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This policy review introduces the Policy Guidance on Artificial Intelligence (AI) for Children, produced by the United Nations Children's Fund (UNICEF). This Policy Guidance is the first international‐level output to boost the development of child‐centred AI and relevant policies. A main contribution of this Policy Guidance is that it outlines the foundations, requirements and specific recommendations for developing child‐centred AI and surrounding policies. The shortcomings of this Policy Guidance are also introduced, especially the insufficient gender responsiveness and age sensitivity, plus relatively low representation of the developing world. Possible suggestions for future updates of the Policy Guidance and improving policies on child‐centred AI are provided in this review, such as the inclusion of a broader age range of children during the consultation process. The coexistence of contributions and limitations of this Policy Guidance reflects the situation of development of child‐centred AI and relevant policies, which is currently immature but promising. [ABSTRACT FROM AUTHOR]

Broadband lasers, e.g., ultrashort lasers, optical supercontinuum, and frequency combs, are revolutionary coherent light sources, which enable a plethora of state‐of‐the‐art applications ranging from precision spectroscopy to optical clocks. However, the spectral broadening of these coherent light sources mainly relies on the third‐order nonlinearity (χ(3)$\left(\chi\right)^{\left(\right. 3 \left.\right)}$) and is difficult to extend to the visible or shorter wavelength regime. Second‐order nonlinearity (χ(2)$\left(\chi\right)^{\left(\right. 2 \left.\right)}$), which is orders of magnitude larger than χ(3)$\left(\chi\right)^{\left(\right. 3 \left.\right)}$, becomes a powerful tool for the frequency translation if its broadband operation is well addressed. Herein, an octave‐spanning second‐harmonic generation scheme is experimentally demonstrated beyond an extremely large frequency range of 135 THz and high conversion efficiency of 1% for sub‐100 pJ for the near‐infrared picosecond supercontinuum in a fiber–waveguide–fiber configuration. The process relies on ultrabroadband birefringence phase matching in the dispersion‐engineered lithium niobate‐on‐insulator ridge microwaveguide. The mode area of microwaveguide well matches with single‐mode lens fiber, reducing coupling loss and ensuring easy packaging. The method provides a new approach to span the wavelength range of coherent light with χ(2)$\left(\chi\right)^{\left(\right. 2 \left.\right)}$‐based wavelength translation for supercontinuum or frequency combs into the visible regime. The result would find applications in spectroscopy, astrophysics, atomic optics, optical synthesis, etc. [ABSTRACT FROM AUTHOR]

Two‐dimensional material (2DM)/conducting polymer (CP) composites with excellent electrical transport behavior, functional multidimensional structure, and good flexibility have attracted widespread attention as potential composite thermoelectric (TE) materials in the field of energy conversion. Appropriate preparation strategies determine the interface microstructure of 2DM/CP composites, which would influence the optimization degree of TE performance and practical applications. This review describes the recent progress in preparing advanced 2DM/CP composites by different design strategies for improving TE performance. In addition, some typical 2DM/CP composites applied to TE generators are also presented. Finally, other challenges and opportunities toward high‐performance 2DM/CP composites are discussed, including precise structural regulation, an in‐depth understanding of the interfacial transport mechanism, and the development of practical 2DM/CP‐based flexible TE devices. [ABSTRACT FROM AUTHOR]

