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Electrocatalytic alkynes semi-hydrogenation to produce alkenes with high yield and Faradaic efficiency remains technically challenging because of kinetically favorable hydrogen evolution reaction and over-hydrogenation. Here, we propose a hierarchically nanoporous Cu50Au50 alloy to improve electrocatalytic performance toward semi-hydrogenation of alkynes. Using Operando X-ray absorption spectroscopy and density functional theory calculations, we find that Au modulate the electronic structure of Cu, which could intrinsically inhibit the combination of H* to form H2 and weaken alkene adsorption, thus promoting alkyne semi-hydrogenation and hampering alkene over-hydrogenation. Finite element method simulations and experimental results unveil that hierarchically nanoporous catalysts induce a local microenvironment with abundant K+ cations by enhancing the electric field within the nanopore, accelerating water electrolysis to form more H*, thereby promoting the conversion of alkynes. As a result, the nanoporous Cu50Au50 electrocatalyst achieves highly efficient electrocatalytic semi-hydrogenation of alkynes with 94% conversion, 100% selectivity, and a 92% Faradaic efficiency over wide potential window. This work provides a general guidance of the rational design for high-performance electrocatalytic transfer semi-hydrogenation catalysts.
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BACKGROUND: DNA methylation contributes to the epigenetic regulation of nuclear gene expression, and is associated with plant growth, development, and stress responses. Compelling evidence has emerged that long non-coding RNA (lncRNA) regulates DNA methylation. Previous genetic and physiological evidence indicates that lncRNA-CRIR1 plays a positive role in the responses of cassava plants to cold stress. However, it is unclear whether global DNA methylation changes with CRIR1-promoted cold tolerance. RESULTS: In this study, a comprehensive comparative analysis of DNA methylation and transcriptome profiles was performed to reveal the gene expression and epigenetic dynamics after CRIR1 overexpression. Compared with the wild-type plants, CRIR1-overexpressing plants present gained DNA methylation in over 37,000 genomic regions and lost DNA methylation in about 16,000 genomic regions, indicating a global decrease in DNA methylation after CRIR1 overexpression. Declining DNA methylation is not correlated with decreased/increased expression of the DNA methylase/demethylase genes, but is associated with increased transcripts of a few transcription factors, chlorophyll metabolism and photosynthesis-related genes, which could contribute to the CRIR1-promoted cold tolerance. CONCLUSIONS: In summary, a first set of transcriptome and epigenome data was integrated in this study to reveal the gene expression and epigenetic dynamics after CRIR1 overexpression, with the identification of several TFs, chlorophyll metabolism and photosynthesis-related genes that may be involved in CRIR1-promoted cold tolerance. Therefore, our study has provided valuable data for the systematic study of molecular insights for plant cold stress response.
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Metilação de DNA , Epigênese Genética , Regulação da Expressão Gênica de Plantas , Transcriptoma , RNA Longo não Codificante/genética , Epigenoma , Resposta ao Choque Frio/genética , Temperatura BaixaRESUMO
The regenerative potential of injured axons displays considerable heterogeneity. However, the molecular mechanisms underlying the heterogeneity have not been fully elucidated. Here, we establish a method that can separate spinal motor neurons (spMNs) with low and high regenerative capacities and identify a set of transcripts revealing differential expression between two groups of neurons. Interestingly, oligodendrocyte transcription factor 1 (Olig1), which regulates the differentiation of various neuronal progenitors, exhibits recurrent expression in spMNs with enhanced regenerative capabilities. Furthermore, overexpression of Olig1 (Olig1 OE) facilitates axonal regeneration in various models, and down-regulation or deletion of Olig1 exhibits an opposite effect. By analyzing the overlapped differentially expressed genes after expressing individual Olig factor and functional validation, we find that the role of Olig1 is at least partially through the neurite extension factor 1 (Nrsn1). We therefore identify Olig1 as an intrinsic factor that promotes regenerative capacity of injured axons.
