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This is an Accepted Manuscript of an article published by Taylor & Francis Group in International Journal of Architectural Heritage on 2022, available online at: http://www.tandfonline.com/10.1080/15583058.2022.2096513 This paper presents the historical development of the vertical extensions of unreinforced masonry buildings in the Eixample district of Barcelona and their impact on the seismic behaviour. Existing masonry buildings of Eixample present significant seismic risk because, despite the low to moderate seismic hazard of Barcelona, they show a marked vulnerability given their average height of six storeys and the substantial slenderness of the walls. Between the end of the 19th century and the beginning of the 20th century, the vertical extensions, known as remuntes in Catalan, were a common solution to the increasing demographic demand of the city. In their majority, these vertical extensions add a structural irregularity that represents a potential vulnerability factor not yet investigated. The present study focuses on Eixample’s remuntes, including their historical development, the description of their structural features, and the identification of their most representative configurations in the existing building stock. A seismic analysis based on the Finite Element Method is presented on a reference model without extensions and three others with the most recurrent configurations of remuntes. The seismic response is investigated through pushover analysis. The results provide a better understanding of the negative impact of the vertical extensions on the seismic performance. This work was supported by the Ministry of Science, Innovation and Universities of the Spanish Government (MCIU) [RTI2018-099589-B-I00], the State Agency of Research (AEI) [RTI2018-099589-B-I00] and the European Regional Development Fund [RTI2018-099589-B-I00]; through the project SEVERUS (Multilevel evaluation of seismic vulnerability and risk mitigation of masonry buildings in resilient historical urban centres [RTI2018-099589-B-I00]; Agència de Gestió d'Ajuts Universitaris i de Recerca; MSc SAHC Consortium scholarship; Sapienza University of Rome.

Both experimental and theoretical studies on the microscale and fast physical phenomena occurring during the growth of vapor bubbles in nucleate pool boiling are reported. The focus is on the liquid film of micrometric thickness (``microlayer'') that can form between the heater and the liquid-vapor interface of a bubble on the millisecond time scale. The microlayer strongly affects the macroscale heat transfer and is thus important to be understood. It is shown that the microlayer can be seen as the Landau-Levich film deposited by the bubble foot edge during its receding when the bubble grows. The microlayer profile measured with white-light interferometry, the temperature distribution over the heater, and the bubble shape were observed with synchronized high-speed cameras. The microlayer consists of two regions: a ridge near the contact line followed by a longer and flatter part. The ridge could not be measured because of the intrinsic limitation of interferometry, which is analyzed. The simulations show that the ridge grows over time due to collection of liquid at contact line receding, the theoretical dynamics of which agrees with the experiment. The flatter part of the microlayer is bumped and its physical origin is explained.

The directed migration of cellular clusters enables morphogenesis, wound healing and collective cancer invasion. Gradients of substrate stiffness direct the migration of cellular clusters in a process called collective durotaxis, but the underlying mechanisms remain unclear. Here we unveil a connection between collective durotaxis and the wetting properties of cellular clusters. We show that clusters of cancer cells dewet soft substrates and wet stiff ones. At intermediate stiffness—at the crossover from low to high wettability—clusters on uniform-stiffness substrates become maximally motile, and clusters on stiffness gradients exhibit optimal durotaxis. Durotactic velocity increases with cluster size, stiffness gradient and actomyosin activity. We demonstrate this behaviour on substrates coated with the cell–cell adhesion protein E-cadherin and then establish its generality on substrates coated with extracellular matrix. We develop an active wetting model that explains collective durotaxis in terms of a balance between in-plane active traction and tissue contractility and out-of-plane surface tension. Finally, we show that the distribution of cluster displacements has a heavy tail, with infrequent but large cellular hops that contribute to durotactic migration. Our study demonstrates a physical mechanism of collective durotaxis, through both cell–cell and cell–substrate adhesion ligands, based on the wetting properties of active droplets., This paper was funded by the Generalitat de Catalunya (AGAUR SGR-2017-01602 to X.T., AGAUR SGR-2017-1061 to J.C., the CERCA Programme and ‘ICREA Academia’ awards to P.R.-C. and J.C.); the Spanish Ministry for Science and Innovation MICCINN/FEDER (PGC2018-099645-B-I00 to X.T., PID2019-110298GB-I00 to P.R.-C., PID2019-108842GB-C21 to J.C., RTI2018-101256-J-I00 and RYC2019-026721-I to R.S., FPU19/05492 to I.P.-J., FPU15/06516 to M.-E.P.); Fondo Social de la DGA (grupos DGA) to V.G. and J.M.d.l.F.; European Research Council (Adv-883739 to X.T.); Fundació la Marató de TV3 (project 201903-30-31-32 to X.T.); the European Commission (H2020-FETPROACT-01-2016-731957 to P.R.-C. and X.T.); the European Union’s Horizon 2020 research and innovation programme (under the Marie Skłodowska-Curie grant agreement no. 797621 to M.G.-G.); the European Foundation for the Study of Chronic Liver Failure (EF-Clif); and the La Caixa Foundation (LCF/PR/HR20/52400004 to P.R.-C. and X.T.). IBEC is the recipient of a Severo Ochoa Award of Excellence from MINECO. R.S. is a Serra Húnter fellow.

