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Coastal wetlands are important blue carbon ecosystems that play a significant role in the global carbon cycle. However, there is insufficient understanding of the variations in soil organic carbon (SOC) stocks and the mechanisms driving these ecosystems. Here we analyze a comprehensive multi-source dataset of SOC in topsoil (0-20 cm) and subsoil (20-100 cm) across 31 coastal wetlands in China to identify the factors influencing their distribution. Structural equation models (SEMs) reveal that hydrology has the greatest overall effect on SOC in both soil layers, followed by vegetation, soil properties, and climate. Notably, the mechanisms driving SOC density differ between the two layers. In topsoil, vegetation type and productivity directly impact carbon density as primary sources of carbon input, while hydrology, primarily through seawater salinity, exerts the largest indirect influence. Conversely, in subsoil, hydrology has the strongest direct effect on SOC, with seawater salinity also influencing SOC indirectly through soil and vegetation mediation. Soil properties, particularly pH, negatively affect carbon accumulation, while climate influences SOC indirectly via its effects on vegetation and soil, with a diminishing impact at greater depths. Using Random Forest, we generate high-resolution maps (90 m × 90 m) of topsoil and subsoil carbon density (R 2 of 0.53 and 0.62, respectively), providing the most detailed spatial distribution of SOC in Chinese coastal wetlands to date. Based on these maps, we estimate that SOC storage to a depth of 1 m in Chinese coastal wetlands totals 74.58 ± 3.85 Tg C, with subsoil carbon storage being 2.5 times greater than that in topsoil. These findings provide important insights into mechanism on driving spatial pattern of blue carbon and effective ways to assess carbon status on a national scale, thus contributing to the advancement of global blue carbon monitoring and management.
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Background: This study investigated the midterm primary patency of drug-coated balloons (DCBs), directional atherectomy plus balloon angioplasty (DA), and bare metal stent (BMS) angioplasty for the treatment of femoropopliteal lesions. Methods: This two-center retrospective cohort study included 105 patients (110 limbs) undergoing DCB, DA, and BMS angioplasty-32 patients (34 limbs), 31 patients (32 limbs), and 42 patients (44 limbs), respectively. The demographic, baseline, and procedure data were collected, and the complications and midterm outcomes (patency, amputation-free survival, and clinically driven target lesion revascularization rates) were analyzed. Results: All three procedures achieved a 100% success rate. Significant improvements were noted in ankle brachial index, walking distance, and Rutherford classification at 30 days post-procedure (p < 0.001), with no differences or severe complications among the groups. The all-cause mortality rate during the follow-up period, was 5.5%, and amputation-free survival rates at 24 months were 97.0%, 90.6% and 90.9% in the DCB, DA, and BMS angioplasty groups, respectively. The primary patency rate for the DCB group (79.4%) exceeded those of the DA (56.2%) and BMS (52.2%) groups (p < 0.05), with no significant difference between the DA and BMS groups at 24 months. The secondary patency and clinically driven target lesion revascularization rates were similar among the three groups. A runoff number ≤1, Trans-Atlantic Intersociety Consensus (TASC) D, and severe calcification were found to be independent risk factors for primary patency. Conclusions: The DCB procedure demonstrated superior primary patency, compared to both BMS and DA procedures, in the treatment of femoropopliteal lesions.