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Axônios , Fatores de Transcrição Hélice-Alça-Hélice Básicos , Perfilação da Expressão Gênica , Regeneração Nervosa , Animais , Axônios/metabolismo , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Regeneração Nervosa/genética , Regeneração Nervosa/fisiologia , Camundongos , Neurônios Motores/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Proteínas do Tecido Nervoso/genética , Camundongos Endogâmicos C57BL , Transcriptoma/genéticaRESUMO
Arsenic is a toxic element widely distributed in the Earth's crust and ranked as a class I human carcinogen. Microbial metabolism makes significant contributions to arsenic detoxification, migration and transformation. Nowadays, research on arsenic is primarily in areas affected by arsenic pollution associated with human health activities. However, the biogeochemical traits of arsenic in the global marine ecosystem remain to be explicated. In this study, we revealed that seawater environments were primarily governed by the process of arsenate reduction to arsenite, while arsenite methylation was predominant in marine sediments which may serve as significant sources of arsenic emission into the atmosphere. Significant disparities existed in the distribution patterns of the arsenic cycle between surface and deep seawaters at middle and low latitudes, whereas these situations tend to be similar in the Arctic and Antarctic oceans. Significant variations were also observed in the taxonomic diversity and core microbial community of arsenic cycling across different marine environments. Specifically, γ-proteobacteria played a pivotal role in the arsenic cycle in the whole marine environment. Temperature, dissolved oxygen and phosphate were the crucial factors that related to these differentiations in seawater environments. Overall, our study contributes to a deeper understanding of the marine arsenic cycle.
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Arsênio , Bactérias , Sedimentos Geológicos , Água do Mar , Poluentes Químicos da Água , Água do Mar/microbiologia , Água do Mar/química , Arsênio/metabolismo , Arsênio/análise , Bactérias/metabolismo , Bactérias/genética , Bactérias/classificação , Sedimentos Geológicos/microbiologia , Sedimentos Geológicos/química , Poluentes Químicos da Água/metabolismo , Poluentes Químicos da Água/análise , Arseniatos/metabolismo , MicrobiotaRESUMO
Heusler alloys are a series of well-established intermetallic compounds with abundant structure and elemental substitutions, which are considered as potentially valuable catalysts for integrating multiple reactions owing to the features of ordered atomic arrangement and optimized electronic structure. Herein, a nanoporous copper titanium tin (np-Cu2TiSn) Heusler alloy is successfully prepared by the (electro)chemical dealloying transformation method, which exhibits high nitrate (NO3-) reduction performance with an NH3 Faradaic efficiency of 77.14 %, an NH3 yield rate of 11.90 mg h-1 mg-1cat, and a stability for 100 h under neutral condition. Significantly, we also convert NO3- to high-purity ammonium phosphomolybdate with NH4+ collection efficiency of 83.8 %, which suggests a practical approach to convert wastewater nitrate into value-added ammonia products. Experiments and theoretical calculations reveal that the electronic structure of Cu sites is modulated by the ligand effect of surrounding Ti and Sn atoms, which can simultaneously enhance the activation of NO3-, facilitate the desorption of NH3, and reduce the energy barriers, thereby boosting the electrochemical nitrate reduction reaction.
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Human cortical neurons (hCNs) exhibit high dendritic complexity and synaptic density, and the maturation process is greatly protracted. However, the molecular mechanism governing these specific features remains unclear. Here, we report that the hominoid-specific gene TBC1D3 promotes dendritic arborization and protracts the pace of synaptogenesis. Ablation of TBC1D3 in induced hCNs causes reduction of dendritic growth and precocious synaptic maturation. Forced expression of TBC1D3 in the mouse cortex protracts synaptic maturation while increasing dendritic growth. Mechanistically, TBC1D3 functions via interaction with MICAL1, a monooxygenase that mediates oxidation of actin filament. At the early stage of differentiation, the TBC1D3/MICAL1 interaction in the cytosol promotes dendritic growth via F-actin oxidation and enhanced actin dynamics. At late stages, TBC1D3 escorts MICAL1 into the nucleus and downregulates the expression of genes related with synaptic maturation through interaction with the chromatin remodeling factor ATRX. Thus, this study delineates the molecular mechanisms underlying human neuron development.
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Mitochondria are pivotal in the modulation of macrophage activation, differentiation, and survival. Furthermore, macrophages are instrumental in the onset and progression of cardiovascular diseases. Hence, it is imperative to investigate the role of mitochondria within macrophages in the context of cardiovascular disease. In this review, we provide an updated description of the origin and classification of cardiac macrophages and also focused on the relationship between macrophages and mitochondria in cardiovascular diseases with respect to (1) proinflammatory or anti-inflammatory macrophages, (2) macrophage apoptosis, (3) macrophage pyroptosis, and (4) macrophage efferocytosis. Clarifying the relationship between mitochondria and macrophages can aid the exploration of novel therapeutic strategies for cardiovascular disease.
