Lanthanide-Free Infinite Coordination Polymer Nanoparticles for Real-Time Monitoring of Alkaline Phosphatase and Its Application for Digital Algal Bloom Detection

In this study, 1,1,2,2-tetra­(4-carboxylphenyl)­ethylene (H4TCPE) with the aggregation-induced emission (AIE) feature and sulforhodamine 101 (SR101) with the aggregation-caused quenching (ACQ) feature were rationally selected and introduced into a lanthanide-free infinite coordination polymer (ICP) host consisting of copper ions (Cu2+) and guanosine-5-monophosphate (GMP). The host–guest effect empowered the H4TCPE/SR101/Cu-GMP ICP nanoparticles with opposite emission characteristics and a blue color. Under the stimuli of alkaline phosphatase (ALP), the ligand GMP was hydrolyzed and the network structure of the Cu-GMP ICP host was destructed, resulting in the state change of both guests and the corresponding ratiometric emission changes: the AIE of H4TCPE at 450 nm (blue fluorescence) was quenched, while the ACQ of SR101 at 625 nm (red fluorescence) was recovered. As the signal response directly stemmed from the substrate, the H4TCPE/SR101/Cu-GMP ICP nanoparticles not only allowed for ALP detection with high sensitivity and specificity but also enabled ALP activity monitoring in a real-time fashion. Based on the great analytical performance, the H4TCPE/SR101/Cu-GMP ICP nanoparticles could be successfully applied for the dynamical monitoring of ALP in environmental samples under different spatial–temporal conditions. Furthermore, besides the spectral response, the blue color H4TCPE/SR101/Cu-GMP ICP nanoparticles turned pink, while dual-wavelength emissions led to a purple-blue to red fluorescence color change. These color changes could be recognized using a smartphone in the form of the R/B ratio, which offers great field application potential for the establishment of a new digital analytical platform with reliability in algal bloom warning with surging ALP as an effective indicator

Image_1_Comparison of dynamic visual acuity after implantation of toric bifocal or trifocal intraocular lens in age-related cataract patients: a randomized controlled trial.TIF

PurposeTo investigate the dynamic visual acuity (DVA) after implantation of toric bifocal or trifocal intraocular lens in age-related cataract patients.MethodsThis was a prospective randomized controlled trial. Of one hundred and twenty-four patients enrolled and randomized to receive unilateral phacoemulsification and toric trifocal (939 M/MP, Carl Zeiss Meditec AG, Jena, Germany) or toric bifocal (909 M, Carl Zeiss Meditec AG, Jena, Germany) intraocular lenses (IOL) implantation, ninety-nine patients completed the follow-up and were included in final analysis. Postoperatively, uncorrected and corrected distance (UDVA and CDVA), intermediate (UIVA and DCIVA) and near (UNVA and DCNVA) static visual acuity, manifest refraction and uncorrected and corrected distance DVA (UDDVA and CDDVA) at 20, 40 and 80 degrees per second (dps) were evaluated at one week, one month and three months.ResultsThree months postoperatively, the UDVA were 0.13 ± 0.11 and 0.14 ± 0.13 in the toric trifocal and bifocal IOL group, respectively. Significant better UIVA (trifocal, 0.17 ± 0.13 vs. bifocal, 0.23 ± 0.13, p = 0.037) and DCIVA (trifocal, 0.16 ± 0.11 vs. bifocal, 0.20 ± 0.12, p = 0.048) were observed in patients implanting toric trifocal than bifocal IOL at three months postoperatively. Patients implanted with toric bifocal IOL obtained better CDDVA at 80 dps (0.5607 ± 0.2032) than the trifocal group (0.6573 ± 0.2450, p = 0.039) at three months. Postoperative UDDVA and CDDVA at 20, 40 and 80 dps were significantly associated with age (p ConclusionToric trifocal IOL provides better static intermediate visual acuity, and toric bifocal IOL implantation provides better distance dynamic visual acuity at high speed.</p

Lab-on-a-ZnO-Submicron-Particle Sensor Array for Monitoring AD upon Cd²⁺ Exposure with CSF Tau441% as an Effective Hallmark

