RESUMO
Objective: This study aimed to determine the risk factors associated with fluctuations in nucleic acid CT values in patients infected with the Omicron variant during an outbreak at a hospital in Changchun city. Methods: A retrospective analysis was conducted on general information, medical history, vaccination history, and laboratory test data of COVID-19 patients infected with the Omicron variant and admitted to the hospital in Changchun from March 2022 to April 2022. The study aimed to explore the factors influencing nucleic acid CT value fluctuations in COVID-19 patients infected with the Omicron variant in Changchun city. Results: Fluctuations in nucleic acid CT values were significantly correlated with occupation composition (p = 0.030), hospital stay duration (p = 0.000), heart rate (p = 0.026), creatinine (p = 0.011), platelet count (p = 0.000), glutamic-pyruvic transaminase (p = 0.045), and glutamic oxaloacetic transaminase (p = 0.017). Binary logistic regression analysis revealed significant correlations between hospital stay duration (p = 0.000), platelet count (p = 0.019), heart rate (p = 0.036), and nucleic acid CT value fluctuations (p < 0.05), indicating that they were independent risk factors. Red blood cell count was identified as a factor influencing nucleic acid CT value fluctuations in Group A patients. Occupation composition, direct bilirubin, and platelet count were identified as factors influencing nucleic acid CT value fluctuations in Group B patients. Further binary logistic regression analysis indicated that occupational composition and direct bilirubin are significant independent factors for nucleic acid CT value fluctuations in Group B patients, positively correlated with occupational risk and negatively correlated with direct bilirubin. Conclusion: Therefore, enhancing patients' immunity, increasing physical exercise to improve myocardial oxygen consumption, reducing the length of hospital stays, and closely monitoring liver function at the onset of hospitalization to prevent liver function abnormalities are effective measures to control fluctuations in nucleic acid CT values.
Assuntos
COVID-19 , SARS-CoV-2 , Humanos , COVID-19/diagnóstico por imagem , Estudos Retrospectivos , Masculino , Feminino , Pessoa de Meia-Idade , China/epidemiologia , Adulto , Fatores de Risco , IdosoRESUMO
Background: Cervical cancer (CC) is a highly malignant gynecological cancer with a direct causal link to inflammation, primarily resulting from persistent high-risk human papillomavirus (HPV) infection. Given the challenges in early detection and mid to late-stage treatment, our research aims to identify inflammation-associated immune biomarkers in CC. Methods: Using a bioinformatics approach combined with experimental validation, we integrated two CC datasets (GSE39001 and GSE63514) in the Gene Expression Omnibus (GEO) to eliminate batch effects. Immune-related inflammation differentially expressed genes (DGEs) were obtained by R language identification. Results: This analysis identified 37 inflammation-related DEGs. Subsequently, we discussed the different levels of immune infiltration between CC cases and controls. Weighted gene co-expression network analysis (WGCNA) identified seven immune infiltration-related modules in CC. We identified 15 immune DEGs associated with inflammation at the intersection of these findings. In addition, we constructed a protein interaction network using the String database and screened five hub genes using "CytoHubba": CXC chemokine ligand 8 (CXCL8), CXC chemokine ligand 10 (CXCL10), CX3C chemokine receptor 1 (CX3CR1), Fc gamma receptors 3B (FCGR3B), and SELL. The expression of these five genes in CC was determined by PCR experiments. In addition, we assessed their diagnostic value and further analyzed the association of immune cells with them. Conclusions: Five inflammation- and immune-related genes were identified, aiming to provide new directions for early diagnosis and mid to late-stage treatment of CC from multiple perspectives.
