Altered epitopes enhance macrophage-mediated anti-tumour immunity to low-immunogenic tumour mutations.

Personalized neoantigen therapy has shown long-term and stable efficacy in specific patient populations. However, not all patients have sufficient levels of neoantigens for treatment. Although somatic mutations are commonly found in tumours, a significant portion of these mutations do not trigger an immune response. Patients with low mutation burdens continue to exhibit unresponsiveness to this treatment. We propose a design paradigm for neoantigen vaccines by utilizing the highly immunogenic unnatural amino acid p-nitrophenylalanine (pNO2Phe) for sequence alteration of somatic mutations that failed to generate neoepitopes. This enhances the immunogenicity of the mutations and transforms it into a suitable candidate for immunotherapy. The nitrated altered epitope vaccines designed according to this paradigm is capable of activating circulating CD8+ T cells and inducing immune cross-reactivity against autologous mutated epitopes in different MHC backgrounds (H-2Kb, H-2Kd, and human HLA-A02:01), leading to the elimination of tumour cells carrying the mutation. After immunization with the altered epitopes, tumour growth was significantly inhibited. It is noteworthy that nitrated epitopes induce tumour-infiltrating macrophages to differentiate into the M1 phenotype, surprisingly enhancing the MHC II molecule presenting pathway of macrophages. Nitrated epitope-treated macrophages have the potential to cross-activate CD4+ and CD8+ T cells, which may explain why pNO2Phe can enhance the immunogenicity of epitopes. Meanwhile, the immunosuppressive microenvironment of the tumour is altered due to the activation of macrophages. The nitrated neoantigen vaccine strategy enables the design of vaccines targeting non-immunogenic tumour mutations, expanding the pool of potential peptides for personalized and shared novel antigen therapy. This approach provides treatment opportunities for patients previously ineligible for new antigen vaccine therapy.

Empagliflozin protects against heart failure with preserved ejection fraction partly by inhibiting the senescence-associated STAT1-STING axis.

Heart failure with preserved ejection fraction (HFpEF) is a mortal clinical syndrome without effective therapies. Empagliflozin (EMPA) improves cardiovascular outcomes in HFpEF patients, but the underlying mechanism remains elusive. Here, mice were fed a high-fat diet (HFD) supplemented with L-NAME for 12 weeks and subsequently intraperitoneally injected with EMPA for another 4 weeks. A 4D-DIA proteomic assay was performed to detect protein changes in the failing hearts. We identified 310 differentially expressed proteins (DEPs) (ctrl vs. HFpEF group) and 173 DEPs (HFpEF vs. EMPA group). The regulation of immune system processes was enriched in all groups and the interferon response genes (STAT1, Ifit1, Ifi35 and Ifi47) were upregulated in HFpEF mice but downregulated after EMPA administration. In addition, EMPA treatment suppressed the increase in the levels of aging markers (p16 and p21) in HFpEF hearts. Further bioinformatics analysis verified STAT1 as the hub transcription factor during pathological changes in HFpEF mice. We next treated H9C2 cells with IFN-γ, a primary agonist of STAT1 phosphorylation, to investigate whether EMPA plays a beneficial role by blocking STAT1 activation. Our results showed that IFN-γ treatment caused cardiomyocyte senescence and STAT1 activation, which were inhibited by EMPA administration. Notably, STAT1 inhibition significantly reduced cellular senescence possibly by regulating STING expression. Our findings revealed that EMPA mitigates cardiac inflammation and aging in HFpEF mice by inhibiting STAT1 activation. The STAT1-STING axis may act as a pivotal mechanism in the pathogenesis of HFpEF, especially under inflammatory and aging conditions.

High-temperature rotation-vibration spectrum of iminosilylene (HNSi).