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Background: Chemotherapy (CT) remains the primary treatment for locally advanced unresectable pancreatic cancer (LAUPC) and metastatic pancreatic cancer (MPC). The role of radiotherapy (RT) in these conditions remains unclear. This study compares the outcomes of CT alone versus CT combined with RT (combined-modality therapy [CMT]) in LAUPC and MPC patients. Materials and methods: We conducted a retrospective analysis of LAUPC and MPC patients treated with either CT or CMT from a single institution and Surveillance, Epidemiology, and End Results (SEER) database. Kaplan-Meier curves and Cox hazards models evaluated the association between treatment modalities and overall survival (OS). Propensity score matching (PSM) ensured balanced comparisons. Landmark analysis addressed immortal time bias. Subgroup analyses were based on clinical characteristics. eXtreme Gradient Boosting (XGBoost) and Shapley Additive Explanations (SHAP) assessed outcome prediction and influence of significant predictors. Results: The study included 102 patients receiving CMT and 155 receiving CT at single institution, along with 1733 CMT and 9310 CT patients from the SEER dataset. In the single-institution cohort, CMT showed superior survival compared to CT both before (median OS: 20.5 vs. 11.5 months, hazard ratio [HR]: 0.47, 95% CI: 0.34-0.65, P=0.001) and after PSM (median OS: 22.2 vs. 11.8 months, HR: 0.49, 95% CI: 0.30-0.79, P=0.003). Multivariate analyses confirmed that CMT was independently associated with improved OS both before (HR: 0.54, 95% CI: 0.38-0.77, P=0.001) and after PSM (HR: 0.45, 95% CI: 0.27-0.73, P=0.001). Landmark analysis indicated better OS for patients receiving CMT compared to CT alone. Subgroup analysis revealed an OS benefit for CMT across most subgroups. SHAP value analysis indicated that CMT was the most significant contributor to survival outcomes. SEER database validation confirmed these findings. Conclusions: This study demonstrates that CMT significantly improves OS in LAUPC and MPC patients compared to CT alone. Integrating RT with CT could be beneficial for treating LAUPC and MPC.
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With continuous advancements in interventional radiology, considerable progress has been made in transarterial therapies for hepatocellular carcinoma (HCC) in recent years, and an increasing number of research papers on transarterial therapies for HCC have been published. In this editorial, we comment on the article by Ma et al published in the recent issue of the World Journal of Gastro intestinal Oncology: "Efficacy and predictive factors of transarterial chemoembolization combined with lenvatinib plus programmed cell death protein-1 inhibition for unresectable HCC". We focus specifically on the current research status and future directions of transarterial therapies. In the future, more studies are needed to determine the optimal transarterial local treatment for HCC. With the emergence of checkpoint immunotherapy modalities, it is expected that the results of trials of transarterial local therapy combined with systemic therapy will bring new hope to HCC patients.
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BACKGROUND: Bladder neuroendocrine tumors are few and exhibit a high degree of aggressiveness. The bladder is characterized by four distinct forms of neuroendocrine tumors. Among them, large-cell neuroendocrine carcinoma is the least prevalent, but has the highest level of aggressiveness. The 5-year survival rate for large-cell neuroendocrine carcinoma of the bladder is exceedingly poor. To date, only a few dozen cases have been reported. CASE SUMMARY: Here, we report the case of a 65-year-old man with large-cell neuroendocrine carcinoma of the bladder. The patient presented to the Department of Urology at our hospital due to the presence of painless hematuria without any identifiable etiology. During hospitalization, abdominal computed tomography revealed the presence of an irregular mass on the right anterior wall of the bladder. A cystoscopic non-radical resection of the bladder lesion was performed. The postoperative pathological examination revealed large-cell neuroendocrine bladder cancer. Previous reports on cases of large-cell neuroendocrine carcinoma cases were retrieved from PubMed, and the present paper discusses the currently recognized best diagnostic and treatment options for large-cell neuroendocrine carcinoma based on the latest research progress. CONCLUSION: Large-cell neuroendocrine carcinoma of the bladder is an uncommon malignancy with a highly unfavorable prognosis. Despite ongoing efforts to prolong patient survival through multidisciplinary therapy, the prognosis remains unfavorable. Large-cell neuroendocrine carcinoma continues to be a subject of uncertainty.
