Metformin Ameliorates Postoperative Cognitive Dysfunction through Regulation of the AMPK/SIRT1 Pathway.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is a common postoperative complication in elderly patients. The purpose of this study was to investigate the mechanism through which metformin improves postoperative cognitive function. METHODS: In the in vivo experiment, 18-month-old Sprague-Dawley (SD) rats were randomly divided into four groups (n = 12 in each group): the control, metformin, operation, and operation plus metformin groups. The animals were pretreated with metformin by gavage once daily for two weeks. The Morris water maze (MWM) was used to measure cognitive ability. In the in vitro experiment, BV2 cells were divided into five groups: the control, metformin, lipopolysaccharide (LPS), LPS plus metformin, and LPS plus metformin plus compound C groups. We stimulated microglia with LPS (500 ng/mL). Immunofluorescence and Western blotting were used to assess ROS (reactive oxygen species) levels, autophagy-associated protein levels and adenosine monophosphate-activated protein kinase (AMPK)/regulator factor 2-related enzyme 1 (SIRT1) signaling pathway activity in the rat cortex and microglial cells. RESULTS: In the MWM test, the metformin-pretreated rats spent a higher proportion of time in the target quadrant. Immunofluorescence showed that the fluorescence intensity of LC3 in the cortex was increased in rats pretreated with metformin. Western blotting indicated that metformin upregulated the expression of autophagy-related and AMPK/SIRT1 signaling pathway-related proteins in the cortex after surgery. By activating the AMPK/SIRT1 signaling pathway in vitro, metformin reduced microglial activation and oxidative stress and promoted autophagy. CONCLUSIONS: Through the AMPK/SIRT1 pathway, metformin can boost autophagy and reduce oxidative stress in cortical microglia in older rats, in turn improving postoperative cognitive function.

Knockdown of CD146 promotes endothelial-to-mesenchymal transition via Wnt/ß-catenin pathway.

PURPOSE: Cardiac fibrosis is characterized by the excessive deposition of extracellular matrix (ECM) proteins and leads to the maladaptive changes in myocardium. Endothelial cells (ECs) undergoing mesenchymal transition contributes to the occurrence and development of cardiac fibrosis. CD146 is an adhesion molecule highly expressed in ECs. The present study was performed to explore the role of CD146 in modulating endothelial to mesenchymal transition (EndMT). METHODS: C57BL/6 mice were subjected to subcutaneous implantation of osmotic minipump infused with angiotensin II (Ang Ⅱ). Adenovirus carrying CD146 short hairpin RNA (shRNA) or CD146 encoding sequence were infected into cultured human umbilical vein endothelial cells (HUVECs) followed by stimulation with Ang II or transforming growth factor-ß1 (TGF-ß1). Differentially expressed genes were revealed by RNA-sequencing (RNA-Seq) analysis. Gene expression was measured by quantitative real-time PCR, and protein expression and distribution were determined by Western blot and immunofluorescence staining, respectively. RESULTS: CD146 was predominantly expressed by ECs in normal mouse hearts. CD146 was upregulated in ECs but not fibroblasts and myocytes in hearts of Ang II-infused mice and in HUVECs stimulated with Ang Ⅱ. RNA-Seq analysis revealed the differentially expressed genes related to EndMT and Wnt/ß-catenin signaling pathway. CD146 knockdown and overexpression facilitated and attenuated, respectively, EndMT induced by Ang II or TGF-ß1. CD146 knockdown upregulated Wnt pathway-related genes including Wnt4, LEF1, HNF4A, FOXA1, SOX6, and CCND3, and increased the protein level and nuclear translocation of ß-catenin. CONCLUSIONS: Knockdown of CD146 exerts promotional effects on EndMT via activating Wnt/ß-catenin pathway and the upregulation of CD146 might play a protective role against EndMT and cardiac fibrosis.

WNT1 expression influences the development of dysplasia of the hip via regulating RBPMS2/NOG-BMP2/4-GDF5- WISP2 pathway.

