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Although multiscale filament eruptions serve as significant triggers for various energetic release processes in the solar atmosphere, the underlying mechanisms remain elusive. Using coordinated observations from the New Vacuum Solar Telescope, Solar Dynamics Observatory, and Chinese Hα Solar Explorer, we present a unique two-sided loop jet and evidence of magnetic reconnection driven by a medium-scale filament eruption within a lantern-like structure. Reconnection between the brightening part of the erupting filament and the overlying S-shaped magnetic loops produced the two-sided loop jet. This jet exhibited asymmetric spires, an S-shaped morphology, coexistence of hot and cool components, and a threefold speed difference between spires resulting from uneven magnetic confinement. Clockwise rotation indicates twists transferred from the filament to the S-shaped loops. The eruption also induced reconnection between adjacent coronal loops, forming a current sheet near the postflare loops. Concurrently, the rotation and descent of the dark part of the erupting filament drove the reconfiguration of the ambient chromospheric magnetic field through secondary effects, resulting in the appearance of a new set of chromospheric fibrils. Subsequent reconnection between these new and preexisting fibrils was confirmed by reconnection inflows and outflows, a current sheet, cusp-shaped structures, and expelled plasma blobs. Therefore, both eruptive events are directly or indirectly involved in driving the reconfiguration of the local magnetic field, facilitating the release and transfer of mass and energy across the solar atmosphere via jet and magnetic reconnection.

We used high-resolution observations from the New Vacuum Solar Telescope and the Solar Dynamics Observatory to perform a detailed multiwavelength analysis of the fine structures in the flare ribbon of a C3.9-class flare on 2021 April 22. A segment of the flare ribbon was rooted in a sunspot light bridge and exhibited discrete substructures that we term “burrs,” with equivalent diameters of 233–895 km and intercore separations of 1129–1739 km. These structures are characterized by discrete redshifted cores, accompanied by “tails” (length 700–1370 km and width 310–600 km) exhibiting faint blueshifts. These structures exhibit systematic slipping motions along the ribbon, with apparent velocities decelerating from about 40–21 km s−1, and display a distinct quasiperiodicity of ∼6 minutes in Hα and extreme-ultraviolet passbands. Differential emission measure (DEM) analysis confirms the emitting plasma is multithermal, dominated by temperatures of 1–2 MK. The observed morphology and kinematics are consistent with the scenario of impulsive energy deposition by precipitating plasmoids (oblique flux ropes) originating from tearing-mode fragmentation in the coronal current sheet. The specific spatiotemporal correlation between the tails and blueshifts supports the hypothesis of untwisting magnetic flux ropes. Furthermore, the ∼6 minute periodicity suggests that the reconnection process may be modulated by photospheric p-mode oscillations coupled with the tearing-mode instability. Our findings provide observational evidence that these light-bridge-anchored fine structures constitute elementary units of flare energy release.

To better understand the characteristics, driving mechanisms, and potential heating contributions of chromospheric jets, we analyze two contrasting types: one originating from within the sunspot penumbra (inside jets) and the other originating from outside the penumbra (outside jets). Statistical analysis of 100 jets (50 inside jets and 50 outside jets) reveals that inside jets have a projected velocity range of 4–14 km s−1, a length range of 1–4 Mm, a width range of 0.2–0.6 Mm, and a lifetime range of 135–450 s, with mean values of 7.90 km s−1, 2.61 Mm, 0.41 Mm, and 260 s, respectively. About 52% of inside jets are associated with brightenings in Hα blue wing images, and some show high-temperature signatures, suggesting a connection with localized energy release. In contrast, outside jets have higher velocities (8–50 km s−1, average 19.04 km s−1), greater lengths (average 6.26 Mm, up to 27.27 Mm), slightly larger widths (average 0.46 Mm), and longer lifetimes (135–630 s, average 327 s). They typically originate from regions of opposite magnetic polarities and are associated with magnetic flux emergence and extreme-ultraviolet brightenings. Some outside jets correspond to coronal jets with inverted Y-shaped structures and temperatures exceeding one million Kelvin. Our results suggest that both jet types are driven by magnetic reconnection occurring in distinct magnetic field configurations and contribute to chromospheric and coronal heating.

We investigate the interaction between two filaments (F1 and F2) and their subsequent magnetic reconnection in active region (AR) NOAA 13296 and AR NOAA 13293 on 2023 May 9, utilizing high spatial and temporal resolution and multiwavelength observational data from the Solar Dynamics Observatory, the New Vacuum Solar Telescope, and the Chinese Hα Solar Explorer. The movement of F1 from the southeast toward the northwest, driven by the motion of the positive magnetic polarity (P1), leads to a collision and reconnection with F2. This reconnection exchanges their footpoints, resulting in the formation of two new filaments (F3 and F4) consistent with “slingshot” type filament interaction. During the interaction, the current sheet, moving due to the motion of F1, and the reconnection outflows, moving along F3 and F4, were both observed. The current sheet is rarely observed in the slingshot type filament interaction, measuring approximately 2.17 Mm in length and 0.84 Mm in width. After the interaction, the F1 disappears, whereas a portion of F2 remains, indicating that the interaction involves partial slingshot reconnection, due to the unequal magnetic flux between the filaments. The residual part of F2 will undergo another magnetic reconnection in the same interaction region with the magnetic loops connecting polarities N1 and P1. The material generated by the reconnection is continuously injected into F4, leading to its final morphology. The findings enhance our understanding of slingshot-type filament interactions, indicating that partial slingshot reconnections between filaments may be more common than full slingshot events.

