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Electric-field manipulation of giant vesicles: new frontiers in membrane electromechanics. 巨大囊泡的电场操纵:膜电力学的新前沿。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-09-30 DOI: 10.1007/s00249-026-01869-w
Rumiana Dimova, Elias Sabri

Giant unilamellar vesicles (GUVs) are a powerful model system whose response to electric fields constitutes a strategy to directly assess membrane material properties. In the last few years, the field has advanced in both conceptual scope and experimental precision. Electric-field manipulation of GUVs remains a versatile platform for extracting membrane mechanical, electrical, and rheological properties with single-vesicle resolution, while increasingly extending from a diagnostic tool into an actuation mechanism. Here, we summarize classical electrodeformation and electroporation methodologies and review recent developments that push these approaches toward greater biological realism, including compound vesicles as nucleate-cell mimics, resting-membrane-potential- and ion-dependent poration, phase-transition electromechanics, and cytoskeleton-loaded, field-responsive membranes. We also discuss how electric fields are combined with other stimuli, such as light and biochemical cues, and repurposed to drive active, motile vesicle assemblies and to fabricate tailored lipid architectures at high throughput. We further highlight theoretical work on electromechanical coupling, membrane charging dynamics, and vesicle shape landscapes under electric stress. We close by outlining remaining challenges, from reproducibility across preparation protocols to bridging model membranes and living cells, and future opportunities for automated, high-throughput, and multimodal electromechanical studies of biomimetic membranes.

巨型单层囊泡(GUVs)是一个强大的模型系统,其对电场的响应构成了直接评估膜材料性能的策略。在过去几年中,该领域在概念范围和实验精度方面都取得了进展。电场操作的guv仍然是一个通用的平台,用于提取膜的力学、电学和流变性能,同时越来越多地从诊断工具扩展到驱动机制。在这里,我们总结了经典的电变形和电穿孔方法,并回顾了将这些方法推向更大生物学现实的最新进展,包括作为核细胞模拟物的复合囊泡、静止膜电位和离子依赖的穿孔、相变电力学和细胞骨架负载、场响应膜。我们还讨论了电场如何与其他刺激(如光和生化信号)相结合,并重新用于驱动活跃的、可移动的囊泡组装,并以高通量制造量身定制的脂质结构。我们进一步强调了在电应力下机电耦合、膜充电动力学和囊泡形状景观的理论研究。最后,我们概述了仍然存在的挑战,从制备方案的可重复性到桥接模型膜和活细胞,以及仿生膜自动化、高通量和多模态机电研究的未来机会。
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引用次数: 0
A hydrophobic vector association model of nucleosomes in chromatin. 核小体在染色质中的疏水载体关联模型。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-09-25 DOI: 10.1007/s00249-026-01863-2
Ángel Mozo-Villarías, Enrique Querol, Juan A Cedano

The structure of chromatin and its association mechanisms are studied using the biological membrane (BM) model with a formalism of electric and hydrophobic dipole interactions. This model establishes that hydrophobic moments attract each other, associating in parallel in a manner analogous to how phospholipids associate to form a biological membrane. The structure of DNA is reviewed as the stacking of the hydrophobic dipole moments of its bases in relation to their separation distances. Archaeal chromatin is revisited, which is associated with a structure resembling a continuous coil of DNA, in which each turn contains three protohistone dimers hydrophobically attached to it. A description follows of the hydrophobic association of histones H2A, H2B, H3, and H4, forming the well-known octamer, and its binding to two DNA strands that constitute the nucleosome. This association is nuanced with electrostatic interactions, highlighting the fundamental role of hydrophobic interactions. Simulated alternative forms of histone association are compared, and it is confirmed that the structure present in the nucleosome is the most energetically stable. This type of interaction is also the basis of the hydrophobic association mechanisms of nucleosome stacking, by the parallel alignment of their hydrophobic dipole moments. These associations in parallel stacks have variable strengths, depending on their specific sequence compositions. Also the role of histone H1 and linker DNAs is addressed in its mechanisms of joining the extensions of nucleosomal DNA to join another nucleosome.