OBJECTIVE: To explore the role of WNT family member 1 (WNT1) in the development of dysplasia of the hip (DDH) and the molecular mechanism involved in this process. Methods: Si-WNT1, pcDNA3.1-WNT1 or corresponding negative controls were transfected into human osteoblast hFOB1.19 and human chondrocyte C28/I2, respectively. The proliferation of cells was measured by EdU assay. The relative expressions of human noggin gene (NOG), growth differentiating factor 5 (GDF5), WNT1, and WNT1-inducible-signaling pathway protein 2 (WISP2) were determined by immunofluorescence analysis. The protein expressions of RNA-binding protein of multiple splice forms 2 (RBPMS2), NOG, bone morphogenetic protein 2 (BMP2), BMP4, WNT1 and WISP2 were determined by western blot. Animal experiment was also performed and the morphological development of hip joint was observed. Results: Overexpression of WNT1 promoted osteoblast proliferation and inhibited chondrocyte proliferation, while knockdown of WNT1 inhibited osteoblast proliferation. In chondrocytes, knockdown of WNT1 upregulated NOG expression, while overexpression of WNT1 downregulated its expression. In osteoblasts and chondrocytes, overexpression of WNT1 increased BMP2, BMP4, WNT1, and WISP2 expression. RBPMS2 and NOG were slightly expressed in each group. Conclusion: Overexpression of WNT1 promoted osteoblast proliferation, inhibited chondrocyte proliferation, and increased the expressions of BMP2, BMP4, WNT1, and WISP2. Therefore, WNT1 may be a new therapeutic target for DDH.

Clinical observation of different dosages of dexmedetomidine combined with a target-controlled infusion of propofol in hysteroscopic submucosal myomectomy.

Objective: This study aimed to explore the clinical effects of different dosages of dexmedetomidine (Dex) combined with a target-controlled infusion of propofol in hysteroscopic submucosal myomectomy. Methods: Ninety patients who underwent hysteroscopic submucosal myomectomy between September 2021 and March 2022 were enrolled and randomly divided into three groups, with 30 patients in each group. Patients in Groups A, B, and C received injections of 0.25, 0.5, or 0.75 µg/kg of Dex, respectively, by intravenous pump over 10 min. After this time, a maintenance dosage of 0.5 µg/kg/h was administered by intravenous infusion until the end of the surgery. Anesthesia was induced using 1.5 mg/kg of propofol and 0.3 µg/kg of sufentanil that were introduced through a laryngeal mask. The plasma concentration of propofol was maintained at 3 µg/ml by target-controlled infusion until the end of the surgery. The mean arterial pressure (MAP), heart rate (HR), and electroencephalographic bispectral index (BIS) were observed when the patient entered the operating room (T0), after catheter indwelling for anesthesia (T1), at the time of cervical dilation (T2), at the time of hysteroscopic surgery (T3), and at the end of the surgery (T4) in all three groups. The total dosage of propofol for induction and maintenance, anesthesia awakening time, orientation recovery time, Visual Analog Scale (VAS) score of the post-awakening uterine contraction pain, and adverse reactions were recorded. Results: The intraoperative reductions of MAP and HR in patients were significant in Group C when compared with those in Groups A and B (P < 0.05), and BIS was significantly lower in Group C at T2 and T3 when compared with the baseline measurement at T0 (P < 0.05). The dosage of propofol was significantly higher for Group A than for Groups B and C (P < 0.05). The anesthesia awakening time and orientation recovery time were significantly longer for patients in Group C when compared with patients in Groups A and B (P < 0.05). Within 5-30 min after awakening, the VAS scores in Groups B and C were significantly lower than those for Group A (P < 0.05). The incidence of adverse reactions in Group B was significantly less than that for Groups A and C (P < 0.05). Conclusion: The continuous pumping of 0.5 µg/kg of Dex combined with a target-controlled infusion of propofol in hysteroscopic submucosal myomectomy resulted in positive anesthetic and analgesia effects and fewer adverse reactions. It therefore has high clinical significance.

Engineering the Redox-Driven Channel for Precisely Regulating Nanoconfined Glutathione Identification and Transport.

Bioinspired artificial nanochannels for molecular and ionic transport have extensive applications. However, it is still a huge challenge to achieve an intelligent transport system with high selectivity/efficiency and controllability. Inspired by glutathione transport across the plasma membrane via redox regulation, we herein designed and fabricated a redox-reactive artificial nanochannel based on the host-guest chemical strategy. The nanochannel platform achieved high selectivity/efficiency for the identification and transmission of glutathione in the confined space. In addition, this nanochannel can switch between the ON and OFF states through the redox reaction. This redox-regulated system can provide a potential application for detection/binding of biological analytes and redox-controlled drug release.

Monteggia equivalent lesion in children: a narrative review.

