Abstract This paper introduces a nonlinear, magnetically charged, singularity-free black hole model. The Ricci scalar, Kretschmann scalar, horizon, energy conditions, and Hawking radiation corresponding to the singularity-free metric are presented, and the asymptotic behavior and quantum correction of the model are examined. The model was constructed by coupling a mass function with the regular black hole solution under nonlinear electrodynamics in general relativity. Aside from resolving the problem of singularities in Einstein’s theory of general relativity, the model asymptotically meets the quantum correction under an effective field theory. This obviates the need for additional correction terms; in this regard, the model outperforms the black hole models developed by Bardeen and Hayward. Regarding the nonlinear magnetic monopole source of the gravitational field of the black hole, the energy-momentum tensors fulfill weak energy conditions. The model constitutes a novel, spherically symmetric solution to regular black holes.

A new noninvasive screening tool for colorectal neoplasia detects epigenetic alterations exhibited by gastrointestinal tumor cells shed into stool. There is insufficient existing data to determine temporal associations between colorectal cancer (CRC) progression and aberrant DNA methylation. To evaluate the feasibility of using fecal DNA methylation status to determine CRC progression, we collected stool samples from 14 male SD rats aged six weeks, and administered subcutaneous injections of either 1,2-dimethylhydrazine or saline weekly. p16 DNA methylation statuses in tumorous and normal colon tissue, and from stool samples were determined using methylation-specific PCR. Additionally, p16 methylation was detected in stool DNA from 85.7% of the CRC rats. The earliest change in p16 methylation status in the DMH-treated group stool samples occurred during week nine; repeatabilities were 57.1% in week 19 (p = 0.070) and 85.7% in week 34 (p = 0.005). A temporal correlation was evidenced between progression of CRC and p16 methylation status, as evidenced by DMH-induced rat feces. Using fecal DNA methylation status to determine colorectal tissue methylation status can reveal CRC progression. Our data suggests that p16 promoter methylation is a feasible epigenetic marker for the detection and may be useful for CRC screening.