RESUMO
OBJECTIVE: Coronary artery lesions (CALs) are a major complication of Kawasaki disease (KD); however, data on CAL incidence and risk factors in recurrent KD are limited. METHODS: Ninety-seven children with recurrent KD were retrospectively enrolled from 2013 to 2022, and CAL incidence was tracked during admission, discharge, and during follow-up. RESULTS: Initially, 27.8% had CAL at admission and discharge, declining to 7.2% at 12 months post-discharge. Most patients (66 of 97, 68.0%) did not exhibit CAL at any of the time points, 7 cases presented CAL at all time points, indicating a persistent CAL. The remaining 20 cases presented CAL at admission but recovered at discharge or during follow-up. Notably, transient CALs had presented at discharge, or during the follow-up, but finally resolved at 12 months after discharge. Notably, prior IVIG resistance and increased prothrombin time seemed associated with CAL in recurrent KD, suggesting they could help identify patients needing close monitoring. CONCLUSION: The study highlights decreasing CAL incidence over time in recurrent KD but with diverse patterns, emphasizing the importance of monitoring and further investigations to confirm these findings.
Assuntos
Síndrome de Linfonodos Mucocutâneos , Recidiva , Humanos , Síndrome de Linfonodos Mucocutâneos/epidemiologia , Masculino , Incidência , Feminino , Pré-Escolar , Estudos Retrospectivos , Lactente , Criança , Doença da Artéria Coronariana/epidemiologia , Imunoglobulinas Intravenosas/uso terapêutico , Fatores de Risco , Vasos Coronários/patologia , Vasos Coronários/diagnóstico por imagem , SeguimentosRESUMO
The issue of material failure attributed to microbiologically influenced corrosion (MIC) is escalating in seriousness. Microorganisms not only facilitate corrosion but certain beneficial microorganisms also impede its occurrence. This study explored the impact of marine B. velezensis on the corrosion behavior of X65 steel in simulated offshore oilfield produced water. B. velezensis exhibited rapid growth in the initial stages, and the organic acid metabolites were found to promote corrosion. Subsequently, there was an increase in cross-linked "networked" biofilms products, a significant rise in the prismatic shape of corrosion products, and a tendency for continuous development in the middle and late stages. The organic/inorganic mineralized film layer formed on the surface remained consistently complete. Metabolic products of amino acid corrosion inhibitors were also observed to be adsorbed into the film. B. velezensis altered the kinetics of the X65 steel cathodic reaction, resulting in a deceleration of the electrochemical reaction rate. The mineralization induced by B. velezensis effectively slowed down the corrosion rate of X65 steel.
Assuntos
Bacillus , Aço , Aço/química , Água , Corrosão , Biomineralização , Campos de Petróleo e Gás , BiofilmesRESUMO
Late flowering is a serious bottleneck in pumpkin (Cucurbita moschata Duch.) agriculture production. Although key genes governing flowering time have been reported in many species, the regulatory network of flowering in pumpkin remains largely obscure, thereby impeding the resolution of industry-wide challenges associated with delayed fruit ripening in pumpkin cultivation. Here, we report an early flowering pumpkin germplasm accession (LXX-4). Using LXX-4 and a late flowering germplasm accession (HYM-9), we constructed an F2 segregation population. A significant difference in FLOWERING LOCUS T-LIKE 2 (FTL2) expression level was identified to be the causal factor of the flowering time trait discrepancy in LXX-4 and HYM-9. Moreover, we have shown that a 21 bp InDel in the FTL2 promoter was the key reason for the waxing and waning of its transcript level. The 21 bp deletion excluded a repressor-AGL19 and recruited activators-BBX7, WRKY40 and SVP to the FTL2 promoter in LXX-4. Together, our data add a useful element to our knowledge which could be used to simplify breeding efforts for early-maturing pumpkin.