Iminosilylene (HNSi) has been observed in the laboratory and is expected to occur in the envelopes of carbon-rich stars. However, the lack of spectroscopic information for HNSi has hampered its further astrophysical detection. Using robust ab initio methods, we present the first and comprehensive molecular line list for HNSi (X 1Σ+). The new line list contains almost 3.36 billion transitions between 1.57 million levels with rotational excitation up to J = 160. It is suitable for temperatures up to 3000 K and covers the wavenumber range of 0-9000 cm-1 (wavelengths λ > 1.11 µm). This new line list can be helpful for the future spectroscopic characterization and molecular detection of HNSi in the laboratory and interstellar space.

High-temperature molecular line list of hydroboron monoxide (HBO).

Hydroboron monoxide (HBO) is expected to occur in envelopes of the asymptotic giant branch (AGB), but a lack of spectroscopic data is hampering its possible detection. Using the state-of-the-art ab initio method, we present the first, comprehensive molecular line list for HBO which is suitable for temperatures up to T = 3000 K. This new line list covers the wavenumber range of 0-9000 cm-1 (wavelengths of λ ≥ 1.11 µm), and it contains almost 75 million transitions between 435 631 energy levels with rotational excitation up to J = 120. The new line list of HBO can facilitate its future molecular detection in the laboratory and interstellar space.

Selective sp3 C-H alkylation via polarity-match-based cross-coupling.

The functionalization of carbon-hydrogen (C-H) bonds is one of the most attractive strategies for molecular construction in organic chemistry. The hydrogen atom is considered to be an ideal coupling handle, owing to its relative abundance in organic molecules and its availability for functionalization at almost any stage in a synthetic sequence. Although many C-H functionalization reactions involve C(sp3)-C(sp2) coupling, there is a growing demand for C-H alkylation reactions, wherein sp3 C-H bonds are replaced with sp3 C-alkyl groups. Here we describe a polarity-match-based selective sp3 C-H alkylation via the combination of photoredox, nickel and hydrogen-atom transfer catalysis. This methodology simultaneously uses three catalytic cycles to achieve hydridic C-H bond abstraction (enabled by polarity matching), alkyl halide oxidative addition, and reductive elimination to enable alkyl-alkyl fragment coupling. The sp3 C-H alkylation is highly selective for the α-C-H of amines, ethers and sulphides, which are commonly found in pharmaceutically relevant architectures. This cross-coupling protocol should enable broad synthetic applications in de novo synthesis and late-stage functionalization chemistry.

Topologies of synthetic gene circuit for optimal fold change activation.

Computations widely exist in biological systems for functional regulations. Recently, incoherent feedforward loop and integral feedback controller have been implemented into Escherichia coli to achieve a robust adaptation. Here, we demonstrate that an indirect coherent feedforward loop and mutual inhibition designs can experimentally improve the fold change of promoters, by reducing the basal level while keeping the maximum activity high. We applied both designs to six different promoters in E. coli, starting with synthetic inducible promoters as a proof-of-principle. Then, we examined native promoters that are either functionally specific or systemically involved in complex pathways such as oxidative stress and SOS response. Both designs include a cascade having a repressor and a construct of either transcriptional interference or antisense transcription. In all six promoters, an improvement of up to ten times in the fold change activation was observed. Theoretically, our unitless models show that when regulation strength matches promoter basal level, an optimal fold change can be achieved. We expect that this methodology can be applied in various biological systems for biotechnology and therapeutic applications.

Speckle-type POZ protein could play a potential inhibitory role in human renal cell carcinoma.