Background: Preterm complications and neonatal asphyxia are the leading causes of death in those under 5 years of age. However, little information exists for the province of Henan, China. The purpose of this study was to explore changes in the live birth profile in a provincial hospital over the past 32 years in Henan, China. Methods: A retrospective analysis was conducted to reveal the characteristics of live neonates from 1987 to 2018. Results: There were 118 253 live births during the period, including 19 798 (16.74%) preterm births. The neonatal death rate was 6.45‰, and the top risk factor was preterm birth complications and birth asphyxia. Before 1998, neonatal death occurred primarily among term infants. Between 1999 and 2018, preterm infants, especially extreme and very preterm infants with very low birthweight, constituted more than half of all mortalities, and the preterm birth rate increased from 5.94% in 1999 to 16.69% in 2018. The risk factors associated with preterm birth were being male (aOR = 1.18, P < 0.001), advanced maternal age (>35 years old; aOR = 1.08, P = 0.008), gravidity ≥2 (aOR = 1.15, P < 0.001), parity ≥2 (aOR = 1.50, P < 0.001), placenta previa (aOR = 7.41, P < 0.001), twin or multiple births (aOR = 10.63, P < 0.001), hypertension (aOR = 2.08, P < 0.001), and rupture of membrane (aOR = 5.03, P < 0.001). Conclusions: The preterm birth rate has increased over the past 32 years from 4.98% to 16.69% in a provincial hospital in China. Preterm birth was the leading reason for neonatal death, and birth asphyxia was the major risk factor for death in term infants. [ABSTRACT FROM AUTHOR]

This is reflected by the fact that Geneva has a long history of hosting IOs as well as the large number of IOs that are headquartered in Geneva (Dairon & Badache, [2]). A response to "Understanding International Organizations" Headquarters as Ecosystems: The Case of Geneva' Emilie Dairon and Fanny Badache In the paper "Understanding International Organizations" Headquarters as Ecosystems: The Case of Geneva', authors Dairon and Badache ([2]) proposed the concept of "ecosystem" to explore the influence of host cities on international organisations (IOs), which is a relatively understudied topic. Although the density of IOs varies across different areas of Geneva, it can be observed that IOs are scattered largely in almost all parts of the city of Geneva (Dairon & Badache, [2]). [Extracted from the article]

Based on the energy evolution of limestone and acoustic emission evolution law, this paper takes the limestone unloading energy evolution law and acoustic emission cumulative ringing count, cumulative energy, RA value, acoustic emission information entropy, and acoustic emission damage as precursor discrimination indicators for the occurrence of rock explosion. Study of the impact of the unloading rate on the rock explosion precursors indicates that with increasing unloading rate there are more dramatic changes in the degree of each precursor discrimination indicators and rock ruptures within a short period of time before the completion of the indicators. The establishment of the precursor response coefficient reveals that the precursor response is the strongest when the rock rupture acoustic emission RA value time is the earliest. The remaining four precursor discrimination indicators of rock rupture with different loading paths show fluctuations in the identification capacity of the state. The research results can provide some reference for identifying rockburst precursor information. [ABSTRACT FROM AUTHOR]

Background. Mitral subvalvular procedures have acquired a major role during hypertrophic obstructive cardiomyopathy (HOCM) surgery. However, few studies have focused on characterizing the clinical feature of HOCM patients without intrinsic mitral valve (MV) diseases undergoing mitral subvalvular procedures in addition to myectomy. Additionally, scant data about the results of mitral subvalvular procedures during HOCM surgery are available. This single-center study aims to characterize the clinical feature and surgical results of HOCM patients without intrinsic MV diseases undergoing mitral subvalvular procedures in addition to myectomy in comparison with those receiving myectomy alone. Methods. Among 181 eligible patients, 50 (27.6%) patients undergoing myectomy plus mitral subvalvular procedures were entered into the combined group, and the remaining 131 patients receiving myectomy alone were included in the alone group. Baseline and surgical characteristics were investigated, and surgical results were compared. Results. Comparatively, the combined group was younger (52.9 ± 11.2 years vs. 56.8 ± 11.8 years, p = 0.045) and had a better New York Heart Association (NYHA) class (p = 0.034) and less septal hypertrophy (16.4 ± 2.3 mm vs. 18.5 ± 3.2 mm, p < 0.001). Septal thickness was independently associated with combined procedures in multivariable logistic regression analysis (OR = 0.887, 95% CI 0.612–0.917). No surgical death or iatrogenic septal perforation occurred in the combined group. Two (6.5%) patients in the combined group developed complete atrioventricular block and required permanent pacemaker implantation. During a median follow-up of 10 months, no deaths or reoperations were observed with the symptom of relief and NYHA class I or II in either group. Patients in the combined group as compared to the alone group had lower outflow tract gradients and a lower incidence of residual systolic anterior motion (SAM) syndrome. Conclusions. For HOCM patients without intrinsic MV diseases who are scheduled for surgery, a less pronounced septal hypertrophy may be closely associated with myectomy with concomitant mitral subvalvular procedures instead of myectomy alone. Mitral subvalvular procedures during myectomy are safe and allow the reduction of outflow tract gradients and freedom from SAM more effectively in comparison with myectomy alone. [ABSTRACT FROM AUTHOR]

