Neutrophil Count and the Inflammation-based Glasgow Prognostic Score Predict Survival in Patients with Advanced Gastric Cancer Receiving First-line Chemotherapy

Li, Qing-Qing,Lu, Zhi-Hao,Yang, Li,Lu, Ming,Zhang, Xiao-Tian,Li, Jian,Zhou, Jun,Wang, Xi-Cheng,Gong, Ji-Fang,Gao, Jing,Li, Jie,Li, Yan,Shen, Lin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.2

Purpose: To explore the value of systemic inflammatory markers as independent prognostic factors and the extent these markers improve prognostic classification for patients with inoperable advanced or metastatic gastric cancer (GC) receiving palliative chemotherapy. Methods: We studied the prognostic value of systemic inflammatory factors such as circulating white blood cell count and its components as well as that combined to form inflammation-based prognostic scores (Glasgow Prognostic Score (GPS), Neutrophil-Lymphocyte Ratio (NLR), Platelet Lymphocyte Ratio (PLR), Prognostic Index (PI) and Prognostic Nutritional Index (PNI)) in 384 patients with inoperable advanced or metastatic gastric cancer (GC) receiving first-line chemotherapy. Univariate and multivariate analyses were performed to examine the impact of inflammatory markers on overall survival (OS). Results: Univariate analysis revealed that an elevated white blood cell, neutrophil and/or platelet count, a decreased lymphocyte count, a low serum albumin concentration, and high CRP concentration, as well as elevated NLR/PLR, GPS, PI, PNI were significant predictors of shorter OS. Multivariate analysis demonstrated that only elevated neutrophil count (HR 3.696, p=0.003) and higher GPS (HR 1.621, p=0.01) were independent predictors of poor OS. Conclusion: This study demonstrated elevated pretreatment neutrophil count and high GPS to be independent predictors of shorter OS in inoperable advanced or metastatic GC patients treated with first-line chemotherapy. Upon validation of these data in independent studies, stratification of patients using these markers in future clinical trials is recommended.

Protective Effect of Magnolol on TBHP-Induced Injury in H460 Cells Partially via a p53 Dependent Mechanism

Gao, Jian-Mei,Ying, Xi-Xiang,Wang, Shu-Peng,Li, Jian-Chun,Li, Hai-Bo 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.7

The aim is to investigate the effect of Magnolol preserved H460 cells from an oxidative agent tert-butylhydroperoxide (TBHP)-induced cell death. Magnolol augmented cell survival ratio after TBHP challenged. The protective action of this drug was more efficacious than that of N-acetylcysteine (NAC) which is a putative antioxidant. DNA damage, detected by the comet assay, was diminished after treatment of Magnolol. The cells viability decreased after treatment with 0.15 mM TBHP for 24 h, accompanied by inducing apoptotic death of the cells. Cytotoxicity and apoptosis induced by TBHP were significantly inhibited or attenuated after pretreatment with $20\;{\mu}M$ Magnolol. Magnolol contributes to the cells survival through downregulated the p53 phosphorylation and PTEN expression, and upregulated Akt phosphorylation. Taken together, Magnolol was effective against DNA single strand breaks (SSB) formation, cytotoxicity and lipid peroxidation induced by TBHP, and its effects on p53 phosphorlation, PTEN and Akt phosphorylation were due to its antioxidative function, and partially via a p53 dependent mechanism in this protective effects.

Magnolol-Induced H460 Cells Death via Autophagy but Not Apoptosis

Li, Hai-Bo,Yi, Xin,Gao, Jian-Mei,Ying, Xi-Xiang,Guan, Hong-Quan,Li, Jian-Chun 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.12

We have reported that the protective effect of Magnolol on TBHP-induced injury in human non-small lung cancer H460 cells is partially via a p53 dependent mechanism. In this study, we found that Magnolol displayed a stimulatory effect at low concentrations $(\leq20{\mu}M)$ whilst inhibitory effect at high concentrations $(\geq20{\mu}M)$ in H460 cells. To investigate the mechanism of inducing the biphasic effect in H460 cells with Magnolol, we showed that Magnolol stimulated DNA synthesis at low concentrations and displayed an inhibition effect at high concentrations in H460 cells. More importantly, the inhibition of DNA synthesis was accompanied by the S phase cell cycle arrest and the appearance of intense intracytoplasmic vacuoles. These vacuoles can be labeled by autophagic marker monodansylcadaverin (MDC), 3-methyladenine (3-MA), an inhibitor of autophagy, was able to inhibit the occurrence of autophagy. The results of the LDH activity assay and TUNEL assay also showed that Magnolol at high concentrations inhibiting H460 cell growth was not via apoptotic pathway. Furthermore, accompanied by the occurrence of autophagy, the expression of phospho-Akt was down-regulated but PTEN significantly was up-regulated. In conclusion, Magnolol induces H460 cells death by autophagy but not apoptotic pathway. Blockade of PI3K/PTEN/Akt pathway is maybe related to Magnolol-induced autophagy. Autophagic cells death induction by Magnolol underlines the potential utility of its induction as a new cancer treatment modality.

