Recent Progress in Resonant Acoustic Metasurfaces.

Acoustic metasurfaces, as two-dimensional acoustic metamaterials, are a current research topic for their sub-wavelength thickness and excellent acoustic wave manipulation. They hold significant promise in noise reduction and isolation, cloaking, camouflage, acoustic imaging, and focusing. Resonant structural units are utilized to construct acoustic metasurfaces with the unique advantage of controlling large wavelengths within a small size. In this paper, the recent research progresses of the resonant metasurfaces are reviewed, covering the design mechanisms and advances of structural units, the classification and application of the resonant metasurfaces, and the tunable metasurfaces. Finally, research interest in this field is predicted in future.

Design a flower-like magnetic graphite carbon microsphere for enhanced adsorption of 2,4-dichlorophenol.

2,4-Dichlorophenol (2,4-DCP) is a hazardous chlorinated organic chemical, so its removal is an important task to protect the whole ecosystem and human health. During the material preparation, the magnetic graphitic carbon adsorbent (HFMCM) with a sparse sheet-like stacking structure was formed by interlayer assembly of nickel hydroxide nanosheets and hydrothermal glucose carbon. The conditions for optimal performance of the adsorbent are 45 °C and pH 5. The maximum adsorption capacity of HFMCM-180 for 2,4-DCP is 147.06 mg·g-1. Adsorption behavior in accordance with Langmuir isothermal model and pseudo-second-order kinetic models. The adsorbent remains selective for 2,4-DCP in metal ion solutions. More than 75% of the adsorption capacity is maintained after five cycles of adsorption. Electrostatic interaction, hydrogen bonding, and π-π bonding play a major role in the adsorption of 2,4-DCP by HFMCM. The adsorbent was glucose as the carbon source, nickel sulfate as the magnetic source, and hexamethylenetetramine as the precipitant. Its carbonization after pretreatment with different hydrothermal temperatures resulted in the synthesis of flower-like graphitic carbon spheres with magnetic properties. The interconnected pore channels on the adsorbent surface conferred large specific surface area to the material. 2,4-DCP was efficiently adsorbed by π-π stacking, hydrogen bonding, and electrostatic attraction within the pore channels with low spatial potential resistance.

Flexible Manipulation of the Reflected Wavefront Using Acoustic Metasurface with Split Hollow Cuboid.

This work proposes a method for actively constructing acoustic metasurface (AMS) based on the split hollow cuboid (SHC) structure of local resonance, with the designed AMS flexibly manipulating the direction of reflected acoustic waves at a given frequency range. The AMS was obtained by precisely adjusting any one or two types of structural parameters of the SHC unit, which included the diameter of the split hole, the length, width, height, and shell thickness of the SHC. The simulation results showed that the AMS can flexibly manipulate the direction of the reflected acoustic waves, and the anomalous reflection angle obeys the generalized Snell's law. Furthermore, among the five structural parameters, the AMS's response frequency band is widest with the hole diameter and height, followed by the length and width, and narrowest with the shell thickness. It is worth noting that comprehensive manipulation of two parameters not only broadens the response frequency band, but also strengthens the effect of the anomalous reflection at the same response frequency. The subwavelength size of the AMS constructed with such a comprehensive method has the advantages of a small size, wide response band, simple preparation, and flexible modulation, and can be widely used in various fields, such as medical imaging and underwater stealth.

Anti-ATR001 monoclonal antibody ameliorates atherosclerosis through beta-arrestin2 pathway.

