Salsolinol as an RNA m6A methylation inducer mediates dopaminergic neuronal death by regulating YAP1 and autophagy.

JOURNAL/nrgr/04.03/01300535-202503000-00032/figure1/v/2024-06-17T092413Z/r/image-tiff Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, Sal) is a catechol isoquinoline that causes neurotoxicity and shares structural similarity with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, an environmental toxin that causes Parkinson's disease. However, the mechanism by which Sal mediates dopaminergic neuronal death remains unclear. In this study, we found that Sal significantly enhanced the global level of N6-methyladenosine (m6A) RNA methylation in PC12 cells, mainly by inducing the downregulation of the expression of m6A demethylases fat mass and obesity-associated protein (FTO) and alkB homolog 5 (ALKBH5). RNA sequencing analysis showed that Sal downregulated the Hippo signaling pathway. The m6A reader YTH domain-containing family protein 2 (YTHDF2) promoted the degradation of m6A-containing Yes-associated protein 1 (YAP1) mRNA, which is a downstream key effector in the Hippo signaling pathway. Additionally, downregulation of YAP1 promoted autophagy, indicating that the mutual regulation between YAP1 and autophagy can lead to neurotoxicity. These findings reveal the role of Sal on m6A RNA methylation and suggest that Sal may act as an RNA methylation inducer mediating dopaminergic neuronal death through YAP1 and autophagy. Our results provide greater insights into the neurotoxic effects of catechol isoquinolines compared with other studies and may be a reference for assessing the involvement of RNA methylation in the pathogenesis of Parkinson's disease.

ECM-mimetic glucomannan hydrogel promotes pressure ulcer healing by scavenging ROS, promoting angiogenesis and regulating macrophages.

Pressure ulcers (PUs) have emerged as a significant burden on both individuals and society. Effective treatment of PUs is a significant clinical challenge due to the compromised tissue microenvironment characterized by extracellular matrix (ECM) depletion, increased levels of reactive oxygen species (ROS), excessive inflammation and impaired angiogenesis. To this end, we have developed a glucomannan hydrogel (GM-Pgel) that mimics the skin's extracellular matrix to accelerate wound healing by regulating chronic inflammation in the PUs. This hydrogel not only faithfully replicates the components and nanofibrous architecture of ECM-like glycoproteins but also exhibits remarkable capabilities in enhancing neovascularization, scavenging ROS, and promoting macrophage polarization toward the M2 phenotype. In summary, this ECM-mimetic multifunctional hydrogel emerges as a promising dressing with diverse functionalities, capable of reshaping the compromised tissue environment without the need for additional drugs, exogenous cytokines, or cells. This presents a compelling and effective strategy for the repair and regeneration of chronic cutaneous wounds.

Stepwise de novo establishment of inactive X chromosome architecture in early development.

X chromosome inactivation triggers a dramatic reprogramming of transcription and chromosome architecture. However, how the chromatin organization of inactive X chromosome is established de novo in vivo remains elusive. Here, we identified an Xist-separated megadomain structure (X-megadomains) on the inactive X chromosome in mouse extraembryonic lineages and extraembryonic endoderm (XEN) cell lines, and transiently in the embryonic lineages, before Dxz4-delineated megadomain formation at later stages in a strain-specific manner. X-megadomain boundary coincides with strong enhancer activities and cohesin binding in an Xist regulatory region required for proper Xist activation in early embryos. Xist regulatory region disruption or cohesin degradation impaired X-megadomains in extraembryonic endoderm cells and caused ectopic activation of regulatory elements and genes near Xist, indicating that cohesin loading at regulatory elements promotes X-megadomains and confines local gene activities. These data reveal stepwise X chromosome folding and transcriptional regulation to achieve both essential gene activation and global silencing during the early stages of X chromosome inactivation.

Outdoor light at night, air pollution and risk of incident type 2 diabetes.

