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Zhao J.,Zhengzhou University | Zhao J.,Henan Provincial People Hospital | Cheng Z.,Zhengzhou University | Cheng Z.,Henan Provincial People Hospital | And 6 more authors.
Journal of Surgical Research | Year: 2014

Background The transmural biodegradable polycaprolactone/poly(D,L-lactic/ glycolic acid) (PCL/PLGA) scaffold is a promising modality for diffuse coronary atherosclerosis cases that are not suitable for bypass grafting. The purpose of this study was to evaluate the long-term performance of the PCL/PLGA scaffold in vivo in the setting of polymer and heparin degradation. Materials and methods After mechanical drilling through the ventricular wall was performed in the whole ventricular wall, two scaffolds were implanted into the ventricular wall. Animals were grouped into the single drilling group (SD group), the blank scaffold group (BS group), and the heparinized scaffold group (HS group) and were allowed to survived for 6 mo. Next, the patency and integrity of the scaffolds were evaluated by echocardiography and 3D-DOCTOR software. Endothelium coverage of the lumen was evaluated by scanning electron microscopy. Neovessels and collagen fiber within the scaffolds were identified by histologic staining. Metabolite production of prostacyclin (PGI2) and thromboxane A 2 (TXA2) in the plasma was measured by an enzyme-linked immunosorbent assay. The expression levels of PGI2 synthase and cyclooxygenase 2 (COX-2) involved in PGI2 production and COX-1 involved in TXA2 production were measured by Western blot analysis. Results The heparinized scaffolds were patent for up to 6 mo and the lumen was covered with confluent endothelial cells. Histologic staining revealed collagen fiber remodeling and reconstruction of the neovascular network immediately surrounding the lumen. The expression of PGI2 synthase and COX-2 in the HS group was significantly higher compared with the SD and BS groups (P < 0.01). The expression of COX-1 was similar in the three groups (P > 0.05). Consistent with synthetase expression, a PGI2 metabolite (6-keto-PGF1a) also showed a significant increase in the HS group relative to the SD and BS groups (P = 0.021 and P = 0.015, respectively). Concomitantly, as a PGI2 antagonist, the TXA2 metabolite (TXB2) did not exhibit a significant difference among the three groups (P = 0.17). Conclusions Despite polymer and heparin degradation, the scaffold could continuously maintain the structural integrity and lumen patency for up to 6 mo by reinforcement of host collagen fiber and the balance of PGI 2/TXA2. © 2014 Elsevier Inc. All rights reserved.


Zhang Y.,Jining Medical University | Ma X.,Jining Medical University | Xie X.,North Sichuan Medical College | Sun G.,Jining Medical University | And 6 more authors.
Renal Failure | Year: 2015

Tubular epithelial-myofibroblast transition (TEMT) is an important process in renal tubulointerstitial fibrosis. Interleukin-1α (IL-1α) and transforming growth factor-β1 (TGF-β1) have been demonstrated to be key inducers of TEMT. In mouse embryonic fibroblast cells (NIH3T3), P311 protein induces phenotypic changes that are consistent to myofibroblast transformation. In the present study, we investigated the role of P311 gene and protein as well as potential mechanisms underlying TEMT in normal rat kidney tubular epithelial cells (NRK52E). Morphological and molecular changes were determined in NRK52E cells that were treated with IL-1α and/or P311 antibodies. The results showed that the NRK52E cells triggered by IL-1α became fibroblast-like cells, exhibiting hypertrophy of elongated and fusiform-shaped cells. IL-1α induced a time-dependent increase in P311 gene expression in NRK52E cells, with a peak time at 4 days. The expression levels of P311 gene were positively correlated withα-SMA and TGF-β1 gene expression levels. Anti-P311 antibody inhibited P311 andα-SMA expression in the presence of IL-1α. In contrast, anti-P311 antibody increased the expression of TGF-β1 gene in cells cultured with IL-1α. Therefore, P311 gene, together withα-SMA and TGF-β1 genes, was induced in the process of TEMT. P311 protein triggered by interleukin-1α may promote TEMT through a TGF-β1-independent pathway. © 2015 Taylor & Francis.


