Abstract Background Post-traumatic wound infection (PTWI) is a major challenge in trauma, burns, and surgeries. The skin microbiota is crucial for defense and may influence PTWI occurrence, though the relationship is unclear. This study explores the causal link between the skin microbiome and PTWI using bidirectional two-sample Mendelian randomization (MR) analysis. Methods A two-sample MR analysis was conducted using genome wide association studies (GWAS) data of 147 skin microbiota taxa and PTWI. The inverse-variance weighted (IVW) method was the primary analysis technique, while the MR-Egger and weighted median were used as supplementary analysis methods. Cochran’s Q test was used to perform heterogeneity analysis. The MR-Egger intercept test and MR-PRESSO were employed to assess potential horizontal pleiotropy. The leave-one-out method was utilized to evaluate the impact of individual SNPs on the overall causal effect. Results The two-sample MR analysis identified significant causal relationships between 12 skin microbiota species and PTWI. Five species were potentially beneficial: asv045 [Acinetobacter (unc.)] (OR = 0.971, P = 0.044), asv092 [C. kroppenstedtii] (OR = 0.966, P = 6.88e − 03), asv093 [Staphylococcus (unc.)] (OR = 0.911, P = 0.044), genus Finegoldia (OR = 0.965, P = 0.043), and genus Kocuria (OR = 0.95, P = 0.025). Seven species were potentially harmful: asv001 [P. acnes] (OR = 1.187, P = 0.041), asv005 [P. granulosum] (OR = 1.259, P = 6.06e − 03), family Micrococcaceae (OR = 1.24, P = 0.014), family Neisseriaceae (OR = 1.161, P = 0.038), genus Enhydrobacter (OR = 1.039, P = 0.013; OR = 1.202, P = 0.017), and order Bacteroidales (OR = 1.202, P = 0.012). PTWI may also induce skin microenvironment changes, disrupting homeostasis and increasing the likelihood of pathogenic microbiota, such as class Betaproteobacteria, genus Chryseobacterium, asv007 [Anaerococcus (unc.)], and family Flavobacteriaceae. Conversely, PTWI might promote beneficial microbiota, like asv005 [P. granulosum]. Conclusions This study provides strong evidence of a causal link between the skin microbiome and PTWI, emphasizing their complex interactions. These findings offer new insights for preventing and treating PTWI. Further research on the underlying mechanisms and similar studies in different populations are essential.
To explore the potential biological function of XPA (Xeroderma pigmentosum group A) in hepatic neoplasms and the underlying molecular mechanisms.Liver cells were used as experimental models to establish HCC (hepatocellular carcinoma) in vitro. Protein extractions were subjected to Western blotting to detect the proteins expression. The lentivirus transfection efficiency was confirmed by Western blot and RT-qPCR, Tunnel staining was used to detect apoptosis, and Transwell assays were used to observe cell migration and invasion. Cell proliferation was detected with colony formation and CCK-8 (cell counting kit-8) assays.XPA expression was obviously lower in HCC tissue and liver cancer cell lines. XPA overexpression induced autophagy and apoptosis by increasing LC3B II/I, Beclin1, cleaved-caspase-3, and Bax expression and decreasing p62 and Bcl2 protein levels. XPA also suppressed HCC EMT (Epithelial-Mesenchymal Transition) by increasing E-cadherin and decreasing N-cadherin and vimentin protein expression. Cell proliferation, migration and invasion in vivo were significantly inhibited by the overexpression of XPA, and p-PI3K, p-Akt, and p-mTOR expression were decreased in LV-XPA cells. In general, XPA inhibited HCC by inducing autophagy and apoptosis and by modulating the expression of PI3K/Akt/mTOR proteins.XPA overexpression was found to suppress HCC by inducing autophagy and apoptosis and repressing EMT and proliferation. Each of these effects may be involved in modulating the PI3K/Akt/mTOR signaling pathway.
