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Background Enhancing health intervention for floating populations has become an essential aspect of public health around the world. China launched a policy reform aimed at implementing immediate reimbursement for trans-provincial inpatient treatments. The objective of this study was to investigate the effects of this policy change on socioeconomic inequality in health among the floating population. Methods This study used two waves of individual-level data from the China Migrants Dynamic Survey (CMDS) collected in 2017 and 2018 as well as administrative hospital data at the city level. The sample included 122061 individuals and 262 cities. Under a quasi-experimental research design, we built up the framework to employ the generalized and multi-period difference-in-differences estimation strategy. We used the number of qualified hospitals that could provide immediate reimbursement to represent the degree and intensity of the implementation of this policy change. We also calculated the Wagstaff Index (WI) to measure socioeconomic inequality in health. Results This policy change and income level had a negative joint impact on the health status of floating population (odds ratio = 0.955, P  < 0.01), that is, the lower the income, the better the number of qualified hospitals' effect on health improvement. Furthermore, as the number of qualified tertiary hospitals increased, the health inequality would decrease significantly on average at the city level ( P  < 0.05). In addition, inpatient utilization as well as total expenditure and reimbursement significantly improved after the policy change, and the magnitude of increase was greater in the relatively lower-income group ( P  < 0.01). Finally, only inpatient spending could obtain immediate reimbursement in the early stage, thus, compared with primary care, these impacts were greater in tertiary care. Conclusions Our study revealed that after the implementation of immediate reimbursement, the floating population could obtain greater and more timely reimbursement, which significantly increased its inpatient utilization, promoted health, and reduced the health inequality caused by socioeconomic factors. These results suggest that a more accessible and friendly medical insurance scheme should be promoted for this group.

Recently, quantum anomalous Hall effect with spontaneous ferromagnetism was observed in twisted bilayer graphenes (TBG) near 3/4 filling. Importantly, it was observed that an extremely small current can switch the direction of the magnetization. This offers the prospect of realizing low energy dissipation magnetic memories. However, the mechanism of the current-driven magnetization switching is poorly understood as the charge currents in graphenes are generally believed to be non-magnetic. In this work, we demonstrate that in TBG, the twisting and substrate induced symmetry breaking allow an out of plane orbital magnetization to be generated by a charge current. Moreover, the large Berry curvatures of the flat bands give the Bloch electrons large orbital magnetic moments so that a small current can generate a large orbital magnetization. We further demonstrate how the charge current can switch the magnetization of the ferromagnetic TBG near 3/4 filling as observed in the experiments. The mechanism of current-driven magnetization switching in twisted bilayer graphene (TBG) is poorly understood. Here, He et al. show that a small current can generate a large orbital magnetization due to symmetry breaking by the twisting and substrate in TBG, leading to a giant orbital magnetoelectric effect.

Rare earth (RE 3+ )-doped phosphors generally suffer from thermal quenching, in which their photoluminescence (PL) intensities decrease at high temperatures. Herein, we report a class of unique two-dimensional negative-thermal-expansion phosphor of Sc 2 (MoO 4 ) 3 :Yb/Er. By virtue of the reduced distances between sensitizers and emitters as well as confined energy migration with increasing the temperature, a 45-fold enhancement of green upconversion (UC) luminescence and a 450-fold enhancement of near-infrared downshifting (DS) luminescence of Er 3+ are achieved upon raising the temperature from 298 to 773 K. The thermally boosted UC and DS luminescence mechanism is systematically investigated through in situ temperature-dependent Raman spectroscopy, synchrotron X-ray diffraction and PL dynamics. Moreover, the luminescence lifetime of 4 I 13/2 of Er 3+ in Sc 2 (MoO 4 ) 3 :Yb/Er displays a strong temperature dependence, enabling luminescence thermometry with the highest relative sensitivity of 12.3%/K at 298 K and low temperature uncertainty of 0.11 K at 623 K. These findings may gain a vital insight into the design of negative-thermal-expansion RE 3+ -doped phosphors for versatile applications. Rare-earth doped phosphors with negative thermal expansion (NTE) may display thermally-enhanced emission, but their performance is generally limited. Here the authors report thermally-boosted green upconversion luminescence and near-infrared downshifting luminescence in Sc 2 (MoO 4 ) 3 :Yb/Er phosphors with two-dimensional NTE, and their application in temperature sensing.

The laurel family within the Magnoliids has attracted attentions owing to its scents, variable inflorescences, and controversial phylogenetic position. Here, we present a chromosomelevel assembly of the Litsea cubeba genome, together with low-coverage genomic and transcriptomic data for many other Lauraceae. Phylogenomic analyses show phylogenetic discordance at the position of Magnoliids, suggesting incomplete lineage sorting during the divergence of monocots, eudicots, and Magnoliids. An ancient whole-genome duplication (WGD) event occurred just before the divergence of Laurales and Magnoliales; subsequently, independent WGDs occurred almost simultaneously in the three Lauralean lineages. The phylogenetic relationships within Lauraceae correspond to the divergence of inflorescences, as evidenced by the phylogeny of FUWA, a conserved gene involved in determining panicle architecture in Lauraceae. Monoterpene synthases responsible for production of specific volatile compounds in Lauraceae are functionally verified. Our work sheds light on the evolution of the Lauraceae, the genetic basis for floral evolution and specific scents.

