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Background: The nucleolar MSP58 protein is a candidate oncogene implicated in cellular transformation.Results: MSP58 is associated with BRG1 and induces cellular senescence through the p53/p21 pathway.Conclusion: MSP58 has both tumor-suppressing and -promoting functions.Significance: This work reveals a novel role for MSP58 in cellular senescence and suggests that MSP58 may have further prognostic and therapeutic implications.

SummaryHelicobacter pylori inhabits the gastric mucosa where it senses and responds to various stresses via a twocomponent systems (TCSs) that enable its persistent colonization. The aim of this study was to investigate whether any of the three paired TCSs (ArsRS, FleRS and CrdRS) in H. pylori respond to nitrosative stress. The results showed that the expression of crdS was significantly increased upon exposure to nitric oxide (NO). crdS-knockout (ΔcrdS) and crdR/crdS-knockout (ΔcrdRS) H. pylori, but not arsS-knockout (ΔarsS) or fleS-knockout (ΔfleS) H. pylori, showed a significant loss of viability upon exposure to NO compared with wild-type strain. Knockin crdS (ΔcrdS-in) significantly restored viability in the presence of NO. Global transcriptional profiling analysis of wild-type and ΔcrdS H. pylori in the presence or absence of NO showed that 101 genes were differentially expressed, including copper resistance determinant A (crdA), transport, binding and envelope proteins. The CrdR binding motifs were investigated by competitive electrophoretic mobility shift assay, which revealed that the two AC-rich regions in the crdA promoter region are required for binding. These results demonstrate that CrdR-crdA interaction enables H. pylori to survive under nitrosative stress.

DBE-ERC was effective for both populations with biliary disorders. Reaching the blind end was more difficult but ERC was easier for patients with BEA in terms of procedure time rather than success rates.