An Ionic Assisted Enhancement Strategy Enabled High Performance Flexible Pressure-Temperature Dual Sensor.

Flexible pressure sensors with a broad range and high sensitivity are greatly desired yet challenging to build. Herein, we have successfully fabricated a pressure-temperature dual sensor via an ionic assisted charge enhancement strategy. Benefiting from the immobilization effect for [EMIM+] [TFSI-] ion pairs and charge transfer between ionic liquid (IL) and HFMO (H10Fe3Mo21O51), the formed IL-HFMO-TPU pressure sensor shows a high sensitivity of 25.35 kPa-1 and broad sensing range (∼10 MPa), respectively. Furthermore, the sensor device exhibits high durability and stability (5000 cycles@1 MPa). The IL-HFMO-TPU sensor also shows the merit of good temperature sensing properties. Attributed to these superior properties, the proposed sensor device could detect pressure in an ultrawide sensing range (from Pa to MPa), including breathe and biophysical signal monitoring etc. The proposed ionic assisted enhancement approach is a generic strategy for constructing high performance flexible pressure-temperature dual sensor.

Pancreatic α- and ß-cellular clocks have distinct molecular properties and impact on islet hormone secretion and gene expression.

A critical role of circadian oscillators in orchestrating insulin secretion and islet gene transcription has been demonstrated recently. However, these studies focused on whole islets and did not explore the interplay between α-cell and ß-cell clocks. We performed a parallel analysis of the molecular properties of α-cell and ß-cell oscillators using a mouse model expressing three reporter genes: one labeling α cells, one specific for ß cells, and a third monitoring circadian gene expression. Thus, phase entrainment properties, gene expression, and functional outputs of the α-cell and ß-cell clockworks could be assessed in vivo and in vitro at the population and single-cell level. These experiments showed that α-cellular and ß-cellular clocks are oscillating with distinct phases in vivo and in vitro. Diurnal transcriptome analysis in separated α and ß cells revealed that a high number of genes with key roles in islet physiology, including regulators of glucose sensing and hormone secretion, are differentially expressed in these cell types. Moreover, temporal insulin and glucagon secretion exhibited distinct oscillatory profiles both in vivo and in vitro. Altogether, our data indicate that differential entrainment characteristics of circadian α-cell and ß-cell clocks are an important feature in the temporal coordination of endocrine function and gene expression.

A developmental lineage-based gene co-expression network for mouse pancreatic ß-cells reveals a role for Zfp800 in pancreas development.

To gain a deeper understanding of pancreatic ß-cell development, we used iterative weighted gene correlation network analysis to calculate a gene co-expression network (GCN) from 11 temporally and genetically defined murine cell populations. The GCN, which contained 91 distinct modules, was then used to gain three new biological insights. First, we found that the clustered protocadherin genes are differentially expressed during pancreas development. Pcdhγ genes are preferentially expressed in pancreatic endoderm, Pcdhß genes in nascent islets, and Pcdhα genes in mature ß-cells. Second, after extracting sub-networks of transcriptional regulators for each developmental stage, we identified 81 zinc finger protein (ZFP) genes that are preferentially expressed during endocrine specification and ß-cell maturation. Third, we used the GCN to select three ZFPs for further analysis by CRISPR mutagenesis of mice. Zfp800 null mice exhibited early postnatal lethality, and at E18.5 their pancreata exhibited a reduced number of pancreatic endocrine cells, alterations in exocrine cell morphology, and marked changes in expression of genes involved in protein translation, hormone secretion and developmental pathways in the pancreas. Together, our results suggest that developmentally oriented GCNs have utility for gaining new insights into gene regulation during organogenesis.

TRPM7 is a crucial regulator of pancreatic endocrine development and high-fat-diet-induced ß-cell proliferation.

The melastatin subfamily of the transient receptor potential channels (TRPM) are regulators of pancreatic ß-cell function. TRPM7 is the most abundant islet TRPM channel; however, the role of TRPM7 in ß-cell function has not been determined. Here, we used various spatiotemporal transgenic mouse models to investigate how TRPM7 knockout influences pancreatic endocrine development, proliferation and function. Ablation of TRPM7 within pancreatic progenitors reduced pancreatic size, and α-cell and ß-cell mass. This resulted in modestly impaired glucose tolerance. However, TRPM7 ablation following endocrine specification or in adult mice did not impact endocrine expansion or glucose tolerance. As TRPM7 regulates cell proliferation, we assessed how TRPM7 influences ß-cell hyperplasia under insulin-resistant conditions. ß-Cell proliferation induced by high-fat diet was significantly decreased in TRPM7-deficient ß-cells. The endocrine roles of TRPM7 may be influenced by cation flux through the channel, and indeed we found that TRPM7 ablation altered ß-cell Mg2+ and reduced the magnitude of elevation in ß-cell Mg2+ during proliferation. Together, these findings revealed that TRPM7 controls pancreatic development and ß-cell proliferation, which is likely due to regulation of Mg2+ homeostasis.

