Abstract Background Ischemia-reperfusion (IR) induces increased release of extracellular vesicles in the heart and exacerbates myocardial IR injury. We have previously shown that propofol attenuates hypoxia/reoxygenation (HR)-induced injury in human umbilical vein endothelial cells (HUVECs) and that microvesicles derived from propofol-treated HUVECs inhibit oxidative stress in endothelial cells. However, the role of microvesicles derived from propofol post-treated HUVECs ((HR + P)-EMVs) in IR-injured cardiomyocytes is unclear. In this study, we aimed to investigate the role of (HR + P)-EMVs in cardiac IR injury compared to microvesicles derived from hypoxic/reoxygenated HUVECs (HR-EMVs) and to elucidate the underlying mechanisms. Methods Hypoxia/reoxygenation (HR) models of HUVECs and AC16 cells and a mouse cardiac IR model were established. Microvesicles from HR-injured HUVECs, DMSO post-treated HUVECs and propofol post-treated HUVECs were extracted by ultra-high speed centrifugation, respectively. The above EMVs were co-cultured with HR-injured AC16 cells or injected intracardially into IR mice. Flow cytometry and immunofluorescence were used to determine the levels of oxidative stress and apoptosis in cardiomyocytes. Apoptosis related proteins were detected by Western blot. Echocardiography for cardiac function and Evans blue-TTC staining for myocardial infarct size. Expression of lncCCT4-2 in EMVs and AC16 cells was analysed by whole transcriptome sequencing of EMVs and RT-qPCR. The molecular mechanism of inhibition of myocardial injury by (HR + P)-EMVs was elucidated by lentiviral knockdown of lncCCT4-2, plasmid overexpression or knockdown of CCT4, and actinomycin D assay. Results In vitro and in vivo experiments confirmed that HR-EMVs exacerbated oxidative stress and apoptosis in IR-injured cardiomyocytes, leading to increased infarct size and worsened cardiac function. Notably, (HR + P)-EMVs induced significantly less oxidative stress and apoptosis in IR-injured cardiomyocytes compared to HR-EMVs. Mechanistically, RNA sequencing of EMVs and RT-qPCR showed that lncCCT4-2 was significantly upregulated in (HR + P)-EMVs and cardiomyocytes co-cultured with (HR + P)-EMVs. Reduction of lncCCT4-2 in (HR + P)-EMVs enhanced oxidative stress and apoptosis in IR-injured cardiomyocytes. Furthermore, the anti-apoptotic activity of lncCCT4-2 from (HR + P)-EMVs was achieved by increasing the stability of CCT4 mRNA and promoting the expression of CCT4 protein in cardiomyocytes. Conclusions Our study showed that (HR + P)-EMVs uptake by IR-injured cardiomyocytes upregulated lncCCT4-2 in cardiomyocytes and promoted CCT4 expression, thereby inhibiting HR-EMVs induced oxidative stress and apoptosis. Highlights Microvesicles from hypoxic/reoxygenated HUVECs (HR-EMVs) exacerbated oxidative stress and apoptosis in IR-injured cardiomyocytes. Microvesicles from propofol post-treated HUVECs ((HR + P)-EMVs) induced diminished oxidative stress and apoptosis in IR-injured cardiomyocytes compared with microvesicles from hypoxic/reoxygenated HUVECs (HR-EMVs). lncCCT4-2 was significantly highly expressed in (HR + P)-EMVs and cardiomyocytes co-cultured with (HR + P)-EMVs, and reduction of lncCCT4-2 in (HR + P)-EMVs enhanced oxidative stress and apoptosis in IR-injured cardiomyocytes. lncCCT4-2 inhibited HR-EMVs induced oxidative stress and apoptosis in HR-injured AC16 cells by increasing the stability of CCT4 mRNA and promoting the expression of CCT4 protein in AC16 cells.

Abstract Compared with central penetration, the eccentric penetration of jet into a liquid-filled composite armor (LCA) shows a more obvious lateral displacement due to the asymmetric impact by the shock wave and liquid radial reflux. Based on this characteristic, the reaming process in the liquid layer during the shaped charge jet (SCJ) penetrates into the strongly-constrained liquid-filled composite armor (SLCA) eccentrically, the interference process of jet is subjected to the asymmetric impact by the shock wave and liquid radial reflux, and the lateral movement process of the SCJ under lateral force loading is analyzed to study the influence of SLCA on the stability of incoming SCJ during eccentric penetration. Theoretical and X-ray experimental results show that when the eccentricity distance is [0 mm, 12 mm], the severely disturbed velocity range and total disturbed velocity range of the SCJ increase with the increase of the eccentricity distance, while the maximum lateral displacement of the SCJ decreases slightly with the increase of the eccentricity distance at [1 mm, 12 mm].