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BACKGROUND: Schizotypy, a multidimensional construct with positive, negative, and disorganized dimensions, represents a vulnerability marker for the development of schizophrenia. Although there has been increasing evidence linking schizotypy to emotion regulation (ER) deficits, the specific association between different schizotypal dimensions and alterations in ER strategy use in daily life remains poorly understood. METHODS: Using the experience sampling method (ESM), the present study examined the associations between positive, negative, and disorganized schizotypy and ER strategy use in daily life in a nonclinical young adult sample (N = 258). Participants were instructed to report their ER strategy use 5 times a day for 14 days. Four adaptive ER strategies (reflection, reappraisal, social sharing, and distraction) and two maladaptive ER strategies (suppression and rumination) were included. RESULTS: Multilevel modeling analyses showed that positive schizotypal traits predicted greater use of adaptive ER strategies, while negative schizotypal traits predicted less use of adaptive ER strategies and more frequent use of emotional suppression in daily life. No associations between disorganized schizotypal traits and any ER strategy use were found. CONCLUSION: Schizotypy dimensions are differentiated by preferences for different ER strategies in daily life. The findings suggest a strong association between negative schizotypy and notable dysfunctions in ER, emphasizing the significance of negative schizotypy as a vulnerability factor for psychosis.
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Avaliação Momentânea Ecológica , Regulação Emocional , Transtorno da Personalidade Esquizotípica , Humanos , Transtorno da Personalidade Esquizotípica/fisiopatologia , Regulação Emocional/fisiologia , Feminino , Masculino , Adulto Jovem , Adulto , AdolescenteRESUMO
Nine jatrophane diterpenoids were isolated from the whole plant Euphorbia helioscopia, including two new ones, helioscopnins A (1) and B (2). Comprehensive spectroscopic data analysis and ECD calculations elucidated their structures, including absolute configurations. All compounds were evaluated for bioactivity towards autophagic flux by flow cytometry using HM mCherry-GFP-LC3 cells. Compounds 1, 3, 4, 5, 8, and 9 significantly increased autophagic flux.
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Autofagia , Diterpenos , Euphorbia , Euphorbia/química , Diterpenos/farmacologia , Diterpenos/química , Diterpenos/isolamento & purificação , Autofagia/efeitos dos fármacos , Estrutura Molecular , HumanosRESUMO
Learning, an important activity for both human and animals, has long been a focal point of research. During the learning process, subjects assimilate not only their own information but also information from others, a phenomenon known as social learning. While numerous studies have explored the impact of social feedback as a reward/punishment during learning, few studies have investigated whether social feedback facilitates or inhibits the learning of environmental rewards/punishments. This study aims to test the effects of social feedback on economic feedback and its cognitive processes by using the Iowa Gambling Task (IGT). One hundred ninety-two participants were recruited and categorized into one non-social feedback group and four social feedback groups. Participants in the social feedback groups were informed that after the outcome of each choice, they would also receive feedback from an online peer. This peer was a fictitious entity, with variations in identity (novice or expert) and feedback type (random or effective). The Outcome-Representation Learning model (ORL model) was used to quantify the cognitive components of learning. Behavioral results showed that both the identity of the peer and the type of feedback provided significantly influenced the deck selection, with effective social feedback increasing the ratio of chosen good decks. Results in the ORL model showed that the four social feedback groups exhibited lower learning rates for gain and loss compared to the nonsocial feedback group, which suggested, in the social feedback groups, the impact of the recent outcome on the update of value decreased. Parameters such as forgetfulness, win frequency, and deck perseverance in the expert-effective feedback group were significantly higher than those in the non-social feedback and expert-random feedback groups. These findings suggest that individuals proactively evaluate feedback providers and selectively adopt effective feedback to enhance learning.
