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As the core of high-voltage direct-current transmission technology, the DC converter valve and its key power device thyristor face a high risk of failure caused by atmospheric neutron when operating in high-altitude areas. The atmospheric neutron failure rate of thyristors used at high altitudes can be quantitatively evaluated by conducting accelerated irradiation tests. The accelerated irradiation experiments of 8.5 kV/5 kA thyristor for DC transmission were carried out at different temperatures by using the China spallation neutron source. The atmospheric neutron-induced single-event burnout (SEB) for thyristor was verified by experiments. It is manifested as a sudden surge in reverse bias leakage current during irradiation, and the device loses its high voltage blocking ability. The failure rates of thyristor caused by atmospheric neutrons were also evaluated based on the accelerated irradiation experimental results. The reverse bias voltages and junction temperatures of thyristor are the key factors affecting the failure rates. The atmospheric neutron-induced failure rates increase exponentially with the reverse bias voltage. The atmospheric neutron failure rate of the 8 500 V thyristor operating at 4 350 V will reach 673 FIT at room temperature at sea level; when the bias voltage drops to 4 100 V (a decrease of about 5.7%), the atmospheric neutron failure rate can be reduced to 11 FIT. In addition, the failure rate increases with the decrease of temperature. The failure rate at 5℃ is nearly 6 times higher than that at 25℃ when the device is biased at 50% of the rated voltage. Based on TCAD simulations, the failure mechanism of thyristor caused by irradiation is further verified. The simulation results show that the SEB failure is directly related to the avalanche breakdown effect-induced by the incident radiation particles. For radiation-induced SEB failure of thyristors, the sensitive region is the N-drift/P-substrate junction depletion region (corresponding to the electric field concentration region under reverse bias of thyristors). When radiation particles are incident into the sensitive region, it can cause the concentration of electric field near the incident location, resulting in additional electric field spikes. If the peak of the electric field exceeds the critical electric field Ec (about 1.64×105 V/cm), it will induce avalanche breakdown. The high voltage reverse bias high current state caused by avalanche breakdown ultimately leads to the failure of the thyristor. The avalanche breakdown effect is positively correlated with the reverse bias voltage of thyristor and negatively correlated with the junction temperature. This is consistent with the variation of atmospheric neutron failure rates with bias voltages and junction temperatures.

In this paper, the total ionize dose (TID) irradiations for NPN bipolar transistors were carried out by 60Co γ rays. Obvious degradations were observed after irradiation, which are manifested as the increase of base current and the decrease of current gain. A more obvious increase of base current was observed at lower emitter junction bias. It shows that the degradation of the base current mainly origins from the increase of the recombination current of the emitter junction, since the recombination current component in base current is dominant at lower emitter junction bias. It can be concluded that the performance degradations of bipolar transistors are mainly due to the increase of recombination current caused by radiationinduced traps in the oxide. It is found that the bias condition during irradiation is the key factor affecting the TID effect of NPN transistor. The reverse bias is a worse bias condition than the zero bias during irradiation. Furthermore, the TID effect of two kinds of NPN bipolar transistors was compared. The two kinds of transistors have the same structure, except that one of the devices is radiation hardened by improving the surface state of the base region. The radiation induced degradations in radiation hardened devices are less than that in unhardened devices. For the unhardened device, the base current increases from 882×10-8 A to 367×10-7 A at |VEB|=05 V after 50 krad(Si) irradiation, increased by 316%. While for the hardened device, the base current increases from 751×10-8 A to 119×10-7 A at |VEB|=05 V after 50 krad(Si) irradiation, increased by 584%. Finally, the deep level traps in NPN transistors were measured by deep level transient spectrum (DLTS) before and after irradiation. The radiation will increase the trap densities and alter the energy level of the traps for the unhardened devices. By comparing the DLTS results of hardened and unhardened devices, it is found that there are great differences in their native traps. The energy level of the traps in the hardened devices is farther away from the center of the band gap than the unhardened devices. It may implies that the radiation hardness of the device can be achieved by improving the native trap states of the device.

Based on the test site at the Qinghai�Tibet Plateau with an altitude of 4 300 m, atmospheric neutron single event effects of a 65 nm high�speed large�area static random access memory (SRAM) array were measured in real�time. By breaking through key technologies such as effect screening, intelligent remote measurement and control, a total of 39 single�event upset were observed during the 153 d test period, of which multiple�cell upset (MCU) accounts for 23%, and the largest MCU is 9 bits. The contribution ratios of high�energy neutron, thermal neutron and alpha particle were analyzed in detail, and based on the multi�ground neutron flux data, the single�bit upset (SBU) and MCU failure in time (FIT) at Beijing ground and 10 km high�altitude application were deduced. It is found that the main cause of soft error on the ground is the alpha particle. As the altitude increases, the contribution of atmospheric neutron to soft error increases significantly. All MCUs are caused by high�energy neutron, and the MCU FIT value at an altitude of 10 km in Beijing is obviously increased. Its proportion increases from 8% of the ground to 26%. In combination with the device layout, an in�depth analysis of the MCU generation mechanism was carried out. Finally, a goal�oriented optimization method of memory soft error hardening strategy was proposed.

