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。

Longitudinal assessment of peripheral organ metabolism and the gut microbiota in an APP/PS1 transgenic mouse model of Alzheimer’s disease

Alzheimer’s disease not only affects the brain,but also induces metabolic dysfunction in peripheral organs and alters the gut microbiota.The aim of this study was to investigate systemic changes that occur in Alzheimer’s disease,in particular the association between changes in peripheral organ metabolism,changes in gut microbial composition,and Alzheimer’s disease development.To do this,we analyzed peripheral organ metabolism and the gut microbiota in amyloid precursor protein-presenilin 1(APP/PS1)transgenic and control mice at 3,6,9,and 12 months of age.Twelve-month-old APP/PS1 mice exhibited cognitive impairment,Alzheimer’s disease-related brain changes,distinctive metabolic disturbances in peripheral organs and fecal samples(as detected by untargeted metabolomics sequencing),and substantial changes in gut microbial composition compared with younger APP/PS1 mice.Notably,a strong correlation emerged between the gut microbiota and kidney metabolism in APP/PS1 mice.These findings suggest that alterations in peripheral organ metabolism and the gut microbiota are closely related to Alzheimer’s disease development,indicating potential new directions for therapeutic strategies.

微生物菌群调控人畜共患结核病的研究进展

目前,人畜共患结核病(zTB)仍是世界上最重要的细菌传染性疫病之一,严重威胁人和动物健康以及公共卫生安全。机体数量庞大的微生物菌群积极参与着机体的发育、免疫调控、代谢等。研究发现微生物菌群和zTB的发生、发展、治疗、疫苗免疫具有紧密的相关性,现已成为诸多领域中的研究热点。菌群对zTB进程的调控可通过诸多途径直接或间接地进行,如菌群稳态、代谢物及对免疫的调控等。基于此,论文综述了目前微生物菌群与zTB相关研究的最新进展,重点讨论了肠道菌群和肺部菌群与zTB的关联及调节机制,分析了肠-肺轴相互作用、菌群代谢产物对zTB的影响,探讨了通过调节宿主的菌群组成和功能对预防和辅助治疗结核病的潜在价值,旨在为zTB防控提供理论基础和借鉴。

基于CT影像儿童枢椎正常发育与变异的解剖特征

背景:枢椎发育演变过程复杂,研究报道较少。CT成像可以显示枢椎的正常发育过程、解剖结构、发育变异与畸形,明确枢椎骨化中心出现与骺板闭合时间及其演变过程和规律具有重要的临床价值。目的:基于CT影像展示儿童枢椎正常发育与变异的解剖结构。方法:回顾性分析2016年6月至2019年11月行颈部扫描的732例0-15岁儿童CT图像。观察指标包括枢椎齿状突、双侧椎弓、椎体骨化中心,齿突尖部二次骨化中心,椎弓、齿突基底部及后正中骺板,以及枢椎发育变异或畸形。分析与比较各项指标在不同年龄下的变化情况,并利用SPSS 17.0统计学软件包进行数据分类处理及统计学分析。结果与结论:(1)732例研究对象包括枢椎正常发育718例(98.1%),畸形或发育异常14例(1.9%);(2)枢椎5个骨化中心,其中双侧椎弓及齿突、椎体骨化中心在出生时已出现;齿突尖部二次骨化中心出现的中位年龄是5.7岁,年龄四分位差(IQR)是4.1-7岁,最早出现的为8个月22 d,最迟未出现的为12岁10个月;(3)齿突尖骺板融合的中位年龄是6岁,IQR是5-8岁,未融合最大年龄是8岁9个月,融合的最小年龄是4岁3个月;(4)双侧椎弓骺板闭合的中位年龄约3.8岁,IQR约2.9-4.6岁,闭合的最小年龄是2岁3个月,未闭合的最大年龄是6岁;(5)齿突基底部骺板闭合的中位数5.2岁,IQR为3.5-6.8岁,闭合最小年龄是2岁6个月,最晚未闭合年龄是9岁6个月;(6)后正中骺板闭合年龄中位数为1.5岁,IQR为1.0-2.1岁,最晚未闭合2例分别为2岁5个月、14岁,最早闭合为6个月20 d;(7)枢椎畸形或发育异常,包括出现副骨化中心及副骺板7例、枢椎游离骨化小骨3例、后正中骺板不闭合2例、无齿突尖部二次骨化中心2例及枢椎齿突骨化中心未出现1例;(8)提示多层螺旋CT扫描、结合多平面重组技术可以完整显示枢椎的解剖结构,评估其正常发育变异及畸形。

