subjected to Lateral Collisions[J]. Marine Structures, 2009, 22 (1): 84-95.[7]ALSOS H S, AMADH J, HOPPERSTAD O S. On theResistance to Penetration of Stiffened Plates, Part II: Numerical Analysis[J]. International Journal of Impact Engineering, 2009, 36 (7): 875-887.[8]DNV. Design Against Accidental Loads, RecommendedPractice: DNV-RP-C204[S]. 2010.[9]BV. Rules for the Classification of Offshore Units[S].2013.[10]彭大炜, 张世联. 结构极限强度分析的三种有限元解法研究[J]. 中国海洋平台, 2010, 25(2): 1-5.《海洋工程结构设计和评估环境条件应用指南（2021）》发布《海洋工程结构设计和评估环境条件应用指南（2021）》于2021年2月22日发布，于2021年4月1日生效。

中华行为医学与脑科学杂志2021年4月第30卷第4期Chin J Behav M e d Brain Sci，April 2021，V〇1.30，N〇.4•289••临床研究•重度抑郁症患者嗜睡症状与快感缺失的相关性张佳佳1张玉'储召学1王婷1余家快1朱鹏2张京婧2朱道民11安徽医科大学附属心理医院，合肥市第四人民医院，安徽省精神卫生中心睡眠医学科，合肥230000;2安徽医科大学，合肥230032通信作者：朱道民，Email:hfsyzdm7778@ 163. com【摘要】目的探讨重度抑郁症患者嗜睡症状与快感缺失的相关性。

方法2018年11月至2019年5月，以符合ICD-10诊断标准的重度抑郁症住院患者为研究对象，根据Epworth嗜睡量表(Epworth sleepiness scale，ESS)，将ESS為7分定为白天嗜睡组，共纳入46例;将ESS<7分定为无嗜睡组，共纳人171例。

采用中文版修订社会快感缺失量表（revised social anhedonia scale,RSAS)、中文版修订躯体快感缺失量表（revised physical anhedonia scale,RPAS)评估患者的快感缺失症状，采用双因素方差分析、Pearscm相关分析进行数据处理。

结果（1)有无嗜睡和性别对躯体快感缺失得分的影响不存在交互作用（F=0. 274,P=0. 601),主效应分析提示性别对躯体快感缺失的影响差异有统计学意义（尸=10.948，户<0.05)。

（2)有无嗜睡和年龄对躯体快感缺失得分的影响存在交互作用（^"=4.396,P=0. 013)，进一步做简单效应分析，在白天嗜睡组中，40~49年龄段的患者躯体快感缺失得分[(21.M±12.37)分]低于5〇〜64岁年龄段[(34. 13±12.53)分](P<0.05)。

（3)有无嗜睡和坐躺时间对社会快感缺失得分的影响存在交互作用（F= 4. 247,P=0. 041 )，进一步做简单效应分析，在白天嗜睡组中，坐躺时间<2 h的患者社会快感缺失得分[(13.71±5. 18)分]低于坐躺时间3=2 h的患者[(19. 75±6. 39)分](/><0. 05)。

论著急性脑出血患者颅内血肿及其周边区局部脑血流量与躯体感觉神经诱发电位的研究孔令斌,杨志寅,安锐 作者单位:430030华中科技大学同济医学附属院协和医院核医学科,济宁医学院(孔令斌);济宁医学院,行为医学研究所(杨志寅);华中科技大学同济医学院附属协和医院校医学科(安锐) 【摘要】　目的　研究急性脑出血患者血肿区、周边区和对侧脑组织局部脑血流量以及躯体感觉神经诱发电位(si -m atosensory evoked pot ential ,SSEP )的变化。

方法　利用单光子发射计算机断层(si ngle photon e m issi on computed t omo -graphy ,SPECT )显像技术检查25例急性基底核区出血患者,根据中国卒中评分分型,轻型组16例,中型组9例,发病后1～5d 、13～19d 各做1次SPECT 检查。

采用感兴趣区模型分析法,分别于局部脑血流量(regional cerebral blood flo w ,r CBF )减低区的中心和其周围额顶叶、小脑中心及上述区域的对侧镜像区做放射性摄取计数,并计算病变侧与对侧放射性计数的摄取比(R ),同时测定两组患者的SSEP 各波潜伏时。