BACKGROUND: Air pollution and outdoor light at night (LAN) have been reported to be related to type 2 diabetes (T2D). However, their interaction with risk of T2D remains uncertain. Therefore, our study aimed to explore the relationship between outdoor LAN, air pollution and incident T2D. METHODS: Our study included a cohort of 24,147 subjects recruited from 2015 to 2018 in Ningbo, China. Land use regression models were used to evaluate particulate matter with a diameter ≤2.5µm (PM2.5), ≤10µm (PM10) and nitrogen dioxide (NO2). Satellite images data with a spatial resolution of 500m was used to estimate outdoor LAN levels. T2D new cases were identified by medical records based on health information system. Cox proportional hazards models were used to estimate Hazard ratios (HRs) and 95% confidence intervals (CIs). Moreover, we investigated the multiplicative and additive interactions between air pollution and outdoor LAN. RESULTS: During 108,908 person-years of follow-up period, 1,016 T2D incident cases were identified. The HRs (95% CIs) were 1.22 (1.15, 1.30) for outdoor LAN, 1.20 (1.00, 1.45) for PM2.5, 1.23 (1.11, 1.35) for PM10 and 1.19 (1.04, 1.37) for NO2 in every interquartile range increase, respectively. Furthermore, significant interactions were observed between outdoor LAN and NO2. CONCLUSIONS: Our findings indicated that air pollution and outdoor LAN were positively associated with T2D. Moreover, we observed an interaction between outdoor LAN and NO2 suggesting that stronger associations for outdoor LAN and T2D in areas with higher levels of NO2, and for NO2 and T2D in areas with higher levels of outdoor LAN.

High-performance hydrogen evolution reaction in quadratic nodal line semimetal Na2CdSn.

Topological nodal line semimetals (TNLSMs), which exhibit one-dimensional (1D) band crossing in their electronic band structure, have been predicted to be potential catalysts in electrocatalytic processes. However, the current studies are limited to the TNLSMs where the dispersion around the nodal line is linear in all directions. Here, the potential application of the quadratic nodal line (QNL) semimetal Na2CdSn in hydrogen evolution reaction is explored. Based on the bulk-boundary correspondence, we find that the topological surface states (TSSs) of the QNL are extended in the entire Brillouin zone. A linear relationship between the density of states of the TSSs and the Gibbs free energy is established in Na2CdSn. Remarkably, the best performance of Na2CdSn can be comparable to that of the noble metal Pt. Therefore, our work not only identifies an innovative type of topological catalyst with a QNL state but also confirms the relationship between TSSs and catalytic performance.

The role of ß2-AR/PI3K/AKT pathway in the proliferation, migration and invasion of THLE-2 cells induced by nicotine.

Nicotine, the primary constituent of tobacco, is one of the important factors that induce the occurrence of hepatocellular carcinoma (HCC). The ß2-adrenergic receptor (ß2-AR) is implicated in the growth and advancement of tumors. However, the role of ß2-AR and its mediated cascades in nicotine-induced HCC remains unclear. This present study aims to observe the effects of nicotine on the proliferation, migration, and invasion of immortalized human liver epithelial (THLE-2) cells, as well as to explore the underlying mechanisms of action. The results of cell counting kit-8 (CCK-8) assay showed that 0.3125 µM nicotine had the ability to promote the proliferation of THLE-2 cells with a significant time-dependent manner. Therefore, THLE-2 cells were mainly selected for chronic treatment with 0.3125 µM nicotine in the later stage to cause transformation. After 30 passages of THLE-2 cells with 0.3125 µM nicotine treatment, chronic exposure to nicotine significantly enhanced the proliferation, metastasis, and invasion of cells. Besides, it also upregulated the intracellular levels of ß2-AR, phosphoinositide 3-kinase (PI3K), AKT, matrix metalloproteinase-2 (MMP-2) and Cyclin D1, as well as downregulated the expression of p53. More importantly, the ß2-AR/PI3K/AKT pathway was found to mediate the expression of MMP-2, Cyclin D1, and p53 in THLE-2 cells, playing a crucial role in their proliferation, migration, and invasion after continuous exposure to nicotine. Simply put, it demonstrated the role of ß2-AR/PI3K/AKT pathway in the transformation of THLE-2 cells induced by nicotine. This study could provide valuable insights into the relationship between nicotine and HCC. Additionally, it lays the groundwork for investigating potential anticancer treatments for liver cancer linked to tobacco consumption.

