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Background and PurposeTransnational nurse migration is a growing phenomenon. This study explored the experiences of China-educated nurses working in Australia.DesignUsing a constructivist grounded theory method, 46 in-depth interviews were conducted with 28 China-educated nurses in two major cities in Australia.ResultsThe core category emerged was “reconciling different realities”. Three phases of reconciling were conceptualised: realising, struggling, and reflecting. Realising refers to an awareness of the discrepancies between different realities. Struggling reflects the dilemma of the “middle position” and how being situated as “the other” is experienced. Reflecting is the process of making sense of the experience and rationalising the gains and losses associated with immigration.ConclusionsThis study produced a theoretical understanding of the experience of China-educated nurses working in Australia. The findings not only inform Chinese nurses who wish to migrate but contribute to the implementation of more effective support services for immigrant nurses.

Aim To deeply explore the experience of front‐line nurses who participated in rescuing Wuhan during the early stage of coronavirus disease 2019 (COVID‐19) epidemic. Methods Using a descriptive qualitative design, individual semi‐structured interviews were conducted between February 25 and March 5, 2020. A conventional content analysis method was used in data analysis to extract themes and sub‐themes. Results Six themes emerged after data analysis: (a) worries and stress during rescue; (b) difficulties encountered during rescue; (c) experience of team work; (d) experience of interaction with COVID‐19 patients; (e) experience of logistic support and widespread concern; and (f) value and significance of the experience. Conclusions Nurses took on difficult missions in the rescue and played an irreplaceable role. They experienced remarkable psychological changes over the intensive work. It was necessary to understand the feelings and problems of the nurses so as to establish a healthcare system that can protect medical staff effectively in future disasters.

The Mainland Chinese IBDQ proved to be a valid, discriminative, and reliable instrument for assessing health-related quality of life in patients with UC and CD in Mainland China.

Castration-resistant prostate cancer (CRPC) is difficult to treat in current clinical practice. Hypoxia is an important feature of the CRPC microenvironment and is closely associated with the progress of CRPC invasion. However, no research has been performed on the immune escape of CRPC from NK cells. The present study focused on this subject. Firstly, when the CRPC cell lines C4-2 and CWR22Rv1 were induced by hypoxia, the expression of the UL16 binding protein (ULBP) ligand family of natural killer (NK) group 2D (NKG2D; ULBP-1, ULBP-2 and ULBP-3) and MHC class I chain-related proteins A and B (MICA/MICB) decreased. NKG2D is the main activating receptor of NK cells. Tumor cells were then co-cultured with NK cells to conduct NK cell-mediated cytotoxicity experiments, which revealed the decreased immune cytolytic activity of NK cells on hypoxia-induced CRPC cells. In exploring the mechanism behind this observation, an increase in programmed death-ligand 1 (PD-L1) expression in CRPC cells induced by hypoxia was observed, while the addition of PD-L1 antibody effectively reversed the expression of NKG2D ligand and enhanced the cytotoxic effect of NK cells on CRPC cells. In the process of exploring the upstream regulatory factors of PD-L1, inhibition of the Janus kinase (JAK)1,2/signal transducer and activator of transcription 3 (Stat3) signaling pathway decreased the expression of PD-L1 in CRPC cells. Finally, it was observed that combined inhibition of JAK1,2/PD-L1 or Stat3/PD-L1 was more effective than inhibition of a single pathway in enhancing the immune cytolytic activity of NK cells. Taking these results together, it is thought that combined inhibition of the JAK1,2/PD-L1 and Stat3/PD-L1 signaling pathways may enhance the immune cytolytic activity of NK cells toward hypoxia-induced CRPC cells, which is expected to provide novel ideas and targets for the immunotherapy of CRPC.

The results suggest that any interventions that produce a stable clinical remission, whether medical or surgical, allowing patients to return to their usual work position can decrease the disease impact on their daily lives.

Store-operated calcium entry (SOCE) plays an important role in the invasion and migration of cancer cells. Stromal-interacting molecule 1 (STIM1) is a critical component in the SOCE. STIM1 has been attracting more and more attention due to its oncogenic potential. STIM1 inhibition suppresses cell proliferation, migration and invasion in a variety of cancer models both in vitro and in vivo. However, the role of STIM1 in prostate carcinogenesis, in particular, in tumor migration and invasion is unclear. Herein, we downregulated STIM1 in prostate cancer cells by lentivirus-mediated short hairpin (shRNA), and then studied its impacts on cell migration and invasion. We found that migration and invasion of prostate cancer cells were significantly inhibited after the suppression of STIM1. Furthermore, we demonstrated that the PI3K/Akt signaling pathway was inactivated by STIM1 knockdown. The PI3K inhibitor LY294002 synergized with STIM1 knockdown to inhibit cell motility. Our results revealed that STIM1 may act as a novel regulator to promote migration and invasion of prostate cancer cells and is associated with the activation of the PI3K/Akt signaling pathway.

Castration-resistant prostate cancer (CRPC), also known as androgen-independent prostate cancer, frequently develops local and distant metastases, the underlying mechanisms of which remain undetermined. In the present study, surgical specimens obtained from patients with clinical prostate cancer were investigated, and it was revealed that the expression levels of ataxia telangiectasia mutated kinase (ATM) were significantly enhanced in prostate cancer tissues isolated from patients with CRPC compared with from patients with hormone-dependent prostate cancer. CRPC C4-2 and CWR22Rv1 cells lines were subsequently selected to establish prostate cancer models, and ATM knockout cells were established via lentivirus infection. The results of the present study demonstrated that the migration and epithelial-mesenchymal transition (EMT) of ATM knockout cells were significantly decreased, which suggested that ATM is closely associated with CRPC cell migration and EMT. To further investigate the mechanisms underlying this process, programmed cell death 1 ligand 1 (PD-L1) expression was investigated in ATM knockout cells. In addition, inhibitors of Janus kinase (JAK) and signal transducer and activator of transcription 3 (STAT3; Stattic) were added to C4-2-Sc and CWR22Rv1-Sc cells, and the results demonstrated that PD-L1 expression was significantly decreased following the addition of JAK inhibitor 1; however, no significant change was observed following the addition of Stattic. Furthermore, a PD-L1 antibody and JAK inhibitor 1 were added to C4-2-Sc and CWR22Rv1-Sc cells, and it was revealed that cell migration ability was significantly decreased and the expression of EMT-associated markers was effectively reversed. The results of the present study suggested that via inhibition of the ATM-JAK-PD-L1 signaling pathway, EMT, metastasis and progression of CRPC may be effectively suppressed, which may represent a novel therapeutic approach for targeted therapy for patients with CRPC.