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The online detection of fertilizer solution information is a crucial link in the implementation of intelligent and precise variable fertilization techniques. However, achieving simultaneous rapid online detection of multiple fertilizer components is still challenging. Therefore, a rapid detection method based on spectrophotometry for qualitative and quantitative identification of four fertilizers (typical N, P, and K fertilizers: KNO3, (NH4)2SO4, KH2PO4, and K2SO4) was proposed in this work. Full-scan absorption spectra of fertilizer solutions at varying concentrations were obtained using a UV–visible/near-infrared spectrophotometer. By assessing the linear fit between fertilizer concentration and absorbance at each wavelength within the characteristic band, the characteristic wavelengths for KNO3, (NH4)2SO4, KH2PO4, and K2SO4 were identified as 214 nm, 410 nm, 712 nm, and 1708 nm, respectively. The identification method of fertilizer type and the prediction model of concentration were constructed based on characteristic wavelength and the Lambert–Beer law. Based on the above analysis, a four-channel photoelectric sensor was designed with four LEDs emitting wavelengths closely matched to characteristic wavelengths for fertilizer detection. A detection strategy of "qualitative analysis followed by quantitative detection" was proposed to realize the online detection of four fertilizer types and their concentrations. Evaluation of the sensor's performance showed its high stability, with an accuracy of 81.5% in recognizing fertilizer types. Furthermore, the relative error of the sensor detection was substantially less than ±15% for the fertilizer concentrations not exceeding 80 mg/L. These results confirm the capability of the sensor to meet the practical requirements for online detection of four fertilizer types and concentrations in the field of agricultural engineering. [ABSTRACT FROM AUTHOR]

Loneliness is associated with various negative mental and physical health outcomes. Studies on factors associated with loneliness can inform its early screening and prevention. However, little is known about what factors are associated with loneliness among Chinese young children. The present study aimed to identify the various loneliness-associated factors (demographic, personal, school-related, and family-related) among primary school students in Hong Kong. A total of 258 students and their parents from six primary schools in Hong Kong completed an online anonymous survey from June to October 2020. Loneliness (i.e., UCLA Loneliness Scale 3 total score ≥ 3) was reported by 14% of the students. Multivariable mixed effects logistic regression suggested loneliness was positively associated with a lower happiness level at school, poorer independence skills, a lower level of satisfaction with parents, and lower child-rearing expenditure. There was no clustering effect of school on the associations. The current study found important demographic, personal, school-related, and family-related factors of loneliness among school-age children, with caution suggested in their interpretation considering the cross-sectional nature of this study. Future studies with a larger sample, preferably longitudinal ones, are needed to substantiate these associations and uncover their underlying mechanisms. [ABSTRACT FROM AUTHOR]

Using a static chamber-gas chromatography method, we investigate the characteristics of soil CO2, CH4, and N2O fluxes and their relationships with environmental factors during the growing season in four typical Larix gmelinii forests (moss–Larix gmelinii forest, Ledum palustre–Larix gmelinii forest, herbage–Larix gmelinii forest, and Rhododendron dauricum–Larix gmelinii forest) in the Greater Khingan Mountains. Our results show that all four forest types are sources of CO2 emissions, with similar average emission fluxes (146.71 mg·m−2 h−1–211.81 mg·m−2 h−1) and no significant differences. The soil in the moss–Larix gmelinii forest emitted CH4 (43.78 μg·m−2 h−1), while all other forest types acted as CH4 sinks (−56.02 μg·m−2 h−1–−28.07 μg·m−2 h−1). Although all forest types showed N2O uptake at the beginning of the growing season, the N2O fluxes (4.03 μg·m−2 h−1–5.74 μg·m−2 h−1) did not differ significantly among the four forest types for the entire growing season, and all acted as sources of N2O emissions. The fluxes of CO2, CH4, and N2O were significantly correlated with soil temperature and soil pH for all four forest types. Multiple regression analysis shows that considering the interactive effects of soil temperature and moisture could better explain the changes in greenhouse gas emissions among different forest types. The average Q10 value (8.81) of the moss–Larix gmelinii forest is significantly higher than that of the other three forest types (3.16–3.54) (p < 0.05), indicating that the soil respiration in this forest type is more sensitive to temperature changes. [ABSTRACT FROM AUTHOR]

