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Background: There is increasing evidence that macrophages are involved in the development of carotid atherosclerosis (CAS), but the specific mechanism is still unclear. We aimed to explore the key genes that play a regulatory role on macrophages in the progression of CAS. Methods: From 2021 August to 2023 August, GEO datasets GSE100927 and GSE43292 were downloaded and the key gene modules related to CAS were identified by weighted Gene co-expression network analysis (WGCNA). Kyoto Encyclopedia of Genes and Genes (KEGG) pathway analysis was performed on the genes of the key modules to identify common gene enrichment pathways. Differential expression analysis of pathway-related genes was performed by the "limma" package of R software. Case groups were categorized into high and low expression groups based on the expression levels of key genes, and ssGSEA immune infiltration analysis was performed. Results: The turquoise module of GSE100924 (threshold=12) and the brown module of GSE43292 (threshold=7) were obtained through WGCNA analysis. The analysis of KEGG showed that the differentially expressed genes in the turquoise and brown modules were co-enriched in the staphylococcus aureus infection signaling pathway. Differential expression analysis identified 18 common differentially expressed genes, all of which were highly expressed in the case group. C1QA is the gene of interest. According to ssGSEA analysis, the high expression group of C1QA showed a significant increase in the number of macrophages (GSE43292, P=0.0011; GSE100927, P=0.025). Conclusion: This study identified the key gene C1QA involved in regulating macrophage functional activity during the CAS process, providing new ideas for effective control of CAS.
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Ameloblastoma (AB) is a common odontogenic tumor that develops in the mouth. Despite its benign nature, AB exhibits significant invasiveness leading to tumor metastasis and high postoperative recurrence rates. Studies have shown a relationship between the occurrence and development of various tumors and non-coding RNA (ncRNA). NcRNA, transcribed from the genomes of mammals and other complex organisms, are often products of alternative splicing and processing into smaller products. MicroRNA (miRNA), circular RNA (circRNA), and long non-coding RNA (lncRNA) are the main types of ncRNA. NcRNA play increasingly significant roles in the pathogenesis of human cancers, regulating their occurrence and progression as oncogenes or tumor suppressors. They are involved in tumor development and progression through alternative splicing of pre-mRNA, transcriptional regulation, mRNA stability, protein translation, and chromatin remodeling and modification. The importance of ncRNA in AB has received significant attention in recent years. However, the biological functions and mechanisms of ncRNA in AB remain largely unknown. In this review, we not only explore the functions and roles of ncRNA in AB, but also describe and envision their potential functional roles as biomarkers in AB diagnosis. In particular, we highlight the potential of miR-29a as a molecular marker for diagnosis and therapy. As promising novel therapeutic targets, the biological functions of ncRNA need further study, which is indispensable.
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Excessive abdominal fat deposition negatively impacts poultry meat production and carcass yield. Identification of novel adipogenesis regulators may help improve production performance declines caused by excessive fat deposition. NUMB Endocytic Adaptor Protein (NUMB) typically functions as a cell fate determinant and plays a significant role in cell development and various diseases. Here, we found that NUMB is abundantly expressed in chicken abdominal fat depots and is induced in cultured adipocytes following adipogenic treatment. The gain- and loss-of-function experiments demonstrated that NUMB promotes the proliferation and G1/S transition of chicken adipocytes, enhances adipocyte differentiation, and increases the expression of PPARγ1 transcript. Through mRNA-seq analysis and molecular experiments, we further confirmed that NUMB inhibits the transcriptional activation of the NOTCH1 pathway and the expression of the downstream transcription factor HES1 by inducing NOTCH1 degradation. Nevertheless, the inhibition of the NOTCH1/HES1 axis alone cannot fully explain NUMB's role in adipogenesis, as NUMB also regulates the expression of multiple adipogenic transcription factors such as E2F1, EGR2, and NR4A3. Our data suggest that NUMB is a potent activator of adipogenesis and enhances our understanding of its regulatory mechanisms in chicken abdominal fat deposition.