Dysfunctional APPL1-Mediated Epigenetic Regulation in Diabetic Vascular Injury.

BACKGROUND: APN (adiponectin) and APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1) are potent vasculoprotective molecules, and their deficiency (eg, hypoadiponectinemia) contributes to diabetic vascular complications. However, the molecular mechanisms that govern their vasculoprotective genes as well as their alteration by diabetes remain unknown. METHODS: Diabetic medium-cultured rat aortic endothelial cells, mouse aortic endothelial cells from high-fat-diet animals, and diabetic human aortic endothelial cells were used for molecular/cellular investigations. The in vivo concept-prove demonstration was conducted using diabetic vascular injury and diabetic hindlimb ischemia models. RESULTS: In vivo animal experiments showed that APN replenishment caused APPL1 nuclear translocation, resulting in an interaction with HDAC (histone deacetylase) 2, which inhibited HDAC2 activity and increased H3Kac27 levels. Based on transcriptionome pathway-specific real-time polymerase chain reaction profiling and bioinformatics analysis, Angpt1 (angiopoietin 1), Ocln (occludin), and Cav1 (caveolin 1) were found to be the top 3 vasculoprotective genes suppressed by diabetes and rescued by APN in an APPL1-dependent manner. APN reverses diabetes-induced inhibition of Cav1 interaction with APPL1. APN-induced Cav1 expression was not affected by Angpt1 or Ocln deficiency, whereas APN-induced APPL1 nuclear translocation or upregulation of Angpt1/Ocln expression was abolished in the absence of Cav1 both in vivo and in vitro, suggesting Cav1 is upstream molecule of Angpt1/Ocln in response to APN administration. Chromatin immunoprecipitation-qPCR (quantitative polymerase chain reaction) demonstrated that APN caused significant enrichment of H3K27ac in Angpt1 and Ocln promoter region, an effect blocked by APPL1/Cav1 knockdown or HDAC2 overexpression. The protective effects of APN on the vascular system were attenuated by overexpression of HDAC2 and abolished by knocking out APPL1 or Cav1. The double knockdown of ANGPT1/OCLN blunted APN vascular protection both in vitro and in vivo. Furthermore, in diabetic human endothelial cells, HDAC2 activity is increased, H3 acetylation is decreased, and ANGPT1/OCLN expression is reduced, suggesting that the findings have important translational implications. CONCLUSIONS: Hypoadiponectinemia and dysregulation of APPL1-mediated epigenetic regulation are novel mechanisms leading to diabetes-induced suppression of vasculoprotective gene expression. Diabetes-induced pathological vascular remodeling may be prevented by interventions promoting APPL1 nuclear translocation and inhibiting HDAC2.

Inducible Fgf13 ablation alleviates cardiac fibrosis via regulation of microtubule stability.

Fibroblast growth factor (FGF) isoform 13, a distinct type of FGF, boasts significant potential for therapeutic intervention in cardiovascular dysfunctions. However, its impact on regulating fibrosis remains unexplored. This study aims to elucidate the role and mechanism of FGF13 on cardiac fibrosis. Here, we show that following transverse aortic constriction (TAC) surgery, interstitial fibrosis and collagen content increase in mice, along with reduced ejection fraction and fractional shortening, augmented heart mass. However, following Fgf13 deletion, interstitial fibrosis is decreased, ejection fraction and fractional shortening are increased, and heart mass is decreased, compared with those in the TAC group. Mechanistically, incubation of cardiac fibroblasts with transforming growth factor ß (TGFß) increases the expressions of types I and III collagen proteins, as well as α-smooth muscle actin (α-SMA) proteins, and enhances fibroblast proliferation and migration. In the absence of Fgf13, the expressions of these proteins are decreased, and fibroblast proliferation and migration are suppressed, compared with those in the TGFß-stimulated group. Overexpression of FGF13, but not FGF13 mutants defective in microtubule binding and stabilization, rescues the decrease in collagen and α-SMA protein and weakens the proliferation and migration function of the Fgf13 knockdown group. Furthermore, Fgf13 knockdown decreases ROCK protein expression via microtubule disruption. Collectively, cardiac Fgf13 knockdown protects the heart from fibrosis in response to haemodynamic stress by modulating microtubule stabilization and ROCK signaling pathway.

