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BACKGROUND: The aim of this study was to investigate the associations of blood phosphorus levels with the risk of developing medial arterial calcification (MAC) in lower-limb arteries and diabetic foot (DF) in diabetes patients. We sought to enhance the understanding of the pathophysiology of diabetic complications and develop strategies to mitigate diabetes-related risks. METHODS: We conducted a retrospective analysis of 701 diabetic patients from the Department of Endocrinology at Sun Yat-Sen Memorial Hospital (2019-2023). We utilized multimodel-adjusted logistic regression to investigate the associations of serum phosphorus levels and the risk of developing MAC and DF. Restricted cubic spline plots were employed to model the relationships, and threshold analysis was used to identify inflection points. Subgroup analyses were performed to explore variations across different demographics. The diagnostic utility of phosphorus concentrations was assessed via the C index, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). RESULTS: Of the 701 patients (mean age 63.9 years; 401 (57.20%) were male), 333 (47.50%) had MAC, and 329 (46.93%) had DF. After controlling for numerous confounding variables, each one-unit increase in phosphorus concentrations was associated with an increased risk of developing MAC (OR 2.65, 95% CI 1.97-3.57, p < 0.001) and DF (OR 1.54, 95% CI 1.09-2.18, p = 0.014). Phosphorus levels demonstrated a linear risk association, with risk not being uniform on either side of the inflection point, which was approximately 3.28 mg/dL for MAC and varied for DF (3.26 to 3.81 mg/dL). Adding the phosphorus as an independent component to the diagnostic model for MAC and DF increased the C index, NRI, and IDI to varying degrees. CONCLUSIONS: Elevated serum phosphorus levels are significantly associated with an increased risk of developing MAC and DF among diabetic people. These findings suggest that phosphorus management could be integrated into routine diagnostic processes to improve the identification and management of lower-extremity diabetic complications.
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Biomarcadores , Pé Diabético , Doença Arterial Periférica , Fósforo , Calcificação Vascular , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Feminino , Estudos Transversais , Fósforo/sangue , Calcificação Vascular/sangue , Calcificação Vascular/epidemiologia , Calcificação Vascular/diagnóstico por imagem , Calcificação Vascular/diagnóstico , Idoso , Fatores de Risco , Doença Arterial Periférica/diagnóstico , Doença Arterial Periférica/sangue , Doença Arterial Periférica/epidemiologia , Pé Diabético/diagnóstico , Pé Diabético/sangue , Pé Diabético/epidemiologia , Medição de Risco , Biomarcadores/sangue , Prognóstico , Extremidade Inferior/irrigação sanguíneaRESUMO
Dispersion management is vital for nonlinear optics and ultrafast lasers. We demonstrate that group velocity dispersion (GVD, or second-order dispersion, i.e., ß2) and group delay dispersion (GDD) in optical microfibers can be tuned simply by stretch due to their remarkable features of small diameter and diameter-dependent dispersion. We experimentally demonstrate that a pulling force of just a few mN would elongate the optical microfibers by up to 5%, bringing a significant change in the ß2 and GDD. This change can be increment or decrement, lying on the diameter of optical microfibers. Therefore, 10-cm-long optical microfibers would provide a GDD change of 104 fs2 when elongated by 5%, well in the elastic limit. Remarkably, this change is equivalent to the GDD (not GDD change) provided by a 0.5-m-long single-mode fiber. Experimental results and simulations show that the GDD change is due to the interplay between elongation, diameter shrink, and refractive index decrease. Benefited from the easy manipulation, tiny pulling force required, and full integration with conventional optical fibers, stretch tuning of dispersion in optical microfibers would find applications in dispersion management for ultrafast lasers and nonlinear optics.
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Considering the established pharmacokinetics and toxicity profiles, drug repurposing has emerged as an alternative therapeutic approach for treating cancer. Mefloquine has previously demonstrated inhibitory effects on multiple cancer types. This study aims to explore the impact of mefloquine on nasopharyngeal carcinoma (NPC). We found that mefloquine, at pharmacologically achievable concentrations, displayed anti-NPC activity while sparing normal counterparts. Mefloquine inhibits proliferation and induces death by reducing the levels of Cyclin A2, Bcl-2, and Bcl-xL. Intriguingly, we observed an increase in the levels of the anti-apoptotic protein Mcl-1. Mefloquine exerts its effects on NPC cells by inducing lysosomal-mediated ROS production, and the heightened expression of Mcl-1 is a consequence of ROS generation in mefloquine-treated NPC cells. The combination of an Mcl-1 inhibitor with mefloquine synergistically inhibits NPC growth in mice without causing substantial toxicity. These findings demonstrate the effectiveness and limited toxicity of mefloquine as a monotherapy and in combination with an Mcl-1 inhibitor. Our research underscores the promise of the mefloquine and Mcl-1 inhibitor combination as a potential treatment for NPC. Additionally, the elevation of Mcl-1 is a compensatory response in cells exposed to oxidative stress, offering a potential target to overcome resistance induced by pro-oxidant therapies.