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INTRODUCTION: Autologous hematopoietic stem cell transplantation (ASCT) has gained extensive application in the treatment of lymphoma and multiple myeloma (MM). Plenty of studies demonstrate that peripheral blood indicators could be considered potential predictive biomarkers for hematopoietic stem cells (HSCs) collection efficiency, including white blood cell count (WBC), monocyte count (Mono), platelet count (PLT), hematocrit, and hemoglobin levels. Currently, clinically practical predictive models based on these peripheral detection indicators to quickly, conveniently, and accurately predict collection efficiency are lacking. METHODS: In total, 139 patients with MM and lymphoma undergoing mobilization and collection of ASCT were retrospectively studied. The study endpoint was successful collection of autologous HSCs. We analyzed the effects of clinical characteristics and peripheral blood markers on collection success, and screened variables to establish a prediction model. We determined the optimal cutoff value of peripheral blood markers for predicting successful stem cell collection and the clinical value of a multi-marker prediction approach. We also established a prediction model for collection efficacy. RESULTS: Univariate and multivariate logistic regression analyses showed that the mobilization regimen, Mono, PLT, mononuclear cell count (MNC), and peripheral blood CD34+ cell count (PB CD34+ counts) were significant predictors of successful collection of peripheral blood stem cells (PBSC). Two predictive models were constructed based on the results of multivariate logistic analyses. Model 1 included the mobilization regimen, Mono, PLT, and MNC, whereas Model 2 included the mobilization regimen, Mono, PLT, MNC, and PB CD34+ counts. Receiver operating characteristic (ROC) curve analysis showed that the PB CD34+ counts, Model 1, and Model 2 could predict successful HSCs collection, with cutoff values of 26.92 × 106/L, 0.548, and 0.355, respectively. Model 1 could predict successful HSCs collection with a sensitivity of 84.62%, specificity of 75.73%, and area under the curve (AUC) of 0.863. Model 2 could predict successful HSCs collection with a sensitivity of 83.52%, specificity of 94.17%, and AUC of 0.946; thus, it was superior to the PB CD34+ counts alone. CONCLUSION: Our findings suggest that the combination of the mobilization regimen, Mono, PLT, MNC, and PB CD34+ counts before collection has predictive value for the efficacy of autologous HSCs collection in patients with MM and lymphoma. Using models based on these predictive markers may help to avoid over-collection and improve patient outcomes.
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Mimicking the dissipative assemblies found in living systems fueled by bioenergy, we present a novel chemical fuel-driven transient 2D SOF, formed via the redox reaction-driven transient self-assembly of tetraphenylene-based structural units and cucurbit[8]uril (CB[8]). The system was initiated by adding sodium dithionite (SDT) as the fuel, leading to the formation of 2D SOFs through 2 : 1 host-guest complexation between the viologen cation radical and CB[8]. These 2D SOFs then spontaneously disassemble over time as the radicals are oxidized by air. The temporal assembly and lifetimes of these transient SOFs can be controlled by adjusting the concentrations of the fuel. Moreover, the resulting transient 2D SOFs exhibited remarkable potential as catalysts for the green synthesis of benzyl sulfones in water.
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The release of phosphorous (P) via chemical weathering is a vital process that regulates the global cycling of numerous key elements and shapes the size of the Earth's biosphere. It has long been postulated that global climate should theoretically play a prominent role in governing P weathering rates. Yet, there is currently a lack of direct evidence for this relationship based on empirical data at the global scale. Here, using a compilation of temperature and P content data of global surface soils (0 to 30 cm), we demonstrate that P release does enhance at high mean annual surface temperatures. We propose that this amplification of nutrient supply with warming is a critical component of Earth's natural thermostat, and that this relationship likely caused expanded oceanic anoxia during past climate warming events. The potential acceleration of phosphorus loss from soils due to anthropogenic climate warming may pose threats to agricultural production, terrestrial and marine ecosystems, and alter marine redox landscapes.
