Effect of CeO2-Reinforcement on Pb Absorption by Coconut Coir-Derived Magnetic Biochar.

Magnetic separable biochar holds great promise for the treatment of Pb2+-contaminated wastewater. However, the absorption effect of unmodified magnetic biochar is poor. Considering this gap in knowledge, CeO2-doped magnetic coconut coir biochar (Ce-MCB) and magnetic coconut coir biochar (MCB) for Pb2+ absorption were prepared by the impregnation method, and the efficiency of Ce-MCB for Pb2+ absorption was evaluated in comparison with MCB. Conducting the absorption experiments, the study provided theoretical support for the exploration of the absorption mechanism. The quantitative analysis exposed that the enhanced absorption capacity of Ce-MCB was attributed to the increase in oxygen-containing functional groups and mineral precipitation. The Langmuir and Freundlich isotherm model showed that Ce-MCB is a suitable adsorbent for Pb2+. The absorption characteristics of Ce-MCB was fit well with the pseudo-second-order (PSO) and Langmuir models, which revealed that the absorption of Pb2+ in water was monolayer chemisorption with a maximum theoretical adsorption capacity of 140.83 mg·g-1. The adsorption capacity of Ce-MCB for Pb(II) was sustained above 70% after four cycles. In addition, the saturation magnetization intensity of Ce-MCB was 7.15 emu·g-1, which was sufficient to separate out from the solution. Overall, Ce-MCB has wide application prospects in terms of biomass resources recycling and environmental conservation.

Mismatch repair deficiency is associated with specific morphologic features and frequent loss of ARID1A expression in ovarian clear cell carcinoma.

BACKGROUND: Ovarian clear cell carcinoma (OCCC) is the second subtype of ovarian epithelial carcinoma reported to be closely related to Lynch syndrome (LS). ARID1A mutation is an important pathogenetic mechanism in OCCC that leads to loss of ARID1A expression in approximately half of OCCCs. However, the correlation of MMR status and ARID1A deficiency is unclear. The current study aimed to identify the clinical and histopathological characteristics of OCCC associated with dMMR and to further explore the association between dMMR and ARID1A deficiency. METHODS: A cohort of 176 primary OCCC patients was enrolled and review included histological characteristics (nuclear atypia, necrosis, mitosis, stromal hyalinization, and background precursors) and host inflammatory response (tumor-infiltrating lymphocytes, peritumoral lymphocytes, intratumoral stromal inflammation and plasma cell infiltration). Immunohistochemical staining of MLH1, PMS2, MSH2, MSH6 and ARID1A was performed using tissue microarrays. RESULTS: dMMR was detected in 10/176 tumors (6 %), followed by MSH2/MSH6 (6/176), MLH1/PMS2 (3/176), and MSH6 (1/176). The average age of patients with dMMR was younger than that of patients with intact MMR (46 y vs. 53 y). Tumors with diffuse intratumoral stromal inflammation remained significantly associated after multivariate analysis. ARID1A expression was absent in 8 patients with dMMR (8/10), which is a significantly higher frequency than that observed in patients with intact MMR (80 % vs. 43.2 %). CONCLUSIONS: Our study indicates that diffuse intratumoral stromal inflammation of OCCCs is associated with dMMR, with loss of MSH2/MSH6 expression being most frequent. dMMR is strongly associated with the loss of ARID1A expression in OCCC.