Keeping an appropriate level of trust in automated driving (AD) is critical to safe driving. Although ample studies have investigated factors affecting trust in AD, few studies have investigated whether the personality of drivers influences the trust in AD system. Considering that trust measured at a given point in time lies on a continuum between dispositional and history-based trust, the current research investigated the relationship between driver's personality and dispositional as well as history-based trust. We revealed that personality affected the two types of trust in different ways: A significant negative correlation emerged between Neuroticism and dispositional trust of AD (Study 1), whereas a significant negative correlation between Openness and history-based trust was found when participants interacted with the AD system (Study 2). These results suggest that drivers' personality has an impact on the trust in AD, which is further modulated by the experience of driver's interaction with the AD system. [ABSTRACT FROM AUTHOR]

Thermoelectric (TE) energy converters have attracted great interest due to their maintenance-free, long-life, and high-reliability properties. However, improving the output power of TE devices remains a huge challenge. In this work, a high-efficient photo-TE coupling generator based on cuprous iodide (CuI) film is proposed to increase the output power of TE devices. Here, CuI film was prepared by the successive ionic layer adsorption and reaction method. The influence of the photovoltaic (PV) effect on the TE output voltage of CuI film was investigated by an analysis of the experimental results. The results showed that the output voltage of the photo-TE coupling generator had a maximum increment of 83.47% at 343 K compared to the sum of TE and PV voltages. The increase in the output voltage was mainly because of the PV effect rather than the TE effect, while the photo-generated electrons also induce a considerable change in the TE figure of merit. Hence, the strategy proposed in this work might be a potential approach to further improve the output performance of other TE materials. [ABSTRACT FROM AUTHOR]

UV radiation has been recognized as a direct driver of litter decomposition by photodegrading organic matter in dryland ecosystems. However, the importance and mechanism of UV radiation on litter decomposition, especially on standing litter, in humid forest ecosystems remain unclear.We conducted a factorial experiment in a humid subtropical forest gap, manipulating the effects of UV radiation on the decomposition of standing litter under different microbial conditions.After 366 days of standing incubation, under normal conditions (UV pass with microorganisms), up to 40.63% of the litter mass was lost. However, under a UV pass without microorganisms, litter mass loss was only 16.30%. Under a UV block, the mass loss of litter with microorganisms was 27.68% and that of litter without microorganisms was 15.54%. Without microorganisms, UV radiation had no significant effect on the mass loss of litter carbon. However, UV radiation increased the DOC concentration of litter. And in the presence of microorganisms, UV radiation contributed to an increased mass loss of lignin by 16.72% and of cellulose by 14.75%. No negative effects of UV radiation on microorganisms were observed. These results suggest that UV radiation increased the net mass loss of litter by 106.67%, and this doubling promotion was achieved through microbial degradation.Synthesis. The increase in microbial degradation under UV radiation may be linked to the increased degradability of lignin and cellulose caused by photodegradation. Our study indicates that direct photodegradation by UV radiation could be weak in subtropical forests, but UV photofacilitation generates rapid turnover of carbon in this system. [ABSTRACT FROM AUTHOR]

Hyperlipidemia is an important factor in the induction of cardiovascular diseases. However, the molecular mechanisms underlying the vascular injury involved in hyperlipidemia remains unclear. This study aimed to investigate the Notch pathway of endothelial progenitor cells (EPCs) in reendothelialization after vascular injury and to explore the involvement of Notch pathway in the senescence of EPCs. Our results demonstrated that high-fat diet (HFD) treatment inhibited reendothelialization after vascular injury in the mice model. In vitro studies showed that 7-ketocholesterol (7-keto) stimulation induced senescence in the isolated EPCs from mice. In addition, 7-keto markedly upregulated the protein expression of Notch1 and Delta-like ligand 4 and induced the transport of notch intracellular domain (NICD) to the nucleus. Mechanistically, treatment with NICD inhibitor reduced the senescence of the EPCs stimulated by cholesterol. In summary, our results showed that HFD treatment caused the disruption of reendothelialization after vascular injury in the mouse model. In vitro studies indicated that 7-keto-induced senescence of EPCs was at least via the activation of the Notch1 pathway. Mechanistic data suggested that 7-keto may activate the Notch1 pathway by regulating the generation and transport of NICD to the nucleus. Future investigations are warranted to confirm the role of Notch1 in the dysfunction of EPCs during obesity. [ABSTRACT FROM AUTHOR]

