Search

In order to meet the requirements of high accuracy and low energy consumption of time synchronization among massive nodes of coal mine underground network, a distributed accurate time synchronization algorithm is proposed based on the time-sensitive network (TSN) of coal mine with non-uniform clustering structure of multiple Sink nodes. The underground coal mine TSN is divided into 3 layers, including the TSN convergence layer containing all Sink nodes, the main network consisting of Sink nodes and all cluster head nodes within their respective communication radius, and the secondary network consisting of cluster head nodes and common nodes in the cluster. The TSN convergence layer uses the gPTP algorithm to achieve nanosecond time synchronization among Sink nodes. The main network uses an optimized algorithm based on Kalman filter to predict and compensate for frequency offset, phase offset and noise errors so as to improve the network time synchronization accuracy. The secondary network uses the broadcast-based single and two way hybrid synchronization algorithm to reduce the number of synchronization message packets. The simulation results show that the proposed algorithm can improve the accuracy and stability of network time synchronization effectively and reduce the energy consumption of network time synchronization.

Recent evidence suggests that glia maturation factor β (GMFβ) is important in the pathogenesis of pulmonary arterial hpertension (PAH), but the underlying mechanism is unknown. To clarify whether GMFβ can be involved in pulmonary vascular remodeling and to explore the role of the IL‐6‐STAT3 pathway in this process, the expression of GMFβ in PAH rats is examined and the expression of downstream molecules including periostin (POSTN) and interleukin‐6 (IL‐6) is measured using real‐time quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis. The location and expression of POSTN is also tested in PAH rats using immunofluorescence. It is proved that GMFβ is upregulated in the lungs of PAH rats. Knockout GMFβ alleviated the MCT‐PAH by reducing right ventricular systolic pressure (RVSP), mean pulmonary arterial pressure (mPAP), and pulmonary vascular remodeling. Moreover, the inflammation of the pulmonary vasculature is ameliorated in PAH rats with GMFβ absent. In addition, the IL‐6‐STAT3 signaling pathway is activated in PAH; knockout GMFβ reduced POSTN and IL‐6 production by inhibiting the IL‐6‐STAT3 signaling pathway. Taken together, these findings suggest that knockout GMFβ ameliorates PAH in rats by inhibiting the IL‐6‐STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Doxorubicin (DOX) is a highly efficient chemotherapeutic drug limited by its cardiotoxicity. Galectin-3 (Gal-3) overexpression is associated with several cardiovascular diseases. In this study, the in vivo models of DOX-treated rats and the in vitro model of DOX-treated H9C2 cells were used. DOX induced cardiac injury and dysfunction accompanied with the upregulation of Gal-3 at the end of the experiment, while inhibition of Gal-3 with modified citrus pectin (MCP) exhibited a dramatic improvement in cardiac function of the DOX-treated rats, as manifested by increased left ventricular systolic pressure and [+ or -]dp/[dt.sb.max] and decreased left ventricular end-diastolic pressure. The plasma levels of myocardial injury markers such as lactate dehydrogenase, creatine kinase, creatine kinase-MB, and cardiac troponin I were decreased after MCP treatment. In parallel, MCP attenuated myocardial tissue markers of oxidative stress such as hydrogen peroxide and malondialdehyde restored the activities of superoxide dismutase, catalase, and glutathione peroxidase and upregulated antioxidant peroxiredoxin-4 (Prx-4). To further verify the role of Prx-4, it was downregulated by siRNA-mediated knockdown in H9C2 cells. MCP could not reverse DOX-induced oxidative stress in Prx-4-knock-down cells. In conclusion, Gal-3 mediated DOX-induced cardiotoxicity and Gal-3 inhibition attenuated DOX-induced cardiac dysfunction by upregulating the expression of Prx-4 to reduce myocardial oxidative stress. Key words: galectin-3, doxorubicin, cardiac dysfunction, oxidative stress, peroxiredoxin-4, modified citrus pectin, siRNA. La doxorubicine (DOX) est un medicament chimiotherapeutique tres efficace dont la cardiotoxicite limite l'utilisation. La surexpression de la galectine-3 (Gal-3) est associee a plusieurs maladies cardiovasculaires. Dans cette etude, nous avons utilise les modeles in vivo d'administration de DOX chez le rat ainsi que le modele in vitro d'administration de DOX a des cellules H9C2. La DOX entrainait des lesions et des dysfonctionnements cardiaques accompagnes d'une regulation a la hausse de la Gal-3 a la fin de l'experience. L'inhibition de la Gal-3 a l'aide de pectine d'agrume modifiee (PAM) chez des rats auxquels etait administree de la DOX permettait d'obtenir des ameliorations impressionnantes sur le plan de la fonction cardiaque, lesquelles se manifestaient par une augmentation de la pression systolique ventriculaire gauche et du [+ or -]dp/[dt.sub.max], avec une diminution de la pression telediastolique ventriculaire gauche. Apres l'administration de PAM, nous avons observe une diminution des taux plasmatiques des marqueurs de lesions cardiaques suivants : deshydrogenase lactique, creatine kinase, creatine kinase MB et troponine cardiaque I. En parallele, le PAM permettait d'attenuer la hausse des marqueurs tissulaires myocardiques de stress oxydatif comme le peroxyde d'hydrogene et le malonyldialdehyde, de retablir l'activite de la superoxyde dismutase, de la catalase et de la glutathion peroxydase, ainsi que de reguler a la hausse la peroxyredoxine-4 (Prx-4), un antioxydant. Pour une meilleure verification du role du Prx-4, il etait regule a la baisse par le << knock-down >> medie par le siARN dans des cellules H9C2. Il n'etait pas possible d'inverser le stress oxydatif engendre par la DOX dans les cellules knock-down-Prx-4 a l'aide de PAM. En conclusion, la Gal-3 participait a la mediation de la cardiotoxicite engendree par la DOX et l'inhibition de la Gal-3 permettait d'attenuer les dysfonctionnements cardiaques engendres par la DOX par l'intermediaire d'une regulation a la hausse de l'expression de la Prx-4 avec attenuation du stress oxydatif myocardique. [Traduit par la Redaction] Mots-cles: galectine-3, doxorubicine, dysfonctionnement cardiaque, stress oxydatif, peroxiredoxine-4, pectine d'agrume modifiee, siARN., Introduction Doxorubicin (DOX) as an effective anti-cancer agent is widely used for the treatment of patients with haematological malignancies or solid tumors (Rivankar 2014; Zhao et al. 2018c). However, its [...]