In this study, based on the posttreatment strategy, blue-color-emissive ZnO submicron particles (B-ZnO SMPs) and red-color-emissive ZnO submicron particles (R-ZnO SMPs) were obtained from rationally designed Zn-infinite coordination polymer (ICP) precursors. After modification of thiol-containing aptamers, diverse spectral changes in the ultraviolet and visible regions of B- and R-ZnO SMPs toward different tau species were explored to construct a lab-on-a-ZnO-submicron-particle sensor array. Assisted by principal component analysis (PCA), the unique fingerprints of the sensor array enabled the simultaneous differentiation and quantitative detection of different tau species (tau381, tau410, and tau441) for the first time. Furthermore, the dynamic changes of tau441% (the ratio of the two most reported representative 4R isoform (full-length tau441) and 3R isoform (tau381)) in cerebrospinal fluid (CSF) during the Alzheimer’s disease (AD) onset of Cd2+-exposed rats could also be monitored by the lab-on-a-ZnO-submicron-particle sensor array, which was supposed to be an effective hallmark and highly correlated with the formation of neurofibrillary tangles (NFTs). This study not only provides a further insight into the involvement of subchronic Cd2+ exposure in the tau etiology of AD but also offers more comprehensive and effective information about the asymptomatic stage of AD upon environmental risk, which has potential applications in the early diagnosis and therapy

Lab-on-a-ZnO-Submicron-Particle Sensor Array for Monitoring AD upon Cd²⁺ Exposure with CSF Tau441% as an Effective Hallmark

In this study, based on the posttreatment strategy, blue-color-emissive ZnO submicron particles (B-ZnO SMPs) and red-color-emissive ZnO submicron particles (R-ZnO SMPs) were obtained from rationally designed Zn-infinite coordination polymer (ICP) precursors. After modification of thiol-containing aptamers, diverse spectral changes in the ultraviolet and visible regions of B- and R-ZnO SMPs toward different tau species were explored to construct a lab-on-a-ZnO-submicron-particle sensor array. Assisted by principal component analysis (PCA), the unique fingerprints of the sensor array enabled the simultaneous differentiation and quantitative detection of different tau species (tau381, tau410, and tau441) for the first time. Furthermore, the dynamic changes of tau441% (the ratio of the two most reported representative 4R isoform (full-length tau441) and 3R isoform (tau381)) in cerebrospinal fluid (CSF) during the Alzheimer’s disease (AD) onset of Cd2+-exposed rats could also be monitored by the lab-on-a-ZnO-submicron-particle sensor array, which was supposed to be an effective hallmark and highly correlated with the formation of neurofibrillary tangles (NFTs). This study not only provides a further insight into the involvement of subchronic Cd2+ exposure in the tau etiology of AD but also offers more comprehensive and effective information about the asymptomatic stage of AD upon environmental risk, which has potential applications in the early diagnosis and therapy

Lab-on-a-ZnO-Submicron-Particle Sensor Array for Monitoring AD upon Cd²⁺ Exposure with CSF Tau441% as an Effective Hallmark

In this study, based on the posttreatment strategy, blue-color-emissive ZnO submicron particles (B-ZnO SMPs) and red-color-emissive ZnO submicron particles (R-ZnO SMPs) were obtained from rationally designed Zn-infinite coordination polymer (ICP) precursors. After modification of thiol-containing aptamers, diverse spectral changes in the ultraviolet and visible regions of B- and R-ZnO SMPs toward different tau species were explored to construct a lab-on-a-ZnO-submicron-particle sensor array. Assisted by principal component analysis (PCA), the unique fingerprints of the sensor array enabled the simultaneous differentiation and quantitative detection of different tau species (tau381, tau410, and tau441) for the first time. Furthermore, the dynamic changes of tau441% (the ratio of the two most reported representative 4R isoform (full-length tau441) and 3R isoform (tau381)) in cerebrospinal fluid (CSF) during the Alzheimer’s disease (AD) onset of Cd2+-exposed rats could also be monitored by the lab-on-a-ZnO-submicron-particle sensor array, which was supposed to be an effective hallmark and highly correlated with the formation of neurofibrillary tangles (NFTs). This study not only provides a further insight into the involvement of subchronic Cd2+ exposure in the tau etiology of AD but also offers more comprehensive and effective information about the asymptomatic stage of AD upon environmental risk, which has potential applications in the early diagnosis and therapy

Data_Sheet_1_The impact of different corneal refractive surgeries on binocular dynamic visual acuity.DOCX