Heteropolyacids: An Ultrasensitive Ionic Volume-Enhanced Raman Scattering Platform.

Surface-enhanced Raman scattering (SERS) is regarded as the most direct and powerful tool to identify chemical fingerprints. However, current SERS substrate materials still face some critical challenges, including low molecular utilization efficiency and low selectivity. Herein, a novel oxygen vacancy heteropolyacid─H10Fe3Mo21O51 (HFMO)─is developed as a high-performance volume-enhanced Raman scattering (VERS)-active platform. Due to its merit of water solubility, HFMO forms a special coordination bond with the probe molecule at the molecular level, which allows its enhancing ability to be comparable to that of noble metals. An enhancement factor of 1.26 × 109 and a very low detection limit of 10-13 M for rhodamine 6G were obtained. A robust O-N coordination bond was formed between the anion of HFMO and the probe molecule, resulting in a special electron transfer path (Mo-O-N) with high selectivity, which is verified using X-ray photoelectron spectroscopy analysis and density functional theory calculations. That is to say, the proposed HFMO platform has excellent VERS enhancing effect, specifically for the molecules containing the imino group (e.g., methyl blue, detection limit: 10-11 M), offering the merits of high reproducibility and uniformity, high-temperature resistance, long-time laser irradiation, and strong acid resistance. Such an initial effort on the ionic type VERS platform may enable the further development of highly sensitive, highly selective, and water-soluble VERS technology.

Different hydration methods for the prevention of contrast-induced nephropathy in patients with elective percutaneous coronary intervention: a retrospective study.

BACKGROUND: Hydration is currently the main measure to prevent contrast-induced nephropathy (CIN). We aimed to compare the preventive effect of preprocedure and postprocedure hydration on CIN in patients with coronary heart disease undergoing elective percutaneous coronary intervention (PCI). METHODS: A retrospective study included 198 cases of postprocedure hydration and 396 cases of preprocedure hydration using propensity score matching. The incidence of CIN 48 h after PCI and adverse events within 30 days after contrast media exposure were compared between the two groups. Logistic regression analysis was used to analyse the risk factors for CIN. RESULTS: The incidence of CIN in the postprocedure hydration group was 3.54%, while that in the preprocedure hydration group was 4.8%. There was no significant difference between the two groups (p = 0.478). Multivariate logistic regression analysis showed that diabetes mellitus, baseline BNP and cystatin C levels, and contrast agent dosage were independent risk factors for CIN. There was no significant difference in the incidence of major adverse events between the two groups (3.03% vs. 2.02%, p = 0.830). CONCLUSIONS: Postprocedure hydration is equally effective compared to preoperative hydration in the prevention of CIN in patients with coronary heart disease undergoing elective PCI.

A new alternative technique for the guidance of transjugular intrahepatic portosystemic shunt creation using DSA overlay reference.

BACKGROUND: Portal vein puncture (PVP) is a critical step during transjugular intrahepatic portosystemic shunt (TIPS) and correlates to several complications. Techniques guiding PVP are needed. PURPOSE: To evaluate the safety, feasibility, and efficiency of digital subtraction angiography (DSA) overlay reference during TIPS creation and compare it with transhepatic portal vein (THPV) guiding. MATERIAL AND METHODS: The clinical records of 185 patients at three medical centers who underwent TIPS placement were reviewed. Portal vein access was guided by THPV guiding in 120 cases and DSA overlay reference in 60 cases. The number of punctures, portal vein entry time, procedural adverse events, technical and hemodynamic success rate were analyzed to compare the safety, feasibility, and efficiency of the two methods. RESULTS: The median numbers of punctures in group 1 and group 2 were 2 (1-4) and 2 (1-5), respectively (P = 0.094). There was no statistical difference between two groups in needle passes. The median portal vein entry time of group 1 was 12 min (8-16 min) and 13 min (8-16 min) in group 2. No significant difference was found in the PVP time (P = 0.802). Arterioportal fistula formation occurred in 15 patients in group 1; two patients in group 2 had hepatic artery injury. The patients in group 2 had lower rates of procedural adverse events (P = 0.047). Median dose area product of G1 was lower than G2 statistically (P<0.001). There was no significant difference in total fluoroscopy time (P = 0.856). CONCLUSION: DSA overlay reference has lower procedural adverse events rates compared with THPV guiding TIPS. It seems to be a safe and effective method for guiding PVP.