利用具有电疏水偶极子相互作用形式的生物膜(BM)模型研究了染色质的结构及其关联机制。该模型建立了疏水时刻相互吸引,以类似磷脂结合形成生物膜的方式平行结合。DNA的结构被认为是其碱基的疏水偶极矩与它们的分离距离的关系。古菌染色质被重新审视,它与一个类似于DNA连续线圈的结构有关,其中每转包含三个疏水连接的原组蛋白二聚体。下面描述了组蛋白H2A、H2B、H3和H4的疏水结合,形成了众所周知的八聚体,并与构成核小体的两条DNA链结合。这种关联与静电相互作用微妙,突出了疏水相互作用的基本作用。模拟替代形式的组蛋白结合进行比较,并证实,核小体存在的结构是最稳定的能量。这种类型的相互作用也是核小体堆叠的疏水结合机制的基础,通过它们的疏水偶极矩的平行排列。这些关联在并行堆栈中有不同的强度,这取决于它们特定的序列组成。此外,组蛋白H1和连接体DNA的作用在其连接核小体DNA延伸连接另一个核小体的机制中得到了解决。
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引用次数: 0
Biophysics Austria: from molecular mechanisms to complex biological systems 奥地利生物物理学:从分子机制到复杂的生物系统。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-09-25 DOI: 10.1007/s00249-026-01868-x
Elena E. Pohl, Thomas Stockner
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引用次数: 0
Biophysics Austria: 65 years history 奥地利生物物理学:65年的历史。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-09-22 DOI: 10.1007/s00249-026-01866-z
Elena E. Pohl, Klaus Groschner

The Austrian Biophysical Society (Biophysics Austria) was founded in 1961, making it one of the oldest national biophysical societies in Europe. It hosted the first European Meeting in Biophysics in Baden near Vienna in 1971 and celebrated its 60th anniversary by hosting the 13th European Biophysics Congress in Vienna as a hybrid event during the COVID-19 pandemic in 2021. In 2026, the society is celebrating its 65th anniversary. This review reflects on the society´s history and highlights events, milestones, and people who have contributed to its development.

奥地利生物物理学会(Biophysics Austria)成立于1961年,是欧洲最古老的国家生物物理学会之一。1971年在维也纳附近的巴登举办了第一届欧洲生物物理学大会,并于2021年在维也纳举办了第13届欧洲生物物理学大会,作为混合活动庆祝了60周年。2026年,该协会将庆祝成立65周年。这篇评论反映了社会的历史,突出了对社会发展做出贡献的事件、里程碑和人物。
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引用次数: 0
BIF-1 expression in human cancers: roles in apoptosis, autophagy, and therapeutic potential. BIF-1在人类癌症中的表达:在细胞凋亡、自噬和治疗潜力中的作用
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-09-18 DOI: 10.1007/s00249-026-01867-y
Hasti Rahimi, Fatemeh Dehghani, Mahta Rabani, Fatemeh Shafiee

Bax-interacting factor-1 (BIF-1), also known as endophilin B1 (SH3GLB1), is a membrane-associated protein involved in apoptosis, autophagy, and membrane dynamics. There is growing evidence of a context-dependent role in tumor biology, mainly associated with tumor-suppressive functions in several cancers. In this narrative review, we summarize current evidence regarding BIF-1 expression patterns and its functional relevance in cancer-related pathways. Downregulation of BIF-1 has been consistently reported in melanoma, breast cancer, prostate cancer, gastric carcinoma, colorectal cancer, urinary bladder cancer and gallbladder cancer, where reduced expression is associated with impaired apoptosis, altered autophagy and tumor progression, supporting its potential value as a tumor suppressor-associated biomarker. On the other hand, hepatocellular carcinoma shows a context-dependent expression pattern and inconsistent associations with clinical outcomes. Its clinical utility in these tumors is limited because diagnostic and prognostic significance has not been consistently demonstrated. Therapeutic studies suggest that modulation of BIF-1-related pathways could influence autophagy, apoptosis and cellular metabolism, implying indirect participation in cancer treatment strategies. In general, BIF-1 seems to be a potential biomarker linked to tumor suppression in various epithelial cancers, especially in melanoma, breast, and prostate cancers. However, it's clinical utility remains limited or appears variable in pancreatic ductal adenocarcinoma and Merkel cell carcinoma. These findings highlight the context-dependent role of BIF-1 in tumor biology.