Reasonable heterostructure design can effectively improve the thermoelectric performance of composite materials. High‐conductivity and high‐stability MXenes are expected for the application of thermoelectric conversion benefiting from their diverse electronic properties. In this work, the 2D MXene and 1D SWCNTs are employed to construct layered composite films with 2D–3D sandwich structures in the vertical direction by the wet‐chemical assembly strategy. As a result, sandwich Ti3C2Tx–SWCNTs–Ti3C2Tx film shows a higher power factor than that of Ti3C2Tx/SWCNTs film with interlaced structure, further 25 times higher than that of Ti3C2Tx film, which mainly due to the considerable electrical conductivity (750.9 S cm−1) and enhanced Seebeck (−32.2 µV K−1) coefficient. This study provides a feasible and valuable reference for expanding the application field of MXenes‐based materials and reasonably improving their thermoelectric conversion performance. [ABSTRACT FROM AUTHOR]

Background and Aim: Ischemic mitral regurgitation (IMR) recurrence after combined coronary artery bypass grafting (CABG) and mitral valve repair does occur, with a prevalence of 20% to 30% at the 2- to 4-year follow-up. This single-center study aims to identify the predictors of IMR improvement after surgical revascularization plus mitral valve repair for moderate IMR.Methods: A total of 201 eligible patients were entered into an improved group (n = 141) or a control group (n = 60) according to whether moderate or more mitral regurgitation occurred at the 2-year postoperative time point. Clinical outcomes between groups were compared.Results: The left ventricular endo-diastolic diameter (LVEDD), type of ring (rigid complete ring), and the use of repair techniques (restrictive annuloplasty associated with subvalvular and/or leaflet repair) were three predictors of IMR improvement after surgery (odds ratio [OR] = 0.921, 95% confidence interval [CI], 0.865-0.976, P = .025; OR = 7.753, 95% CI, 3.168-17.742, P < .001; and OR = 0.168, 95% CI, 0.076-0.423, P = .004, respectively). The cutoff value of the LVEDD was 65 mm with a sensitivity of 80.0% and a specificity of 65.2%. Patients in the improved group compared with those in the control group demonstrated better cumulative survival during a median follow-up of 41.0 months (χ2  = 4.559, logrank P = .033) and a reduced ratio of the New York Heart Association class III-IV at the latest follow-up (5.7% vs 38.4%, P < .001).Conclusions: An LVEDD of less than 65 mm, the use of a rigid complete ring, and combined restrictive annuloplasty and subvalvular and/or leaflet repair are associated with IMR improvement after CABG plus mitral valve repair for the treatment of moderate IMR; IMR improvement 2 years after surgery is associated with improved midterm outcomes. [ABSTRACT FROM AUTHOR]

