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A tunnel junction is constructed with an asymmetrically hydrogenated 8-ZGNR and the spin-dependent electron transport in it is studied. Due to the spin-semiconducting ZGNR, giant magnetoresistance and bipolar spin filtering effects are achieved.

Automatic segmentation of lesion, organ, and tissue from the medical image is an important part of medical image analysis, which are useful for improving the accuracy of disease diagnosis and clinical analysis. For skin melanomas lesions, the contrast ratio between lesions and surrounding skin is low and there are many irregular shapes, uneven distribution, and local and boundary features. Moreover, some hair covering the lesions destroys the local context. Polyp characteristics such as shape, size, and appearance vary at different development stages. Early polyps with small sizes have no distinctive features and could be easily mistaken for other intestinal structures, such as wrinkles and folds. Imaging positions and illumination conditions would alter polyps' appearance and lead to no visible transitions between polyps and surrounding tissue. It remains a challenging task to accurately segment the skin lesions and polyps due to the high variability in the location, shape, size, color, and texture of the target object. Developing a robust and accurate segmentation method for medical images is necessary.To achieve better segmentation performance while dealing with the difficulties above, a U-shape network based on the encoder and decoder structure is proposed to enhance the segmentation performance in target regions.In this paper, a novel deep network of the encoder-decoder model that combines HarDNet, dual attention (DA), and reverse attention (RA) is proposed. First, HarDNet68 is employed to extract the backbone features while improving the inference speed and computational efficiency. Second, the DA block is adopted to capture the global feature dependency in spatial and channel dimensions, and enrich the contextual information on local features. At last, three RA blocks are exploited to fuse and refine the boundary features to obtain the final segmentation results.Extensive experiments are conducted on a skin lesion dataset which consists of ISIC2016, ISIC2017, and ISIC 2018, and a polyp dataset which consists of several public datasets, that is, Kvasir, CVC-ClinicDB, CVC-ColonDB, ETIS, Endosece. The proposed method outperforms some state-of-art segmentation models on the ISIC2018, ISIC2017, and ISIC2016 datasets, with Jaccard's indexes of 0.846, 0.881, and 0.894, mean Dice coefficients of 0.907, 0.929, and 03939, precisions of 0.908, 0.977, and 0.968, and accuracies of 0.953, 0.975, and 0.972. Additionally, the proposed method also performs better than some state-of-art segmentation models on the Kvasir, CVC-ClinicDB, CVC-ColonDB, ETIS, and Endosece datasets, with mean Dice coefficients of 0.907, 0.935, 0.716, 0.667, and 0.887, mean intersection over union coefficients of 0.850, 0.885, 0.644, 0.595, and 0.821, structural similarity measures of 0.918, 0.953, 0.823, 0.807, and 0.933, enhanced alignment measures of 0.952, 0.983, 0.850, 0.817, and 0.957, mean absolute errors of 0.026, 0.007, 0.037, 0.030, and 0.009.The proposed deep network could improve lesion segmentation performance in polyp and skin lesion images. The quantitative and qualitative results show that the proposed method can effectively handle the challenging task of segmentation while revealing the great potential for clinical application.

Acute pancreatitis (AP) is one of the leading causes of hospital admission for gastrointestinal disorders. Although lipid peroxides are produced in AP, it is unknown if targeting lipid peroxides prevents AP. This study aimed to investigate the role of mitochondrial aldehyde dehydrogenase 2 (ALDH2), a critical enzyme for lipid peroxide degradation, in AP and the possible underlying mechanisms. Cerulein was used to induce AP in C57BL/6 J male mice and pancreatic acinar cells were used to elucidate underlying mechanisms in vitro. Pancreatic enzymes in the serum, lipid peroxidation products malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), and Bcl-2, Bax and cleaved caspase-3 were measured. ALDH2 activation with a small-molecule activator, Alda-1, reduced the levels of the pancreatic enzymes in the serum and the lipid peroxidation products MDA and 4-HNE. In addition, Alda-1 decreased Bax and cleaved caspase-3 expression and increased Bcl-2 expression in vivo and in vitro. In conclusion, ALDH2 activation by Alda-1 has a protective effect in cerulein-induced AP by mitigating apoptosis in pancreatic acinar cells by alleviating lipid peroxidation.