bax相互作用因子-1 (BIF-1),也被称为嗜内肽B1 (SH3GLB1),是一种参与细胞凋亡、自噬和膜动力学的膜相关蛋白。越来越多的证据表明,在肿瘤生物学中,环境依赖的作用主要与几种癌症的肿瘤抑制功能有关。在这篇叙述性综述中,我们总结了目前关于BIF-1表达模式及其在癌症相关途径中的功能相关性的证据。BIF-1的下调已在黑色素瘤、乳腺癌、前列腺癌、胃癌、结直肠癌、膀胱癌和胆囊癌中得到持续报道,其中表达下调与细胞凋亡受损、自噬改变和肿瘤进展有关,支持其作为肿瘤抑制相关生物标志物的潜在价值。另一方面,肝细胞癌表现出上下文依赖的表达模式,与临床结果的关联不一致。它在这些肿瘤中的临床应用是有限的,因为诊断和预后的意义尚未得到一致的证明。治疗研究表明,bif -1相关通路的调节可以影响自噬、凋亡和细胞代谢,暗示间接参与癌症治疗策略。总的来说,BIF-1似乎是一种潜在的生物标志物,与各种上皮癌,特别是黑色素瘤、乳腺癌和前列腺癌的肿瘤抑制有关。然而,它在胰腺导管腺癌和默克尔细胞癌中的临床应用仍然有限或出现变化。这些发现强调了BIF-1在肿瘤生物学中的环境依赖性作用。
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引用次数: 0
Beyond stiffness: interfacial slippage and active cellular matrix remodelling in focal adhesion dynamics. 超越刚度:界面滑移和活跃的细胞基质重塑焦点粘附动力学。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-09-15 DOI: 10.1007/s00249-026-01864-1
Ivana Pajic-Lijakovic, Milan Milivojevic, Boris Martinac, Massimo Vassalli, Peter V E McClintock

Focal adhesion (FA) dynamics and cell migration depend sensitively on the mechanical properties of the extracellular matrix, yet substrate stiffness alone cannot account for the distinct behaviours observed on natural versus artificial materials. In this review, we synthesize experimental findings on cells interacting with collagen I matrices and viscoelastic hydrogels, and identify the key physical mechanisms that govern adhesion stability, turnover, and migratory efficiency. Collagen I substrates are characterized by structural anisotropy, spatial heterogeneity, and a broad spectrum of relaxation times, in contrast to the simplified and often isotropic response of artificial hydrogels. Based on these observations, we highlight the central role of interfacial slippage at the FA-substrate biointerface enabled by matrix remodelling and multi-timescale viscoelastic dissipation. We further discuss how cell-generated forces can induce collagen reorganization and surface tension gradients, potentially driving Marangoni-like flows that contribute to dynamic matrix redistribution. These processes collectively maintain adhesions in a state between stabilization and turnover, favourable for persistent migration. Finally, we consider the interplay between these mechanical mechanisms and mechanosensitive signalling, particularly involving Piezo1 ion channels. This perspective emphasizes that effective cell-matrix coupling arises from the ability of the substrate to dissipate and reorganize distribution of mechanical energy, rather than from stiffness alone.

焦点黏附(FA)动力学和细胞迁移敏感地依赖于细胞外基质的机械特性,但基体刚度本身不能解释在天然材料和人工材料上观察到的不同行为。在这篇综述中,我们综合了细胞与胶原I基质和粘弹性水凝胶相互作用的实验结果,并确定了控制粘附稳定性,周转和迁移效率的关键物理机制。胶原I底物具有结构各向异性、空间异质性和广谱弛豫时间的特点,与人工水凝胶的简化和各向同性反应形成鲜明对比。基于这些观察结果,我们强调了通过基质重塑和多时间尺度粘弹性耗散实现的FA-substrate生物界面界面滑移的核心作用。我们进一步讨论了细胞产生的力如何诱导胶原蛋白重组和表面张力梯度,潜在地驱动有助于动态基质再分配的马兰戈尼样流动。这些过程共同维持黏附在稳定和周转之间的状态,有利于持续迁移。最后,我们考虑了这些机械机制和机械敏感信号之间的相互作用,特别是涉及压电离子通道。这种观点强调,有效的细胞-基质耦合源于基底耗散和重组机械能分布的能力,而不仅仅是刚度。
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引用次数: 0
vascr: An R-based toolkit for rapid and robust analysis of cellular impedance sensing data. vascr:一个基于r的工具包,用于快速和稳健地分析细胞阻抗传感数据。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-08-18 DOI: 10.1007/s00249-026-01852-5
James J W Hucklesby, Charles P Unsworth, E Scott Graham, Catherine E Angel

Electrical impedance sensing offers a powerful, non-invasive method for real-time monitoring of cellular behaviour; with applications spanning immunology, cancer biology and drug discovery. Adoption of impedance-sensing approaches has been accelerated by the commercial availability of the ECIS, xCELLigence, ScioSpec and cellZscope platforms; however, the complexity and volume of impedance datasets produced has limited rigorous analysis. vascr, an open-source R-based toolkit designed to streamline the processing of impedance sensing datasets was created to facilitate rapid and simplified handling of cellular impedance sensing data. vascr can import multi-frequency data from multiple instrument manufacturers and includes robust analysis tools for resampling, outlier detection, and statistical testing using ANOVA and cross-correlation. Using the vascr workflow, impedance sensing data can be rapidly and robustly interpreted, allowing for real-time investigation of the effects of biological agents on cellular processes such as endothelial barrier integrity.

