Liu H.,Harbin Medical University |
Zhao S.,Harbin Medical University |
Jiao M.,Harbin Medical University |
Jiao M.,Jian Guo |
And 8 more authors.
International Journal of Environmental Research and Public Health | Year: 2015
Using a cross-sectional survey design from 11 public tertiary hospitals (a specialist hospital, four Chinese medicine hospitals, and six general hospitals) in the urban areas of Heilongjiang, we determined the nature of workplace violence that medical staff have encountered in Chinese hospitals and identified factors associated with those experiences of violence. A total of 1129 health workers participated. The specialist hospital had the highest prevalence of physical violence (35.4%), while the general hospitals had the highest prevalence of non-physical violence (76%). Inexperienced medical staff (p < 0.001) were more likely to suffer non-physical violence than physical violence in Chinese medicine hospitals compared to experienced staff. Medical units (p = 0.001) had a high risk of non-physical violence, while surgical units (p = 0.005) had a high risk of physical violence. In general hospitals, staff with higher levels of anxiety about workplace violence were more vulnerable to both physical violence (1.67, 95% CI 1.36–2.10) and non-physical violence (1.309, 95% CI 1.136–1.508) compared to those with lower levels of anxiety, while rotating shift workers had a higher odds of physical violence (2.2, 95% CI 1.21–4.17) and non-physical violence (1.65, 95% CI 1.13–2.41) compared to fixed day shift workers. Thus, prevention should focus not only on high-risk sections of hospitals, but also on the nature of the hospital itself. © 2015 by the authors; licensee MDPI, Basel, Switzerland.
Kong J.,Harbin Medical University |
Zhang H.-N.,Heilongjiang University of Chinese Medicine |
Jia D.,Harbin Medical University |
Wang D.,Harbin Medical University |
And 10 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2013
Background: The incidence of spinal cord injury shows an increasing tendency, but the repair mechanism after spinal cord injury is not fully understood. Objective: To investigate the effect of oligodendrocyte precursor cells in repair of spinal cord injury. Methods: According to Allen's method, models of spinal cord injury were established in mice. The morphological change of spinal cord was detected by pathological method. Oligodendrocyte precursor cells were isolated and purified from green fluorescence protein transgenic mice in vitro, and induced to differentiate into oligodendrocytes. Furthermore, oligodendrocyte precursor cells were transplanted into mice model of spinal cord injury. The experiment was divided into four groups according to different treatment methods: model group, sham-operation group, treatment group and control group. Results and Conclusion: The success rate for establishing the mice model of spinal cord injury was 100%. The cultured oligodendrocyte precursor cells had the ability to self-proliferate and differentiate into oligodendrocytes. After being transplanted, oligodendrocyte precursor cells could not only integrate with the host tissue of spinal cord, but also could migrate to the injury zone and replace the damaged tissue. Motor function of mice was significantly recovered by oligodendrocyte precursor cells transplantation. Exogenous oligodendrocyte precursor cells can survive in the injury zone and integrate with the host tissue of the mice after spinal cord injury.
Meng F.-Y.,Guangxi Medical University |
Ning Y.-L.,Guangxi Medical University |
Ning Y.-L.,Wu Jieping Medical Foundation Cell and Molecular Clinical Research Center |
Qi J.,Heilongjiang Nursing College |
And 6 more authors.