Background: Progression of nontarget lesions (NTLs) after percutaneous coronary intervention (PCI) has been reported. However, it remains unknown whether progression of NTLs was causally related to stenting. This study was undertaken to test the hypothesis that stent implantation triggers acute phase response and systemic inflammation which may be associated with progression of NTLs. Methods: Thirty New Zealand rabbits receiving endothelial denudation and atherogenic diet were randomly divided into stenting, sham, and control groups. Angiography and intravascular ultrasonography were performed in the stenting and sham groups, and stent implantation performed only in the stenting group. Histopathologic study was conducted and serum levels of APPs (acute phase proteins) measured in all rabbits. Proteomics analysis was performed to screen the potential proteins related to NTLs progression after stent implantation. The serum levels of APPs and inflammatory cytokines were measured in 147 patients undergoing coronary angiography or PCI. Results: Plaque burden in the NTLs was significantly increased 12 weeks after stent implantation in the stenting group versus sham group. Serum levels of APPs and their protein expression in NTLs were significantly increased and responsible for stenting-triggered inflammation. In patients receiving PCI, serum levels of SAA-1 (serum amyloid A protein 1), CRP (C-reactive protein), TNF (tumor necrosis factor)-α, and IL (interleukin)-6 were substantially elevated up to 1 month post-PCI. Conclusions: In a rabbit model of atherosclerosis, stent implantation triggered acute phase response and systemic inflammation, which was associated with increased plaque burden and pathological features of unstable plaque in NTLs. The potential mechanism involved vessel injury-triggered acute phase response manifested as increased serum levels of SAA-1, CRP, and LBP (lipopolysaccharide-binding protein) and their protein expression in NTLs. These findings provided a new insight into the relation between stent implantation and progression of NTLs, and further studies are warranted to clarify the detailed mechanism and clinical significance of these preliminary results. Registration: URL: http://www.chictr.org.cn ; Unique identifier: ChiCTR1900026393. Graphic Abstract: A graphic abstract is available for this article.

This paper presents a bandwidth expansion method for dual-mass microelectromechanical system (MEMS) gyroscopes based on the pole–zero temperature compensation method. When the sense loop operates under open conditions, the mechanical sensitivity of the gyroscope structure conflicts with the bandwidth and is governed by the frequency difference between the drive and the sense modes (min {Δ ω 1, Δ ω 2}), which is proven to change with temperature during the experiment. The pole–zero temperature compensation proportional controller (PZTCPC) is proposed to expand the bandwidth under different temperatures based on the pole–zero compensation method. The force rebalancing combs stimulation method (FRCSM) is used to achieve accurate gyroscope bandwidth characteristics. The mechanical bandwidth of the gyroscope is proven to be approximately 13 Hz when the sense-mode loop is open, and the simulation results show that the PZTCPC method expands the bandwidth to greater than 91.7 Hz after the sense-mode loop is closed. The FRCSM experiments indicate that gyroscope bandwidth is expanded to 95 Hz at –40 °C, 94 Hz at 20 °C and 92 Hz at 60 °C, while the bandwidths at –40, 20, and 60 °C are all 93 Hz with the turntable method. The experimental curves match the simulation curves well and verify the simulation results. The new limiting condition of the closed-loop bandwidth is the trough generated by conjugate zeros, formed by superposition of in-phase and anti-phase sense modes.

Many businesses and organisations have found that the application of Knowledge Management (KM)has enabled them to improve their performance and enhance their development. It has been emphasised in various studies related to KM that the most central activity in managing knowledge is to ensure that knowledge is transferred between different parties. The practice of Knowledge Transfer (KT) is extremely valuable in the healthcare sector, and this especially applies to hospitals and nursing teams. Hence, the ability to transfer knowledge in the nursing workforce has a critical impact on the development of the healthcare system, particularly newborn health care in the New-born Intensive Care Unit (NICU). Therefore, the aim of this paper is to identify and understand the key concepts involved in Social Networks and Knowledge Transfer Mechanisms in a new-born Intensive Care Unit (NICU) in order to develop a knowledge transfer framework for NICUs in future research.