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BACKGROUND: Delayed cerebral ischemia (DCI) is a common and serious complication of subarachnoid hemorrhage (SAH). Its pathogenesis is not fully understood. Here, we developed a predictive model based on peripheral blood biomarkers and validated the model using several bioinformatic multi-analysis methods. METHODS: Six datasets were obtained from the GEO database. Characteristic genes were screened using weighted correlation network analysis (WGCNA) and differentially expressed genes. Three machine learning algorithms, elastic networks-LASSO, support vector machines (SVM-RFE) and random forests (RF), were also used to construct diagnostic prediction models for key genes. To further evaluate the performance and predictive value of the diagnostic models, nomogram model were constructed, and the clinical value of the models was assessed using Decision Curve Analysis (DCA), Area Under the Check Curve (AUC), Clinical Impact Curve (CIC), and validated in the mouse single-cell RNA-seq dataset. Mendelian randomization(MR) analysis explored the causal relationship between SAH and stroke, and the intermediate influencing factors. We validated this by retrospectively analyzing the qPCR levels of the most relevant genes in SAH and SAH-DCI patients. This experiment demonstrated a statistically significant difference between SAH and SAH-DCI and normal group controls. Finally, potential small molecule compounds interacting with the selected features were screened from the Comparative Toxicogenomics Database (CTD). RESULTS: The fGSEA results showed that activation of Toll-like receptor signaling and leukocyte transendothelial cell migration pathways were positively correlated with the DCI phenotype, whereas cytokine signaling pathways and natural killer cell-mediated cytotoxicity were negatively correlated. Consensus feature selection of DEG genes using WGCNA and three machine learning algorithms resulted in the identification of six genes (SPOCK2, TRRAP, CIB1, BCL11B, PDZD8 and LAT), which were used to predict DCI diagnosis with high accuracy. Three external datasets and the mouse single-cell dataset showed high accuracy of the diagnostic model, in addition to high performance and predictive value of the diagnostic model in DCA and CIC. MR analysis looked at stroke after SAH independent of SAH, but associated with multiple intermediate factors including Hypertensive diseases, Total triglycerides levels in medium HDL and Platelet count. qPCR confirmed that significant differences in DCI signature genes were observed between the SAH and SAH-DCI groups. Finally, valproic acid became a potential therapeutic agent for DCI based on the results of target prediction and molecular docking of the characterized genes. CONCLUSION: This diagnostic model can identify SAH patients at high risk for DCI and may provide potential mechanisms and therapeutic targets for DCI. Valproic acid may be an important future drug for the treatment of DCI.
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Biomarcadores , Isquemia Encefálica , Ácido Valproico , Humanos , Animales , Isquemia Encefálica/tratamiento farmacológico , Isquemia Encefálica/genética , Isquemia Encefálica/sangre , Isquemia Encefálica/inmunología , Ácido Valproico/uso terapéutico , Ratones , Biomarcadores/sangre , Hemorragia Subaracnoidea/sangre , Hemorragia Subaracnoidea/inmunología , Hemorragia Subaracnoidea/genética , Hemorragia Subaracnoidea/tratamiento farmacológico , Biología Computacional , Bases de Datos Genéticas , Aprendizaje AutomáticoRESUMEN
Neonicotinoids (NEOs) are currently the fastest-growing and most widely used insecticide class worldwide. Increasing evidence suggests that long-term NEO residues in the environment have toxic effects on non-target soil animals. However, few studies have conducted surveys on the effects of NEOs on soil animals, and only few have focused on global systematic reviews or meta-analysis to quantify the effects of NEOs on soil animals. Here, we present a meta-analysis of 2940 observations from 113 field and laboratory studies that investigated the effects of NEOs (at concentrations of 0.001-78,600.000 mg/kg) on different soil animals across five indicators (i.e., survival, growth, behavior, reproduction, and biochemical biomarkers). Furthermore, we quantify the effects of NEOs on different species of soil animals. Results show that NEOs inhibit the survival, growth rate, behavior, and reproduction of soil animals, and alter biochemical biomarkers. Both the survival rate and longevity of individuals decreased by 100 % with NEO residues. The mean values of juvenile survival, cocoon number, and egg hatchability were reduced by 97 %, 100 %, and 84 %, respectively. Both individual and cocoon weights were reduced by 82 %, while the growth rate decreased by 88 % with NEO residues. Our meta-analysis confirms that NEOs pose significant negative impacts on soil animals.
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Insecticidas , Neonicotinoides , Contaminantes del Suelo , Animales , Contaminantes del Suelo/toxicidad , Insecticidas/toxicidad , Neonicotinoides/toxicidad , Residuos de Plaguicidas/toxicidad , Residuos de Plaguicidas/análisis , Reproducción/efectos de los fármacos , Suelo/química , Conducta Animal/efectos de los fármacosRESUMEN
[This corrects the article DOI: 10.3389/fgene.2024.1343411.].
