As a major component of the human body, the extracellular matrix (ECM) is a complex biopolymer network. The ECM not only hosts a plethora of biochemical interactions but also defines the physical ...microenvironment of cells. The physical properties of the ECM, such as its geometry and mechanics, are critical to physiological processes and diseases such as morphogenesis, wound healing, and cancer. This review provides a brief introduction to the recent progress in understanding the mechanics of ECM for researchers who are interested in learning about this relatively new subject of biophysics. This review covers the mechanics of a single ECM fiber (nanometer scale), the micromechanics of ECM (micrometer scale), and bulk rheology (greater than millimeter scale). Representative experimental measurements and basic theoretical models are introduced side by side. After discussing the physics of ECM mechanics, the review concludes by commenting on the role of ECM mechanics in healthy and tumorigenic tissues and the open questions that call for future studies at the interface of fundamental physics, engineering, and medical sciences.
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The extracellular matrix (ECM), with its major component fibrillar collagen, defines the physical microenvironment of cells. In this review, Sun provides a summary of the structural and mechanical properties of fibrillar collagen matrices at various scales and the roles of these physical cues in tissue maintenance and in cancer progression.
Metasurfaces, planer artificial materials composed of subwavelength unit cells, have shown superior abilities to manipulate the wavefronts of electromagnetic waves. In the last few years, ...metasurfaces have been a burgeoning field of research, with a large variety of functional devices, including planar lenses, beam deflectors, polarization converters, and metaholograms, being demonstrated. Up to date, the majority of metasurfaces cannot be tuned postfabrication. Yet, the dynamic control of optical properties of metasurfaces is highly desirable for a plethora of applications including free space optical communications, holographic displays, and depth sensing. Recently, much effort has been made to exploit active materials, whose optical properties can be controlled under external stimuli, for the dynamic control of metasurfaces. The tunability enabled by active materials can be attributed to various mechanisms, including but not limited to thermo‐optic effects, free‐carrier effects, and phase transitions. This short review summarizes the recent progress on tunable metasurfaces based on various approaches and analyzes their respective advantages and challenges to be confronted with. A number of potential future directions are also discussed at the end.
Various mechanisms to achieve dynamic control of metasurfaces enabled by active materials are discussed. Recent works on tunable metasurfaces based on thermo‐optic effects, free carrier effects, and phase transitions are summarized. Their respective advantages and challenges are analyzed and an outlook on the potential development of tunable metasurfaces is presented.
Actuators that can convert environmental stimuli into mechanical work are widely used in intelligent systems, robots, and micromechanics. To produce robust and sensitive actuators of different ...scales, efforts are devoted to developing effective actuating schemes and functional materials for actuator design. Carbon‐based nanomaterials have emerged as preferred candidates for different actuating systems because of their low cost, ease of processing, mechanical strength, and excellent physical/chemical properties. Especially, due to their excellent photothermal activity, which includes both optical absorption and thermal conductivities, carbon‐based materials have shown great potential for use in photothermal actuators. Herein, the recent advances in photothermal actuators based on various carbon allotropes, including graphite, carbon nanotubes, amorphous carbon, graphene and its derivatives, are reviewed. Different photothermal actuating schemes, including photothermal effect–induced expansion, desorption, phase change, surface tension gradient creation, and actuation under magnetic levitation, are summarized, and the light‐to‐heat and heat‐to‐work conversion mechanisms are discussed. Carbon‐based photothermal actuators that feature high light‐to‐work conversion efficiency, mechanical robustness, and noncontact manipulation hold great promise for future autonomous systems.
This review highlights the recent advances in carbon‐based photothermal actuators. Physical properties and light‐to‐heat conversion mechanisms of various carbon‐based functional materials are summarized. Photothermal actuating schemes such as photothermal expansion, desorption, phase change, surface tension effect, and magnetic susceptibility are reviewed. The current challenges and future perspectives of this field are also discussed.
•Taxifolin improved diastolic dysfunction in streptozotocin-induced diabetic mice.•Taxifolin inhibited oxidative stress by enhancing antioxidative enzymes’ activities.•Taxifolin inhibited NADPH ...oxidase activities and reduced ROS level.•JAK/STAT pathway was involved in the protective effects of taxifolin.
Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. The objective of this study was to investigate the potential protective effects and mechanisms of taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that taxifolin inhibited 33mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm. In conclusion, taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy.