PubMed | Chengdu First People Hospital, North Sichuan Medical College, Henan Provincial People Hospital, Jining Medical University and University of Sichuan
Type: Journal Article | Journal: Renal failure | Year: 2015

Tubular epithelial-myofibroblast transition (TEMT) is an important process in renal tubulointerstitial fibrosis. Interleukin-1 (IL-1) and transforming growth factor-1 (TGF-1) have been demonstrated to be key inducers of TEMT. In mouse embryonic fibroblast cells (NIH3T3), P311 protein induces phenotypic changes that are consistent to myofibroblast transformation. In the present study, we investigated the role of P311 gene and protein as well as potential mechanisms underlying TEMT in normal rat kidney tubular epithelial cells (NRK52E). Morphological and molecular changes were determined in NRK52E cells that were treated with IL-1 and/or P311 antibodies. The results showed that the NRK52E cells triggered by IL-1 became fibroblast-like cells, exhibiting hypertrophy of elongated and fusiform-shaped cells. IL-1 induced a time-dependent increase in P311 gene expression in NRK52E cells, with a peak time at 4 days. The expression levels of P311 gene were positively correlated with -SMA and TGF-1 gene expression levels. Anti-P311 antibody inhibited P311 and -SMA expression in the presence of IL-1. In contrast, anti-P311 antibody increased the expression of TGF-1 gene in cells cultured with IL-1. Therefore, P311 gene, together with -SMA and TGF-1 genes, was induced in the process of TEMT. P311 protein triggered by interleukin-1 may promote TEMT through a TGF-1-independent pathway.


Liu Y.,Zhengzhou University | Yue H.,The First Peoples Hospital Of Zhengzhou City | Xu S.,Zhengzhou University | Wang F.,Zhengzhou University | And 4 more authors.
International Journal of Clinical Oncology | Year: 2015

Background: Because of the poor prognosis of unresectable or metastatic hepatocellular carcinoma there is a need for effective systemic therapy. The purpose of this study was to assess the efficacy and safety of gemcitabine and oxaliplatin (GEMOX) combined with sorafenib, as first-line therapy, followed by sorafenib as maintenance therapy for patients with advanced hepatocellular carcinoma (HCC). Methods: In this open-label, multicenter, single-group, prospective study, eligible patients with advanced HCC received oral sorafenib 400 mg twice daily, gemcitabine 1,000 mg/m2 intravenously (i.v.) on day 1 and oxaliplatin 85 mg/m2 i.v. on day 2 every 14 days for up to six cycles. Patients without disease progression were then treated further with sorafenib as maintenance therapy until disease progression. Results: All forty-nine patients completed six cycles of combined GEMOX and sorafenib therapy. The objective response was 26.5 %. The median time to progression was 10.3 months (95 % CI: 8.7–11.9 months) and median overall survival was 15.7 months (95 % CI: 13.0–18.4 months). During the combination therapy, the most common grade 3/4 hematologic toxicity was neutropenia (22.4 %, 11/49 patients) and thrombocytopenia (14.3 %, 7/49 patients); grade 3/4 non-hematologic toxicity was fatigue (22.4 %, 11/49 patients) and appetite loss (18.4 %, 9/49 patients). During the maintenance therapy, grade 3/4 adverse events were nonhematologic toxicity, for example fatigue (16.0 %, 4/25 patients) and appetite loss (16.0 %, 4/25 patients). Conclusions: GEMOX combined with sorafenib as first-line therapy followed by sorafenib as maintenance therapy was effective with manageable toxicity for patients with advanced hepatocellular carcinoma. However, the results should be further validated in controlled phase II trials. © 2015, Japan Society of Clinical Oncology.