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Proliferação de Células , Mefloquina , Proteína de Sequência 1 de Leucemia de Células Mieloides , Carcinoma Nasofaríngeo , Neoplasias Nasofaríngeas , Espécies Reativas de Oxigênio , Animais , Humanos , Camundongos , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Reposicionamento de Medicamentos , Sinergismo Farmacológico , Mefloquina/farmacologia , Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo , Proteína de Sequência 1 de Leucemia de Células Mieloides/antagonistas & inibidores , Carcinoma Nasofaríngeo/tratamento farmacológico , Carcinoma Nasofaríngeo/patologia , Neoplasias Nasofaríngeas/tratamento farmacológico , Neoplasias Nasofaríngeas/patologia , Espécies Reativas de Oxigênio/metabolismo , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
This study aimed to explore the regulatory effect of remifentanil-mediated mitochondrial autophagy on osteoclast formation and further investigate its mechanism. Macrophage cell line RAW264.7 was taken and induced to differentiate into mature osteoclasts using nuclear factor kB receptor activating factor ligand (RANKL). The cell model was treated with different concentrations of remifentanil or down-regulated expression of mitochondrial autophagy-related gene PINK1. The survival, death and ROS production of osteoclasts were detected by CCK8 kit and flow cytometry, MMP level was detected by JC-1 method, mitochondrial morphology and autophagy were observed by transmission electron microscopy, and mitochondrial autophagy-related protein expression was detected by Western blot. The number of osteoclasts in the remifentanil-treated group was significantly reduced compared to the control group, accompanied by a reduction in reactive oxygen species (ROS) and mitochondrial membrane potential levels (MMP). Further results showed that remifentanil could significantly up-regulate the activity of PINK1/Parkin pathway, promote the occurrence of mitochondrial autophagy, and damaged mitochondria, and inhibit the formation of osteoclasts. Remifentanil successfully inhibited osteoclast formation by regulating mitochondrial autophagy mediated by PINK1/Parkin pathway. The results of this study revealed that remifentanil plays an important role in the physiology and pathology of osteoclasts, which may provide new ideas and strategies for the clinical treatment of remifentanil in tibial fractures.
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Autofagia , Potencial da Membrana Mitocondrial , Mitocôndrias , Osteoclastos , Proteínas Quinases , Espécies Reativas de Oxigênio , Remifentanil , Ubiquitina-Proteína Ligases , Camundongos , Osteoclastos/efeitos dos fármacos , Osteoclastos/metabolismo , Animais , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Proteínas Quinases/metabolismo , Proteínas Quinases/genética , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Remifentanil/farmacologia , Ubiquitina-Proteína Ligases/metabolismo , Ubiquitina-Proteína Ligases/genética , Células RAW 264.7 , Autofagia/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Diferenciação Celular/efeitos dos fármacosRESUMO
BACKGROUND: In recent years, compression therapy has attracted gradually increasing clinical attention in lower extremity venous diseases. However, basic concepts and clear nomenclature, standard treatment methods, and consistent product standards for pressure equipment are lacking. Therefore, developing clinical guidelines for compression therapy is essential to improving the treatment of venous diseases. METHODS: Our panel generated strong (Grade I), moderate (Grade IIa and IIb), and weak (Grade III) recommendations based on high quality (Class A), moderate quality (Class B), and low quality (Class C) evidence, using the Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) approach and the European Society of Cardiology (ESC) grading system. RESULTS: The panels made 30 recommendations from current evidence, focusing on seven fields of lower extremity venous disease (venous thromboembolism, post-thrombotic syndrome, chronic venous insufficiency, varicose veins, hemangioma and vascular malformations, lymphedema, and venous ulcers) and 18 topics. CONCLUSIONS: Of the 30 recommendations made across the 18 topics, 7 were strong (Grade I) and 17 were based on high quality (Class A) evidence, highlighting the need for further research of the use of compression therapy for .
