Intravenous Flurbiprofen Axetil Enhances Analgesic Effect of Opioids in Patients with Refractory Cancer Pain by Increasing Plasma β-Endorphin

Wu, Ting-Ting,Wang, Zhi-Gang,Ou, Wu-Ling,Wang, Jun,Yao, Guo-Qing,Yang, Bo,Rao, Zhi-Guo,Gao, Jian-Fei,Zhang, Bi-Cheng Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.24

Background: The study aimed to investigate the analgesic effect of a combination of intravenous flurbiprofen axetil and opioids, and evaluate the relationship between refractory pain relief and plasma ${\beta}$-endorphin levels in cancer patients. Materials and Methods: A total of 120 cancer patients was randomly divided into two groups, 60 patients took orally morphine sulfate sustained-release tablets in group A, and another 60 patients receiving the combination treatment of intravenous flurbiprofen axetil and opioid drugs in group B. After 7 days, pain relief, quality of life improvement and side effects were evaluated. Furthermore, plasma ${\beta}$-endorphin levels were measured by radioimmunoassay. Results: With the combination treatment of intravenous intravenous flurbiprofen axetil and opioids, the total effective rate of pain relief rose to 91.4%, as compared to 82.1% when morphine sulfate sustained-release tablet was used alone. Compared with that of group A, the analgesic effect increased in group B (p=0.031). Moreover, satisfactory pain relief was associated with a significant increase in plasma ${\beta}$-endorphin levels. After the treatment, plasma ${\beta}$-endorphin level in group B was $62.4{\pm}13.5pg/ml$, which was higher than that in group A ($45.8{\pm}11.2pg/ml$) (p<0.05). Conclusions: Our results suggest the combination of intravenous flurbiprofen axetil and opioids can enhance the analgesic effect of opioid drugs by increasing plasma ${\beta}$-endorphin levels, which would offer a selected and reliable strategy for refractory cancer pain treatment.

Imbalanced Data Classification Based on AdaBoost-SVM

Li Peng,Bi Ting-ting,Yu Xiao-yang,Li Si-ben 보안공학연구지원센터 2014 International Journal of Database Theory and Appli Vol.7 No.5

The classification of imbalanced data is one of the most challenging problems in data mining and machine learning research. Imbalanced dataset is a form that exists in reality area, which describes truly and objectively the essential characters of something. There will appear paucity of data and flooded in the classification of imbalanced dataset. Beside problems such as loss of information and data splitting phenomenon will also appear when using the traditional machine learning methods. So how to solve the classification problem of imbalanced data will be challenging. In this paper, aiming at the above problems, a classification algorithm based on AdaBoost-SVM is proposed. In the experiments with four typical forms of imbalanced data sets in UCI were validated the effectiveness of this strategy.

SVM Classification for High-dimensional Imbalanced Data based on SNR and Under-sampling

Li Peng,Bi Ting-ting,Liu Yang 보안공학연구지원센터 2015 International Journal of Multimedia and Ubiquitous Vol.10 No.4

Support vector machine (SVM) is biased towards the majority class, in some case dataset is class-imbalanced and the bias is even larger for high-dimensional. In order to improve the classification accuracy of SVM on high-dimensional imbalanced data, we combine signal-noise ratio (SNR) and under-sampling technique based on K-means. In this article firstly we apply SNR into feature selection to reducing the feature amount then solve the problem of data imbalance using under-sampling technique based on K-means. To verify the feasibility of the proposed strategy, we utilize some metrics such as receiver operating characteristic curve (ROC curve) and area under the receiver operating characteristic curve (AUC value).As a result, the AUC value increased by 4%~16% before and after the process. The experimental results show that our strategy is feasible and effective exactly.

