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Wang L.,Guangdong Pharmaceutical University | Wang L.,Jinan University | Tian X.,Jinan University | Wang B.,The First Peoples Hospital of Foshan City | Yin M.,Guangdong Pharmaceutical University
Acta Medica Mediterranea | Year: 2016

In order to improve quality of life for infertility patients and relieve their adverse emotional state, this paper conducted in-depth analysis and research of the clinical effect of implementation of comprehensive nursing intervention on the treatment process of infertility patients. A total of 3800 patients who had been treated for infertility in some 10 hospitals from June 2014 to June 2015 were selected as study subjects. Among them, 2500 patients who decided to receive fine nursing in the treatment process after discussion with doctors and family members were selected as observation group; the remaining 1300 patients who didn't receive comprehensive nursing intervention due to various reasons but received routine nursing care in the treatment process were selected as a control group. The preferred infertility patients in this study received 8 weeks of nursing intervention. After completion of nursing, a comparison of the psychological state of anxiety and depression and quality of life of the two groups of patients revealed that various indicators of the observation group patients with comprehensive nursing intervention improved, patient psychological mood moved in a more positive direction, life attitude was more positive and patients were more willing to cooperate in the treatment. Hence, the therapeutic effect was significantly better than that of the control group. Therefore, this clinical research fully confirms the great role of comprehensive nursing intervention in the clinical treatment of infertility patients. It is recommended that comprehensive nursing intervention should be promoted in the actual clinical process.


Liu J.,Sun Yat Sen University | Xie X.,Sun Yat Sen University | Zhou C.,Sun Yat Sen University | Peng S.,The First Peoples Hospital of Foshan City | And 2 more authors.
European Journal of Cardio-thoracic Surgery | Year: 2012

Objectives: The demographic and clinicopathologic factors associated with 5-year survivors have not been well documented in oesophageal squamous cell carcinoma (OSCC). We evaluated factors predictive of actual 5-year survival in the present research. Methods: We analysed 1241 patients underwent oesophagectomy for invasive OSCC retrospectively. The demographic and clinicopathologic characteristics were compared between patients who were alive >5 years after oesophagectomy and patients who died within 5 years of oesophagectomy. Results: Univariate analysis showed significant differences between the two groups regarding 11 different factors. Further analysis by logistic regression showed that eight factors were identified as independent predictors of actual 5-year survival. Conclusions: The independent positive predictors for actual 5-year survival are younger patients, female gender, absence of weight loss, R0 resection, lower pathological T stage, lower pathological N stage, higher histologic grade and more resected lymph nodes. © The Author 2012. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.


Cai S.,Sun Yat Sen University | Chen R.,Sun Yat Sen University | Li X.,Sun Yat Sen University | Cai Y.,Sun Yat Sen University | And 15 more authors.
Oncotarget | Year: 2015

Here we found that levels of miR-23a were decreased in prostate cancer cell lines and tumor tissues. These low levels were associated with poor patients' prognosis. MiR-23a inhibited migration and invasion of prostate cancer in vivo and in orthotopic prostate cancer mice model. MiR-23a decreased levels of p21-activated kinase 6 (PAK6). Expression of miR-23a inhibited phosphorylation of LIM kinase 1 (LIMK1) and cofilin, in turn suppressing formation of stress fibers and actin filaments, which was required for cell motility and invasion. PAK6 bound to LIMK1 and activated it via phosphorylation at Thr-508. Also, PAK6 and LIMK1 were colocalized in the cytoplasma. Thus, miR-23a regulated cytoskeleton by affecting LIMK1 and cofilin. In summary, we have identified the miR-23a-PAK6-LIMK1 pathway of prostate cancer metastasis. Potential therapeutic approach by targeting miR-23 is suggested.


