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Comparing RNA-sequencing datasets from astrocytes, oligodendrocytes, and microglia in multiple sclerosis identifies novel dysregulated genes relevant to inflammation and myelination. 比较多发性硬化症中星形胶质细胞、少突胶质细胞和小胶质细胞的rna测序数据集,发现了与炎症和髓鞘形成相关的新的失调基因。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-03-01 DOI: 10.1002/wsbm.1594
Sienna S Drake, Aliyah Zaman, Tristan Simas, Alyson E Fournier

Central nervous system (CNS) inflammation is a key factor in multiple sclerosis (MS). Invasion of peripheral immune cells into the CNS resulting from an unknown signal or combination of signals results in activation of resident immune cells and the hallmark feature of the disease: demyelinating lesions. These lesion sites are an amalgam of reactive peripheral and central immune cells, astrocytes, damaged and dying oligodendrocytes, and injured neurons and axons. Sustained inflammation affects cells directly located within the lesion site and further abnormalities are apparent diffusely throughout normal-appearing white matter and grey matter. It is only relatively recently, using animal models, new tissue sampling techniques, and next-generation sequencing, that molecular changes occurring in CNS resident cells have been broadly captured. Advances in cell isolation through Fluorescence Activated Cell Sorting (FACS) and laser-capture microdissection together with the emergence of single-cell sequencing have enabled researchers to investigate changes in gene expression in astrocytes, microglia, and oligodendrocytes derived from animal models of MS as well as from primary patient tissue. The contribution of some dysregulated pathways has been followed up in individual studies; however, corroborating results often go unreported between sequencing studies. To this end, we have consolidated results from numerous RNA-sequencing studies to identify and review novel patterns of differentially regulated genes and pathways occurring within CNS glial cells in MS. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology.

中枢神经系统(CNS)炎症是多发性硬化症(MS)的关键因素。由未知信号或信号组合引起的外周免疫细胞侵入中枢神经系统导致常驻免疫细胞的激活和疾病的标志性特征:脱髓鞘病变。这些病变部位是反应性外周和中枢免疫细胞、星形胶质细胞、受损和死亡的少突胶质细胞以及受损的神经元和轴突的混合体。持续的炎症影响直接位于病变部位的细胞,进一步的异常在正常的白质和灰质中弥漫性表现明显。直到最近,使用动物模型、新的组织取样技术和下一代测序技术,才广泛地捕捉到发生在中枢神经系统驻留细胞中的分子变化。通过荧光活化细胞分选(FACS)和激光捕获显微解剖分离细胞的进展,以及单细胞测序的出现,使研究人员能够研究来自多发性硬化症动物模型和原发患者组织的星形胶质细胞、小胶质细胞和少突胶质细胞基因表达的变化。一些失调通路的贡献在个体研究中得到了跟进;然而,在测序研究之间,证实的结果往往没有报道。为此,我们整合了大量rna测序研究的结果,以鉴定和回顾多发性硬化症中中枢神经胶质细胞内发生的差异调节基因和通路的新模式。
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引用次数: 2
In silico modeling for the hepatic circulation and transport: From the liver organ to lobules. 肝脏循环和运输的计算机模拟:从肝器官到小叶。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-03-01 DOI: 10.1002/wsbm.1586
Harvey Ho, Shawn Means, Soroush Safaei, Peter John Hunter

The function of the liver depends critically on its blood supply. Numerous in silico models have been developed to study various aspects of the hepatic circulation, including not only the macro-hemodynamics at the organ level, but also the microcirculation at the lobular level. In addition, computational models of blood flow and bile flow have been used to study the transport, metabolism, and clearance of drugs in pharmacokinetic studies. These in silico models aim to provide insights into the liver organ function under both healthy and diseased states, and to assist quantitative analysis for surgical planning and postsurgery treatment. The purpose of this review is to provide an update on state-of-the-art in silico models of the hepatic circulation and transport processes. We introduce the numerical methods and the physiological background of these models. We also discuss multiscale frameworks that have been proposed for the liver, and their linkage with the large context of systems biology, systems pharmacology, and the Physiome project. This article is categorized under: Metabolic Diseases > Computational Models Metabolic Diseases > Biomedical Engineering Cardiovascular Diseases > Computational Models.