Assuntos
Cucurbita , Cucurbita/genética , Cucurbita/metabolismo , FenótipoRESUMO
During heart development, a well-characterized network of transcription factors initiates cardiac gene expression and defines the precise timing and location of cardiac progenitor specification. However, our understanding of the post-initiation transcriptional events that regulate cardiac gene expression is still incomplete. The PAF1C component Rtf1 is a transcription regulatory protein that modulates pausing and elongation of RNA Pol II, as well as cotranscriptional histone modifications. Here we report that Rtf1 is essential for cardiogenesis in fish and mammals, and that in the absence of Rtf1 activity, cardiac progenitors arrest in an immature state. We found that Rtf1's Plus3 domain, which confers interaction with the transcriptional pausing and elongation regulator Spt5, was necessary for cardiac progenitor formation. ChIP-seq analysis further revealed changes in the occupancy of RNA Pol II around the transcription start site (TSS) of cardiac genes in rtf1 morphants reflecting a reduction in transcriptional pausing. Intriguingly, inhibition of pause release in rtf1 morphants and mutants restored the formation of cardiac cells and improved Pol II occupancy at the TSS of key cardiac genes. Our findings highlight the crucial role that transcriptional pausing plays in promoting normal gene expression levels in a cardiac developmental context.
RESUMO
Adipose-derived mesenchymal stem cells (ADSCs) are multipotent stromal cells and play huge role in forming and repairing bone tissues. Emerging evidence shows that MicroRNAs (miRNAs) are involved in ADSCs differentiation. Here, we explored the role of miR-150-5p and its related mechanisms in ADSCs osteogenesis. Real-time PCR was used to determine miR-150-5p expression during ADSCs osteogenesis. miR-150-5p inhibitors, miR-150-5p ADV or short hairpin RNA (shRNA) of Notch3 were transfected to ADSCs for analyzing the effects on osteogenesis. The mixture of hydroxyapatite/tricalcium phosphate (HA/TCP) ceramic powders and transfected ADSCs was implanted into BALB/C nude mice. Micro-CT and histological methods were performed to evaluate the new bone formation. Compared with negative control (NC) and miR-150-5p overexpression, inhibition of miR-150-5p increased ADSCs osteogenesis by regulating Notch3. MiR-150-5p overexpression decreased the expression of pFAK, pERK1/2, and RhoA, while these were up-regulated when miR-150-5p was inhibited, or notch3 was silenced. Furthermore, miR-150-5p inhibition partially reversed the suppression effect of notch3 knockdown on osteogenesis in vitro and in vivo. This study demonstrated the critical function of miR-150-5p during osteogenesis. The combination of ADSCs with miR-150-5p inhibition and HA/TCP might be a promising strategy for bone damage repair. STATEMENT OF SIGNIFICANCE: Osteoporosis is a common chronic metabolic bone disease in humans. Bone tissue engineering based on mesenchymal stem cells, biomaterials, and growth factors, provides a promising way to treat osteoporosis and bone defects. ADSCs commonly differentiate into adipose cells, they can also differentiate into osteogenic cell lineages. Nucleic acids and protein have usually been considered as regulators of ADSCs osteogenic differentiation. In the current study, we demonstrated the combination of ADSCs with miR-150-5p inhibition and hydroxyapatite/tricalcium phosphate ceramic powders enhanced bone regeneration. Furthermore, miR-150-5p/Notch3 axis regulating osteogenesis via the FAK/ERK1/2 and RhoA pathway was assessed. The current study showed the application of ADSCs in bone regeneration might be a promising strategy for osteoporosis and bone damage repairing.