The mechanical properties of the extracellular matrix (ECM) determine cell differentiation, proliferation and migration through mechanoresponsive proteins including YAP. However, how different mechanical signals cooperate, synergize or compete to steer cell behavior remains poorly understood. Here, we have examined competition between the two major ECM mechanical cues, i.e. rigidity, which activates cell mechanosensing, and viscous energy dissipation, which reduces stiffness blunting cell mechanotransduction. To trigger competition, we have engineered protein hydrogels allowing concomitant modulation of stiffness and viscosity by mechanisms characteristic of native ECM. Culturing cells on these hydrogels, we have found that substrate energy dissipation attenuates YAP mechanosensing prevailing over stiffness cues. Hampered YAP activation on more dissipative substrates correlates with faster actin flow and smaller focal adhesions. Mechanistically, inhibition of actomyosin contractility reverses the outcome of the competition between rigidity and energy dissipation. Our results highlight the dominating contribution of substrate viscosity to the biology of the cell.

The term 'mechanosensation' describes the capacity of cells to translate mechanical stimuli into the coordinated regulation of intracellular signals, cellular function, gene expression and epigenetic programming. This capacity is related not only to the sensitivity of the cells to tissue motion, but also to the decryption of tissue geometric arrangement and mechanical properties. The cardiac stroma, composed of fibroblasts, has been historically considered a mechanically passive component of the heart. However, the latest research suggests that the mechanical functions of these cells are an active and necessary component of the developmental biology programme of the heart that is involved in myocardial growth and homeostasis, and a crucial determinant of cardiac repair and disease. In this Review, we discuss the general concept of cell mechanosensation and force generation as potent regulators in heart development and pathology, and describe the integration of mechanical and biohumoral pathways predisposing the heart to fibrosis and failure. Next, we address the use of 3D culture systems to integrate tissue mechanics to mimic cardiac remodelling. Finally, we highlight the potential of mechanotherapeutic strategies, including pharmacological treatment and device-mediated left ventricular unloading, to reverse remodelling in the failing heart.

This study addresses the evaluation of the confinement effect in the experimental determination of compressive strength in solid fired clay units. The experimental campaign has focused on two different types of solid fired clay bricks, namely mechanically extruded and handmade, with a total amount of 458 specimens. The research considers different standard specimens, such as whole or half brick, and 100 × 100 × 40 mm3 specimen, and nonstandard 40 × 40 × 40 mm3 specimen, subjected to different standard bearing surface treatments, i.e. grinding, capping with cement mortar or gypsum plaster, placing with birch plywood or fibreboard. Additionally, two novel bearing surface treatments are proposed, i.e. covering with gypsum powder, and placing two oiled PTFE leaves. The experimental campaign has focused on four main aspects. First, the evaluation of the compressive strength value in specimens with hardening response. Second, the influence of the cross section’s aspect ratio, defined as the ratio between the specimen’s length and width. Third, the influence of the bearing surface treatment on the determination of the compressive strength. Fourth, the evaluation of the standard compressive strength through the comparison amongst reference standards. The results highlight and quantify the different factors that influence the confinement, while detecting differences depending on the manufacturing process of the unit. In addition, the results reveal the use of oiled PTFE leaves as a promising and fast possibility of low boundary friction to obtain the strength regardless of the specimen shape. The authors gratefully acknowledge the financial support from the Ministry of Science, Innovation and Universities of the Spanish Government (MCIU), the State Agency of Research (AEI) as well as that of the ERDF (European Regional Development Fund) through the project SEVERUS (Multilevel evaluation of seismic vulnerability and risk mitigation of masonry buildings in resilient historical urban centres, ref. Num. RTI2018-099589-B-I00). Support from MCIU through a predoctoral grant awarded to the first author is also gratefully acknowledged.