A new geopolymeric grout blended completely weathered granite with blast-furnace slag

Zhang, Jian,Li, Shucai,Li, Zhaofeng,Li, Hengtian,Du, Junqi,Gao, Yifan,Liu, Chao,Qi, Yanhai,Wang, Wenlong Techno-Press 2020 Advances in concrete construction Vol.9 No.6

In order to reduce the usage of cement slurry in grouting engineering and consume the tunnel excavation waste soil, a new geopolymeric grouting material (GGM) was prepared by combine completely weathered granite (CWG) and blast-furnace slag (BFS), which can be applied to in-situ grouting treatment of completely weathered granite strata. The results showed CWG could participate in the geopolymerization process, and GGM slurry has the characteristics of short setting time, high flowability, low viscosity, high stone rate and high mechanical strength, and a design method of grouting pressure based on viscosity evolution was proposed. By adjusted the content of completely weathered granite and alkali activator concentration, the setting time of GGM were ranged from 5 to 30 minutes, the flowability was more than 23.5 cm, the stone rate was higher than 90%, the compressive strength of 28 days were 7.8-16.9 MPa, the porosity were below 30%. This provides a novel grouting treatment and utilizing excavated soil of tunnels in the similar strata.

BCC-DPSO Algorithm for Task Scheduling on NOC

Wei Gao,Yubai Li,Song Chai,Jian Wang 보안공학연구지원센터 2014 International Journal of Grid and Distributed Comp Vol.7 No.5

In this paper, a BCC-DPSO scheduling algorithm is proposed to solve multi-objective optimization problem for task scheduling on Network-on-Chip (NoC). In our proposal, the relative advantage of the solution is evaluated by calculating its efficiency using BCC model in Data Envelopment Analysis (DEA), and the referred-time method is introduced to rank the BCC-efficient solution. Moreover, a sub-swarm strategy is adopted to reduce the high computational requirement introduced by the DEA. There are four sub-swarms, each of which optimizes one of four observed metrics, namely makespan, energy, link load and workload balance. Meanwhile, the speed vector updating formulation is modified to comply with the sub-swarm strategy. By conducting comparative simulations, the results show that our proposal produces more efficient schedule solution than other multi-objective Particle Swarm Optimization (PSO).

Magnolol-Induced H460 Cells Death via Autophagy but Not Apoptosis

Hai-bo Li,Xin Yi,Jian-mei Gao,Xi-xiang Ying,Hong-quan Guan,Jian-chun Li 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.12

We have reported that the protective effect of Magnolol on TBHP-induced injury in human nonsmall lung cancer H460 cells is partially via a p53 dependent mechanism. In this study, we found that Magnolol displayed a stimulatory effect at low concentrations (≤20 µM) whilst inhibitory effect at high concentrations (≥40 µM) in H460 cells. To investigate the mechanism of inducing the biphasic effect in H460 cells with Magnolol, we showed that Magnolol stimulated DNA synthesis at low concentrations and displayed an inhibition effect at high concentrations in H460 cells. More importantly, the inhibition of DNA synthesis was accompanied by the S phase cell cycle arrest and the appearance of intense intracytoplasmic vacuoles. These vacuoles can be labeled by autophagic marker monodansylcadaverin (MDC), 3-methyladenine (3- MA), an inhibitor of autophagy, was able to inhibit the occurrence of autophagy. The results of the LDH activity assay and TUNEL assay also showed that Magnolol at high concentrations inhibiting H460 cell growth was not via apoptotic pathway. Furthermore, accompanied by the occurrence of autophagy, the expression of phospho-Akt was down-regulated but PTEN significantly was up-regulated. In conclusion, Magnolol induces H460 cells death by autophagy but not apoptotic pathway. Blockade of PI3K/PTEN/Akt pathway is maybe related to Magnololinduced autophagy. Autophagic cells death induction by Magnolol underlines the potential utility of its induction as a new cancer treatment modality.

Protective Effect of Magnolol on TBHP-Induced Injury in H460 Cells Partially via a p53 Dependent Mechanism

Hai-bo Li,Jian-mei Gao,Xi-xiang Ying,Shu-Peng Wang,Jian-chun Li 대한약학회 2007 Archives of Pharmacal Research Vol.30 No.7

The aim is to investigate the effect of Magnolol preserved H460 cells from an oxidative agent tert-butylhydroperoxide (TBHP)-induced cell death. Magnolol augmented cell survival ratio after TBHP challenged. The protective action of this drug was more efficacious than that of Nacetylcysteine (NAC) which is a putative antioxidant. DNA damage, detected by the comet assay, was diminished after treatment of Magnolol. The cells viability decreased after treatment with 0.15 mM TBHP for 24 h, accompanied by inducing apoptotic death of the cells. Cytotoxicity and apoptosis induced by TBHP were significantly inhibited or attenuated after pretreatment with 20 µM Magnolol. Magnolol contributes to the cells survival through downregulated the p53 phosphorylation and PTEN expression, and upregulated Akt phosphorylation. Taken together, Magnolol was effective against DNA single strand breaks (SSB) formation, cytotoxicity and lipid peroxidation induced by TBHP, and its effects on p53 phosphorylation, PTEN and Akt phosphorylation were due to its antioxidative function, and partially via a p53 dependent mechanism in this protective effects.

