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During the electrical discharge machining (EDM) process, the tool electrode wear is inevitable, which affects the process precision of the micro-hole. In the present experimental investigation, a fixed reference axial compensation (FRAC) method is proposed to enhance the machining precision of micro-hole. The effect of pulse power, compensation methods, and electrode materials on the depth and roundness factor of micro-hole are explored. The experiment results show that the FRAC method can realize the accurate compensation and reach the expected depth hole processing. When the FRAC is used, the depth deviation is less than 0.43%, and the minimum difference from the expected depth is only 0.106 µm. In addition, the micro-holes of tungsten steel and brass electrodes machine by the FRAC method were close to the expected depth, the difference from the expected depth less than 0.7%, but the bottom of micro-hole produced a cone. However, compared to tungsten steel and brass electrodes, the copper electrode has a better processing performance, the roundness factor is up to 79.8%. When the long-pulse power supply is applied, the expected depth of 400–1,600 µm blind holes with a better processing shape, and the phenomenon of the cone at the bottom are not apparent. Therefore, the proposed FRAC method can be utilized in many high-end manufacturing fields to improve the precision of the micro-hole for micro features.

In femoral neck fractures the secondary damage caused by repeated multiple reductions needs to be prevented. Accordingly, the aim of this study was to achieve an anatomical reduction in the first manipulation of reduction in femoral neck fractures. We propose a new reduction strategy using the x-ray morphology of femoral neck fractures for preoperative planning. In the present study we compared this approach to conventional operation procedures for the treatment of femoral neck fractures. From 2020 to 2021, 35 patients with femoral neck fractures were operated with this reduction strategy. Those were compared with 34 patients treated without the proposed preoperative method. All patients were compared for consistency between the preoperative assessment and the intraoperative execution of the reduction approach, number of reductions, operative time, number of fluoroscopies, intraoperative bleeding, and reduction quality. The operative time of patients in the study group was significantly shorter (38.40 ± 10.26 min) than that of the control group (47.26 ± 9.09 min), and the number of reductions [1.0 (1.0, 1.0)] was significantly less than that of the control group [2.0 (1.75, 2.25)]. The number of fluoroscopies (10.27 ± 2.84) was also significantly less than that of the control group (13.53 ± 2.59) times. The KAPPA value = 0.886 shows the good agreement between the preoperative proposed protocol and the intraoperative protocol about the study group.The bleeding, quality of repositioning, Harris Hip score, MOS 12-item Short Form Survey (SF-12), and early complication rate were not statistically different between the groups (P > 0.05). The selection of the appropriate repositioning method based on the analysis of femoral neck fracture X-ray morphology can improve the efficiency and accuracy of preoperative planning. This reduces the secondary damage that may be caused by multiple reduction, shortens the operation time and reduces the exposure to radiation. [ABSTRACT FROM AUTHOR]

Background: Massive hemoptysis is characterized by its life-threatening nature, potentially leading to airway obstruction and asphyxia. The objective of this study was to evaluate the clinical effectiveness of combining endobronchial tamponade with bronchial artery embolization (BAE) in the treatment of massive hemoptysis. Methods: Between March 2018 and March 2022, a total of 67 patients with massive hemoptysis who underwent BAE were divided into two groups: the combination group (n = 26) and the BAE group (n = 41). Technical and clinical success rates were assessed, and adverse events were monitored following the treatment. Blood gas analysis and coagulation function indicators were collected before and after the treatment, and recurrence and survival rates were recorded during the follow-up period. Results: All patients achieved technical success. There were no significant differences in the clinical success rate, recurrence rates at 3 and 6 months, and mortality rates at 3 months, 6 months, and 1 year between the combination group and the BAE group. However, the hemoptysis recurrence rate at 1 year was significantly lower in the combination group compared to the BAE group (15.4% vs. 39.0%, P = 0.039). No serious adverse events were reported in either group. After treatment, the combination group showed higher levels of arterial partial pressure of oxygen (PaO2), oxygenation index (PaO2/FiO2), fibrinogen (FIB), and D-dimer (D-D) compared to the BAE group (P < 0.05). Multivariate regression analysis demonstrated a significant correlation between combined therapy and hemoptysis-free survival. Conclusion: Combination therapy, compared to embolization alone, exhibits superior efficacy in improving respiratory function, correcting hypoxia, stopping bleeding, and preventing recurrence. It is considered an effective and safe treatment for massive hemoptysis. [ABSTRACT FROM AUTHOR]

The innate immune response to viruses is formed in part by interferon (IFN)-induced restriction factors, including ISG15, p21, and SAMHD1. IFN production can be blocked by the ISG15-specific protease USP18. HIV-1 has evolved to circumvent host immune surveillance. This mechanism might involve USP18. In our recent studies, we demonstrate that HIV-1 infection induces USP18, which dramatically enhances HIV-1 replication by abrogating the antiviral function of p21. USP18 downregulates p21 by accumulating misfolded dominant negative p53, which inactivates wild-type p53 transactivation, leading to the upregulation of key enzymes involved in de novo dNTP biosynthesis pathways and inactivated SAMHD1. Despite the USP18-mediated increase in HIV-1 DNA in infected cells, it is intriguing to note that the cGAS-STING-mediated sensing of the viral DNA is abrogated. Indeed, the expression of USP18 or knockout of ISG15 inhibits the sensing of HIV-1. We demonstrate that STING is ISGylated at residues K224, K236, K289, K347, K338, and K370. The inhibition of STING K289-linked ISGylation suppresses its oligomerization and IFN induction. We propose that human USP18 is a novel factor that potentially contributes in multiple ways to HIV-1 replication. [ABSTRACT FROM AUTHOR]