Intestinal organoids capture essential features of the intestinal epithelium such as crypt folding, cellular compartmentalization and collective movements. Each of these processes and their coordination require patterned forces that are at present unknown. Here we map three-dimensional cellular forces in mouse intestinal organoids grown on soft hydrogels. We show that these organoids exhibit a non-monotonic stress distribution that defines mechanical and functional compartments. The stem cell compartment pushes the extracellular matrix and folds through apical constriction, whereas the transit amplifying zone pulls the extracellular matrix and elongates through basal constriction. The size of the stem cell compartment depends on the extracellular-matrix stiffness and endogenous cellular forces. Computational modelling reveals that crypt shape and force distribution rely on cell surface tensions following cortical actomyosin density. Finally, cells are pulled out of the crypt along a gradient of increasing tension. Our study unveils how patterned forces enable compartmentalization, folding and collective migration in the intestinal epithelium.

Cells sense and respond to the extracellular matrix (ECM) milieu through integrin proteins. Integrin availability on the plasma membrane, regulated by endosomal receptor uptake and recycling, has been extensively studied and regulates cell dynamics in various normal and pathological contexts1–5. In contrast, the role of integrin transport through the biosynthetic pathway has been considered primarily as a mechanism to replenish the receptor pool and too slow to influence cell dynamics6. Here, we adopted the RUSH (Retention Using Selective Hooks) assay to synchronize integrin anterograde transport from the endoplasmic reticulum (ER), allowing spatial and temporal analysis of newly synthesized receptor traffic. We observe that the delivery of new integrins to the plasma membrane is polarized in response to specific ECM ligands, facilitates integrin recruitment specifically to the membrane-proximal tip of focal adhesions (FA) and contributes to cell protrusion and FA growth. We explain the augmented adhesion growth using a computational molecular clutch model7, where increased integrin availability drives recruitment of additional integrins. Notably, a subset of newly synthesized integrins undergo rapid traffic from the ER to the cell surface to facilitate localized cell spreading, seemingly bypassing the Golgi. This unconventional secretion is dependent on cell adhesion and mediated by Golgi reassembling stacking proteins (GRASPs) association with the PDZ-binding motif in the integrin α5 cytoplasmic tail. This spatially targeted delivery of integrins through the biosynthetic pathway may propel cell dynamics by rapidly altering adhesion receptor availability, providing cells with an additional degree of plasticity to respond to their environment.

The function of organs such as lungs, kidneys and mammary glands relies on the three-dimensional geometry of their epithelium. To adopt shapes such as spheres, tubes and ellipsoids, epithelia generate mechanical stresses that are generally unknown. Here we engineered curved epithelial monolayers of controlled size and shape and mapped their state of stress. We designed pressurized epithelia with circular, rectangular and ellipsoidal footprints. We developed a computational method to map the stress tensor in these epithelia. This method establishes a direct correspondence between epithelial shape and mechanical stress without assumptions of material properties. In epithelia with spherical geometry spanning more than one order of magnitude in radius, we show that stress weakly increases with areal strain in a size-independent manner. In epithelia with rectangular and ellipsoidal cross-section we found pronounced stress anisotropies consistent with the asymmetric distribution of tractions measured at the cell-substrate contact line. In these anisotropic profiles, cell shape tended to align with the direction of maximum principal stress but this alignment was non-universal and depended on epithelial geometry. Besides interrogating the fundamental mechanics of epithelia over a broad range of sizes and shapes, our approach will enable a systematic study of how geometry and stress influence epithelial fate and function in three-dimensions.

The mechanical properties of the extracellular matrix (ECM) dictate tissue behaviour. In epithelial tissues, laminin is both a very abundant ECM component, and a key supporting element. Here we show that laminin hinders the mechanoresponses of breast epithelial cells by shielding the nucleus from mechanical deformation. Coating substrates with laminin-111, unlike fibronectin or collagen I, impairs cell response to substrate rigidity, and YAP nuclear localization. Blocking the laminin-specific integrin β4 increases nuclear YAP ratios in a rigidity dependent manner, without affecting cell forces or focal adhesions. By combining mechanical perturbations and mathematical modelling, we show that β4 integrins establish a mechanical linkage between the substrate and the keratin cytoskeleton, which stiffens the network and shields the nucleus from actomyosin-mediated mechanical deformation. In turn, this affects nuclear YAP mechanoresponses and chromatin methylation. Our results demonstrate a mechanism by which tissues can regulate their sensitivity to mechanical signals.