结果　两组患者行第1、2次SPECT 检查时,血肿区病变侧放射性计数均显著低于对侧(P <0.01)。

第1、2次检查时两组患者病变侧血肿区放射性计数均低于周边区(P <0.01)。

病变对侧小脑的放射性计数低于病变侧,差异有显著性意义(P <0.01)。

轻型组患者病变侧SSEP 各波在P40、N60潜伏时及中型组患者病变侧SSEP 各波在P25、N30、P40、N60潜伏时均较相应的对侧延长,差异有显著性意义(P <0.05);中型组患者病变侧SSEP 各波在P25、N30、P40、N60潜伏时较轻型组相应波的潜伏时长,差异有显著性意义(P <0.05)。

NEURAL REGENERATION RESEARCH ^REVIEWAmyotrophic lateral sclerosis: a complex syndrome that needs an integrated research approachJavier Riancho1,2 *, Francisco J. Gil-Bea2,3, Ana Santurtun4, Adolfo Lopez de Munain2,3,5,61Service of Neurology, Hospital Sierrallana-Idival, Torrelavega, Spain2 CIBERNED (Center for Networked Biomedical Research on Neurodegenerative Diseases, Ministry of Economy and Competitiveness, Institute Carlos III), Madrid, Spain3 Neurosciences Area, Institute Biodonostia, San Sebastian, Spain4 Department of Physiology and Pharmacology, University of Cantabria-Idival, Santander, Spain5 Department of Neurology, University Hospital Donostia, San Sebastian, Spain6 Department of Neurosciences, University of the Basque Country, Universidad Pais Vasco-Euskal Herria Unibertsitatea, San Sebastian, SpainAbstractAmyotrophic lateral sclerosis, the most common neurodegenerative disease affecting motor neu­rons, lacks an effective treatment. A small fraction of amyotrophic lateral sclerosis cases have a familial origin, related to m utations in causative genes, while the vast majority of amyotrophic lateral sclerosis cases are considered to be sporadic, resulting from the interaction between genes and environmental factors in predisposed individuals. During the past few years, dozens of drugs have been postulated as promising strategies for the disease after showing some beneficial effects in preclinical cellular and murine models. However, the translation into clinical practice has been largely unsuccessful and the compounds failed when were tested in clinical trials. This might be explained, at least partially, by the enormous complexity of the disease both from clinico-ep- idemiological and a pathogenic points of view. In this review, we will briefly comment on the complexity of the disease focusing on some recent findings, and we will suggest how amyotrophic lateral sclerosis research might be reoriented to foster the advance in the diagnostic and therapeu­tic questions.* C orrespondence to:Javier Riancho, MD, PhD, rianchozj@unican.es,javier.riancho86@.orcid:〇〇〇〇-〇〇〇1-7929-1055 (Javier Riancho)doi: 10.4103/1673-5374.244783 Received: July 17, 2018 Accepted: September 17, 2018Key Words: amyotrophic lateral sclerosis; ALS; environment; epidemiology; genes; phenotype; therapyAmyotrophic lateral sclerosis (ALS) is the most common neurodegenerative disease affecting motor neurons (Riancho et al. 2016c; Zufiria et al. 2016). With an annual incidence that ranges from 1to 2 cases per 100,000 habitants, it is characterised by progressive muscle wasting which usually leads to death during the first 3 years after diagnosis, com­monly related to respiratory failure (Riancho et al. 2016c; Zufiria et al. 2016). More than 90 percent of cases are thought to be sporadic ALS, in which the disease likely results from the interaction between individual genetic predisposition, environment and aging (Figure 1) (Riancho et al., 2016b). Currently, riluzole and more recently edaravone, both with a very modest effect on survival, are the only approved drugs for the disease. Therefore, there is a need to find new therapies for the disease. For preparing this article, we reviewed the literature and selected rele­vant studies published from 2000 to 2018, prioritiz­ing the most recent ones.During the past few years, dozens of drugs have been postulated as promising strategies for the dis­ease (Riancho et al., 2016a; Al Chalabi et al., 2017). However, despite the fascinating results in basic research with both neuronal cells and murine ALS models, there have existed important difficulties in the translation of these findings into patients with ALS, since all these new compounds failed when tested in clinical trials with ALS patients (Ittner et al., 2015). A potential explanation for this failure might depend on the enormous complexity of the disease.First, from a clinical point of view, ALS is a com­plex syndrome with a variable phenotype. Both clin­ical onset patterns and survival rates markedly differ between the different forms (classic spinal onset, bulbar, flailed-arm, pseudomyopathic) of the disease (Al Chalabi et al., 2016). This, as well as the absence of useful validated biomarkers, substantially difficult the correct stratification of patients in clinical tri­als, therefore masking potential positive outcomes in some groups of patients (Brown and Al Chalabi, 2017). In recent years, an extensive list of potential biomarkers has been studied (Benatar et al., 2016),193A BFigure 1Main involved components in the genesis of amyotrophic lateral sclerosis (ALS).Each individual has a determined prenatal genetic load and during life accumulates a number of environmental exposures and some