BackgroundIn China, the growing prevalence of bronchopulmonary dysplasia (BPD) in increased number of survived very preterm and extremely preterm infants, seriously endangers the life and impairs quality of life in this population. There are different degrees of hemodynamic changes in preterm infants in the process of developing BPD, however, there are relatively few studies about the correlation between the occurrence of BPD and hemodynamic indicators in preterm infant.ObjectiveTo examine predictive value of the hemodynamic indexes for BPD in premature infants.MethodsOne hundred and sixty-one premature infants (hospitalized within 1 hour of birth, gestational age 0.05) . Preterm infants with BPD had higher incidence of neonatal asphyxia, neonatal respiratory distress syndrome, neonatal pneumonia, and retinopathy of prematurity than those without (P0.05) . PI values at 1, 12 and 24 hours after birth differed significantly between the two groups (P0.05) . In predicting BPD, the PI at 1-hour, 12-hour, and 24-hour was 0.847〔95%CI (0.788, 0.906) , P

Objective: This study aimed to investigate the effect of METTL3 knockdown on osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) in the weak inflammation microenvironments, as well as the underlying mechanisms. Materials and Methods: PDLSCs were stimulated by lipopolysaccharide from Escherichia coli (E. coli LPS), followed by quantification of METTL3. METTL3 expression was assessed using RT‐qPCR and Western blot analysis in periodontitis. METTL3 knockdown PDLSCs were stimulated with or without E. coli LPS. The evaluation included proinflammatory cytokines, osteogenic markers, ALP activity, and mineralized nodules. Bioinformatics analysis and Western blot determined the association between METTL3 and the PI3K/Akt pathway. Results: METTL3 was overexpressed in periodontitis. METTL3 knockdown in PDLSCs reduced proinflammatory cytokines, osteogenic markers, ALP activity, and mineralized nodules in both environments. Bioinformatics analysis suggested a link between METTL3 and the PI3K/Akt pathway. METTL3 knockdown inhibited PI3K/Akt signaling pathway activation. Conclusion: METTL3 knockdown might inhibit osteogenesis in PDLSCs through the inactivation of PI3K/Akt signaling pathway. Concomitant findings might shed novel light on the roles and potential mechanisms of METTL3 in the LPS‐stimulated inflammatory microenvironments of PDLSCs. [ABSTRACT FROM AUTHOR]

Surface α-particle emissivity testing and spectral characterization of two leaded tin spheres (Sn10%Pb90%, Sn63%Pb37%) and one lead-free tin sphere (Sn96.5%Ag3.0%Cu0.5%, SAC305) were carried out. The results show that Sn10%Pb90% Sn spheres have the highest α-particle emissivity; Sn63%Pb37% Sn spheres are the next highest, which is an order of magnitude lower than the α-particle emissivity of Sn10%Pb90% Sn spheres; and SAC305 Sn spheres have the lowest emissivity, which is reduced by about 55.6% compared to the emissivity of Sn63%Pb37% Sn spheres. All three types of tin spheres, after purification treatment, achieved the grade of ultra-low alpha particle emissivity (<0.002 α/(cm2·h)). The internal radionuclide traceability of the tin sphere, combined with the energy spectrum, reveals that the emission spectrum of the tin sphere exhibits an obvious "single peak" characteristic, with the peak energy in the interval of 5 MeV~5.5 MeV. Comparative analyses revealed that 210Po is the main nuclide that produces alpha particles, and 210Po originates from the decay of 210Pb. Further Monte Carlo simulations show that α-particles with energies greater than 4.1 MeV in the measured energy spectrum all come from the contribution of radionuclides within 5 μm of the surface layer of the tin sphere, which accounts for 60% of the total radioactivity. Combining the experimental and simulation results, it is found that the internal radionuclides of the tin sphere are characterized by more surface layer and less internal layer. The above results are of great significance for the establishment of α-particle mitigation methods for tin spheres. [ABSTRACT FROM AUTHOR]

Aim: This Mendelian randomization (MR) study was performed to explore the potential bidirectional causal relationship between the gut microbiome (GM) and periodontitis. Materials and Methods: We used genetic instruments from the genome‐wide association study of European descent for periodontitis from the GeneLifestyle Interactions in Dental Endpoints (GLIDE) consortium (17,353 cases and 28,210 controls) and the FinnGen consortium (4434 cases and 259,234 controls) to investigate the causal relationship with GM (the MiBioGen consortium, 18,340 samples), and vice versa. Several MR techniques, which include inverse variance weighting (IVW), MR‐Egger, weighted median, simple mode and weighted mode approaches, were employed to investigate the causal relationship between the exposures and the outcomes. Cochran's Q‐test was performed to detect heterogeneity. The MR‐Egger regression intercept and MR pleiotropy residual sum and outlier test (MR‐PRESSO) were conducted to test potential horizontal pleiotropy. Leave‐one‐out sensitivity analyses were used to assess the stabilities of single nucleotide polymorphisms (SNPs). Finally, the IVW results from the two databases were analysed using meta‐analysis. Results: We confirmed three potential causal relationships between GM taxa and periodontitis at the genus level. Among them, the genera Alistipes and Holdemanella were genetically associated with an increased risk of periodontitis. In reverse, periodontitis may lead to a decreased abundance of the genus Ruminococcaceae UCG014. Conclusions: The demonstration of a causal link between GM and periodontitis provides compelling evidence, highlighting the interconnectivity and interdependence of the gut–oral and oral–gut axes. [ABSTRACT FROM AUTHOR]

