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This study aims to clarify the influence of H2S concentration and temperature on the sulfide stress corrosion cracking (SSCC) susceptibility of 20# steel weld joints. 20# steel is a commonly selected pipe material for ground gas pipelines, and there is a risk of welds cracking after years of service. The selection of a corrosive environment is based on the working conditions of high-sulfur oil fields on site. Slow strain rate tensile (SSRT) tests were conducted under simulated high-sulfur gathering and transportation conditions across varying temperatures and H2S concentrations. The mechanical properties, SSCC susceptibility, fracture morphology, and elemental composition of fracture surfaces were systematically analyzed. As H2S concentration increased (5%, 7.5%, 10%) and temperature decreased (30–60 °C), the elongation after fracture and the reduction in area of 20# steel decreased, while the yield strength and SSCC susceptibility increased. The H2S concentration range of 0–5% represented a critical sensitivity interval for the material, where elongation after fracture decreased by up to 74%. Within the 5–10% H2S range, elongation decreased by only 2.11%, indicating a slowing trend of fracture toughness deterioration, though SSCC susceptibility still increased by 12%. Increasing the temperature from 30 °C to 60 °C reduced SSCC susceptibility by approximately 30%, confirming higher susceptibility at lower temperatures. Temperature exerts a lesser influence on material performance than H2S concentration. Also, 20# steel remains within the SSCC brittle fracture sensitivity zone in sulfur-containing environments, necessitating strict quality control to avoid defects and stress concentrations. In high-sulfur environments (H2S > 5%), further increases in H2S concentration have a diminished effect on cracking susceptibility.

Carbon dioxide (CO2) is a non-toxic asphyxiant gas that, once released, can pose severe risks, including suffocation, poisoning, frostbite, and even death. As a critical component of carbon capture, utilization, and storage (CCUS) technology, CO2 pipeline transportation requires reliable leakage detection and precise localization to safeguard the environment, ensure pipeline operational safety, and support emergency response strategies. This study proposes an inversion model that integrates wireless sensor networks (WSNs) with the Gaussian plume model for CO2 pipeline leakage monitoring. The WSN is employed to collect real-time CO2 concentration data and environmental parameters around the pipeline, while the Gaussian plume model is used to simulate and invert the dispersion process, enabling both leak source localization and emission rate estimation. Simulation results demonstrate that the proposed model achieves a source localization error of 12.5% and an emission rate error of 3.5%. Field experiments further confirm the model’s applicability, with predicted concentrations closely matching the measurements, yielding an error range of 3.5–14.7%. These findings indicate that the model satisfies engineering accuracy requirements and provides a technical foundation for emergency response following CO2 pipeline leakage.

This study aims to clarify the influence of H S concentration and temperature on the sulfide stress corrosion cracking (SSCC) susceptibility of 20# steel weld joints. 20# steel is a commonly selected pipe material for ground gas pipelines, and there is a risk of welds cracking after years of service. The selection of a corrosive environment is based on the working conditions of high-sulfur oil fields on site. Slow strain rate tensile (SSRT) tests were conducted under simulated high-sulfur gathering and transportation conditions across varying temperatures and H S concentrations. The mechanical properties, SSCC susceptibility, fracture morphology, and elemental composition of fracture surfaces were systematically analyzed. As H S concentration increased (5%, 7.5%, 10%) and temperature decreased (30-60 °C), the elongation after fracture and the reduction in area of 20# steel decreased, while the yield strength and SSCC susceptibility increased. The H S concentration range of 0-5% represented a critical sensitivity interval for the material, where elongation after fracture decreased by up to 74%. Within the 5-10% H S range, elongation decreased by only 2.11%, indicating a slowing trend of fracture toughness deterioration, though SSCC susceptibility still increased by 12%. Increasing the temperature from 30 °C to 60 °C reduced SSCC susceptibility by approximately 30%, confirming higher susceptibility at lower temperatures. Temperature exerts a lesser influence on material performance than H S concentration. Also, 20# steel remains within the SSCC brittle fracture sensitivity zone in sulfur-containing environments, necessitating strict quality control to avoid defects and stress concentrations. In high-sulfur environments (H S > 5%), further increases in H S concentration have a diminished effect on cracking susceptibility.