The formation mechanism of spicules is fundamentally important for understanding mass and energy transport from the chromosphere into the corona. Recent studies suggested that spicules may be powered by microfilament eruptions. However, direct observational evidence remains limited due to insufficient spatial resolution. Using high-resolution Hα broadband observations from the Visible Broadband Imager on board the Daniel K. Inouye Solar Telescope, we identify 30 spicule events triggered by microfilament eruptions in a quiet-Sun region near the solar disk center on 2023 August 29. The detected microfilaments have an average length of 0.93 ± 0.46 Mm and a minimum length of 0.17 Mm, substantially smaller than previously reported minifilaments. We identify two distinct morphological classes of ejecta: individual spicules associated with smaller microfilaments and enhanced spicular activities associated with larger microfilaments. Moreover, some events exhibit apparent twisting motions. All these high-resolution observations provide compelling evidence that spicules can be triggered by microfilament eruptions.

Background Atherosclerosis is characterized by complex pathological processes, including endothelial dysfunction and inflammation. The underlying pathogenic mechanisms have been well elucidated; however, effective treatments are yet to be validated. Our study explored the novel application of a recognized antiviral agent, remdesivir, focusing on its impact on endothelial activation and atherosclerosis. Methods Pharmacological treatment with remdesivir significantly reduced atherosclerotic lesions in the total aorta and decreased VCAM-1 expression in aortic roots of ApoE−/− mice. Remdesivir notably attenuated ox-LDL-induced endothelial cell (EC) activation, monocyte adhesion, and ROS production. In HUVECs, TAL1 interference via siRNA significantly increased TRAF6 protein levels, which was reversed by remdesivir. Remdesivir also reduced both total and K63-linked ubiquitination of TRAF6 in HUVECs. Immunoprecipitation assays revealed diminished co-localization of the two proteins under ox-LDL treatment, but this effect was reversed by remdesivir. Importantly, ectopic adeno-associated virus (AAV)-mediated overexpression of TAL1 reduced atherosclerotic lesions and VCAM-1 expression in the aorta of ApoE−/− mice. Results In ApoE –/– mice fed with a Western diet, remdesivir greatly attenuated atherosclerosis progression. At the cellular level, remdesivir suppressed oxidative stress, THP-1 adhesion, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1 via oxidized low-density lipoprotein in human umbilical vein endothelial cells. T-cell acute lymphoblastic leukemia 1 (TAL1) functions by interacting with the ubiquitin E3 ligase TNF receptor-associated factor 6 (TRAF6) to ubiquitinate TRAF6, inhibiting nuclear factor kappa B activation. Remdesivir also restored the TAL1-TRAF6 interaction and decreased endothelial activation. Endothelial-specific TAL1 over-expression in ApoE –/– mice significantly reduced aortic plaque formation. Conclusions Remdesivir impedes atherosclerosis progression by re-establishing the interaction between TAL1 and TRAF6, diminishing endothelial activation. These findings offer an innovative therapeutic approach for atherosclerosis.

Identification of cytotoxic T lymphocyte (CTL) epitopes from tumor antigens is essential for the development of peptide vaccines against tumor immunotherapy. Among all the tumor antigens, the caner-testis (CT) antigens are the most widely studied and promising targets. PLAC1 (placenta-specific 1, CT92) was considered as a novel member of caner-testis antigen, which expressed in a wide range of human malignancies, most frequently in breast cancer. In this study, three native peptides and their analogues derived from PLAC1 were predicted by T cell epitope prediction programs including SYFPEITHI, BIMAS and NetCTL 1.2. Binding affinity and stability assays in T2 cells showed that two native peptides, p28 and p31, and their analogues (p28-1Y9 V, p31-1Y2L) had more potent binding activity towards HLA-A*0201 molecule. In ELISPOT assay, the CTLs induced by these four peptides could release IFN-γ. The CTLs induced by these four peptides from the peripheral blood mononuclear cells (PBMCs) of HLA-A*02 + healthy donor could lyse MCF-7 breast cancer cells (HLA-A*0201 + , PLAC1 + ) in vitro. When immunized in HLA-A2.1/K b transgenic mice, the peptide p28 could induce the most potent peptide-specific CTLs among these peptides. Therefore, our results indicated that the peptide p28 (VLCSIDWFM) could serve as a novel candidate epitope for the development of peptide vaccines against PLAC1-positive breast cancer.

