Laser additively manufactured (LAM) Ti–6Al–4V alloy has huge application potential in aerospace structural parts such as turbine blades. However, there are few studies on the fatigue properties of such LAM parts under vibration loading, particularly with regard to anisotropy. In this paper, vibration fatigue properties of LAM Ti-6Al-4V by laser melted deposition process were investigated along the transversely deposited (TD) direction and parallelly deposited (PD) direction. Through the first-order bending vibration experiments, LAM Ti-6Al-4V alloy exhibits obvious anisotropic fatigue properties and significant dispersion in fracture position. The fracture morphology analysis reveals that the vibration fatigue failure was mainly dominated by the LAM process-induced defects and the microstructure. For the LAM samples without defects at crack initiation sites, the fatigue behavior is controlled by the prior β columnar grains with preferential orientation, which leads to enhanced fatigue crack propagation resistance for the PD samples. For the LAM samples with defects at initiation sites, having lower fatigue lives, the fatigue anisotropy strongly depends on the projection area of the lack-of-fusion defects relative to the loading direction, resulting in better fatigue performance for the TD samples.

The establishment of an isolation layer in submarine mining has long presented an enduring challenge. In the context of this research, we conducted a similarity simulation test to preliminarily ascertain the interplay between the thickness and extent of the isolation layer. Subsequently, we introduce an innovative approach that integrates fractal theory and the bonded block model (BBM) to simulate undersea isolation layer mining. The validation of this method hinges on on-site borehole scanning and displacement monitoring, which serve to depict the intricate fractal evolution of fractures and predict the optimal thickness of the isolation layer. Our findings affirm the robustness and validity of this method. Evaluation of the fractal dimensions of fractures reveals that a critical threshold of 1.7 exists to prevent structural failure of the isolation layer, while a limit of 1.5 is necessary to avert significant water ingress. Remarkably, the correlation dimension of the settlement time series closely aligns with the fractal dimension of the fractures, underscoring the feasibility of ensuring the safety of isolation layer mining through real-time settlement monitoring.

There are many theories of carcinogenesis arguing against the orthodox mutation theory, debating on such as “epigenetic alteration” that is inheritable and yet, theoretically, reversible. Our integrated theory describes that any extracellular, intracellular, or intranuclear stressors, mutagenic or not, can initiate a lengthy tumorigenesis to engender a benign or malignant tumor, but the aberrations directly establishing cellular immortality and autonomy may be epigenetic or genetic alterations in the genomic DNA. A neoplasm is considered a semi-new organism with autonomy; it therefore should have genetic mutations to be “new”. We may be able to direct cancer cells towards differentiation as a remedy, because the extracellular milieu may control the phenotype of a cell and the tissue or organ made of the cell’s progenies, and the cytoplasm of a cell may override the nucleus in the phenotypic control. However, the nucleus retains the capacity to manifest itself if allowed by the microenvironment, which then allows the already reversed cells to revert back to tumor cells again. Neoplasms are malignant if they bear epigenetic or genetic anomalies in mutator genes defined as those whose alterations allow or accelerate alterations to occur in other genes, whereas neoplasms are benign if they bear epigenetic or genetic aberrations only in non-mutator genes. It is imperative to identify the immediate tumor-causing cellular alterations defined as those directly responsible for immortality and autonomy, and for treatment purposes to identify the extracellular and intracellular factors that control the phenotype of cancer cells.

Chrysoeriol (CHE) is a flavonoid substance that exists in many plants and has various physiological and pharmacological effects, including anti-inflammatory, antioxidant, anti-tumor, and protective activity, especially for the cardiovascular system and liver. This study aimed to analyze the results and possible mechanisms of CHE on early porcine embryo development. Adding CHE to the culture media can improve the development quality of early porcine embryos. CHE significantly increased the blastocyst rate and total cell number of embryos in vitro. The apoptosis of blastocyst in CHE-treated culture also decreased significantly compared with untreated culture. Furthermore, CHE downregulated intracellular reactive oxygen species (ROS) and increased glutathione (GSH) in embryos. CHE was also shown to improve the activity of mitochondria and inhibit the occurrence of autophagy. In addition, antioxidant-related genes (SOD1, SOD2, and CAT) and cell pluripotency-related genes (SOX2, OCT4, and NANOG) were upregulated, while those related to apoptosis (Caspase 3) and autophagy (LC3B) showed a downward trend after supplementation with CHE. These results indicated that CHE improved the development of porcine embryos in vitro by reducing oxidative stress and autophagy levels.