The overestimated prevalence of hypertension in a population survey: a cross-sectional study from Hebei province, China.

OBJECTIVE: Currently, the prevalence of hypertension is mainly ascertained using a one-visit population survey, which may lead to overestimation. The purpose of this study was to assess the accuracy of hypertension prevalence determined by a one-visit population survey. METHODS: For this cross-sectional study, we continuously enrolled 1116 volunteers without a hypertension history in Hebei province from January 2018 to December 2019. The study population included 511 (45.80%) males and 605 (54.20%) females with a mean age of 48 years. The hypertension prevalence was assessed using two methods: one-visit screening and daytime ambulatory blood pressure (BP) monitoring. We directly compared the performances of daytime ambulatory BP monitoring and one-visit screening in the same group of subjects. In addition, we explored possible thresholds to improve the detection of hypertension. RESULTS: During the one-visit survey, the mean BP value was about 8 mmHg higher than that determined by daytime ambulatory BP monitoring. The prevalence of hypertension was 29.84% and 14.07% during the one-visit and daytime multiple visit surveys, respectively. The risk factors for overestimated hypertension were female sex, body mass index < 24.00 kg/m2, and diastolic BP of 100 mmHg. The positive predictive value of the one-visit population survey for diagnosing hypertension was 36.34%. Furthermore, receiver operating characteristic analysis showed that in males, the best diagnostic threshold for hypertension diagnosis was 148/96 mmHg. CONCLUSION: The hypertension prevalence was likely overestimated by 2-fold in the one-visit survey group compared to the daytime ambulatory BP monitoring group. Thus, the threshold for one-visit BP screening should be raised to 148/96 mmHg to improve the accuracy of hypertension diagnosis.

FGF13 enhances resistance to platinum drugs by regulating hCTR1 and ATP7A via a microtubule-stabilizing effect.

Platinum-based regimens are the most widely used chemotherapy regimens, but cancer cells often develop resistance, which impedes therapy outcome for patients. Previous studies have shown that fibroblast growth factor 13 (FGF13) is associated with resistance to platinum drugs in HeLa cells. However, the mechanism and universality of this effect have not been clarified. Here, we found that FGF13 was associated with poor platinum-based chemotherapy outcomes in a variety of cancers, such as lung, endometrial, and cervical cancers, through bioinformatics analysis. We then found that FGF13 simultaneously regulates the expression and distribution of hCTR1 and ATP7A in cancer cells, causes reduced platinum influx, and promotes platinum sequestration and efflux upon cisplatin exposure. We subsequently observed that FGF13-mediated platinum resistance requires the microtubule-stabilizing effect of FGF13. Only overexpression of FGF13 with the -SMIYRQQQ- tubulin-binding domain could induce the platinum resistance effect. This phenomenon was also observed in SK-MES-1 cells, KLE cells, and 5637 cells. Our research reveals the mechanism of FGF13-induced platinum drug resistance and suggests that FGF13 can be a sensibilization target and prognostic biomarker for chemotherapy.

ROCK-nmMyoII, Notch and Neurog3 gene-dosage link epithelial morphogenesis with cell fate in the pancreatic endocrine-progenitor niche.

During mouse pancreas organogenesis, endocrine cells are born from progenitors residing in an epithelial plexus niche. After a period in a lineage-primed Neurog3LO state, progenitors become endocrine committed via upregulation of Neurog3 We find that the Neurog3LO to Neurog3HI transition is associated with distinct stages of an epithelial egression process: narrowing the apical surface of the cell, basalward cell movement and eventual cell-rear detachment from the apical lumen surface to allow clustering as nascent islets under the basement membrane. Apical narrowing, basalward movement and Neurog3 transcriptional upregulation still occur without Neurog3 protein, suggesting that morphogenetic cues deployed within the plexus initiate endocrine commitment upstream or independently of Neurog3. Neurog3 is required for cell-rear detachment and complete endocrine-cell birth. The ROCK-nmMyoII pathway coordinates epithelial-cell morphogenesis and the progression through Neurog3-expressing states. NmMyoII is necessary for apical narrowing, basalward cell displacement and Neurog3 upregulation, but all three are limited by ROCK activity. We propose that ROCK-nmMyoII activity, Neurog3 gene-dose and Notch signaling integrate endocrine fate allocation with epithelial plexus growth and morphogenesis, representing a feedback control circuit that coordinates morphogenesis with lineage diversification in the endocrine-birth niche.

