Objective:To assess the impact of self-guidance manual combined with one-to-one training on the knowledge and practice of caregivers of patients in neurosurgery.Methods:Ninety pairs of inpatients and their caregivers in the second Neurosurgery Ward of the First Hospital of China Medical University were randomly selected and divided into two groups, the control group and the research group. The research group trained caregivers with self-guidance manual combined with one-to-one training, while the control group trained caregivers with self-guidance manual. The demographic data of the two groups were recorded. According to the practice test of nursing staff, the number of completed 6 items before and after the training was recorded and compared between the two groups.Results:The study group's caregiver correctly turned over the buckle after 3 months of intervention, correct skin care, correct functional exercise, correct tracheotomy care, and the number of people who correctly sanitized their hands were 35 (94.6%, 35/37), 35 (94.6%, 35/37), 32 (86.5%, 32/37), 25 (67.6%, 25/37), 22 (59.5%, 22/37). The control caregiver correctly turned over the buckle back after 3 months of intervention, correct skin care, correct functional exercise, correct tracheotomy care, and the number of correct hygiene hands washing was 9 (27.3%, 9/33), 7 (21.2%, 7/33), 8 (24.2%, 8/33), 13 (39.4%, 13/33), 9 (27.3%, 9/33). There was a statistically significant difference between the two ( χ2 value was 5.58-39.14, P<0.05). Conclusion:Guidance manual combined with one-to-one training can significantly improve the knowledge and skills of caregivers of neurosurgery patients.

We measured the interleukin-34 (IL-34) level in sera from patients with systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE) using an enzyme-linked immunosorbent assay (ELISA). Blood tests, including assays to determine C-reactive protein (CRP), complement (C) 3, C4, immunoglobulin (Ig) A, IgG, IgM, anti-double-stranded DNA antibody (Anti-dsDNA Ab) and hemoglobin (Hb) levels and white blood cell (WBC) and platelet (PLT) counts, were performed using standard methods. Lupus nephritis (LN) was diagnosed according to the American College of Rheumatology (ACR) renal criteria. The SLE disease activity was scored using the SLE Disease Activity Index (SLEDAI). Among the 110 SLE cases, IL-34 could be detected in 79 cases (71.8%). IL-34 was barely detected in the control group. The serum level of IL-34 was significantly higher in the SLE group. No change was observed in the serum IL-34 concentration in the SLE patients regardless of LN status. Correlations were observed between the serum IL-34 level and the disease activity parameters. The SLE patients with detectable IL-34 levels had higher SLEDAI and IgG concentrations and lower C3 and Hb levels than patients with undetectable IL-34 levels. Therefore, IL-34 could be a potential disease activity marker for SLE.

To explore the immunological mechanisms underlying the effect of exogenous interleukin-34 (IL-34) on collagen-induced arthritis (CIA) in mouse. We established a CIA mouse model and injected exogenous recombination mouse IL-34 (rmIL-34) intraperitoneally. The articular index (AI) was measured according to the amount of erythema, swelling, or joint rigidity. The concentrations of TNF-α, IL-17, and IL-6 in CIA mice sera were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of TNF-α, IL-17, and IL-6 in CIA synovial tissue were detected by reverse transcription PCR. The CIA mice dosed with rmIL-34 exhibited increased AI. Neutralization of endogenous IL-17 with anti-IL-17 antibody reduced the effect of IL-34. TNF-α, IL-17, and IL-6 levels in serum in IL-34-treated CIA mice were increased compared to those in CIA mice. IL-34 increased the expression of TNF-α and IL-17 mRNA in synovial tissues of CIA mice, but the gene expression of IL-6 was not affected. The effects of IL-34 on TNF-α, IL-17, and IL-6 expression were abolished by anti-IL-17 antibody. In conclusion, IL-34 acts as a proinflammatory factor, aggravating the severity of arthritis in CIA mice by inducing the production of IL-17.

Objective To study the effect of exogenous IL-34 on peripheral blood mononuclear cells(PBMCs) of RA animal model(collagen-induced arthritis,CIA),explore if IL-34 promotes the production of tumor necrosis factorα (TNF-oα) and IL-6 by Th17 cells.Methods PBMCs of CIA were stimulated by recombination mouse(rm) IL-34,the frequency of IL-17+CD4+,interferon (IFN)-γ+CD4+,IL-4+CD4+ and IL-10+CD4+T lymphocytes in PBMCs was detected by flow cytometry.The contents of IL-17,IFN-γ,IL-4,IL-10,TNF-α and IL-6 in PBMCs were measured by ELISA following stimulation with anti-CD3/CD28 and rmIL-34.The expressions of TNF-α and IL-6 mRNAs in CIA PBMCs after stimulated with rmIL-34 were detected by RT-PCR;PBMCs were co-cultured with rmIL-34 and anti-IL-17,the secretion of TNF-α and IL-6 were detected by ELISA.Results IL-34 increased the frequency of Th17 cells and stimulated the secretion of IL-17 by PBMCs of CIA.IL-34 increased the secretion of TNF-α and IL-6 and stimulated the expression of TNF-α and IL-6 mRNAs by PBMCs of CIA.Blocking IL-17 by anti-IL-17 antibody decreased the secretion of TNF-α and IL-6 under stimulation with rmIL-34.Conclusion IL-34 promotes the secretion and expression of TNF-α and IL-6 by up-regulated the function of Th17 cells,might be a new treatment target for RA.