Assuntos
Células-Tronco Mesenquimais , MicroRNAs , Humanos , Camundongos , Animais , Osteogênese/genética , Pós/metabolismo , Pós/farmacologia , Tecido Adiposo , Camundongos Nus , Camundongos Endogâmicos BALB C , MicroRNAs/genética , MicroRNAs/metabolismo , Diferenciação Celular/genética , RNA Interferente Pequeno/farmacologia , Hidroxiapatitas/farmacologia , Células Cultivadas , Proteína rhoA de Ligação ao GTPRESUMO
Pulmonary fibrosis is a chronic, progressive lung disease characterized by excessive scarring of lung tissue, and its pathophysiological mechanisms have not been fully elucidated. Immune cells play a key role in many diseases, and this study aims to explore the causal link between immune cell characteristics and pulmonary fibrosis using Mendelian randomization. Utilizing the public GWAS database Open GWAS, this study collected whole-genome association study datasets of peripheral blood immune phenotypes and summary data of GWAS related to pulmonary fibrosis. Through Mendelian randomization (MR) analysis, we identified single nucleotide polymorphisms (SNPs) significantly associated with immune traits as instrumental variables. After pleiotropy and heterogeneity tests, causal effects were assessed using methods such as inverse-variance weighted (IVW), weighted median, and MR-Egger. Comprehensive MR analysis indicated a significant causal relationship between various immune cell types, including regulatory T cells (Tregs), natural killer (NK) cells, and specific monocyte subgroups, with the risk of pulmonary fibrosis. Specifically, phenotypes such as Activated & resting Treg %CD4+, CCR2-positive monocytes, and CD16-CD56 positive NK cells were associated with a reduced risk of pulmonary fibrosis. In contrast, CD8â +â T cell subgroups were associated with an increased risk. This study provides evidence of a causal relationship between immune cell characteristics and pulmonary fibrosis, highlighting the protective role of regulatory T cells and specific NK cell subgroups, as well as the potential harm of CD8â +â T cell subgroups. These findings offer new insights into the immunoregulatory mechanisms of pulmonary fibrosis and the development of novel therapeutic strategies.
Assuntos
Fibrose Pulmonar , Humanos , Fibrose Pulmonar/genética , Análise da Randomização Mendeliana , Fatores Imunológicos , Linfócitos T CD8-Positivos , Causalidade , Estudo de Associação Genômica AmplaRESUMO
Congenital heart defects occur in almost 80% of patients with CHARGE syndrome, a sporadically occurring disease causing craniofacial and other abnormalities due to mutations in the CHD7 gene. Animal models have been generated to mimic CHARGE syndrome; however, heart defects are not extensively described in zebrafish disease models of CHARGE using morpholino injections or genetic mutants. Here, we describe the co-occurrence of craniofacial abnormalities and heart defects in zebrafish chd7 mutants. These mutant phenotypes are enhanced in the maternal zygotic mutant background. In the chd7 mutant fish, we found shortened craniofacial cartilages and extra cartilage formation. Furthermore, the length of the ventral aorta is altered in chd7 mutants. Many CHARGE patients have aortic arch anomalies. It should be noted that the aberrant branching of the first branchial arch artery is observed for the first time in chd7 fish mutants. To understand the cellular mechanism of CHARGE syndrome, neural crest cells (NCCs), that contribute to craniofacial and cardiovascular tissues, are examined using sox10:Cre lineage tracing. In contrast to its function in cranial NCCs, we found that the cardiac NCC-derived mural cells along the ventral aorta and aortic arch arteries are not affected in chd7 mutant fish. The chd7 fish mutants we generated recapitulate some of the craniofacial and cardiovascular phenotypes found in CHARGE patients and can be used to further determine the roles of CHD7.
RESUMO
As the world's biggest carbon dioxide (CO2) emitter and the largest developing country, China faces daunting challenges to peak its emissions before 2030 and achieve carbon neutrality within 40 years. This study fully considered the carbon-neutrality goal and the temperature rise constraints required by the Paris Agreement, by developing six long-term development scenarios, and conducting a quantitative evaluation on the carbon emissions pathways, energy transformation, technology, policy and investment demand for each scenario. This study combined both bottom-up and top-down methodologies, including simulations and analyses of energy consumption of end-use and power sectors (bottom-up), as well as scenario analysis, investment demand and technology evaluation at the macro level (top-down). This study demonstrates that achieving carbon neutrality before 2060 translates to significant efforts and overwhelming challenges for China. To comply with the target, a high rate of an average annual reduction of CO2 emissions by 9.3% from 2030 to 2050 is a necessity, which requires a huge investment demand. For example, in the 1.5 °C scenario, an investment in energy infrastructure alone equivalent to 2.6% of that year's GDP will be necessary. The technological pathway towards carbon neutrality will rely highly on both conventional emission reduction technologies and breakthrough technologies. China needs to balance a long-term development strategy of lower greenhouse gas emissions that meets both the Paris Agreement and the long-term goals for domestic economic and social development, with a phased implementation for both its five-year and long-term plans.