This paper presents two novel three-phase modular SRMs (MSRMs) with the same segmented E-shaped stator modules and different rotor topologies, namely, segmental rotor and conventional rotor. The basic topologies and simplified equivalent magnetic circuit (EMC) are presented first. The static electromagnetic characteristics of two MSRMs such as flux distribution, phase flux linkage and inductance, electromagnetic torque, and so on, are computed and compared by 3D finite-element analysis. Then the dynamic performances including steady-state and transient operations of two MSRM drives are evaluated and compared. Finally, two MSRM prototypes with segmental rotor and conventional rotor are manufactured and tested for experimental verification and comparison. The experimental results of static flux linkage, steady state and transient performances of two MSRM drives are presented and compared, which verify the analytical EMC model, FEA and the corresponding Matlab/Simulink-based predictions.
The finite element magnetic field numerical calculation method is widely used in motor structure design and performance analysis due to its high calculation accuracy and versatility. The permanent magnet swing angle torque motor is studied in this paper which applied to high voltage circuit breaker. Firstly, the topological structure and equivalent circuit equation of coupling circuit are discussed for the permanent magnet swing angle torque motor during the opening and closing, established the field-path-motion coupling time-step finite element model of motor, analyzed the distribution of magnetic flux, magnetic density and air gap magnetic density at the closing position, maximum load and opening position, and calculated the dynamic parameters of motor. The results show that the permanent magnet swing angle torque motor can meet the operating requirements of circuit breaker. In the magnetic field analysis, the magnetic density of stator yoke is 2.5T, the average air gap magnetic density is 1.0T. In the dynamic parameters simulation, the average opening speed is 656r/min, the opening operation time is 33ms, the closing operation time is 40ms. It can provide a theoretical basis for the further research and development of motor.
Dexmedetomidine (Dex) protects different cell types during hypoxia or ischemia-reperfusion injury by inhibiting cell apoptosis. However, the underlying mechanism and its impact on hepatic ischemia reperfusion injury are still not known. In this study, we established a model of oxygen-glucose deprivation/reperfusion (OGD/R) injury in hepatocyte HL7702 cells, and studied the impact of Dex on cell proliferation, apoptosis, and cell cycle during OGD/R. In addition, we explored the role of CCAT1 in this process. We found that Dex increased cell proliferation and inhibited cell apoptosis during OGD/R, in a concentration-dependent manner. Dex partially reversed the OGD-inhibited expression of lncRNA CCAT1. Knockdown of CCAT1 by siRNA inhibited Dex-mediated protection against OGD/R-induced injury and promoted cell apoptosis, caspase-3 expression and cell cycle arrest in the G0/G1 phase, and inhibited cell proliferation and cyclin D1 expression. In contrast, overexpression of CCAT1 by pcDNA3.0-CCAT1 enhanced Dex-mediated protection against OGD/R-induced cell injury. Thus, Dex protects hepatocytes against OGD/R injury by upregulating lncRNA CCAT1. This study suggests a novel role of CCAT1 in ischemia reperfusion injury, and lays the framework for future studies.
Hand–arm vibration syndrome (HAVS) is caused by long-term exposure to hand-transmitted vibration (HTV), and its pathogenesis has not been elucidated fully. We explored the molecular mechanism of HAVS and provided clues and a theoretical basis for the early prevention and treatment of HAVS. After vibration, samples were collected from the plasma of human workers, plasma of rat tails, and human umbilical vein endothelial cells (HUVECs). ELISAs were used to measure the expression of vasoactive factors. Cell Counting Kit-8 and electron microscopy were used to detect cell damage. Flow cytometry was employed to detect apoptosis. Real-time reverse transcription-polymerase chain reaction was used to measure the expression of long non-coding RNAs (lncRNAs). Western blotting was used to measure the expression of apoptosis-related proteins. Vibration could cause cell damage, apoptosis, and changes in the expression vasoactive factors and lncRNAs. The lncRNA maternally expressed gene 3 (MEG3) had a significant regulatory effect on cell damage, apoptotic proteins, and vascular regulatory factors in the HUVEC damage induced by vibration, as shown by the further decrease in viability and aggravation of injury after knockdown of MEG3 expression in HUVECs treated with vibration. Expression of vasoactive factors and apoptosis-related proteins was changed after interfering with MEG3 expression. In conclusion, vibration can affect the expression of vasoactive factors and lncRNA, and cause damage to vascular endothelial cells. MEG3 may be involved in the inflammatory damage to vascular endothelial cells induced by vibration.
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