电阻抗传感为实时监测细胞行为提供了一种强大的非侵入性方法;其应用跨越免疫学,癌症生物学和药物发现。ECIS、xCELLigence、ScioSpec和cellZscope平台的商业可用性加速了阻抗传感方法的采用;然而,产生的阻抗数据集的复杂性和数量限制了严格的分析。vascr是一个基于r的开源工具包,旨在简化阻抗传感数据集的处理,以促进快速和简化蜂窝阻抗传感数据的处理。vascr可以从多个仪器制造商导入多频率数据,并包括强大的分析工具,用于重新采样,离群值检测和使用方差分析和相互关联的统计测试。使用vascr工作流,阻抗传感数据可以快速、可靠地解释,从而可以实时研究生物制剂对细胞过程(如内皮屏障完整性)的影响。
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引用次数: 0
Proton wave propagation along collagen fibers 质子波沿胶原纤维传播。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-07-29 DOI: 10.1007/s00249-026-01856-1
Pedro Costa, Anna Maznichenko, Noam Agmon, Peter Pohl

Collagen deposition and alignment in the tumor stroma stiffen the extracellular matrix and, via integrin signaling, stimulate proton extrusion by cancer cells. In aggressive tumors, migration occurs preferentially along aligned collagen fibers, where proton efflux at the leading edge acidifies and degrades the matrix to facilitate invasion. Whether directional proton diffusion along collagen fibers exacerbates invasion remains uncertain, as it is not known how far protons can travel along a fiber before being released. To characterize the release barrier, we labeled collagen lysine side chains with a pH-sensitive fluorescein derivative and introduced an interfacial proton flux by microinjecting HCl near the surface of self-assembled collagen fibers elevated above the chamber bottom. Proton wave propagation was monitored by wide-field fluorescence microscopy. Quantitative analysis of the fluorescence transients revealed that proton migration is best described by a one-dimensional diffusion model with a finite surface-to-bulk release rate. A single global parameter set consistently described all experiments. From the fitted release rate, we determined a Gibbs activation energy barrier ΔG‡ of approximately 30 kBT, comparable to values reported for membrane–water interfaces. These results demonstrate that protons can travel tens of micrometers along collagen fibers before equilibrating with the bulk solution, suggesting that membrane-anchored collagen fibers may provide an effective pathway for directing acidification along migration tracks in tumor stroma.

肿瘤基质中的胶原沉积和排列使细胞外基质硬化,并通过整合素信号传导刺激癌细胞的质子挤压。在侵袭性肿瘤中,迁移优先沿着排列的胶原纤维发生,其中前缘的质子外排使基质酸化和降解,从而促进侵袭。质子沿着胶原纤维的定向扩散是否会加剧胶原纤维的侵袭仍不确定,因为不知道质子在被释放之前可以沿着纤维传播多远。为了表征释放屏障,我们用ph敏感的荧光素衍生物标记胶原赖氨酸侧链,并通过微注射HCl在腔室底部上方自组装胶原纤维表面附近引入界面质子通量。用宽视场荧光显微镜监测质子波的传播。荧光瞬态的定量分析表明,质子迁移是最好的描述一维扩散模型具有有限的表面到体释放率。单一全局参数集一致地描述了所有实验。根据拟合的释放速率,我们确定了吉布斯活化能势垒ΔG‡约为30 kBT,与报道的膜-水界面值相当。这些结果表明,质子可以沿着胶原纤维行进数十微米,然后与大量溶液平衡,这表明膜锚定的胶原纤维可能为肿瘤基质中沿迁移轨迹指导酸化提供了有效途径。
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引用次数: 0
Stochastic models for cell polarization and crawling: journey from external fluctuations in reaction-diffusion system to internal noise effects. 细胞极化和爬行的随机模型:从反应扩散系统的外部波动到内部噪声效应的历程。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-07-27 DOI: 10.1007/s00249-026-01858-z
Badamasi Bashir Mikailu, Cristina Montañola-Sales, Laureano Ramírez-Piscina, Sergio Alonso