SummaryCircadian rhythms are a key survival mechanism that dictates biological activity according to the day-night cycle. In animals, cell-autonomous circadian clocks can be found in nearly every cell type and are subjected to multi-layered regulation. Although these peripheral clocks are remotely controlled by the master clock in the brain, they are also sensitive to their immediate mechano-chemical microenvironment. Whereas the mechanisms by which biochemical signalling controls the circadian clock at the single cell level are increasingly well understood, mechanisms underlying regulation by mechanical cues are still unknown. Here we show that the circadian clock in fibroblasts is regulated mechanically through YAP/TAZ and TEAD. We use high-throughput analysis of single-cell circadian rhythms and apply controlled mechanical, biochemical, and genetic perturbations to study the expression of the clock gene Rev-erbα. We observe that Rev-erbα circadian oscillations are disrupted concomitantly with the translocation of YAP/TAZ to the nucleus. By targeted mutations and tuning expression levels of YAP we identify TEAD as the transcriptional effector of this mechanosensitive regulatory pathway. Our findings establish a mechanism that links cell mechanobiology and the circadian clock, which could contribute to explain the circadian impairment observed in cancer and ageing, where the regulation of the mechanical environment and YAP/TAZ is lost.

International audience; Because of their innocuity, Au nanowires present an interesting field of applications in biology and, particularly, in cancer therapy. Since their morphology and distribution can greatly affect their performances, being able to control their mode of growth is important. Various elaboration techniques including “top-down” and “bottom-up” approaches have been developed. In this work, we propose an efficient maskless method to grow Au nanowires with the help of hydrogen plasma treatment of Au thin films. We have been able to grow Au nanowires by taking advantage of spinodal dewetting of an Au thin film and the supply of silicon radicals resulting from hydrogen plasma etching of amorphous silicon coating the walls of the reactor. A variety of techniques have been applied to study the microstructure and the optical properties of Au nanowires. A strong photothermal effect of Au nanowires has been demonstrated with the help of visible laser light. In order to study the nanowire growth, the transport of Au atoms is discussed, and a growth mechanism is proposed.

Secretory trafficking from the endoplasmic reticulum (ER) is subject to regulation by extrinsic and intrinsic factors. While much of the focus has been on biochemical triggers, little is known whether and how the ER is subject to regulation by mechanical signals. Here, we show that COPII-dependent ER-export is regulated by mechanical strain. Mechanotransduction to the ER was mediated via a previously unappreciated ER-localized pool of the small GTPase Rac1. Mechanistically, we show that Rac1 interacts with the small GTPase Sar1 to drive budding of COPII carriers and stimulate ER-to-Golgi transport. Altogether, we establish an unprecedented link between mechanical strain and export from the ER.

Modulated photoluminescence (MPL) is a powerful technique for determining the effective minority carrier lifetime (τeff) of semiconductor materials and devices. MPL is based on the measurement of phase shifts between two sinusoidal waves (minimal amplitude excitation; and PL signal). In particular, in situ τeff has been proven to be an effective measurement at showing changes within a plasma-enhanced chemical vapor deposition reactor during fabrication of c-Si solar cells. However, the required time for a single measurement, using the previous method, was 40 s. In this paper a new input signal is proposed, called Dolphin's Wave, providing a method for decreasing the required measurement period to under 2 s, using superposition, frequency sweeps, and wavelets.

We report on the growth of Sn-catalyzed GeSn nanowires (NWs) having a GeSn core and a c-Ge shell in the presence of germane plasma at substrate temperatures (TS) below the GeSn eutectic temperature (TE), containing an exceptional Sn concentration of 30 at. % in their core. The differences between the NWs produced at TS above and below TE of the GeSn alloy are highlighted. Two types of NW growth process are identified: the previously reported in-plane solid–liquid–solid (IPSLS) process for TS ≥ TE and a plasma-assisted IPSLS (PA-IPSLS) method taking place at TS < TE; the crucial role of plasma in providing the energy necessary to melt the Sn catalyst at substrate temperatures lower than TE is discussed. The thermal activation window for each method is determined. The PA-IPSLS process is shown to provide an efficient strategy for the growth of crystalline GeSn NWs with a high Sn incorporation in a growth duration of less than 3 min.