Background: Monteggia equivalent lesion represents a group of injury or combined injury patterns that resemble the Monteggia lesion in its presentations and mechanisms. Unlike Monteggia lesions, the equivalent ones, which share vague definitions and mostly occur as sporadic single case reports in the literature, have not been thoroughly reviewed since Bado first proposed the term, especially in the pediatric population. The objective of this review was to elucidate the definition by elaborating on its clinical styles and thus analyzing the mechanism, diagnosis, and management through related literature. Data sources: Based on the terms of 'Monteggia equivalent', 'radial neck fracture' and 'pediatric', all of the related literature was searched on the PubMed and Google Scholar search engine. Results: The advance of the definitions for pediatric Monteggia equivalent lesion (PMEL) was reviewed. The functional roles of the ulnar and the related mechanism theories in this injury were analyzed. The status of the radiocapitellar joint in this injury was emphasized. According to the previous statements, a new classification model was proposed and proper diagnosis and treatment approaches were suggested. Conclusions: PMEL should be defined as an ulnar fracture at any level combined with a proximal radial fracture. According to the status of the radiocapitellar joint, it could be divided into three groups. The occult ulnar bowing and delayed radial head dislocation should be a serious concern of orthopedists. Surgical need is usually warranted. Maintaining the ulnar length and securing the radiocapitellar joint are highly recommended.

Propofol Protects Against TNF-α-induced Blood-brain Barrier Disruption via the PIM-1/eNOS/NO Pathway.

BACKGROUND: The Inflammatory cytokine, tumor necrosis factor-α (TNF-α), disrupts blood-brain barrier (BBB). Propofol reportedly exerts an anti-inflammatory effect in the central nervous system. OBJECTIVE: We hypothesized that propofol could provide a protective effect against TNF-α-induced disruption in human cerebral microvascular endothelial cells (hCMEC/D3 cells) and explored the underlying mechanisms. METHODS: The hCMEC/D3 cell monolayers were pretreated with propofol, followed by TNF-α treatment. The integrity of BBB was reflected by assessing the trans-endothelial electrical resistance (TEER) and determining the expression of proteins within tight junctions (TJs). The effect of propofol on TNF-α-modulated nitric oxide production was measured by a nitrate reductase assay kit. The expression of ZO-1, claudin-5, occludin, TNF receptor 1 (TNFR1), TNF receptor 2 (TNFR2), proviral-integration site for Moloney murine leukaemia virus (PIM)-1kinase, the phosphorylation of endothelial nitric oxide synthase at ser633 (peNOS-ser633) were detected by western blot. RESULTS: In hCMEC/D3 cells, TNF-α treatment markedly disrupted the integrity of BBB. Further, we found TNF-α treatment could increase the expression of PIM-1, then activate the phosphorylation of eNOS and induce the release of nitric oxide (NO). More importantly, we found that TNF- α-impaired BBB integrity could be reversed by propofol. CONCLUSION: These results suggest that the PIM-1/eNOS/NO pathway plays a vital role, in which Propofol protects against TNF-α-induced blood-brain barrier disruption.

RNA Sequencing Analyses Reveal the Potential Mechanism of Pulmonary Injury Induced by Gallium Arsenide Particles in Human Bronchial Epithelioid Cells.

Extensive use of gallium arsenide (GaAs) has led to increased exposure to humans working in the semiconductor industry. This study employed physicochemical characterization of GaAs obtained from a workplace, cytotoxicity analysis of damage induced by GaAs in 16HBE cells, RNA-seq and related bioinformatic analysis, qRT-PCR verification and survival analysis to comprehensively understand the potential mechanism leading to lung toxicity induced by GaAs. We found that GaAs-induced abnormal gene expression was mainly related to the cellular response to chemical stimuli, the regulation of signalling, cell differentiation and the cell cycle, which are involved in transcriptional misregulation in cancer, the MAPK signalling pathway, the TGF-ß signalling pathway and pulmonary disease-related pathways. Ten upregulated genes (FOS, JUN, HSP90AA1, CDKN1A, ESR1, MYC, RAC1, CTNNB1, MAPK8 and FOXO1) and 7 downregulated genes (TP53, AKT1, NFKB1, SMAD3, CDK1, E2F1 and PLK1) related to GaAs-induced pulmonary toxicity were identified. High expression of HSP90AA1, RAC1 and CDKN1A was significantly associated with a lower rate of overall survival in lung cancers. The results of this study indicate that GaAs-associated toxicities affected the misregulation of oncogenes and tumour suppressing genes, activation of the TGF-ß/MAPK pathway, and regulation of cell differentiation and the cell cycle. These results help to elucidate the molecular mechanism underlying GaAs-induced pulmonary injury.