BACKGROUND: Speckle-type POZ protein(SPOP), a substrate adaptor of Cul3 ubiquitin ligase, plays crucial roles in solid neoplasms by promoting the ubiquitination and degradation of substrates. Limited studies have shown that SPOP is overexpressed in human renal cell carcinoma (RCC) tissue. However, the exact role of SPOP in RCC remains unclear and needs to be further elucidated. The present study showed that SPOP was expressed at different levels in different RCC cell lines. The purpose of this study was to explore the roles of SPOP in the biological features of RCC cells and the expression levels of SPOP in human tissue microarray (TMA) and kidney tissues. METHODS: Here, SPOP was overexpressed by lentiviral vector transfection in ACHN and Caki-1 cells, and SPOP was knocked down in Caki-2 cells with similar transfection methods. The transfection efficiency was evaluated by quantitative PCR and western blotting analyses. The role of SPOP in the proliferation, migration, invasion and apoptosis of cell lines was determined by the MTT, wound-healing, transwell and flow cytometry assays. Moreover, the cells were treated with different drug concentrations in proliferation and apoptosis assays to investigate the effect of sunitinib and IFN-α2b on the proliferation and apoptosis of SPOP-overexpressing cells and SPOP-knockdown RCC cells. Finally, immunohistochemical staining of SPOP was performed in kidney tissues and TMAs, which included RCC tissues and corresponding adjacent normal tissues. RESULTS: Overexpression of SPOP inhibited cell proliferation, migration and invasion and increased cell apoptosis. Interestingly, sunitinib and IFN-α2b at several concentrations increased the proliferation inhibitory rate and total apoptosis rate of cells overexpressing SPOP. The findings of the present study showed that the SPOP protein was significantly expressed at low levels in most clear cell RCC (ccRCC) tissues and at relatively high levels in the majority of adjacent normal tissues and kidney tissues. Kaplan-Meier survival analysis showed that there was no statistically significant difference in cumulative survival based on the data of different SPOP expression levels in TMA and patients. CONCLUSIONS: In contrast to previous studies, our findings demonstrated that overexpression of SPOP might suppress the progression of RCC cells, which was supported by cell experiments and immunohistochemical staining. SPOP could be a potential tumour inhibitor in RCC.

Highly Conformal Polymers for Ambulatory Electrophysiological Sensing.

Stable ambulatory electrophysiological sensing is widely used for smart e-healthcare monitoring, clinical diagnosis of cardiovascular diseases, treatment of neurological diseases, and intelligent human-machine interaction. As the favorable signal interaction platform of electrophysiological sensing, the conformal property of on-skin electrodes is an extremely crucial factor that can affect the stability of long-term ambulatory electrophysiological sensing. From the perspective of materials, to realize conformal contact between electrodes and skin for stable sensing, highly conformal polymers are in great demand and attracting ever-growing attention. This review focuses on the recent progress of highly conformal polymers for ambulatory electrophysiological sensing, including their synthetic methods, conformal property, and potential applications. Specifically, three main types of highly conformal polymers for stable long-term electrophysiological signals monitoring are proposed, including nature silk fibroin based conformal polymers, marine mussels bioinspired conformal polymers, and other conformal polymers such as zwitterionic polymers and polyacrylamides. Furthermore, the future challenges and opportunities in preparing highly conformal polymers for on-skin electrodes are also highlighted.

An accurate NH2(X2A'') CHIPR potential energy surface via extrapolation to the complete basis set limit and dynamics of the N(2D) + H2(X1Σ+g) reaction.

The amidogen radical (NH2) and its associated N(2D) + H2(X1Σ+g) → H(2S) + NH(X3Σ-) reaction have great significance in interstellar chemistry and the accurate potential energy surface (PES) is the basis for studying them. We report a new and accurate PES for the ground state NH2(X2A'') using the combined-hyperbolic-inverse-power-representation methodology based on 7970 ab initio energy points computed at the Davidson-corrected internally contracted multireference configuration interaction level of theory. Both aug-cc-pVTZ and aug-cc-pVQZ basis sets have been employed to extrapolate the energies to the complete basis set limit. The analytical PES reproduces well with the ab initio energy points with a root mean square deviation of 55.7 cm-1. The topographical features of the analytical PES are examined in detail and agree well with the previous theoretical results. The integral cross sections and rate constants of the N(2D) + H2(X1Σ+g) → H(2S) + NH(X3Σ-) reaction are obtained using the quasi-classical trajectory method and the time-dependent wave packet method and then compared with the available theoretical and experimental values.

Electrocardiographic patterns predict the presence of collateral circulation and in-hospital mortality in acute total left main occlusion.