肝脏的功能主要取决于它的血液供应。许多计算机模型已经被开发出来,用于研究肝循环的各个方面,不仅包括器官水平的宏观血流动力学,还包括小叶水平的微循环。此外,在药代动力学研究中,血流和胆汁流量的计算模型已被用于研究药物的转运、代谢和清除。这些计算机模型旨在深入了解健康和患病状态下的肝脏器官功能,并协助定量分析手术计划和术后治疗。本综述的目的是提供最新的最先进的肝脏循环和运输过程的计算机模型。我们介绍了这些模型的数值方法和生理背景。我们还讨论了为肝脏提出的多尺度框架,以及它们与系统生物学、系统药理学和生理组项目的大背景的联系。本文分类如下:代谢疾病>计算模型代谢疾病>生物医学工程心血管疾病>计算模型。
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引用次数: 1
Organoids of the male reproductive system: Challenges, opportunities, and their potential use in fertility research. 男性生殖系统类器官:挑战、机遇及其在生育研究中的潜在应用。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-03-01 DOI: 10.1002/wsbm.1590
Daniela Patrício, Joana Santiago, João F Mano, Margarida Fardilha

Organoids are units of function of a given organ able to reproduce, in culture, a biological structure similar in architecture and function to its counterpart in vivo. Today, it is possible to develop an organoid from a fragment of tissue, a stem cell located in an adult organ, an embryonic stem cell, or an induced pluripotent stem cell. In the past decade, many organoids have been developed which mimic stomach, pancreas, liver and brain tissues, optic cups, among many others. Additionally, different male reproductive system organs have already been developed as organoids, including the prostate and testis. These 3D cultures may be of great importance for urological cancer research and have the potential to be used in fertility research for the study of spermatozoa production and maturation, germ cells-somatic cells interactions, and mechanisms of disease. They also provide an accurate preclinical pipeline for drug testing and discovery, as well as for the study of drug resistance. In this work, we revise the current knowledge on organoid technology and its use in healthcare and research, describe the male reproductive system organoids and other biomaterials already developed, and discuss their current application. Finally, we highlight the research gaps, challenges, and opportunities in the field and propose strategies to improve the use of organoids for the study of male infertility situations. This article is categorized under: Reproductive System Diseases > Stem Cells and Development Reproductive System Diseases > Biomedical Engineering.

类器官是特定器官的功能单位,能够在培养中复制与其体内对应器官在结构和功能上相似的生物结构。如今,从组织碎片、成人器官中的干细胞、胚胎干细胞或诱导多能干细胞中培育出类器官是可能的。在过去的十年里,许多类器官已经被开发出来,它们模仿了胃、胰腺、肝脏和脑组织、视杯等许多其他组织。此外,不同的男性生殖系统器官已经发展成为类器官,包括前列腺和睾丸。这些3D培养物可能对泌尿系统癌症的研究具有重要意义,并有可能用于生殖研究,研究精子的产生和成熟、生殖细胞-体细胞的相互作用以及疾病的机制。它们还为药物测试和发现以及耐药性研究提供了准确的临床前管道。在这项工作中,我们修订了目前关于类器官技术及其在医疗保健和研究中的应用的知识,描述了已经开发的男性生殖系统类器官和其他生物材料,并讨论了它们目前的应用。最后,我们强调了该领域的研究差距、挑战和机遇,并提出了改善类器官在男性不育症研究中的应用的策略。本文分类如下:生殖系统疾病>干细胞与发育生殖系统疾病>生物医学工程。
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引用次数: 5
Determination of the Salmonella intracellular lifestyle by the diversified interaction of Type III secretion system effectors and host GTPases. III型分泌系统效应物与宿主gtpase多种相互作用对沙门氏菌胞内生活方式的影响。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-03-01 DOI: 10.1002/wsbm.1587
Kun Meng, Ping Zhu, Liuliu Shi, Shan Li

Intracellular bacteria have developed sophisticated strategies to subvert the host endomembrane system to establish a stable replication niche. Small GTPases are critical players in regulating each step of membrane trafficking events, such as vesicle biogenesis, cargo transport, tethering, and fusion events. Salmonella is a widely studied facultative intracellular bacteria. Salmonella delivers several virulence proteins, termed effectors, to regulate GTPase dynamics and subvert host trafficking for their benefit. In this review, we summarize an updated and systematic understanding of the interactions between bacterial effectors and host GTPases in determining the intracellular lifestyle of Salmonella. This article is categorized under: Infectious Diseases > Molecular and Cellular Physiology.