degree of age-related cell damage. Regardless the particular “weight” of each one of these components, ALS would develop when the sum of them reach a certain threshold. (A) Healthy subject, (B) sporadic ALS.including biological fluid-based biomarkers, elec- trophysiological biomarkers and neuroimaging bio­markers. Within the first category, phosphorylated neurofilament heavy and neurofilament light seem to be the most promising ones. Based on published data, phosphorylated neurofilament heavy and neu­rofilament light levels in cerebrospinal fluid (and potentially in plasma) may have a role as prognostic biomarkers. Thus, they could be used in clinical tri­als to facilitate the stratification of study participants into treatment arms on the basis of anticipated rates of disease progression (Boylan et al., 2013). Re­garding electrophysiological biomarkers, the motor unit number index (MUNIX) is gaining relevance (Nandedkar et al., 2004). MUNIX is a relatively easy technique which would theoretically allow to capture disease progression very early in the disease course, at a time when common neurophysiological param­eters CMAP remained relatively stable. Unfortu­nately, this potential benefit is offset by the fact that repeatability of MUNIX is usually lowest early in the disease and improves only as the disease progress­es into advanced stages (Felice, 1997; Bromberg, 2007). Among neuroimaging biomarkers, structural imaging analysis such as voxel based morphometry consistently show atrophy in the precentral gyrus in ALS patients compared to healthy volunteers (Menke et al., 2014). MRI tractography has also been evalu­ated revealing changes at corticospinal tract as dis­ease progresses (Keil et al., 2012). However, further studies are needed to validate these results. Finally, fluorodeoxyglucose-positron emission tom ogra­phy studies have revealed hypometabolism in the precentral girus and frontal regions in ALS subjects (Van Laere et al., 2014) and it may be an indepen­dent predictor of shorter survival (Van Laere et al., 2014).It can be anticipated that a combination of val­idated humoral, electrophysiologic and imaging biomarkers will probably provide a dynamic under­standing of the disease and its progression as well as the eventual response to a particular therapy more firmly that any single biomarker (Benatar et al., 2016).Second, from an epidemiological point of view, there is a rapid-growing list of environmental fac­tors that have been associated to ALS (Riancho et al., 2018). In addition to the classical ones, such as exposure to heavy metals, toxicants as parafor­maldehyde or cyanotoxins, new categories of en­vironmental factors and lifestyle characteristic are being including in that list. In recent years, some microorganisms, particularly retroviruses and gut microbiota dysregulation, have been associated with the genesis of the disease (Castanedo-Vazquez et al., 2018). Furthermore, lifestyle and other demographic parameters such as physical activity, nutrition, body mass index, cardiovascular risk factors, autoimmune diseases and cancer are being associated to the dis­ease. Differently from most other neurodegenerative diseases, increased body mass index and metabolic syndrome have been related to an increased risk of ALS (Gallo et al., 2013). The association with au­toimmunity and cancer is also intriguing: patientsRiancho /, Gil-Bea F/, Santurtun A, Lopez de Munain A (2019) Amyotrophic lateral sclerosis: a complex syndrome that needs an integrated research approach. Neural Regen Res 14(2):193-196. doi: 10.4103/1673-5374.244783siv*£1—194Riancho J，Gil-Bea FJ，Santurtun L6pez de Munain A (2019) Amyotrophic lateral sclerosis: a complex syndrome that needs an integratedresearch approach. Neural Regen Res 14(2): 193-196. doi: 10.4103/1673-5374.244783with previous autoimmune diseases and oncological history have been reported to have increased anddecreased risk of ALS，respectively (Turner et al.，2013; Gibson et al., 2016). New research about theassociations between ALS and comorbid conditions will doubtlessly provide new perspectives of the dis­ease and will help us to better understand it (Riancho et al., 2018).Third, from a molecular perspective, ALS should also be considered as a very complex condition. Fa­milial forms of the disease, which represent about 10 percent cases, appear as ''pure^ forms, directly de­rived from mutations not only in the genes encoding neuron-damaging proteins, but also in genes that are involved in a variety of cellular functions, including RNA processing, autophagy, vesicular transport and energy metabolism (Zufiria et al., 2016). The mech­anisms leading to disease in sporadic cases may be much more complex and at least as heterogeneous as those in familial forms. In any case, once the pathogenic process has been initiated, a plethora of metabolic and other cellular alterations precipitate a vicious cycle in ALS and other neurodegenerative diseases favouring disease progression (Zufiria et al., 2016). In other