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The directional transformation of carbon dioxide (CO2) with renewable hydrogen into specific carbon-heavy products (C6+) of high value presents a sustainable route for net-zero chemical manufacture. However, it is still challenging to simultaneously achieve high activity and selectivity due to the unbalanced CO2 hydrogenation and C-C coupling rates on complementary active sites in a bifunctional catalyst, thus causing unexpected secondary reaction. Here we report LaFeO3 perovskite-mediated directional tandem conversion of CO2 towards heavy aromatics with high CO2 conversion (> 60%), exceptional aromatics selectivity among hydrocarbons (> 85%), and no obvious deactivation for 1000 hours. This is enabled by disentangling the CO2 hydrogenation domain from the C-C coupling domain in the tandem system for Iron-based catalyst. Unlike other active Fe oxides showing wide hydrocarbon product distribution due to carbide formation, LaFeO3 by design is endowed with superior resistance to carburization, therefore inhibiting uncontrolled C-C coupling on oxide and isolating aromatics formation in the zeolite. In-situ spectroscopic evidence and theoretical calculations reveal an oxygenate-rich surface chemistry of LaFeO3, that easily escape from the oxide surface for further precise C-C coupling inside zeolites, thus steering CO2-HCOOH/H2CO-Aromatics reaction pathway to enable a high yield of aromatics.
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Glutathione (GSH) depletion, mitochondrial damage, and oxidative stress have been implicated in the pathogenesis of acetaminophen (APAP) hepatotoxicity. Here, we demonstrated that the expression of histone deacetylase 6 (HDAC6) is highly elevated, whereas malate dehydrogenase 1 (MDH1) is downregulated in liver tissues and AML-12 cells induced by APAP. The therapeutic benefits of LT-630, a novel HDAC6 inhibitor on APAP-induced liver injury, were also substantiated. On this basis, we demonstrated that LT-630 improved the protein expression and acetylation level of MDH1. Furthermore, after overexpression of MDH1, an upregulated NADPH/NADP+ ratio and GSH level and decreased cell apoptosis were observed in APAP-stimulated AML-12 cells. Importantly, MDH1 siRNA clearly reversed the protection of LT-630 on APAP-stimulated AML-12 cells. In conclusion, LT-630 could ameliorate liver injury by modulating MDH1-mediated oxidative stress induced by APAP.
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Enfermedad Hepática Crónica Inducida por Sustancias y Drogas , Enfermedad Hepática Inducida por Sustancias y Drogas , Histona Desacetilasa 6 , Leucemia Mieloide Aguda , Animales , Humanos , Ratones , Acetaminofén , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Enfermedad Hepática Crónica Inducida por Sustancias y Drogas/metabolismo , Glutatión/metabolismo , Histona Desacetilasa 6/antagonistas & inhibidores , Leucemia Mieloide Aguda/metabolismo , Hígado/patología , Ratones Endogámicos C57BL , Estrés Oxidativo/efectos de los fármacosRESUMEN
Crop cultivation suitability plays a vital role in determining the distribution, quality, and production of crop and can be greatly affected by climate change. Therefore, evaluating crop cultivation suitability under climate change and identifying the factors influencing it can optimize crop cultivation layout and improve production and quality. Based on comprehensive datasets including geographical distribution points, climate data, soil characteristics, and topography, our study employed the MaxEnt model to simulate the potential distribution of Pu'er tea (Camellia sinensis var. assamica) cultivation suitability in Yunnan Province from 1961 to 2020. Furthermore, we assessed the consistency between the simulated suitable areas and the actual production of Pu'er tea. The results showed that precipitation of the warmest quarter, precipitation of the driest month, and average temperature in January were the three dominant environmental variables affecting the cultivation distribution of Pu'er tea. The high suitable areas for Pu'er tea cultivation in Yunnan Province were mainly distributed in the western and southern regions, accounting for 13.89% of the total area of Yunnan Province. The medium suitable areas are mainly distributed in the central and western regions of Yunnan Province, accounting for 20.07% of the total area of Yunnan Province. Over the past 60 years, the unsuitable area for Pu'er tea has increased, while the suitable area has shown a trend of migration to the southwest. Changes in precipitation and temperature were found to be the main drivers of the changes in the distribution of suitable areas for Pu'er tea. We also found a mismatch between the cultivation suitability and the actual production of Pu'er tea. Our study provides an accurate assessment and zoning analysis of the suitability of Pu'er tea cultivation in Yunnan Province, which can help optimize the layout of Pu'er tea cultivation and reduce potential climate risks.