Background: Visceral adipose tissue derived serine protease inhibitor (vaspin), a secretory adipokine, was reported to play a protective role in insulin resistance. Recent studies have demonstrated that serum vaspin levels are downregulated in patients with coronary artery disease (CAD) and that vaspin has a protective effect on myocardial ischaemia/reperfusion injury (IRI) and atherosclerosis. However, whether vaspin exerts specific effects on pathological cardiac hypertrophy remains unknown.Methods: Pathologic cardiac hypertrophy was induced in male C57BL/6J wild type (WT) and vaspin knockout (vaspin ko) mice. Buparlisib (PI3K inhibitor, 50 mg/kg), rapamycin (mTOR inhibitor, 20 mg/kg), or A 769662 (AMPK agonist, 30 mg/kg) wer e pre and co administered to vaspin ko mice daily for a period of 15 days. Induction of pathological cardiac hypertrophy was performed by the subcutaneous administration of isoproterenol (ISO) (5 mg/kg) into mice from the 7th to the 15th day. Cardiac hype rtrophy, fibrosis, and cardiac function were examined in these mice. Critical characteristics of senescence (senescence associated β galactosidase activity and expression of cyclin dependent kinase inhibitors) were examined in the cardiac hypertrophy modelResults: We provide the first evidence that the serum level of vaspin decreased during pathological cardiac hypertrophy; further, knocking out of vaspin resulted in markedly exaggerated cardiac h ypertrophy and fibrosis, and increased cardiomyocyte senesc senescence in mice treated with ISO. Conversely, the administration of exogenous ence in mice treated with ISO. Conversely, the administration of exogenous recombinant human vaspin in vitro protected myocardial cells against hypertrophy recombinant human vaspin in vitro protected myocardial cells against hypertrophy and senescence caused by ISO. and senescence caused by ISO. MechanisticallyMechanistically, PI3K, PI3K--AKTAKT--mTOR mTOR pathwaypathway--dependent activation of autophadependent activation of autophagic flux was involved in the protective gic flux was involved in the protective effects of vaspin toward cardiac hypertrophy.effects of vaspin toward cardiac hypertrophy.Conclusion: Our results showed for the first time that vaspin functions as a critical Our results showed for the first time that vaspin functions as a critical regulator that alleviates pathological cardiac hypertrophy by regulating regulator that alleviates pathological cardiac hypertrophy by regulating autophagyautophagy--ddependent myocardial senescence, which provides potential preventive and ependent myocardial senescence, which provides potential preventive and therapeutic targets for pathological cardiac hypertrophy.therapeutic targets for pathological cardiac hypertrophy.

Visceral adipose tissue-derived serine protease inhibitor (vaspin), as a secretory adipokine, was reported to exert a protective role on insulin resistance. Recent studies showed that serum vaspin level was downregulated in patients with coronary artery disease. However, whether vaspin exerted specific effects on myocardial injury remains unknown. In this study, we determined to explore the role of vaspin overexpression in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. Our results showed that the systemic delivery of adeno-associated virus-vaspin to mice reduced myocardial infarct size and apoptosis, and improved cardiac function after reperfusion, accompanied with upregulated autophagic flux and restored lysosomal function in the ischaemic heart. Blockage of the autophagic flux with choroquine mitigated the protection of vaspin on myocardial I/R injury. Moreover, we testified that administration of exogenous recombinant human vaspin on cultured cardiomyocytes suppressed hypoxia/reoxygenation-induced apoptosis, through the AMPK-mTOR-upregulated autophagic flux. Overall, we verified that vaspin functions as an adipokine which can alleviate I/R injury in the heart by suppressing myocardial apoptosis through AMPK-mTOR-dependent activation of autophagic flux, and then provided a potential breakthrough in the treatment of myocardial I/R injury and other ischaemic diseases.

In this paper, we revisit the problem of optimal insurance under a general criterion that preserves stop-loss order when the insured faces two mutually dependent risks: background risk and insurable risk. According to the local monotonicity of conditional survival function, we derive the optimal contract forms in different types of interval. Because the conditional survival function reflects the dependence between background risk and insurable risk, the dependence structure between the two risks plays a critical role in the insured’s optimal insurance design. Furthermore, we obtain the optimal insurance forms explicitly under some special dependence structures. It is shown that deductible insurance is optimal and the Mossin’s Theorem is still valid when background risk is stochastically increasing in insurable risk, which generalizes the corresponding results in Lu et al. (2012). Moreover, we show that an individual will purchase no insurance when the sum of the two risks is stochastically decreasing in insurable risk.

Moderate alcohol consumption has been shown to reduce atherosclerosis-associated diseases. As shown in our earlier works, ethanol has a dose-dependent protective effects against endothelial cellular senescence by activating aldehyde dehydrogenase 2 (ALDH2) in vitro. However, whether ethanol administration possesses anti-atherosclerosis properties and whether ALDH2 is involved in the underlying mechanisms are unknown. In the present study, we revealed that the appropriate dose of ethanol reduced atherosclerotic plaque formation, and upregulated ALDH2 expression and activity in ApoE-/- mice. ALDH2 deficiency blocked the protection of ethanol against atherosclerotic plaque formation by inhibiting endothelium senescence. In contrast, Alda-1, which is a specific enzymatic agonist of ALDH2, enhanced the anti-senescence and anti-atherosclerosis effects of the appropriate dose of ethanol. Furthermore, following ALDH2 knockdown, resveratrol (an anti-aging compound) recovered the beneficial effects of ethanol against endothelial senescence in vitro. Thus, these results suggest that the appropriate dose of ethanol has protective effects against endothelial senescence and atherosclerosis by activating ALDH2.