Triple‐negative breast cancer (TNBC) is insensitive to endocrine therapies and targeted therapies to human epidermal growth factor receptor‐2 (HER2), estrogen receptor (ER) and progesterone receptor (PR). New targets and new targeted therapeutic drugs for TNBC are desperately needed. Our study confirmed that DCC‐2036 inhibited the proliferation, invasion, migration and epithelial‐mesenchymal transition (EMT) of TNBC cells as well as induced apoptosis. Moreover, the antiproliferative activity of DCC‐2036 was more efficient than that of most clinical drugs. In addition, the combination of DCC‐2036 and cisplatin or lapatinib had synergistic effects on TNBC cells. Mechanistically, DCC‐2036 targeted AXL/MET, especially AXL, and regulated the downstream PI3K/Akt‐NFκB signaling to exert its antitumor effect in TNBC. DCC‐2036 also inhibited the growth and metastasis of xenografted MDA‐MB‐231 cells (AXL/MET‐high TNBC cells) but not MDA‐MB‐468 cells (AXL‐low TNBC cells) in NSG mice in vivo. Furthermore, DCC‐2036 significantly inhibited tumor growth and invasion of AXL/MET‐high TNBC PDX tumors but not AXL/MET‐low TNBC PDX tumors. These results highlighted the roles of AXL/MET in cancer growth and metastasis and further verified that the critical targets of DCC‐2036 are AXL and MET, especially AXL. In addition, there was no significant toxicity of DCC‐2036 even at a high dosage. Therefore, DCC‐2036 may be a potential compound to treat TNBC, especially for tumors with AXL/MET overexpression. What's new? Triple‐negative breast cancer (TNBC) is not sensitive to hormonal therapies or treatments targeted against HER2. Tyrosine kinases (TKs) could be potential targets due to their activation and high expression in multiple TNBC subtypes. This study shows that DCC‐2036, a third‐generation tyrosine kinase inhibitor with high selective activity for multiple TKs, has potent activity against TNBC. DCC‐2036 targets AXL/MET and regulates the downstream PI3K/Akt‐NFκB pathway in vitro and in vivo, without apparent toxicity. Moreover, DCC‐2036 exhibits more efficient anti‐proliferative activity than most clinical drugs. These data highlight DCC‐2036 as a promising targeting agent for treating TNBC, especially tumors that overexpress AXL/MET. [ABSTRACT FROM AUTHOR]

Abstract: Exposure to particulate matter (PM) leads to kinds of cardiopulmonary diseases, such as asthma, COPD, arrhythmias, lung cancer, etc., which are related to PM‐induced inflammation. We have found that PM2.5 (aerodynamics diameter <2.5 µm) exposure induces inflammatory response both in vivo and in vitro. Since the toxicity of PM is tightly associated with its size and components, PM1 (aerodynamics diameter <1.0 µm) is supposed to be more toxic than PM2.5. However, the mechanism of PM1‐induced inflammation is not clear. Recently, emerging evidences prove that microRNAs play a vital role in regulating inflammation. Therefore, we studied the regulation of miR‐146a in PM1‐induced inflammation in human lung bronchial epithelial BEAS‐2B cells. The results show that PM1 induces the increase of IL‐6 and IL‐8 in BEAS‐2B cells and up‐regulates the miR‐146a expression by activating NF‐κB signaling pathway. Overexpressed miR‐146a prevents the nuclear translocation of p65 through inhibiting the IRAK1/TRAF6 expression, and downregulates the expression of IL‐6 and IL‐8. Taken together, these results demonstrate that miR‐146a can negatively feedback regulate PM1‐induced inflammation via NF‐κB signaling pathway in BEAS‐2B cells. [ABSTRACT FROM AUTHOR]

The aimof this study was to explore the intracellular mechanisms underlying the cardiovascular toxicity of air particulate matter (PM) with an aerodynamic diameter of less than 2.5 µm (PM2.5) in a human umbilical vein cell line, EA.hy926. We found that PM2.5 exposure triggered reactive oxygen species (ROS) generation, resulting in a significant decrease in cell viability. Data from Western blots showed that PM2.5 induced phosphorylation of Jun N-terminal kinase (JNK), extracellular signal regulatory kinase (ERK), p38 mitogen-activated protein kinase (MAPK) and protein kinase B (AKT), and activation of nuclear factor kappa B (NF-κB). We further observed a significant increase in expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) in a time- and dose-dependentmanner. Moreover, the adhesion of monocytic THP-1 cells to EA.hy926 cellswas greatly enhanced in the presence of PM2.5. However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-κB activation aswell as the expression of ICAM-1 and VCAM-1. Furthermore, ERK inhibitor (U0126), AKT inhibitor (LY294002) and NF-κB inhibitor (BAY11-7082) significantly down-regulated PM2.5-induced ICAM-1 and VCAM-1 expression as well as adhesion of THP-1 cells, but not JNK inhibitor (SP600125) and p38 MAPK inhibitor (SB203580), indicating that ERK/AKT/NF-κB is involved in the signaling pathway that leads to PM2.5-induced ICAM-1 and VCAM-1 expression. These findings suggest PM2.5-induced ROSmay function as signalingmolecules triggering ICAM-1 and VCAM-1 expressions through activating the ERK/AKT/NF-κB-dependent pathway, and further promoting monocyte adhesion to endothelial cells. [ABSTRACT FROM AUTHOR]

