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By polymerization of gadolinium methacrylate (Gd (MAA)3), lead methacrylate (Pb(MAA)2) and methyl methacrylate (MMA), Gd and Pb were chemically bonded into polymers. The X-ray shielding performance was evaluated by Monte Carlo simulation method, and the results showed that the more metal functional organic monomer, the better the shielding performance of terpolymers. When the X-ray energy is 65 keV, Gd (MAA)3-containing polymers have better shielding performance than Pb(MAA)2-containing polymers. Gd could compensate for the weak absorption region of Pb. Therefore, polymers containing both Gd and Pb enhanced shielding efficiency against X-ray in various low-energy ranges. For obtaining terpolymers with uniform monomer compositions, the relationship between the monomer composition of the terpolymers and the conversion level was optimized by calculating the reactivity ratios. The value of reactivity ratios of r (Gd (MAA)3/Pb(MAA)2), r (Pb(MAA)2/Gd (MAA)3), r (Gd (MAA)3/MMA), r (MMA/Gd (MAA)3), r (Pb(MAA)2/MMA) and r (MMA/Pb(MAA)2) was 0.483, 0.004, 0.338, 2.508, 0.255, 0.029. The terpolymers with uniform monomer composition could be obtained by controlling the monomer compositions or conversion levels. The results can provide new radiation protection materials and contribute to the improvement in nuclear safety.

ABSTRACT Growing evidence indicates an association between gut dysbiosis and coronary artery disease (CAD). However, the underlying mechanisms relevant to stable CAD (SCAD) pathogenesis, based on microbe-host metabolism interactions, are poorly explored. Here, we constructed a quasi-paired cohort based on the metabolic background of metagenomic samples by the propensity score matching (PSM) principle. Compared to healthy controls (HCs), gut microbiome disturbances were observed in SCAD patients, accompanied by differences in serum metabolome, mainly including elevated acylcarnitine and decreased unsaturated fatty acids in SCAD patients, which implicated the reduced cardiac fatty acid oxidation. Moreover, we identified Ralstonia pickettii as the core strain responsible for impaired microbial homeostasis in SCAD patientsm and may be partly responsible for the decrease of host unsaturated fatty acid levels. These findings highlight the importance of unsaturated fatty acids, R. pickettii, and their interaction in the pathogenesis of SCAD. IMPORTANCE Stable coronary artery disease (SCAD) is an early stage of CAD development. It is important to understand the pathogenesis of SCAD and find out the possible prevention and control targets for delaying the progression of CAD. We observed reduced levels of unsaturated fatty acids (USFAs) in SCAD patients. However, the reduced USFAs may be related to Ralstonia Pickettii, which was the core strain responsible for the impaired gut microbial function in SCAD patients, and further affected the host's cardiovascular health by altering amino acids, vitamin B metabolism, and LPS biosynthesis. These findings not only emphasized the importance of USFAs for cardiovascular health, but also R. Pickettii for maintaining microbial function homeostasis. More importantly, our study revealed, for the first time, that enriched R. Pickettii might be responsible for the reduced USFAs in SCAD patients, which adds new evidence on the role of altered gut microbiota for SCAD formation.

