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Context: Previous studies have discovered a high expression rate of Mucin 1 (MUC1) in pancreatic cancer tissue, and its abnormal glycosylation causes MUC1 to expose new protein epitopes or glycoantigens.Aims: To investigate the therapeutic effect of drug-loaded gemcitabine polybutylcyanoacrylate nanoparticles coupled with anti-human MUC1 monoclonal antibody (mAb) on human pancreatic cancer cell line and xenografts.Settings and Design: Randomized controlled trial.Materials and Methods: Gemcitabine-loaded nanospheres were prepared by emulsion polymerization; then, the anti-MUC1 mAb coupled with gemcitabine polybutylcyanoacrylate nanoparticles (MUC1-GEM-PBCA-NP) was prepared by chemical cross-linking. Cell-killing rates were detected by MTT assay in in vitro study, and changes in tumor cell cycle and apoptosis after treatment were detected by flow cytometry. Furthermore, in in vivo study, MUC1-GEM-PBCA-NP was injected into nude mice through the tail vein. Gemcitabine-loaded polybutylcyanoacrylate nanoparticles (GEM-PBCA-NP), gemcitabine bulk drug and empty nanoparticles (PBCA-NP), and normal saline blank control groups were established. Finally, data obtained were compared between groups.Results: Compared with the control group, the cell-killing rate of each experimental group was significantly different (P < 0.05) in in vitro study, among which the MUC1-GEM-PBCA-NP group was significantly higher than other groups (P < 0.05). In addition, the apoptosis rate of the MUC1-GEM-PBCA-NP treatment group was significantly higher than that of other groups (P < 0.05). Furthermore, in in vivo study, the tumor inhibition rate of the MUC1-GEM-PBCA-NP treatment group was (68.14% ±1.66%), which was significantly higher than other control groups (P < 0.05). Finally, at the end of the treatment, the average tumor mass of the MUC1-GEM-PBCA-NP treatment group was (471.61 mg ± 12.16 mg), which was significantly lower than those of other control groups (P < 0.05).Conclusions: MUC1-GEM-PBCA-NP could have an excellent inhibitory effect on tumors; thus, requiring further study. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the impact of laparoscopic left hepatectomy (LLH) for hepatolithiasis on the T lymphocyte immune changes of elderly patients and to analyze underlying mechanisms of action behind these changes. A total of 164 patients who underwent LLH due to left-sided hepatolithiasis were recruited. In terms of T lymphocyte immune changes, it was found that firstly, the basic quantity of peripheral lymphocytes in the elderly group was significantly lower than that in a younger preoperative group. Secondly, after surgical trauma, the immune function of T lymphocytes had a significant decline and lasted longer when compared with younger patients, which was reflected by the perioperative changes in the T lymphocyte proliferative ability, levels of IL-2 secreted by T lymphocytes and the percentage of CD3 + /CD4 + T lymphocytes in the peripheral blood. Circular RNA (circRNA) 102911 (102911) was upregulated and microRNA (miR)-129-5p was downregulated in CD3 + /CD4 + T lymphocytes from elderly patients with LLH for hepatolithiasis. Furthermore, the overexpression of 102911 inhibited the proliferation of CD3 + /CD4 + T lymphocytes as well as promoting cell apoptosis, with the opposite effects being observed on knockdown of 102911. miR-129-5p is involved in the proliferation and apoptosis of CD3 + /CD4 + T lymphocytes and may be a promising target of 102911. Moreover, SOX6 is a downstream molecule of miR-129-5p. Immune function and number of T lymphocytes decreased significantly after surgical trauma compared to younger patients, and this decline lasted longer in older patients treated with LLH for hepatolithiasis. The 102911/miR-129-5p/SOX6 axis was found to be involved in T lymphocytes immune function, which provided a novel insight for the treatment of elderly patients with hepatolithiasis., (Copyright: © Zhao et al.)