Although the Fe(VI)–sulfite process has shown great potential for the rapid removal of organic contaminants, the major active oxidants (Fe(IV)/Fe(V) versus SO4 •–/•OH) involved in this process are ...still under debate. By employing sparingly soluble CaSO3 as a slow-releasing source of SO3 2–, this study evaluated the oxidation performance of the Fe(VI)–CaSO3 process and identified the active oxidants involved in this process. The process exhibited efficient oxidation of a variety of compounds, including antibiotics, pharmaceuticals, and pesticides, at rates that were 6.1–173.7-fold faster than those measured for Fe(VI) alone, depending on pH, CaSO3 dosage, and the properties of organic contaminants. Many lines of evidence verified that neither SO4 •– nor •OH was the active species in the Fe(VI)–CaSO3 process. The accelerating effect of CaSO3 was ascribed to the direct generation of Fe(IV)/Fe(V) species from the reaction of Fe(VI) with soluble SO3 2– via one-electron steps as well as the indirect generation of Fe(IV)/Fe(V) species from the self-decay of Fe(VI) and Fe(VI) reaction with H2O2, which could be catalyzed by uncomplexed Fe(III). Besides, the Fe(VI)–CaSO3 process exhibited satisfactory removal of organic contaminants in real water, and inorganic anions showed negligible effects on organic contaminant decomposition in this process. Thus, the Fe(VI)–CaSO3 process with Fe(IV)/Fe(V) as reactive oxidants may be a promising method for abating various micropollutants in water treatment.
Nicotinamide phosphoribosyltransferase (NAMPT) maintains mitochondrial function and protects against cerebral ischemic injury by improving energy metabolism. Notoginsenoside R1 (R1), a unique ...constituent of Panax notoginseng, has been shown to promote the proliferation and tube formation of human umbilical vein endothelial cells. Whether R1 has proangiogenesis on the activation of NAMPT in ischemic stroke remains unclear. The purpose of this study was to investigate the pharmacodynamic effect and mechanism of R1 on angiogenesis after ischemic stroke. We used male Sprague-Dawley (SD) rats subjected to middle cerebral artery occlusion/reperfusion (MCAO/R). R1 was administered via intraperitoneal (i.p.) injection immediately after ischemia induction. The promotion of R1 on angiogenesis were detected by immunofluorescence staining, 3D stereoscopic imaging and transmission electron microscopy detection. HBMEC cells were pretreated with different concentrations of R1 for 12 h before oxygen-glucose deprivation/reoxygenation (OGD/R) exposure. Afterward, scratch assay, EdU staining and tube formation were determined. Western blot analyses of proteins, including those involved in angiogenesis, NAMPT-SIRT1 cascade, VEGFR-2, and Notch signaling, were conducted. We showed that R1 significantly restored cerebral blood flow, improved mitochondrial energy metabolism and promoted angiogenesis. More importantly, incubation with 12.5–50 μM R1 significantly increased the migration, proliferation and tube formation of HBMECs in vitro. The promotion of R1 on angiogenesis were associated with the NAMPT-NAD+-SIRT1 cascade and Notch/VEGFR-2 signaling pathway, which was partially eliminated by inhibitors of NAMPT and SIRT1. We demonstrated that R1 promotes post-stroke angiogenesis via activating NAMPT-NAD+-SIRT1 cascade. The modulation of Notch signaling and VEGFR-2 contribute to the post-stroke angiogenesis. These findings offer insight for exploring new therapeutic strategies for neurorestoration via R1 treatment after ischemic stroke.
Schematic diagram of the mechanisms underlying the R1-induced promotion of angiogenesis after ischemia-reperfusion injury. Overall, R1 activates the NAMPT-NAD+-SIRT1 cascade, SIRT1 deacetylates NICD, which led to inhibition of DLL4-Notch signaling. Inhibition of the Dll4-Notch signaling pathway can upregulate the expression of VEGFR-2, thereby promoting angiogenesis after ischemia. Display omitted
•A new therapeutic strategy in the treatment of ischemic stroke was proposed.•The mechanism relies on the promotion of angiogenesis.•A new method for the detection of energy metabolic molecules were proposed.
The Fowan Cliff Carvings are a key part of the Dazu Grottoes. Formed in a southern and northern stretch, the 290 individual niches at Fowan were mostly sculpted from the Late Tang to the Southern ...Song. Previous research by archaeologists and art historians has used typological and iconographic methods to periodize these niches and debate the themes behind particular niche sculptures. This essay employs niche inscriptions in a discussion of typical Fowan niche contents, matching lay feasting activities onto the period background behind their construction. These individual case studies grant an understanding of the overall atmosphere at Fowan through the shared inclinations or connections between niches, also reflecting specific niche sculptures via holistic analysis. This method, repeatedly examining the relationship between the niches and site from the perspective of “venue”, helps us restore a sense of situatedness when facing different eras of Fowan and to understand the choice in statue content, changes in niche content, and the design underlying niche form.
Clinopodium chinense (Benth.) O. Ktze is a traditional Chinese herbal medicine, which comprises the plant's total flavonoids. TFCC plays an important role in the treatment of cardiovascular disease.
...The aim of the study was to study the protective effects and possible mechanism of TFCC against isoproterenol (ISO)-mediated myocardial injury in vivo and anoxia/reoxygenation (A/R)-induced H9c2 cell injury in vitro.