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BACKGROUND: Problematic Internet Use (PIU), characterized by failures to control the overuse of internet, is associated with a range of functional impairments. However, there is limited research on the specific impact of PIU on inhibitory control functions, particularly in terms of differentiating between prepotent response inhibition and interference control. Therefore, the main objective of this study is to investigate these two components of inhibitory control in individuals with PIU. METHODS: Thirty participants who met the PIU criteria and 30 control participants were included in the present study. All participants completed the Go/No-Go and Flanker tasks, in which internet-related images and words were used as task stimuli. RESULTS: In the Go/No-Go task, all participants exhibited poorer performance in inhibiting internet-related stimuli compared to internet-unrelated stimuli, during the No-Go trials. In the Flanker task, results revealed a three-way interaction of Group, Stimulus type and Congruency. Specifically, in the incongruent condition, participants with PIU exhibited slower responses for internet-unrelated targets compared to internet-related targets, whereas no similar effect was observed among individuals with low internet use. CONCLUSIONS: The findings suggest that difficulties in controlling the interference effect of internet-related information represent a key dysfunction in inhibitory control of PIU.
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Comportamento Aditivo , Humanos , Uso da Internet , Inibição Psicológica , InternetRESUMO
BACKGROUND: Severe myocarditis is often accompanied by cardiac fibrosis, but the underlying mechanism has not been fully elucidated. CXCL4 is a chemokine that has been reported to have pro-inflammatory and profibrotic functions. The exact role of CXCL4 in cardiac fibrosis remains unclear. METHODS: Viral myocarditis (VMC) models were induced by intraperitoneal injection of Coxsackie B Type 3 (CVB3). In vivo, CVB3 (100 TCID50) and CVB3-AMG487 (CVB3: 100 TCID50; AMG487: 5 mg/kg) combination were administered in the VMC and VMC+AMG487 groups, respectively. Hematoxylin and eosin staining, severity score, Masson staining, and immunofluorescence staining were performed to measure myocardial morphology in VMC. Enzyme-linked immunosorbent assay (ELISA) and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were performed to quantify inflammatory factors (IL-1ß, IL-6, TNF-α, and CXCL4). Aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine kinase-myocardial band (CK-MB) levels were analyzed by commercial kits. CXCL4, CXCR3B, α-SMA, TGF-ß1, Collagen I, and Collagen III were determined by Western blot and immunofluorescence staining. RESULTS: In vivo, CVB3-AMG487 reduced cardiac injury, α-SMA, Collagen I and Collagen III levels, and collagen deposition in VMC+AMG487 group. Additionally, compared with VMC group, VMC+AMG group decreased the levels of inflammatory factors (IL-1ß, IL-6, and TNF-α). In vitro, CXCL4/CXCR3B axis activation TGF-ß1/Smad2/3 pathway promote mice cardiac fibroblasts differentiation. CONCLUSION: CXCL4 acts as a profibrotic factor in TGF-ß1/Smad2/3 pathway-induced cardiac fibroblast activation and ECM synthesis, and eventually progresses to cardiac fibrosis. Therefore, our findings revealed the role of CXCL4 in VMC and unveiled its underlying mechanism. CXCL4 appears to be a potential target for the treatment of VMC.
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Acetamidas , Infecções por Coxsackievirus , Miocardite , Pirimidinonas , Camundongos , Animais , Fator de Crescimento Transformador beta1/metabolismo , Fator de Necrose Tumoral alfa , Interleucina-6 , Colágeno , FibroseRESUMO
Severe myocarditis is often accompanied by cardiac fibrosis, but the underlying mechanism has not been fully elucidated. NOD-like receptor protein 3 (NLRP3) inflammation is involved in the development of myocarditis and is closely related to the form of cell death. Inhibiting pyroptosis mediated by NLRP3 inflammasome can reduce cardiac fibrosis, although its exact mechanism remains unknown. In this study, we induced Viral myocarditis (VMC) via infection of CVB3 to explore the relationship between pyroptosis and fibrosis. Our results showed that intraperitoneal injection of an NLRP3 inhibitor MCC950 or use of NLRP3-/- mice inhibited cardiac pyroptosis mediated by NLRP3 inflammasome in VMC. CXCL4 is a chemokine that has been reported to have pro-inflammatory and pro-fibrotic functions. In VMC, we further found that pyroptosis of Mouse myocardial fibroblasts (MCF) promoted the secretion of CXCL4 by activating Wnt/ß-Catenin signaling. Subsequently, the transcriptome sequencing data showed that CXCL4 could promote cardiac fibrosis by activating PI3K/AKT pathway. In summary, infection of CVB3 induced host oxidative stress to further activate the NLRP3 inflammasome and ultimately lead to heart pyroptosis, in which MCF secreted CXCL4 by activating Wnt/ß-Catenin signaling and CXCL4 participated in cardiac fibrosis by activating PI3K/AKT pathway. Therefore, our findings revealed the role of CXCL4 in VMC and unveiled its underlying mechanism. CXCL4 appears to be a potential target for the treatment of VMC.