BACKGROUND: Data on the clinical characteristics, electrocardiogram (ECG) findings and outcomes of patients with acute myocardial infarction (AMI) due to total unprotected left main (ULM) artery occlusion is limited. METHODS: Between 2009 and 2021, 44 patients with AMI due to total ULM occlusion underwent primary percutaneous coronary intervention (PCI) at our institution. The ECG, collateral circulation, clinical and procedural characteristics, and in-hospital mortality were retrospectively evaluated. RESULTS: Twenty five patients presented with shock and 18 patients had in-hospital mortality. Nineteen patients presented with ST-segment elevation myocardial infarction (STEMI), while 25 presented with non-ST-segment elevation myocardial infarction (NSTEMI). ST-segment elevation (STE) in I and STEMI were associated with the absence of collateral circulation, while STE in aVR was associated with its presence. In the NSTEMI group, patients with STE in both aVR and aVL showed more collateral filling of the left anterior descending coronary artery (LAD) territory, while patients with STE in aVR showed more collateral filling of the LAD and the left circumflex artery territory. Compared with total ULM occlusion, patients with partial ULM obstruction presented with more STE in aVR, less STE in aVR and aVL, and less STEMI. Shock, post-PCI TIMI 0-2 flow, non-STE in aVR, STEMI, and STE in I predicted in-hospital mortality. STEMI and the absence of collateral flow were significantly associated with shock. CONCLUSIONS: STE in the precordial leads predicted the absence of collateral circulation while STE in aVR and STE in both aVR and aVL predicted different collateral filling territories in ULM occlusion. STE in I, non-STE in aVR, and STEMI predicted in-hospital mortality in these patients.

Effect of AKT silence on malignant biological behavior of renal cell carcinoma cells.

BACKGROUND: As the most common malignant tumor of primary renal tumor, renal cell carcinoma (RCC) is the highly invasive disease with high mortality. AKT is a serine/threonine kinase that play a critical role in the phosphoinositide 3-kinase (PI3K) signaling pathway, and it is an attractive target for RCC treatment. The aim of present study was to investigate the effect of AKT silence on malignant behavior of renal cell carcinoma cells. METHODS: AKT expression was quantified by immunohistochemistry in tumor tissues and normal tissues. The human RCC cell lines Caki-2 cell were chosen for this study. The optimal silencing siRNA was subsequently selected by RT-qPCR and western blot. The effect of AKT silence on RCC cells was investigated by CCK8 assay, transwell assay, scratch test and flow cytometry. The AKT1 expression in human renal cell carcinoma tissue was detected by immunohistochemical staining. RESULTS: The AKT in Caki-2 cells was silenced successfully. The results shown AKT silence could inhibit cell proliferation, invasion, and, migration. In addition, AKT silence could promote Caki-2 cell apoptosis with prevention of RCC cells move from G1 phase to S phase. Immunohistochemical staining revealed significant difference of expression of AKT1 in RCC tissues and normal renal tissues. Taken together, AKT family members might involve in malignant growth of RCC, and might be a potential therapeutic target. CONCLUSION: Our data show that AKT silence inhibited cell proliferation, invasion, and, migration of Caki-2 cell, and promoted Caki-2 cell apoptosis. Moreover, AKT silence prevented RCC cells move from G1 phase to S phase. Therefore, AKT may act as an effective therapeutic target for RCC.

Broadband trifunctional metasurface and its application in a lens antenna.

Multifunctional metasurfaces have attracted extensive attention due to their ability to achieve diversified wavefront controls in flat devices. To date, most designs through metasurface are confined to realize one or two functionalities. In this work, we implement a broadband trifunctional metasurface by using different meta-atoms of the same type. The meta-atoms can independently manipulate the amplitude and phase of transmitted waves and the phase of reflected waves in a wide frequency range. Thus, they help the metasurface achieving the functionalities of beam deflection, diffuse scattering, and beam focusing according to the polarization and the direction of incident waves. The metasurface is applied to a metalens antenna, which features broadband, low side-lobe, and stealth. The metalens antenna works at the frequency range 9.8 GHz to 11.6 GHz with gain over 25 dBi. Experiments verify the functions of the trifunctional metasurface and are in good agreement with the designs. Our approach provides a solid platform for high-efficiency wideband metadevices with diverse functionalities.