Association of Fine Particulate Matter and Residential Greenness With Risk of Pulmonary Tuberculosis Retreatment: Population-Based Retrospective Study.

Background: The evidence on the association of fine particulate matter with an aerodynamic diameter of 2.5 µm or less (PM2.5) with pulmonary tuberculosis (PTB) retreatment is limited. There are no data on whether greenness exposure protects air pollution-related PTB retreatment in patients with prior PTB. Objective: In a population-based retrospective study, we aimed to investigate the influence of PM2.5 and residential greenness on the risk of PTB retreatment. Methods: A total of 26,482 patients with incident PTB, registered in a mandatory web-based reporting system between 2012 and 2019 in Zhengzhou, China, were included in the analysis. The exposure to PM2.5 was assessed based on the China High Air Pollutants dataset, and the level of greenness was estimated using the Normalized Difference Vegetation Index (NDVI) values. The associations of PTB retreatment with exposure to PM2.5 and greenness were evaluated, respectively, considering the local socioeconomic level indicated by the nighttime light index. Results: Among the 26,482 patients (mean age 46.86, SD 19.52 years) with a median follow-up time of 1523 days per patient, 1542 (5.82%) PTB retreatments were observed between 2012 and 2019. Exposure to PM2.5 was observed to be significantly associated with the increased risk of PTB retreatment in fully adjusted models with a hazard ratio of 1.97 (95% CI 1.34-2.83) per 10 µg/m3 increase in PM2.5. Patients living in the regions with relatively high quartiles of NDVI values had a 45% lower risk of PTB retreatment than those living in the regions with the lowest quartile for the 500 m buffers (hazard ratio 0.55, 95% CI 0.40-0.77). Such a protective effect of residential greenness was more pronounced among patients living in lower nighttime light areas. The strength of the association between PM2.5 exposure and the risk of PTB retreatment was attenuated by greenness. No significant association was observed between NDVI and the incidence of drug resistance. Conclusions: Long-term exposure to PM2.5 might be a risk factor for PTB retreatment, while an increased level of residential greenness was found to be associated with reduced risks of PTB retreatment. Our results suggest strengthening the control of ambient air pollution and improving residential greenness may contribute to the reduction of PTB retreatment.

Remote limb ischemic preconditioning alleviated spinal cord injury through inhibiting proinflammatory immune response and promoting the survival of spinal neurons.

STUDY DESIGN: Experimental animal study. OBJECTIVES: To investigate the protective effect of remote limb ischemia preconditioning (RLPreC) on traumatic spinal cord injury (SCI) and explore the underlying biological mechanisms using RNA sequencing. SETTING: China Rehabilitation Science Institute; Beijing; China. METHODS: spinal cord injury was induced in mice using a force of 0.7 N. RLPreC treatment was administered. Motor function, pain behavior, and gene expression were assessed. RESULTS: RLPreC treatment significantly improved motor function and reduced pain-like behavior in SCI mice. RNA-Seq analysis identified 5247 differentially expressed genes (DEGs). GO analysis revealed enrichment of immune response, inflammatory signaling, and synaptic transmission pathways among these DEGs. KEGG analysis indicated suppression of inflammation and promotion of synapse-related pathways. CONCLUSIONS: RLPreC is a promising therapeutic strategy for improving motor function and alleviating pain after traumatic SCI. RNA-Seq analysis provides insights into potential therapeutic targets and warrants further investigation.

Altered Effective Connectivity of the Pain Matrix in Herpes Zoster and Postherpetic Neuralgia Patients: Granger Causality Analysis of Resting-State fMRI.