Background: Alzheimer disease (AD) and traumatic brain injury (TBI) are two devastating brain disorders with complex relationships. Growing evidence supports that early or middle life of TBI may be a risk factor for developing late‐life AD and AD‐related dementias (ADRD). Tau hyperphosphorylation and gliosis may serve as a causative link between TBI and AD as well as ADRD. We have recently identified BCL2 associated athanogene 3 (BAG3) as a hub gene of regulating tau protein homeostasis. The protein level of BAG3 is significantly reduced in neurons, but it is increased in astrocytes of human AD compared to controls. We hypothesized that overexpression of BAG3 in neurons would attenuate tau hyperphosphorylation and gliosis induced by TBI. Method: We injected 500 nL AAV9‐hSYN1‐eGFP‐2A‐hBAG3‐WPRE or AAV9‐hSYN1‐eGFP‐WPRE (control AAV9) into the hippocampal CA1 and DG regions of C57BL6/J and htau knock‐in mice. These mice were subjected to TBI surgery (controlled cortical impact, velocity: 3.00 m/s, depth: 0.8 mm, dwell time: 200 ms) three months post the injection. We then performed behavioral tests (open‐field test, Y‐maze, and Morris Water Maze) on these mice one month after the CCI surgery. Following the behavioral tests, we collected the brain tissues and performed the immunofluorescent staining of ptau (PHF1, pS396/404 tau), BAG3, IBA‐1 (microglia/macrophage marker) and GFAP (astrocyte marker) on fixed mouse brain floating sections. Result: TBI increased the immunoreactivity of PHF1, IBA‐1, GFAP and astrocytic BAG3, whereas reducing neuronal BAG3 compared to sham C57BL6/J and htau knock‐in mice. Furthermore, the immunoreactivity of BAG3 increased, while PHF1, IBA‐1 and GFAP decreased in the ipsilateral hippocampus after the injection of AAV9‐BAG3 compared to those TBI mice injected with control AAVs. Continued immunofluorescent staining and quantification for AAV9‐BAG3‐ and control AAV9‐injected mice is currently ongoing, as is behavior data quantification. Conclusion: TBI induces tau hyperphosphorylation, microglia activation and reactive astrocytes, while reducing neuronal BAG3 in C57BL6/J and htau knock‐in mice. Neuronal overexpression of BAG3 can significantly attenuate tau hyperphosphorylation and gliosis induced by TBI. Our data suggests that targeting neuronal BAG3 may be a therapeutic strategy for preventing or reducing intra‐neuronal tau aggregates and gliosis found in TBI and TBI‐associated AD and ADRD. [ABSTRACT FROM AUTHOR]

Introduction: Previous studies have shown that endothelial cell senescence is involved in cardiovascular diseases such as cardiac fibrosis, atherosclerosis and heart failure. Accumulating evidence indicates that apelin exerts protective effects on ageing-related endothelial dysfunction. In this study, we aim to investigate the role of the apelin/APJ axis in angiotensin II (AngII)-induced endothelium senescence and its associated mechanisms.Material and Methods: Senescence-related β-gal activity assay and western blot were used to evaluate human umbilical vein endothelial cell (HUVEC) senescence. In addition, DCFH-DA staining was carried out to detect the generation of reactive oxygen species (ROS). A validated, high-sensitivity real-time quantitative telomeric repeat amplification protocol (RQ-TRAP) was applied to determine telomerase activity in HUVECs, and a CCK-8 assay was employed to measure cellular viability.Results: AngII induced an increase in SA-β-Gal-positive cells and upregulation on expression of P21 and PAI-1 compared to the control group (p < 0.05), while apelin against this process (p < 0.05). The protective effects were attenuated when APJ, AMPK and SIRT1 expression was knocked down (p < 0.05). Furthermore, apelin reduced AngII-induced ROS generation and enhanced telomerase activity in HUVECs (p < 0.05), which contributed to increased HUVEC viability as assessed by the CCK-8 assay (p < 0.05).Conclusions: The apelin/APJ axis improved AngII-induced HUVEC senescence via the AMPK/SIRT1 signaling pathway, and the underlying mechanisms might be associated with reduced ROS production and enhanced telomerase activity. [ABSTRACT FROM AUTHOR]

