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Background Paris polyphylla var. yunnanensis (PPY) is commonly used in traditional Chinese medicine formulas and folk families. Nearly more than 100 chemical substances with medicinal values have been reported in PPY, among which steroidal saponins are the main active components. Due to its long growth cycle, the resource of PPY has become too scarce, and the current production capacity of PPY is still far from meeting the market demand. Numerous studies have shown that endophytic bacteria not only promote the production of secondary metabolites in the host plant, but some of them are also able to produce the same secondary metabolites as the host. However, little is known about the endophytic bacteria associated with PPY in different geographic conditions and tissues. In order to compare the endophytic bacterial communities associated with PPY in different geographic conditions and plant tissues, the endophytic bacteria from roots, stems, and leaves of PPY collected from five locations were isolated, and the diversity, richness, and homogeneity of bacterial communities were analyzed, and the dominant genera correlation with polyphyllin content was further investigated. Results A total of 268 endophytic bacterial strains were isolated and identified from PPY. The experimental results showed that the isolates belonged to 5 phyla, 7 classes, 14 orders and 39 genera of bacteria, of which the dominant order was Bacillariophyta and the dominant genera were Bacillus , Pseudomonas and Agrobacterium . In general, the differences in the distribution pattern and diversity of endophytic bacteria in PPY were characterized by the highest diversity and richness index of endophytic bacterial communities in Er yuan Qisheng (QS) and the highest evenness index in Dali Fengyi (FY). The diversity, richness and evenness of bacterial communities in terms of tissue state showed a hierarchical pattern of root > stem > leaf. The three optimal genera were positively correlated with polyphyllin content. Conclusion The distribution pattern and diversity of endophytic bacteria in PPY were influenced by tissue type and habitat. In addition, three endophytic bacteria ( Pseudomonas , Bacllius and Agrobacterium ) were positively correlated with the content of polyphylin.

Signal attenuates while Measurement-While-Drilling (MWD) mud pulse is transmited in drill string during high temperature deep well drilling. In this work, an analytical model for the propagation of mud pulse was presented. The model consists of continuity, momentum, and state equations with analytical solutions based on the linear perturbation analysis. The model can predict the wave speed and attenuation coefficient of mud pulse. The calculated results were compared with the experimental data showing a good agreement. Effects of the angular frequency, static velocity, mud viscosity, and mud density behavior on speed and attenuation coefficients were included in this paper. Simulated results indicate that the effects of angular frequency, static velocity, and mud viscosity are important, and lower frequency, viscosity, and static velocity benefit the transmission of mud pulse. Influenced by density behavior, the speed and attenuation coefficients in drill string are seen to have different values with respect to well depth. For different circulation times, the profiles of speed and attenuation coefficients behave distinctly different especially in lower section. In general, the effects of variables above on speed are seen to be small in comparison.

Certain miRNAs can attenuate hypoxia/re-oxygenation-induced autophagic cell death reported in our previous studies, but how these miRNAs regulate the autophagy-related cellular signaling pathway in preventing cell death is largely unknown. In the current study, the autophagy-related miRNAs of hsa-miR-20b were investigated in an in vitro model of hypoxia/re-oxygenation-induced endothelial autophagic cell death. Of these, miR-20b was found to be the most important miRNA which targeted on the key autophagy kinase ULK1 and inhibited hypoxia/re-oxygenation injury-induced autophagy by decreasing both autophagosomes and LC3I to II transition rate and P62 degradation. These processes were reversed by the transfection of an miR-20b inhibitor. Re-expression of ULK1 restores miR-20b-inhibited autophagy. Propofol, a commonly used anesthetic, promoted miR-20b and METTL3 expression and attenuated endothelial autophagic cell death. The inhibited endogenous expression of miR-20b or silenced METTL3 diminished the protective effect of propofol and accentuated autophagy. Additionally, METTL3 knockdown significantly inhibited miR-20b expression but up-regulated pri-miR-20b expression. Together, our data shows that propofol protects against endothelial autophagic cell death induced by hypoxia/re-oxygenation injury, associated with activation of METTL3/miR-20b/ULK1 cellular signaling.

