Interfaces often dictate heat flow in micro- and nanostructured systems. However, despite the growing importance of thermal management in micro- and nanoscale devices, a unified understanding of the atomic-scale structural features contributing to interfacial heat transport does not exist. Herein, we experimentally demonstrate a link between interfacial bonding character and thermal conductance at the atomic level. Our experimental system consists of a gold film transfer-printed to a self-assembled monolayer (SAM) with systematically varied termination chemistries. Using a combination of ultrafast pump-probe techniques (time-domain thermoreflectance, TDTR, and picosecond acoustics) and laser spallation experiments, we independently measure and correlate changes in bonding strength and heat flow at the gold-SAM interface. For example, we experimentally demonstrate that varying the density of covalent bonds within this single bonding layer modulates both interfacial stiffness and interfacial thermal conductance. We believe that this experimental system will enable future quantification of other interfacial phenomena and will be a critical tool to stimulate and validate new theories describing the mechanisms of interfacial heat transport. Ultimately, these findings will impact applications, including thermoelectric energy harvesting, microelectronics cooling, and spatial targeting for hyperthermal therapeutics.

Self-healing of an electrical circuit is demonstrated with nearly full recovery of conductance less than one millisecond after damage. Crack damage breaks a conductive pathway in a multilayer device, interrupting electron transport and simultaneously rupturing adjacent microcapsules containing gallium-indium liquid metal (top). The released liquid metal flows to the area of damage, restoring the conductive pathway (bottom).

Maintenance of periodontal health or transition to a periodontal lesion reflects the continuous and ongoing battle between the vast microbial ecology in the oral cavity and the array of resident and emigrating inflammatory/immune cells in the periodontium. This war clearly signifies many 'battlefronts' representing the interface of the mucosal-surface cells with the dynamic biofilms composed of commensal and potential pathogenic species, as well as more recent knowledge demonstrating active invasion of cells and tissues of the periodontium leading to skirmishes in connective tissue, the locality of bone and even in the local vasculature. Research in the discipline has uncovered a concerted effort of the microbiome, using an array of survival strategies, to interact with other bacteria and host cells. These strategies aid in colonization by 'ambushing, infiltrating and outflanking' host cells and molecules, responding to local environmental changes (including booby traps for host biomolecules), communicating within and between genera and species that provide MASINT (Measurement and Signature Intelligence) to enhance sustained survival, sabotage the host inflammatory and immune responses and by potentially adopting a 'Fabian strategy' with a war of attrition and resulting disease manifestations. Additionally, much has been learned regarding the ever-increasing complexity of the host-response armamentarium at both cellular and molecular levels that is addressed in this review. Knowledge regarding how these systems fully interact requires both new laboratory and clinical tools, as well as sophisticated modeling of the networks that help maintain homeostasis and are dysregulated in disease. Finally, the triggers resulting in a 'coup de main' by the microbiome (exacerbation of disease) and the characteristics of susceptible hosts that can result in 'pyrrhic victories' with collateral damage to host tissues, the hallmark of periodontitis, remains unclear. While much has been learned, substantial gaps in our understanding of the 'parameters of this war' remain elusive toward fulfilling the Sun Tzu adage: 'If you know the enemy and know yourself, you need not fear the result of a hundred battles.'

The cytoskeleton is primarily responsible for providing structural support, localization and transport of organelles, and intracellular trafficking. The structural support is supplied by actin filaments, microtubules, and intermediate filaments, which contribute to overall cell elasticity to varying degrees. We evaluate cell elasticity in five different cell types with drug-induced cytoskeletal derangements to probe how actin filaments and microtubules contribute to cell elasticity and whether it is conserved across cell type. Specifically, we measure elastic stiffness in primary chondrocytes, fibroblasts, endothelial cells (HUVEC), hepatocellular carcinoma cells (HUH-7), and fibrosarcoma cells (HT 1080) subjected to two cytoskeletal destabilizers: cytochalasin D and nocodazole, which disrupt actin and microtubule polymerization, respectively. Elastic stiffness is measured by atomic force microscopy (AFM) and the disruption of the cytoskeleton is confirmed using fluorescence microscopy. The two cancer cell lines showed significantly reduced elastic moduli values (~0.5kPa) when compared to the three healthy cell lines (~2kPa). Non-cancer cells whose actin filaments were disrupted using cytochalasin D showed a decrease of 60-80% in moduli values compared to untreated cells of the same origin, whereas the nocodazole-treated cells showed no change in elasticity. Overall, we demonstrate actin filaments contribute more to elastic stiffness than microtubules but this result is cell type dependent. Cancer cells behaved differently, exhibiting increased stiffness as well as stiffness variability when subjected to nocodazole. We show that disruption of microtubule dynamics affects cancer cell elasticity, suggesting therapeutic drugs targeting microtubules be monitored for significant elastic changes.