RESUMO Introdução: Nos últimos anos, a engenharia genética tem contribuído de forma notável para os esportes, além de ter uma função importante na promoção do desenvolvimento de áreas relacionadas ao esporte. Objetivo: Analisamos a origem de tecidos do crescimento ósseo e sua regeneração através do estudo da proteína morfogenética óssea e fatores de transformação do crescimento em fraturas causadas pela prática do esporte. Métodos: Criamos um modelo de fratura humana para expressar a forma e o conteúdo da proteína morfogenética óssea e de fatores de transformação do crescimento durante a recuperação de fraturas. Resultados: Na fase de recuperação da fratura causada por diversos esportes, os níveis de expressão dos dois genes são diferentes. A proteína morfogenética óssea se apresenta em alta quantidade na fase osteogenetica da membrana, e o fator de transformação de crescimento apresenta alta quantidade na fase de ossificação da cartilagem. Conclusão: A terapia genética para fraturas causadas por exercícios físicos apresenta diversas vantagens. Osteoblastos e condrócitos tem um papel na síntese dos fatores de transformação do crescimento. Nível de evidência II; Estudos terapêuticos – investigação de resultados de tratamento.

ABSTRACT Introduction: In recent years, genetic engineering has made outstanding contributions to sports, and it has played a huge role in promoting the development of sports-related fields. Objective: We analyze the tissue source of bone growth and healing by studying the role of bone morphogenetic protein and transforming growth factors in fracture injuries caused by sports. Methods: We established a human fracture model to express the shape and content of bone morphogenetic protein and transforming growth factor during fracture healing. Results: In the fracture healing stage caused by different sports, the expression levels of the two genes are different. Bone morphogenetic protein has a high content in the osteogenesis stage of the membrane, while transforming growth factor is high in the cartilage ossification stage. Conclusion: Gene therapy for fractures caused by physical exercise has certain advantages. Osteoblasts and chondrocytes are involved in the synthesis of transforming growth factors. Level of evidence II; Therapeutic studies - investigation of treatment results.

RESUMEN Introducción: En los últimos años, la ingeniería genética ha contribuido de forma notable para los deportes, además de tener una función importante en la promoción del desarrollo de áreas relacionadas al deporte. Objetivo: Analizamos el origen de tejidos del crecimiento óseo y su regeneración a través del estudio de la proteína morfogenética ósea y factores de crecimiento transformante en fracturas causadas por la práctica del deporte. Métodos: Creamos un modelo de fractura humana para expresar la forma y el contenido de la proteína morfogenética ósea y de factores de crecimiento transformante durante la recuperación de fracturas. Resultados: En la fase de recuperación de la fractura causada por diversos deportes, los niveles de expresión de los dos genes son diferentes. La proteína morfogenética ósea se presenta en alta cantidad en la fase osteogénica de la membrana, y el factor de crecimiento transformante presenta alta cantidad en la fase de osificación del cartílago. Conclusión: La terapia genética para fracturas causadas por ejercicios físicos presenta diversas ventajas. Osteoblastos y condrocitos tienen un papel en la síntesis de los factores de crecimiento transformante. Nivel de evidencia II; Estudios terapéuticos – investigación de resultados de tratamiento.

Abstract A large number of cracks occur in concrete structure after projectile penetration. The study of crack distribution and propagation process is the basis of damage assessment, structural repair and high dynamic fracture mechanism. In this paper, wire saw cutting, X-ray computed tomography (X-CT) and mechanical property testing of damaged concrete were carried out on deep penetration targets. According to X-CT images of radial core samples in target and the mechanical properties of damaged concrete, the crack distribution in the target was divided into a plastic damage zone and a brittle damage zone, and the microcracks only existed in the plastic damage zone. The initial growth process of three-dimensional cracks was obtained by X-CT images of axial core samples in target, that is, the cracks in the pure mortar target gradually developed from the radial direction to the tangential direction, and the target containing coarse aggregate directly formed tangential cracks. The propagation progress of cracks was obtained through the target section, that is, the tangential cracks bent in the pure mortar target, and were relatively straight in the target containing coarse aggregate. A crack propagation model was established, and the tangential crack formula and the crack propagation velocity were obtained.

Abstract Deep penetration experiments were performed on five types of concrete with different coarse aggregate content. The projectile diameter was 29.9 mm, the initial velocity was 647 m/s, and the volume fraction of the coarse aggregate was between 0% and 59.0%. The damage laws and damage mechanism of the target were analyzed. The pure mortar target had the smallest radial crack origin diameter and crater depth. Too high of the coarse aggregate content led to the formation of many voids, which led to the disappearance of radial cracks, crater surface bypassing the coarse aggregate and a large reduction of crater diameter. The influence laws and mechanism of the coarse aggregate on the penetration depth were also analyzed. The increase of volume fraction of coarse aggregate was beneficial to reducing penetration depth and the increase of voids volume fraction was opposite. The penetration depth was the lowest when the volume fraction of the coarse aggregate reached the maximum and no voids formed. By modifying the static resistance stress in the Forrestal penetration formula, a penetration depth model considering the volume fractions of the coarse aggregate and voids was established. The predicted results were in good agreement with the experimental results.