Objective: We examine how state spending on children is associated with the size of socioeconomic gaps in maternal childcare time. Background: Persistent socioeconomic divides in the amount and nature of parental time with children have prompted consideration of the factors that mitigate inequalities within the family. At both the national and local levels, the welfare state plays an important role in structuring opportunities for children. Thus, it is important to understand the institutional factors that shape parental behavior. Yet, little research examines how the social safety net is associated with family processes. Method: Using rich data on maternal time with children from the American Time Use Surveys (2003–2016), combined with longitudinal data on public spending in states on major programs affecting children and families, we examine how state spending on children is associated with the size of socioeconomic gaps in maternal childcare time. Results: We found that higher levels of state spending were associated with significant increases in childcare time among low‐educated mothers at both the extensive and intensive margin, increasing the likelihood of spending any minutes on primary childcare in a typical day, as well as increasing the number of minutes spent on childcare. In contrast, we observed no variation in the behavior of highly educated mothers as state spending changes. Implications: State‐level investments could meaningfully narrow socioeconomic gaps in maternal time with children. [ABSTRACT FROM AUTHOR]

Ref.: Can. J. Physiol. Pharmacol. 98(10): 700-707 (2020). dx.doi.org/10.1139/cjpp-2020-0700. The last author's name should read 'Haoming Song' in the online HTML version and in the 'corresponding author' line in the [...]

Purpose: To develop a weakly supervised deep learning (WSDL) method that could utilize incomplete/missing survival data to predict the prognosis of extranodal natural killer/T cell lymphoma, nasal type (ENKTL) based on pretreatment 18F-FDG PET/CT results. Methods: One hundred and sixty-seven patients with ENKTL who underwent pretreatment 18F-FDG PET/CT were retrospectively collected. Eighty-four patients were followed up for at least 2 years (training set = 64, test set = 20). A WSDL method was developed to enable the integration of the remaining 83 patients with incomplete/missing follow-up information in the training set. To test generalization, these data were derived from three types of scanners. Prediction similarity index (PSI) was derived from deep learning features of images. Its discriminative ability was calculated and compared with that of a conventional deep learning (CDL) method. Univariate and multivariate analyses helped explore the significance of PSI and clinical features. Results: PSI achieved area under the curve scores of 0.9858 and 0.9946 (training set) and 0.8750 and 0.7344 (test set) in the prediction of progression-free survival (PFS) with the WSDL and CDL methods, respectively. PSI threshold of 1.0 could significantly differentiate the prognosis. In the test set, WSDL and CDL achieved prediction sensitivity, specificity, and accuracy of 87.50% and 62.50%, 83.33% and 83.33%, and 85.00% and 75.00%, respectively. Multivariate analysis confirmed PSI to be an independent significant predictor of PFS in both the methods. Conclusion: The WSDL-based framework was more effective for extracting 18F-FDG PET/CT features and predicting the prognosis of ENKTL than the CDL method. [ABSTRACT FROM AUTHOR]