BACKGROUND: Shingles can cause long-term pain and negative emotions, along with changes in brain function. In this study, Granger Causality Analysis (GCA) was used to compare herpes zoster (HZ) and postherpetic neuralgia (PHN) differences in effective connections within the "pain matrix" between patients and healthy controls to further understand patterns of interaction between brain regions and explore the relationship between changes in effective connections and clinical features. METHODS: Resting-state functional magnetic resonance imaging (fMRI) scans were performed on 55 HZ; 55 PHN; and 50 age-, sex- matched healthy controls (HCs). The brain regions associated with the pain matrix are used as the seeds of effective connectivity. GCA was used to analyze effective connections in brain regions that differed significantly between groups. Then the correlation between GCA values and clinical indicators was studied. RESULTS: Compared with HC, GCA values between the thalamus and the amygdala, between the thalamus and the precentral gyrus, from the thalamus to the postcentral gyrus, and from the parahippocampal gyrus to the amygdala, anterior cingulate gyrus were significantly reduced in HZ patients. Compared with HC, GCA values between the insular and the postcentral gyrus, from the insular to the inferior parietal lobe, and from the postcentral gyrus to the amygdala were significantly reduced in PHN patients. Compared with HZ, GCA values between the inferior parietal lobe and the parahippocampal gyrus, between the inferior parietal lobe and the anterior cingulate gyrus, and from the anterior cingulate gyrus to the amygdala were significantly increased in PHN patients. The visual analogue scale (VAS) score of PHN patients was positively correlated with the GCA value from the central posterior lobe to the insula. CONCLUSIONS: PHN and HZ patients showed a broad reduction in effective connections, mainly reflected in abnormal pain pathway regulation, pain perception, negative emotion and memory production, providing new perspectives to understand the neuroimaging mechanisms of shingles.

CRISPR screens reveal convergent targeting strategies against evolutionarily distinct chemoresistance in cancer.

Resistance to chemotherapy has been a major hurdle that limits therapeutic benefits for many types of cancer. Here we systematically identify genetic drivers underlying chemoresistance by performing 30 genome-scale CRISPR knockout screens for seven chemotherapeutic agents in multiple cancer cells. Chemoresistance genes vary between conditions primarily due to distinct genetic background and mechanism of action of drugs, manifesting heterogeneous and multiplexed routes towards chemoresistance. By focusing on oxaliplatin and irinotecan resistance in colorectal cancer, we unravel that evolutionarily distinct chemoresistance can share consensus vulnerabilities identified by 26 second-round CRISPR screens with druggable gene library. We further pinpoint PLK4 as a therapeutic target to overcome oxaliplatin resistance in various models via genetic ablation or pharmacological inhibition, highlighting a single-agent strategy to antagonize evolutionarily distinct chemoresistance. Our study not only provides resources and insights into the molecular basis of chemoresistance, but also proposes potential biomarkers and therapeutic strategies against such resistance.

Exploiting viral vectors to deliver genome editing reagents in plants.

Genome editing holds great promise for the molecular breeding of plants, yet its application is hindered by the shortage of simple and effective means of delivering genome editing reagents into plants. Conventional plant transformation-based methods for delivery of genome editing reagents into plants often involve prolonged tissue culture, a labor-intensive and technically challenging process for many elite crop cultivars. In this review, we describe various virus-based methods that have been employed to deliver genome editing reagents, including components of the CRISPR/Cas machinery and donor DNA for precision editing in plants. We update the progress in these methods with recent successful examples of genome editing achieved through virus-based delivery in different plant species, highlight the advantages and limitations of these delivery approaches, and discuss the remaining challenges.

Prognoses and risk stratification of thrombus-associated events in heart failure patients without atrial fibrillation.