PubMed | Henan Provincial People Hospital, The First Peoples Hospital of Zhengzhou City and Zhengzhou University
Type: Clinical Study | Journal: International journal of clinical oncology | Year: 2015

Because of the poor prognosis of unresectable or metastatic hepatocellular carcinoma there is a need for effective systemic therapy. The purpose of this study was to assess the efficacy and safety of gemcitabine and oxaliplatin (GEMOX) combined with sorafenib, as first-line therapy, followed by sorafenib as maintenance therapy for patients with advanced hepatocellular carcinoma (HCC).In this open-label, multicenter, single-group, prospective study, eligible patients with advanced HCC received oral sorafenib 400 mg twice daily, gemcitabine 1,000 mg/m(2) intravenously (i.v.) on day 1 and oxaliplatin 85 mg/m(2) i.v. on day 2 every 14 days for up to six cycles. Patients without disease progression were then treated further with sorafenib as maintenance therapy until disease progression.All forty-nine patients completed six cycles of combined GEMOX and sorafenib therapy. The objective response was 26.5 %. The median time to progression was 10.3 months (95 % CI: 8.7-11.9 months) and median overall survival was 15.7 months (95 % CI: 13.0-18.4 months). During the combination therapy, the most common grade 3/4 hematologic toxicity was neutropenia (22.4 %, 11/49 patients) and thrombocytopenia (14.3 %, 7/49 patients); grade 3/4 non-hematologic toxicity was fatigue (22.4 %, 11/49 patients) and appetite loss (18.4 %, 9/49 patients). During the maintenance therapy, grade 3/4 adverse events were nonhematologic toxicity, for example fatigue (16.0 %, 4/25 patients) and appetite loss (16.0 %, 4/25 patients).GEMOX combined with sorafenib as first-line therapy followed by sorafenib as maintenance therapy was effective with manageable toxicity for patients with advanced hepatocellular carcinoma. However, the results should be further validated in controlled phase II trials.


Sun M.,Central South University | Sun M.,Henan Provincial People Hospital | Liao Q.,Central South University | Wen L.,Central South University | And 3 more authors.
Journal of Central South University (Medical Sciences) | Year: 2013

Objective: To explore whether perioperative intravenous flurbiprofen axetil can reduce the incidence and intensity of chronic pain for breast cancer after surgical treatment. Methods: This randomized, double-blind, controlled trial enrolled 60 patients undergoing mastectomy and axillary lymph node dissection under general anesthesia. All patients accepted Hospital Anxiety and Depression Scale (HAD) tests the day before the surgery to evaluate depression and anxiety. The patients were randomly assigned to receive either 50 mg flurbiprofen axetil intravenously 15 minutes before the surgical incision and 6 hours later (group F) or intravenous 5 mL intralipid as a control (group C). All patients received patient-controlled intravenous analgesia (PCLA) with fentanyl postoperatively. Peripheral venous blood samples were drawn before the surgery, at 4 and 24 h after the surgery to detect the plasma level of PGE2 and tumor necrosis factor-α (TNF-α). Postoperative fentanyl consumption, Numerical Rating Scale (NRS) scores and adverse effects were recorded at 2, 6, 12, 24 and 48 h after the surgery. The duration and intensity of pain were followed up by telephone at the 2nd-12th month after the surgery. Results: The incidence of pain at 2, 4, 6, and 12 months after the breast surgery was 33%, 20%, 15%, and 10%, respectively, and the average pain score was 0.77, 0.57, 0.28, and 0.18, respectively. Compared with group C, the scores of pain in group F were significantly lower at 2, 4, 6 and 12 months postoperatively (F=7.758, P=0.007). The incidence of pain in group F was significantly lower at 2, 4 and 6 months postoperatively (P<0.05). There was no significant difference in the incidence of pain between the groups at 12 months postoperatively (P>0.05). Preoperatively and at 4 and 24 h after the surgery, there was no significant difference in the level of TNF-α between the two groups (F=0.530, P=0.470); but plasma concentration of PGE2 in group F was significantly lower than that in group C (F=S.646, P=0.021). No patients developed abnormal bleeding, peptic ulcer, impaired liver or renal function and respiratory depression. Conclusion: Perioperative intravenous infusion of 100 mg flurbiprofen axetil can decrease the intensity and incidence of chronic pain for breast cancer after surgical treatment.

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