Background Stress‐induced cell premature senescence participates in a variety of tissue and organ remodeling by secreting such proteins as proinflammatory cytokines, chemokines, and growth factors. However, the role of cardiomyocyte senescence in heart remodeling after acute myocardial infarction has not been thoroughly elucidated to date. Therefore, we sought to clarify the impact of premature myocardial senescence on postinfarction heart function. Methods and Results Senescence markers, including p16 INK 4a , p21 CIP 1/ WAF 1 , and SA ‐β‐gal staining, were analyzed in several heart disease models by immunostaining. Both postinfarction mouse hearts and ischemic human myocardium demonstrated increased senescence markers. Additionally, senescence‐related secretory phenotype was activated after acute myocardial infarction, which upregulated senescence‐related secretory phenotype factors, including CCN family member 1 ( CCN 1), interleukin‐1α, tumor necrosis factor α, and monocyte chemoattractant protein‐1. In vivo, a tail vein injection of AAV 9‐ Gata4 ‐sh RNA significantly attenuated senescence‐related secretory phenotype secretion and aggravated postinfarction heart dysfunction. Furthermore, among activated senescence‐related secretory phenotype factors, CCN 1 administration reduced myofibroblast viability in vitro and rescued the deleterious effect of AAV 9‐ Gata4 ‐sh RNA in vivo. Conclusions Myocardial premature senescence was observed in the ischemic hearts and improved postinfarction heart function, partly through the GATA‐binding factor 4‐ CCN 1 pathway.

Aldehyde dehydrogenase 2 (ALDH2) plays essential roles in drinking-associated diseases or effects. As we have previously reported, ALDH2 mediates acute ethanol-induced eNOS activation in vitro. However, whether chronic ethanol treatment has a dose-response endothelial protection, as well as the possible mediating role of ALDH2 involved, is unclear. Here, we show that appropriate dose of ethanol preserved the expression and activity of ALDH2 and eNOS, and alleviated senescence-associated phenotypes in human aortic endothelial cells. Furthermore, ALDH2 deficiency impairs the dose-response protection of ethanol against endothelial senescence by promoting the accumulation of 4-HNE, the formation of 4-HNE-SIRT1 protein adducts and the subsequent decrease in SIRT1-dependent p53 deacetylation. Collectively, our data indicate that ALDH2 mediates the protection of appropriate ethanol by modulating SIRT1/p53-dependent endothelial senescence.

This study presents a microelectromechanical systems S-springs vibration ring gyroscope (MSVRG), which is driven by electrostatic force and detected by capacitance. First, a ring resonator structure with eight S-shaped symmetrical supporting springs is developed, and the capacitor electrodes are designed according to the vibration characteristics of the ring resonator. Then, a precise equivalent stiffness model of MSVRG is established based on the vibration mechanics and the Cassette theorem, which can be employed for any other ring gyroscope with differently shaped springs. Moreover, the mode resonant frequency error of between experiments, finite-element analysis (FEA) and theory calculation, is 10.54% and 3.76%, respectively. After that, the process of MSVRG structure is introduced and the structure is manufactured, and the theory calculation and FEA value with processed parameters have 1.19% and 4.59% difference with resonant frequency tested value, respectively. Finally, the static performance of the fabricated MSVRG is tested, and the bias instability is about 0.0119 deg/s and angle random walk is about 0.0359 deg/s1/2 at room temperature.

A facial biotemplate-directed synthetic route for fabricating mesoporous multiwall ZnO nanotubes (ZnO-MMNTs) was proposed. Owing to the mesoporous multiwall based matrix, one dimensional (1D) tubes based channels and high isoelectric point (IEP), the prepared ZnO-MMNTs are wonderful platform to immobilize glucose oxidase (GOx) for glucose biosensing. Scale-adaptive cells are constructed to hold enzymes molecules, maintain enzymatic activity and keep stability. The prepared enzymatic electrode (chitosan/GOx/ZnO/Au) exhibits high sensitivity (47.2 μA mM(-1)cm(-2)), very fast response (