Introduction For investigating the mechanism of brain injury caused by chronic fluorosis, this study was designed to determine whether NRH:quinone oxidoreductase 2 (NQO2) can influence autophagic disruption and oxidative stress induced in the central nervous system exposed to a high level of fluoride. Methods Sprague–Dawley rats drank tap water containing different concentrations of fluoride for 3 or 6 months. SH‐SY5Y cells were either transfected with NQO2 RNA interference or treated with NQO2 inhibitor or activator and at the same time exposed to fluoride. The enrichment of gene signaling pathways related to autophagy was evaluated by Gene Set Enrichment Analysis; expressions of NQO2 and autophagy‐related protein 5 (ATG5), LC3‐II and p62, and mammalian target of rapamycin (mTOR) were quantified by Western‐blotting or fluorescent staining; and the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) assayed biochemically and reactive oxygen species (ROS) detected by flow cytometry. Results In the hippocampal CA3 region of rats exposed to high fluoride, the morphological characteristics of neurons were altered; the numbers of autophagosomes in the cytoplasm and the levels of NQO2 increased; the level of p‐mTOR was decreased, and the levels of ATG5, LC3‐II and p62 were elevated; and genes related to autophagy enriched. In vitro, in addition to similar changes in NQO2, p‐mTOR, ATG5, LC3 II, and p62, exposure of SH‐SY5Y cells to fluoride enhanced MDA and ROS contents and reduced SOD activity. Inhibition of NQO2 with RNAi or an inhibitor attenuated the disturbance of the autophagic flux and enhanced oxidative stress in these cells exposed to high fluoride. Conclusion Our findings indicate that NQO2 may be involved in regulating autophagy and oxidative stress and thereby exerts an impact on brain injury caused by chronic fluorosis. We reported for the first time that NQO2 may be involved in regulating autophagy and oxidative stress and thereby exert an impact on brain injury caused by chronic fluorosis. Suppressing NQO2 expression relieves oxidative stress and restores autophagy flux in fluoride‐treated neuron cells.

Realizing non-trivial topological effects is challenging in acoustic systems. It is now shown that inversion symmetry breaking can be used to create acoustic analogues of the topological Haldane model. Following the discovery of the quantum Hall effect 1 , 2 and topological insulators 3 , 4 , the topological properties of classical waves began to draw attention 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 . Topologically non-trivial bands characterized by non-zero Chern numbers are realized through either the breaking of time-reversal symmetry using an external magnetic field 5 , 6 , 7 , 15 , 16 or dynamic modulation 8 , 17 . Owing to the absence of a Faraday-like effect, the breaking of time-reversal symmetry in an acoustic system is commonly realized with moving background fluids 20 , 22 , which drastically increases the engineering complexity. Here we show that we can realize effective inversion symmetry breaking and create an effective gauge flux in a reduced two-dimensional system by engineering interlayer couplings, achieving an acoustic analogue of the topological Haldane model 2 , 23 . We show that the synthetic gauge flux is closely related to Weyl points 24 , 25 , 26 in the three-dimensional band structure and the system supports chiral edge states for fixed values of k z .

We examined the mechanism by which lithium chloride (LiCl) attenuates the impaired learning capability and memory function of dual‐transgenic APP/PS1 mice. Six‐ or 12‐month‐old APP/PS1 and wild‐type (WT) mice were randomized into four groups, namely WT, WT+Li (100 mg LiCl/kg body weight, gavage once daily), APP/PS1 and APP/PS1+Li. Primary rat hippocampal neurons were exposed to β‐amyloid peptide oligomers (AβOs), LiCl and/or XAV939 (inhibitor of Wnt/β‐catenin) or transfected with small interfering RNA against the β‐catenin gene. In the cerebral zone of APP/PS1 mice, the level of Aβ was increased and those of α7 nicotinic acetylcholine receptors (nAChR), phosphor‐GSK3β (ser9), β‐catenin and cyclin D1 (protein and/or mRNA levels) reduced. Two‐month treatment with LiCl at ages of 4 or 10 months weakened all of these effects. Similar expression variations were observed for these proteins in primary neurons exposed to AβOs, and these effects were attenuated by LiCl and aggravated by XAV939. Inhibition of β‐catenin expression lowered the level of α7 nAChR protein in these cells. LiCl attenuates the impaired learning capability and memory function of APP/PS1 mice via a mechanism that might involve elevation of the level of α7 nAChR as a result of altered Wnt/β‐catenin signalling.