BACKGROUND: Our previous study developed ATRQß-001 vaccine, which targets peptide ATR001 from angiotensin Ⅱ (Ang Ⅱ) receptor type 1 (AT1R). The ATRQß-001 vaccine could induce the production of anti-ATR001 monoclonal antibody (McAb-ATR) and inhibit atherosclerosis without feedback activation of the renin-angiotensin system (RAS). This study aims at investigating the underexploited mechanisms of McAb-ATR in ameliorating atherosclerosis. METHODS: AT1R-KO HEK293T cell lines were constructed to identify the specificity of McAb-ATR and key sites of ATRQß-001 vaccine. Beta-arrestin1 knock-out (Arrb1-/-) mice, Beta-arrestin2 knock-out (Arrb2-/-) mice, and low-density lipoprotein receptor knock-out (LDLr-/-) mice were used to detect potential signaling pathways affected by McAb-ATR. The role of McAb-ATR in beta-arrestin and G proteins (Gq or Gi2/i3) signal transduction events was also investigated. RESULTS: McAb-ATR could specifically bind to the Phe182-His183-Tyr184 site of AT1R second extracellular loop (ECL2). The anti-atherosclerotic effect of McAb-ATR disappeared in LDLr-/- mice transplanted with Arrb2-/- mouse bone marrow (BM) and BM-derived macrophages (BMDMs) from Arrb2-/- mice. Furthermore, McAb-ATR inhibited beta-arrestin2-dependent extracellular signal regulated kinase1/2 (ERK1/2) phosphorylation, and promoted beta-arrestin2-mediated nuclear factor kappa B p65 (NFκB p65) inactivity. Compared with conventional AT1R blockers (ARBs), McAb-ATR did not inhibit Ang Ⅱ-induced uncoupling of heterotrimeric G proteins (Gq or Gi2/i3) and Gq-dependent intracellular Ca2+ release, nor cause RAS feedback activation. CONCLUSIONS: Through regulating beta-arrestin2, McAb-ATR ameliorates atherosclerosis without affecting Gq or Gi2/i3 pathways. Due to high selectivity for AT1R and biased interaction with beta-arrestin2, McAb-ATR could serve as a novel strategy for treating atherosclerosis.

Inhibition of Sphingosine-1-Phosphate Receptor 2 Prevents Thoracic Aortic Dissection and Rupture.

Background: Numerous pieces of evidence have indicated that thoracic aortic dissection (TAD) is an inflammatory disease. Sphingosine-1-phosphate receptor 2 (S1PR2) signaling is a driver in multiple inflammatory diseases. Here, we examined the S1PR2 expression in TAD lesions and explored the effect of interfering with S1PR2 on TAD formation and progression. Methods: Aorta specimens and blood samples were collected from patients with TAD and matched controls. The expression of S1PR1, S1PR2, and S1PR3 was examined. The effect of inhibiting S1PR2 on TAD was evaluated in a TAD mouse model induced by ß-aminopropionitrile fumarate (BAPN) and AngII. The presence of sphingosine kinase 1 (SPHK1), S1P, and neutrophil extracellular traps (NETs) was investigated. Further, the possible association between S1PR2 signaling and NETs in TAD was analyzed. Results: In the aortic tissues of patients with TAD and a mouse model, the S1PR2 expression was significantly up-regulated. In the TAD mouse model, JTE013, a specific S1PR2 antagonist, not only blunted the TAD formation and aortic rupture, but also preserved the elastic fiber architecture, reduced the smooth muscle cells apoptosis level, and mitigated the aortic wall inflammation. Augmented tissue protein expression of SPHK1, citrullinated histone H3 (CitH3, a specific marker of NETs), and serum S1P, CitH3 were detected in TAD patients. Surgical repair normalized the serum S1P and CitH3 levels. Immunofluorescence staining revealed that S1PR2 colocalized with NETs. The protein expression levels of SPHK1 and serum S1P levels positively correlated with the protein expression and serum levels of CitH3, separately. Furthermore, JTE013 treatment reduced NETs accumulation. Conclusion: Inhibiting S1PR2 attenuates TAD formation and prevents aortic rupture. Targeting S1PR2 may provide a promising treatment strategy against TAD.

A bivalent antihypertensive vaccine targeting L-type calcium channels and angiotensin AT1 receptors.