Quantitative assessment of cell population diversity in single-cell landscapes.

Single-cell RNA sequencing (scRNA-seq) has become a powerful tool for the systematic investigation of cellular diversity. As a number of computational tools have been developed to identify and visualize cell populations within a single scRNA-seq dataset, there is a need for methods to quantitatively and statistically define proportional shifts in cell population structures across datasets, such as expansion or shrinkage or emergence or disappearance of cell populations. Here we present sc-UniFrac, a framework to statistically quantify compositional diversity in cell populations between single-cell transcriptome landscapes. sc-UniFrac enables sensitive and robust quantification in simulated and experimental datasets in terms of both population identity and quantity. We have demonstrated the utility of sc-UniFrac in multiple applications, including assessment of biological and technical replicates, classification of tissue phenotypes and regional specification, identification and definition of altered cell infiltrates in tumorigenesis, and benchmarking batch-correction tools. sc-UniFrac provides a framework for quantifying diversity or alterations in cell populations across conditions and has broad utility for gaining insight into tissue-level perturbations at the single-cell resolution.

Relationship among atrial fibrillation, the CHA2DS2-VASc score and ischaemic stroke in patients with coronary artery disease: a propensity score matching study in Hebei, China.

BACKGROUND: Recent evidence has shown that the pathogenesis of ischaemic stroke associated with atrial fibrillation (AF) is complex and involves other factors in addition to arrhythmias. The purpose of this study was to investigate the relationship among AF, CHA2DS2-VASc score and ischaemic stroke in patients with coronary artery disease (CAD) in Hebei, China. METHODS: A total of 2,335 patients with CAD from September 2016 to May 2019 at the Second Hospital of Hebei Medical University were included (mean age 62.73 ± 10.35 years, range 26-92 years; 41.58% female). This was a cross-sectional study, and participants were divided into non-stroke (n = 1997) and ischaemic stroke groups (n = 338). Propensity score matching (PSM) was performed to match ischaemic stroke patients with non-stroke patients in a 1:4 ratio. The relationship among AF, the CHA2DS2-VASc score and ischaemic stroke was evaluated using univariable generalized linear models for different sex, age, body mass index (BMI), CAD and CHA2DS2-VASc score subgroups. Univariable and multivariable generalized linear models were used to evaluate the relationship between AF and ischaemic stroke in the different models. RESULTS: Compared with that in the non-stroke group, the prevalence of AF (8.81% vs. 14.20%, P = 0.002) in the ischaemic stroke group was higher. The proportion of patients with ischaemic stroke was significantly different between the AF group and the non-AF group (28.74% vs. 19.04%, P = 0.003). An increasing CHA2DS2-VASc score was associated with a gradual increase in the prevalence of AF (P for trend < 0.001). Subgroup analysis showed that the trend towards increased stroke risk in the AF group was consistent across the various subgroups. The multivariable analysis demonstrated that AF was not associated with ischaemic stroke compared with the absence of AF (OR = 1.55, 95% CI 0.94-2.56, P = 0.087). CONCLUSION: In our cross-sectional study, after adjustment for confounding factors, there was no association between AF and ischaemic stroke. The increased risk of ischaemic stroke associated with AF was attenuated by atherosclerotic factors. Our study supports the current view that enhanced control of modifiable cardiovascular risk factors in patients with AF is essential.

SD + SV4 diagnosis of left ventricular hypertrophy, a revaluation of ECG criterion by cardiac magnetic resonance imaging.