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OBJECTIVE: To evaluate the efficacy of a new mechanochemical ablation (MOCA) device versus endovenous laser ablation (EVLA) for primary great saphenous vein (GSV) reflux. MATERIALS AND METHODS: Prospectively analyze the demographics, treatment detail and outcomes data of 57 primary GSV reflux patients. Patients were randomly assigned to MOCA or EVLA group with random envelope method. Primary endpoint was 6-month closure rate of GSV. Secondary endpoint including technical success rate, the venous clinical severity score (VCSS), chronic venous insufficiency questionnaire (CIVIQ-20) score and visual analogue scale (VAS) for pain. RESULTS: The procedures were well tolerated according to the VAS score. The 6-month closure rate was 85.71% in MOCA and 96.55% in EVLA group (p = .194). Significant changes were observed in regard of VCSS and CIVIQ-20 score at 6-month follow-up. Skin paresthesia occurred in 0 in MOCA and 5 in EVLA group. CONCLUSION: The new MOCA device is safe and effective in treating primary great saphenous vein reflux. The 6-month closure rate is non-inferior compared with EVLA. However, the long-term results need further follow-up.
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The adverse impacts of chronic hypoxia on maternal and infant health at high altitudes warrant significant attention. However, effective protective measures against the resultant growth restrictions and neurodevelopmental disorders in infants and young children are still lacking. This study investigated the neurodevelopment of mice offspring under hypoxic conditions by exposing pregnant mice to a hypobaric oxygen chamber that simulated the hypobaric hypoxia at an altitude of 4000â¯m until 28 days after delivery. Our findings suggested that prolonged exposure to hypoxia might result in emotional abnormalities and social disorders in offspring. The significant reduction in astrogliogenesis was a characteristic feature associated with neurodevelopmental disorders induced by hypoxia. Further studies demonstrated that cold-induced RNA-binding protein (CIRBP) was a key transcriptional regulator in astrogliogenesis, which downregulated astrocytic differentiation under hypoxia through its crosstalk with the NFIA. Our study emphasized the crucial role of CIRBP in regulating astrogliogenesis and highlighted its potential as a promising target for therapeutic interventions in neurodevelopmental disorders associated with hypoxia.
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Astrócitos , Regulação para Baixo , Hipóxia , Proteínas de Ligação a RNA , Animais , Proteínas de Ligação a RNA/genética , Proteínas de Ligação a RNA/metabolismo , Camundongos , Feminino , Gravidez , Diferenciação Celular , Altitude , Transtornos do Neurodesenvolvimento , Camundongos Endogâmicos C57BL , Masculino , Fatores de Transcrição NFIRESUMO
The deleterious impact of lead (Pb) pollution on human health is evident in both domestic and occupational settings, provoking an inflammatory response across multiple tissue, limited attention has been devoted to its adverse effects on colitis and the underlying mechanisms. Peiminine (PMI) has been recognized for its anti-inflammatory properties, yet its specific anti-inflammatory effects in lead-induced colitis models remain elusive. Through the establishment of both in vivo and in vitro lead exposure models, suggests that lead exposure can induce colitis and that PMI regulates lead exposure-induced colitis by inhibiting the NF-kB signaling pathway, and alleviates the ability of lead to apoptosis and inflammation levels in intestinal epithelial cells. Consequently, these results present a promising avenue for further exploration of the molecular mechanisms underlying lead-induced colitis, evaluation of the associated risks linked to lead exposure, and the development of therapeutic interventions for colitis resulting from lead exposure.
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The role of PARKIN in Parkinson's disease is well established but its role in cancer has recently emerged. PARKIN serves as a tumor suppressor in many cancers and loses the tumor-suppressive function due to loss of heterozygosity and DNA copy number. But how PARKIN protects against cancer is poorly understood. Through the analysis of PARKIN substrates and their association with mitochondria, this viewpoint discussed that PARKIN exerts its anti-cancer activity through targeting mitochondria. Mitochondria function as a convergence point for many signaling pathways and biological processes, including apoptosis, cell cycle, mitophagy, energy metabolism, oxidative stress, calcium homeostasis, inflammation, and so forth. PARKIN participates in these processes through regulating its mitochondrial targets. Conversely, these mitochondrial substrates also influence the function of PARKIN under different cellular circumstances. We believe that future studies in this area may lead to novel therapeutic targets and strategies for cancer therapy.