Abstract Introduction Long noncoding RNA Mirt2 has been proven to be a suppressor of lipopolysaccharide (LPS) (a key player in sepsis)‐induced inflammation responses. Therefore, Mirt2 may also participate in sepsis. This study was carried out to analyze the interactions between Mirt2 and microRNA‐1246 (miR‐1246) in sepsis, with a specific focus on sepsis‐induced acute lung injury (sepsis‐ALI). Methods Forty sepsis patients (sepsis group; 23 males and 17 females; 40–65 years, 48.6 ± 6.3 years), 40 sepsis patients with acute lung injury (sepsis‐ALI group, 23 males and 17 females; 40–65 years, 48.7 ± 6.4 years), and 40 healthy controls (control group, 23 males and 17 females; 40–65 years, 48.6 ± 6.1 years) were included. Mirt2 and miR‐1246 expression in plasma samples from these patients were determined by a reverse transcription‐quantitative polymerase chain reaction (PCR). Overexpression of Mirt2 and miR‐1246 was achieved in human bronchial epithelial cells (HBEpCs) to explore the interaction between them. The effects of Mirt2 overexpression on miR‐1246 methylation were analyzed by methylation‐specific PCR. Cell apoptosis analysis was performed to analyze the role of Mirt2 and miR‐1246 in the apoptosis of HBEpCs. Results Mirt2 expression was downregulated in sepsis and was further downregulated in patients with sepsis‐ALI. Mirt2 and miR‐1246 found to be positively correlated. Downregulation of Mirt2 and miR‐1246 was observed in HBEpCs with LPS treatment. In HBEpCs, Mirt2 overexpression increased miR‐1246 expression but decreased its gene methylation. Cell apoptosis analysis showed that Mirt2 and miR‐1246 negatively regulated the apoptosis of HBEpCs induced by LPS. In addition, miR‐1246 inhibition reduced the inhibitory effects of Mirt2 overexpression on cell apoptosis. Conclusions Mirt2 may upregulate miR‐1246 through methylation to suppress lung cell apoptosis.

Abstract Whistler mode chorus, characterized by frequency chirping, is an important type of waves in planetary magnetospheres. To investigate the role of nonlinear wave particle interactions in excitation of chorus, analysis of electron phase space dynamics is required. While electron phase hole associated with rising tone chorus has been well studied, the phase space structure corresponding to falling tone chorus is less understood. Here, we investigate in detail the electron phase space dynamics in a spontaneously generated falling tone chorus with a parabolic type magnetic field, where field strength decreases away from the equator. We demonstrate the formation and evolution of electron phase space clump from downstream to upstream regions, and show that the variation of frequency chirping rate is caused by the movement of the source region. The results are consistent with the recently proposed Trap‐Release‐Amplify model, and should be useful to understand the mechanism of chorus frequency chirping.

The single-pass second-harmonic generation (SHG) of a vortex beam under low fundamental wave depletion is systematically studied. Vortex modes at 1064 nm with integer topological charges from ±1 to ±9 and fractional ones at ±0.75 are generated by modulating the fundamental Gaussian beam with different spiral phase plates. The frequency doubling of these fundamental vortex modes is realized via single-pass SHG through the KTP. A detailed theoretical model is set up in the single-pass SHG of the vortex beams. Theoretical analysis indicates that the higher the order of the vortex beams, the lower the SHG efficiency, when the beam waists and fundamental power are given. The experimentally measured SHG output characteristics verify those obtained via theoretical analysis. Conservation of the orbital angular momentum during the SHG process is also verified, regardless of the fractional or integer vortex beams. SH LG0,2l vortex beams with high mode purity are obtained. The beam waists of fundamental/SH in KTP measured using a 4f system demonstrate that the Rayleigh ranges of the fundamental wave and SH wave are the same. The paper comprehensively presents some basic laws in the single-pass SHG of a vortex beam. In addition, it also indicates that SHG is an effective method to improve the mode purity of vortex beam.

Skeletal muscle, which comprises a significant portion of the body, is responsible for vital functions such as movement, metabolism, and overall health. However, severe injuries often result in volumetric muscle loss (VML) and compromise the regenerative capacity of the muscle. Tissue-engineered muscles offer a potential solution to address lost or damaged muscle tissue, thereby restoring muscle function and improving patients’ quality of life. Induced pluripotent stem cells (iPSCs) have emerged as a valuable cell source for muscle tissue engineering due to their pluripotency and self-renewal capacity, enabling the construction of tissue-engineered artificial skeletal muscles with applications in transplantation, disease modelling, and bio-hybrid robots. Next-generation iPSC-based models have the potential to revolutionize drug discovery by offering personalized muscle cells for testing, reducing reliance on animal models. This review provides a comprehensive overview of iPSCs in tissue-engineered artificial skeletal muscles, highlighting the advancements, applications, advantages, and challenges for clinical translation. We also discussed overcoming limitations and considerations in differentiation protocols, characterization methods, large-scale production, and translational regulations. By tackling these challenges, iPSCs can unlock transformative advancements in muscle tissue engineering and therapeutic interventions for the future.