In and Sn are the type of catalysts which do not introduce deep level electrical defects within the bandgap of germanium (Ge). However, Ge nanowires produced using these catalysts usually have a large diameter, a tapered morphology, and mixed crystalline and amorphous phases. In this study, we show that plasma-assisted vapor–liquid–solid (PA-VLS) method can be used to synthesize Ge nanowires. Moreover, at certain parameter domains, the sidewall deposition issues of this synthesis method can be avoided and long, thin tapering-free monocrystalline Ge nanowires can be obtained with In and Sn catalysts. We find two quite different parameter domains where Ge nanowire growth can occur via PA-VLS using In and Sn catalysts: (i) a low temperature-low pressure domain, below ∼235 °C at a GeH4 partial pressure of ∼6 mTorr, where supersaturation in the catalyst occurs thanks to the low solubility of Ge in the catalysts, and (ii) a high temperature-high pressure domain, at ∼400 °C and a GeH4 partial pressure above ∼20 mTorr, where supersaturation occurs thanks to the high GeH4 concentration. While growth at 235 °C results in tapered short wires, operating at 400 °C enables cylindrical nanowire growth. With the increase of growth temperature, the crystalline structure of the nanowires changes from multi-crystalline to mono-crystalline and their growth rate increases from ∼0.3 nm s−1 to 5 nm s−1. The cylindrical Ge nanowires grown at 400°C usually have a length of few microns and a radius of around 10 nm, which is well below the Bohr exciton radius in bulk Ge (24.3 nm). To explain the growth mechanism, a detailed growth model based on the key chemical reactions is provided.

Blood vessel formation generates unique vascular patterns in each individual. The principles governing the apparent stochasticity of this process remain to be elucidated. Using mathematical methods, we find that the transition between two fundamental vascular morphogenetic programs – sprouting angiogenesis and vascular remodeling – is established by a shift on collective front-rear polarity of endothelial cells. We demonstrate that the competition between biochemical (VEGFA) and mechanical (blood flow-induced shear stress) cues controls this collective polarity shift. Shear stress increases tension at focal adhesions overriding VEGFA-driven collective polarization, which relies on tension at adherens junctions. We propose that vascular morphogenetic cues compete to regulate individual cell polarity and migration through tension shifts that translates into tissue-level emergent behaviors, ultimately leading to uniquely organized vascular patterns.

Hydrogenated microcrystalline silicon (µc-Si:H) and epitaxial silicon (epi-Si) films have been produced from SiF4, H2 and Ar mixtures by plasma enhanced chemical vapor deposition (PECVD) at 200 °C. Here, both films were produced using identical deposition conditions, to determine if the conditions for producing µc-Si with the largest crystalline fraction (XC), will also result in epi-Si films that encompass the best quality and largest crystalline silicon (c-Si) fraction. Both characteristics are of importance for the development of thin film transistors (TFTs), thin film solar cells and novel 3D devices since epi-Si films can be grown or etched in a selective manner. Therefore, we have distinguished that the H2/SiF4 ratio affects the XC of µc-Si, the c-Si fraction in epi-Si films, and the structure of the epi-Si/c-Si interface. Raman and UV-Vis ellipsometry were used to evaluate the crystalline volume fraction (Xc) and composition of the deposited layers, while the structure of the films were inspected by high resolution transmission electron microscopy (HRTEM). Notably, the conditions for producing µc-Si with the largest XC are different in comparison to the fabrication conditions of epi-Si films with the best quality and largest c-Si fraction.

Cell nuclei are submitted to mechanical forces, which in turn affect nuclear and cell functions. Recent evidence shows that a crucial mechanically regulated nuclear function is nucleocytoplasmic transport, mediated by nuclear pore complexes (NPCs). Mechanical regulation occurs at two levels: first, by force application to the nucleus, which increases NPC permeability likely through NPC stretch. Second, by the mechanical properties of the transported proteins themselves, as mechanically labile proteins translocate through NPCs faster than mechanically stiff ones. In this perspective, we discuss this evidence and the associated mechanisms by which mechanics can regulate the nucleo-cytoplasmic partitioning of proteins. Finally, we analyze how mechanical regulation of nucleocytoplasmic transport can provide a systematic approach to the study of mechanobiology and open new avenues both in fundamental and applied research.