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Neoplasias , Doença de Parkinson , Humanos , Mitocôndrias/metabolismo , Neoplasias/patologia , Proteínas Quinases/genética , Proteínas Quinases/metabolismo , Transdução de Sinais , Ubiquitina-Proteína Ligases/metabolismoRESUMO
BACKGROUND: Sunflower is an important ornamental plant, which can be used for fresh cut flowers and potted plants. Plant architecture regulation is an important agronomic operation in its cultivation and production. As an important aspect of plant architecture formation, shoot branching has become an important research direction of sunflower. RESULTS: TEOSINTE-BRANCHED1/CYCLOIDEA/PCF (TCP) transcription factors are essential in regulating various development process. However, the role of TCPs in sunflowers has not yet been studied. This study, 34 HaTCP genes were identified and classified into three subfamilies based on the conservative domain and phylogenetic analysis. Most of the HaTCPs in the same subfamily displayed similar gene and motif structures. Promoter sequence analysis has demonstrated the presence of multiple stress and hormone-related cis-elements in the HaTCP family. Expression patterns of HaTCPs revealed several HaTCP genes expressed highest in buds and could respond to decapitation. Subcellular localization analysis showed that HaTCP1 was located in the nucleus. Paclobutrazol (PAC) and 1-naphthylphthalamic acid (NPA) administration significantly delayed the formation of axillary buds after decapitation, and this suppression was partially accomplished by enhancing the expression of HaTCP1. Furthermore, HaTCP1 overexpressed in Arabidopsis caused a significant decrease in branch number, indicating that HaTCP1 played a key role in negatively regulating sunflower branching. CONCLUSIONS: This study not only provided the systematic analysis for the HaTCP members, including classification, conserved domain and gene structure, expansion pattern of different tissues or after decapitation. But also studied the expression, subcellular localization and function of HaTCP1. These findings could lay a critical foundation for further exploring the functions of HaTCPs.
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Arabidopsis , Decapitação , Helianthus , Fatores de Transcrição/metabolismo , Helianthus/genética , Helianthus/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Filogenia , Regulação da Expressão Gênica de Plantas , Arabidopsis/metabolismoRESUMO
Van der Waals heterojunction (vdWs) of 2D materials with integrated or extended superior characteristics, opening up new opportunities in functional electronic and optoelectric device applications. Exploring methods to achieve multifunctional vdWs heterojunction devices is one of the most promising prospects in this area. Herein, a diverse function of forward rectifying diode, Zener tunneling diode, and backward rectifying diodes are realized in GeAs/ReS2 heterojunction by modulating the doping level of GeAs. The tunneling diode presents an interesting trend forward negative differential resistance (NDR) behavior which may facilitate the application of multi-value logic. More importantly, the GeAs/ReS2 forward rectifying diode exhibits highly sensitive photodetection in the wide-spectrum range up to 1550 nm corresponding to a short-wave infrared (SWIR) region. In addition, as two strong anisotropic 2D materials of GeAs and ReS2 , the heterojunction exhibits strong polarization-sensitive photodetection behavior with a dichroic photocurrent ratio of 1.7. This work provides an effective strategy to achieve multifunctional 2D vdW heterojunction devices and develops more possibilities to broaden their functionalities and applications.
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Preferentially expressed antigen in melanoma (PRAME) is a cancer/testis antigen (CTA) that is predominantly expressed in normal male gonad tissues and a variety of tumors. PRAME proteins are present in the acrosome and sperm tail, but their role in sperm function is unknown. The objective of this study was to examine the function of the bovine Y-linked PRAME (PRAMEY) during spermatozoal capacitation, the acrosome reaction (AR), and fertilization. Freshly ejaculated spermatozoa were induced to capacitate and undergo AR in vitro. Western blotting results revealed a decrease in the PRAMEY protein in capacitated spermatozoa, and the release of the PRAMEY protein from the acrosome during the AR, suggesting its involvement in sperm capacitation and AR. IVF was performed using in vitro matured bovine oocytes and cauda epididymal spermatozoa either treated with PRAMEY antibody, rabbit IgG, or DPBS. Sperm-egg binding and early embryos were examined at 6 and 45 h post IVF, respectively. The number of spermatozoa that bound per oocyte was nearly two-fold greater in the PRAMEY antibody treatment group (34.4) when compared to both the rabbit IgG (17.6) and DPBS (18.1) controls (P < 0.01). Polyspermy rate in the antibody-treated group (18.9%) was three-fold greater than the rabbit IgG control (6.0%) (P < 0.01). The results indicate that PRAMEY may play a role in anti-polyspermy defense. This study thus provides the initial evidence for the involvement of the PRAME protein family in sperm function and fertilization.