Background: To evaluate association of 24 h-systolic blood pressure (SBP) variability and obstructive sleep apnea (OSA) as defined by the apnea-hypopnea index ≥5/h; and association of 24 h-SBP variability and prevalent cardiovascular disease (CVD) in OSA patients.Methods: Participants underwent polysomongraphy to evaluate the presence of OSA, and 24 h-ambulatory blood pressure monitoring was applied to evaluate 24 h-SBP variability as indexed by weighted 24 h-standard deviation (SD) of SBP. Between-group differences were evaluated in participants with and without OSA. Participants with OSA were divided into high and low 24 h-SBP variability groups and between-group differences were evaluated.Results: Mean age of 384 participants was 50 years old and 42.2% had OSA. Mean 24 h-systolic/diastolic BP were 130/78 mmHg, with mean weighted 24 h-SD of systolic/diastolic BP were 12.9/7.3 mmHg. Compared to those without OSA, OSA participants had higher clinic-, 24 h-, daytime- and nighttime-SBP, and weighted 24 h, daytime- and nighttime-SD of SBP. Age, prevalent CVD and OSA, usage of angiotensin converting enzyme inhibitor/angiotensin receptor blocker, calcium channel blocker and diuretic were significantly associated with 24 h-SBP variability. In OSA patients, compared to those with low variability, participants with high variability had higher weighted 24 h, daytime- and nighttime-SD of SBP. After adjusted for covariates including clinic-SBP and 24 h-SBP, per 1-SD increment weighted 24 h-SD of SBP was associated with 21% increased prevalent CVD.Conclusions: Patients with newly-diagnosed OSA have higher 24 h-SBP variability compared to those without OSA; in OSA patients, increased 24 h-SBP variability is associated with increased prevalence of CVD. [ABSTRACT FROM AUTHOR]

Myocardial fibrosis is a characteristic feature of cardiomyopathies. However, no effective strategies to attenuate cardiac fibrosis are currently available. Late-stage endothelial progenitor cells (EPCs) are precursors of endothelial cells (ECs) that repair the heart through a paracrine mechanism. In the present study, we tested whether EPC-derived exosomes regulate the differentiation of fibroblasts into ECs. We isolated late-stage EPCs from human peripheral blood (PB) and used immunofluorescence and flow cytometry to confirm their identity. Next, we isolated exosomes from the EPCs and characterized their morphology using electron microscopy and confirmed the expression of exosome-specific marker proteins using Western blots. We then investigated the in vitro effects of exosomes on the proliferation and angiogenesis of cardiac fibroblasts (CFs) and on the expression of the mesenchymal-endothelial transition (MEndT)-related genes and the myocardial fibrosis-regulated protein, high mobility group box 1 protein B1 (HMGB1). We found that human PB-EPC-derived exosomes enhanced the proliferation and angiogenesis of CFs in vitro. Furthermore, CFs stimulated with these exosomes showed increased expression of the EC-specific markers, like cluster of differentiation 31 and vascular endothelial growth factor receptor 2, and decreased expression of proteins involved in fibrosis, like alpha-smooth muscle actin, vimentin, collagen I, transforming growth factor-beta, and tumor necrosis factor-alpha. In addition, CFs stimulated with human PB-EPC-derived exosomes, inhibited the expression of HMGB1. Taken together, our study demonstrated that EPC-derived exosomes promote the proliferation and angiogenesis of CFs by inhibiting MEndT and decreasing the expression of HMGB1. [ABSTRACT FROM AUTHOR]