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Fibrose , Miocardite , Proteína 3 que Contém Domínio de Pirina da Família NLR , Fator Plaquetário 4 , Piroptose , Animais , Humanos , Masculino , Camundongos , Fibroblastos/metabolismo , Furanos/farmacologia , Indenos , Inflamassomos/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Knockout , Miocardite/metabolismo , Miocárdio/patologia , Miocárdio/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Fator Plaquetário 4/metabolismo , Transdução de Sinais , Sulfonamidas/farmacologia , Sulfonas/farmacologiaRESUMO
Peripheral artery disease (PAD) shares common clinical risk factors, for example, endothelial dysfunction, with preserved ejection fraction (LVEF) heart failure (HFpEF). Whether PAD is associated with preclinical systolic dysfunction and higher HF risk among individuals presenting preserved LVEF remains uncertain. We retrospectively included outpatients with at least one known or established cardiovascular (CV) risk factor with LVEF ≥ 50%. Patients were categorized into high risk and low risk of developing PAD (PAD vs Non-PAD) by ankle-brachial index (ABI) (≤ 0.90 or > 1.4) and further stratified based on their history of HFpEF (HFpEF vs. Non-HFpEF), resulting in the formation of four distinct strata. Preclinical systolic dysfunction was defined using dedicated speckle-tracking algorithm. A total of 2130 consecutive patients were enrolled in the study, with a median follow-up of 4.4 years. The analysis revealed a higher prevalence of high risk of developing PAD in patients with HFpEF compared to those without HFpEF (25.1% vs. 9.4%). Both high risk of developing PAD and HFpEF were independently associated with preclinical systolic dysfunction (global longitudinal strain, GLS ≥ - 18%) (odds ratio, OR: 1.38; 95% confidence interval, CI: 1.03-1.86). In comparison to patients at low risk of developing PAD without HFpEF (Non-PAD/Non-HFpEF group), those categorized as having a high risk of developing PAD with HFpEF (PAD/HFpEF group) exhibited the most impaired GLS and a heightened susceptibility to heart failure hospitalization (hazard ratio, HR: 6.51; 95% CI: 4.43-9.55), a twofold increased risk of all-cause mortality (HR: 2.01; 95% CI: 1.17-3.38), cardiovascular mortality (HR: 2.44; 95% CI: 1.08-5.51), and non-cardiovascular mortality (HR: 1.78; 95% CI: 0.82-3.84). A high risk of developing PAD was strongly linked to impaired preclinical systolic function and an increased likelihood for subsequent hospitalization for HF, all-cause mortality, CV mortality and non-CV mortality. There is a clear need for preventive strategies aimed at reducing hospitalizations for HF and mortality in this high-risk population.