Background Although many studies have validated the diagnostic performance of Ovarian-Adnexal Reporting and Data Systems ultrasound (O-‎RADS US), most have been observed by experienced sonologists, and relatively few by junior sonologists. The purpose of this study was to compare the diagnostic performance of the O-RADS US and the International Ovarian Tumor Analysis (IOTA) Simple Rules (SRs) in senior and junior sonologists to determine a more suitable assessment model for general clinical use. Methods We prospectively recruited 228 patients diagnosed with adnexal masses (AMs). Two senior sonologists acquired images and evaluated them following the O-RADS US and IOTA guidelines, and two junior sonologists reviewed and analyzed images and evaluated them following the same guidelines. In this research, pathological findings were used as the reference standard. Comparisons of categorical variables were made using the chi-square test, and comparisons of continuous variables were made using the two independent-samples t-test. The diagnostic performance of the models was compared by analyzing the receiver operating characteristic (ROC) curve. The kappa value (κ) was used to compare the interobserver agreement between the senior and junior sonologists and the agreement between each ultrasound method and the reference standard. Results Of 228 AMs, 176 were benign and 52 malignant. The junior adjusted O-RADS US (> O-RADS 4a represents malignancy) had the highest diagnostic validity, with a sensitivity, specificity, and accuracy of 94.23%, 87.5%, and 89.04%, respectively, and ROC curve of 0.959 (95% CI, 0.924–0.980). Both junior unadjusted (> O-RADS 3 represents malignancy) and adjusted O-RADS US had significantly higher diagnostic performance than the junior SRs (AUC 0.951 and 0.959 vs. 0.840, P  = 0.0003, 0.0001, respectively). Interobserver agreement between senior and junior sonologists using O-RADS US was moderate (κ = 0.465), and interobserver agreement between senior and junior sonologists using SRs, unadjusted, and adjusted O-RADS US was good (κ = 0.618, 0.657, and 0.718, respectively). The junior unadjusted O-RADS US, adjusted O-RADS US, and SRs showed good agreement with the pathological results (κ = 0.648, 0.724, 0.716, respectively). Conclusions When assisting sonologists in AM diagnosis, the O-RADS US, especially the adjusted O-RADS US, had higher diagnostic performance than the SRs, and it would be more suitable for general clinical application.

Background Ischemia-reperfusion (IR) induces increased release of extracellular vesicles in the heart and exacerbates myocardial IR injury. We have previously shown that propofol attenuates hypoxia/reoxygenation (HR)-induced injury in human umbilical vein endothelial cells (HUVECs) and that microvesicles derived from propofol-treated HUVECs inhibit oxidative stress in endothelial cells. However, the role of microvesicles derived from propofol post-treated HUVECs ((HR + P)-EMVs) in IR-injured cardiomyocytes is unclear. In this study, we aimed to investigate the role of (HR + P)-EMVs in cardiac IR injury compared to microvesicles derived from hypoxic/reoxygenated HUVECs (HR-EMVs) and to elucidate the underlying mechanisms. Methods Hypoxia/reoxygenation (HR) models of HUVECs and AC16 cells and a mouse cardiac IR model were established. Microvesicles from HR-injured HUVECs, DMSO post-treated HUVECs and propofol post-treated HUVECs were extracted by ultra-high speed centrifugation, respectively. The above EMVs were co-cultured with HR-injured AC16 cells or injected intracardially into IR mice. Flow cytometry and immunofluorescence were used to determine the levels of oxidative stress and apoptosis in cardiomyocytes. Apoptosis related proteins were detected by Western blot. Echocardiography for cardiac function and Evans blue-TTC staining for myocardial infarct size. Expression of lncCCT4-2 in EMVs and AC16 cells was analysed by whole transcriptome sequencing of EMVs and RT-qPCR. The molecular mechanism of inhibition of myocardial injury by (HR + P)-EMVs was elucidated by lentiviral knockdown of lncCCT4-2, plasmid overexpression or knockdown of CCT4, and actinomycin D assay. Results In vitro and in vivo experiments confirmed that HR-EMVs exacerbated oxidative stress and apoptosis in IR-injured cardiomyocytes, leading to increased infarct size and worsened cardiac function. Notably, (HR + P)-EMVs induced significantly less oxidative stress and apoptosis in IR-injured cardiomyocytes compared to HR-EMVs. Mechanistically, RNA sequencing of EMVs and RT-qPCR showed that lncCCT4-2 was significantly upregulated in (HR + P)-EMVs and cardiomyocytes co-cultured with (HR + P)-EMVs. Reduction of lncCCT4-2 in (HR + P)-EMVs enhanced oxidative stress and apoptosis in IR-injured cardiomyocytes. Furthermore, the anti-apoptotic activity of lncCCT4-2 from (HR + P)-EMVs was achieved by increasing the stability of CCT4 mRNA and promoting the expression of CCT4 protein in cardiomyocytes. Conclusions Our study showed that (HR + P)-EMVs uptake by IR-injured cardiomyocytes upregulated lncCCT4-2 in cardiomyocytes and promoted CCT4 expression, thereby inhibiting HR-EMVs induced oxidative stress and apoptosis. Highlights Microvesicles from hypoxic/reoxygenated HUVECs (HR-EMVs) exacerbated oxidative stress and apoptosis in IR-injured cardiomyocytes. Microvesicles from propofol post-treated HUVECs ((HR + P)-EMVs) induced diminished oxidative stress and apoptosis in IR-injured cardiomyocytes compared with microvesicles from hypoxic/reoxygenated HUVECs (HR-EMVs). lncCCT4-2 was significantly highly expressed in (HR + P)-EMVs and cardiomyocytes co-cultured with (HR + P)-EMVs, and reduction of lncCCT4-2 in (HR + P)-EMVs enhanced oxidative stress and apoptosis in IR-injured cardiomyocytes. lncCCT4-2 inhibited HR-EMVs induced oxidative stress and apoptosis in HR-injured AC16 cells by increasing the stability of CCT4 mRNA and promoting the expression of CCT4 protein in AC16 cells.