胞内细菌已经发展出复杂的策略来破坏宿主的膜系统,以建立一个稳定的复制生态位。小gtpase在调节膜运输事件的每个步骤中都起着关键作用,例如囊泡生物发生、货物运输、系结和融合事件。沙门氏菌是一种被广泛研究的兼性细胞内细菌。沙门氏菌提供了几种毒力蛋白,称为效应物,以调节GTPase动力学和破坏宿主运输为他们的利益。在这篇综述中,我们总结了细菌效应物和宿主gtpase在决定沙门氏菌细胞内生活方式中的相互作用的最新和系统的理解。本文分类为:感染性疾病>分子与细胞生理学。
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引用次数: 0
Neurodegeneration in multiple sclerosis. 多发性硬化症的神经变性。
IF 4.6 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-01-01 Epub Date: 2022-08-10 DOI: 10.1002/wsbm.1583
Gabrielle M Mey, Kedar R Mahajan, Tara M DeSilva

Axonal loss in multiple sclerosis (MS) is a key component of disease progression and permanent neurologic disability. MS is a heterogeneous demyelinating and neurodegenerative disease of the central nervous system (CNS) with varying presentation, disease courses, and prognosis. Immunomodulatory therapies reduce the frequency and severity of inflammatory demyelinating events that are a hallmark of MS, but there is minimal therapy to treat progressive disease and there is no cure. Data from patients with MS, post-mortem histological analysis, and animal models of demyelinating disease have elucidated patterns of MS pathogenesis and underlying mechanisms of neurodegeneration. MRI and molecular biomarkers have been proposed to identify predictors of neurodegeneration and risk factors for disease progression. Early signs of axonal dysfunction have come to light including impaired mitochondrial trafficking, structural axonal changes, and synaptic alterations. With sustained inflammation as well as impaired remyelination, axons succumb to degeneration contributing to CNS atrophy and worsening of disease. These studies highlight the role of chronic demyelination in the CNS in perpetuating axonal loss, and the difficulty in promoting remyelination and repair amidst persistent inflammatory insult. Regenerative and neuroprotective strategies are essential to overcome this barrier, with early intervention being critical to rescue axonal integrity and function. The clinical and basic research studies discussed in this review have set the stage for identifying key propagators of neurodegeneration in MS, leading the way for neuroprotective therapeutic development. This article is categorized under: Immune System Diseases > Molecular and Cellular Physiology Neurological Diseases > Molecular and Cellular Physiology.

多发性硬化症(MS)的轴突丢失是疾病进展和永久性神经残疾的关键因素。多发性硬化症是中枢神经系统(CNS)的一种异质性脱髓鞘和神经退行性疾病,表现、病程和预后各不相同。免疫调节疗法可降低作为多发性硬化症标志的炎症性脱髓鞘事件的频率和严重程度,但治疗进展性疾病的疗法很少,而且无法治愈。来自多发性硬化症患者、死后组织学分析和脱髓鞘疾病动物模型的数据阐明了多发性硬化症的发病模式和神经变性的潜在机制。核磁共振成像和分子生物标志物已被提出用于确定神经变性的预测因子和疾病进展的风险因素。轴突功能障碍的早期迹象已经显现,包括线粒体贩运受损、轴突结构变化和突触改变。随着炎症的持续以及再髓鞘化受损,轴突会发生退化,导致中枢神经系统萎缩和疾病恶化。这些研究凸显了中枢神经系统慢性脱髓鞘在轴突缺失中的作用,以及在持续的炎症损伤中促进再髓鞘化和修复的困难。再生和神经保护策略对于克服这一障碍至关重要,早期干预对于挽救轴突的完整性和功能至关重要。本综述中讨论的临床和基础研究为确定多发性硬化症神经退行性变的关键传播因素奠定了基础,为神经保护疗法的开发指明了方向。本文归类于免疫系统疾病 > 分子和细胞生理学 神经系统疾病 > 分子和细胞生理学。
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引用次数: 0
Evolution of precision oncology-guided treatment paradigms. 精准肿瘤指导治疗模式的演变。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1585
Ramanuj DasGupta, Aixin Yap, Elena Yong Yaqing, Shumei Chia