International Journal of Molecular Sciences | Year: 2014
A new water-soluble polysaccharide (longan polysaccharide 1 (LP1)) was extracted and successfully purified from Dimocarpus longan pulp via diethylaminoethyl (DEAE)-cellulose anion-exchange and Sephacryl S-300 HR gel chromatography. The chemical structure was determined using Infrared (IR), gas chromatography (GC) and nuclear magnetic resonance (NMR) analysis. The results indicated that the molecular weight of the sample was 1.1 × 105 Da. Monosaccharide composition analysis revealed that LP1 was composed of Glc, GalA, Ara and Gal in a molar ratio of 5.39:1.04:0.74:0.21. Structural analysis indicated that LP1 consisted of a backbone of →4)-α-D-Glcp-(1→4)-α-D-Galp A-(1→4)-α-D-Glcp -(1→4)-Β-D-Glcp -(1→ units with poly saccharide side chains composed of →2)-Β-D-Fruf-(1→2)-L-sorbose-(1→ attached to the O-6 position of the α-D-Glcp residues. In vitro experiments indicated that LP1 had significantly high antitumor activity against SKOV3 and HO8910 tumor cells, with inhibition percentages of 40% and 50%, respectively. In addition, LP1 significantly stimulated the production of the cytokine interferon-γ (IFN-γ), increased the activity of murine macrophages and enhanced B- and T-lymphocyte proliferation. The results of this study demonstrate that LP1 has potential applications as a natural antitumor agent with immunomodulatory activity. © 2014 by the authors; licensee MDPI, Basel, Switzerland.
Li J.,Jilin University |
Yao L.,Harbin Medical University |
Li G.,Harbin Medical University |
Ma D.,Harbin Medical University |
And 4 more authors.
PLoS ONE | Year: 2015
Extrahepatic cholangiocarcinoma (EHCC) is a refractory malignancy with poor prognosis due to its early invasion, metastasis and recurrence after operation. Therefore, understanding the mechanisms of invasion and metastasis is the key to the development of new and effective therapeutic strategies for EHCC. In the present study we demonstrated that miR-221 promoted EHCC invasion and metastasis through targeting PTEN and formed a positive feedback loop with β-catenin/c-Jun signaling pathway. We found miR-221 was upregulated in EHCC specimens and CC cell lines. Moreover, miR-221 was found strongly associated with the metastasis and prognosis of EHCC patients. The expression of PTEN was downregulated in EHCC patients and CC cell lines, and was further demonstrated as one of the downstream targets of miR-221. In addition, our data indicated that β-catenin activated miR-221 through c-jun, while miR-221 enhanced β-catenin signaling induced-epithelial-mesenchymal transition (EMT) by targeting PTEN, hence forming a positive feedback loop in EHCC cell lines. In conclusion, our results suggested that miR-221 promotes EMT through targeting PTEN and forms a positive feedback loop with β-catenin/c-Jun signaling pathway in EHCC. © 2015 Li et al.
Yao L.,Harbin Medical University |
Li F.,Harbin Medical University |
Tang Z.,Harbin Medical University |
Gao S.,Heilongjiang Nursing College |
Wu D.,Harbin Medical University
Asian Pacific Journal of Cancer Prevention | Year: 2012
Aims: Primary hepatocellular carcinoma (HCC) is a common malignancy often related to hepatitis viral infection. Smad4 is known to mediate the TGF-β pathway to suppress tumorigenesis. However, the function of Smad4 in HCC is still controversial. In this study we compared levels of Smad4 in HCC tissues with or without hepatitis virus infection and adjacent normal-appearing liver. Methods: Samples from HCC patients were analyzed for Smad4 protein and mRNA expression by immunohistochemistry (IHC), RT-PCR and Western blotting. Results: We found that tumor tissues expressed less Smad4 mRNA and protein than the adjacent tissues. Most HCC tumor tissues were negative for Smad4 in IHC staining, while the majority of adjacent tissues were positively stained. Interestingly, protein levels were higher in HCC tissues with viral hepatitis than those without virus infection. Suppression of expression appeared closely related to HCC, so that Smad4 appears to function as a tumor suppressor gene (TSG). Conclusion: Patients with hepatitis viral infection, at higher risk for HCC, exhibited increased Smad4 protein expression suggesting hepatitis virus may modulate Smad4 expression, which is functionally distinct from its putative role as a TSG. Smad4 expression may thus be an applicable marker for diagnosis and/or a target to develop therapeutic agents for HCC.