Invasive lobular breast carcinoma (ILC) is characterized by proliferative indolence and long-term latency relapses. This study aimed to identify how disseminating ILC cells control the balance between quiescence and cell cycle re-entry. In the absence of anchorage, ILC cells undergo a sustained cell cycle arrest in G0/G1 while maintaining viability. From the genes that are upregulated in anchorage independent ILC cells, we selected Inhibitor of DNA binding 2 (Id2), a mediator of cell cycle progression. Using loss-of-function experiments, we demonstrate that Id2 is essential for anchorage independent survival (anoikis resistance) in vitro and lung colonization in mice. Importantly, we find that under anchorage independent conditions, E-cadherin loss promotes expression of Id2 in multiple mouse and (organotypic) human models of ILC, an event that is caused by a direct p120-catenin/Kaiso-dependent transcriptional de-repression of the canonical Kaiso binding sequence TCCTGCNA. Conversely, stable inducible restoration of E-cadherin expression in the ILC cell line SUM44PE inhibits Id2 expression and anoikis resistance. We show evidence that Id2 accumulates in the cytosol, where it induces a sustained and CDK4/6-dependent G0/G1 cell cycle arrest through interaction with hypo-phosphorylated Rb. Finally, we find that Id2 is indeed enriched in ILC when compared to other breast cancers, and confirm cytosolic Id2 protein expression in primary ILC samples. In sum, we have linked mutational inactivation of E-cadherin to direct inhibition of cell cycle progression. Our work indicates that loss of E-cadherin and subsequent expression of Id2 drive indolence and dissemination of ILC. As such, E-cadherin and Id2 are promising candidates to stratify low and intermediate grade invasive breast cancers for the use of clinical cell cycle intervention drugs.

As cells migrate and experience forces from their surroundings, they constantly undergo mechanical deformations which reshape their plasma membrane (PM). To maintain homeostasis, cells need to detect and restore such changes, not only in terms of overall PM area and tension as previously described, but also in terms of local, nano-scale topography. Here we describe a novel phenomenon, by which cells sense and restore mechanically induced PM nano-scale deformations. We show that cell stretch and subsequent compression reshape the PM in a way that generates local membrane evaginations in the 100 nm scale. These evaginations are recognized by the I-BAR protein IRSp53, which triggers a burst of actin polymerization mediated by Rac1 and Arp2/3. The actin polymerization burst subsequently re-flattens the evagination, completing the mechanochemical feedback loop. Our results demonstrate a new mechanosensing mechanism for PM shape homeostasis, with potential applicability in different physiological scenarios.TeaserCell stretch cycles generate PM evaginations of ≈100 nm which are sensed by IRSp53, triggering a local event of actin polymerization that flattens and recovers PM shape.

SUMMARYAdherens junctions allow cell contact to inhibit epithelial migration. But a long-standing puzzle is how locomotion is downregulated when E-cadherin adhesions form at surfaces perpendicular, but not those parallel, to the direction of migration. We now show that this arises from coupling between E-cadherin adhesions and the retrograde cortical flows of leader cells in migrating epithelia. At interfaces perpendicular to the direction of motion, such flows are antiparallel, which generates a tensile signal that induces the actin-binding domain of α-catenin to promote lateral growth of nascent adhesions and inhibit the lamellipodial activity necessary for migration. At interfaces parallel to the direction of motion, by contrast, cortical flows are aligned and no such mechanical inhibition takes place. Therefore, α-catenin mechanosensitivity in the clutch between E-cadherin and cortical F-actin allows cells to interpret the direction of motion via cortical flows and trigger the first signal for contact to inhibit locomotion.

Mechanical force controls fundamental cellular processes in health and disease, and increasing evidence shows that the nucleus both experiences and senses applied forces. Here we show that nuclear forces differentially control passive and facilitated nucleocytoplasmic transport, setting the rules for the mechanosensitivity of shuttling proteins. We demonstrate that nuclear force increases permeability across nuclear pore complexes, with a dependence on molecular weight that is stronger for passive than facilitated diffusion. Due to this differential effect, force leads to the translocation into or out of the nucleus of cargoes within a given range of molecular weight and affinity for nuclear transport receptors. Further, we show that the mechanosensitivity of several transcriptional regulators can be both explained by this mechanism, and engineered exogenously by introducing appropriate nuclear localization signals. Our work sets a novel framework to understand mechanically induced signalling, with potential general applicability across signalling pathways and pathophysiological scenarios.One sentence summaryForce application to the nucleus leads to nuclear accumulation of proteins by differentially affecting passive versus facilitated nucleocytoplasmic transport.