Epithelial-mesenchymal transition (EMT) plays a pivotal role in the invasion and metastasis of breast cancer. Livin is a recently identified member of the inhibitors of the apoptosis protein family, which has been revealed to facilitate the progression of several types of cancer. However, the role of Livin in EMT and metastasis of breast cancer and its underlying mechanisms are not fully elucidated. In the present study, the levels of Livin mRNA and protein expression were found to be elevated in breast cancer tissues and cell lines. In addition, Livin expression was positively correlated with TNM stage and lymph node metastasis in total and triple-negative breast cancer (TNBC) cases. Livin overexpression enhanced the migratory and invasive abilities of the MCF-7 cells, accompanied by increases in vimentin, N-cadherin, Snail, MMP-2 and MMP-7 and a decrease in E-cadherin. Conversely, the downregulation of Livin had the opposite effect in MDA-MB-231 cells. Furthermore, the upregulation of Livin expression markedly stimulated the activation of the p38/GSK3β pathway, while the downregulation of Livin expression clearly suppressed the activation of the p38/GSK3β pathway. In conclusion, our results revealed that Livin induced EMT through the activation of the p38/GSK3β pathway, which in turn promoted the progression and metastasis of breast cancer, especially for TNBC.

The aim of this study was to detect the expression of BRCA-1 and BAG-1 in Triple Negative Breast Cancer (TNBC), and analyse the correlation between protein expression and sensitivity to Platinumbased Chemotherapy (PbC). Malignant tissues from 72 TNBC patients who were treated according to the NP and GP programs; then, the relationships between BRCA-1 and BAG-1 protein expression and the survival period (median Overall Survival (OS) and Progression-Free Survival (PFS)) were examined. In TNBC, BRCA-1 expression was related to lymph node metastasis and clinical stage (P<0.01); whereas BAG-1 expression was only related to lymph node metastasis. In TNBC tissues, the expression of BRCA-1 and BAG-1 proteins was significantly positively correlated (r=0.845, P=0.001), and the median OS and PFS of the BRCA-1 and BAG-1-negative group were significantly longer than those of the BRCA-1 and BAG-1-positive group after PbC (P<0.05). In TNBC, the expression of BRCA-1 and BAG-1 was significantly positively correlated, suggesting that these two have synergistic roles in the development of TNBC. The survival rate of TNBC patients with non-BRCA-1 and BAG-1-expressing tumours was higher than that of patients with BRCA-1 and BAG-1-expressing tumours; thus, negativity for BRCA-1 and BAG-1 expression could be used to predict chemo sensitivity of TNBC to PbC.

Leukocytoclastic vasculitis (LCV) is a neutrophilic inflammation of the blood vessels. LCV may present as a paraneoplastic syndrome occurring before, synchronously with, or after the diagnosis of malignancy. In this study, we report a unique case of multiple malignancies developing simultaneously in a patient with a long history of LCV. The patient was originally diagnosed with LCV and received long-term glucocorticoid treatment. After 11 years of therapy, the patient developed three primary malignancies, including small-cell lung carcinoma, gastric adenocarcinoma and colonic adenocarcinoma. It is likely that LCV was not a paraneoplastic syndrome in this case, but rather an independent process, and the development of multiple cancers is likely associated with the long-term glucocorticoid treatment, which caused imbalance of the immune system. Although the development of cancer during the course of glucocorticoid treatment is very rare, clinicians must be aware of this possible association and immunodysregulation may play a role in this context.

We have reported that SIAH1 is down-regulated and associated with apoptosis and invasion in human breast cancer. However, the molecular mechanisms leading to SIAH1 down-regulation remain to be elucidated. Here, we demonstrated that miR-107 directly down-regulates SIAH1 expression in human breast cancer cells. Over- expression of miR-107 reduced SIAH1 expression, promoted human breast cancer cell proliferation, colony formation, migration and invasion, and inhibited apoptosis. On the contrary, silencing of miR-107 increased SIAH1 expression and inhibited the tumor growth of MDA-MB-231 cells, a kind of triple-negative breast cancer (TNBC) cells, in vitro and in vivo. Our results reveal that miR-107 is an upstream regulator for SIAH1 down-regulation in human breast cancer cells and miR-107 provides a potential effective target for the treatment of TNBC. (c) 2015 Wiley Periodicals, Inc.