NPD1 inhibits excessive autophagy by targeting RNF146 and wnt/ß-catenin pathway in cerebral ischemia-reperfusion injury.

Objective: Cerebral ischemia-reperfusion (I/R) injury is a common pathological feature in ischemic stroke. Autophagy plays a key role in I/R-induced neuronal death. Neuroprotectin D1 (NPD1) is a docosahexaenoic acid derivative with neuroprotective and anti-inflammatory properties. The purpose of this study was to investigate the mediatory role of NPD1 on I/R-induced injury and to elucidate the underlying mechanisms involved in this process.Methods: An I/R injury model was established in PC12 cells induced by oxygen and glucose deprivation/reoxygenation (OGD/R). NPD1 at increasing doses (5, 10, 20, 50, 100 nM) were added to cells one hour before OGD/R. To investigate the effect of ring finger protein 146 (RFP146) deficiency in I/R injury, PC12 cells were transiently transfected with small interfering RNF146 before further experiment.Results: Compared to the controls, OGD/R-challenged cells exhibited significantly decreased cell viability, induced oxidative stress, and excessive autophagic cell death following OGD/R. Pretreatment with NPD1 protected cells against ischemic injury as evidenced by enhanced cell survival, decreased oxidative stress markers, and a lower level of autophagy compared to drug-free group. OGD/R also increased the level of RFP146 and inhibited the expression of ß-catenin in PC12 cells. NPD1 treatment promoted the production of RNF146 and ß-catenin in cells following OGD/R experiment. Moreover, RNF146 deficiency significantly inhibited ß-catenin expression and reversed the protective effects of NPD1 in OGD/R-induced cells.Conclusion: NPD1 alleviated excessive autophagy via regulating RNF146 and Wnt/ß-catenin signaling, suggesting the potential therapeutic use of NPD1 for the protection against cerebral I/R injury.

3D printed multi-scale scaffolds with ultrafine fibers for providing excellent biocompatibility.

It is a dilemma that both strength and biocompatibility are requirements for an ideal scaffold in tissue engineering. The normal strategy is mixing or coating another material to improve the biocompatibility. Could we solve this dilemma by simply adjusting the scaffold structure? Here, a novel multi-scale scaffold was designed, in which thick fibers provide sufficient strength for mechanical support while the thin fibers provide a cell-favorable microenvironment to facilitate cell adhesion. Moreover, we developed a promising multi-scale direct writing system (MSDWS) for printing the multi-scale scaffolds. By switching the electrostatic field, scaffolds with fiber diameters from 3 µm to 600 µm were fabricated using one nozzle. Using this method, we proved that PCL scaffolds could also have excellent biocompatibility. BMSCs seeded on the scaffolds readily adhered to the thin fibers and maintained a high proliferation rate. Moreover, the cells bridged across the pores to form a cell sheet and gradually migrated to the thick fibers to cover the entire scaffold. We further combined the scaffolds with hydrogel for 3D cell culture and found that the fibers enhanced the strength and induced cell migration. We believe that the multi-scale scaffolds fabricated by an innovative 3D printing system have great potential for tissue engineering.

Rhomboidal Pt(II) metallacycle-based NIR-II theranostic nanoprobe for tumor diagnosis and image-guided therapy.

Fluorescent theranostics probes at the second near-IR region (NIR-II; 1.0-1.7 µm) are in high demand for precise theranostics that minimize autofluorescence, reduce photon scattering, and improve the penetration depth. Herein, we designed and synthesized an NIR-II theranostic nanoprobe 1 that incorporates a Pt(II) metallacycle 2 and an organic molecular dye 3 into DSPE-mPEG5000 (1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene glycol)-5000]). This design endows 1 with good photostability and passive targeting ability. Our studies show that 1 accurately diagnoses cancer with high resolution and selectively delivers the Pt(II) metallacycle to tumor regions via an enhanced permeability and retention effect. In vivo studies reveal that 1 efficiently inhibits the growth of tumor with minimal side effects. At the same time, improved fluorescent imaging quality and signal-to-noise ratios are shown due to the long emission wavelengths. These studies demonstrate that 1 is a potential theranostic platform for tumor diagnosis and treatment in the NIR-II region.