Background: Pathological tau accumulates in patients with Alzheimer's disease (AD) and related tauopathies. However, it remains unclear why specific neuronal subtypes and brain regions are vulnerable to pathological tau in early AD. Recently we found excitatory neurons expressing the Wolframin (WFS1) in the entorhinal cortex and the CA1 of hippocampus are particularly vulnerable to pathological tau in tau transgenic mice and human AD. However, the role of WFS1 in mediating this selective neuronal vulnerability is unknown. Method: The tau aggregates in live cells were imaged as individual tiles and stitched via the Zeiss Observer 7 fluorescent microscope, and then the area with tau aggregates in each stitched image was quantitated by Image J. The tau pathology in mouse brain was visualized by MC1‐positive and conformation‐dependent tau via the immunofluroscent staining. The protein interaction between WFS1 and tau was measured by the Duolink Proximity ligation assay (PLA) and co‐immunoprecipitation (CO‐IP) assay. Result: Here we reported that overexpression of human WFS1 significantly reduced DS9 tau seeding in SH‐SY5Y cells stably transfected with P301S mutant tau, while overexpression of mutant P724L WFS1 did not. Also, overexpression of human WFS1 significantly reduced exogenous tau aggregation in primary mouse mixed neurons treated with P301S tau‐YFP lentivirus, while overexpression of mutant WFS1 did not. Furthermore, the heterozygotes of PS19 tau;NestinCre/+; Wfs1f/+ brain‐specific knock‐out mice and PS19 tau;Wfs1+/‐ knock‐out mice have much more tau pathology in the Dentate gyrus, CA1 and entorhinal cortex compared with PS19 tau and PS19 tau;Wfs1f/+mice. The homozygotes of PS19 tau;NestinCre/+;Wfs1f/f brain‐specific knock‐out mice and PS19 tau;Wfs1‐/‐ knock‐out mice have even more tau pathology than those heterozygotes. We further identified that WFS1 interacts with both total tau and pathological tau in primary cultured neurons, wild‐type and tau transgenic mice, and human non‐AD and AD cases. The interaction is first enhanced as tau pathology increases, however, it is reduced as tau pathology further increases. Conclusion: Taken together, we demonstrate that deficiency of Wfs1 increases vulnerability to pathological tau in vitro and in vivo, indicating WFS1 may be a therapeutic target for preventing or delaying the tau pathology in AD. [ABSTRACT FROM AUTHOR]

A new operating approach by reducing the aeration time while keeping high intensity was evaluated for enhanced nutrients removal and maintenance of granular stability. Three aerobic granular sequencing batch reactors (SBR) performing simultaneous nitrification, denitrification and phosphorus removal (SNDPR) were run at different aeration time (120, 90, and 60 min). Aerobic granules could remain their integrity and stability over long-term operation under high aeration intensity and different time, and shorter aeration time favored the retention of biomass, better settleability, and more production of extracellular polymeric substances (EPS). Besides, efficient and stable reactor performance for carbon and phosphorus were achieved, especially, enhanced nitrogen removal was obtained due to reduction of aeration time. Further exploration revealed that the aeration time shaped the bacterial community in terms of diversity, composition, as well as the distribution of functional groups involving carbon, nitrogen and phosphorus removal. [ABSTRACT FROM AUTHOR]

Electromagnetic source imaging (ESI) requires solving a highly ill-posed inverse problem. To seek a unique solution, traditional ESI methods impose various forms of priors that may not accurately reflect the actual source properties, which may hinder their broad applications. To overcome this limitation, in this article, a novel data-synthesized spatiotemporally convolutional encoder-decoder network (DST-CedNet) method is proposed for ESI. The DST-CedNet recasts ESI as a machine learning problem, where discriminative learning and latent-space representations are integrated in a CedNet to learn a robust mapping from the measured electroencephalography/magnetoencephalography (E/MEG) signals to the brain activity. In particular, by incorporating prior knowledge regarding dynamical brain activities, a novel data synthesis strategy is devised to generate large-scale samples for effectively training CedNet. This stands in contrast to traditional ESI methods where the prior information is often enforced via constraints primarily aimed for mathematical convenience. Extensive numerical experiments as well as analysis of a real MEG and epilepsy EEG dataset demonstrate that the DST-CedNet outperforms several state-of-the-art ESI methods in robustly estimating source signals under a variety of source configurations.