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Ground-level ozone (O3) has been shown to induce airway inflammation, the underlying mechanisms remain unclear. The aim of this study was to determine whether gut and airway microbiota dysbiosis, and airway metabolic alterations were associated with O3-induced airway inflammation. Thirty-six 8-week-old male C57BL/6â¯N mice were divided into 2 groups: sterile water group and broad-spectrum antibiotics group (Abx). Each group was further divided into two subgroups, filtered air group (Air) and O3 group (O3), with 9 mice in each subgroup. Mice in the Air and O3 groups were exposed to filtered air or 1â¯ppm O3, 4â¯h/d for 5 consecutive days, respectively. Mice in Abxâ¯+â¯Air and Abxâ¯+â¯O3 groups were exposed to filtered air or O3, respectively, after drinking broad-spectrum Abx. 24â¯h after the final O3 exposure, mouse feces and bronchoalveolar lavage fluids (BALF) were collected and subjected to measurements of airway oxidative stress and inflammation biomarkers, 16S rRNA sequencing and metabolite profiling. Hematoxylin-eosin staining of lung tissues was applied to examine the pathological changes of lung tissue. The results showed that O3 exposure resulted in airway oxidative stress and inflammation, as well as gut and airway microbiota dysbiosis, and airway metabolism alteration. Abx pre-treatment markedly changed gut and airway microbiota and promoted O3-induced metabolic disorder and airway inflammation. Spearman correlation analyses indicated that inter-related gut and airway microbiota dysbiosis and airway metabolic disorder were associated with O3-induced airway inflammation. Together, inhaled O3 causes airway inflammation, which may implicate gut and airway microbiota dysbiosis and airway metabolic alterations.
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Small-cell lung cancer (SCLC) transformation accounts for 3-14% of resistance in EGFR-TKI relapsed lung adenocarcinomas (LUADs), with unknown molecular mechanisms and optimal treatment strategies. We performed transcriptomic analyses (including bulk and spatial transcriptomics) and multiplex immunofluorescence on pre-treated samples from LUADs without transformation after EGFR-TKI treatment (LUAD-NT), primary SCLCs (SCLC-P) and LUADs with transformation after EGFR-TKI treatment (before transformation: LUAD-BT; after transformation: SCLC-AT). Our study found that LUAD-BT exhibited potential transcriptomic characteristics for transformation compared with LUAD-NT. We identified several pathways that shifted during transformation, and the transformation might be promoted by epigenetic alterations (such as HDAC10, HDAC1, DNMT3A) within the tumor cells instead of within the tumor microenvironment. For druggable pathways, transformed-SCLC were proved to be less dependent on EGF signaling but more relied on FGF signaling, while VEGF-VEGFR pathway remained active, indicating potential treatments after transformation. We also found transformed-SCLC showed an immuno-exhausted status which was associated with the duration of EGFR-TKI before transformation. Besides, SCLC-AT exhibited distinct molecular subtypes from SCLC-P. Moreover, we constructed an ideal 4-marker model based on transcriptomic and IHC data to predict SCLC transformation, which obtained a sensitivity of 100% and 87.5%, a specificity of 95.7% and 100% in the training and test cohorts, respectively. We provided insights into the molecular mechanisms of SCLC transformation and the differences between SCLC-AT and SCLC-P, which might shed light on prevention strategies and subsequent therapeutic strategies for SCLC transformation in the future.
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Adenocarcinoma de Pulmão , Transformação Celular Neoplásica , Receptores ErbB , Neoplasias Pulmonares , Humanos , Receptores ErbB/genética , Receptores ErbB/metabolismo , Adenocarcinoma de Pulmão/genética , Adenocarcinoma de Pulmão/patologia , Adenocarcinoma de Pulmão/tratamento farmacológico , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Neoplasias Pulmonares/tratamento farmacológico , Transformação Celular Neoplásica/genética , Carcinoma de Pequenas Células do Pulmão/genética , Carcinoma de Pequenas Células do Pulmão/patologia , Carcinoma de Pequenas Células do Pulmão/tratamento farmacológico , Mutação , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/genética , Feminino , Masculino , Inibidores de Proteínas Quinases/farmacologiaRESUMO
Traumatic main bronchus rupture is a relatively rare injury in thoracic trauma, which is extremely critical, with a mortality rate as high as 70% - 80%. The complete rupture and displacement of the traumatic cervical trachea can lead to asphyxia, hypoxia, and cardiac arrest, even death of the patient in a short time. We performed emergency surgery with the support of extracorporeal membrane oxygenation for a case of traumatic cervical tracheal trunk complete rupture and displacement combined with cardiac arrest and achieved a successful rescue. We summarized our experience and found that timely surgical reconstruction of the airway is the key to increasing the traumatic main bronchus rupture survival of patients.