PEGylation Regulates Self-Assembled Small-Molecule Dye-Based Probes from Single Molecule to Nanoparticle Size for Multifunctional NIR-II Bioimaging.

To date, small-molecule dye-based probes have been at the forefront of research in biomedical imaging, especially in the second near-infrared (NIR-II) window (1.0-1.7 µm). However, how to precisely regulate the synthesized size of NIR-II organic dye-based probes remains challenging. Moreover, systematic studies on whether the size of NIR-II probes affects optical/pharmacokinetic properties are still rare. Here, an ingenious PEGylation strategy is developed to regulate the self-assembly size of organic dye-based (CH1055 scaffold) NIR-II probes (SCH1-SCH4) from nanoparticles to the single molecule, and the relationship between their size and chemical/physical properties is thoroughly investigated. Based on their own merits, nanoprobe SCH1 (≈170 nm), with outstanding fluorescent brightness (quantum yield ≈0.14%), performs accurate tracing of the lymphatic system as well as identification of vessel networks in mice brains with excellent signal-to-background ratio images. Meanwhile, rapidly excreted SCH4, showing fast and high passive liver tumor uptake and promising tumor/normal tissue ratios (>7), is capable of facilitating precise image-guided tumor surgery, and also demonstrates the first example of the assessment of liver fibrosis in the NIR-II window.

Chiral Selective Transport of Proteins by Cysteine-Enantiomer-Modified Nanopores.

Chirality is an intriguing and intrinsic feature of life and is highly associated with many significant biological processes. However, whether it influences the translocation behavior of proteins remains unclear. Herein, based on biomimetic strategies, we made chiral nanopores modified with cysteine enantiomers, and studied the chirality gating effects on protein transport. The results show that protein is preferentially transported through nanopores modified with l-cysteine because of chiral interaction, indicating chirality strongly influences protein transport process. This study presents a new method for better understanding the role of chirality in selective protein transport processes and provides a convenient approach for studying protein chiral separation and targeted treatments.

Single Nanochannel Platform for Detecting Chiral Drugs.

Chiral drugs play an essential role in medical and biochemical systems, and thus enantioselective analysis of chiral molecules has become a central focus in chemical, biological, medical, and pharmaceutical research. The design of chiral drug-detecting systems is a long-term and challenging task. Here we report the use of a modification-free nanochannel method for enantioselective recognition of S-naproxen from R-naproxen using N-acetyl-l-cysteine-capped gold nanoparticles as a chiral selector. The chiral discrimination is based on a drug-induced nanoparticle diastereoselective aggregation mechanism that blocks ion transport through the nanochannel. We demonstrated that high S-Npx selectivity in both water and biological samples can be achieved. This simple method has potential applications as a general platform for the detection of chiral molecules.

Construction of three-dimensional graphene interfaces into carbon fiber textiles for increasing deposition of nickel nanoparticles: flexible hierarchical magnetic textile composites for strong electromagnetic shielding.

Since manipulating electromagnetic waves with electromagnetic active materials for environmental and electric engineering is a significant task, here a novel prototype is reported by introducing reduced graphene oxide (RGO) interfaces in carbon fiber (CF) networks for a hierarchical carbon fiber/reduced graphene oxide/nickel (CF-RGO-Ni) composite textile. Upon charaterizations of the microscopic morphologies, electrical and magnetic properties, the presence of three-dimensional RGO interfaces and bifunctional nickel nanoparticles substantially influences the related physical properties in the resulting hierarchical composite textiles. Eletromagnetic interference (EMI) shielding performance suggests that the hierarchical composite textiles hold a strong shielding effectiveness greater than 61 dB, showing greater advantages than conventional polymeric and foamy shielding composites. As a polymer-free lightweight structure, flexible CF-RGO-Ni composites of all electromagnetic active components offer unique understanding of the multi-scale and multiple mechanisms in electromagnetic energy consumption. Such a novel prototype of shielding structures along with convenient technology highlight a strategy to achieve high-performance EMI shielding, coupled with a universal approach for preparing advanced lightweight composites with graphene interfaces.

[Effects of Plasmid Fibroblast Growth Factor-2 Magnetic Chitosan Gelatin Microspheres on Proliferation and Differentiation of Mesenchymal Stem Cells].