Wang P.-p.,Sun Yat Sen University | Xie D.-y.,Sun Yat Sen University | Liang X.-J.,Jinan University | Peng L.,Sun Yat Sen University | And 4 more authors.
PLoS ONE | Year: 2012

Aims: Bone marrow-derived mesenchymal stem cells (BMSCs) can reduce liver fibrosis. Apart from the paracrine mechanism by which the antifibrotic effects of BMSCs inhibit activated hepatic stellate cells (HSCs), the effects of direct interplay and juxtacrine signaling between the two cell types are poorly understood. The purpose of this study was to explore the underlying mechanisms by which BMSCs modulate the function of activated HSCs. Methods: We used BMSCs directly and indirectly co-culture system with HSCs to evaluate the anti-fibrosis effect of BMSCs. Cell proliferation and activation were examined in the presence of BMSCs and HGF. c-met was knockdown in HSCs to evaluate the effect of HGF secreted by BMSCs. The TLR4 and Myeloid differentiation primary response gene 88(MyD88) mRNA levels and the NF-kB pathway activation were determined by real-time PCR and western blotting analyses. The effect of BMSCs on HSCs activation was investigated in vitro in either MyD88 silencing or overexpression in HSCs. Liver fibrosis in rats fed CCl4 with and without BMSCs supplementation was compared. Histopathological examinations and serum biochemical tests were compared between the two groups. Results: BMSCs remarkably inhibited the proliferation and activation of HSCs by interfering with LPS-TLR4 pathway through a cell-cell contact mode that was partially mediated by HGF secretion. The NF-kB pathway is involved in HSCs activation inhibition by BMSCs. MyD88 over expression reduced the BMSC inhibition of NF-kB luciferase activation. BMSCs protected liver fibrosis in vivo. Conclusion: BMSCs modulate HSCs in vitro via TLR4/MyD88/NF-kB signaling pathway through cell-cell contact and secreting HGF. BMSCs have therapeutic effects on cirrhosis rats. Our results provide new insights into the treatment of hepatic fibrosis with BMSCs. © 2012 Wang et al.


PubMed | TPM DTI Foundation, Sun Yat Sen University, The First Peoples Hospital of Foshan City, Guangzhou University and 4 more.
Type: Journal Article | Journal: American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons | Year: 2015

Reliable prediction of time of death after withdrawal of life-sustaining treatment in patients with devastating neurological injury is crucial to successful donation after cardiac death. Herein, we conducted a study of 419 neurocritical patients who underwent life support withdrawal at four neurosurgical centers in China. Based on a retrospective cohort, we used multivariate Cox regression analysis to identify prognostic factors for patient death, which were then integrated into a nomogram. The model was calibrated and validated using data from an external retrospective cohort and a prospective cohort. We identified 10 variables that were incorporated into a nomogram. The C-indexes for predicting the 60-min death probability in the training, external validation and prospective validation cohorts were 0.96 (0.93-0.98), 0.94 (0.91-0.97), and 0.99 (0.97-1.00), respectively. The calibration plots after WLST showed an optimal agreement between the prediction of time to death by the nomogram and the actual observation for all cohorts. Then we identified 22, 26 and 37 as cut-points for risk stratification into four groups. Kaplan-Meier curves indicated distinct prognoses between patients in the different risk groups (p<0.001). In conclusion, we have developed and validated a nomogram to accurately identify potential cardiac death donors in neurocritical patients in a Chinese population.


PubMed | Sun Yat Sen University and The First Peoples Hospital of Foshan City
Type: Journal Article | Journal: Oncology reports | Year: 2015

The Raf kinase inhibitor protein (RKIP) is a novel metastasis suppressor. RKIP was previously found to have low expression in a colorectal cancer (CRC) patient cohort by immunohistochemistry. However, the role of RKIP in CRC remains undetermined. In the present study, immunohistochemistry was performed to compare RKIP expression between 129 paired stage II CRC and adjacent non-tumorous tissues. The correlations between clinical parameters, prognosis and RKIP expression were evaluated. To investigate the effect of RKIP on proliferation and metastasis, RKIP was overexpressed and knocked down in colon cancer cell lines. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Transwell and wound-healing assays were performed. Murine models were established to confirm the influence of RKIP on malignant tumor phenotypes in vivo. Our results showed that RKIP expression was significantly decreased in the CRC tissues compared to the adjacent noncancerous tissues (p<0.001) and was correlated with the risk of relapse in stage II CRC (p<0.05). Overexpression of RKIP suppressed HCT116 cell metastasis in vitro and in vivo, whereas knockdown of RKIP expression in SW480 cells and its murine model increased metastatic ability (p<0.05). No effect of RKIP on cell proliferation in CRC was observed. These data suggest that RKIP is an important metastasis-suppressor gene in CRC. The re-expression of RKIP could be a potential therapeutic target for antimetastatic strategies for CRC.