Berberine (BBR) has been confirmed to have multiple bioactivities in clinic, such as cholesterol-lowering, anti-diabetes, cardiovascular protection and anti- inflammation. However, BBR's plasma level is very low; it cannot explain its pharmacological effects in patients. We consider that the in vivo distribution of BBR as well as of its bioactive metabolites might provide part of the explanation for this question. In this study, liquid chromatography coupled to ion trap time-of-flight mass spectrometry (LC/MS(n)-IT-TOF) as well as liquid chromatography that coupled with tandem mass spectrometry (LC-MS/MS) was used for the study of tissue distribution and pharmacokinetics of BBR in rats after oral administration (200 mg/kg). The results indicated that BBR was quickly distributed in the liver, kidneys, muscle, lungs, brain, heart, pancreas and fat in a descending order of its amount. The pharmacokinetic profile indicated that BBR's level in most of studied tissues was higher (or much higher) than that in plasma 4 h after administration. BBR remained relatively stable in the tissues like liver, heart, brain, muscle, pancreas etc. Organ distribution of BBR's metabolites was also investigated paralleled with that of BBR. Thalifendine (M1), berberrubine (M2) and jatrorrhizine (M4), which the metabolites with moderate bioactivity, were easily detected in organs like the liver and kidney. For instance, M1, M2 and M4 were the major metabolites in the liver, among which the percentage of M2 was up to 65.1%; the level of AUC (0-t) (area under the concentration-time curve) for BBR or the metabolites in the liver was 10-fold or 30-fold higher than that in plasma, respectively. In summary, the organ concentration of BBR (as well as its bioactive metabolites) was higher than its concentration in the blood after oral administration. It might explain BBR's pharmacological effects on human diseases in clinic.

Notch receptors (Notch1–4) play critical roles in tumorigenesis and metastasis of malignant tumors, including breast cancer. Although abnormal Notch activation is related to various tumors, the importance of single receptors and their mechanism of activation in distinct breast cancer subtypes are still unclear. Previous studies by our group demonstrated that Notch3 may inhibit the emergence and progression of breast cancer. PTEN is a potent tumor suppressor, and its loss of function is sufficient to promote the occurrence and progression of tumors. Intriguingly, numerous studies have revealed that Notch1 is involved in the regulation of PTEN through its binding to CBF-1, a Notch transcription factor, and the PTEN promoter. In this study, we found that Notch3 and PTEN levels correlated with the luminal phenotype in breast cancer cell lines. Furthermore, we demonstrated that Notch3 transactivated PTEN by binding CSL-binding elements in the PTEN promoter and, at least in part, inhibiting the PTEN downstream AKT-mTOR pathway. Notably, Notch3 knockdown downregulated PTEN and promoted cell proliferation and tumorigenesis. In contrast, overexpression of the Notch3 intracellular domain upregulated PTEN and inhibited cell proliferation and tumorigenesis in vitro and in vivo. Moreover, inhibition or overexpression of PTEN partially reversed the promotion or inhibition of cell proliferation induced by Notch3 alterations. In general, Notch3 expression positively correlated with elevated expression of PTEN, ER, lower Ki-67 index, and incidence of involved node status and predicted better recurrence-free survival in breast cancer patients. Therefore, our findings demonstrate that Notch3 inhibits breast cancer proliferation and suppresses tumorigenesis by transactivating PTEN expression.

Background The use of indirect calorimetry (IC) is increasing due to its precision in resting energy expenditure (REE) measurement in critically ill patients. Thus, we aimed to evaluate the clinical outcomes of an IC-guided nutrition therapy compared to predictive equations strategy in such a patient population. Methods We searched PubMed, EMBASE, and Cochrane library databases up to October 25, 2020. Randomized controlled trials (RCTs) were included if they focused on energy delivery guided by either IC or predictive equations in critically ill adults. We used the Cochrane risk-of-bias tool to assess the quality of the included studies. Short-term mortality was the primary outcome. The meta-analysis was performed with the fixed-effect model or random-effect model according to the heterogeneity. Results Eight RCTs with 991 adults met the inclusion criteria. The overall quality of the included studies was moderate. Significantly higher mean energy delivered per day was observed in the IC group, as well as percent delivered energy over REE targets, than the control group. IC-guided energy delivery significantly reduced short-term mortality compared with the control group (risk ratio = 0.77; 95% CI 0.60 to 0.98; I 2  = 3%, P  = 0.03). IC-guided strategy did not significantly prolong the duration of mechanical ventilation (mean difference [MD] = 0.61 days; 95% CI − 1.08 to 2.29; P  = 0.48), length of stay in ICU (MD = 0.32 days; 95% CI − 2.51 to 3.16; P  = 0.82) and hospital (MD = 0.30 days; 95% CI − 3.23 to 3.83; P  = 0.87). Additionally, adverse events were similar between the two groups. Conclusions This meta-analysis indicates that IC-guided energy delivery significantly reduces short-term mortality in critically ill patients. This finding encourages the use of IC-guided energy delivery during critical nutrition support. But more high-quality studies are still needed to confirm these findings.