Bayi Hospital

Bayi’awati, China

Bayi Hospital

Bayi’awati, China
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Qin S.,Bayi Hospital | Cheng Y.,Jilin Province Cancer Hospital | Liang J.,Qingdao University | Shen L.,Peking University | And 11 more authors.
Oncologist | Year: 2014

Background. The EACH study assessed the efficacy of oxali-platin, 5-fluorouracil, and leucovorin (the FOLFOX4 regimen) compared with doxorubicin alone in terms of overall survival (OS), progression-free survival (PFS), and safety in patients with advanced hepatocellular carcinoma (HCC). We present the results of this study in Chinese patients.Methods. In a multicenter, open-label, randomized, phase III study (NCT00471965), 371 patients (279 patients from the People’s Republic of China) were randomized 1:1 to receive either FOLFOX4 or doxorubicin until disease progression, intolerable toxicity, death, or surgical resection.Results. Baseline characteristics of the Chinese patients enrolled in the study were similar for the 2 treatment groups and in comparison with the whole EACH cohort. Median OS at the prespecified time point of treatment was 5.7 months with FOLFOX4 and 4.3 months with doxorubicin (hazard ratio [HR]: 0.74; 95% confidence interval [CI]: 0.55-0.98; p 5.03). At the end of the follow-up period, median OS was 5.9 months with FOLFOX4 and 4.3 months with doxorubicin (HR: 0.75; 95% CI: 0.58-0.98; p 5.03). Median PFS was 2.4 months and 1.7 months in the FOLFOX4 and doxorubicin groups, respectively (HR: 0.55; 95% CI: 0.45-0.78;p 5.0002).The response rate (RR) and disease control rate (DCR) were significantly higher in the FOLFOX4group than in the doxorubicin group (RR: 8.6% vs. 1.4%, p 5.006; DCR: 47.1% vs. 26.6%, p 5.0004). Hematological toxicity was more frequently reported in the FOLFOX4 group.Conclusion. For Chinese HCC patients enrolled in the EACH study, FOLFOX4 significantly improved the RR and DCR and prolonged survival compared with doxorubicin. Systemic chemotherapy with oxaliplatin-based regimens may play an important role in the treatment of Chinese patients with advanced HCC. © AlphaMed Press 2014.

Guo B.,Bayi hospital | Wang Y.,General Hospital of Coal Industry Ministry of China | Hui Y.,PLA Fourth Military Medical University | Yang X.,No 4 Hospital Of Xian | Fan Q.,Bayi hospital
Molecular Vision | Year: 2010

Purpose: To evaluate the effects of an anti-rat vascular endothelial growth factor antibody (ARVA) and bevacizumab (Avastin) on rat retinal Müller glial cells (RMGCs) in vivo and in vitro. Methods: Rat RMGCs were identified and cultivated, and were then treated with bevacizumab (0.1, 0.25, and 1 mg/ml), ARVA (0.1, 0.5, and 1 μg/ml), or 1 mg/ml of rat immunoglobulin G (IgG) for 12, 24, 48, and 72 h. The numbers of viable RMGCs were determined using a trypan blue dye exclusion assay and a methyl thiazolyl tetrazolium colorimetric assay. In the in vivo study, the rats received intravitreal injections of 5 μl bevacizumab (3.75 mg/ml), ARVA (15 μg/ml), and rat IgG (1 mg/ml). The electroretinogram was recorded. Seven days after the injections, histopathologic changes and glial fibrillary acidic protein expression of RMGCs in the retina were analyzed by immunohistochemistry with hematoxylineosin and fluorescent staining. Results: After exposure to bevacizumab at various concentrations for various periods of time, the stained cell numbers and optical density values of mitochondrial dehydrogenase activity of RMGCs had no significant differences (p>0.05) from those of the control group and IgG medium. In the stained cells, ARVA demonstrated a dose-dependent increase. Compared with those treated for 12 and 24 h, the increase of stained cells treated with 0.5 and 1 μg/ml ARVA at 48 and 72 h was very significant (p<0.01). The optical densities of RMGCs exposed to 0.5 and 1 μg/ml of ARVA at 48 and 72 h were significantly lower than cells exposed to a fresh culture medium (p<0.01). The histology of both treated and control eyes after intravitreal injection was similar and showed no anatomic signs of toxicity. There were no obvious glial fibrillary acidic protein upregulations of RMGCs in all groups. The scotopic electroretinogram responses to flashes of light in the control and treated eyes had similar b-wave amplitudes. Conclusions: Intravitreal bevacizumab and ARVA had no short-term, direct retinal toxicity in rats. Bevacizumab exerts no inhibition on rat RMGCs, while ARVA at higher doses (over 0.5 μg/ml) may be harmful to the growth of RMGCs © 2010 Molecular Vision.