Synthetic metabolic computation in a bioluminescence-sensing system.

Bioluminescence is visible light produced and emitted by living cells using various biological systems (e.g. luxCDABE cassette). Today, this phenomenon is widely exploited in biological research, biotechnology and medical applications as a quantitative technique for the detection of biological signals. However, this technique has mostly been used to detect a single input only. In this work, we re-engineered the complex genetic structure of luxCDABE cassette to build a biological unit that can detect multi-inputs, process the cellular information and report the computation results. We first split the luxCDABE operon into several parts to create a genetic circuit that can compute a soft minimum in living cells. Then, we used the new design to implement an AND logic function with better performance as compared to AND logic functions based on protein-protein interactions. Furthermore, by controlling the reverse reaction of the luxCDABE cassette independently from the forward reaction, we built a comparator with a programmable detection threshold. Finally, we applied the redesigned cassette to build an incoherent feedforward loop that reduced the unwanted crosstalk between stress-responsive promoters (recA, katG). This work demonstrates the construction of genetic circuits that combine regulations of gene expression with metabolic pathways, for sensing and computing in living cells.

Compact patch antenna enabled by a metasurface with stereo elements.

We implemented a novel compact antenna by applying a metasurface with stereo elements (stereo-MS) as the superstrate of a patch antenna. The stereo-MS, an array of stereo patches printed on a grooved dielectric substrate, enabled the footprint miniaturization and bandwidth enhancement of the patch antenna. The overall size reduction of the stereo-MS antenna is over 38% compared with the conventional plane metasurface (plane-MS) antenna working in the same frequency range. A prototype antenna working at 5.3 GHz was designed, fabricated, and measured. Experiments demonstrated the fractional impedance bandwidth of the antenna was 44.5% at criteria |S11 |< -10 dB, covering the frequencies 4.18 to 6.56 GHz, and the average gain about 6.9 dBi in the band. Experimental results were found in very good agreement with the design, which confirms the functionality of stereo-MS in antenna minimization. Our antenna features a compact size (0.409 λ02) and low profile (3.024 mm). The stereo-MSs provide a new way for the size miniaturization of microwave and optical devices, such as antennas.

The metabolic role of PFKFB4 in androgen-independent growth in vitro and PFKFB4 expression in human prostate cancer tissue.

BACKGROUND: It is well known that androgen-deprivation therapy (ADT) can inevitably drive prostate cancer (PCa) cells into a castration-resistant state. According to the "Warburg effect", the metabolism of aggressive tumor cells increases significantly. The growth of cancer cells depends on glycolysis, which may be a potential target for cancer control. 6-Phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) plays key roles in the proliferation and metastasis of PCa cells. However, there is very limited knowledge on the role of PFKFB4 in the conversion to castration resistance. The present study aimed to determine the changes in glucose consumption and PFKFB4 expression in LNCaP cells and androgen-independent LNCaP (LNCaP-AI) cells during the whole process of androgen-independent growth. Additionally, PFKFB4 expression in human PCa tissues was evaluated. METHODS: We established an androgen-independent LNCaP-AI cell line derived from LNCaP cells to mimic the traits of castration resistance in vitro. LNCaP-AI and LNCaP cells were cultured in the corresponding medium containing the same amount of glucose. At the end of experiments, the medium supernatant and blank medium were collected, and absorbance was measured. LNCaP-AI and LNCaP cells were harvested to detect PFKFB4 expression by Western blotting. Prostate tissue samples including PCa tissue, carcinoma-adjacent tissue and benign prostatic hyperplasia (BPH) tissue specimens were evaluated for PFKFB4 expression using immunohistochemistry. RESULTS: In 18 h supernatant samples, the glucose consumption and lactate secretion of LNCaP-AI cells were higher than those of LNCaP cells. The Western blot results indicated that PFKFB4 expression was increased in LNCaP-AI cells compared with LNCaP cells. Immunohistochemistry revealed that the expression of PFKFB4 in PCa tissue specimens was higher than that in BPH and adjacent tissue specimens. However, the differences in PCa tissue before and after ADT were not statistically significant. CONCLUSION: PFKFB4 may be associated with enhanced glycolysis during the androgen-independent growth of PCa cells in vitro. PFKFB4 may be a marker of PCa progression. Our results provide a rationale for further clinical investigation of PCa treatment focused on controlling PFKFB4 expression.