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Cytidine base editors (CBEs) hold significant potential in genetic disease treatment and in breeding superior traits into animals. However, their large protein sizes limit their delivery by adeno-associated virus (AAV), given its packing capacity of <4.7 kb. To overcome this, we employed a web-based fast generic discovery (WFG) strategy, identifying several small ssDNA deaminases (Sdds) and constructing multiple Sdd-CBE 1.0 versions. SflSdd-CBE 1.0 demonstrated high C-to-T editing efficiency, comparable to AncBE4max, while SviSdd-CBE 1.0 exhibited moderate C-to-T editing efficiency with a narrow editing window (C3 to C5). Utilizing AlphaFold2, we devised a one-step miniaturization strategy, reducing the size of Sdds while preserving their efficiency. Notably, we administered AAV8 expressing PCSK9 targeted sgRNA and SflSdd-CBEs (nSaCas9) 2.0 into mice, leading to gene-editing events (with editing efficiency up to 15%) and reduced serum cholesterol levels, underscoring the potential of Sdds in gene therapy. These findings offer new single-stranded editing tools for the treatment of rare genetic diseases.
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BACKGROUND: Breast tumorigenesis is a complex and multistep process accompanied by both genetic and epigenetic dysregulation. In contrast to the extensive studies on DNA epigenetic modifications 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC) in malignant breast tumors, their roles in the early phases of breast tumorigenesis remain ambiguous. RESULTS: DNA 5hmC and 5mC exhibited a consistent and significant decrease from usual ductal hyperplasia to atypical ductal hyperplasia and subsequently to ductal carcinoma in situ (DCIS). However, 5hmC showed a modest increase in invasive ductal breast cancer compared to DCIS. Genomic analyses showed that the changes in 5hmC and 5mC levels occurred around the transcription start sites (TSSs), and the modification levels were strongly correlated with gene expression levels. Meanwhile, it was found that differentially hydroxymethylated regions (DhMRs) and differentially methylated regions (DMRs) were overlapped in the early phases and accompanied by the enrichment of active histone marks. In addition, TET2-related DNA demethylation was found to be involved in breast tumorigenesis, and four transcription factor binding sites (TFs: ESR1, FOXA1, GATA3, FOS) were enriched in TET2-related DhMRs/DMRs. Intriguingly, we also identified a certain number of common DhMRs between tumor samples and cell-free DNA (cfDNA). CONCLUSIONS: Our study reveals that dynamic changes in DNA 5hmC and 5mC play a vital role in propelling breast tumorigenesis. Both TFs and active histone marks are involved in TET2-related DNA demethylation. Concurrent changes in 5hmC signals in primary breast tumors and cfDNA may play a promising role in breast cancer screening.
