RESUMO
Deep-space optical communication has garnered increasing attention for its high data transfer rate, wide bandwidth, and high transmission speed. However, coronal plasma turbulence severely degrades optical signals during superior solar conjunction. In this study, we introduce the models for plasma density and generalized non-Kolmogorov turbulence power spectrum. Based on these models, we derive the variance of the phase fluctuations with the assistance of the Rytov theory in the weak turbulence regime involving various variables, such as turbulence outer scale, spectral index, relative fluctuation factor, and wavelength. Subsequently, we evaluate the bit error ratio (BER) performance of the deep-space optical communication system, considering phase fluctuations and intensity scintillations, under binary phase shift keying modulation. Numerical calculations reveal that small heliocentric distance, large relative fluctuation factor and spectral index, could induce severe phase fluctuations and high BER. Fortunately, the effects of the plasma irregularities on the BER performance can be mitigated by short optical wavelength under large outer scale.
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Endothelial permeability deterioration is involved in ventilator-induced lung injury (VILI). The integrality of vascular endothelial glycocalyx (EG) is closely associated with endothelial permeability. The hypothesis was that vascular EG shedding participates in VILI through promoting endothelial permeability. In the present study, male Sprague-Dawley (SD) rats were ventilated with high tidal volume (VT =40 ml/kg) or low tidal volume (VT =8 ml/kg) to investigate the effects of different tidal volume and ventilation durations on EG in vivo. We report disruption of EG during the period of high tidal volume ventilation characterized by increased glycocalyx structural components (such as syndecan-1, heparan sulfate, hyaluronan) in the plasma and decreased the expression of syndecan-1 in the lung tissues. Mechanistically, the disruption of EG was associated with increased proinflammatory cytokines and matrix metalloproteinase in the lung tissues. Collectively, these results demonstrate that the degradation of EG is involved in the occurrence and development of VILI in rats, and the inflammatory mechanism mediated by activation of the NF-κB signaling pathway may be partly responsible for the degradation of EG in VILI in rats. This study enhances our understanding of the pathophysiological processes underlying VILI, shedding light on potential therapeutic targets to mitigate VILI.
Assuntos
Sindecana-1 , Lesão Pulmonar Induzida por Ventilação Mecânica , Ratos , Masculino , Animais , Ratos Sprague-Dawley , Glicocálix/metabolismo , Lesão Pulmonar Induzida por Ventilação Mecânica/tratamento farmacológico , Lesão Pulmonar Induzida por Ventilação Mecânica/metabolismo , Pulmão/metabolismoRESUMO
OBJECTIVES: In order to assist junior doctors in better diagnosing apical periodontitis (AP), an artificial intelligence AP grading system was developed based on deep learning (DL) and its reliability and accuracy were evaluated. METHODS: 120 cone-beam computed tomography (CBCT) images were selected to construct a classification dataset with four categories, which were divided by CBCT periapical index (CBCTPAI), including normal periapical tissue, CBCTPAI 1-2, CBCTPAI 3-5 and young permanent teeth. Three classic algorithms (ResNet50/101/152) as well as one self-invented algorithm (PAINet) were compared with each other. PAINet were also compared with two recent Transformer-based models and three attention models. Their performance was evaluated by accuracy, precision, recall, balanced F score (F1-score) and the area under the macro-average receiver operating curve (AUC). Reliability was evaluated by Cohen's kappa ââto compare the consistency of model predicted labels with expert opinions. RESULTS: PAINet performed best among the four algorithms. The accuracy, precision, recall, F1-score and AUC on the test set were 0.9333, 0.9415, 0.9333, 0.9336 and 0.9972, respectively. Cohen's kappa was 0.911, which represented almost perfect consistency. CONCLUSIONS: PAINet can accurately distinguish between normal periapical tissues, CBCTPAI 1-2, CBCTPAI 3-5 and young permanent teeth. Its results were highly consistent with expert opinions. It can help junior doctors diagnose and score AP, reducing the burden. It can also be promoted in areas where experts are lacking to provide professional diagnostic opinions.
