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Control of damaged zone caused by impact load is the challenging issue in blasting engineering. In this paper, a new rock breaking method using carbon dioxide ice powder is developed, which is characterized by weak disturbance. Then experiments on the CO 2 pneumatic fracturing of concrete specimens were conducted. Generally, the CO 2 -driven fracturing process generates medium strain rate ( ε · = 10 0 to 10 1 1/s), the large concrete specimen was fractured into 3–5 blocks, and no crushing damage occurred. The transient failure modes in the shock wave event were discussed, and the fragment size-strain rate relationship was established based on the cusp mutation theory. The theoretical calculation results are consistent with the experimental results. The research achievement may provide a new and safe rock-fracturing method for geological engineering.

Two review articles published in 2000 and 2011 by Hanahan and Weinberg have dominated the discourse about carcinogenesis among researchers in the recent past. The basic tenets of their arguments favour considering cancer as a cell-based, genetic disease whereby DNA mutations cause uncontrolled cell proliferation. Their explanation of cancer phenotypes is based on the premises adopted by the somatic mutation theory (SMT) and its cell-centered variants. From their perspective, eight broad features have been identified as so-called ‘Hallmarks of Cancer’. Here, we criticize the value of these features based on the numerous intrinsic inconsistencies in the data and in the rationale behind SMT. An alternative interpretation of the same data plus data mostly ignored by Hanahan and Weinberg is proposed, based instead on evolutionarily relevant premises. From such a perspective, cancer is viewed as a tissue-based disease. This alternative, called the tissue organization field theory, incorporates the premise that proliferation and motility are the default state of all cells, and that carcinogenesis is due to alterations on the reciprocal interactions among cells and between cells and their extracellular matrix. In this view, cancer is development gone awry.

In this paper, after analyzing the VAR model, we design the Gram causality test between human resource management and enterprise performance and establish a structural equation combining multiple regression and factor analysis to explore the interrelationship between the two, in addition to evaluating enterprise performance based on mutation theory. In order to study the relationship between human resource management and enterprise performance, assumptions are made about the relationship between the two, a conceptual model of the role path relationship between human resource management and enterprise performance is established, and the proposed assumptions are empirically analyzed based on the existing literature and actual data. The results show that the coefficient of HR practices is 10.048343, which is significant at the 0.0031 level, and the goodness of fit is 0.403881, and HR practices do have a relatively significant impact on business performance, and the marginal impact is 10.048343, which indicates that HR practices significantly amplify business performance. This study confirms that human resource management is positively correlated with firm performance and that firms can optimize their human resource management strategies, which in turn will enhance their performance and provide impetus for their progress and development.

Despite methodological issues, this seems to be a multifactorial omission insofar as original references are increasingly not read and/or cited with a lack of critical analysis resulting in the dominance of erroneous conclusions from research data [3] as has been pointed out recently [4]. Hereditary cancers occur in some 10% of all cancers and genetically triggered primary cancers represent some 8% of breast and ovarian cancers, which are causally linked to genetic changes such as breast cancer 1, early onset (BRCA1) or breast cancer 2, early onset (BRCA2) mutations; the corresponding figure for gastric cancer is less than 1%, for colorectal cancers it is somewhere between 3 and 5%,and infection-associated cancers are estimated to represent some 15% of all cancers [6, 7, 8]. Even these estimates seem misleading since no one knows why this ratio is about 60% in gastric cancers with Helicobacter pylori (H. pylori) infection and as high as 80% in liver cancers with chronic Hepatitis B or C viruses [9]. [...]broadly speaking about 80% of cancers are referred to as being ‘sporadic', meaning their cause remains unknown Figure 1 and Figure 2. [...]the term, ‘post-zygotic mosaicism' was coined as a unifying term for all DNA changes acquired during life from single base pair mutations to aberrations at the chromosomal level [47].

It is of great significance for ecological environment protection to clarify the regional evolution characteristics of shallow water under the disturbance of multi-working face mining. In this paper, the catastrophe theory method, GIS spatial analysis function and FEFLOW numerical calculation method were comprehensively used to study the instability risk and evolution law of shallow water systems in the Zhuan Longwan Coal Mine. The results show that: the Zhuan Longwan Coal Mine is divided into five areas (small risk area, light risk area, middle risk area, heavy risk area and special risk area) based on catastrophe theory, among which the middle risk area has the largest area of 16,616,880 m2, and the special risk area has the smallest area of 1,769,488 m2. Based on the results of catastrophe zoning, the evolution law of shallow water under multi-surface disturbance in different zones is expounded. In the middle-risk area, the water level drop at measuring point 4 is the largest, which is 0.525 m, and the water level drop at measuring point 5 is the smallest, which is 0.116 m. The study aims to provide a basis for regional coal development planning and research on the method of water-retaining coal mining.

As open-pit mining extends to greater depths, slope stability is becoming a critical factor in ensuring safe production. This issue is particularly pronounced in geological settings with weak interlayers, where sudden slope failures are more likely to occur, demanding precise and reliable stability assessment methods. In this study, a typical open-pit slope with weak interlayers was investigated. Acoustic testing and ground-penetrating radar were employed to identify rock mass structural features and delineate loose zones, enabling detailed rock mass zoning and the development of numerical simulation models for stability analysis. The results indicate that (1) the slope exhibits poor overall integrity, dominated by blocky to fragmented structures with well-developed joints and significant weak interlayers, posing a severe threat to stability; (2) in the absence of support, the slope’s dissipated energy, displacement, and plastic zone volume all exceeded the failure threshold (Δ < 0), and the safety factor was only 0.962, indicating a near-failure state; after implementing support measures, the safety factor increased to 1.31, demonstrating a significant improvement in stability; (3) prior to excavation, the energy damage index (ds) in the 1195–1240 m platform zone reached 0.82, which dropped to 0.48 after reinforcement, confirming the effectiveness of support in reducing energy damage and enhancing slope stability; (4) field monitoring data of displacement and anchor rod forces further validated the stabilizing effect of the support system, providing strong assurance for safe mine operation. By integrating cusp catastrophe theory with energy-based analysis, this study establishes a comprehensive evaluation framework for slope stability under complex geological conditions, offering substantial practical value for deep open-pit mining projects.