Cancer treatment is gradually evolving from the classical use of nonspecific cytotoxic drugs targeting generic mechanisms of cell growth and proliferation. Instead, new "patient-specific treatment paradigms" that are based on an individual patient's tumor-specific molecular features are emerging, and these include "druggable" genomic alterations such as oncogenic driver mutations, downstream activities of cancer-signaling pathways, and the expression of specific genes involved in tumorigenesis and cancer progression. This evolving landscape of making evidence-based treatment decisions forms the foundation of precision oncology, which aims to deliver "the right drug, to the right patient and at the right time". The long-term vision for this approach is to maximize the treatment efficacy while minimizing exposure to ineffective therapy and reducing co-morbidity-related side effects. Successful clinical translation and implementation of this vision have the potential to revolutionize treatment paradigms from predominantly reactive, to more evidence-based, proactive and predictive care. In this article, we review the past and current approaches in precision oncology, and describe their remarkable power and limitations. We also speculate on the evolution of newly emerging methodologies of the future that can be used to address some of the key challenges associated with the existing paradigms. This article is categorized under: Cancer > Genetics/Genomics/Epigenetics Cancer > Molecular and Cellular Physiology Cancer > Computational Models.

癌症治疗正逐渐从传统的使用非特异性细胞毒性药物来靶向一般的细胞生长和增殖机制演变而来。相反,基于个体患者肿瘤特异性分子特征的新的“患者特异性治疗范式”正在出现,其中包括“可药物”的基因组改变,如致癌驱动突变,癌症信号通路的下游活动,以及参与肿瘤发生和癌症进展的特定基因的表达。这种不断发展的以证据为基础的治疗决策构成了精确肿瘤学的基础,其目标是“在正确的时间给正确的病人提供正确的药物”。这种方法的长期目标是最大限度地提高治疗效果,同时最大限度地减少无效治疗的暴露,并减少与合并症相关的副作用。成功的临床翻译和实施这一愿景有可能彻底改变治疗模式,从主要的被动治疗,到更多的循证、主动和预测性护理。在这篇文章中,我们回顾了过去和现在的精确肿瘤学方法,并描述了它们显著的力量和局限性。我们还推测了未来新出现的方法的演变,这些方法可用于解决与现有范式相关的一些关键挑战。本文分类如下:癌症>遗传学/基因组学/表观遗传学癌症>分子和细胞生理学癌症>计算模型。
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引用次数: 3
Computational models for generating microvascular structures: Investigations beyond medical imaging resolution. 生成微血管结构的计算模型:超越医学成像分辨率的研究。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1579
Cameron Apeldoorn, Soroush Safaei, Julian Paton, Gonzalo D Maso Talou

Angiogenesis, arteriogenesis, and pruning are revascularization processes essential to our natural vascular development and adaptation, as well as central players in the onset and development of pathologies such as tumoral growth and stroke recovery. Computational modeling allows for repeatable experimentation and exploration of these complex biological processes. In this review, we provide an introduction to the biological understanding of the vascular adaptation processes of sprouting angiogenesis, intussusceptive angiogenesis, anastomosis, pruning, and arteriogenesis, discussing some of the more significant contributions made to the computational modeling of these processes. Each computational model represents a theoretical framework for how biology functions, and with rises in computing power and study of the problem these frameworks become more accurate and complete. We highlight physiological, pathological, and technological applications that can be benefit from the advances performed by these models, and we also identify which elements of the biology are underexplored in the current state-of-the-art computational models. This article is categorized under: Cancer > Computational Models Cardiovascular Diseases > Computational Models.