Background: The incidence of thyroid carcinoma (THCA), the most common endocrine tumor, is continuously increasing worldwide. Although the overall prognosis of THCA is good, patients with distant metastases exhibit a mortality rate of 5-20%., Methods: To improve the diagnosis and overall prognosis of patients with thyroid cancer, we screened specific candidate neoantigen genes in early- and late-stage THCA by analyzing the transcriptome and somatic cell mutations in this study., Results: The top five early-stage neoantigen-related genes (NRGs) were G protein-coupled receptor 4 [ GPR4 ], chondroitin sulfate proteoglycan 4 [ CSPG4 ], teneurin transmembrane protein 1 [ TENM1 ], protein S 1 [ PROS1 ], and thymidine kinase 1 [ TK1 ], whereas the top five late-stage NRGs were cadherin 6 [ CDH6 ], semaphorin 6B [ SEMA6B ], dysferlin [ DYSF ], xenotropic and polytropic retrovirus receptor 1 [ XPR1 ], and ABR activator of RhoGEF and GTPase [ ABR ]. Subsequently, we used machine learning models to verify their ability to screen NRGs and analyze the correlations among NRGs, immune cell types, and immune checkpoint regulators. The use of candidate antigen genes resulted in a better diagnostic model (the area under the curve [AUC] value of the early-stage group [0.979] was higher than that of the late-stage group [0.959]). Then, a prognostic model was constructed to predict NRG survival, and the 1-, 3- and 5-year AUC values were 0.83, 0.87, and 0.86, respectively, which were closely related to different immune cell types. Comparison of the expression trends and mutation frequencies of NRGs in multiple tumors revealed their potential for the development of broad spectrum therapeutic drugs., Conclusion: In conclusion, the candidate NRGs identified in this study could potentially be used as therapeutic targets and diagnostic biomarkers for the development of novel broad spectrum therapeutic agents., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Jia, Liang, Li, Qin, Li, Wang and Lu.)

Accurate reconstruction of the brain activities from electroencephalography and magnetoencephalography (E/MEG) remains a long-standing challenge for the intrinsic ill-posedness in the inverse problem. In this study, to address this issue, we propose a novel data-driven source imaging framework based on sparse Bayesian learning and deep neural network (SI-SBLNN). Within this framework, the variational inference in conventional algorithm, which is built upon sparse Bayesian learning, is compressed via constructing a straightforward mapping from measurements to latent sparseness encoding parameters using deep neural network. The network is trained with synthesized data derived from the probabilistic graphical model embedded in the conventional algorithm. We achieved a realization of this framework with the algorithm, source imaging based on spatio-temporal basis function (SI-STBF), as backbone. In numerical simulations, the proposed algorithm validated its availability for different head models and robustness against distinct intensities of the noise. Meanwhile, it acquired superior performance compared to SI-STBF and several benchmarks in a variety of source configurations. Additionally, in real data experiments, it obtained the concordant results with the prior studies.

Accurate reconstruction of cortical activation from electroencephalography and magnetoencephalography (E/MEG) is a long-standing challenge because of the inherently ill-posed inverse problem. In this paper, a novel algorithm under the empirical Bayesian framework, source imaging with smoothness in spatial and temporal domains (SI-SST), is proposed to address this issue. In SI-SST, current sources are decomposed into the product of spatial smoothing kernel, sparseness encoding coefficients, and temporal basis functions (TBFs). Further smoothness is integrated in the temporal domain with the employment of an underlying autoregressive model. Because sparseness encoding coefficients are constructed depending on overlapped clusters over cortex in this model, we derived a novel update rule based on fixed-point criterion instead of the convexity based approach which becomes invalid in this scenario. Entire variables and hyper parameters are updated alternatively in the variational inference procedure. SI-SST was assessed by multiple metrics with both simulated and experimental datasets. In practice, SI-SST had the superior reconstruction performance in both spatial extents and temporal profiles compared to the benchmarks.