BACKGROUD: Present electrocardiogram (ECG) criteria for diagnosing left ventricular hypertrophy (LVH) usually have low sensitivity, while the newly proposed SD + SV4 criterion, namely the deepest S-wave amplitude in any lead (SD) plus SV4 amplitude, has been reported to have higher sensitivity and accuracy compared with other existing criteria. We aimed to further evaluate the diagnostic value of the SD + SV4 criterion in reference to the gold standard cardiac magnetic resonance imaging (CMR) in LVH diagnosis. METHODS: This retrospective study enrolled 138 patients who received CMR examination-60 patients with reduced ejection fraction (EF) and 78 patients with preserved EF. The left ventricular mass index (LVMI) measured by CMR was used as the gold standard for diagnosing LVH. RESULT: The diagnostic value of the SD + SV4 criterion was compared with other 4 commonly used criteria. By CMR, 29 out of 138 people (21%) were diagnosed with LVH in reference to CMR. The SD + SV4 criterion had markedly higher sensitivity in diagnosing LVH compared with other criteria, but no higher specificity. There was no significant difference in area under receiver operating characteristic (ROC) curve among these criteria. The SD + SV4 criterion was not markedly consistent with CMR in diagnosing LVH. Compared to the other criteria, the SD + SV4 criterion had the highest sensitivity in patients with reduced ejection fraction; however, the area under the curve (AUC) of the SD + SV4 criterion in patients with reduced EF was significantly lower than in patients with preserved EF. CONCLUSION: The newly proposed SD + SV4 criterion did not have a better diagnostic value compared with other existing criteria, and the statistical power of the SD + SV4 criterion was influenced by EF.

Diabetes recovery by age-dependent conversion of pancreatic δ-cells into insulin producers.

Total or near-total loss of insulin-producing ß-cells occurs in type 1 diabetes. Restoration of insulin production in type 1 diabetes is thus a major medical challenge. We previously observed in mice in which ß-cells are completely ablated that the pancreas reconstitutes new insulin-producing cells in the absence of autoimmunity. The process involves the contribution of islet non-ß-cells; specifically, glucagon-producing α-cells begin producing insulin by a process of reprogramming (transdifferentiation) without proliferation. Here we show the influence of age on ß-cell reconstitution from heterologous islet cells after near-total ß-cell loss in mice. We found that senescence does not alter α-cell plasticity: α-cells can reprogram to produce insulin from puberty through to adulthood, and also in aged individuals, even a long time after ß-cell loss. In contrast, before puberty there is no detectable α-cell conversion, although ß-cell reconstitution after injury is more efficient, always leading to diabetes recovery. This process occurs through a newly discovered mechanism: the spontaneous en masse reprogramming of somatostatin-producing δ-cells. The juveniles display 'somatostatin-to-insulin' δ-cell conversion, involving dedifferentiation, proliferation and re-expression of islet developmental regulators. This juvenile adaptability relies, at least in part, upon the combined action of FoxO1 and downstream effectors. Restoration of insulin producing-cells from non-ß-cell origins is thus enabled throughout life via δ- or α-cell spontaneous reprogramming. A landscape with multiple intra-islet cell interconversion events is emerging, offering new perspectives for therapy.

Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation.

BACKGROUND: Platelet activation occurs upon ischemia/reperfusion and is related to the generation of reactive oxygen species (ROS) during this process. Vitamin C (VC) is a powerful antioxidant. VC scavenges ROS, reduces platelet activation, and attenuates reperfusion injury. However, the effects of VC on platelets undergoing hypoxia/reoxygenation (H/R) remain unclear. OBJECTIVES: Herein, we evaluated the effects of VC on platelets in vitro following H/R and the related mechanisms. METHOD: Fresh platelets were collected from 67 volunteers at the Blood Center of Hebei Province. Platelets were diluted with saline to a concentration of 2.00 × 1011/L. Aggregation and the curve slope were evaluated within 4 h with a whole-blood impedance analyzer. To determine the optimal experimental time, platelets were treated with hypoxia or reoxygenation for different times, and impedance aggregometry was carried out by measuring changes in electrical impedance induced by arachidonic acid (0.5 mM) and adenosine diphosphate (10 µM), thereby establishing the H/R model. Three antioxidants (VC, melatonin, and probucol) were used to treat platelets after H/R, and impedance aggregometry was used to determine their effects on platelet aggregation. The influence of VC on apoptosis-related indicators was detected. ROS and the mitochondrial membrane potential were observed by inverted fluorescence microscopy and flow cytometry, respectively. Related protein levels were detected by Western blotting. RESULTS: ROS scavengers inhibited platelet activation and aggregation in a concentration-dependent manner. VC post-conditioning scavenged ROS, downregulated cytochrome C, Bax, and caspase-9 proteins, and upregulated Bcl-2 protein. These effects collectively blocked platelet apoptosis and inhibited platelet aggregation. CONCLUSIONS: VC inhibited platelet aggregation by blocking apoptosis. Thus, VC may have applications in the treatment of platelet-related diseases.