Background Anemia remains a critical global health challenge, affecting 24.3% of the global population. While air pollution and depressive symptoms are recognized as potential risk factors, their combined effects and underlying mechanisms on anemia risk remain underexplored. This study aims to explore the associations between air pollution (PM₁, PM₂.₅ and O₃), depressive symptoms, and anemia risk using data from the China Health and Retirement Longitudinal Study. Methods Data from 6,526 participants in the CHARLS database from 2011 to 2015 were analyzed. Air pollution exposure was assessed using geospatial modeling, while depressive symptoms were measured by the CESD-10 scale. Anemia was defined based on hemoglobin concentrations. Logistic regression models, restricted cubic spline analysis and mediating effect analysis were used to examine the relationships between air pollutants, depressive symptoms and anemia risk. Results Long-term exposure to PM₁ (OR = 1.12, 95% CI: 1.05–1.19, P  < 0.001) and PM₂.₅ (OR = 1.10, 95% CI: 1.03–1.17, P  = 0.004) was associated with elevated anemia risk, whereas O₃ exhibited a protective effect (OR = 0.68, 95% CI: 0.64–0.73, P  < 0.001). Depressive symptoms mediated 5.6% of the PM₁-anemia association ( P  = 0.020) and 3.1% of the O₃-anemia pathway ( P  < 0.001). Stratified analyses revealed stronger PM-related anemia risks in rural residents (vs. urban) and western China (vs. eastern) while O₃’s protective effect was pronounced in populations with lower education or pre-existing digestive diseases. Conclusion This study provides novel evidence that depressive symptoms partially mediate the effects of PM₁ and O₃ on anemia, underscoring the intertwined roles of environmental and mental health in hematological outcomes.

This study was intended to investigate the effect of SAMD1 on antiphospholipid syndrome (APS)-induced pregnancy complications in mice. The mRNA and protein expression of SAMD1 in APS patients and healthy controls was detected by qRT-PCR and western blot. Anti-B GPI and ACA levels were tested by ELISA, MMP-9, iNOS, ICAM-1 and MCP-1 mRNA and protein levels determined by qRT-PCR and western blot, cellular senescence detected by β-galactosidase staining, cell proliferation ability detected by CCK-8 assay, cell viability detected by trypan blue staining, cell mobility detected by Transwell, and cell angiogenesis ability detected by matrigel tube formation assay. An APS pregnant mouse model was constructed, and the embryo absorption rate was calculated. SAMD1 expression was low in serum of APS patients, which was correlated with the history of thrombosis and the number of adverse pregnancies. Anti-B GPI and ACA levels were increased in APS. The expressions of MMP-9, iNOS, ICAM-1, and MCP-1 were also significantly upregulated in HUVECs treated with APS serum. APS promoted HUVEC senescence and inhibited cell proliferation, migration and angiogenesis. Overexpression of SAMD1 reversed the above results. Experiments on the APS pregnant mouse model confirmed that overexpression of SAMD1 reduced the rate of fetal loss. SAMD1 may reduce APS-induced embryo loss by regulating cellular senescence, proliferation, migration, and angiogenesis.

We deliberated a case report of seven cases to investigate whether inhibitors of tumor necrosis factor-α (TNF-) could reduce pregnancy dangers caused by antiphospholipid syndrome (APS). Patient 1 was diagnosed with NC-OAPS and Hashimoto, Patient 3 was with SN-APS and Hashimoto, Patient 2, 3, 4 were with SN-APS, Patient 5 and 6 were with OAPS, and Patient 7 was with OAPS and PCOS. Patient 4 took the longest period to report the disappearance of symptoms (7 days), followed by patients 1 and 5, and lastly, 2, 3, 6 and 7; after treatment, TNF-α decreased to varying degrees in 7 patients, among which Patient 1, 3, 6, 7 reached the ideal level (< 8.1) and Patient 5 reached the highest level (123.04); Patient 6 and 7 were ongoing pregnancies. The fetuses were born to the desired gestational age except the fetus from Patient 1. A total of 5 patients underwent cesarean delivery. The average height of the newborns was 48.20 cm and the average weight was 2.50 kg. The Apgar scores ranged between 8 and 10. The ongoing pregnancies as a limitation of the dataset. Collectively, we found that TNF-α Inhibitors could prolong gestational period.