words, abnormalities in neuronal functions are often related to the combination of alterations at several levels, including alterations of gene processing (impaired DNA/RNA regulation, epigenetic aberrations), increased oxidative stress, mitochondrial dysfunction, proteostasic abnormal­ities, energetic imbalance, axonal transport deficits and glial cell dysfunction (Riancho et al., 2016b). Based on this perception of the disease, several disease models, including cellular models and more complex animal models have been created by us­ing molecular biology tools. Unfortunately, after accumulating a huge amount of data, experimental outcomes have not been translated into effective preventive or therapeutic strategies. This lack of suc­cess might respond to several reasons. Perhaps, we should consider that extrapolations and inferences may have been made in a too simplistic manner, as animal models of the disease commonly reproduce just a particular feature, rather than the whole pro­cess. In addition, we may have not paid enough at­tention to other factors of the internal and external environmental that influence the disease course.If we do agree with the idea that in ALS thereare several pathways involved, with multiple inter­actions building a complex pathogenic network, we should consider a modern perspective about causation (Rothman and Greenland, 2005). In this model, a causative factor could be unique (such as mutation in a causative gene) but more frequently could also be composed of several causal compo­nents that could be grouped in different manners constituting different sufficient causes (which may or may not share some of the component causes). When a component cause is present in all the suffi­cient causes it must be considered a necessary cause (Rothman and Greenland, 2005). It seems clear that according to this model, research focused on just one or two component causes will continue yielding very partial results with serious difficulties in refor­mulating a theory that generates valid predictive models.These focused approaches derive, at least partially, from the structure of research funding programs. According to this new concept, research funding strategies should firmly support integrated p ro­grams of investigation considering ALS as a global neurodegenerative process rather than the result of a variety of isolated pathogenic events. These integrat­ed projects should doubtlessly involve multi-disci­plinary groups that focus together on the same prob- lem by using different models and analytical tools, but always subordinated to a common hypothesis (Figure 2).In conclusion, we think that a multidisciplinary holistic approach to ALS-related questions is needed to better understand the pathogenesis of the disease and advance into more effective therapies. An open, honest and cooperative relationship between aca­demia and industry, as well as between industry and health regulatory authorities will foster translational research programs leasing to effective therapies.Author contributions: M anuscript conception and writting: JR; m an­uscript writting: FJGB; m anuscript revision: AS; fin a l revision: ALM.C onflicts o f interest: A ll authors declare that they have no conflicts o f interest.Financial support: None.C opyright licen se agreem ent: The Copyright License A greem ent has been signed by all authors before publication.Plagiarism check: Checked twice by iThenticate.Peer review: Externally peer reviewed.O pen access statem ent: This is an open access journal, and articles are distributed under the term s o f the Creative C om m ons A ttrib u-tion-N onC om m ercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-com m erdallyy as long as appropriate credit is given and the new creations are licensed under the identical terms.195Riancho /, Gil-Bea FJ, Santurtun A, Lopez de Munain A (2019) Amyotrophic lateral sclerosis: a complex syndrome that needs an integrated research approach. Neural Regen Res 14(2):193-196. doi: 10.4103/1673-5374.244783New hypothesisClinicalEpidemiologyCell biologyMetabolcTranscriptomicsNew resultsCellular models (IPSCs, fibroblasts..ValidationPatients (clinical trials...)，Animal models {mice, zebra fish, flies) Figure 2 An integrated vision of amyotrophic lateral sclerosis research.Integrated projects must include multi-disciplinary groups that focus together on the same problem by using different models and analytical tools, being always subordinated to a common hypothesis. IPSCs: In­duced pluripotent stem cells.ReferencesAl-Chalabi A, Hardiman O, Kiernan MC, Chio A, Rix-Brooks B, van den Berg LH (2016) Amyotrophic lateral sclerosis: moving towards a new classification system. Lancet Neurol 15:1182- 1194.Al-Chalabi A, van den Berg LH, Veldink J (2017) Gene discovery in amyotrophic lateral sclerosis: implications for clinical man­agement. 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神经系统（nervous system）是机体内对生理功能活动的调节起主导作用的系统，主要由神经组织组成，分为中枢神经系统（central nervous system）和周围神经系统（peripheral nervous system）两大部分。