RESUMO
BACKGROUND: Lung cancer is a high-incidence cancer, and it is also the most common cause of cancer death worldwide. 80-85% of lung cancer cases can be classified as non-small cell lung cancer (NSCLC). METHODS: NSCLC transcriptome data and clinical information were downloaded from the TCGA database and GEO database. Firstly, we analyzed and identified the differentially expressed genes (DEGs) between non-metastasis group and metastasis group of NSCLC in the TCGA database, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) were consulted to explore the functions of the DEGs. Thereafter, univariate Cox regression and LASSO Cox regression algorithms were applied to identify prognostic metastasis-related signature, followed by the construction of the risk score model and nomogram for predicting the survival of NSCLC patients. GSEA analyzed that differentially expressed gene-related signaling pathways in the high-risk group and the low-risk group. The survival of NSCLC patients was analyzed by the Kaplan-Meier method. ROC curve was plotted to evaluate the accuracy of the model. Finally, the GEO database was further applied to verify the metastasisrelated prognostic signature. RESULTS: In total, 2058 DEGs were identified. GO functions and KEGG pathways analysis results showed that the DEGs mainly concentrated in epidermis development, skin development, and the pathway of Neuro active ligand -receptor interaction in cancer. A six-gene metastasis-related risk signature including C1QL2, FLNC, LUZP2, PRSS3, SPIC, and GRAMD1B was constructed to predict the overall survival of NSCLC patients. The reliability of the gene signature was verified in GSE13213. The NSCLC patients were grouped into low-risk and high-risk groups based on the median value of risk scores. And low-risk patients had lower risk scores and longer survival time. Univariate and multivariate Cox regression verified that this signature was an independent risk factor for NSCLC. CONCLUSION: Our study identified 6 metastasis biomarkers in the NSCLC. The biomarkers may contribute to individual risk estimation, survival prognosis.
Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Carcinoma Pulmonar de Células não Pequenas/patologia , Proteínas de Ligação a DNA/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/patologia , Prognóstico , Reprodutibilidade dos Testes , Tripsina/genética , Tripsina/metabolismoRESUMO
Non-Hermitian topological edge states have many intriguing properties, however, to date, they have mainly been discussed in terms of bulk-boundary correspondence. Here, we propose using a bulk property of diffusion coefficients for probing the topological states and exploring their dynamics. The diffusion coefficient was found to show unique features with the topological phase transitions driven by parity-time (PT)-symmetric non-Hermitian discrete-time quantum walks as well as by Hermitian ones, despite the fact that artificial boundaries are not constructed by an inhomogeneous quantum walk. For a Hermitian system, a turning point and abrupt change appears in the diffusion coefficient when the system is approaching the topological phase transition, while it remains stable in the trivial topological state. For a non-Hermitian system, except for the feature associated with the topological transition, the diffusion coefficient in the PT-symmetric-broken phase demonstrates an abrupt change with a peak structure. In addition, the Shannon entropy of the quantum walk is found to exhibit a direct correlation with the diffusion coefficient. The numerical results presented herein may open up a new avenue for studying the topological state in non-Hermitian quantum walk systems.
RESUMO
Quantum key distribution (QKD) can share an unconditional secure key between two remote parties, but the deviation between theory and practice will break the security of the generated key. In this paper, we evaluate the security of QKD with weak basis-choice flaws, in which the random bits used by Alice and Bob are weakly controlled by Eve. Based on the definition of Li et al. (Sci Rep 5:16200, 2015) and GLLP's analysis, we obtain a tight and analytical bound to estimate the phase error and key rate for both the single photon source and the weak coherent source. Our approach largely increases the key rate from that of the original approach. Finally, we investigate and confirm the security of BB84-QKD with a practical commercial devices.