Basiliximab

Kidney transplantation programs in developing countries chiefly depends on live donors, and waiting lists are long for patients lacking ABO compatible ( ABOc ) donors. ABO incompatible ( ABOi ) transplantation enhances the donor pool. We report our experience of ABOi kidney transplantation in children.

We screened medical records of ABOi and ABOc kidney transplantation performed at this center between January 2019 to December 2023. For desensitization of ABOi kidney allograft recipients a combination of rituximab and either immunoadsorption or plasma exchange along with IVIg was used. Induction regimen comprised either basiliximab or ATG , followed by maintenance therapy with tacrolimus, mycophenolate mofetil and prednisolone. We retrieved data on recipient and donor characteristics, immunosuppression, and post‐transplant complications. Allograft and patient survival were estimated using Kaplan–Meier survival analysis.

During the 5‐years, 7 ABOi and 46 ABOc kidney transplantation were performed. The mean follow up duration was 24.9 ± 17.1 months in ABOi group and 30.3 ± 18.8 months in ABOc group. Patient age, native kidney disease, donor profile and other characteristics were comparable. Rejection free graft survival was similar between ABOi and ABOc groups ( p  = 0.88). Median ( IQR ) eGFR at last follow up was 61.4 (46.6, 74.3) ml/min/1.73 m 2 in ABOi group and 50.9 (39.7, 68.9) ml/min/1.73 m 2 in ABOc group ( p  = 0.23). Patients and graft survival rates were similar in both groups.

Our findings suggest that ABOi kidney transplantation in children in India is feasible and associated with satisfactory outcomes P.

Diffuse large B‐cell lymphoma (DLBCL), a heterogeneous malignancy characterized by distinct genetic and clinical subtypes, remains a therapeutic challenge despite standard R‐CHOP chemotherapy. This study systematically investigated the synergistic anti‐tumor efficacy and mechanism of the histone deacetylase inhibitor chidamide (CHI) combined with doxorubicin (DOX) in DLBCL models. Through multimodal experimental approaches including CCK8 proliferation assays, senescence‐associated β‐galactosidase (SA‐β‐gal) staining analysis, comet assay for DNA damage quantification, and comprehensive western blotting for molecular mechanism elucidation, we identified a potent synergistic interaction between CHI and DOX. By constructing a xenograft tumor model, the synergistic effect of the two drugs and its mechanism in vivo were confirmed. Our research found that CHI showed cell cycle inhibition and apoptosis induction effects on DLBCL cells. When combined with DOX, both synergistically inhibited the proliferation of DLBCL cells and promoted death of DOX‐induced senescent cells. Preliminary mechanism studies revealed that CHI can reduce the level of mutant p53, inhibit cell senescence, and induce irreparable DNA damage in DOX‐induced senescent tumor cells, ultimately leading them into programmed apoptosis. Thus, the “One‐two punch” strategy increased the sensitivity of p53‐mutated DLBCL cells to CHI. In summary, our study demonstrates that CHI synergizes with DOX to suppress DLBCL and presents a promising strategy to augment the therapeutic efficacy of DOX.