中枢神经系统又包括脑（brain）和脊髓（spinal cord），周围神经系统包括颅神经（cranial nerves，也称“脑神经”）和脊神经（spinal nerves）。

神经组织是由神经细胞和神经胶质细胞（glial cell）组成的，它们都是有突起的细胞。

神经细胞是神经系统的结构和功能单位，亦称神经元（neuron）。

神经元数量庞大，它们具有接受刺激、传导冲动和整合信息的能力。

有些神经元还有内分泌功能。

01 常见词根词缀合集neur神经，神经系统（neurotoxic神经毒性的）encephal脑（encephaledema脑水肿）cerebr大脑（decerebrate切除大脑，消除大脑功能）cerebell小脑（cerebellospinal小脑脊髓的）mening脑膜（meningorrhagia脑膜出血）ventricul脑室thalam丘脑ax轴突（axonal轴突的）dendr树突（dendriceptor树突受体的；dendriform树状的）gangli/gonglion神经节neuron神经元gli神经胶质（gliophagia神经胶质细胞吞噬作用）cortic皮质medull髓（medullary髓质的，延髓的；medulloculture骨髓培养）myel脊髓（poliomyelosis脊髓灰质炎；myelosis骨髓瘤形成; 骨髓组织增生）psych精神的（psychosomatic身心的，心身失调的；psychotropic作用于精神的）somn睡眠（somnolence嗜睡）-algia痛（arthralgia关节痛）-esthesia感觉，知觉（anesthesia麻醉，麻木）-lepsy突然发作（epilepsy癫痫）-lexia阅读-paresis偏瘫（左/右边的一半）（hemiparesis轻偏瘫）-phasia言语-plegia瘫痪（quadriplegia四肢麻痹，四肢瘫痪；facioplegia面瘫；paraplgia截瘫，半身不遂）-phobia恐惧hemi-一半（hemianesthesia偏侧感觉缺失）intra-内02 单词词组学习*神经系统&大脑neuron神经元ganglion神经节glial神经胶质的axon轴突dendrite树突sympathetic交感神经parasympathetic副交感神经innervate 使受神经支配的medulla oblongata延髓cerebrum大脑hemisphere大脑半球cerebellum小脑thalamus丘脑hypothalamus 下丘脑；丘脑下部pons脑桥meninges脑膜cavity/ventricle脑室词根cerebell/o: cerebellum 小脑cerebellar 小脑的cerebellitis 小脑炎cerebellopontine 小脑脑桥cerebr/o: cerebrum 大脑cerebral 大脑的cerebrospinal fluid 脑脊液cerebral artery 大脑动脉cerebral cortex 大脑皮层encephala/: brain 脑encephalitis 脑炎encephalopathy 脑病（hepatic encephalopathy肝性脑病）electroencephalogram 脑电图Mening/o：脑膜Meningitis 脑膜炎Meningeal 脑膜的Meningioma 脑膜瘤Kinesia: movement 运动Bradykinesia 运动徐缓（见于Parkison disease）Dyskinesia 运动障碍Esthesia: 感觉Hyperesthesia 感觉过敏Anaesthesia 麻醉（没有感觉）Paresis: 无力Hemiparesis 轻偏瘫Plegia: 瘫痪Hemiplegia 偏瘫Paraplegia 截瘫Quadriplegia 四肢瘫这几个看下图就明白了（但要学会掌握这些词根：hemi -, para -, quadra-）神经系统有个很有意思的词是arachoid，有个经典的疾病是subarachoid hemorrhage(蛛网膜下腔出血).Arachoid 这个词来源于希腊神话。