Abstract Background Ischemia-reperfusion (IR) induces increased release of extracellular vesicles in the heart and exacerbates myocardial IR injury. We have previously shown that propofol attenuates hypoxia/reoxygenation (HR)-induced injury in human umbilical vein endothelial cells (HUVECs) and that microvesicles derived from propofol-treated HUVECs inhibit oxidative stress in endothelial cells. However, the role of microvesicles derived from propofol post-treated HUVECs ((HR + P)-EMVs) in IR-injured cardiomyocytes is unclear. In this study, we aimed to investigate the role of (HR + P)-EMVs in cardiac IR injury compared to microvesicles derived from hypoxic/reoxygenated HUVECs (HR-EMVs) and to elucidate the underlying mechanisms. Methods Hypoxia/reoxygenation (HR) models of HUVECs and AC16 cells and a mouse cardiac IR model were established. Microvesicles from HR-injured HUVECs, DMSO post-treated HUVECs and propofol post-treated HUVECs were extracted by ultra-high speed centrifugation, respectively. The above EMVs were co-cultured with HR-injured AC16 cells or injected intracardially into IR mice. Flow cytometry and immunofluorescence were used to determine the levels of oxidative stress and apoptosis in cardiomyocytes. Apoptosis related proteins were detected by Western blot. Echocardiography for cardiac function and Evans blue-TTC staining for myocardial infarct size. Expression of lncCCT4-2 in EMVs and AC16 cells was analysed by whole transcriptome sequencing of EMVs and RT-qPCR. The molecular mechanism of inhibition of myocardial injury by (HR + P)-EMVs was elucidated by lentiviral knockdown of lncCCT4-2, plasmid overexpression or knockdown of CCT4, and actinomycin D assay. Results In vitro and in vivo experiments confirmed that HR-EMVs exacerbated oxidative stress and apoptosis in IR-injured cardiomyocytes, leading to increased infarct size and worsened cardiac function. Notably, (HR + P)-EMVs induced significantly less oxidative stress and apoptosis in IR-injured cardiomyocytes compared to HR-EMVs. Mechanistically, RNA sequencing of EMVs and RT-qPCR showed that lncCCT4-2 was significantly upregulated in (HR + P)-EMVs and cardiomyocytes co-cultured with (HR + P)-EMVs. Reduction of lncCCT4-2 in (HR + P)-EMVs enhanced oxidative stress and apoptosis in IR-injured cardiomyocytes. Furthermore, the anti-apoptotic activity of lncCCT4-2 from (HR + P)-EMVs was achieved by increasing the stability of CCT4 mRNA and promoting the expression of CCT4 protein in cardiomyocytes. Conclusions Our study showed that (HR + P)-EMVs uptake by IR-injured cardiomyocytes upregulated lncCCT4-2 in cardiomyocytes and promoted CCT4 expression, thereby inhibiting HR-EMVs induced oxidative stress and apoptosis. Highlights Microvesicles from hypoxic/reoxygenated HUVECs (HR-EMVs) exacerbated oxidative stress and apoptosis in IR-injured cardiomyocytes. Microvesicles from propofol post-treated HUVECs ((HR + P)-EMVs) induced diminished oxidative stress and apoptosis in IR-injured cardiomyocytes compared with microvesicles from hypoxic/reoxygenated HUVECs (HR-EMVs). lncCCT4-2 was significantly highly expressed in (HR + P)-EMVs and cardiomyocytes co-cultured with (HR + P)-EMVs, and reduction of lncCCT4-2 in (HR + P)-EMVs enhanced oxidative stress and apoptosis in IR-injured cardiomyocytes. lncCCT4-2 inhibited HR-EMVs induced oxidative stress and apoptosis in HR-injured AC16 cells by increasing the stability of CCT4 mRNA and promoting the expression of CCT4 protein in AC16 cells.

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