The plasma membrane hosts a diverse set of proteins whose attachment, detachment, and lateral diffusion give rise to complex spatiotemporal patterns that regulate essential cellular processes. In motile eukaryotic cells, localized protein patterns at the membrane control actin organization and thereby establish a front-rear axis that drives locomotion. While persistent migration following a chemotactic signal can be captured by deterministic reaction-diffusion models coupled to a phase-field description of cell shape, amoeboid motion in cells such as neutrophils and Dictyostelium discoideum is markedly more irregular and requires the inclusion of stochastic effects. Existing modeling approaches typically introduce external noise into pattern-forming mechanisms or, alternatively, although much less frequently, they account for intrinsic fluctuations arising from the small number of participating molecules. Here, we compare and connect these two complementary modeling strategies for membrane protein dynamics driving cell locomotion in Dictyostelium discoideum. We present a stochastic reaction-diffusion model coupled to a phase field, previously calibrated to experimental data, alongside a related formulation in which fluctuations emerge intrinsically from molecular discreteness. Through systematic numerical simulations, we characterize the resulting membrane patterns and dynamical behaviors. Our results test the hypothesis that externally imposed fluctuations can be effectively reduced to intrinsic noise derived from first principles. We highlight the critical role of temporal correlation, a key feature of the original phenomenological formulation, and contrast it with the behavior of internal fluctuations. Finally, we discuss the relative strengths, differences, and physical limitations of both stochastic approaches.

质膜承载着多种蛋白质,它们的附着、分离和侧向扩散产生了复杂的时空模式,调节着基本的细胞过程。在可运动的真核细胞中,膜上的局部蛋白模式控制肌动蛋白组织,从而建立一个驱动运动的前后轴。虽然趋化信号后的持续迁移可以通过确定性反应扩散模型与细胞形状的相场描述相结合来捕捉,但中性粒细胞和盘状盘状肌等细胞中的变形虫运动明显更加不规则,需要包含随机效应。现有的建模方法通常将外部噪声引入模式形成机制,或者,尽管频率要低得多,但它们可以解释由少量参与分子引起的内在波动。在此,我们比较并连接了这两种互补的膜蛋白动力学建模策略,以驱动盘状盘齿龙的细胞运动。我们提出了一个与相场耦合的随机反应扩散模型,该模型先前已校准为实验数据,以及一个相关的公式,其中波动本质上来自分子离散性。通过系统的数值模拟,我们描述了所得到的膜模式和动力学行为。我们的结果验证了一个假设,即外部施加的波动可以有效地减少为来自第一性原理的固有噪声。我们强调了时间相关性的关键作用,这是原始现象学公式的一个关键特征,并将其与内部波动的行为进行了对比。最后,我们讨论了两种随机方法的相对优势、差异和物理限制。
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引用次数: 0
Clustering of the T-cell receptor complex may facilitate T-cell activation by stretching of CD3(zeta) cytoplasmic tails t细胞受体复合体的聚集可能通过伸展CD3ζ细胞质尾部来促进t细胞的激活。
IF 2.3 4区 生物学 Q3 BIOPHYSICS Pub Date : 2026-07-27 DOI: 10.1007/s00249-026-01861-4
Steven Siegl, Sebastian Fürthauer, Gerhard J. Schütz

Motivated by experimental observations that T-cells can activate as a consequence of clustering of T-cell receptors, we hypothesize that steric confinement between the intracellular chains of the TCR could play a role. Using coarse-grained simulations, we show that steric interactions between TCRs are sufficient to induce appreciable stretch of the intracellular domains of CD3(zeta) chains. We propose a model, in which the difference in membrane distances between the phosphatase CD45 and the kinases lck and fyn is able to sense the clustering-induced CD3(zeta) stretch: we estimate a 1.5- to 2-fold increase in phosphorylation of immunoreceptor tyrosine-based activation motifs (ITAMs) at CD3(zeta) upon TCR clustering.

根据实验观察,t细胞可以作为t细胞受体聚集的结果而激活,我们假设TCR细胞内链之间的空间限制可能起作用。使用粗粒度模拟,我们表明,tcr之间的空间相互作用足以诱导CD3ζ链的胞内结构域的明显拉伸。我们提出了一个模型,在这个模型中,CD45和激酶之间的膜距离差异能够感知聚类诱导的CD3ζ拉伸:我们估计在TCR聚类时,CD3ζ上免疫受体酪氨酸基激活基(ITAMs)的磷酸化增加了1.5到2倍。
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引用次数: 0
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European Biophysics Journal
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