短链脂肪酸介导的肠骨轴在骨代谢中的研究进展

随着全球老龄化加剧,骨质疏松症等与年龄相关的骨骼代谢疾病发病率不断上升,寻求安全有效的治疗干预方法至关重要。目前肠道微生物及其代谢产物调节骨代谢已成为研究的热点。短链脂肪酸(short-chain fatty acids,SCFAs)如乙酸、丙酸和丁酸等,能够通过肠-骨轴发挥骨形成和骨吸收的调节作用,对骨稳态调节具有一定的积极作用,并能改善炎症性骨丢失。本文综述SCFAs通过内分泌、免疫、改善营养吸收等途径调控骨代谢稳态,以期为老年代谢性骨病的预防和治疗提供科学依据。

软硬件协同的RapidIO接口带宽测试方法

RapidIO是一种高性能嵌入式系统互联技术。FPGA的SRIO控制器实现了RapidIO二代协议,在工程中经常需要得到其实际带宽性能以确定其是否满足应用需求。采用FPGA的嵌入式软核,配合FPGA内部硬件电路可搭建软硬件协同SOPC测试系统。该系统既具有硬件可裁剪、可定制、扩展性强的特点,又具备软件灵活性的特点。此系统在硬件层面设计了周期采样单元、周期配置接口、锁存接口、上传接口;软件层面具备采样参数配置、采样控制、采样数据分析、结果呈现功能。通过软硬件代码的编写和验证,表明此方法可实时监测接口的带宽及抖动性能指标。

密度胁迫对珍珠龙胆石斑鱼生长和生理的影响

养殖密度是影响工厂化循环水养殖的重要因素之一,为探究密度胁迫对珍珠龙胆石斑鱼(Epinephelus fuscoguttatus♀×Epinephelus lanceolatus♂)幼鱼生长、消化代谢酶活性、抗氧化酶活性和下丘脑-垂体-肾间组织(HPI)轴相关激素水平及基因表达的影响,实验选取1800尾规格一致、体格健康的珍珠龙胆石斑鱼,随机分为3个密度梯度:低密度100尾[(3.14±0.13)kg/m3,LD]、中密度200尾[(6.31±0.13)kg/m3,MD]和高密度300尾[(9.56±0.24)kg/m3,HD]进行实验。研究表明,HD组特定增长率、肥满度及存活率显著低于其他各组(P<0.05);饵料系数和变异系数随密度的升高显著上升(P<0.05);HD组抗氧化酶和代谢酶活性显著高于其他各组(P<0.05),而消化酶活性显著低于其他各组(P<0.05);HD组HPI轴相关激素水平显著高于其他各组(P<0.05),HPI轴相关基因(crhr1、nr3c1及nr3c2)的表达量随密度的升高显著上调(P<0.05),crh-bp表达量则相反(P<0.05)。本研究结果可为深入认识密度胁迫对珍珠龙胆石斑鱼生长、消化代谢、氧化应激及内分泌的影响提供科学依据,为实际生产过程中珍珠龙胆石斑鱼幼鱼养殖密度的设定提供理论参考。