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5-Metilcitosina , Neoplasias da Mama , Proteínas de Ligação a DNA , Dioxigenases , Proteínas Proto-Oncogênicas , Humanos , 5-Metilcitosina/análogos & derivados , 5-Metilcitosina/metabolismo , Feminino , Neoplasias da Mama/genética , Proteínas de Ligação a DNA/genética , Dioxigenases/genética , Proteínas Proto-Oncogênicas/genética , Proteínas Proto-Oncogênicas/metabolismo , Carcinogênese/genética , Metilação de DNA/genética , Epigênese Genética/genética , Regulação Neoplásica da Expressão Gênica , Desmetilação do DNARESUMO
Background: Even with significant advancements, treating multiple myeloma (MM) remains difficult. At present, the main treatment methods include combined treatment of stem cell transplantation, drug treatment, etc. With the clarification of the molecular biological mechanism of MM, as well as the in-depth study of the internal signal of myeloma cells and the microenvironment of MM patients, more and more new drugs targeting myeloma and microenvironment are gradually used in clinical maintenance treatment, such as inhibit the proteosome: ixazomib, bortezomib and carfilzomib, immune - modulators: thalidomide and lenalidomide, monoclonal antibodies, etc. have made great progress in MM maintenance treatment. With the continuous development of proteasome inhibitor maintenance treatment in MM, the prognosis of the disease has been significantly improved. Our aim is to evaluate the effectiveness and adverse reactions of proteasome inhibitors in maintenance therapy for multiple myeloma, providing new ideas for clinical medication. Methods: Four databases containing randomized controlled studies on the effectiveness and safety of proteasome inhibitors in the maintenance therapy of multiple myeloma are retrieved by the computer. Once the quality of the literature has been thoroughly evaluated, run the data via the RevMan 5.3 software. Results: Eventually 8 studies were added in this systematic review. Compared with the placebo group, proteasome inhibitor in maintenance treatment of multiple myeloma patients with prolonged the survival without progression and overall existence. 5 studies reported the peripheral neuropathy of multiple myeloma in the treatment group compared to placebo group, which was remarkably greater (OR: 1.98; 95 % Cl: 1.35, 2.92; P < 0.001) compared to placebo group, Serious adverse events (OR: 1.60; 95 % Cl: 1.19, 2.14; P < 0.01), Rash (OR: 2.23; 95 % Cl: 1.62, 3.05; P < 0.001) and Vomiting (OR: 5.12; 95 % Cl: 3.36, 7.80; P < 0.001). The Serious adverse events of the treatment group were remarkably greater compared with the untreated group (OR: 1.60; 95 % Cl: 1.19, 2.14; P < 0.01). Conclusion: The study results proposed that proteasome inhibitors are effective in the multiple myeloma maintenance treatment compared with the placebo group. Bortezomib has certain advantages in prolonging PFS, followed by ixazomib and carfilzomib in terms of efficacy. Bortezombib may be superior to carfilzombib in extending OS. However, the adverse reactions caused by proteasome inhibitors, such as Peripheral neuropathy, Serious adverse events, Rash, Vomiting, etc., should be paid enough attention.
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Lycorma delicatula, a globally invasive pest, has caused considerable economic losses in many countries. Determining the potential distribution range of L. delicatula is crucial for its effective management and control; however, our understanding of this species remains limited. In this study, Maxent model with occurrence records and environmental variables were fit first and then optimized by selecting the best combination of feature classes and regularization multipliers using the lowest score of corrected Akaike information criterion. Subsequently, we predicted global suitable areas for L. delicatula both currently and in the future (2041-2060, 2061-2080, and 2081-2100). The results indicated that the mean temperature of the driest quarter is the most important environmental variable limiting L. delicatula distribution. Currently, the suitable areas are concentrated in East Asia (mainly in China, South Korea, and Japan), central and eastern United States, and southern Europe. Compared with current environmental conditions, in all future climate scenarios, the number of suitable areas for L. delicatula increased. In addition, we revealed that suitable areas are likely to expand northward in the future. Our study results suggest that policymakers and governments should prioritize the development of pest management measures in suitable areas for L. delicatula, especially in high suitable areas, to control this invasive pest and minimize global economic losses.