Photonic hooks from Janus microcylinders.

Recently, a type of curved light beams, photonic hooks (PHs), was theoretically predicted and experimentally observed. The production of photonic hook (PH) is due to the breaking of structural symmetry of a plane-wave illuminated microparticle. Herein, we presented and implemented a new approach of utilizing the symmetry-broken of the microparticles in material composition for the generation of PHs from Janus microcylinders. Finite element method-based numerical simulation and energy flow-represented theoretical analysis were used to investigate the field distribution characteristics and formation mechanism of the PHs. The full width at half-maximum (FWHM) of the PH (∼0.29λ) is smaller than the FWHM of the photonic nanojet (∼0.35λ) formed from a circular microcylinder with the same geometric radius. By changing the refractive index contrasts between upper and lower half-cylinders or rotating the Janus microcylinder relative to the central axis, the shape profiles of the PHs can be efficiently modulated. The tunability of the PHs through simple stretching or compression operations for the Janus microcylinder constituted by one solid inorganic half-cylinder and the other flexible polymer half-cylinder was studied and discussed as well.

Elevated high-sensitivity C-reactive protein combined with procalcitonin predicts high risk of contrast-induced nephropathy after percutaneous coronary intervention.

BACKGROUND: Contrast-induced nephropathy (CIN) is common after percutaneous coronary intervention (PCI) and always leads to a poor prognosis. Compared with conventional detection methods, either high-sensitivity C-reactive protein (hs-CRP) or procalcitonin have higher sensitivity and specificity for predicting CIN, but their combination has not been explored. This prospective study investigated the value of hs-CRP combined with procalcitonin for predicting CIN after PCI. METHODS: All patients undergoing PCI admitted to our hospital during the year 2016 were consecutively enrolled (n = 343). The patients received adequate hydration before PCI and 20 mg furosemide after the procedure. CIN was diagnosed by a 25% elevation in serum creatinine or ≥ 44.2 µmol/L (0.5 mg/dL) serum creatinine within 48 to 72 h after intravenous injection of contrast media. RESULTS: Patients with high hs-CRP or procalcitonin had higher rates of CIN relative to those patients with low values. For predicting CIN, hs-CRP combined with procalcitonin showed an area under the receiver operating characteristic curve of 0.67, with optimal cut-off value 0.0643610, and the sensitivity and specificity were higher than hs-CRP or procalcitonin alone. The logistic regression analysis showed that high-risk factors of CIN were acute myocardial infarction and highly elevated hsCRP and procalcitonin. CONCLUSIONS: Prior to PCI, an elevation of the inflammatory biomarkers hsCRP and procalcitonin are a risk factor for postoperative CIN. This study suggests that the combination of hsCRP and procalcitonin is a better predictor of CIN after PCI then either hsCRP or procalcitonin alone. TRIAL REGISTRATION NUMBER: ChiCTR-IOR-14005250. Date of registration 2014-09-24.

Large-scale synthesis of single-crystalline self-standing SnSe2 nanoplate arrays for wearable gas sensors.

Advances in two-dimensional semiconducting thin films enable the realization of wearable electronic devices in the form factor of flexible substrate/thin films that can be seamlessly adapted in our daily lives. For wearable gas sensing, two-dimensional materials, such as SnSe2, are particularly favorable because of their high surface-to-volume ratio and strong adsorption of gas molecules. Chemical vapor deposition and liquid/mechanical exfoliation are the widely applied techniques to obtain SnSe2 thin films. However, these methods normally result in non-uniform and isolated flakes which cannot apply to the practical industrial-scale wearable electronic devices. Here, we demonstrate large-scale (10 cm × 10 cm), uniform, and self-standing SnSe2 nanoplate arrays by co-evaporation process on flexible polyimide substrates. Both structural and morphological properties of the resulting SnSe2 nanoplates are systematically investigated. Particularly, the single-crystalline SnSe2 nanoplates are achieved. Furthermore, we explore the application of the polyimide/SnSe2 nanoplate arrays as wearable gas sensors for detecting methane. The wearable gas sensors show high sensitivity, fast response and recovery, and good uniformity. Our approach not only provides an efficient technique to obtain large-area, uniform and high-quality single-crystalline SnSe2 nanoplates, but also impacts on the future developments of layered metal dichalcogenides-based wearable devices.