肠道菌群在葡萄膜炎中的作用与研究进展

葡萄膜炎是一种涉及眼部多个结构的致盲性炎性疾病,严重时威胁患者的视力和心理健康。目前,针对葡萄膜炎的治疗以糖皮质激素以及免疫抑制剂为主,其存在副作用较多、易复发且治疗费用高昂等问题。近年来的研究表明,肠道菌群可通过肠-眼轴在葡萄膜炎的发展中起作用,其相关代谢物也对该疾病的进展具有重要影响,调节肠道菌群或相关代谢物可能成为治疗葡萄膜炎的新途径。文章综述了肠道菌群与各葡萄膜炎相关疾病如系统性结节病、Vogt-小柳原田病、白塞病、多发性硬化症、鸟枪弹样葡萄膜炎的联系,介绍益生菌和益生元、抗生素、免疫调节剂、噬菌体疗法和粪便微生物移植等菌群相关治疗的研究进展,旨在为推动针对葡萄膜炎特异菌群及相关基因标志物的新疗法发展提供参考,促进精准医疗的实现。

Gut-brain axis as a bridge in obesity and depression:Mechanistic exploration and therapeutic prospects

A recent study by Wang et al,published in the World Journal of Psychiatry,provided preventative and therapeutic strategies for the comorbidity of obesity and depression.The gut-brain axis,which acts as a two-way communication system between the gastrointestinal tract and the central nervous system,plays a pivotal role in the pathogenesis of these conditions.Evidence suggests that metabolic byproducts,such as short-chain fatty acids,lipopolysaccharide and bile acids,which are generated by the gut microbiota,along with neurotransmitters and inflammatory mediators within the gut-brain axis,modulate the host's metabolic processes,neuronal regulation,and immune responses through diverse mechanisms.The interaction between obesity and depression via the gut-brain axis involves disruptions in the gut microbiota balance,inflammatory immune responses,and alterations in the neuroendocrine system.Modulating the gut-brain axis,for example,through a ketogenic diet,the use of probiotics,and the supplementation of antioxidants,offers new remedial approaches for obesity and depression.Future research that explores the mechanisms of the gut-brain axis is needed to provide more evidence for clinical treatment.

Glucocorticoid receptor signaling in the brain and its involvement in cognitive function

The hypothalamic-pituitary-adrenal axis regulates the secretion of glucoco rticoids in response to environmental challenges.In the brain,a nuclear receptor transcription fa ctor,the glucocorticoid recepto r,is an important component of the hypothalamicpituitary-a d renal axis's negative feedback loop and plays a key role in regulating cognitive equilibrium and neuroplasticity.The glucoco rticoid receptor influences cognitive processes,including glutamate neurotransmission,calcium signaling,and the activation of brain-derived neurotrophic factor-mediated pathways,through a combination of genomic and non-genomic mechanisms.Protein interactions within the central nervous system can alter the expression and activity of the glucocorticoid receptor,there by affecting the hypothalamic-pituitary-a d renal axis and stress-related cognitive functions.An appropriate level of glucocorticoid receptor expression can improve cognitive function,while excessive glucocorticoid receptors or long-term exposure to glucoco rticoids may lead to cognitive impairment.Patients with cognitive impairment-associated diseases,such as Alzheimer's disease,aging,depression,Parkinson's disease,Huntington's disease,stroke,and addiction,often present with dysregulation of the hypothalamic-pituitary-adrenal axis and glucocorticoid receptor expression.This review provides a comprehensive overview of the functions of the glucoco rticoid receptor in the hypothalamic-pituitary-a d renal axis and cognitive activities.It emphasizes that appropriate glucocorticoid receptor signaling fa cilitates learning and memory,while its dysregulation can lead to cognitive impairment.This provides clues about how glucocorticoid receptor signaling can be targeted to ove rcome cognitive disability-related disorders.