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BACKGROUND: Epigenetic age accelerations (EAAs) are a promising new avenue of research, yet their investigation in subacute thyroiditis (SAT) remains scarce. Our study endeavors to fill this void by exploring the potential causal association between EAAs and SAT. METHODS: Our study utilized publicly available genome-wide association study (GWAS) data of European ancestry to conduct a bidirectional Mendelian randomization (MR) study. Five MR methods were employed to measure causal association between EAAs and SAT multiple analyses were utilized to perform quality control. RESULTS: Our study evaluated causal association between SAT and four EAAs, included GrimAge acceleration (GrimAA), Hannum age acceleration (HannumAA), PhenoAge acceleration (PhenoAA), intrinsic epigenetic age acceleration (IEAA). Results showed that there is a significant causal association between PhenoAA and SAT (OR 1.109, 95% CI 1.000-1.228, p = 0.049, by IVW method). On the contrary, SAT was associated with IEAA (OR 0.933, 95% CI 0.884-0.984, p = 0.011, by IVW method; OR 0.938, 95% CI 0.881-0.998, p = 0.043, by weighted median method). Leave-one-out sensitivity analysis, heterogeneity test, pleiotropy test, and MR-PRESSO analysis provide good quality control. CONCLUSION: The bidirectional MR analysis concluded that an increase in PhenoAA was correlated with a higher risk of SAT, indicating a potential causal relationship between PhenoAA and risk of SAT. Conversely, SAT was found to be closely associated with IEAA, suggesting that SAT may accelerate the aging process. Slowing down biological aging has emerged as a new research direction in curbing SAT.
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Epigênese Genética , Estudo de Associação Genômica Ampla , Análise da Randomização Mendeliana , Tireoidite Subaguda , Humanos , Análise da Randomização Mendeliana/métodos , Estudo de Associação Genômica Ampla/métodos , Epigênese Genética/genética , Tireoidite Subaguda/genética , Predisposição Genética para Doença , Polimorfismo de Nucleotídeo Único , Feminino , Metilação de DNA/genética , Masculino , Fatores de Risco , Envelhecimento/genéticaRESUMO
Necrotizing enterocolitis (NEC) is a microbiota- and feeding-related gut inflammatory disease in preterm infants. The standard of care (SOC) treatment for suspected NEC is antibiotic treatment and reduced enteral feeding, but how SOC treatment mitigates NEC remains unclear. We explored whether SOC treatment alone or combined with an anti-inflammatory protein (inter-alpha inhibitor protein, IAIP) supplementation improves outcomes in a preterm piglet model of formula-induced NEC. Seventy-one cesarean-delivered preterm piglets were initially fed formula, developing NEC symptoms by day 3, and then randomized into CON (continued feeding) or SOC groups (feeding cessation and antibiotics), each with or without human IAIP (2×2 factorial design). By day 5, IAIP treatment did not significantly influence outcomes, whereas SOC treatment effectively reduced NEC lesions, diarrhea, and bloody stools. Notably, SOC treatment improved gut morphology and function, dampened gut inflammatory responses, altered the colonic microbiota composition, and modulated systemic immune responses. Plasma proteomic analysis revealed the effects of SOC treatment on organ development and systemic inflammatory responses. Collectively, these findings suggest that SOC treatment significantly prevents NEC progression in preterm piglets via effects on gut structure, function, and microbiota, as well as systemic immune and inflammatory responses. Timely feeding cessation and antibiotics are critical factors in preventing NEC progression in preterm infants, while the benefits of additional human IAIP treatment remain to be established.