Purpose A large number of high-frequency harmonic voltages exist in the output voltage of the inverter, which will affect the performance of the motor. The purpose of this paper is to obtain the influence of high frequency harmonic voltage on the performance of the line start permanent magnet synchronous motor (LSPMSM) and reveal the mechanism of influence. The research results can provide help for the design of LSPMSM driven by inverter drives. Design/methodology/approach First, the actual output voltage data of the inverter is collected, and then the fundamental voltage and high frequency harmonic voltage data can be obtained by performing the fast Fourier transformation method on the voltage data. Second, the finite element model is established. During the finite element calculation, the obtained fundamental voltage and the main harmonic voltage components are used as the voltage source. To research the effect of high frequency harmonic voltage on the performance of motor, a reference group without high frequency harmonic voltage is set up, which is used to compare and analyze the effect of high-frequency harmonics on the performance of the motor. To verify the correctness of the model, a prototype based on the model parameters is manufactured, and then the back EMF experiment and load experiment are performed. The test data and calculation results are compared and analyzed. Findings The coupling relationship between high frequency time harmonic magnetic field and low frequency space harmonic magnetic field is obtained. The stator copper loss and rotor eddy-current loss are calculated and analyzed under normal supply voltage and abnormal supply voltage, and the influence mechanism is revealed Originality/value The coupling relationship between high frequency time harmonic magnetic field and low frequency space harmonic magnetic field is obtained. The sensitivity of the high frequency harmonic voltage to the stator copper loss and rotor eddy-current loss is obtained, and the mechanism of losses change is revealed.

Activation of microglia is closely associated with neuroinflammation. However, the cell‐intrinsic molecular mechanisms translating microglia activation into neuroinflammation are only partially understood. Here, it is shown that deubiquitinating enzyme A (DUBA) is upregulated in microglia under neuroinflammatory conditions in both mice and humans. Mechanistically, activation of microglia induces DUBA self‐deubiquitination and stabilization, leading to the rapid upregulation of DUBA protein levels. In turn, stabilized DUBA increases proinflammatory gene induction in activated microglia by enhancing the activation of nuclear factor‐κB (NF‐κB) and mitogen‐activated protein kinase (MAPK) signaling. Of note, DUBA promotes NF‐κB and MAPK activation by stabilizing interleukin‐1 receptor activated kinase 1 (IRAK1) through K48 deubiquitination. Importantly, specific ablation of DUBA in microglia mitigates lipopolysaccharide‐induced depression‐like behavior and ischemic stroke injury in mice by limiting neuroinflammation. Collectively, these findings establish DUBA as a key regulator of microglia in neuroinflammation and uncover novel molecular mechanisms for DUBA in inflammatory signal transduction. The protein levels of deubiquitinating enzyme A (DUBA) are rapidly upregulated in microglia after activation of Toll‐like receptor 4 (TLR4). In turn, DUBA potentiates TLR4‐induced proinflammatory signal transduction in microglia by stabilizing interleukin‐1 receptor activated kinase 1 (IRAK1) through K48 deubiquitination. Targeted ablation of microglial DUBA attenuates lipopolysaccharide‐induced depression‐like behavior and ischemic stroke injury in mice by reducing neuroinflammation.

Objective This study was intended to investigate the effect of SAMD1 on antiphospholipid syndrome (APS)‐induced vascular injury in human umbilical vein endothelial cells (HUVECs) and pregnancy complications in mice. Methods The expression of SAMD1 in APS patients and healthy controls was detected by quantitative real‐time polymerase chain reaction (qRT‐PCR). Anti‐B2GPI and anticardiolipin antibody (ACA) levels were tested by enzyme‐linked immunosorbent assay, MMP‐9, iNOS, ICAM‐1, and MCP‐1 mRNA and protein levels determined by qRT‐PCR and Western blot, cellular senescence detected by β‐galactosidase staining, cell proliferation ability detected by CCK‐8 assay, cell viability detected by trypan blue staining, cell mobility detected by Transwell, and cell angiogenesis ability detected by matrigel tube formation assay. An APS pregnant mouse model was constructed, and the embryo absorption rate was calculated. Results SAMD1 expression was low in serum of APS patients, which was correlated with the history of thrombosis and the number of adverse pregnancies. Anti‐B2GPI and ACA levels were increased in APS. The expressions of MMP‐9, iNOS, ICAM‐1, and MCP‐1 were also significantly upregulated in HUVECs treated with APS serum. APS promoted HUVEC senescence and inhibited cell proliferation, migration, and angiogenesis. Overexpression of SAMD1 reversed the above results. Experiments on the APS pregnant mouse model confirmed that overexpression of SAMD1 reduced the rate of fetal loss. Conclusion SAMD1 may reduce APS‐induced vascular injury and embryo loss by regulating cellular senescence, proliferation, migration, and angiogenesis. The expression of SAMD1 decreased and the levels of anti‐B2GPI, anticardiolipin antibody, MMP‐9, iNOS, ICAM‐1, and MCP‐1 increased in human umbilical vein endothelial cells incubated with 10% peripheral blood serum of antiphospholipid syndrome (APS) patients, with enhanced cell senescence and reduced cell proliferation, viability, migration, and angiogenesis. An increase in placental resorption was detected in the pregnant mouse model of APS.