miR-378a Modulates Macrophage Phagocytosis and Differentiation through Targeting CD47-SIRPα Axis in Atherosclerosis.

BACKGROUND: Signal regulatory protein alpha (SIRPa) is an essential signalling molecule that modulates inflammatory responses in macrophages. However, the regulation of SIRPs and its dynamic changes in macrophages under inflammatory stimulation in atherosclerosis remain uncertain. OBJECTIVE: The study aimed to identify the miRNAs that regulate SIRPa transcription and their roles in modulating phagocytosis, differentiation and cholesterol efflux in macrophages. METHODS: ApoE knockout mice were fed with a high-fat diet for 12 weeks. Intimal lesion areas and lipid accumulation were assessed by haematoxylin and eosin (HE) and oil red O staining. The expression of mRNAs/miRNAs was assessed by RNA-seq (RNA sequencing) and RT-qPCR (real-time quantitative polymerase chain reaction). The identification of miR-378a associated with SIRPa regulation in macrophages induced by ox-LDL was confirmed by RT-qPCR and Western blot. The phagocytosis and differentiation of macrophages were detected to figure out the role of miR-378a and SIRPa. RESULTS: SIRPa was proved to be a target of miR-378a. Reduced miR-378a can promote the expression of SIRPa. RNA-seq data showed that the levels of mRNA associated with macrophage phenotypes and SIRPa-CD47 axis were increasing significantly with a decreasing phagocytic phenotype in ApoE-/- mice vs wild-type (WT) mice (P < 0.01). The level of miR-378a was reduced in the aorta of ApoE-/- mice vs WT mice. The experiment in vitro showed that overexpression of miR-378a in macrophages decreased the level of Sirpa mRNA obviously vs control (P < 0.01). The phagocytic activity of miR-378a-transfected macrophages was promoted vs control (P < 0.05). miR-378a significantly depleted Sirpa levels in oxidized low-density lipoprotein (ox-LDL)-stimulated macrophages (P < 0.05), and depletion of miR-378a reversed Sirpa reduction obviously (P < 0.05). miR-378a promoted the secretion of TNF-a and IL-6 indirectly. CONCLUSION: It has been demonstrated that miR-378a regulates SIRPa-mediated phagocytosis and polarization of macrophages by a direct or indirect way. This research may provide a new path to promote reverse cholesterol transport of macrophages and hinder the progress of atherosclerosis.

Biophysical attributes that affect CaMKII activation deduced with a novel spatial stochastic simulation approach.

Calcium/calmodulin-dependent protein kinase II (CaMKII) holoenzymes play a critical role in decoding Ca2+ signals in neurons. Understanding how this occurs has been the focus of numerous studies including many that use models. However, CaMKII is notoriously difficult to simulate in detail because of its multi-subunit nature, which causes a combinatorial explosion in the number of species that must be modeled. To study the Ca2+-calmodulin-CaMKII reaction network with detailed kinetics while including the effect of diffusion, we have customized an existing stochastic particle-based simulator, Smoldyn, to manage the problem of combinatorial explosion. With this new method, spatial and temporal aspects of the signaling network can be studied without compromising biochemical details. We used this new method to examine how calmodulin molecules, both partially loaded and fully loaded with Ca2+, choose pathways to interact with and activate CaMKII under various Ca2+ input conditions. We found that the dependence of CaMKII phosphorylation on Ca2+ signal frequency is intrinsic to the network kinetics and the activation pattern can be modulated by the relative amount of Ca2+ to calmodulin and by the rate of Ca2+ diffusion. Depending on whether Ca2+ influx is saturating or not, calmodulin molecules could choose different routes within the network to activate CaMKII subunits, resulting in different frequency dependence patterns. In addition, the size of the holoenzyme produces a subtle effect on CaMKII activation. The more extended the subunits are organized, the easier for calmodulin molecules to access and activate the subunits. The findings suggest that particular intracellular environmental factors such as crowding and calmodulin availability can play an important role in decoding Ca2+ signals and can give rise to distinct CaMKII activation patterns in dendritic spines, Ca2+ channel nanodomains and cytoplasm.