血管生成、动脉生成和剪枝是血管再生过程中必不可少的自然血管发育和适应过程,也是肿瘤生长和中风恢复等病理发生和发展的核心参与者。计算建模允许对这些复杂的生物过程进行可重复的实验和探索。在这篇综述中,我们介绍了对发芽血管生成、肠套管血管生成、吻合、修剪和动脉生成等血管适应过程的生物学理解,并讨论了对这些过程的计算建模做出的一些更重要的贡献。每个计算模型都代表了生物学如何运作的理论框架,随着计算能力的提高和对问题的研究,这些框架变得更加准确和完整。我们强调了可以从这些模型的进步中受益的生理、病理和技术应用,并且我们还确定了当前最先进的计算模型中未充分探索的生物学要素。本文分类如下:癌症>计算模型心血管疾病>计算模型。
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引用次数: 3
Models of the cardiac L-type calcium current: A quantitative review. 心脏 L 型钙电流模型:定量综述。
IF 4.6 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-01-01 Epub Date: 2022-08-26 DOI: 10.1002/wsbm.1581
Aditi Agrawal, Ken Wang, Liudmila Polonchuk, Jonathan Cooper, Maurice Hendrix, David J Gavaghan, Gary R Mirams, Michael Clerx

The L-type calcium current ( I CaL ) plays a critical role in cardiac electrophysiology, and models of I CaL are vital tools to predict arrhythmogenicity of drugs and mutations. Five decades of measuring and modeling I CaL have resulted in several competing theories (encoded in mathematical equations). However, the introduction of new models has not typically been accompanied by a data-driven critical comparison with previous work, so that it is unclear which model is best suited for any particular application. In this review, we describe and compare 73 published mammalian I CaL models and use simulated experiments to show that there is a large variability in their predictions, which is not substantially diminished when grouping by species or other categories. We provide model code for 60 models, list major data sources, and discuss experimental and modeling work that will be required to reduce this huge list of competing theories and ultimately develop a community consensus model of I CaL . This article is categorized under: Cardiovascular Diseases > Computational Models Cardiovascular Diseases > Molecular and Cellular Physiology.

L 型钙电流(I CaL)在心脏电生理学中起着至关重要的作用,I CaL 模型是预测药物和突变致心律失常性的重要工具。五十年来,对 I CaL 的测量和建模产生了多种相互竞争的理论(以数学公式编码)。然而,在引入新模型的同时,通常并没有与之前的工作进行数据驱动的批判性比较,因此目前还不清楚哪种模型最适合任何特定应用。在这篇综述中,我们描述并比较了已发表的 73 个哺乳动物 I CaL 模型,并通过模拟实验表明,这些模型的预测结果存在很大的变异性,按物种或其他类别分组后,这种变异性并没有明显减弱。我们提供了 60 个模型的模型代码,列出了主要的数据来源,并讨论了为减少这一庞大的相互竞争的理论清单并最终开发出一个群体共识的 I CaL 模型所需的实验和建模工作。本文归类为心血管疾病 > 计算模型 心血管疾病 > 分子和细胞生理学。
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引用次数: 0
The cardiac wound healing response to myocardial infarction. 心肌梗死后心脏伤口愈合的反应。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1584
Upendra Chalise, Mediha Becirovic-Agic, Merry L Lindsey

Myocardial infarction (MI) is defined as evidence of myocardial necrosis consistent with prolonged ischemia. In response to MI, the myocardium undergoes a series of wound healing events that initiate inflammation and shift to anti-inflammation before transitioning to tissue repair that culminates in scar formation to replace the region of the necrotic myocardium. The overall response to MI is determined by two major steps, the first of which is the secretion of proteases by infiltrating leukocytes to breakdown extracellular matrix (ECM) components, a necessary step to remove necrotic cardiomyocytes. The second step is the generation of new ECM that comprises the scar; and this step is governed by the cardiac fibroblasts as the major source of new ECM synthesis. The leukocyte component resides in the middle of the two-step process, contributing to both sides as the leukocytes transition from pro-inflammatory to anti-inflammatory and reparative cell phenotypes. The balance between the two steps determines the final quantity and quality of scar formed, which in turn contributes to chronic outcomes following MI, including the progression to heart failure. This review will summarize our current knowledge regarding the cardiac wound healing response to MI, primarily focused on experimental models of MI in mice. This article is categorized under: Cardiovascular Diseases > Molecular and Cellular Physiology Immune System Diseases > Molecular and Cellular Physiology.