Uncertainty exists about whether lowering systolic blood pressure to less than 120 mm Hg is superior to that of less than 140 mm Hg, particularly in patients with diabetes and patients with previous stroke. In this open-label, blinded-outcome, randomised controlled trial, participants with high cardiovascular risk were enrolled from 116 hospitals or communities in China. We used minimised randomisation to assign participants to intensive treatment targeting standard office systolic blood pressure of less than 120 mm Hg or standard treatment targeting less than 140 mm Hg. The primary outcome was a composite of myocardial infarction, revascularisation, hospitalisation for heart failure, stroke, or death from cardiovascular causes, assessed by the intention-to-treat principle. This trial was registered with ClinicalTrials.gov, NCT04030234. Between Sept 17, 2019, and July 13, 2020, 11 255 participants (4359 with diabetes and 3022 with previous stroke) were assigned to intensive treatment (n=5624) or standard treatment (n=5631). Their mean age was 64·6 years (SD 7·1). The mean systolic blood pressure throughout the follow-up (except the first 3 months of titration) was 119·1 mm Hg (SD 11·1) in the intensive treatment group and 134·8 mm Hg (10·5) in the standard treatment group. During a median of 3·4 years of follow-up, the primary outcome event occurred in 547 (9·7%) participants in the intensive treatment group and 623 (11·1%) in the standard treatment group (hazard ratio [HR] 0·88, 95% CI 0·78–0·99; p=0·028). There was no heterogeneity of effects by diabetes status, duration of diabetes, or history of stroke. Serious adverse events of syncope occurred more frequently in the intensive treatment group (24 [0·4%] of 5624) than in standard treatment group (eight [0·1%] of 5631; HR 3·00, 95% CI 1·35–6·68). There was no significant between-group difference in the serious adverse events of hypotension, electrolyte abnormality, injurious fall, or acute kidney injury. For hypertensive patients at high cardiovascular risk, regardless of the status of diabetes or history of stroke, the treatment strategy of targeting systolic blood pressure of less than 120 mm Hg, as compared with that of less than 140 mm Hg, prevents major vascular events, with minor excess risk. The Ministry of Science and Technology of China and Fuwai Hospital. For the Mandarin translation of the abstract see Supplementary Materials section.

Whelming evidence has demonstrated that WW domain containing E3 ubiquitin protein ligase 1 (WWP1) participates in a wide variety of biological processes and is tightly related to the initiation and progression of many tumors. Currently, although mounting evidence supports a role of WWP1 in tumor promotion and tumorigenesis, the potential roles of WWP1 and its biological functions in gastric carcinoma are not fully understood. Here, we found that WWP1 messenger RNA (mRNA) and protein were highly expressed in gastric carcinoma tissues and cells. High WWP1 mRNA and protein levels were tightly related to differentiation status, TNM stage, invasive depth, lymph node metastasis, and poor prognosis in gastric carcinoma. Furthermore, WWP1 siRNA significantly decreased WWP1 protein level in MKN-45 and AGS cells; meanwhile, WWP1 depletion markedly inhibited tumor proliferation in vitro and in vivo, arrested cell cycle at G0/G1 phase, and induced cell apoptosis in MKN-45 and AGS cells. Most notably, WWP1 downregulation both inactivated PTEN-Akt signaling pathway in MKN-45 and AGS cells. Taken altogether, our findings suggest that WWP1 acts as an oncogenic factor and should be considered as a novel interfering molecular target for gastric carcinoma.

Depression has been well established as an independent predictor of mortality and cardiac morbidity rates in patients with coronary artery disease (CAD). Evidence has shown that single nucleotide polymorphisms located in pre-microRNA (miRNA) or mature miRNA may modify various biological processes and affect the process of carcinogenesis, and the downregulation of neuronal nitric oxide synthase 1 (NOS1) can induce depression. It has been shown that NOS1 is the target gene of miR-146a, and that the rs2910164 G/C polymorphism can downregulate the expression of miR-146a. In the present study, computational analysis was used to identify the target of miR-146a, and a luciferase reporter assay system was used to validate NOS1 as a target gene of miR-146a. In addition, U251 cells were treated with miR-146a mimics/inhibitors to verify the negative regulatory association between miR-146a and NOS1. Reverse transcription-quantitative polymerase chain reaction analysis and western blot analysis were used to estimate the mRNA expression of NOS1 and the expression of miR-146a. The results showed that the 'seed sequence' was located within the 3′-untranslated region of NOS1 by searching an online miRNA database (www.mirdb.org), and the luciferase reporter assay confirmed that NOS1 was a direct target gene of miR-146a. It was also found that the mRNA and protein expression levels of NOS1 in U251 cells treated with miR-146a mimics and NOS1 small interfering RNA were substantially downregulated, compared with cells treated with the scramble control. The cells treated with miR-146a inhibitors showed increased expression of NOS1. In addition, the presence of a minor allele of the rs2910164 polymorphism was significantly associated with risk of depression in patients with CAD. Taken together, the findings indicated a decreased risk of depression in the patients with CAD who were carriers of the miR-146a rs2910164 C allele, and this association may be attributed to its ability to compromise the expression of miR-146a, and thereby increase the expression of its target gene, NOS1.