Bao W.,Peking Union Medical College | Bao W.,Nanjing University | Bao W.,Bayi Hospital | Jin L.,Nanjing University | And 7 more authors.
PLoS ONE | Year: 2013

Background:In recent years, the fungal infectious disease zygomycosis has increased in incidence worldwide, especially among the immunodeficient population. Despite the rates of zygomycosis-related death and deformation being very high, the mechanism(s) by which the fungal pathogens cause these severe manifestations remain unknown.Methods:Using the associated Rhizomucor variabilis species, which can selectively induce cutaneous zygomycosis in otherwise healthy individuals, we investigated the host mechanisms of infection-related responses, including cytokine and chemokine expression as well as contributions of particular T cell subsets. siRNA specifically targeting IL-22,IL-17 and IFN-γ were used to down-regulate expression of those molecules.Results:In mouse models of infection, IL-22 was implicated in development of Rhizomucor spp.-induced skin lesions. In cultured human peripheral blood monocytes, R. pusilluscan, which is often found in immunodeficient patients, induced the production of IL-22, while R. variabilis did not. Moreover, Rhizomucor spp.-induced secretion of Il-22 from CCR6+CCR4+CCR10+ cells was down-regulated by knockdown of IL-22 related signaling receptors, RORC and ARH.Conclusion:Our data strongly suggest that avoidance of IL-22 may be one mechanism by which mucor species produce morbidity and mortality in infected individuals. © 2013 Bao et al.

Chan S.L.,Chinese University of Hong Kong | Wong V.W.S.,Chinese University of Hong Kong | Qin S.,Chinese University of Hong Kong | Chan H.L.Y.,Chinese University of Hong Kong | Chan H.L.Y.,Bayi Hospital
Journal of Clinical Oncology | Year: 2016

Infection is a well-described cause of cancer in humans. Being one of the most common infections worldwide, hepatitis B virus (HBV) is the leading cause of hepatocellular carcinoma (HCC), particularly in Asian countries. The etiological link betweenHBV andHCCprovides an important opportunity for health care policy makers and clinicians to intervenewithHBVinfection to prevent cancer development and improve the outcomes of cancer. This review aims to use HBV as an example to illustrate the potential of tackling infection-related conditions to help improve cancer outcomes. This article is divided into four parts: In thefirst part, an overview is given on the epidemiologic data and risk factors of HCC development in patients with chronic hepatitis B. In the second part, recent progress on the anti-HBV strategies for preventing HCC is updated. In the third part, approaches to improve the outcomes of established HBV-related HCC are covered. Thesemethods include surveillance strategies to identify asymptomaticHCC among patientswith chronicHBV infection, and use of antiviral treatment to avoid HBV reactivation during treatment forHCC and reduce the recurrence of HCC after curative treatment. Finally, the status of the development of targeted drugs specifically for HBV-related HCC is discussed in the section on future development. © 2015 by American Society of Clinical Oncology.

Ma X.,Bayi Hospital | Cheng Y.,Bayi Hospital | Huang Y.,Bayi Hospital | Tian Y.,Nanjing University | And 2 more authors.
RSC Advances | Year: 2015

This paper developed small-sized PEGylated gold nanoprisms (GNPs) to induce photothermal therapy at low laser power density. Upon irradiation of the laser at low power density (2 W cm-2), these PEGylated GNPs showed ultrahigh photothermal conversion efficacy (η ≈ 70%) and produced enough heat to kill human breast cancer cells. © The Royal Society of Chemistry 2015.