BACKGROUND AND PURPOSE: Hypertension has been the leading preventable cause of premature death worldwide. The aim of this study was to design a more efficient vaccine against novel targets for the treatment of hypertension. EXPERIMENTAL APPROACH: The epitope CE12, derived from the human L-type calcium channel (CaV 1.2), was designed and conjugated with Qß bacteriophage virus-like particles to test the efficacy in hypertensive animals. Further, the hepatitis B core antigen (HBcAg)-CE12-CQ10 vaccine, a bivalent vaccine based on HBcAg virus-like particles and targeting both human angiotensin AT1 receptors and CaV 1.2 channels, was developed and evaluated in hypertensive rodents. KEY RESULTS: The Qß-CE12 vaccine effectively decreased the BP in hypertensive rodents. A monoclonal antibody against CE12 specifically bound to L-type calcium channels and inhibited channel activity. Injection with monoclonal antibody against CE12 effectively reduced the BP in angiotensin II-induced hypertensive mice. The HBcAg-CE12-CQ10 vaccine showed antihypertensive effects in hypertensive mice and relatively superior antihypertensive effects in spontaneously hypertensive rats and ameliorated L-NAME-induced renal injury. In addition, no obvious immune-mediated damage or electrophysiological adverse effects were detected. CONCLUSION AND IMPLICATIONS: Immunotherapy against both AT1 receptors and CaV 1.2 channels decreased the BP in hypertensive rodents effectively and provided protection against hypertensive target organ damage without obvious feedback activation of renin-angiotensin system or induction of dominant antibodies against the carrier protein. Thus, the HBcAg-CE12-CQ10 vaccine may provide a novel and promising therapeutic approach for hypertension.

Tunable Two-Layer Dual-Band Metamaterial with Negative Modulus.

A tunable dual-band acoustic metamaterial (AM) with nested two-layer split hollow spheres (TLSHSs) is presented here, which was achieved by adjusting the hole diameter and the ratio of the two layers' volumes. This work comprises theoretical and numerical studies. Based on sound-force analogy (SFA), TLSHSs can be considered equivalent to a model of two spring oscillators in series. The equations of two resonant frequencies were derived, which precisely provided the relation between two resonant frequencies and the hole diameter as well as the ratio of the two layers' volumes. The analytical formulas and simulation results by the finite element method (FEM) showed that there were two resonant frequencies for the TLSHSs, and their dynamic modulus became negative near the resonant frequencies. As the the diameter of two holes increased, both of the resonant frequencies underwent a blue shift. As the relative volume ratio increased, both of the resonant frequencies underwent a red shift. The calculation and simulation results were in good agreement. This kind of precisely controllable dual-band AM with negative modulus can easily be coupled to other structures with negative mass density, thereby achieving a double-negative AM in an expected frequency range.

Vaccine Targeted Alpha 1D-Adrenergic Receptor for Hypertension.

The α1-AR (α1 adrenergic receptor) blockers currently on the market cannot meet clinical needs because of low-selectivity for subtypes of α1-ARs, short half-life, and uncertain role in cardiovascular end point events. The study sought to find a vaccine specifically against α1D-AR (α1D-adrenergic receptor) for treating hypertension. A short peptide ADR-004 (cgiteeagy) belonging to α1D-AR was screened, and the ADRQß-004 vaccine was produced and injected into spontaneously hypertensive rats model (including a short-term study, 10 weeks, and a long-term observation study, 39 weeks) and NG-nitro-l-arginine methyl ester + spontaneously hypertensive rats model (15 weeks). The antihypertensive effect and target organ protection of the ADRQß-004 vaccine were carefully evaluated. The possible immune-mediated damage was detected in normal vaccinated Sprague Dawley rats. The ADR-004 peptide has perfect immunogenicity, and the ADRQß-004 vaccine could induce strong antibody production. In the short-term study, the ADRQß-004 vaccine averagely decreased the systolic blood pressure of spontaneously hypertensive rats up to 15 mm Hg and that of NG-nitro-l-arginine methyl ester+spontaneously hypertensive rats up to 29 mm Hg. In the long-term observation model, the antihypertensive effect of the ADRQß-004 vaccine was quite stable, and the average decline of systolic blood pressure was 22 mm Hg. The ADRQß-004 vaccine effectively prevented vascular structural remodeling, cardiac hypertrophy and fibrosis, and renal injury of hypertensive animals, superior to prazosin at renal level. Moreover, the ADRQß-004 vaccine obviously downregulated the expression of α1D-AR, but not α1A-AR. Additionally, no significant immune-mediated damage was detected in immunized animals. The present results demonstrate that the ADRQß-004 vaccine may provide a novel and promising method for the treatment of hypertension.