AIMS: We aim to assess the risk of thrombus-associated events (TAE) in patients with heart failure (HF) without atrial fibrillation (AF) and develop an effective scoring system for a risk stratification model. METHODS AND RESULTS: This retrospective study included 450 patients (median age 64.0 years, interquartile range [55.0, 75.0]; 31.6% women) hospitalized for HF without AF and atrial flutter, but with a left ventricular ejection fraction (LVEF) ≤ 55% and New York Heart Association (NYHA) functional class of III-IV. A median follow-up of 47 months was conducted. In the present study, TAE during follow-up was independently associated with both all-cause death [hazard ratio (HR) 1.756, 95% confidence interval (CI) 1.324-2.328, P < 0.001] and readmission for HF (HR 1.574, 95% CI 1.122-2.208, P = 0.009) after adjustment for covariates. Hypertension (HR 1.573, 95% CI 1.018-2.429, P = 0.041), atrial arrhythmia excluding AF (AAexAF) (HR 2.041, 95% CI 1.066-3.908, P = 0.031), previous ischaemic stroke (HR 2.469, 95% CI 1.576-3.869, P < 0.001), and vascular disease (HR 1.658, 95% CI 1.074-2.562, P = 0.023) were independently associated with TAE. Age (HR 1.021, 95% CI 1.008-1.033, P = 0.001), previous ischaemic stroke (HR 1.685, 95% CI 1.248-2.274, P = 0.001), LVEF ([10, 25] vs. [40, 55]) HR 1.925, 95% CI 1.311-2.826, P = 0.001; (25, 40] vs. (40, 55] HR 1.084, 95% CI 0.825-1.424, P = 0.563), and creatinine clearance rate (Ccr) (HR 0.991, 95% CI 0.986-0.996, P = 0.001) were independently associated with composite events of TAE and death (TAE-D). CHA2DS2VASc modestly predicted 5-year TAE [area under the receiver operating characteristic curves (AUC) 0.660, P < 0.001 compared with 0.5] and TAE-D (AUC 0.639, P < 0.001 compared with 0.5). (C)ACE, formed by incorporating AAexAF, LVEF, and Ccr into CHA2DS2VASc, had higher AUC for predicting 5-year TAE (0.694 vs. 0.660, P = 0.018) and TAE-D (0.708 vs. 0.639, P < 0.001) compared with CHA2DS2VASc. In patients with HF with reduced ejection fraction (HFrEF), (C)ACE and (C)ACEN [formed by incorporating NYHA into (C)ACE] had higher AUC compared with CHA2DS2VASc in predicting 5-year TAE (0.700 and 0.707 vs. 0.649, P = 0.013 and 0.030, respectively) and TAE-D (0.712 and 0.713 vs. 0.622, P < 0.001 and <0.001, respectively). The AUC did not improve statistically from (C)ACE to (C)ACEN (0.700 vs. 0.707, P = 0.600 for TAE; 0.712 vs. 0.713, P = 0.917 for TAE-D). CONCLUSIONS: In HF without AF, TAE during follow-up was associated with adverse prognoses. The independent risk factors of TAE or TAE-D improved CHA2DS2-VASc predictive ability, especially in patients with HFrEF. Our findings provide new evidence for TAE risk stratification in HF without AF, potentially guiding prophylactic anticoagulation.

Surface photogalvanic effect in Ag2Te.

The bulk photovoltaic effect (BPVE) in non-centrosymmetric materials has attracted significant attention in recent years due to its potential to surpass the Shockley-Queisser limit. Although these materials are strictly constrained by symmetry, progress has been made in artificially reducing symmetry to stimulate BPVE in wider systems. However, the complexity of these techniques has hindered their practical implementation. In this study, we demonstrate a large intrinsic photocurrent response in centrosymmetric topological insulator Ag2Te, attributed to the surface photogalvanic effect (SPGE), which is induced by symmetry reduction of the surface. Through diverse spatially-resolved measurements on specially designed devices, we directly observe that SPGE in Ag2Te arises from the difference between two opposite photocurrent flows generated from the top and bottom surfaces. Acting as an efficient SPGE material, Ag2Te demonstrates robust performance across a wide spectral range from visible to mid-infrared, making it promising for applications in solar cells and mid-infrared detectors. More importantly, SPGE generated on low-symmetric surfaces can potentially be found in various systems, thereby inspiring a broader range of choices for photovoltaic materials.

The critical role of SETDB1-mediated CCND1/PI3K/AKT pathway via p53-RS di-methylation at K370 in the proliferation of WRL68 cells induced by nicotine.