Molecular targeting of nanoparticle drug carriers promises maximized therapeutic impact to sites of disease or injury with minimized systemic effects. Precise targeting demands addressing to subcellular features. Caveolae, invaginations in cell membranes implicated in transcytosis and inflammatory signaling, are appealing subcellular targets. Caveolar geometry has been reported to impose a ≈50 nm size cutoff on nanocarrier access to plasmalemma vesicle associated protein (PLVAP), a marker found in caveolae in the lungs. The use of deformable nanocarriers to overcome that size cutoff is explored in this study. Lysozyme-dextran nanogels (NGs) are synthesized with ≈150 or ≈300 nm mean diameter. Atomic force microscopy indicates the NGs deform on complementary surfaces. Quartz crystal microbalance data indicate that NGs form softer monolayers (≈60 kPa) than polystyrene particles (≈8 MPa). NGs deform during flow through microfluidic channels, and modeling of NG extrusion through porous filters yields sieving diameters less than 25 nm for NGs with 150 and 300 nm hydrodynamic diameters. NGs of 150 and 300 nm diameter target PLVAP in mouse lungs while counterpart rigid polystyrene particles do not. The data in this study indicate a role for mechanical deformability in targeting large high-payload drug-delivery vehicles to sterically obscured targets like PLVAP.

Thin films of mechanochemically active polymer were subjected to laser-generated, high amplitude acoustic pulses. Stress wave propagation through the film produced large amplitude stresses (>100 MPa) in short time frames (10-20 ns), leading to very high strain rates (ca. 1 × 10(7) to 1 × 10(8) s(-1)). The polymer system, spiropyran (SP)-linked polystyrene (PS), undergoes a force-induced chemical reaction causing fluorescence and color change. Activation of SP was evident via a fluorescence signal in thin films subject to high strain-rates. In contrast, quasi-static loading of bulk SP-linked PS samples failed to result in SP activation. Mechanoresponsive coatings have potential to indicate deformation under shockwave loading conditions.

The cell interior is a crowded chemical space, which limits the diffusion of molecules and organelles within the cytoplasm, affecting the rates of chemical reactions. We provide insight into the relationship between non-specific intracellular diffusion and cytoskeletal integrity. Quantum dots entered the cell through microinjection and their spatial coordinates were captured by tracking their fluorescence signature as they diffused within the cell cytoplasm. Particle tracking revealed significant enhancement in the mobility of biocompatible quantum dots within fibrosarcoma cells versus their healthy counterparts, fibroblasts, as well as in actin destabilized fibroblasts versus untreated fibroblasts. Analyzing the displacement distributions provided insight into how the heterogeneity of the cell cytoskeleton influences intracellular particle diffusion. We demonstrate that intracellular diffusion of non-specific nanoparticles is enhanced by disrupting the actin network, which has implications for drug delivery efficacy and trafficking.

Laser-induced spallation is a process in which a stress wave generated from a rapid, high-energy laser pulse initiates the ejection of surface material opposite the surface of laser impingement. Through knowledge of the stress wave amplitude that causes film separation, the adhesion and interfacial properties of a film-on-substrate system are determined. Some advantages of the laser spallation technique are the non-contact loading, development of large stresses (on the order of GPa) and high strain rates, up to 108 /s. The applicability to both relatively thick films, tens of microns, and thin films, tens of nm, make it a unique technique for a wide range of materials and applications. This review combines the available knowledge and experience in laser spallation, as a state-of-the-art measurement tool, in a comprehensive pedagogical publication for the first time. An historical review of adhesion measurement by the laser-induced spallation technique, from its inception in the 1970s through the present day, is provided. An overview of the technique together with the physics governing the laser-induced spallation process, including functions of the absorbing and confining materials, are also discussed. Special attention is given to applications of laser spallation as an adhesion quantification technique in metals, polymers, composites, ceramics, and biological films. A compendium of available experimental parameters is provided that summarizes key laser spallation experiments across these thin film materials. This review concludes with a future outlook for the laser spallation technique, which approaches its semicentennial anniversary.