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Sêmen , Espermatozoides , Coelhos , Masculino , Animais , Bovinos , Espermatozoides/metabolismo , Fertilização in vitro , Acrossomo , Capacitação Espermática , Imunoglobulina G , FertilizaçãoRESUMO
Acetylcholine (ACh) is found not only in cholinergic nerve termini but also in the nonneuronal cholinergic system (NNCS). ACh is released from cholinergic nerves by vesicular ACh transporter (VAChT), but ACh release from the NNCS is mediated by organic cation transporter (OCT). Recent studies have suggested that components of the NNCS are located in intestinal epithelial cells (IECs), crypt-villus organoids, immune cells, intestinal stem cells (ISCs), and vascular endothelial cells (VECs). When ACh enters the interstitial space, its self-modulation or effects on adjacent tissues are part of the range of its biological functions. This review focuses on the current understanding of the mechanisms of ACh synthesis and release in the NNCS. Furthermore, studies on ACh functions in colonic disorders suggest that ACh from the NNCS contributes to immune regulation, IEC and VEC repair, ISC differentiation, colonic movement, and colonic tumor development. As indicated by the features of some colonic disorders, ACh and the NNCS have positive and negative effects on these disorders. Furthermore, the NNCS is located in multiple colonic organs, and the specific effects and cross-talk involving ACh from the NNCS in different colonic tissues are explored.
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Colina/metabolismo , Doenças do Colo/metabolismo , Mucosa Intestinal/metabolismo , Animais , Humanos , Proteínas de Membrana Transportadoras/genética , Proteínas de Membrana Transportadoras/metabolismo , Receptores Colinérgicos/genética , Receptores Colinérgicos/metabolismoRESUMO
Neurotoxicity caused by environmental lead (Pb) pollution is a worldwide public health concern, and developing a therapeutic strategy against Pb-induced neurotoxicity is an important area in the current research. Our prior research has demonstrated the significant involvement of microglia-mediated inflammatory responses in the manifestation of Pb-induced neurotoxicity. Additionally, the suppression of proinflammatory mediator activity significantly mitigated the toxic effects associated with Pb exposure. Recent studies have highlighted the critical role of the triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of neurodegenerative disorders. TREM2 exerted protective effects on inflammation, but whether TREM2 is involved in Pb-induced neuroinflammation is poorly understood. In the present study, cell culture experiments and animal models were designed to investigate the role of TREM2 in Pb's neuroinflammation. We examined the impact of pro- and anti-inflammatory cytokines involved in Pb-induced neuroinflammation. Flow cytometry and microscopy techniques were applied to detect microglia phagocytosis and migration ability. Our results showed that Pb treatment significantly downregulated TREM2 expression and altered the localization of TREM2 expression in microglia. The protein expression of TREM2 was restored, and the inflammatory responses provoked by Pb exposure were ameliorated upon the overexpression of TREM2. Furthermore, the phagocytosis and migratory capabilities of microglia, which were impaired due to Pb exposure, were alleviated by TREM2 overexpression. Our in vitro findings were corroborated in vivo, demonstrating that TREM2 regulates the anti-inflammatory functions of microglia, thereby mitigating Pb-induced neuroinflammation. Our results provide insights into the detailed mechanism by which TREM2 alleviates Pb-induced neuroinflammation and suggest that activating the anti-inflammatory functions of TREM2 may represent a potential therapeutic strategy against environmental Pb-induced neurotoxicity.