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The scarcity of hematopoietic stem cells (HSCs) restricts their use in both clinical settings and experimental research. Here, we examined a recently developed method for expanding rigorously purified murine HSCs ex vivo. After 3 weeks of culture, only 0.1% of cells exhibited the input HSC phenotype, but these accounted for almost all functional long-term HSC activity. Input HSCs displayed varying potential for ex vivo self-renewal, with alternative outcomes revealed by single-cell multimodal RNA and ATAC sequencing profiling. While most HSC progeny offered only transient in vivo reconstitution, these cells efficiently rescued mice from lethal myeloablation. The amplification of functional HSC activity allowed for long-term multilineage engraftment in unconditioned hosts that associated with a return of HSCs to quiescence. Thereby, our findings identify several key considerations for ex vivo HSC expansion, with major implications also for assessment of normal HSC activity.
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Células-Tronco Hematopoéticas , RNA , Animais , Camundongos , Divisão Celular , FenótipoRESUMO
Human amniotic epithelial cells (hAECs) are novel and promising therapeutic agents for patients suffering from degenerative diseases. Studies have demonstrated that the therapeutic effects of hAECs mainly depend on their paracrine components. Currently, appropriate pretreatment is a widely confirmed strategy for enhancing the repair potential of stem cells; however, the effect of proinflammatory factor pretreatment on hAECs and their secretome is still unclear. In this study, we used the well-characterized proinflammatory factors tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) to stimulate hAECs and analyzed the effect of TNF-α and IFN-γ on hAECs, including gene expression profile, paracrine proteins, and microRNAs (miRNAs) in exosomes. Results showed that TNF-α and IFN-γ pretreatment improved the viability of hAECs but inhibited the proliferation of hAECs. TNF-α and IFN-γ pretreatment altered the gene expression profile of hAECs, and upregulated differentially expressed genes were predominantly enriched in biological adhesion, antioxidant activity, and response to IFN-beta. In addition, TNF-α and IFN-γ pretreatment enhanced the paracrine secretion of cytokines by hAECs. The upregulated differentially expressed proteins were mainly enriched in tissue remodeling proteins and cytokine-cytokine receptor. Notably, the expression of miRNAs in exosomes from hAECs was also changed by TNF-α and IFN-γ pretreatment. The target genes of upregulated exosomal miRNAs substantially contributed to the response to stimulus, metabolic pathways, and PI3K-Akt signaling pathway. Our findings improve our understanding of the biological characteristics of hAECs after proinflammatory factor pretreatment and provide novel insights to strengthen and optimize the therapeutic potential of hAECs and their secretome in regenerative medicine.
Assuntos
Âmnio , Células Epiteliais , Humanos , Âmnio/citologia , Âmnio/metabolismo , Células Epiteliais/metabolismo , Células Epiteliais/efeitos dos fármacos , Secretoma , Exossomos/metabolismo , Interferon gama/farmacologia , Interferon gama/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Fator de Necrose Tumoral alfa/farmacologia , Proliferação de Células/efeitos dos fármacos , MicroRNAs/metabolismo , MicroRNAs/genética , Sobrevivência Celular/efeitos dos fármacos , Feminino , Citocinas/metabolismo , Células Cultivadas , Mediadores da Inflamação/metabolismoRESUMO
Infant and adult MLL1/KMT2A-rearranged (MLLr) leukemia represents a disease with a dismal prognosis. Here, we present a functional and proteomic characterization of in utero-initiated and adult-onset MLLr leukemia. We reveal that fetal MLL::ENL-expressing lymphomyeloid multipotent progenitors (LMPPs) are intrinsically programmed towards a lymphoid fate but give rise to myeloid leukemia in vivo, highlighting a complex interplay of intra- and extracellular factors in determining disease subtype. We characterize early proteomic events of MLL::ENL-mediated transformation in fetal and adult blood progenitors and reveal that whereas adult pre-leukemic cells are mainly characterized by retained myeloid features and downregulation of ribosomal and metabolic proteins, expression of MLL::ENL in fetal LMPPs leads to enrichment of translation-associated and histone deacetylases signaling proteins, and decreased expression of inflammation and myeloid differentiation proteins. Integrating the proteome of pre-leukemic cells with their secretome and the proteomic composition of the extracellular environment of normal progenitors highlights differential regulation of Igf2 bioavailability, as well as of VLA-4 dimer and its ligandome, upon initiation of fetal- and adult-origin leukemia, with implications for human MLLr leukemia cells' ability to communicate with their environment through granule proteins. Our study has uncovered opportunities for targeting ontogeny-specific proteomic vulnerabilities in in utero-initiated and adult-onset MLLr leukemia.