Exposure to atmospheric particulate matter PM2.5 (aerodynamic diameter < 2.5 lm) has been epidemiologically associated with respiratory illnesses. However, recent data have suggested that PM2.5 is able to infiltrate into circulation and elicit a systemic inflammatory response. Potential adverse effects of air pollutants to the central nervous system (CNS) have raised concerns, but whether PM2.5 causes neurotoxicity remains unclear. In this study, we have demonstrated that PM2.5 impairs the tight junction of endothelial cells and increases permeability and monocyte transmigration across endothelial monolayer in vitro, indicating thatPM2.5 is able to disrupt blood-brain barrier integrity and gain access to the CNS. Exposure of primary neuronal cultures to PM2.5 resulted in decrease in cell viability and loss of neuronal antigens. Furthermore, supernatants collected from PM2.5-treated macrophages and microglia were also neurotoxic. These macrophages and microglia significantly increased extracellular levels of glutamate following PM2.5 exposure, which were negatively correlated with neuronal viability. Pre-treatment with NMDA receptor antagonist MK801 alleviated neuron loss, suggesting that PM2.5 neurotoxicity is mediated by glutamate. To determine the potential source of excess glutamate production, we investigated glutaminase, the main enzyme for glutamate generation. Glutaminase was reduced in PM2.5-treated macrophages and increased in extracellular vesicles, suggesting that PM2.5 induces glutaminase release through extracellular vesicles. In conclusion, these findings indicatePM2.5 as a potential neurotoxic factor, crucial to understanding the effects of air pollution on the CNS. [ABSTRACT FROM AUTHOR]

Exposure to ambient airborne particulate matter (PM) with an aerodynamic diameter less than 10 μm (PM10) links with public health hazards and increases risk for lung cancer and other diseases. Recent studies have suggested that oxidative stress is a key mechanism underlying the toxic effects of exposure to PM10. Several components of water-soluble fraction of PM10 (sPM10) have been known to be capable of inducing oxidative stress in in vitro studies. In this study, we investigated if water-insoluble fraction of PM10 (iPM10) could be also capable of inducing oxidative stress and oxidative damage. Human lung epithelial A549 cells were exposed to 10 μg/mL of sPM10, iPM10 or total PM10 (tPM10) preparation for 24 h. Here, we observed that all three PM10 preparations reduced cell viability and induced apoptotic cell death in A549 cells. We further found that, similar to the exposure to sPM10 and tPM10, the intracellular level of hydrogen peroxide (H2O2) in the iPM10-exposed cells was increased significantly; meanwhile the activity of catalase was decreased significantly as compared with the unexposed control cells, resulting in significant DNA damage. Our data obtained from inductively coupled plasma-mass spectrometry (ICP-MS) assays showed that iron is the most abundant metal in all three PM10 preparations. Thus, we have demonstrated that, similar to sPM10, iPM10 is also capable of inducing oxidative stress by probably inducing generation of H2O2 and impairing enzymatic antioxidant defense, resulting in oxidative DNA damage and even apoptotic cell death through the iron-catalyzed Fenton reaction. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 226-233, 2014. [ABSTRACT FROM AUTHOR]