Influence of gut bacteria on type 2 diabetes:Mechanisms and therapeutic strategy

The onset and progression of type 2 diabetes mellitus(T2DM)are strongly associated with imbalances in gut bacteria,making the gut microbiome a new potential therapeutic focus.This commentary examines the recent publication in World Journal of Diabetes.The article explores the association between T2DM and gut microbiota,with a focus on the pathophysiological changes related to dysbiosis.It proposes innovative microbiome-targeted therapeutic strategies and evaluates the challenges and future directions of such approaches.This editorial summarizes the key points of their discussion of the role of the gut microbiome in T2DM and elaborates on the influence of specific gut microbial species on the disease through the host–microbiota metabolic axis.It provides new insights for future research on gut-microbiota-based interventions for T2DM.

The gut-eye axis:from brain neurodegenerative diseases to age-related macular degeneration

Age-related macular degeneration is a serious neurodegenerative disease of the retina that significantly impacts vision.Unfortunately,the specific pathogenesis remains unclear,and effective early treatment options are consequently lacking.The microbiome is defined as a large ecosystem of microorganisms living within and coexisting with a host.The intestinal microbiome undergoes dynamic changes owing to age,diet,genetics,and other factors.Such dysregulation of the intestinal flora can disrupt the microecological balance,resulting in immunological and metabolic dysfunction in the host,and affecting the development of many diseases.In recent decades,significant evidence has indicated that the intestinal flora also influences systems outside of the digestive tract,including the brain.Indeed,several studies have demonstrated the critical role of the gut-brain axis in the development of brain neurodegenerative diseases,including Alzheimer’s disease and Parkinson’s disease.Similarly,the role of the“gut-eye axis”has been confirmed to play a role in the pathogenesis of many ocular disorders.Moreover,age-related macular degeneration and many brain neurodegenerative diseases have been shown to share several risk factors and to exhibit comparable etiologies.As such,the intestinal flora may play an important role in age-related macular degeneration.Given the above context,the present review aims to clarify the gut-brain and gut-eye connections,assess the effect of intestinal flora and metabolites on age-related macular degeneration,and identify potential diagnostic markers and therapeutic strategies.Currently,direct research on the role of intestinal flora in age-related macular degeneration is still relatively limited,while studies focusing solely on intestinal flora are insufficient to fully elucidate its functional role in age-related macular degeneration.Organ-on-a-chip technology has shown promise in clarifying the gut-eye interactions,while integrating analysis of the intestinal flora with research on metabolites through metabolomics and other techniques is crucial for understanding their potential mechanisms.

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.

Bidirectional regulation of the brain-gut-microbiota axis following traumatic brain injury

Traumatic brain injury is a prevalent disorder of the central nervous system.In addition to primary brain parenchymal damage,the enduring biological consequences of traumatic brain injury pose long-term risks for patients with traumatic brain injury;however,the underlying pathogenesis remains unclear,and effective intervention methods are lacking.Intestinal dysfunction is a significant consequence of traumatic brain injury.Being the most densely innervated peripheral tissue in the body,the gut possesses multiple pathways for the establishment of a bidirectional“brain-gut axis”with the central nervous system.The gut harbors a vast microbial community,and alterations of the gut niche contribute to the progression of traumatic brain injury and its unfavorable prognosis through neuronal,hormonal,and immune pathways.A comprehensive understanding of microbiota-mediated peripheral neuroimmunomodulation mechanisms is needed to enhance treatment strategies for traumatic brain injury and its associated complications.We comprehensively reviewed alterations in the gut microecological environment following traumatic brain injury,with a specific focus on the complex biological processes of peripheral nerves,immunity,and microbes triggered by traumatic brain injury,encompassing autonomic dysfunction,neuroendocrine disturbances,peripheral immunosuppression,increased intestinal barrier permeability,compromised responses of sensory nerves to microorganisms,and potential effector nuclei in the central nervous system influenced by gut microbiota.Additionally,we reviewed the mechanisms underlying secondary biological injury and the dynamic pathological responses that occur following injury to enhance our current understanding of how peripheral pathways impact the outcome of patients with traumatic brain injury.This review aimed to propose a conceptual model for future risk assessment of central nervous system-related diseases while elucidating novel insights into the bidirectional effects of the“brain-gut-microbiota axis.”