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Animais Recém-Nascidos , Antibacterianos , Enterocolite Necrosante , Microbioma Gastrointestinal , Animais , Enterocolite Necrosante/tratamento farmacológico , Enterocolite Necrosante/prevenção & controle , Enterocolite Necrosante/patologia , Antibacterianos/farmacologia , Suínos , Microbioma Gastrointestinal/efeitos dos fármacos , Feminino , Inflamação/tratamento farmacológico , Inflamação/patologia , Modelos Animais de Doenças , Nutrição Enteral , HumanosRESUMO
In recent years, the integration of radiotherapy and nanocatalytic medicine has gained widespread attention in the treatment of breast cancer. Herein, the glucose oxidase (GOx) and MnO2 nanoparticles co-modified multifunctional liposome of GOx-MnO2@Lip was constructed for enhanced radiotherapy. Introduction of GOx would not only elevate the glucose consumption to starve the cancer cells, but also increased the endogenous H2O2 level. Meanwhile, high intracellular GSH concentration facilitated the release of Mn2+ to amplify the cytotoxic ·OH through cascade catalytic reactions within the tumor microenvironment, resulting in a favorable tumor suppression rate of 74.45â¯%. Furthermore, the blood biochemical and blood routine demonstrated that GOx-MnO2@Lip had no obvious toxic side effects. Therefore, this work provided a potential vehicle for synergistic cancer starving therapy, chemodynamic therapy and radiotherapy for improving therapeutic efficacy of breast cancer.
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Neoplasias da Mama , Glucose Oxidase , Lipossomos , Compostos de Manganês , Óxidos , Radiossensibilizantes , Compostos de Manganês/química , Compostos de Manganês/farmacologia , Glucose Oxidase/metabolismo , Feminino , Óxidos/química , Óxidos/farmacologia , Neoplasias da Mama/patologia , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/radioterapia , Radiossensibilizantes/farmacologia , Animais , Humanos , Linhagem Celular Tumoral , Peróxido de Hidrogênio/metabolismo , Camundongos Endogâmicos BALB C , Catálise , Camundongos , Nanopartículas/química , Microambiente Tumoral/efeitos dos fármacosRESUMO
It has been widely acknowledged that high temperatures and heatwaves promote ozone concentration, worsening the ambient air quality. However, temperature can impact ozone via multiple pathways, and quantifying each path is challenging due to environmental confounders. In this study, we frame the problem as a treatment-outcome issue and utilize a machine learning-aided causal inference technique to disentangle the impact of temperature on ozone formation. Our approach reveals that failing to account for the covariations of solar radiation and other meteorological factors leads to an overestimation of the O3-temperature response. Through process evaluation, we find that temperature influences local ozone formation mainly by accelerating chemical reactions and enhancing precursor production and changing boundary layer heights. The O3 response to temperature via enhancing soil NOx and changing relative humidity and wind field is however observable. A better appreciation of O3-temperature response is critical for improving air quality regulation in the warming future.
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BACKGROUND: This study aimed to investigate the epidemiological changes in scarlet fever before, during and after the COVID-19 pandemic (2005-2023) and predict the incidence of the disease in 2024 and 2025 in Chongqing Municipality, Southwest China. METHODS: Descriptive analysis was used to summarize the characteristics of the scarlet fever epidemic. Spatial autocorrelation analysis was utilized to explore the distribution pattern of the disease, and the seasonal autoregressive integrated moving average (SARIMA) model was constructed to predict its incidence in 2024 and 2025. RESULTS: Between 2005 and 2023, 9,593 scarlet fever cases were reported in Chongqing, which resulted in an annual average incidence of 1.6694 per 100,000 people. Children aged 3-7 were the primary victims of this disease, with the highest average incidence found among children aged 6 (5.0002 per 100,000 people). Kindergarten children were the dominant infected population, accounting for as much as 54.32% of cases, followed by students (34.09%). The incidence for the male was 1.51 times greater than that for the female. The monthly distribution of the incidence showed a bimodal pattern, with one peak occurring between April and June and another in November or December. The spatial autocorrelation analysis revealed that scarlet fever cases were markedly clustered; the areas with higher incidence were mainly concentrated in Chongqing's urban areas and its adjacent districts, and gradually spreading to remote areas after 2020. The incidence of scarlet fever increased by 106.54% and 39.33% in the post-upsurge period (2015-2019) and the dynamic zero-COVID period (2020-2022), respectively, compared to the pre-upsurge period (2005-2014) (P < 0.001). During the dynamic zero-COVID period, the incidence of scarlet fever decreased by 68.61%, 25.66%, and 10.59% (P < 0.001) in 2020, 2021, and 2022, respectively, compared to the predicted incidence. In 2023, after the dynamic zero-COVID period, the reported cases decreased to 1.5168 per 100,000 people unexpectedly instead of increasing. The cases of scarlet fever are predicted to increase in 2024 (675 cases) and 2025 (705 cases). CONCLUSIONS: Children aged 3-7 years are the most affected population, particularly males, and kindergartens and primary schools serving as transmission hotspots. It is predicted that the high incidence of scarlet fever in Chongqing will persist in 2024 and 2025, and the outer districts (counties) beyond urban zone would bear the brunt of the impact. Therefore, imminent public health planning and resource allocation should be focused within those areas.