Researchers have explored the influence of visual working memory (VWM) load on visual perception in the past decade. One of their key findings is that a high VWM load leads to reduced visual detection sensitivity to incoming visual stimuli. However, recent studies imply that persistent sensory processing continues after the memory array is offset. It is possible that the impaired visual detection is due to the sensory load of the residual sensory processing of the memory array (sensory load account) rather than the working memory load of the VWM task (VWM load account). We performed four experiments to examine the impacts on visual detection. Experiment 1 manipulated the retention time of the memory array while keeping the VWM load constant, revealing reduced visual detection along with retention time. Experiments 2 and 3 manipulated the VWM load while maintaining a constant sensory load, and visual detection was not affected. Experiment 4 affirmed that the findings in Experiments 1-3 were reliable. Together, the results of the current study suggest that the residual sensory load, rather than the VWM load of the VWM task, impairs visual detection. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Vascular dysfunction is a key hallmark of hypertension and related cardiovascular outcomes. As a well-known hemodynamic disease, hypertension is characterized by abnormal ventricular-vascular interactions. Complementing non-invasive systemic hemodynamics in hypertensive vascular risk assessment is of promising significance. We aimed to investigate the effects of abnormal hemodynamic states other than elevated blood pressure on vascular damage and establish a united index of systemic hemodynamics for generalized vascular risk evaluation. Non-invasive systemic hemodynamics, assessed by impedance cardiography, was compared among blood pressure stages. Vascular function was evaluated by flow-mediated dilation (FMD) and brachial-ankle pulse wave velocity (baPWV). Systemic hemodynamics was obtained from a total of 88 enrollees with a mean (±SD) systolic blood pressure 140 (±17) mm Hg, and aged 17 to 91 years. Both stroke systemic vascular resistance index and left stroke work index exhibited a significant alteration among blood pressure stages ( p < 0.001; p = 0.01, respectively), whereas heterogeneous hemodynamic and vascular function subsets existed within similar blood pressure. In addition, blood pressure categories failed to recognize between-group differences in endothelial dysfunction ( p = 0.88) and arterial stiffness ( p = 0.26). An increase in myocardial contractility and a parallel decrease in afterload was associated with the decline of vascular dysfunction. Systemic Hemodynamic Index (SHI), as a surrogate marker, demonstrated a significantly negative correlation with vascular damage index (VDI, r = -0.49, p < 0.001). These findings illustrate that systemic hemodynamics underlying hypertensives provides more vascular information. The SHI/VDI score may be a feasible tool for cardiovascular function assessment., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Zhang, Liang, Zhang, Su, He, Qiu, Zhou, Wang, Dong, Tu, Xu, Xia and Tao.)

Introduction: Previous studies have shown that endothelial cell senescence is involved in cardiovascular diseases such as cardiac fibrosis, atherosclerosis and heart failure. Accumulating evidence indicates that apelin exerts protective effects on ageing-related endothelial dysfunction. In this study, we aim to investigate the role of the apelin/APJ axis in angiotensin II (AngII)-induced endothelium senescence and its associated mechanisms., Material and Methods: Senescence-related β-gal activity assay and western blot were used to evaluate human umbilical vein endothelial cell (HUVEC) senescence. In addition, DCFH-DA staining was carried out to detect the generation of reactive oxygen species (ROS). A validated, high-sensitivity real-time quantitative telomeric repeat amplification protocol (RQ-TRAP) was applied to determine telomerase activity in HUVECs, and a CCK-8 assay was employed to measure cellular viability., Results: AngII induced an increase in SA-β-Gal-positive cells and upregulation on expression of P21 and PAI-1 compared to the control group ( p < 0.05), while apelin against this process ( p < 0.05). The protective effects were attenuated when APJ, AMPK and SIRT1 expression was knocked down ( p < 0.05). Furthermore, apelin reduced AngII-induced ROS generation and enhanced telomerase activity in HUVECs ( p < 0.05), which contributed to increased HUVEC viability as assessed by the CCK-8 assay ( p < 0.05)., Conclusions: The apelin/APJ axis improved AngII-induced HUVEC senescence via the AMPK/SIRT1 signaling pathway, and the underlying mechanisms might be associated with reduced ROS production and enhanced telomerase activity., Competing Interests: The authors declare no conflict of interest.