针刺联合神经干细胞修复脊髓损伤的科学依据

背景:脊髓损伤是由创伤性或非创伤性事件引起的一种神经系统疾病,常导致损伤节段以下严重功能障碍。近年来,神经干细胞移植被认为在调控脊髓损伤后的炎症反应、抑制胶质瘢痕的过度增生以及促进神经再生方面具有显著的治疗潜力。目的:综述并讨论针刺及神经干细胞移植疗法在抑制脊髓损伤诱导的继发性损伤中的潜在作用机制,深入探讨其治疗脊髓损伤的科学依据。方法:以“脊髓损伤,针刺,神经干细胞,SDF-1α/CXCR4轴”为中文检索词,以“Spinal cord injury,acupuncture,neural stem cells,SDF-1α/CXCR4 axis”为英文检索词,分别检索PubMed、Elsevier、万方及中国知网数据库,最终纳入96篇文献,汇总分析了针刺联合神经干细胞治疗脊髓损伤的相关研究成果,总结了这一联合疗法在治疗脊髓损伤后继发性损伤中的相关机制。结果与结论:①基质细胞衍生因子1α(stromal-derived factor 1α,SDF-1α)/CXC趋化因子受体4(chemokine receptor 4,CXCR4)轴在神经干细胞移植治疗脊髓损伤中扮演着至关重要的角色,该信号传导机制不仅影响神经干细胞的迁移、增殖和分化,更是决定干细胞归巢至损伤部位效率的关键因素。因此,针对该轴线的调控,对于提升脊髓损伤的治疗效果具有重要意义。②针刺作为一种传统中医疗法,在脊髓损伤的继发性损伤调控中展现出独特的优势,它能够通过调节炎症反应、抑制细胞凋亡、改善微循环、减少神经胶质瘢痕形成以及对抗氧化应激等多种途径,有效减轻脊髓损伤后的继发性损伤。③针刺还能够影响SDF-1α/CXCR4轴的表达与功能,从而增强神经干细胞的归巢和存活能力,促进神经再生和功能恢复。④结合针刺与干细胞移植的疗法,是一种创新且较好的脊髓损伤治疗策略,适用于修复神经环路,它结合了传统中医的智慧与现代生物技术的优势,为脊髓损伤患者提供了新的治疗选择。然而,目前这种联合疗法仍处于研究和探索阶段,其长期疗效和安全性尚需进一步验证。⑤综合而言,针刺及神经干细胞移植治疗脊髓损伤具有巨大的临床应用潜力,但仍需深入研究和优化治疗方案。未来,期待通过更多的临床试验和机制研究,进一步揭示这一疗法的疗效机制和最佳适应证,为脊髓损伤患者带来更好的康复希望和更高效的治疗效果。

Inhibition of the cGAS–STING pathway:contributing to the treatment of cerebral ischemia-reperfusion injury

The cGAS–STING pathway plays an important role in ischemia-reperfusion injury in the heart,liver,brain,and kidney,but its role and mechanisms in cerebral ischemia-reperfusion injury have not been systematically reviewed.Here,we outline the components of the cGAS–STING pathway and then analyze its role in autophagy,ferroptosis,cellular pyroptosis,disequilibrium of calcium homeostasis,inflammatory responses,disruption of the blood–brain barrier,microglia transformation,and complement system activation following cerebral ischemia-reperfusion injury.We further analyze the value of cGAS–STING pathway inhibitors in the treatment of cerebral ischemia-reperfusion injury and conclude that the pathway can regulate cerebral ischemia-reperfusion injury through multiple mechanisms.Inhibition of the cGAS–STING pathway may be helpful in the treatment of cerebral ischemia-reperfusion injury.