Water-Stable Metal-Organic Frameworks with Selective Sensing on Fe3+ and Nitroaromatic Explosives, and Stimuli-Responsive Luminescence on Lanthanide Encapsulation.

Three water-stable luminescent MOFs [Zn4(bptc)2(NMP)3(DMF)(H2O)2] n (1-a), [Cd4(bptc)2(NMP)3(DMF)2(H2O)1] n (1-b), and {[Zn2(bptc)(DMA)(H2O)2]·(DMA)2·H2O} n (2), possessing similar chemical components (M2:L1:Sol3) and topology structures, were synthesized by solvents control. Their excellent sensing on iron(III) cation and nitroaromatic explosives (NACs) with great selectivity, sensitivity and a high Ksv (4.54 × 104 for 1-b on PNP) were observed by quenching effects. Furthermore, Zn-MOFs exhibit interesting stimuli-responsive luminescence enhancement after the encapsulation of a series of IIIB cations stimulated different luminescent emitting and intensity enhancement through host-guest processes of the pores in MOFs, especially for two distinct responses of Zn-MOF on a Tb3+ cation.

Non-uniaxial stress-assisted fabrication of nanoconstriction on vertical nanostructured Si.

Vertically aligned Si nanoconstrictions have potential for applications of electronic, photonic and phononic nanodevices. Herein, we report a featured method by utilizing the non-uniaxial tangential tension stress (σ T ) at the Si surface of a vertical hyperbolic Si/SiO2 core-shell nanostructure during thermal oxidation to achieve well defined Si nanoconstrictions. A thermal oxidation model was proposed to describe the correlations between σ T and the structural parameters of the hyperbolic nanostructure, i.e. oxide thickness (t ox ), sidewall curvature radius (R 0) and neck diameter (2r A0). Numerical simulations indicated that the Si surface at the position with the narrowest diameter (neck position) has the highest σ T (∼GPa) and presents a gradient distribution at both ends. By means of stress regulation, an array of well defined Si nanoconstrictions about 10 nm in diameter and about 34 nm in length was obtained. The experimental findings demonstrated that the high σ T would induce a nanofracture and thus a local oxidation to form a nanoconstriction, self-aligned at the neck position. The finding notably extends the capability of stress-assisted 'nanofabrication' of Si via thermal oxidation.

Compact and broadband antenna based on a step-shaped metasurface.

A metasurface (MS) is highly useful for improving the performance of patch antennae and reducing their size due to their inherent and unique electromagnetic properties. In this paper, a compact and broadband antenna based on a step-shaped metasurface (SMS) at an operating frequency of 4.3 GHz is presented, which is fed by a planar monopole and enabled by selecting an SMS with high selectivity. The SMS consists of an array of metallic step-shaped unit cells underneath the monopole, which provide footprint miniaturization and bandwidth expansion. Numerical results show that the SMS-based antenna with a maximum size of 0.42λ02 (where λ0 is the operating wavelength in free space) exhibits a 22.3% impedance bandwidth (S11 < -10 dB) and a high gain of more than 7.15 dBi within the passband. Experimental results at microwave frequencies verify the performance of the proposed antenna, demonstrating substantial consistency with the simulation results. The compact and broadband antenna therefore predicts numerous potential applications within modern wireless communication systems.