IL-12 Regulates B7-H1 Expression in Ovarian Cancer-associated Macrophages by Effects on NF-κB Signalling

Xiong, Hai-Yu,Ma, Ting-Ting,Wu, Bi-Tao,Lin, Yan,Tu, Zhi-Guang Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.14

Background and Aim: B7-H1, a co-inhibitory molecule of the B7 family, is found aberrantly expressed in ovarian cancer cells and infiltrating macrophage/dendritic-like cells, and plays a critical role in immune evasion by ovarian cancer. IL-12, an inducer of Th1 cell development, exerts immunomodulatory effects on ovarian cancer. However, whether IL-12 regulates B7-H1 expression in human ovarian cancer associated-macrophages has not been clarified. Therefore, we investigated the effects of IL-12 on the expression of B7-H1 in ovarian cancer-associated macrophages and possible mechanisms. Methods: PMA induced THP-1-derived macrophages or human monocyte-derived macrophages were treated with recombinant IL-12 (rIL-12) or infected with adenovirus carrying human IL-12 gene (Ad-IL-12-GFP) for 24 h, then cocultured with the SKOV3 ovarian cancer cell line for another 24 h. Macrophages were collected for real-time PCR and Western blot to detect the expression of B7-H1, and activation of the NF-${\kappa}B$ signaling pathway. Moreover, supernatants were collected to assay for IL-12, IFN-${\gamma}$ and IL-10 by ELISA. In addition, monocyte-derived macrophages treated with IFN-${\gamma}$ were cocultured with SKOV3 and determined for the expression of B7-H1. Furthermore, the expression of B7-H1 in monocyte-derived macrophages was also evaluated after blocking NF-${\kappa}B$ signaling. Results: The expression of B7-H1 was significantly upregulated in monocyte-derived macrophages treated with rIL-12 or Ad-IL-12-GFP compared with the control groups (p<0.05), accompanied by a remarkable upregulation of IFN-${\gamma}$ (p<0.05), a marked downregulation of IL-10 (p<0.05) and activation of NF-${\kappa}B$ signaling. However, the upregulation of B7-H1 was inhibited by blocking the NF-${\kappa}B$ signaling pathway (p<0.05). Expression of B7-H1 was also increased (p<0.05) in monocyte-derived macrophages treated with IFN-${\gamma}$ and cocultured with SKOV3. By contrast, the expression of B7-H1 in THP-1-derived macrophages was significantly decreased when treated in the same way as monocyte-derived macrophages (p<0.05), and IL-10 was also significantly decreased but IFN-${\gamma}$ was almost absent. Conclusions: IL-12 upregulates the expression of B7-H1 in monocyte-derived macrophages, which is possible though inducing the secretion of IFN-${\gamma}$ and further activating the NF-${\kappa}B$ signal pathway. However, IL-12 downregulates the expression of B7-H1 in THP-1-derived macrophages, associated with a lack of IFN-${\gamma}$ and inhibition of expression of IL-10.

Genomic Analysis of the Xanthoria elegans and Polyketide Synthase Gene Mining Based on the Whole Genome

Xiaolong Yuan,Yunqing L,Ting Luo,Wei Bi,Jiaojun Yu,Yi Wang 한국균학회 2023 Mycobiology Vol.51 No.1

Xanthoria elegans is a lichen symbiosis, that inhabits extreme environments and can absorb UV-B. We reported the de novo sequencing and assembly of X. elegans genome. The whole genome was approximately 44.63 Mb, with a GC content of 40.69%. Genome assembly gen- erated 207 scaffolds with an N50 length of 563,100 bp, N90 length of 122,672 bp. The gen- ome comprised 9,581 genes, some encoded enzymes involved in the secondary metabolism such as terpene, polyketides. To further understand the UV-B absorbing and adaptability to extreme environments mechanisms of X. elegans, we searched the secondary metabolites genes and gene-cluster from the genome using genome-mining and bioinformatics analysis. The results revealed that 7 NR-PKSs, 12 HR-PKSs and 2 hybrid PKS-PKSs from X. elegans were isolated, they belong to Type I PKS (T1PKS) according to the domain architecture; phylogen- etic analysis and BGCs comparison linked the putative products to two NR-PKSs and three HR-PKSs, the putative products of two NR-PKSs were emodin xanthrone (most likely parietin) and mycophelonic acid, the putative products of three HR-PKSs were soppilines, (þ)-asperlin and macrolactone brefeldin A, respectively. 5 PKSs from X. elegans build a correlation between the SMs carbon skeleton and PKS genes based on the domain architecture, phylo- genetic and BGC comparison. Although the function of 16 PKSs remains unclear, the findings emphasize that the genes from X. elegans represent an unexploited source of novel polyke- tide and utilization of lichen gene resources.