The purpose of this study is to investigate the effect of superparamagnetic chitosan FGF-2 gelatin microspheres (SPCFGM) on the proliferation and differentiation of mouse mesenchymal stem cells. The superparamagnetic iron oxide chitosan nanoparticles (SPIOCNs) were synthesized by means of chemical co-precipitation, combined with FGF-2. Then The SPCFGM and superparamagnetic chitosan gelatin microspheres (SPCGM) were prepared by means of crosslinking-emulsion. The properties of SPCFGM and SPIONs were measured by laser diffraction particle size analyser and transmisson electron microscopy. The SPCFGM were measured for drug loading capacity, encapsulation efficiency and release pharmaceutical properties in vitro. The C3H10 cells were grouped according to the different ingredients being added to the culture medium: SPCFGM group, SPCGM group and DMEM as control group. Cell apoptosis was analyzed by DAPI staining. The protein expression level of FGF-2 was determined by Western blot. The proliferation activity and cell cycle phase of C3H10 were examined by CCK8 and flow cytometry. The results demonstrated that both of the SPIOCNs and SPCFGM were exhibited structure of spherical crystallization with a diameter of (25 ± 9) nm and (140 ± 12) µm, respectively. There were no apoptosis cells in the three group cells. Both the protein expression level of FGF-2 and cell proliferation activity increased significantly in the SPCFGM group cells (P < 0.05). The SPCFGM is successfully constructed and it can controlled-release FGF-2, remained the biological activity of FGF-2, which can promote proliferation activity of C3H10 cells, and are non-toxic to the cell.

Polyphylla saponin I has antiviral activity against influenza A virus.

OBJECTIVE: In the present study, the antiviral effects of polyphylla saponin I isolated from Parispolyphylla on influenza A virus are investigated both in vitro and in vivo. METHODS: Column chromatography and reversed phase liquid chromatography separation technology were used to extract and purify polyphylla saponin I. The purity of polyphylla saponin I was assayed by high performance liquid chromatography. Methyl thiazolyl tetrazolium assay and analyses of cytopathic effects were performed to examine the antiviral activity of polyphylla saponin I upon MDCK cells infected with influenza A virus. Model mice were made by intranasal inoculation of influenza a virus. Mice infected with influenza A virus were orally administered polyphylla saponin I and oseltamivir twice a day for 5 days to study their antiviral efficacy in vivo. RESULTS: Polyphylla saponin I had no cytotoxicity on MDCK cells at the concentration of 50 µg/mL. Polyphylla saponin I (6.25, 12.5, 25 and 50 µg/mL) and oseltamivir (40 µg/mL) had remarkable inactivation effects on influenza A virus, prevention effects on influenza A virus adsorption on MDCK cells, and inhibitory effects on the reproduction of influenza A virus in MDCK cells. In addition, polyphylla saponin I (5 and 10 mg/kg), and oseltamivir (3 mg/kg) significantly reduced viral hemagglutination titer, improved the pathologic histology of lung tissues, and decreased the mortality of mice infected with influenza A virus. Polyphylla saponin I (5 and 10 mg/kg) prolonged the survival time of mice from 8.5±0.3 days to 13.2±0.5 days, with the prolonged life rates being 49.4% and 55.3%, respectively. CONCLUSION: Polyphylla saponin I has antiviral activity on influenza A virus both in vitro and in vivo.

Fabrication of cysteine-responsive biomimetic single nanochannels by a thiol-yne reaction strategy and their application for sensing in urine samples.

A photoinitiated thiol-yne click reaction strategy is used to fabricate a novel responsive biomimetic nanochannel platform. It displays a selective response for Cys by way of covalent bond formation on the channel surface. This system can be applied for Cys sensing with high specificity and non-interference performance in complex matrices and human urine samples.

Hg2+ wettability and fluorescence dual-signal responsive switch based on a cysteine complex of piperidine-calix[4]arene.

The recognition of the mercury(II) ion (Hg(2+)) is essential because of its extreme toxicity in the environment and food. Hence we reported a novel cysteine (Cys) complex of piperidine-calix[4]arene (L) as a convenient and effective dual-signal responsive switch for Hg(2+). This switch system exhibited excellent selectivity toward Hg(2+) by fluorescence (FL), (1)H NMR spectroscopy and the atomic force microscopy (AFM). More importantly, the Hg(2+)-responsive switch had an important and potential application by water contact angle (CA) on a functional micro-nano silicon surface, including intelligent microfluidic and laboratory-on-chip devices, controllable drug delivery, and self-cleaning surfaces.