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Chumbo , Doenças Neuroinflamatórias , Animais , Chumbo/metabolismo , Microglia , Inflamação/metabolismo , Anti-Inflamatórios/farmacologiaRESUMO
As increasing number of people migrated to high altitude, highland encephalopathy and hypoxia-induced cognitive impairment arouse public attention. Yet, its underlying mechanisms remain unclear. Emerging evidence has implied neuroinflammation and neuronal loss may be involved. In the present study, we investigated the neuroinflammation and neuronal loss in mice after hypoxic insult. Our reports showed hypobaric hypoxia exposure for 3 weeks led to impaired spatial exploration and short-term memory in mice, concomitant with neuron loss. In addition, hypoxia induced neuroinflammation and NLRP3 inflammasome activation. Besides, to explore the role of the inflammasome in hypoxia-induced cognitive dysfunction, NLRP3 knockout mice were applied and the results showed that NLRP3 could negatively regulate GPX4 to modify antioxidant capacity. In summary, our work demonstrated that hypoxia exposure led to neuroinflammation and neuronal-deletion, which may be the key events in the process of hypoxia induced cognitive impairment. NLRP3 inflammasome promoted antioxidant deficiency by negatively regulating GPX4.
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Disfunção Cognitiva , Inflamassomos , Camundongos , Animais , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Doenças Neuroinflamatórias , Antioxidantes , Camundongos Knockout , Disfunção Cognitiva/etiologia , HipóxiaRESUMO
BACKGROUND: Lead contamination is a major public health concern. Previous studies have demonstrated that lead exposure could affect the hippocampus, which is a complex and heterogeneous structure composed of 12 subregions. Here, we explored volumetric and functional changes in hippocampal subfields and neuropsychological alterations after lead exposure. METHODS: We performed a cross-sectional study at a smelting company between September 2020 and December 2021. Blood lead level was recorded, and neuropsychological functions were assessed by Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), Self-rating Anxiety Scale (SAS), and Self-rating Depression Scale (SDS). The hippocampus was segmented into 12 subfields in each hemisphere in magnetic resonance images (MRIs). Then, the effect of altered hippocampal subfield volumes on brain functions were studied by seed-based functional connectivity (FC) analysis. Finally, the relationships between the lead level with hippocampal subfield volumes and neuropsychological functions were investigated. Baseline characteristics, hippocampal subfield volumes, and FC analysis were compared between lead-exposed (≥ 300 µg/L) and the control group (≤ 100 µg/L). RESULTS: In 76 participants, lead level positively correlated with SDS(r = 0.422) and negatively correlated with MoCA(r = -0.414), MMSE(r = -0.251), Concentration(r = -0.331), Recall(r = -0.319), Orientation(r = -0.298) and Executive Function/Visuospatial abilities(r = -0.231). Lead group (26 participants) had lower MoCA and MMSE and higher SDS than control group (23 participants). A significantly decreased volume in the left CA4 and GC-ML-DG subfields was found in the lead group compared with the control group. The left GC-ML-DG of the lead group showed a decreased FC with the bilateral postcentral gyrus. The left CA4(r = -0.409) and left GC-ML-DG (r = -0.383) volumes negatively correlated with lead level. The FC between left GC-ML-DG and left postcentral gyrus positively correlated with MoCA(r = 0.318), MMSE(r = 0.379) and Recall(r = 0.311). The FC between left GC-ML-DG and right postcentral gyrus positively correlated with MoCA(r = 0.326), Executive Function/Visuospatial abilities(r = 0.307) and Concentration(r = 0.297). CONCLUSION: High blood lead level was associated with neuropsychological alterations, hippocampal structural and functional changes. The left GC-ML-DG and CA4 atrophy might serve as predictive imaging markers for neurological damage associated with high lead exposure.
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Chumbo , Doenças Neurodegenerativas , Humanos , Chumbo/toxicidade , Estudos Transversais , Hipocampo/patologia , Imageamento por Ressonância Magnética/métodos , Doenças Neurodegenerativas/patologia , Atrofia/patologiaRESUMO
OBJECTIVES: To construct a valid and reliable Nutritional Literacy Scale for patients with end-stage kidney disease (ESKD) receiving dialysis and evaluate associations between nutrition literacy and quality of life. METHODS: A total of 208 ESKD patients receiving dialysis were selected for this study. Nutrition literacy evaluation items were drafted based on dietary guidelines for chronic kidney disease (CKD), Literature reviews and expert consultation. Scale reliability and validity were then assessed. Factors influencing nutrition literacy and the associations among nutrition literacy, nutritional status, and quality of life were evaluated. RESULTS: The scale consists of 28 items with a scale-level content validity index of 0.91 and item-level content validity indices ranging from 0.83 to 1.00. Factor analysis identified 4 common factors (dimensions) named nutrition knowledge, cognitive attitude, behavioral practice, and information acquisition ability that collectively explained 56.31% of literacy score variation. The overall Cronbach's α coefficient of the scale was 0.83, the dimensional Cronbach's α coefficients ranged from 0.79 to 0.87, and the retest reliability was r = 0.73 (p < 0.05). Age, education level, residence (urban vs. Rural) , occupational status and dialysis modalities were significant factors influencing nutrition literacy. Nutrition literacy score was negatively correlated with SGA score and positively correlated with serum albumin and prealbumin concen- trations, and with SF-36 quality of life score (all p < 0.05). CONCLUSIONS: This new Nutrition Literacy Scale demonstrates high reliability and validity for Chinese ESKD patients undergoing dialysis. The nutrition literacy is influenced by age, education level, residence, occupational status and dialysis modalities, associated not only with nutritional status but also with quality of life.