Addition of trace Zn can impose notable effect on the deformation behavior of Mg–Gd–Y–Zr alloy, while the underlying mechanisms have not been revealed. In the present work, Mg–8.5Gd–2.5Y–0.3Zr (wt%) (0Zn) and Mg–8.5Gd–2.5Y–0.5Zn–0.3Zr (wt%) (0.5Zn) alloys are fabricated by casting and extrusion, to obtain a bimodal microstructure containing fine dynamic recrystallized (DRXed) grains and coarse unDRXed grains. The as‐extruded 0Zn and 0.5Zn alloys are studied by in situ synchrotron diffraction under uniaxial tension and compression to clarify the effect of trace Zn on the deformation mechanisms. It is found that both alloys exhibit stress softening in the basal slip‐favored grains under both tension and compression, and adding trace Zn highly enhances the stress softening. Furthermore, the addition of Zn stimulates the occurrence of discontinuous yielding which is in connection with the stress softening, resulting from the interaction between basal dislocations and solute atmospheres. The tension–compression‐yielding symmetry of the alloy is improved by adding Zn, which is mainly attributed to the suppression effect of γ′ phases and Gd/Y–Zn dimers on tensile twinning. Finally, the addition of Zn can promote the tensile and compressive strength, owing to the strength enhancement of the relevant deformation modes and the increase of the fraction of unDRXed regions. [ABSTRACT FROM AUTHOR]

The quadrilateral reassortant IAV A/(H1N1) pdm09 is the pathogen responsible for the first influenza pandemic of the 21st century. The virus spread rapidly among hosts causing high mortality within human population. Efficient accumulation of virions is known to be important for the rapid transmission of virus. However, the mechanism by which A/(H1N1) pdm09 promotes its rapid replication has not been fully studied. Here, we found the NS1 of A/(H1N1) pdm09 mediated complete macroautophagy/autophagy, and then facilitated self-replication, which may be associated with the more rapid spread of this virus compared with H1N1WSN and H3N8JL89. We found that the promotion of self-replication could be mainly attributed to NS1pdm09 strongly antagonizing the inhibitory effect of LRPPRC on autophagy. The interaction between NS1pdm09 and LRPPRC competitively blocked the interaction of LRPPRC with BECN1/Beclin1, resulting in increased recruitment of BECN1 for PIK3C3 (phosphatidylinositol 3-kinase catalytic subunit type 3) and induction of the initiation of autophagy. In conclusion, we uncover the unique molecular mechanism by which A/(H1N1) pdm09 utilizes autophagy to promote self-replication, and we provide theoretical basics for the analysis of the etiological characteristics of the A/(H1N1) pdm09 pandemic and the development of anti-influenza drugs and vaccines. Abbreviations: 293T: human embryonic kidney 293 cells; 293T_LRPPRC: stable LRPPRC expression 293T cells; 3-MA: 3-methyladenine; A549 cells: human non-small cell lung cancer cells; AA: amino acid; ACTB: actin beta; BECN1: beclin 1; BECN1 KO: BECN1 knockout 293T cells; Cal: calyculin A; Co-IP: co-immunoprecipitation; CQ: chloroquine; DC: dendritic cell; Eug: eugenol; GFP: green fluorescent protein; HA: hemagglutinin; HIV: human immunodeficiency virus; IAVs: Influenza A viruses; IFN: interferon; JL89: A/equine/Jilin/1/1989 (H3N8); LAMP2: lysosomal associated membrane protein 2; LRPPRC: leucine rich pentatriicopeptide repeat containing; LRPPRC KO: LRPPRC knockout 293T cells; M2: matrix 2; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MDCK: Madin-Darby canine kidney cells; MOI: multiplicity of infection; MS: mass spectrometry; NP: nucleoprotein; NS1: non-structural protein 1; NS1JL89: non-structural protein 1 of A/equine/Jilin/1/1989 (H3N8); NS1pdm09: non-structural protein 1 of A/(H1N1) pdm09; NS1SC09: non-structural protein 1 of A/Sichuan/2009 (H1N1); NS1WSN: non-structural protein 1 of A/WSN/1933 (H1N1); PB1: polymerase basic protein 1; PB1-F2: alternate reading frame discovered in PB1 gene segment; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PR8: A/PR/8/34 (H1N1); Rapa: rapamycin; RFP: red fluorescent protein; SC09: A/Sichuan/2009 (H1N1); SQSTM1/p62: sequestosome 1; STK4/MST1: serine/threonine kinase 4; TEM: transmission electron microscopy; TOMM20: translocase of outer mitochondrial membrane 20; WHO: World Health Organization; WSN: A/WSN/1933 (H1N1); WSN-NS1JL89: WSN recombinant strain in which NS1 was replaced with that of JL89; WSN-NS1SC09: WSN recombinant strain in which NS1 was replaced with that of SC09. [ABSTRACT FROM AUTHOR]