Protein Tyrosine Phosphatase 1B Inhibition and Glucose Uptake Potentials of Mulberrofuran G, Albanol B, and Kuwanon G from Root Bark of <i>Morus alba</i> L. in Insulin-Resistant HepG2 Cells: An In Vitro and In Silico Study

Paudel, Pradeep,Yu, Ting,Seong, Su Hui,Kuk, Eun Bi,Jung, Hyun Ah,Choi, Jae Sue MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.5

<P>Type II diabetes mellitus (T2DM) is the most common form of diabetes and has become a major health problem across the world. The root bark of <I>Morus alba</I> L. is widely used in Traditional Chinese Medicine for treatment and management of diabetes. The aim of the present study was to evaluate the enzyme inhibitory potentials of three principle components, mulberrofuran G (<B>1</B>), albanol B (<B>2</B>), and kuwanon G (<B>3</B>) in <I>M. alba</I> root bark against diabetes, establish their enzyme kinetics, carry out a molecular docking simulation, and demonstrate the glucose uptake activity in insulin-resistant HepG2 cells. Compounds <B>1</B>–<B>3</B> showed potent mixed-type enzyme inhibition against protein tyrosine phosphatase 1B (PTP1B) and α-glucosidase. In particular, molecular docking simulations of <B>1</B>–<B>3</B> demonstrated negative binding energies in both enzymes. Moreover, <B>1</B>–<B>3</B> were non-toxic up to 5 µM concentration in HepG2 cells and enhanced glucose uptake significantly and decreased PTP1B expression in a dose-dependent manner in insulin-resistant HepG2 cells. Our overall results depict <B>1</B>–<B>3</B> from <I>M. alba</I> root bark as dual inhibitors of PTP1B and α-glucosidase enzymes, as well as insulin sensitizers. These active constituents in <I>M. alba</I> may potentially be utilized as an effective treatment for T2DM.</P>

Imbalanced Data SVM Classification Method Based on Cluster Boundary Sampling and DT-KNN Pruning

Li Peng,Yu Xiao-yang,Bi Ting-ting,Huang Jiu-ling 보안공학연구지원센터(IJSIP) 2014 International Journal of Signal Processing, Image Vol.7 No.2

The role of ginsenoside Rb1, a potential natural glutathione reductase agonist, in preventing oxidative stress-induced apoptosis of H9C2 cells

Hui-Jie Fan,Zhang-Bin Tan,Yu-Ting Wu,Xiao-Reng Feng,Yi-Ming Bi,Ling-Peng Xie,Wen-Tong Zhang,Zhi Ming,Bin Liu,Ying-Chun Zhou 고려인삼학회 2020 Journal of Ginseng Research Vol.44 No.2

Background: Oxidative stress-induced cardiomyocytes apoptosis is a key pathological process inischemic heart disease. Glutathione reductase (GR) reduces glutathione disulfide to glutathione (GSH) toalleviate oxidative stress. Ginsenoside Rb1 (GRb1) prevents the apoptosis of cardiomyocytes; however,the role of GR in this process is unclear. Therefore, the effects of GRb1 on GR were investigated in thisstudy. Methods: The antiapoptotic effects of GRb1 were evaluated in H9C2 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, annexin V/propidium iodide staining, and Western blotting. Theantioxidative effects were measured by a reactive oxygen species assay, and GSH levels and GR activitywere examined in the presence and absence of the GR inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea. Molecular docking and molecular dynamics simulations were used to investigate the binding of GRb1 toGR. The direct influence of GRb1 on GR was confirmed by recombinant human GR protein. Results: GRb1 pretreatment caused dose-dependent inhibition of tert-butyl hydroperoxide-induced cellapoptosis, at a level comparable to that of the positive control N-acetyl-L-cysteine. The binding energybetween GRb1 and GR was positive ( 6.426 kcal/mol), and the binding was stable. GRb1 significantlyreduced reactive oxygen species production and increased GSH level and GR activity without altering GRprotein expression in H9C2 cells. Moreover, GRb1 enhanced the recombinant human GR protein activityin vitro, with a half-maximal effective concentration of z2.317 mM. Conversely, 1,3-bis-(2-chloroethyl)-1-nitrosourea co-treatment significantly abolished the GRb1’s apoptotic and antioxidative effects of GRb1in H9C2 cells. Conclusion: GRb1 is a potential natural GR agonist that protects against oxidative stresseinducedapoptosis of H9C2 cells.