PubMed | Zhongshan Peoples Hospital, Qingyuan Peoples Hospital, Sun Yat Sen University, Taishan Peoples Hospital and The First Peoples Hospital of Foshan City
Type: Journal Article | Journal: Oncotarget | Year: 2015

Here we found that levels of miR-23a were decreased in prostate cancer cell lines and tumor tissues. These low levels were associated with poor patients prognosis. MiR-23a inhibited migration and invasion of prostate cancer in vivo and in orthotopic prostate cancer mice model. MiR-23a decreased levels of p21-activated kinase 6 (PAK6). Expression of miR-23a inhibited phosphorylation of LIM kinase 1 (LIMK1) and cofilin, in turn suppressing formation of stress fibers and actin filaments, which was required for cell motility and invasion. PAK6 bound to LIMK1 and activated it via phosphorylation at Thr-508. Also, PAK6 and LIMK1 were colocalized in the cytoplasma. Thus, miR-23a regulated cytoskeleton by affecting LIMK1 and cofilin. In summary, we have identified the miR-23a-PAK6-LIMK1 pathway of prostate cancer metastasis. Potential therapeutic approach by targeting miR-23 is suggested.


Wang Y.-Z.,Central South University | Wang Y.-Z.,Affiliated Hospital of Jining Medical College | Tian F.-F.,Central South University | Yan M.,The First Peoples Hospital of Foshan City | And 6 more authors.
Clinical and Experimental Immunology | Year: 2014

Summary: MicroRNA-155 (miR155) is required for antibody production after vaccination with attenuated Salmonella. miR155-deficient B cells generated reduced germinal centre responses and failed to produce high-affinity immunoglobulin (Ig)G1 antibodies. In this study, we observed up-regulation of miR155 in the peripheral blood mononuclear cells (PBMCs) of patients with myasthenia gravis (MG), and miR155 was also up-regulated in torpedo acetylcholine receptor (T-AChR)-stimulated B cells. We used an inhibitor of miR155 conjugated to anti-CD20 single-chain antibody to treat both the cultured B cells and the experimental autoimmune MG (EAMG) mice. Our results demonstrated that silencing of miR155 by its inhibitor impaired the B cell-activating factor (BAFF)-R-related signalling pathway and reduced the translocation of nuclear factor (NF)-κB into the nucleus. Additionally, AChR-specific autoantibodies were reduced, which may be related to the altered amounts of marginal zone B cells and memory B cells in the spleens of EAMG mice. Our study suggests that miR155 may be a promising target for the clinical therapy of MG. © 2014 British Society for Immunology.


PubMed | The First Peoples Hospital of Foshan City, Biomedical Technology Co., Wuhan University of Science and Technology, China Three Gorges University and 2 more.
Type: | Journal: European journal of pharmacology | Year: 2016

A brain ischemia rat model was established by middle cerebral artery occlusion (MCAO) for 2h and reperfusion for 4h to investigate the underlying mechanism of the neuroprotection action of clonidine, a classical alpha-2 adrenergic agonist, on cerebral ischemia. Clonidine and yohimbine were intraperitoneally given to the rats each day for a week before ischemia. Neurological deficits evaluations were carried out at 6h after operation. TTC staining method was used to measure the volume of brain infarction. Expression levels of NMDAR1, NMDAR2A, NMDAR2B were assayed by western blotting. Our data demonstrated that clonidine pretreatment significantly improved the neurological deficit scores and reduced the brain infarct volumes of the rats. Furthermore, protein expression level of p-NMDAR2B in cortex was significantly up-regulated whereas that of p-NMDAR1 was decreased when compared with the sham-operated rats. Remarkably, clonidine treatment led to significant down-regulation of p-NMDAR2B and NMDAR2A in addition to enhancement of the expression level of p-NMDAR1 in cortex. This is the first report illustrating the neuroprotective role of clonidine may be mediated through modulation of the expression levels of p-NMDAR2B, NMDAR2A and p-NMDAR1 during cerebral ischemia.

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