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Dieta Saudável , Falência Renal Crônica , Avaliação Nutricional , Estado Nutricional , Diálise Renal , Humanos , Falência Renal Crônica/terapia , Qualidade de Vida , Reprodutibilidade dos Testes , Inquéritos e QuestionáriosRESUMO
Generally, solvents used to synthesize perovskite NCs are toxic, which leads to waste liquid pollution and environmental degradation. Herein, we developed a novel environmentally friendly polar solvent method to synthesize CsPbBr3 nanocrystals (NCs). Over 65% photoluminescence quantum yield (PLQYs) for NCs could be maintained over 45-850 h of storage time, and a maximum was 78% at 750 h. Such amazing stability in polar solvents is dominated by a ripening process, which heals surface defects. Additionally, their solid films also exhibited good moisture stability. Furthermore, CsPbBr3 NCs were applied to inkjet-printing to prepare high-quality patterned films.
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Two coordination polymers (CPs), namely, [Mn3(L)2(4,4'-bipy)2(H2O)2]n (1) and [Ni(L1)(1,4-bib)(H2O)]n (2) (H3L = 5-(3-bromo-4-carboxyphenoxy)isophthalic acid, H2L1 = 5-(3-hydroxyphenoxy)isophthalic acid, 4,4'-bpy = 4,4'-bipyridine, and 1,4-bib = 1,4-bis(1H-imidazol-1-yl)benzene), were synthesized under hydrothermal conditions. Most notably, with the help of the bromine atom-inducing effect, ligand transformation was observed in the structure of complex 2, which was scrutinized thoroughly by single crystal X-ray crystallography and X-ray photoelectron spectroscopy (XPS). Strikingly, Ni(II) ions were utilized as both coordinated atoms and as a catalyst for in situ Br-OH exchange of H3L in the process, as a result of which the product would have preferred to form a one-dimensional chain. The same reaction cannot happen in 1, leading to form a two-dimensional structure. Moreover, Ni(II)-catalyzed and magnetic exchange mechanisms were well interpreted using density functional theory (DFT) calculations. Finally, complexes 1-2 show three-dimensional (3D) supramolecular structures because of intermolecular weak interactions (C-Br···π, C-H···π, C-H···O, and π···π stacking) and exhibit utterly different antiferrimagnetic coupling interactions.
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Ácidos Ftálicos , Modelos Moleculares , Teoria da Densidade Funcional , Fenômenos MagnéticosRESUMO
Langdu, known as a traditional Chinese medicine, was identified as the roots of species of Euphorbia ebracteolata Hayata and Euphorbia fischeriana Steud, displaying anti-tuberculosis activity. To clarify the potent quality markers of Langdu, this research first developed a fast and sensitive ultrahigh-performance liquid chromatography-tandem mass spectrometry method for the quantification of 13 diterpenoids in Langdu. The developed method was further applied in the analyses of 12 authentic E. ebracteolata and E. fischeriana samples collected in northern and southeastern China. Then, the anti-tuberculosis evaluation of 12 batches of Langdu samples was performed in vitro. Finally, partial least squares discrimination analysis was used in the discrimination of E. ebracteolata and E. fischeriana from different origins and processing methods. Jolkinolide A (1), jolkinolide E (3), yuexiandajisu D (6), and ebractenone A (11) were identified as key, potent diterpenoids for the quality control of E. ebracteolata Hayata and E. fischeriana Steud. The present study established a qualitative chemical analysis method for Langdu (E. ebracteolata and E. fischeriana) and suggested the key bioactive components that will improve qualitative control methodology for this important medicine.