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Camellia sinensis , Té , China , Monitoreo del Ambiente , TemperaturaRESUMEN
Metastasis promotes the development of tumors and is a significant cause of gastric cancer death. For metastasis to proceed, tumor cells must become mobile by modulating their cytoskeleton. MICAL1 (Molecule Interacting with CasL1) is known as an actin cytoskeleton regulator, but the mechanisms by which it drives gastric cancer cell migration are still unclear. Analysis of gastric cancer tissues revealed that MICAL1 expression is dramatically upregulated in stomach adenocarcinoma (STAD) samples as compared to noncancerous stomach tissues. Patients with high MICAL1 expression had shorter overall survival (OS), post-progression survival (PPS) and first-progression survival (FPS) compared with patients with low MICAL1 expression. RNAi-mediated silencing of MICAL1 inhibited the expression of Vimentin, a protein involved in epithelial-mesenchymal transition. This effect correlates with a significant reduction in gastric cancer cell migration. MICAL1 overexpression reversed these preventive effects. Immunoprecipitation experiments and immunofluorescence assays revealed that PlexinA1 forms a complex with MICAL1. Importantly, specific inhibition of PlexinA1 blocked the Rac1 activation and ROS production, which, in turn, impaired MICAL1 protein stability by accelerating MICAL1 ubiquitin/proteasome-dependent degradation. Overexpression of PlexinA1 enhanced Rac1 activation, ROS production, MICAL1 and Vimentin expressions, and favored cell migration. In conclusion, this study identified MICAL1 as an important facilitator of gastric cancer cell migration, at least in part, by affecting Vimentin expression and PlexinA1 promotes gastric cancer cell migration by binding to and suppressing MICAL1 degradation in a Rac1/ROS-dependent manner.
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Neoplasias Gástricas , Humanos , Calponinas , Línea Celular Tumoral , Proteínas de Microfilamentos/metabolismo , Oxigenasas de Función Mixta/metabolismo , Complejo de la Endopetidasa Proteasomal/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Neoplasias Gástricas/metabolismo , Ubiquitina/metabolismo , Vimentina/genética , Vimentina/metabolismoRESUMEN
The evolution of oxygen cycles on Earth's surface has been regulated by the balance between molecular oxygen production and consumption. The Neoproterozoic-Paleozoic transition likely marks the second rise in atmospheric and oceanic oxygen levels, widely attributed to enhanced burial of organic carbon. However, it remains disputed how marine organic carbon production and burial respond to global environmental changes and whether these feedbacks trigger global oxygenation during this interval. Here, we report a large lithium isotopic and elemental dataset from marine mudstones spanning the upper Neoproterozoic to middle Cambrian [~660 million years ago (Ma) to 500 Ma]. These data indicate a dramatic increase in continental clay formation after ~525 Ma, likely linked to secular changes in global climate and compositions of the continental crust. Using a global biogeochemical model, we suggest that intensified continental weathering and clay delivery to the oceans could have notably increased the burial efficiency of organic carbon and facilitated greater oxygen accumulation in the earliest Paleozoic oceans.
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Dilatation of soft skin tissue is a common surgical procedure in plastic surgery. M2 macrophages play a critical role in reducing inflammation, promoting epithelial and vascular endothelial cell proliferation, enhancing collagen synthesis in fibroblasts, and orchestrating extracellular matrix remodelling by promoting angiogenesis, epithelialisation, and fibrosis. Macrophages improve flap survival by promoting microangiogenesis and collagen remodelling. However, the role of macrophages in flap expansion has not yet been investigated. Improving the expansion efficiency of dilatation flaps and promoting flap vascularisation are the pressing problems in the fields of plastic and reconstruction surgery. In the present study, we used a mouse model to assess the effects of macrophage activation on skin expansion, thickness, ultrastructure, intradermal angiogenesis, and collagen and cytokine levels. Our findings revealed dynamic changes in the macrophage content and subtypes within the expansion flaps. The enrichment of M2 macrophages significantly enhanced the efficiency of flap expansion, vascularisation, and collagen synthesis. Our findings underline the pivotal role of M2 macrophages in tissue regeneration at the molecular and biochemical levels. These findings provide a basis for improving flap expansion efficiency using M2 macrophages.
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Introduction: Blepharophimosis, ptosis, and epicanthus inversus syndrome (BPES) is a rare inherited disorder. This study was aimed to identify and functionally validate FOXL2 variants in two Chinese families with BPES. Methods: The proband and his family members were subjected to whole-exome sequencing to identify disease-associated variants. Several bioinformatic tools were used to computationally predict altered proteins. In vitro functional assays were conducted by transfecting wild-type and mutant FOXL2 cDNAs into HEK-293 cells, followed by subcellular localization assays, luciferase reporter gene assays, and quantitative real-time polymerase chain reaction. Results: The clinical features of BPES, including small palpebral fissures, ptosis, telecanthus, and epicanthus inversus, were present in all affected patients. Two novel mutations were detected, c.292T>A and c.383G>T. Whole-exome sequencing analysis and prediction software suggested that these mutations were pathogenic. Functional studies showed that these two point mutations decreased FOXL2 protein expression, resulting in subcellular mislocalization and aberrant transcriptional activity of the steroidogenic acute regulatory protein gene promoter. Conclusion: Our results add to the current understanding of known FOXL2 variants in, and our in vitro experiments provide reference data and insights into the etiology of BPES. Further studies are needed to identify the possible mechanisms underlying the action of this mutation on the development of BPES.