心肌梗死(MI)被定义为心肌坏死与长时间缺血一致的证据。心肌对心肌梗死的反应是,心肌经历一系列的伤口愈合事件,开始炎症并转变为抗炎症,然后过渡到组织修复,最终形成疤痕以取代坏死心肌区域。心肌梗死的总体反应由两个主要步骤决定,第一个步骤是通过浸润的白细胞分泌蛋白酶来分解细胞外基质(ECM)成分,这是去除坏死心肌细胞的必要步骤。第二步是生成新的ECM,包括疤痕;这个步骤是由心脏成纤维细胞控制的,它是新ECM合成的主要来源。白细胞成分位于两步过程的中间,在白细胞从促炎细胞表型向抗炎细胞表型和修复细胞表型转变的过程中,对两者都有贡献。这两个步骤之间的平衡决定了最终形成的疤痕的数量和质量,这反过来又有助于心肌梗死后的慢性结局,包括进展为心力衰竭。这篇综述将总结我们目前关于心肌梗死的心脏伤口愈合反应的知识,主要集中在小鼠心肌梗死的实验模型上。本文分类如下:心血管疾病>分子与细胞生理学>免疫系统疾病>分子与细胞生理学。
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引用次数: 6
Fluids and flows in brain cancer and neurological disorders. 脑癌和神经系统疾病的体液流动。
IF 3.1 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Pub Date : 2023-01-01 DOI: 10.1002/wsbm.1582
Peng Jin, Jennifer M Munson

Interstitial fluid (IF) and cerebrospinal fluid (CSF) are an integral part of the brain, serving to cushion and protect the brain parenchymal cells against damage and aid in their function. The brain IF contains various ions, nutrients, waste products, peptides, hormones, and neurotransmitters. IF moves primarily by pressure-dependent bulk flow through brain parenchyma, draining into the ventricular CSF. The brain ventricles and subarachnoid spaces are filled with CSF which circulates through the perivascular spaces. It also flows into the IF space regulated, in part, by aquaporin channels, removing waste solutes through a process of IF-CSF mixing. During disease development, the composition, flow, and volume of these fluids changes and can lead to brain cell dysfunction. With the improvement of imaging technology and the help of genomic profiling, more information has been and can be obtained from brain fluids; however, the role of CSF and IF in brain cancer and neurobiological disease is still limited. Here we outline recent advances of our knowledge of brain fluid flow in cancer and neurodegenerative disease based on our understanding of its dynamics and composition. This article is categorized under: Cancer > Biomedical Engineering Neurological Diseases > Biomedical Engineering.

间质液(IF)和脑脊液(CSF)是大脑不可分割的一部分,起到缓冲和保护脑实质细胞免受损伤的作用,并有助于它们的功能。脑中脑含有各种离子、营养物质、废物、多肽、激素和神经递质。脑脊液主要通过压力依赖的大流量通过脑实质,流入脑脊液。脑室和蛛网膜下腔充满脑脊液,脑脊液通过血管周围腔循环。它也流入中频空间,部分由水通道蛋白调节,通过中频-脑脊液混合过程去除废溶质。在疾病发展过程中,这些液体的组成、流量和体积发生变化,并可能导致脑细胞功能障碍。随着成像技术的进步和基因组图谱的帮助,已经可以从脑液中获得更多的信息;然而,CSF和IF在脑癌和神经生物学疾病中的作用仍然有限。在这里,我们概述了基于我们对其动力学和组成的理解,我们在癌症和神经退行性疾病中脑液流动的知识的最新进展。本文分类为:癌症>生物医学工程神经系统疾病>生物医学工程。
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引用次数: 2
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