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Ultra-high-pressure tubular reactors are crucial pieces of equipment for polyethylene production. Long-term operation under high temperature, high pressure, and other extremely harsh conditions can lead to various defects, with circumferential cracks posing a major safety risk. Detecting cracks is challenging, particularly when they are under a protective layer of a certain thickness. This study designed a pulsed eddy current differential probe to detect circumferential cracks in ultra-high-pressure tubular reactors, with the lift-off distance acting as a protective layer. Detection models for traditional cylindrical and semi-circular excitation differential probes were established using finite element simulations. Corresponding experiments under different lift-off conditions were carried out, and the model’s accuracy was verified by the consistency between the simulation results and experimental data. The distribution of the eddy current field under different conditions and the disturbances caused by cracks at various positions to the detection signal were then calculated in the simulations. The simulation results showed that the cracks significantly disturbed the eddy current field of the semi-circular excitation differential probe compared with that of the traditional cylindrical probe. The designed differential probe effectively detected circumferential cracks of specific lengths and depths using the difference in the voltage signals. The experimental results were in agreement with the simulation results, showing that the designed probe could effectively detect 20 mm-long circumferential cracks at a lift-off of 60 mm. The experimental results also show that the probe’s detection coverage area in the axial direction varied with the lift-off height. The probe design and findings are valuable for detecting cracks in ultra-high-pressure tubular reactors with protective layers.

Diffuse large B-cell lymphoma (DLBCL) is the most frequent lymphoma in adults, and is characterized as clinically and biologically heterogeneous lymphomas with diverse response to therapy and variation in clinical behavior. It's well-established that c-MYC and BCL2 play important roles in normal B-cell differentiation and tumorigenesis. B cell lymphoma with dual expression of c-MYC and BCL2 (double-expressor lymphoma, DEL) accounts for approximately one-third of DLBCL cases. DEL patients have poor outcomes after chemoimmunotherapy or autologous stem-cell transplantation. Lack of a genetic mouse tool for DEL hinders us from understanding the lymphogenesis mechanism and developing therapeutic strategies. Here, we investigated whether ectopic expression of c-MYC and BCL2 in different stages of B cells could lead to lymphoma and generate a mouse model for DEL. We observed that Co-expression of c-MYC and BCL2 in germinal center (GC) B cells, or pan-B cells could induce B cell lymphomas. The tumor-bearing mice have enlarged lymphoid organs, and B cells massively infiltrate into non-lymphoid organs including lung, liver and kidney. The tumor-bearing mice also manifested significantly shorter lifespan than the controls. In addition, adoptive transfer of Co-expression B cells leads to B cell lymphoma and host mice death. This model will provide us a tool to further explore the pathogenesis and treatment approaches for DEL.