We present results from the application of a novel, contactless patterning technique to form the doped fingers required for interdigitated back contact silicon heterojunction (IBC-SHJ) solar cells. The technique involves patterning the RF powered electrode in a custom-designed RF-PECVD chamber. The patterned powered electrode – which has 1 mm wide opening-slits in it - is brought in close proximity to the substrate surface, to localize the plasma and the process it performs. In this work, the localized plasma process being employed is an NF3/Ar etching, and is used to form doped fingers that are sub-mm wide and 60 mm long. The interdigitated structure (alternating electron and hole collection zones) is created by first uniformly depositing an intrinsic/n-type a-Si:H passivation stack, followed by an n-type/p-type µc-Si:H recombination junction on the rear side. A passivation layer is also deposited on the front side. The regions for the hole collection zones are then etched down to the intrinsic a-Si:H layer, and finally, a uniform p-type a-Si:H layer is deposited everywhere. The etched finger areas are first investigated by profilometry and spectroscopic ellipsometry, showing that the process can be controlled to leave as little as a few nanometers of passivating intrinsic a-Si:H. This fine control is achieved by pulsing the plasma, to slow the etching rate to a few A/s. To evaluate the detailed opto-electronic properties of the structure, the samples are mapped out using two contactless techniques: Photoluminescence and Surface Photovoltage measurements (done with a macroscopic scanning Kelvin probe performed under dark and illuminated conditions). These measurements enable one to see both zones of degraded passivation, and the effectiveness of the doped regions in generating an open circuit voltage under illumination.

In this work, we report the same trends for the contact potential difference measured by Kelvin probe force microscopy and the effective carrier lifetime on crystalline silicon (c-Si) wafers passivated by AlOx layers of different thicknesses and submitted to annealing under various conditions. The changes in contact potential difference values and in the effective carrier lifetimes of the wafers are discussed in view of structural changes of the c-Si/SiO2/AlOx interface thanks to high resolution transmission electron microscopy. Indeed, we observed the presence of a crystalline silicon oxide interfacial layer in as-deposited (200 °C) AlOx, and a phase transformation from crystalline to amorphous silicon oxide when they were annealed in vacuum at 300 °C.

Flexibility and power-to-weight (PTW) ratio are the key factors for promoting wearable or portable solar cell applications. Planar hydrogenated amorphous silicon (a-Si:H) thin films deposited directly on soft aluminum foils (AF) are usually subject to easy cracking and delamination due to the mechanical instability on AF surface. Here, an exceptionally robust three-dimensional (3D) construction of a-Si:H radial p-i-n junction solar cells on soft supermarket-available AF of 15 µm thick is reported, where the discrete and firmly standing Si nanowire (SiNW) cores, grown and rooted on the soft AF surface, frame up a 3D architecture that protects the protrusive photo-active radial junctions from the unstable a-Si/Al bottom layer. An excellent flexibility and integrity of the 3D a-Si:H radial junctions have been achieved, even under bending to radius of 5 mm. Remarkably, without any diffusion barrier protection, a power conversion efficiency of 5.6% has been recorded, with an open-circuit voltage of 0.71 V and photo-current density of 14.2 mA/cm2, leading to a high PTW ratio of > 1300 W/kg. Importantly, the overall fabrication cost can be largely slashed off, by ~46% compared to conventional a-Si:H solar cells, as the need for a bottom TCO contact/texturing layer, for a back-reflection coating and for a glass/polymer substrate are all exempted.

Alloying Ge with Sn is one of the promising ways for achieving Si compatible optoelectronics. Here, GeSn nanowires (NWs) are realized via nano-crystallization of a hydrogenated amorphous Ge (a-Ge:H) layer with the help of metal Sn droplets. The full process consists of three steps: (1) SnO

Two methods specifically designed for the analysis of masonry arch bridges - the Cardiff Energy Method and the Non-linear Generalised Matrix Formulation - are presented and discussed with regard to their ability to simulate the ultimate response of several different experiments carried out on arch bridges. Both methods are intended to provide versatile tools of analysis, well adapted to the ultimate analysis of masonry constructions, but requiring very moderate computer resources. (A) For the covering abstract, see IRRD E100543.