Shi Y.,Nanjing University | Gao Y.,Nanjing University | Wang R.,Massey University | Zhang Y.,Bayi Hospital | Wang D.,Bayi Hospital
Applied Intelligence | Year: 2013

Previous computer-aided lung cancer image classification methods are all cost-blind, which assume that the misdiagnosis (categorizing a cancerous image as a normal one or categorizing a normal image as a cancerous one) costs are equal. In addition, previous methods usually require experienced pathologists to label a large amount of images as training samples. To this end, a novel transductive cost-sensitive method is proposed for lung cancer image classification on needle biopsies specimens, which only requires the pathologist to label a small amount of images. The proposed method analyzes lung cancer images in the following procedures: (i) an image capturing procedure to capture images from the needle biopsies specimens; (ii) a preprocessing procedure to segment the individual cells from the captured images; (iii) a feature extraction procedure to extract features (i.e. shape, color, texture and statistical information) from the obtained individual cells; (iv) a codebook learning procedure to learn a codebook on the extracted features by adopting k-means clustering, which aims to represent each image as a histogram over different codewords; (v) an image classification procedure to predict labels for testing images using the proposed multi-class cost-sensitive Laplacian regularized least squares (mCLRLS). We evaluate the proposed method on a real-image set provided by Bayi Hospital, which contains 271 images including normal ones and four types of cancerous ones (squamous carcinoma, adenocarcinoma, small cell cancer and nuclear atypia). The experimental results demonstrate that the proposed method achieves a lower cancer-misdiagnosis rate and lower total misdiagnosis costs comparing with previous methods, which includes the supervised learning approach (kNN, mcSVM and MCMI-AdaBoost), semi-supervised learning approach (LapRLS) and cost-sensitive approach (CS-SVM). Meanwhile, the experiments also disclose that both transductive and cost-sensitive settings are useful when only a small amount of training images are available. © 2012 Springer Science+Business Media, LLC.

Shi Y.,Nanjing University | Gao Y.,Nanjing University | Yang Y.,Nanjing University | Zhang Y.,Bayi Hospital | Wang D.,Bayi Hospital
IEEE Transactions on Biomedical Engineering | Year: 2013

Lung needle biopsy image classification is a critical task for computer-aided lung cancer diagnosis. In this study, a novel method, multimodal sparse representation-based classification (mSRC), is proposed for classifying lung needle biopsy images. In the data acquisition procedure of our method, the cell nuclei are automatically segmented from the images captured by needle biopsy specimens. Then, features of three modalities (shape, color, and texture) are extracted from the segmented cell nuclei. After this procedure, mSRC goes through a training phase and a testing phase. In the training phase, three discriminative subdictionaries corresponding to the shape, color, and texture information are jointly learned by a genetic algorithm guided multimodal dictionary learning approach. The dictionary learning aims to select the topmost discriminative samples and encourage large disagreement among different subdictionaries. In the testing phase, when a new image comes, a hierarchical fusion strategy is applied, which first predicts the labels of the cell nuclei by fusing three modalities, then predicts the label of the image by majority voting. Our method is evaluated on a real image set of 4372 cell nuclei regions segmented from 271 images. These cell nuclei regions can be divided into five classes: four cancerous classes (corresponding to four types of lung cancer) plus one normal class (no cancer). The results demonstrate that the multimodal information is important for lung needle biopsy image classification. Moreover, compared to several state-of-the-art methods (LapRLS, MCMI-AB, mcSVM, ESRC, KSRC), the proposed mSRC can achieve significant improvement (mean accuracy of 88.1\%$, precision of 85.2\%$, recall of 92.8\%$, etc.), especially for classifying different cancerous types. © 1964-2012 IEEE.

Qin S.,Bayi Hospital
Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2013

To determine whether FOLFOX4 (infusional fluorouracil, leucovorin, and oxaliplatin) administered as palliative chemotherapy to patients with advanced hepatocellular carcinoma (HCC) provides a survival benefit and efficacy versus doxorubicin. This multicenter, open-label, randomized, phase III study in mainland China, Taiwan, Korea, and Thailand involved 371 patients age 18 to 75 years who had locally advanced or metastatic HCC and were ineligible for curative resection or local treatment. They were randomly assigned at a ratio of one to one to receive either FOLFOX4 (n = 184) or doxorubicin (n = 187). The primary end point was overall survival (OS); secondary end points included progression-free survival (PFS), response rate (RR) by RECIST (version 1.0), and safety. At the prespecified final analysis, median OS was 6.40 months with FOLFOX4 (95% CI, 5.30 to 7.03) and 4.97 months with doxorubicin (95% CI, 4.23 to 6.03; P = .07; hazard ratio [HR], 0.80; 95% CI, 0.63 to 1.02). Median PFS was 2.93 months with FOLFOX4 (95% CI, 2.43 to 3.53), and 1.77 months with doxorubicin (95% CI, 1.63 to 2.30; P < .001; HR, 0.62; 95% CI, 0.49 to 0.79). RR was 8.15% with FOLFOX4 and 2.67% with doxorubicin (P = .02). On continued follow-up, the trend toward increased OS with FOLFOX4 was maintained (P = .04; HR, 0.79; 95% CI, 0.63 to 0.99). Toxicity was consistent with previous experiences with FOLFOX4; proportions of grade 3 to 4 adverse events were similar between treatments. Although the study did not meet its primary end point, the trend toward improved OS with FOLFOX4, along with increased PFS and RR, suggests that this regimen may confer some benefit to Asian patients, but an OS benefit cannot be concluded from these data.