Naringin and Naringenin Relax Rat Tracheal Smooth by Regulating BKCa Activation

Rui Shi,Jia-Wen Xu,Zi-Ting Xiao,Ruo-Fei Chen,Yi-Lin Zhang,Jia-Bi Lin,Ke-Ling Cheng,Gu-Yi Wei,Pei-Bo Li,Wen-Liang Zhou,Wei-Wei Su 한국식품영양과학회 2019 Journal of medicinal food Vol.22 No.9

Naringin and its aglycone, naringenin, occur naturally in our regular diet and traditional Chinese medicines. This study aimed to detect an effective therapeutic approach for cough variant asthma (CVA) through evaluating the relaxant effect of these two bioactive herbal monomers as antitussive and antiasthmatic on rat tracheal smooth muscle. The relaxant effect was determined by measuring muscular tension with a mechanical recording system in rat tracheal rings. Cytosolic Ca2+ concentration was measured using a confocal imaging system in primary cultured tracheal smooth muscle cells. In rat tracheal rings, addition of both naringin and naringenin could concentration dependently relax carbachol (CCh)-evoked tonic contraction. This epithelium-independent relaxation could be suppressed by BaCl2, tetraethylammonium, and iberiotoxin (IbTX), but not by glibenclamide. After stimulating primary cultured tracheal smooth muscle cells by CCh or high KCl, the intracellular Ca2+ increase could be inhibited by both naringin and naringenin, respectively. This reaction was also suppressed by IbTX. These results demonstrate that both naringin and naringenin can relax tracheal smooth muscle through opening big conductance Ca2+-activated K+ channel, which mediates plasma membrane hyperpolarization and reduces Ca2+ influx. Our data indicate a potentially effective therapeutic approach of naringin and naringenin for CVA.

The role of ginsenoside Rb1, a potential natural glutathione reductase agonist, in preventing oxidative stress-induced apoptosis of H9C2 cells

Fan, Hui-Jie,Tan, Zhang-Bin,Wu, Yu-Ting,Feng, Xiao-Reng,Bi, Yi-Ming,Xie, Ling-Peng,Zhang, Wen-Tong,Ming, Zhi,Liu, Bin,Zhou, Ying-Chun The Korean Society of Ginseng 2020 Journal of Ginseng Research Vol.44 No.2

Background: Oxidative stress-induced cardiomyocytes apoptosis is a key pathological process in ischemic heart disease. Glutathione reductase (GR) reduces glutathione disulfide to glutathione (GSH) to alleviate oxidative stress. Ginsenoside Rb1 (GRb1) prevents the apoptosis of cardiomyocytes; however, the role of GR in this process is unclear. Therefore, the effects of GRb1 on GR were investigated in this study. Methods: The antiapoptotic effects of GRb1 were evaluated in H9C2 cells by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, annexin V/propidium iodide staining, and Western blotting. The antioxidative effects were measured by a reactive oxygen species assay, and GSH levels and GR activity were examined in the presence and absence of the GR inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea. Molecular docking and molecular dynamics simulations were used to investigate the binding of GRb1 to GR. The direct influence of GRb1 on GR was confirmed by recombinant human GR protein. Results: GRb1 pretreatment caused dose-dependent inhibition of tert-butyl hydroperoxide-induced cell apoptosis, at a level comparable to that of the positive control N-acetyl-L-cysteine. The binding energy between GRb1 and GR was positive (-6.426 kcal/mol), and the binding was stable. GRb1 significantl reduced reactive oxygen species production and increased GSH level and GR activity without altering GR protein expression in H9C2 cells. Moreover, GRb1 enhanced the recombinant human GR protein activity in vitro, with a half-maximal effective concentration of ≈2.317 μM. Conversely, 1,3-bis-(2-chloroethyl)-1-nitrosourea co-treatment significantly abolished the GRb1's apoptotic and antioxidative effects of GRb1 in H9C2 cells. Conclusion: GRb1 is a potential natural GR agonist that protects against oxidative stress-induced apoptosis of H9C2 cells.