Male Sprague–Dawley (SD) rats were intragastrically pretreated with TFCC for 15 days. After 2 h of TFCC administration on days 14 and 15, a myocardial injury model was established with intragastric administration of 120 mg/kg of ISO daily for 2 days. The experiment was stopped 12 h after the last administration of the drugs. ECG recordings were taken after the treatment. Serum samples were assayed to determine the serum cardiac enzymes (e.g., creatine kinase, aspartate aminotransferase, and lactate dehydrogenase). The left ventricle was excised for histopathological examination, and myocardial homogenates were prepared to detection catalase, glutathione peroxidase, and superoxide dismutase. Reactive oxygen species (ROS), heme oxygenase-1(HO-1),and peroxidase were detected by the corresponding ELISA kits. H9c2 cells were pretreated with different concentrations of TFCC for 12 h before A/R exposure. Afterward, cell viability, LDH release, hoechst 33,342, and peromide iodine (PI) double staining, JC-1 staining, and ROS examination were determined. Western blot analyses of B-cell lymphoma-2, Bcl-2associated X protein, cleaved cysteinylaspartate specific protease-3 and-9, nuclear factor 2(Nrf2), HO-1 and serine/threonine protein kinase (AKT), and P-AKT were conducted.
The pretreatment of TFCC (10, 20, and 40 mg/kg) daily for 15 days prevented ISO-induced myocardial damage, including the decrease in serum cardiac enzymes and cardiomyocyte apoptotic index and improvement in the heart rate and vacuolation. TFCC also improved the free radical scavenging and antioxidant potential, thereby suggesting that one possible mechanism of TFCC-induced cardio protection is mediated by blocking the oxidative stress. To clarify these mechanisms, we performed the in vitro study by A/R-induced cytotoxicity model in H9c2 cells. TFCC pretreatment prevented apoptosis, increased the expression of HO-1, and enhanced the nuclear translocation of Nrf2. TFCC also activated phosphorylation of AKT, whereas the addition of LY294002, which is the pharmacologic inhibitor of PI3K, blocked the TFCC-induced Nrf2/HO-1 activation and cytoprotective effect.
TFCC protects against myocardial injury and enhances cellular antioxidant defense capacity by inducing the phosphorylation of AKT, which subsequently activated the Nrf2/HO-1 signaling pathway.
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Folium Ginkgo extract and tetramethylpyrazine sodium chloride injection (Xingxiong injection) is a compound preparation commonly used for treating cerebral ischaemia/reperfusion injury in ischaemic ...stroke in China. However, its potential mechanisms on ischaemic stroke remain unknown.
This study explores the potential mechanisms of Xingxiong injection in vivo or in vitro.
Sprague-Dawley (SD) rats were randomly assigned to five groups: the sham (normal saline), the model (normal saline) and the Xingxiong injection groups (12.5, 25 or 50 mL/kg). The rats were subjected to 2 h of middle cerebral artery occlusion (MCAO) followed by reperfusion for 14 d. Xingxiong injection was administered via intraperitoneal (i.p.) injection immediately after ischaemia induction for 14 d. Afterwards, rats were sacrificed at 14 d induced by administration of Xingxiong injection.
Xingxiong injection significantly reduces infarct volume (23%) and neurological deficit scores (93%) compared with the MCAO/R group. Additionally, Xingxiong injection inhibits the loss in mitochondrial membrane potential (43%) and reduces caspase-3 level (44%), decreases NOX (41%), protein carbonyl (29%), 4-HNE (40%) and 8-OhdG (41%) levels, inhibits the expression of inflammatory factors, such as TNF-α (26%), IL-1β (34%), IL-6 (39%), MCP-1 (36%), CD11a (41%) and ICAM-1 (43%). Moreover, Xingxiong injection can increase p-Akt/Akt (35%) and Nrf2 (47%) protein expression and inhibit NLRP3 (42%) protein expression.
Xingxiong injection prevents cerebral ischaemia/reperfusion injury via activating the Akt/Nrf2 pathway and inhibiting NLRP3 inflammasome. These findings provide experimental evidence for clinical use of drugs in the treatment of ischaemic stroke.
The present study was designed to investigate whether Araloside C, one of the major triterpenoid compounds isolated from Aralia elata known to be cardioprotective, can improve heart function ...following ischaemia/reperfusion (I/R) injury and elucidate its underlying mechanisms. We observed that Araloside C concentration‐dependently improved cardiac function and depressed oxidative stress induced by I/R. Similar protection was confirmed in isolated cardiomyocytes characterized by maintaining Ca2+ transients and cell shortening against I/R. Moreover, the potential targets of Araloside C were predicted using the DDI‐CPI server and Discovery Studio software. Molecular docking analysis revealed that Araloside C could be stably docked into the ATP/ADP‐binding domain of the heat shock protein 90 (Hsp90) protein via the formation of hydrogen bonds. The binding affinity of Hsp90 to Araloside C was detected using nanopore optical interferometry and yielded KD values of 29 μM. Araloside C also up‐regulated the expression levels of Hsp90 and improved cell viability in hypoxia/reoxygenation‐treated H9c2 cardiomyocytes, whereas the addition of 17‐AAG, a pharmacologic inhibitor of Hsp90, attenuated Araloside C‐induced cardioprotective effect. These findings reveal that Araloside C can efficiently attenuate myocardial I/R injury by reducing I/R‐induced oxidative stress and Ca2+i overload, which was possibly related to its binding to the Hsp90 protein.
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