第 2 卷 第 2 期2000 年 6 月沈 阳 医 学 院 学 报JOU RN A L O F SH EN YA N G M ED I CA L COL L E GEV o l . 2 N o. 2J u n . 2000扣 带 回 与 痛 觉吴敏范3 综述 滕国玺 审校( 中国医科大学脑研究所神经生理学研究室, 沈阳 110001)扣带回是边缘系统的重要组成部分,其前部和后部是边缘系统功能及形态结构 不同的两个区域。

扣带回的功能比较复杂, 在痛觉研究中已成为关注的焦点。

本文对 扣带回在痛觉感受中的作用进行综述, 为 进一步研究提供资料。

外, 还有一个感觉成分: 痛觉是一种不愉快 的感觉和情绪体验, 伴有实际或潜在的组 织损伤6 。

2 皮层参与痛觉感受的争议多年来在脑皮层是否完全参与痛觉感受的问题上一直存有争议。

人们已为大脑皮层损伤后痛觉发生变化提供了证据, 但是痛觉缺失不是该损伤的唯一重要的症状7。

在猴体内进行的单细胞记录确定了躯体感觉系统的伤害性通路投射到躯体感觉皮层I 区、¦ 区和邻近的顶叶皮层后部区域8。

自从首次应用阳电子发射断面 X 线照相术 (P E T ) 研究急性热痛刺激在人脑的功能激活以来3, 9 , 痛觉的大脑皮层代表区已成为痛觉研究中最活跃的领域之一。

这两个研究在扣带回前部皮层被激活方面取得一致的看法。

目前争论的焦点已转移到大脑皮层区域在痛觉感受中有什么特异功能的问题。

痛觉的大脑皮层代表区具有多维性, 如痛觉的感觉辨别部分、情绪形成部分和认知评价部分10。

痛觉的感觉辨别部分为躯体感觉皮层I 区和¦ 区, 属于外侧伤害系统; 痛觉的情绪形成部分为扣带回前部皮层, 属于内侧伤害系统。

1 概述长期以来许多学者认为扣带回在痛觉 感受中有重要作用, 是接受和调制痛觉信 号的重要中枢1 ～ 4 。

有报道扣带回内存在 躯体伤害性感受神经元1 , 刺激扣带回可 以提高动物的痛阈2 。

多感觉整合脑机制研究一、本文概述Overview of this article随着神经科学的发展，人类对大脑工作机制的理解逐渐深入。

作为人类感知世界、理解世界的关键环节，多感觉整合在脑机制中的作用日益受到关注。

多感觉整合是指大脑将来自不同感觉通道的信息进行整合，形成统一的感知体验。

这一过程涉及到多个脑区的协同工作，包括感觉皮层、联合皮层以及高级认知皮层等。

本文旨在深入探讨多感觉整合的脑机制，通过综述相关文献和实验研究成果，揭示多感觉整合在神经生理学、认知科学以及神经心理学等领域的重要价值。

With the development of neuroscience, human understanding of the working mechanisms of the brain is gradually deepening. As a crucial link in human perception and understanding of the world, the role of multisensory integration in brain mechanisms is increasingly being studied. Multi sensory integration refers to the brain integrating information from different sensory channels to form a unified perceptual experience. This process involves the collaborative work of multiple brainregions, including the sensory cortex, associative cortex, and advanced cognitive cortex. This article aims to explore the brain mechanisms of multisensory integration in depth, and by reviewing relevant literature and experimental research results, reveal the important value of multisensory integration in fields such as neurophysiology, cognitive science, and neuropsychology.文章首先介绍了多感觉整合的基本概念和研究背景，阐述了多感觉整合在感知、注意、记忆和认知等方面的作用。

通路有关。

为进一步证明上述推测，用PI3K抑制剂 LY294002阻断PI3K/AKT通路。

在七氟烷吸入前同时 给予LY294002和依达拉奉，结果表明LY294002逆 转了依达拉奉对海马神经元保护作用，提示依达拉奉 通过激活PI3K/Akt信号通路抑制海马神经元凋亡。

本研究初步探讨了依达拉奉降低七氟烷致海马 神经元凋亡，并初步揭示了其分子作用机制，但值 得注意的是，凋亡机制是一个涉及多个信号通路的 复杂过程。

因此，需要进一步探究依达拉奉抑制七 氟烷致海马神经元凋亡的具体机制。

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