Rare isolated extra-hepatic bile duct injury: A case report.

BACKGROUND: Extra-hepatic bile duct injury (EHBDI) is very rare among all blunt abdominal injuries. According to literature statistics, it only accounts for 3%-5% of abdominal injuries, most of which are combined injuries. Isolated EHBDI is more rare, with a special injury mechanism, clinical presentation and treatment strategy, so missed diagnosis easily occurs. CASE SUMMARY: We report a case of unexplained abdominal effusion and jaundice following blunt abdominal trauma in our department. Of which, surgical exploration of the case was performed and a large amount of bile leakage in the abdominal cavity was found. No obvious abdominal organ damage or bile duct rupture was found. Surgery was terminated after the common bile duct indwelled with a T tube. After 2 wk, a T-tube angiography revealed the lesion in the common bile duct pancreatic segment, confirming isolated EHBDI. And 2 mo later, the T tube was pulled out with re-examined magnetic resonance cholangiopancreatography, indicating narrowing of the common bile duct injury, with no special treatment due to no clinical symptoms and no abnormality in the current follow-up. CONCLUSION: This case was featured by intraoperative bile leakage and no EHBDI. This type of rare isolated EHBDI is prone to missed and delayed diagnosis due to its atypical clinical manifestations and imaging features. Surgery is still the main treatment, and the indications and principles of bile duct injury repair must be followed.

Blockage of RelB expression by gene silencing enhances the radiosensitivity of androgen­independent prostate cancer cells.

Levels of the nuclear factor­kappa B (NF­κB) alternative pathway member RelB have been shown to correlate with the effect of radiation therapy in prostate cancer. RelB expression was evaluated by immunohistochemistry in normal prostate, benign prostate hyperplasia and prostate cancer specimens. RM­1 cells were pretreated with RelB siRNA prior to radiation therapy, and RelB expression in cytoplasmic and nuclear extracts was detected by real­time polymerase chain reaction and western blot analysis. The apoptotic rates of experimental RM­1 cell groups were assessed by flow cytometry. A clonogenic growth array was used to evaluate the radiosensitivity of RM­1 cell groups. The NF­κB family member RelB was expressed at a high level in prostate cancer specimens. Compared with irradiated control cells, RM­1 cells transfected with RelB siRNA and treated with radiation therapy demonstrated a significant downregulation of RelB expression in the cytoplasm and nucleus. Notably, flow cytometry revealed that pretreatment of RM­1 cells with RelB siRNA enhanced the apoptotic rate in response to radiation therapy compared with controls. Clonogenic growth assay results revealed enhanced radiosensitivity of RelB siRNA cells at various dosage points compared with control groups. Blockage of the alternative NF­κB pathway via RelB silencing is a promising approach to enhance the radiosensitivity of prostate cancer.

Tolerogenic dendritic cells generated by RelB silencing using shRNA prevent acute rejection.

It is well known that adoptive transfer of donor-derived tolerogenic dendritic cells (DCs) helps to induce immune tolerance. RelB, one of NF-κB subunits, is a critical element involved in DC maturation. In the present study, our results showed tolerogenic DCs could be acquired via silencing RelB using small interfering RNA. Compared with imDCs, the tolerogenic DCs had more potent ability to inhibit mixed lymphocyte reaction (MLR) and down-regulate Th1 cytokines and prompt the production of Th2 cytokines. They both mediated immune tolerance via the increased of T cell apoptosis and generation of regulatory T cells. Administration of donor-derived tolerogenic DCs significantly prevented the allograft rejection and prolonged the survival time in a murine heart transplantation model. Our results demonstrate donor-derived, RelB-shRNA induced tolerogenic DCs can significantly induce immune tolerance in vitro and in vivo.

Lentiviral-mediated shRNA against RelB induces the generation of tolerogenic dendritic cells.

OBJECTIVE: Lentiviral-mediated shRNA against RelB was used to produce tolerogenic dendritic cells from murine bone marrow derived dendritic cells (BMDCs). METHOD: RelB expression in the BMDCs was silenced by lentivirus carrying RelB shRNA. The apoptosis rate and surface markers of DCs were assessed by flow cytometry. IL-12,IL-10,TGF-ß1 secreted by DCs and DNA binding capacity of NF-κB subunits in the nucleus were measured by ELISA, independently. MLR was used to analyze the capacity of DCs to inhibit immune response. RESULTS: RelB expression was significantly inhibited in DCs following lentiviral mediated delivery of RelB specific shRNA. The RelB shRNA-DC produced lower IL-12 and higher IL-10 than mature dendritic cells (mDCs) and silencing control DCs. There was no difference in the apoptosis rate between shRNA RelB-DCs and mDCs. The expression levels of co-stimulatory molecules (CD80, CD86 and CD83) and MHC-II class molecule were lower in the RelB shRNA-DCs than in the mDCs and silencing control DCs. In addition, RelB shRNA also inhibited the RelB DNA binding capacity but had no effect on other NF-κB subunits. The shRNA RelB-DCs can significantly inhibit mixed lymphocyte reaction (MLR) and down-regulate Th1 cytokines and prompt the production of Th2 cytokines. CONCLUSION: Our results indicate RelB shRNA transfection of DCs can induce the immature status, and produce tolerogenic DCs.