PurposeTo investigate the influence of different corneal refractive surgeries on dynamic visual acuity (DVA), and explore its potential influence factors.MethodsThis was a prospective non-randomized study. Adult myopic patients undergoing bilateral laser-assisted sub-epithelial keratomileusis (LASEK), femtosecond laser-assisted in situ keratomileusis (FS-LASIK), or small incision lenticule extraction (SMILE) with Plano refraction target were enrolled. Uncorrected and corrected distance visual acuity (UDVA/CDVA), manifest refraction and binocular optotype-moving DVA of 40 and 80 degrees per second (dps) were evaluated pre-operatively and post-operatively up to 3 months.ResultsThe study included 264 eyes of 132 subjects, with an average age of 27.0 ± 6.7 years, and females accounted for 59% of the participants. Significant improvement was observed at the 3-month visit for 40 dps (SMILE, P = 0.001; LASEK, P = 0.006; FS-LASIK, P = 0.010) and 80 dps (SMILE, P = 0.011; LASEK, P = 0.025; FS-LASIK, P = 0.012) DVA. Adjusting for pre-operative DVA, there was no significant difference in DVA among groups at 3 months post-operatively (P > 0.05 for multiple comparisons). Overall, multiple linear models demonstrated that post-operative DVA at 3 months was correlated with pre-operative DVA (40 dps, β = 0.349, P = 0.001; 80 dps, β = 0.447, P ConclusionDynamic visual acuity at 3 months post-operatively of the three corneal refractive surgeries was better than that before the surgery in adult myopic patients, and there was no significant difference among different surgical techniques. Post-operative DVA at 3 months was found correlated with pre-operative DVA, pre-operative SE, and post-operative UDVA. With further improvement, DVA could be a promising functional visual indicator for myopic patients undergoing refractive surgeries.</p

Table_1_Perturbation of Ephrin Receptor Signaling and Glutamatergic Transmission in the Hypothalamus in Depression Using Proteomics Integrated With Metabolomics.DOC

Hypothalamic dysfunction is a key pathological factor in inflammation-associated depression. In the present study, isobaric tags for relative-absolute quantitation (iTRAQ) combined with mass spectrometry and gas chromatography-mass spectrometry (GC-MS) were employed to detect the proteomes and metabolomes in the hypothalamus of the lipopolysaccharide (LPS)-induced depression mouse, respectively. A total of 187 proteins and 27 metabolites were differentially expressed compared with the control group. Following the integration of bi-omics data, pertinent pathways and molecular interaction networks were further identified. The results indicated altered molecules were clustered into Ephrin receptor signaling, glutamatergic transmission, and inflammation-related signaling included the LXR/RXR activation, FXR/RXR activation, and acute phase response signaling. First discovered in the hypothalamus, Ephrin receptor signaling regulates N-methyl-D-aspartate receptor (NMDAR)-predominant glutamatergic transmission, and further acted on AKT signaling that contributed to changes in hypothalamic neuroplasticity. Ephrin type-B receptor 2 (EPHB2), a transmembrane receptor protein in Ephrin receptor signaling, was significantly elevated and interacted with the accumulated NMDAR subunit GluN2A in the hypothalamus. Additionally, molecules involved in synaptic plasticity regulation, such as hypothalamic postsynaptic density protein-95 (PSD-95), p-AKT and brain-derived neurotrophic factor (BDNF), were significantly altered in the LPS-induced depressed group. It might be an underlying pathogenesis that the EPHB2-GluN2A-AKT cascade regulates synaptic plasticity in depression. EPHB2 can be a potential therapeutic target in the correction of glutamatergic transmission dysfunction. In summary, our findings point to the previously undiscovered molecular underpinnings of the pathophysiology in the hypothalamus of inflammation-associated depression and offer potential targets to develop antidepressants.</p

Table_2_Perturbation of Ephrin Receptor Signaling and Glutamatergic Transmission in the Hypothalamus in Depression Using Proteomics Integrated With Metabolomics.DOC

Hypothalamic dysfunction is a key pathological factor in inflammation-associated depression. In the present study, isobaric tags for relative-absolute quantitation (iTRAQ) combined with mass spectrometry and gas chromatography-mass spectrometry (GC-MS) were employed to detect the proteomes and metabolomes in the hypothalamus of the lipopolysaccharide (LPS)-induced depression mouse, respectively. A total of 187 proteins and 27 metabolites were differentially expressed compared with the control group. Following the integration of bi-omics data, pertinent pathways and molecular interaction networks were further identified. The results indicated altered molecules were clustered into Ephrin receptor signaling, glutamatergic transmission, and inflammation-related signaling included the LXR/RXR activation, FXR/RXR activation, and acute phase response signaling. First discovered in the hypothalamus, Ephrin receptor signaling regulates N-methyl-D-aspartate receptor (NMDAR)-predominant glutamatergic transmission, and further acted on AKT signaling that contributed to changes in hypothalamic neuroplasticity. Ephrin type-B receptor 2 (EPHB2), a transmembrane receptor protein in Ephrin receptor signaling, was significantly elevated and interacted with the accumulated NMDAR subunit GluN2A in the hypothalamus. Additionally, molecules involved in synaptic plasticity regulation, such as hypothalamic postsynaptic density protein-95 (PSD-95), p-AKT and brain-derived neurotrophic factor (BDNF), were significantly altered in the LPS-induced depressed group. It might be an underlying pathogenesis that the EPHB2-GluN2A-AKT cascade regulates synaptic plasticity in depression. EPHB2 can be a potential therapeutic target in the correction of glutamatergic transmission dysfunction. In summary, our findings point to the previously undiscovered molecular underpinnings of the pathophysiology in the hypothalamus of inflammation-associated depression and offer potential targets to develop antidepressants.</p