ATRQß-001 Vaccine Prevents Experimental Abdominal Aortic Aneurysms.

Background We have developed a peptide vaccine named ATRQß-001, which was proved to retard signal transduction initiated by angiotensin II (Ang II). Ang II was implicated in abdominal aortic aneurysm (AAA) progression, but whether the ATRQß-001 vaccine would prevent AAA is unknown. Methods and Results Ang II-infused ApoE-/- mice and calcium phosphate-induced AAA in C57BL/6 mice were used to verify the efficiency of ATRQß-001 vaccine in AAA. Results demonstrated that the vaccine effectively restrained the aneurysmal dilation and vascular wall destruction of aorta in both animal models, beyond anti-hypertensive effects. In Ang II-induced AAA vascular sections, Immunohistochemical staining showed that the vaccine notably constrained vascular inflammation and vascular smooth muscle cell (VSMC) phenotypic transition, concurrently reduced macrophages infiltration. In cultured VSMC, the anti-ATR-001 antibody inhibited osteopontin secretion induced by Ang II, thereby impeded macrophage migration while co-culture. Furthermore, metalloproteinases and other matrix proteolytic enzymes were also found to be limited by the vaccine in vivo and in vitro. Conclusions ATRQß-001 vaccine prevented AAA initiation and progression in both Ang II and calcium phosphate-induced AAA models. And the beneficial effects were played beyond decrease of blood pressure, which provided a novel and promising method to take precautions against AAA.

Prognostic and Immunological Role of FUN14 Domain Containing 1 in Pan-Cancer: Friend or Foe?

Background: FUN14 domain containing 1 (FUNDC1) plays a pivotal role in mitochondrial autophagy (mitophagy), which is closely associated with human immunity. However, the role of FUNDC1 in cancers remains unclear. This study aimed to visualize the prognostic landscape of FUNDC1 in pan-cancer and investigate the relationship between FUNDC1 expression and immune infiltration. Methods: In this study, we explored the expression pattern and prognostic value of FUNDC1 in pan-cancer across multiple databases, including ONCOMINE, PrognoScan, GEPIA, and Kaplan-Meier Plotter. Then, using the GEPIA and TIMER databases, we investigated the correlations between FUNDC1 expression and immune infiltration in cancers, especially liver hepatocellular carcinoma (LIHC), and lung squamous cell carcinoma (LUSC). Results: In general, compared with that in normal tissue, tumor tissue had a higher expression level of FUNDC1. Although FUNDC1 showed a protective effect on pan-cancer, a high expression level of FUNDC1 was detrimental to the survival of LIHC patients. Although different from what was found for LUSC, for LIHC, there were significant positive correlations between FUNDC1 expression and immune infiltrates, including B cells, CD8+ T cells, CD4+ T cells, neutrophils, macrophages, and dendritic cells. Furthermore, markers of infiltrating immune cells, such as tumor-associated-macrophages (TAMs), exhibited different FUNDC1-related immune infiltration patterns. Conclusion: The mitophagy regulator FUNDC1 can serve as a prognostic biomarker in pan-cancer and is correlated with immune infiltrates.