Upcycling crab shell waste into biochar for treatment of palm oil mill effluent via microwave pyrolysis and activation.

The escalating consumer demand for crabs results in a growing amount of waste, including shells, claws, and other non-edible parts. The resulting crab shell waste (CSW) is disposed of via incineration or landfills which causes environmental pollution. CSW represents a potential biological resource that can be transformed into valuable resources via pyrolysis technique. In this study, microwave pyrolysis of CSW using self-purging, vacuum, and steam activation techniques was examined to determine the biochar production yield and its performance in treating palm oil mill effluent (POME). The biochar produced through microwave pyrolysis exhibits yields ranging from 50 to 61 wt%, showing a hard texture, low volatile matter content (≤34.1 wt%), and high fixed carbon content (≥58.3 wt%). The KOH-activated biochar demonstrated a surface area of up to 177 m2/g that is predominantly composed of mesopores, providing a good amount of adsorption sites for use as adsorbent. The biochar activated with steam removed 8.3 mg/g of BOD and 42 mg/g of COD from POME. The results demonstrate that microwave pyrolysis of CSW is a promising technology to produce high-quality biochar as an adsorbent for POME treatment.

Integrative analysis of disulfidptosis and immune microenvironment in hepatocellular carcinoma: a putative model and immunotherapeutic strategies.

Background: Hepatocellular carcinoma (HCC) is a malignant tumor with a high rate of recurrence and m metastasis that does not respond well to current therapies and has a very poor prognosis. Disulfidptosis is a novel mode of cell death that has been analyzed as a novel therapeutic target for HCC cells. Methods: This study integrated bulk ribonucleic acid (RNA) sequencing datasets, spatial transcriptomics (ST), and single-cell RNA sequencing to explore the landscape of disulfidptosis and the immune microenvironment of HCC cells. Results: We developed a novel model to predict the prognosis of patients with HCC based on disulfidptosis. The model has good stability, applicability, and prognostic and immune response prediction abilities. N-myc downregulated gene1 (NDRG1) may contribute to poor prognosis by affecting macrophage differentiation, thus allowing HCC cells to evade the immune system. Conclusion: Our study explores the disulfidptosis of HCC cells through multi-omics and establishes a new putative model that explores possible targets for HCC treatment.