Constituents of cigarette smoke are known to be carcinogens. Additionally, there is mounting evidence that the liver is an organ susceptible to tobacco carcinogenicity. Nicotine, the primary constituent of tobacco, plays a role in cancer progression. In our previous study, it was found that nicotine enhances the proliferation of a human normal fetal hepatic (WRL68) cell due to the activation of p53 mutation at Ser249 (p53-RS)/STAT1/CCND1 signaling pathway. Here, we further elucidated the mechanism of regulating this pathway. Firstly, dose-dependent increase of SETDB1 protein level in WRL68 cells upon exposure to nicotine (1.25, 2.5, and 5 µM), significantly enhanced cellular proliferation. In addition, the upregulation of SETDB1 protein was necessary for the nuclear translocation of p53-RS to establish a ternary complex with STAT1 and SETDB1, which facilitated p53-RS di-methylation at K370 (p53-RS/K370me2). After that, the activation of CCND1/PI3K/AKT pathway was initiated when STAT1 stability was enhanced by p53-RS/K370me2, ultimately resulting in cell proliferation. Altogether, the study revealed that the increase in SETDB1 expression could potentially have a significant impact on the activation of CCND1/PI3K/AKT pathway through p53-RS/K370me2, leading to the proliferation of WRL68 cells induced by nicotine, which could contribute to hepatocellular carcinoma for smokers. Besides, the results of this study provided a foundation for the development of anticancer therapies for cancers associated with tobacco use.

Histopathological growth pattern and vessel co-option in intrahepatic cholangiocarcinoma.

Intrahepatic cholangiocarcinoma (iCCA) exhibits different blood imaging features and prognosis depending on histology. To clarity histopathological growth patterns (HGPs) and vascularization processes of iCCA, we collected 145 surgical specimens and histologically classified them into large bile duct (LBD) (20 cases), small bile duct (SBD) (54), cholangiolocarcinoma (CLC) (35), combined SBD-CLC (cSBD-CLC) (26), and ductal plate malformation (DPM) (10) (sub)types. According to the invasive pattern at the interface between tumor and adjacent background liver, HGPs were classified into desmoplastic, pushing, and replacing HGPs. Desmoplastic HGP predominated in LBD type (55.5%), while replacing HGP was common in CLC (82.9%) and cSBD-CLC (84.6%) subtypes. Desmoplastic HGP reflected angiogenesis, while replacing HGP showed vessel co-option in addition to angiogenesis. By evaluating microvessel density (MVD) using vascular markers, ELTD1 identified vessel co-option and angiogenesis, and ELTD1-positive MVD at invasive margin in replacing HGP was significantly higher than those in desmoplastic and pushing HGPs. REDD1, an angiogenesis-related marker, demonstrated preferably higher MVD in the tumor center than in other areas. iCCA (sub)types and HGPs were closely related to vessel co-option and immune-related factors (lymphatic vessels, lymphocytes, and neutrophils). In conclusion, HGPs and vascular mechanisms characterize iCCA (sub)types and vessel co-option linked to the immune microenvironment.

Lignin-derivable block copolymer micelle for effectively reinforcing and toughening polylactic acid.

The development of high-performance biodegradable polylactic acid (PLA) materials integrating high strength, malleability and toughness is desired but an ongoing challenge. In this work, a novel full-biobased block copolymer was designed and synthesized by grafting L (+)-lactide (L-LA) and ε-caprolactone (ε-CL) onto lignin via ring-opening polymerization. The obtained lignin-PLA-PCL block copolymer was composed of rigid lignin and poly (LA-CL) rubber segment, could self-assemble into uniform nano-micelles with average diameters of 80-100 nm regulated by simply altering copolymer content. The incorporation of lignin-PLA-PCL copolymers into PLA matrix induced the formation of many cavities, promoted free volume between PLA matrix and copolymer to accelerate chain mobility, achieving excellent ductility and stretchability with maximum stretching deformation of 64.8 %. The resultant PLA composites with the copolymer content as low as 5 wt% displayed simultaneously improved strength (41.84 MPa) and toughness (8.1 MJ/m3), 6.7 % and 1520 % increment than those of neat PLA, respectively. The reinforcing and toughening mechanisms were explored and verified that the combination of cavity growth and fibrillation, followed by extensive shear yielding of matrix, causing substantial plastic deformation. This study extended the design strategy and the foundation for simultaneous reinforcing and toughening PLA plastics using lignin-derived rubbery micelles.

Uncovering the role of free lanthanum (La3+) ions and La oligomer on the surface of La (oxy)hydroxide particles for phosphate removal.