Psycho-gastroenterological profile of an Italian population of children with disorders of gut-brain interaction:A case-control study

BACKGROUND Disorders of gut-brain interaction(DGBI)are common,but knowledge about their physiopathology is still poor,nor valid tools have been used to evaluate them in childhood.AIM To develop a psycho-gastroenterological questionnaire(PGQ)to assess the psycho-gastroenterological profile and social characteristics of a pediatric population with and without DGBI.METHODS One hundred and nineteen Italian children(age 11-18)were included:28 outpatient patients with DGBI(Rome IV criteria)and 91 healthy controls.They filled the PGQ,faces pain scale revised(FPS-R),Bristol stool chart,ga-strointestinal symptoms rating scale,state-trait anxiety inventory,Toronto alexithymia scale 20,perceived self-efficacy in the management of negative emotions and expression of positive emotions(APEN-G,APEP-G),irritable bowel syndrome-quality of life questionnaire,school performances,tobacco use,early life events,degree of digital-ization.RESULTS Compared to controls,patients had more medical examinations(35%of them went to the doctor more than five times),a higher school performance(23%vs 13%,P<0.05),didn’t use tobacco(never vs 16%,P<0.05),had early life events(28%vs 1%P<0.05)and a higher percentage of pain classified as 4 in the FPS-R during the examination(14%vs 7%,P<0.05).CONCLUSION Pediatric outpatients with DGBI had a higher prevalence of early life events,a lower quality of life,more medical examinations rising health care costs,lower anxiety levels.

基于“肾主水”探讨AVP-V2R-AQP2轴与肾病阴虚水肿的关系

肾病阴虚水肿常见于肾脏病中、后期患者,有着难治性、顽固性的特点,并且随着病情进展、利尿药物的应用而逐渐加重,临床关注度低,治疗措施有限,治疗效果不佳。血管升压素(AVP)-加压素受体2(V2R)-水通道蛋白2(AQP2)轴是机体调节水盐平衡的关键通路,且与肾脏排泄钠失常直接相关。根据中医“象”思维,认为“肾主水”理论推导的肾病阴虚水肿发病机制与AVP-VR2-AQP2轴导致肾病阴虚水肿相类似。故本文将基于“肾主水”理论,结合王悦芬教授临床经验,从中、西医不同的角度及运用中医药调控AVP-VR2-AQP2轴治疗肾病阴虚水肿等方面,深入探讨“肾主水”、AVP-V2R-AQP2轴、肾病阴虚水肿三者之间的联系,进一步认识“肾主水”机制,探讨AQP2作为肾病阴虚水肿新型生物标志物的可能,为肾病阴虚水肿的治疗提供新思路,为中医药现代化研究提供可靠依据。

基于脑-肠-菌轴探讨调补肝脾法治疗功能性消化不良的作用机制

功能性消化不良(FD)作为临床常见疾病,其发病机制在现代医学方面被证实与胃肠动力、内脏敏感性、胃肠微生态等直接相关。脑-肠-菌轴作为一条人体的特殊通路,可较好地阐释其复杂的病理机制。中医药在FD的治疗方面有着十分确切的效果。从中医理论角度,脾胃之“运”“化”与现代医学胃肠动力、营养代谢等具有高度相似之处;而肝主疏泄影响脾胃气机,调畅情志影响思维等功能将中枢系统与胃肠道联系在一起,与现代医学“脑-肠-菌轴”高度相似。文章从中西医两方面论治FD,加强了对其病因病机与治则治法的认识,并拓展了中医调补肝脾法的思路。

新型悬臂式掘进机横轴截割头的研制

作为煤矿采掘机械中破岩落煤的关键部件,横轴式截割头相比纵轴式截割头在硬岩截割时具有更好的破岩效率和适应性。相比山特维克AHM105横轴截割头结构,通过在联接结构、头体结构、齿座结构、大端结构等方面的创新,采用八方结构联接、前后截割头体结合防剪切销组焊、J形坡口齿座、一体化耐磨头体大端等结构,成功研制了新型悬臂式掘进机横轴截割头,通过井下应用验证了该截割头在截割全岩过程中具有较高的可靠性和稳定性。研究内容为横轴式截割头的研发和创新提供了参考,具有一定的实用和推广价值。