Background: To evaluate association of 24 h-systolic blood pressure (SBP) variability and obstructive sleep apnea (OSA) as defined by the apnea-hypopnea index ≥5/h; and association of 24 h-SBP variability and prevalent cardiovascular disease (CVD) in OSA patients., Methods: Participants underwent polysomongraphy to evaluate the presence of OSA, and 24 h-ambulatory blood pressure monitoring was applied to evaluate 24 h-SBP variability as indexed by weighted 24 h-standard deviation (SD) of SBP. Between-group differences were evaluated in participants with and without OSA. Participants with OSA were divided into high and low 24 h-SBP variability groups and between-group differences were evaluated., Results: Mean age of 384 participants was 50 years old and 42.2% had OSA. Mean 24 h-systolic/diastolic BP were 130/78 mmHg, with mean weighted 24 h-SD of systolic/diastolic BP were 12.9/7.3 mmHg. Compared to those without OSA, OSA participants had higher clinic-, 24 h-, daytime- and nighttime-SBP, and weighted 24 h, daytime- and nighttime-SD of SBP. Age, prevalent CVD and OSA, usage of angiotensin converting enzyme inhibitor/angiotensin receptor blocker, calcium channel blocker and diuretic were significantly associated with 24 h-SBP variability. In OSA patients, compared to those with low variability, participants with high variability had higher weighted 24 h, daytime- and nighttime-SD of SBP. After adjusted for covariates including clinic-SBP and 24 h-SBP, per 1-SD increment weighted 24 h-SD of SBP was associated with 21% increased prevalent CVD., Conclusions: Patients with newly-diagnosed OSA have higher 24 h-SBP variability compared to those without OSA; in OSA patients, increased 24 h-SBP variability is associated with increased prevalence of CVD.

Background/aims: The aim of present study was to test the hypothesis that preconditioning with sodium hydrosulfide (NaHS) could enhance the capacity of migration, adhesion and proliferation of endothelial progenitor cells (EPCs) in vitro, and also could improve the efficacy of EPCs transplantation for re-endothelialization in nude mice with carotid artery injury. The paper further addressed the underlying mechanisms., Methods: EPCs were isolated from peripheral blood mononuclear cells of healthy male volunteers and the markers of EPCs were analyzed by flow cytometry. Thereafter, different concentrations of NaHS (25, 50, 100, 200 and 500 uM) were used for preconditioning EPCs. In vitro and in vivo migration, adhesion and proliferation as well as nitric oxide (NO) production of EPCs were evaluated. Carotid artery injury model was produced in nude mice and thereafter, NaHS-preconditioned EPCs were transplanted in order to evaluate their capacity of re-endothelialization., Results: Cellular immuno-staining showed that isolated cells expressed the key markers of EPCs. In vitro, EPCs proliferation rates and NO production were gradually increased in a NaHS-concentration dependent manner, while these benefits were blocked at a concentration of 500 uM NaHS. Similarly, the migration and adhesion rates of EPCs were also increased the most prominently at a concentration of 200 µM NaHS. In vivo, compared to the control group, treatment with NaHS-preconditioned EPCs significantly enhanced the capacity of re-endothelialization of EPCs. Fluorescent microscope revealed that there were more EPCs homing to the injury vessels in the NaHS-preconditioned EPCs group than the non-preconditioned group. With the administration of AMPK or eNOS inhibitors respectively, the above benefits of NaHS-preconditioning were abrogated., Conclusion: These results suggested that NaHS-preconditioning enhanced the biological function and re-endothelialization of EPCs through the AMPK/eNOS signaling pathway., (© 2017 The Author(s). Published by S. Karger AG, Basel.)