Objective To explore the possible way of proline‐serine–threonine phosphatase‐interacting protein 2 (PSTPIP2) influencing diabetes mellitus‐osteoarthritis (DM‐OA) progression. Methods In vivo, eight‐week‐old male Sprague Dawley rats were induced with DM‐OA by intraperitoneal injection of streptozotocin with high‐fat diet feeding and intra‐articular injection of monoiodoacetate. PSTPIP2 overexpression was achieved by intra‐articular injection of lentivirus vectors. PSTPIP2 expression was verified by real‐time polymerase chain reaction and Western blotting. Histological changes were examined by hematoxylin/eosin and safranin‐O/fast‐green staining. In vitro, rat synovial fibroblasts were induced DM‐OA by stimulation of high glucose (HG) and interleukin (IL)‐1β. PSTPIP2 overexpression was achieved by lentivirus infection. U0126 was added as an ERK inhibitor. Levels of tumor necrosis factor (TNF)‐α, IL‐6, and IL‐1β were detected using enzyme‐linked immunosorbent assay. Expression of matrix metalloproteinase (MMP)‐3, MMP‐13, aggrecanase‐2 (ADAMTS‐5), intercellular cell adhesion molecule (ICAM)‐1, extracellular regulated protein kinase (ERK) and phospho‐ERK (p‐ERK) was detected by Western blotting. Results In DM‐OA rats, PSTPIP2 relative messenger RNA (mRNA) level was significantly decreased compared to control rats. The protein expression was also decreased obviously. Inflammation score in synovium was dramatically increased, accompanying with increased TNF‐α, IL‐6, and IL‐1β levels. Osteoarthritis research society international (OARSI) score in cartilage was markedly increased, along with increased MMP‐3, MMP‐13, ADAMTS‐5, ICAM‐1, ERK and p‐ERK expression. In PSTPIP2‐overexpressed DM‐OA rats, PSTPIP2 mRNA level and protein expression was increased compared to DM‐OA rats received negative‐control lentivirus vectors. The inflammation score, as well as TNF‐α, IL‐6, and IL‐1β levels were dramatically decreased. Also, the OARSI score and protein expression of MMP‐3, MMP‐13, ADAMTS‐5, ICAM‐1, ERK and p‐ERK were decreased. In HG+IL‐1β‐treated rat synovial fibroblasts, PSTPIP2 protein expression was decreased compared to normal glucose (NG)‐treated cells. Levels of TNF‐α, IL‐6, and IL‐1β, as well as expression of MMP‐3, MMP‐13, ADAMTS‐5, ICAM‐1, ERK and p‐ERK were increased. After cells were infected with PSTPIP2‐overexpressed lentivirus, levels of TNF‐α, IL‐6, and IL‐1β, and expression of MMP‐3, MMP‐13, ADAMTS‐5, ICAM‐1, ERK and p‐ERK were obviously decreased compared to cells infected with NC lentivirus. In addition, ERK inhibitor U0126 treatment also decreased the TNF‐α, IL‐6, and IL‐1βlevels and MMP‐3, MMP‐13, ADAMTS‐5, ICAM‐1, ERK and p‐ERK expression in HG + IL‐1β treated rat synovial fibroblasts. Conclusion Overexpression of PSTPIP2 alleviates synovial inflammation and cartilage injury during DM‐OA progression via inhibiting ERK phosphorylation.