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The NOTCH signaling pathway plays a pivotal role in diverse developmental processes, including cell proliferation and differentiation. In this study, we investigated whether this signaling molecules also contribute to avian adipogenesis. Using previous mRNA-seq datasets, we examined the expression of 11 signaling members during avian adipocyte differentiation. We found most members are down-regulated throughout differentiation (p < 0.05). As a representative, NOTCH1 was decreased in cultured chicken abdominal adipocytes during adipogenesis at mRNA and protein levels (p < 0.05). Moreover, using an overexpression plasmid for NOTCH1's intracellular domain (NICD1), as well as siRNA and DAPT to activate or deplete NOTCH1 in cells, we investigated the role of NOTCH1 in avian adipogenesis. Our findings illuminate that NOTCH1 activates the expression of HES1 and SOCS3 while it decreases NR2F2 and NUMB (p < 0.05), as well as inhibits oleic acid-induced adipocyte differentiation (p < 0.01). We further demonstrate that HES1, a downstream transcription factor activated by NOTCH1, also significantly inhibits adipogenesis by suppressing PPARγ and C/EBPα (p < 0.01). Collectively, these findings establish NOTCH1 as a negative regulator of avian adipocyte differentiation, unveiling NOTCH signaling as a potential target for regulating avian fat deposition.
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BACKGROUND: Magnetic resonance imaging (MRI) is a handy diagnostic tool for orthopedic disorders, particularly spinal and joint diseases. METHODS: The lumbar intervertebral disc is visible in the T1 and T2 weight sequences of the spine MRI, which aids in diagnosing lumbar disc herniation, lumbar spine tuberculosis, lumbar spine tumors, and other conditions. The lumbar intervertebral disc cannot be seen accurately in the Spectral Attenuated Inversion Recovery (SPAIR) due to weaknesses in the fat and frequency offset parameters, which is not conducive to developing the intelligence diagnosis model of medical image. RESULTS: In order to solve this problem, we propose a composite framework, which is first to use the contrast limited adaptive histogram equalization (CLAHE) method to enhance the SPAIR image contrast of the spine MRI and then use the non-local means method to remove the noise of the image to ensure that the image contrast is uniform without losing details. We employ the Information Entropy (IE), Peak signal-to-noise ratio (PSNR), and feature similarity index measure (FSIM) to quantify image quality after enhancement by the composite framework. CONCLUSION: The outcomes of the experiments' output images and quantitative data indicate that our composite framework is better than others.
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Aumento de la Imagen , Imagen por Resonancia Magnética , Humanos , Aumento de la Imagen/métodos , Imagen por Resonancia Magnética/métodos , Relación Señal-Ruido , Vértebras Lumbares/diagnóstico por imagenRESUMEN
Silver nanoparticles (AgNPs) are among the most widely used metal-based engineered nanomaterials in biomedicine and nanotechnology, and account for >50 % of global nanomaterial consumer products. The increasing use of AgNPs potentially causes marine ecosystem changes; however, the environmental impacts of man-made AgNPs are still poorly studied. This study reports for the first time that man-made AgNPs intruded into cold seeps, which are important marine ecosystems where hydrogen sulfide, methane, and other hydrocarbon-rich fluid seepage occur. Using a combination of electron microscopy, geochemical and metagenomic analyses, we found that in the cold seeps with high AgNPs concentrations, the relative abundance of genes associated with anaerobic oxidation of methane (AOM) was lower, while those related to the sulfide oxidizing and sulfate reducing were higher. This suggests that AgNPs can stimulate the proliferation of sulfate-reducing and sulfide-oxidizing bacteria, likely due to the effects of activating repair mechanisms of the cells against the toxicant. A reaction of AgNPs with hydrogen sulfide to form silver sulfide could also effectively reduce the amount of available sulfate in local ecosystems, which is generally used as the AOM oxidant. These novel findings indicate that man-made AgNPs may be involved in the biogeochemical cycles of sulfur and carbon in nature, and their potential effects on the releasing of methane from the marine methane seeps should not be ignored in both scientific and environmental aspects.