ABSTRACT We investigated whether the implantation of juvenile allograft and minced meniscal fragments could improve the healing of avascular meniscal injuries, which cannot heal spontaneously. Concentric cylindrical explants were excised from the inner two-thirds of swine medial menisci. The inner cylinder consisted of a 'sandwich' structure, with minced juvenile meniscal fragments, juvenile meniscal columns, minced mature meniscal fragments, or mature meniscal columns implanted in the middle. The explants were cultured in vitro for 2, 4, or 6 weeks. Interfacial meniscal repair was assessed by histology, immunohistochemistry, biomechanical testing, and confocal laser scanning microscopy. Histology and confocal microscopy results revealed that tissue repair and cell accumulation at the interface were best at all time points in the juvenile meniscal fragments group, followed by the juvenile columns, minced mature fragments, and mature columns groups, respectively. At 6 weeks, the implantation of juvenile allograft and minced meniscal fragments increased the shear strength, peak force, and energy to failure in the peripheral interface. Picosirius red/polarized light microscopy and immunohistochemistry results showed concurrent expression of type I and II collagen in the interfacial repair tissue. In conclusion, implantation of juvenile allograft and minced meniscal fragments could increase the healing of avascular meniscal injury in vitro. © 2013 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 31:1514-1519, 2013 [ABSTRACT FROM AUTHOR]

Abnormal immunity and its related complications are the major causes of mortality and morbidity in diabetes patients. Macrophages, as one of the important innate cells, play pivotal roles in controlling immune homeostasis, immunity, and tolerance. The effects of hyperglycemia on the function of macrophages in hosts remain to be determined. Here we used mice with streptozotocin (STZ)-induced diabetes for long term to study the changes of macrophages. We found that F4/80+ peritoneal exudate macrophages (PEMs) from mice with diabetes for 4 months displayed significantly reduced CD86 and CD54 expression and tumor necrosis factor (TNF)-α and IL-6 production but enhanced nitric oxide (NO) secretion compared with control mice when treated with interferon (IFN)-γ and lipopolysaccharide (LPS), while the activity of arginase in PEMs from diabetic mice was significantly higher than control mice when stimulating with IL-4. These dysfunctions of macrophages could be efficiently reversed by insulin treatment. Importantly, in vitro bone marrow-derived macrophages showed similar functional changes, indicating the epigenetic alteration of macrophage precursors in these mice. In an in vitro culture system, high glucose and insulin significantly altered TNF-α, IL-6, and NO production and arginase activity of macrophages, which was reversed by the treatment with AKT and ERK inhibitors. Therefore, hyperglycemia and insulin deficiency can modify macrophage function through AKT-mTOR and ERK pathways and through epigenetic effects on macrophage precursors. To further identify different components of diabetes on the dysfunction of macrophages is important for efficient prevention of diabetic complications. J. Cell. Physiol. 227: 1670-1679, 2012. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Background and aim of the study : There is still controversy with regard to adequate therapy for symptomatic patients who are refractory to medical management with myocardial bridges of the left anterior descending artery. This study sought to evaluate the treatment of symptomatic coronary myocardial bridges with coronary artery bypass graft surgery. Methods: Thirteen patients who underwent surgery between October 2005 and May 2008 were included in this study. The mean patient age was 51.3 ± 10.2 years (range, 39-75 years). There were ten men and three women. All 13 patients had angina pectoris preoperatively, and they had myocardial bridges only. Coronary angiography prior to surgery demonstrated myocardial bridging of the left anterior descending artery with systolic compression ≥75% in all patients. They underwent off-pump coronary artery bypass grafting using the internal mammary artery. Results: The acute clinical success rate was 100% with respect to the absence of myocardial infarction, death, or other major in-hospital complications. Postoperative coronary CT angiography studies in seven patients after one year demonstrated no graft stenosis. During follow-up, no patient had symptoms of angina. Conclusions: Coronary artery bypass graft surgery using a LIMA graft is a safe and effective treatment for symptomatic coronary myocardial bridges. (J Card Surg 2012;27:405-407) [ABSTRACT FROM AUTHOR]