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Insuficiência Cardíaca , Doença Arterial Periférica , Disfunção Ventricular Esquerda , Humanos , Volume Sistólico , Função Ventricular Esquerda , Estudos Retrospectivos , Índice Tornozelo-Braço , Fatores de Risco , PrognósticoRESUMO
BACKGROUND: Genetic factors contribute to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Advances in genetic testing have enabled the identification of hereditary kidney diseases, including those caused by LMX1B mutations. LMX1B mutations can lead to nail-patella syndrome (NPS) or nail-patella-like renal disease (NPLRD) with only renal manifestations. CASE PRESENTATION: The proband was a 13-year-old female who was diagnosed with nephrotic syndrome at the age of 6. Then she began intermittent hormone and drug therapy. When she was 13 years old, she was admitted to our hospital due to sudden chest tightness, which progressed to end-stage kidney disease (ESRD), requiring kidney replacement therapy. Whole-Exome Sequencing (WES) results suggest the presence of LMX1B gene mutation, c.737Gâ >â T, p.Arg246Leu. Tracing her family history, we found that her father, grandmother, uncle and 2 cousins all had hematuria, or proteinuria. In addition to the grandmother, a total of 9 members of the family performed WES. The members with kidney involved all carry the mutated gene. Healthy members did not have the mutated gene. It is characterized by co-segregation of genotype and phenotype. We followed the family for 9 year, the father developed ESRD at the age of 50 and started hemodialysis treatment. The rest patients had normal renal function. No extra-renal manifestations associated with NPS were found in any member of the family. CONCLUSIONS: This study has successfully identified missense mutation, c.737Gâ >â T (p.Arg246Leu) in the homeodomain, which appears to be responsible for isolated nephropathy in the studied family. The arginine to leucine change at codon 246 likely disrupts the DNA-binding homeodomain of LMX1B. Previous research has documented 2 types of mutations at codon R246, namely R246Q and R246P, which are known to cause NPLRD. The newly discovered mutation, R246L, is likely to be another novel mutation associated with NPLRD, thus expanding the range of mutations at the crucial renal-critical codon 246 that contribute to the development of NPLRD. Furthermore, our findings suggest that any missense mutation occurring at the 246th amino acid position within the homeodomain of the LMX1B gene has the potential to lead to NPLRD.
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Falência Renal Crônica , Síndrome da Unha-Patela , Nefrite Hereditária , Humanos , Feminino , Adolescente , Fatores de Transcrição/genética , Proteínas com Homeodomínio LIM/genética , Nefrite Hereditária/genética , Mutação , Falência Renal Crônica/genética , Falência Renal Crônica/terapia , Códon , China , Proteínas de Homeodomínio/genéticaRESUMO
Aeration plays a crucial role in accelerating the secondary compression of municipal solid waste (MSW) for the scientific implementation of aerobic bioreactor technology. There are few comparative reports on the secondary compaction characteristics of MSW in aerobic and anaerobic bioreactors. In this study, six long-term compression tests were conducted to analyze the impact of aeration on MSW compression characteristics, considering two degradation conditions (i.e. aerobic and anaerobic conditions) and three overburden stresses (i.e. 30, 50 and 100 kPa). Model-fitting analysis was employed to examine the data from the tests and exiting literatures. The results showed that aeration effectively increased the rate of secondary compression, and slightly enhanced the steady-state secondary compression strain. In addition, these enhancements tended to decrease with increasing stresses. The increment ratio of the secondary compression rate constant (Rk) was concentrated in the range of 25 % to 100 %, and increases with the increase of aeration rate. The increment ratio of the steady-state secondary compression strain (Rε) ranged from 10 % to 90 %, for the MSW with higher content of paper and wood exhibited higher Rε. The advance ratio of the secondary compression stabilization time (Rt) fell within the range of 20-50 %, and Rt is higher when the moisture content is in the range of 50-65 %. These findings provide valuable guidance on the accelerated stabilization in aerobic bioreactors, providing practical references for the application of aerobic technology to informal landfills.
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Eliminação de Resíduos , Resíduos Sólidos , Resíduos Sólidos/análise , Eliminação de Resíduos/métodos , Anaerobiose , Reatores Biológicos , Instalações de Eliminação de ResíduosRESUMO
OBJECT: To obtain Pulmonary Inflammation Index scores from imaging chest CT and combine it with clinical correlates of viral pneumonia to predict the risk and severity of viral pneumonia using a computer learning model. METHODS: All patients with suspected viral pneumonia on CT examination admitted to The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University from December 2022 to March 2023 were retrospectively selected. The respiratory viruses were monitored by RT-PCR and categorized into patients with viral pneumonia and those with non-viral pneumonia. The extent of lung inflammation was quantified according to the Pulmonary Inflammation Index score (PII). Information on patient demographics, comorbidities, laboratory tests, pathogenetic testing, and radiological data were collected. Five machine learning models containing Random Forest(RF), Radial Basis Function Neural Network (RBFNN), Support Vector Machine (SVM), K Nearest Neighbour Algorithm (KNN), and Kernel Ridge Regression (KRR) were used to predict the risk of onset and severity of viral pneumonia based on the clinically relevant factors or PII. RESULTS: Among the five models, the SVM model performed best in ACC (76.75 %), SN (73.99 %), and F1 (72.42 %) and achieved a better area under the receiver operating characteristic curve (ROC) (0.8409) when predicting the risk of developing viral pneumonia. RF had the best overall classification accuracy in predicting the severity of viral pneumonia, especially in predicting pneumonia with a PII classification of grade I, the RF model achieved an accuracy of 98.89%. CONCLUSION: Machine learning models are valuable in assessing the risk of viral pneumonia. Meanwhile, machine learning models confirm the importance in predicting the severity of viral pneumonia through PII. The establishment of machine learning models for predicting the risk and severity of viral pneumonia promotes the further development of machine learning in the medical field.