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COVID-19 , Escarlatina , Humanos , China/epidemiologia , Escarlatina/epidemiologia , COVID-19/epidemiologia , Criança , Masculino , Pré-Escolar , Feminino , Incidência , Adolescente , Adulto , Lactente , Adulto Jovem , Pandemias , Previsões , Pessoa de Meia-IdadeRESUMO
The agonist-antagonist myoneural interface (AMI), a surgical method to reinnervate physiologically-relevant proprioceptive feedback for control of limb prostheses, has demonstrated the ability to provide natural afferent sensations for limb amputees when actuating their prostheses. Following AMI surgery, one potential challenge is atrophy of the disused muscles, which would weaken the reinnervation efficacy of AMI. It is well known that electrical muscle stimulus (EMS) can reduce muscle atrophy. In this study, we conducted an animal investigation to explore whether the EMS can significantly improve the electrophysiological performance of AMI. AMI surgery was performed in 14 rats, in which the distal tendons of bilateral solei donors were connected and positioned on the surface of the left biceps femoris. Subsequently, the left tibial nerve and the common peroneus nerve were sutured onto the ends of the connected donor solei. Two stimulation electrodes were affixed onto the ends of the donor solei for EMS delivery. The AMI rats were randomly divided into two groups. One group received the EMS treatment (designated as EMS_on) regularly for eight weeks and another received no EMS (designated as EMS_off). Two physiological parameters, nerve conduction velocity (NCV) and motor unit number, were derived from the electrically evoked compound action potential (CAP) signals to assess the electrophysiological performance of AMI. Our experimental results demonstrated that the reinnervated muscles of the EMS_on group generated higher CAP signals in comparison to the EMS_off group. Both NCV and motor unit number were significantly elevated in the EMS_on group. Moreover, the EMS_on group displayed statistically higher CAP signals on the indirectly activated proprioceptive afferents than the EMS_off group. These findings suggested that EMS treatment would be promising in enhancing the electrophysiological performance and facilitating the reinnervation process of AMI.
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According to the diagnostic criteria for HHV-8 (human herpesvirus-8) negative/idiopathic multicentric Castleman disease (iMCD) proposed by Castleman Disease Collaborative Network (CDCN) in 2017, there is a group of HHV-8 negative multicentric Castleman disease (MCD) patients who do not have symptoms and hyperinflammatory state and do not meet the iMCD criteria. This retrospective study enrolled 114 such patients, described as asymptomatic MCD (aMCD), from 26 Chinese centers from 2000-2021. With a median follow-up time of 46.5 months (range: 4-279 months), 6 patients (5.3%) transformed to iMCD. The median time between diagnosis of aMCD and iMCD in these 6 patients was 28.5 months (range: 3-60 months). During follow-up, 7 patients died; three of them died from progression of MCD. Despite that 37.7% patients received systemic treatment targeting MCD, this strategy was neither associated with a lower probability of iMCD transformation nor a lower death rate. The 5-year estimated survival of all aMCD patients was 94.1% (95% CI 88.8-99.6%). Transformation to iMCD was an important predictor of death (log-rank p=0.01) (5-year estimated survival 83.3%). This study suggests that aMCD patients may represent a potential early stage of iMCD, who may not require immediate treatment but should be closely monitored.