Data_Sheet_1_Perturbation of Ephrin Receptor Signaling and Glutamatergic Transmission in the Hypothalamus in Depression Using Proteomics Integrated With Metabolomics.docx

Hypothalamic dysfunction is a key pathological factor in inflammation-associated depression. In the present study, isobaric tags for relative-absolute quantitation (iTRAQ) combined with mass spectrometry and gas chromatography-mass spectrometry (GC-MS) were employed to detect the proteomes and metabolomes in the hypothalamus of the lipopolysaccharide (LPS)-induced depression mouse, respectively. A total of 187 proteins and 27 metabolites were differentially expressed compared with the control group. Following the integration of bi-omics data, pertinent pathways and molecular interaction networks were further identified. The results indicated altered molecules were clustered into Ephrin receptor signaling, glutamatergic transmission, and inflammation-related signaling included the LXR/RXR activation, FXR/RXR activation, and acute phase response signaling. First discovered in the hypothalamus, Ephrin receptor signaling regulates N-methyl-D-aspartate receptor (NMDAR)-predominant glutamatergic transmission, and further acted on AKT signaling that contributed to changes in hypothalamic neuroplasticity. Ephrin type-B receptor 2 (EPHB2), a transmembrane receptor protein in Ephrin receptor signaling, was significantly elevated and interacted with the accumulated NMDAR subunit GluN2A in the hypothalamus. Additionally, molecules involved in synaptic plasticity regulation, such as hypothalamic postsynaptic density protein-95 (PSD-95), p-AKT and brain-derived neurotrophic factor (BDNF), were significantly altered in the LPS-induced depressed group. It might be an underlying pathogenesis that the EPHB2-GluN2A-AKT cascade regulates synaptic plasticity in depression. EPHB2 can be a potential therapeutic target in the correction of glutamatergic transmission dysfunction. In summary, our findings point to the previously undiscovered molecular underpinnings of the pathophysiology in the hypothalamus of inflammation-associated depression and offer potential targets to develop antidepressants.</p

Table_3_Perturbation of Ephrin Receptor Signaling and Glutamatergic Transmission in the Hypothalamus in Depression Using Proteomics Integrated With Metabolomics.DOC

Hypothalamic dysfunction is a key pathological factor in inflammation-associated depression. In the present study, isobaric tags for relative-absolute quantitation (iTRAQ) combined with mass spectrometry and gas chromatography-mass spectrometry (GC-MS) were employed to detect the proteomes and metabolomes in the hypothalamus of the lipopolysaccharide (LPS)-induced depression mouse, respectively. A total of 187 proteins and 27 metabolites were differentially expressed compared with the control group. Following the integration of bi-omics data, pertinent pathways and molecular interaction networks were further identified. The results indicated altered molecules were clustered into Ephrin receptor signaling, glutamatergic transmission, and inflammation-related signaling included the LXR/RXR activation, FXR/RXR activation, and acute phase response signaling. First discovered in the hypothalamus, Ephrin receptor signaling regulates N-methyl-D-aspartate receptor (NMDAR)-predominant glutamatergic transmission, and further acted on AKT signaling that contributed to changes in hypothalamic neuroplasticity. Ephrin type-B receptor 2 (EPHB2), a transmembrane receptor protein in Ephrin receptor signaling, was significantly elevated and interacted with the accumulated NMDAR subunit GluN2A in the hypothalamus. Additionally, molecules involved in synaptic plasticity regulation, such as hypothalamic postsynaptic density protein-95 (PSD-95), p-AKT and brain-derived neurotrophic factor (BDNF), were significantly altered in the LPS-induced depressed group. It might be an underlying pathogenesis that the EPHB2-GluN2A-AKT cascade regulates synaptic plasticity in depression. EPHB2 can be a potential therapeutic target in the correction of glutamatergic transmission dysfunction. In summary, our findings point to the previously undiscovered molecular underpinnings of the pathophysiology in the hypothalamus of inflammation-associated depression and offer potential targets to develop antidepressants.</p