John Cairns, a British molecular biologist, has pointed out that biology and cancer research have always developed together, and cancer theories have followed “whatever branch of biology happens at the time to be fashionable and exciting”. Indeed, following the long historical development of biological thought confirms this observation. However, tumour theories have never been merely a “fellow runner” to more modern biology theories. Cancer is an exceptionally large medical and economic problem, and the practical results of cancer research are carefully followed and critically analysed by the community. If the expected results do not arrive and the scientific data do not fit into the old theory, then the theory must be corrected. In other words, tumour theories not only derive from the prevailing biological worldview, but they also influence and, if necessary, actively change it. That is exactly what we are witnessing today–the ruling reductionist Somatic Mutations Theory (SMT) does not explain many new experimental findings and extensive research over the last 50 years has not brought major breakthroughs in cancer treatment. This century brings back the attention to developmental biology (embryology) in connection with the epigenetic revolution in biology, and the causes of tumours are searched for in the disorders of differentiation of cells/tissues and communication between them in the organism.

Cancer research is experiencing 'paradigm instability', since there are two rival theories of carcinogenesis which confront themselves, namely the somatic mutation theory and the tissue organization field theory. Despite this theoretical uncertainty, a huge quantity of data is available thanks to the improvement of genome sequencing techniques. Some authors think that the development of new statistical tools will be able to overcome the lack of a shared theoretical perspective on cancer by amalgamating as many data as possible. We think instead that a deeper understanding of cancer can be achieved by means of more theoretical work, rather than by merely accumulating more data. To support our thesis, we introduce the analytic view of theory development, which rests on the concept of plausibility, and make clear in what sense plausibility and probability are distinct concepts. Then, the concept of plausibility is used to point out the ineliminable role played by the epistemic subject in the development of statistical tools and in the process of theory assessment. We then move to address a central issue in cancer research, namely the relevance of computational tools developed by bioinformaticists to detect driver mutations in the debate between the two main rival theories of carcinogenesis. Finally, we briefly extend our considerations on the role that plausibility plays in evidence amalgamation from cancer research to the more general issue of the divergences between frequentists and Bayesians in the philosophy of medicine and statistics. We argue that taking into account plausibilitybased considerations can lead to clarify some epistemological shortcomings that afflict both these perspectives.

Multiple theories exist to explain cancer initiation, although a consensus on this is crucial for developing effective therapies. ‘Somatic mutation theory’ suggests that mutations in somatic cells during DNA repair initiates cancer but this concept has several attached paradoxes. Research efforts to identify quiescent cancer stem cells (CSCs) that survive therapy and result in metastasis and recurrence have remained futile. In solid cancers, CSCs are suggested to appear during epithelial-mesenchymal transition by the dedifferentiation and reprogramming of epithelial cells. Pluripotent and quiescent very small embryonic-like stem cells (VSELs) exist in multiple tissues but remain elusive owing to their small size and scarce nature. VSELs are developmentally connected to primordial germ cells, undergo rare, asymmetrical cell divisions and are responsible for the regular turnover of cells to maintain tissue homeostasis throughout life. VSELs are directly vulnerable to extrinsic endocrine insults because they express gonadal and gonadotropin hormone receptors. VSELs undergo epigenetic changes due to endocrine insults and transform into CSCs. CSCs exhibit genomic instability and develop mutations due to errors during DNA replication while undergoing excessive proliferation and clonal expansion to form spheroids. Thus tissue-resident VSELs offer a connection between extrinsic insults and variations in cancer incidence reported in various body tissues. To conclude, cancer is indeed a stem cell disease with mutations occurring as a consequence. In addition to immunotherapy, targeting mutations, and Lgr5 + organoids for developing new therapeutics, targeting CSCs (epigenetically altered VSELs) by improving their niche and epigenetic status could serve as a promising strategy to treat cancer.

Contemporary philosophy of science has seen a growing trend towards a focus on scientific practice over the epistemic outputs that such practices produce. This practice-oriented approach has yielded a clearer understanding of how reductive research strategies play a central role in contemporary scientific inquiry. In parallel, a growing body of work has sought to explore the role of non-reductive, or systems-level, research strategies. As a result, the relationship between reductive and non-reductive scientific practices is becoming of increased importance. In this paper, I provide a framework within which research strategies can be compared. I argue that no strategy is reductive or non-reductive simpliciter, rather strategies are more, or are less, reductive than one another according to a frame of reference. That frame of reference is provided by a continuum of possible ways in which the target system might be conceptualised. I illustrate the utility of the framework by deploying it to analyse a recent debate in cancer research. When set within the framework, a prominent reductive strategy—the somatic mutation theory—and a prominent non-reductive strategy—the tissue organisational field theory—do not stand opposed to one another. Rather, they serve as boundary markers to chart the territory of approaches to carcinogenesis within which most strategies in the field fall.