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Pneumonia Viral , Humanos , Estudos Retrospectivos , Algoritmos , Análise por Conglomerados , Aprendizado de MáquinaRESUMO
BACKGROUND: Metabolites play critical roles in regulating nutritional qualities of plants, thereby influencing their consumption and human health. However, the genetic basis underlying the metabolite-based nutrient quality and domestication of root and tuber crops remain largely unknown. RESULTS: We report a comprehensive study combining metabolic and phenotypic genome-wide association studies to dissect the genetic basis of metabolites in the storage root (SR) of cassava. We quantify 2,980 metabolic features in 299 cultivated cassava accessions. We detect 18,218 significant marker-metabolite associations via metabolic genome-wide association mapping and identify 12 candidate genes responsible for the levels of metabolites that are of potential nutritional importance. Me3GT, MeMYB4, and UGT85K4/UGT85K5, which are involved in flavone, anthocyanin, and cyanogenic glucoside metabolism, respectively, are functionally validated through in vitro enzyme assays and in vivo gene silencing analyses. We identify a cluster of cyanogenic glucoside biosynthesis genes, among which CYP79D1, CYP71E7b, and UGT85K5 are highly co-expressed and their allelic combination contributes to low linamarin content. We find MeMYB4 is responsible for variations in cyanidin 3-O-glucoside and delphinidin 3-O-rutinoside contents, thus controlling SR endothelium color. We find human selection affects quercetin 3-O-glucoside content and SR weight per plant. The candidate gene MeFLS1 is subject to selection during cassava domestication, leading to decreased quercetin 3-O-glucoside content and thus increased SR weight per plant. CONCLUSIONS: These findings reveal the genetic basis of cassava SR metabolome variation, establish a linkage between metabolites and agronomic traits, and offer useful resources for genetically improving the nutrition of cassava and other root crops.
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Estudo de Associação Genômica Ampla , Manihot , Humanos , Manihot/genética , Domesticação , Quercetina/metabolismo , Glucosídeos , NutrientesRESUMO
The present study aimed to investigate the effect of Xianglian Pills(XLP) on lipid metabolism in obese mice and explore the underlying mechanism based on network pharmacology and intestinal flora. Firstly, network pharmacology was used to predict the possible effect of XLP on obesity. Secondly, an obese mouse model induced by a high-fat diet was established to observe changes in mouse body weight, adiposity index, liver and adipose tissue pathology. Lipid profiles, liver and kidney function markers, insulin content, and the expression of recombinant uncoupling protein 1(UCP-1) and PR structural domain protein 16(PRDM16) were measured. The 16S rRNA gene sequencing technology was used to analyze the changes in the intestinal flora. Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis showed that XLP mainly played a role in improving obesity by regulating lipolysis, type 2 diabetes mellitus, and insulin resistance. The results of animal experiments showed that XLP significantly reduced body weight, adiposity, blood lipid levels, and serum insulin levels in obese mice, while enhancing the expression of UCP-1 and PRDM16 in adipose tissue without causing damage to the liver or kidneys. The 16S rRNA gene sequencing results showed that XLP decreased the Firmicutes/Bacteroidetes(F/B) ratio at the phylum level, increased the relative abundance of Akkermansia and Bacteroides at the family and genus levels, and reduced the abundance of Allobaculum. Therefore, XLP can effectively improve lipid metabolism disorders in high-fat diet-induced obese mice, and the mechanism is related to the improvement of brown adipose function, the browning of white fat, the accelerated lipid metabolism, and the improvement of intestinal flora. However, its effect on promoting the conversion of white adipose to brown adipose still needs to be further studied.