La (oxy)hydroxide-based materials have been recognized as promising adsorbents for aqueous phosphate (P) removal. However, comprehending the adsorption behavior of P onto La (oxy)hydroxide particles remains challenging, given the heterogeneous low-crystalline surface encompassing La oligomers and free La3+ ions. In this study, a hydrogen (H) bond capping method was developed to construct La (oxy)hydroxide oligomers (LHOs) to simulate the low-crystalline La on the surface of La (oxy)hydroxide particles. The P uptake capacity was compared among free La3+ ions, LHOs, and La nanoparticle (La-NP) with maximum capacities of 1967.3 ± 30.8 mg/g, 461.1 ± 53.7 mg/g and 62.5 ± 6.0 mg/g, respectively. The FT-IR, Raman, in situ-XRD and XPS deconvolution analyses revealed that the removal of P by free La3+ ions mainly involve the process of chemical precipitation to form LaPO4·0.5H2O. Conversely, the elimination of P by LHOs is primarily attributed to inner-sphere complexation and hydroxyl exchange effect between LaOOH and P. Based on this study, the free La3+ ions and La oligomers on the surface of La (oxy)hydroxide particles play a primary role in P adsorption. These results also suggest that the successively decreased adsorption capacity of La (oxy)hydroxide-based adsorbents in the continuously adsorption/desorption cycles might be due to the irreversible inactivation and recrystallization of free La3+ ions and La oligomers on the surface.

Enhancing emotional expression in cat-like robots: strategies for utilizing tail movements with human-like gazes.

In recent years, there has been a significant growth in research on emotion expression in the field of human-robot interaction. In the process of human-robot interaction, the effect of the robot's emotional expression determines the user's experience and acceptance. Gaze is widely accepted as an important media to express emotions in human-human interaction. But it has been found that users have difficulty in effectively recognizing emotions such as happiness and anger expressed by animaloid robots that use eye contact individually. In addition, in real interaction, effective nonverbal expression includes not only eye contact but also physical expression. However, current animaloid social robots consider human-like eyes as the main emotion expression pathway, which results in a dysfunctional robot appearance and behavioral approach, affecting the quality of emotional expression. Based on retaining the effectiveness of eyes for emotional communication, we added a mechanical tail as a physical expression to enhance the robot's emotional expression in concert with the eyes. The results show that the collaboration between the mechanical tail and the bionic eye enhances emotional expression in all four emotions. Further more, we found that the mechanical tail can enhance the expression of specific emotions with different parameters. The above study is conducive to enhancing the robot's emotional expression ability in human-robot interaction and improving the user's interaction experience.

Primary hepatobiliary mucoepidermoid carcinoma: a case report and review of literature.

Hepatobiliary mucoepidermoid carcinoma is a rare malignant tumor comprising mucous, intermediate, and epidermoid cells. Herein, we presented a case of primary liver mucoepidermoid carcinoma preoperatively misdiagnosed as conventional intrahepatic cholangiocarcinoma. A 67-year-old male was admitted to our hospital. Preoperative laboratory tests showed increased aspartate transaminase, alanine transaminase, and carbohydrate antigen 19-9. Abdominal Computer Tomography revealed a 4.8 × 4.9 cm liver mass in segment VI. A preliminary diagnosis of intrahepatic cholangiocarcinoma was made, with undergoing partial hepatectomy. However, on histopathology, the tumor comprised a mixture of epidermoid, mucous, and intermediate cells with diffuse infiltrating at the tumor margin. On special stains, mucous and intermedia cells were positive for mucicarmine and Alcian blue, whereas epidermoid cells were positive for Keratin 5/6 and p63. Intermediate cells are also positive for p63. All tumor cells were positive for Keratin 7. The Ki-67 index was 35%. The final diagnosis was primary hepatic mucoepidermoid carcinoma. Although rare, hepatic mucoepidermoid carcinoma should be considered in the intrahepatic cholangiocarcinoma differential diagnosis. We reviewed previous studies and found that hepatobiliary mucoepidermoid carcinoma is more likely to originate from the biliary tract adjacent to the tumor.

Correction: Study on the temporal and spatial relationship between public health events and the development of air transport scale: A case of the Southwest China.

[This corrects the article DOI: 10.1371/journal.pone.0301461.].