PubMed | Bayi Hospital
Type: Journal Article | Journal: Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2016

e21014 Background: Endostar is a modified rh-endostatin expressed and purified in E.coli, an additional nine-amino acid sequence is added at the N-terminal of the protein, which improves the stability and activity of the protein. A series of studies have demonstrated that endostar strongly inhibits the growth of a variety of murine and xenotransplanted human tumors by suppressing the neovascularization. The present study was designed to investigate inhibitory effects of endostar in mice model.The mice models of tumor ascites with S180 and H22 cells by intraperitoneal inoculation were established. Model animals were randomly distributed into 4 groups with 12 mice respectively. 3 groups received different doses of endostar treatment: 4, 8, and 16 mg/kg, respectively. The control group received 0.9% normal saline.The mice were killed to collect the ascites. Then we analyzed the membrane permeability according to it.Apoptosis and cell cycle of tumor cells in the ascites fluid were detected by flow cytometry. The level of VEGF was determined by ELISA in blood serum and ascites fluid. Kaplan-Meier analysis was performed to determine animal survival time.Establishment of mice model bearing tumor ascites was successful with S180 cells and H22 cells by intraperitoneal inoculation. Doses of 8, 16 mg/kg endostar could suppress volume of ascites, and the number of tumor cells and red cells in the ascites fluid (P<0.05, respectively).The different doses of endostar (dose at 4, 8 and 16mg/kg) could profoundly depress peritoneum permeability (P<0.05, respectively). The 8, 16mg/kg endostar could reduce tumor burden of abdominal cavity, and down-regulate the level of VEGF in blood serum and ascites fluid (P<0.05, respectively). Endostar induced mild apoptosis and cell cycle on S180 and H22 cells (P>0.05, respectively). And survival time of 8, 16mg/kg endostar-treated mice was longer than that of control group mice.Results revealed for the first time that endostar could obviously suppress ascites formation, as well as prolonging survival time of test mice bearing S180 and H22 tumor ascites. Endostar is expected to be a novel therapeutic strategy and drug for treating advanced stage cancer with malignant ascites.

PubMed | Bayi Hospital
Type: Journal Article | Journal: Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2016

e21013 Background: Angiogenesis and vessel hyperpermeability are the two important factors leading to the formation of ascites. Many studies have demonstrated that Endostar strongly inhibits the growth of a variety of murine and xenotransplanted human tumors by suppressing the neovascularization. The study was designed to explore the mechanism of action correlated with tumor ascites in vivo and in vitro.In vivo, the mice models of tumor ascites with S180 and H22 cell lines were established. Model animals were randomly distributed into 4 groups with 12 mice respectively. 3 groups received different doses of endostar treatment.The control group received 0.9% normal saline. Four mice in each group were undertaken peritoneal capillar permeability experiments. The mice were slowly injected with 0.25 ml of 5 % Evan blue dye from vena caudalis. After 2 h, the mice were killed to collect ascites. The optical density of Evan blue was measured at 540 nm wavelength to indirectly reflect the concentration of Evan blue dye. In vitro, MTT assay was performed to evaluate the proliferation of S180 and H22 cells in the absence or presence of endostar. Tumor cells (110In vivo. Results showed that Endostar (dose at 8,16mg/kg) could markedly suppress ascites production and peritoneum permeability, and down-regulated the levels of VEGF, MMP-2 and CD44v6 in blood serum and ascites fluid (P<0.05, respectively). Endostar showed mild apoptosis and cell cycle on S180 and H22 cells (P>0.05). In vitro. Results from incubation of S180 cells and H22 cells with various concentrations of endostar suggested significant inhibition of VEGF, MMP-2 and CD44v6 by ELISA (P<0.05, respectively),and down-regulated the expressions of VEGFmRNA and OPNmRNA by Real-time PCR, and reduced the expressions of OPN, VThose results revealed for the first time that Endostar could profoundly suppress ascites formation through the expressions of VEGF, MMP2, CD44v6, OPN and V

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