Zoonoses are diseases and infections naturally transmitted between humans and vertebrate animals. They form the dominant group of diseases among emerging infectious diseases and represent critical threats to global health security. This dilemma is largely attributed to our insufficient knowledge of the pathogenesis regarding zoonotic spillover. Long non-coding RNAs (lncRNAs) are transcripts with limited coding capacity. Recent technological advancements have enabled the identification of numerous lncRNAs in humans, animals, and even pathogens. An increasing body of literature suggests that lncRNAs function as key regulators in zoonotic infection. They regulate immune-related epigenetic, transcriptional, and post-transcriptional events across a broad range of organisms. In this review, we discuss the recent research progress on the roles of lncRNAs in zoonoses. We address the classification and regulatory mechanisms of lncRNAs in the interaction between host and zoonotic pathogens. Additionally, we explore the surprising function of pathogen-derived lncRNAs in mediating the pathogenicity and life cycle of zoonotic bacteria, viruses, and parasites. Understanding how these lncRNAs influence the zoonotic pathogenesis will provide important therapeutic insights to the prevention and control of zoonoses. [ABSTRACT FROM AUTHOR]

The boom refuelling system has a large refueling flow, and the refueling joint when the refueling is interrupted in an emergency will cause pressure shock and pressure pulsation. In severe cases, it will cause vibration of the pipeline system, reduce system reliability, and seriously endanger flight safety. Adding a device similar to an accumulator at the end of the pipeline where pressure shock occurs can well absorb the shock pressure. This paper uses a certain type of aircraft as a background to simulate the construction of a rigid air refueling pipeline system with a buffer device. The emphasis is on the pressure shock suppression characteristics of the buffer device. The simulation analysis of the opening parameters of the expansion cavity entrance includes the number and size of the buffer device. The impact of pressure shock performance. The results show that: the more openings and the larger the pore size, the larger the first pressure peak and the smaller the second pressure peak; while increasing the total flow area can effectively reduce the pressure shock suppression effect of the buffer device.

Background and Objectives: Periodontitis, a prevalent chronic inflammatory condition, poses a significant risk of tooth loosening and subsequent tooth loss. Within the realm of programmed cell death, a recently recognized process known as necroptosis has garnered attention for its involvement in numerous inflammatory diseases. Nevertheless, its correlation with periodontitis is indistinct. Our study aimed to identify necroptosis‐related lncRNAs and crucial lncRNA‐miRNA‐mRNA regulatory axes in periodontitis to further understand the pathogenesis of periodontitis. Materials and Methods: Gene expression profiles in gingival tissues were acquired from the Gene Expression Omnibus (GEO) database. Selecting hub necroptosis‐related lncRNA and extracting the key lncRNA‐miRNA‐mRNA axes based on the ceRNA network by adding novel machine‐learning models based on conventional analysis and combining qRT‐PCR validation. Then, an artificial neural network (ANN) model was constructed for lncRNA in regulatory axes, and the accuracy of the model was validated by receiver operating characteristic (ROC) curve analysis. The clinical effect of the model was evaluated by decision curve analysis (DCA). Weighted correlation network analysis (WGCNA) and single‐sample gene set enrichment analysis (ssGSEA) was performed to explore how these lncRNAs work in periodontitis. Results: Seven hub necroptosis‐related lncRNAs and three lncRNA‐miRNA‐mRNA regulatory axes (RP11‐138A9.1/hsa‐miR‐98‐5p/ZBP1 axis, RP11‐96D1.11/hsa‐miR‐185‐5p/EZH2 axis, and RP4‐773 N10.4/hsa‐miR‐21‐5p/TLR3 axis) were predicted. WGCNA revealed that RP11‐138A9.1 was significantly correlated with the "purple module". Functional enrichment analysis and ssGSEA demonstrated that the RP11‐138A9.1/hsa‐miR‐98‐5p/ZBP1 axis is closely related to the inflammation and immune processes in periodontitis. Conclusion: Our study predicted a crucial necroptosis‐related regulatory axis (RP11‐138A9.1/hsa‐miR‐98‐5p/ZBP1) based on the ceRNA network, which may aid in elucidating the role and mechanism of necroptosis in periodontitis. [ABSTRACT FROM AUTHOR]