Light-Chain Cardiac Amyloidosis: Cardiac Magnetic Resonance for Assessing Response to Chemotherapy

Guo Yubo,Li Xiao,Gao Yajuan,Shen Kaini,Lin Lu,Wang Jian,Cao Jian,Zhang Zhuoli,Wan Ke,Zhou Xi Yang,Chen Yucheng,Zhang Long Jiang,Li Jian,Wang Yining 대한영상의학회 2024 Korean Journal of Radiology Vol.25 No.5

Objective: Cardiac magnetic resonance (CMR) is a diagnostic tool that provides precise and reproducible information about cardiac structure, function, and tissue characterization, aiding in the monitoring of chemotherapy response in patients with lightchain cardiac amyloidosis (AL-CA). This study aimed to evaluate the feasibility of CMR in monitoring responses to chemotherapy in patients with AL-CA. Materials and Methods: In this prospective study, we enrolled 111 patients with AL-CA (50.5% male; median age, 54 [interquartile range, 49–63] years). Patients underwent longitudinal monitoring using biomarkers and CMR imaging. At followup after chemotherapy, patients were categorized into superior and inferior response groups based on their hematological and cardiac laboratory responses to chemotherapy. Changes in CMR findings across therapies and differences between response groups were analyzed. Results: Following chemotherapy (before vs. after), there were significant increases in myocardial T2 (43.6 ± 3.5 ms vs. 44.6 ± 4.1 ms; P = 0.008), recovery in right ventricular (RV) longitudinal strain (median of -9.6% vs. -11.7%; P = 0.031), and decrease in RV extracellular volume fraction (ECV) (median of 53.9% vs. 51.6%; P = 0.048). These changes were more pronounced in the superior-response group. Patients with superior cardiac laboratory response showed significantly greater reductions in RV ECV (-2.9% [interquartile range, -8.7%–1.1%] vs. 1.7% [-5.5%–7.1%]; P = 0.017) and left ventricular ECV (-2.0% [-6.0%–1.3%] vs. 2.0% [-3.0%–5.0%]; P = 0.01) compared with those with inferior response. Conclusion: Cardiac amyloid deposition can regress following chemotherapy in patients with AL-CA, particularly showing more prominent regression, possibly earlier, in the RV. CMR emerges as an effective tool for monitoring associated tissue characteristics and ventricular functional recovery in patients with AL-CA undergoing chemotherapy, thereby supporting its utility in treatment response assessment.

Weight Loss Correlates with Macrophage Inhibitory Cytokine-1 Expression and Might Influence Outcome in Patients with Advanced Esophageal Squamous Cell Carcinoma

Lu, Zhi-Hao,Yang, Li,Yu, Jing-Wei,Lu, Ming,Li, Jian,Zhou, Jun,Wang, Xi-Cheng,Gong, Ji-Fang,Gao, Jing,Zhang, Xiao-Tian,Li, Jie,Li, Yan,Shen, Lin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.15

Background: Weight loss during chemotherapy has not been exclusively investigated. Macrophage inhibitory cytokine-1 (MIC-1) might play a role in its etiology. Here, we investigated the prognostic value of weight loss before chemotherapy and its relationship with MIC-1 concentration and its occurrence during chemotherapy in patients with advanced esophageal squamous cell carcinoma (ESCC). Materials and Methods: We analyzed 157 inoperable locally advanced or metastatic ESCC patients receiving first-line chemotherapy. Serum MIC-1 concentrations were assessed before chemotherapy. Patients were assigned into two groups according to their weight loss before or during chemotherapy:>5% weight loss group and ${\leq}5%$ weight loss group. Results: Patients with weight loss>5% before chemotherapy had shorter progression-free survival period (5.8 months vs. 8.7 months; p=0.027) and overall survival (10.8 months vs. 20.0 months; p=0.010). Patients with weight loss >5% during chemotherapy tended to have shorter progression-free survival (6.0 months vs. 8.1 months; p=0.062) and overall survival (8.6 months vs. 18.0 months; p=0.022), and if weight loss was reversed during chemotherapy, survival rates improved. Furthermore, serum MIC-1 concentration was closely related to weight loss before chemotherapy (p=0.001) Conclusions: Weight loss both before and during chemotherapy predicted poor outcome in advanced ESCC patients, and MIC-1 might be involved in the development of weight loss in such patients.

Permanent magnet temperature estimation of high power density permanent magnet synchronous machines by considering magnetic saturation

Jian Gao,Chengxu Li,Wenjuan Zhang,Shoudao Huang 전력전자학회 2021 JOURNAL OF POWER ELECTRONICS Vol.21 No.12

This paper develops a method for permanent magnet (PM) temperature estimation in high power density permanent magnet synchronous machines (PMSMs) by considering magnetic saturation. Most of the previous methods in the literature are based on unsaturation. In this paper, the temperature estimation method of PMs is improved by adding a saturation coefficient. Once a machine is assembled, the inner and outer PM surfaces cannot be seen. Thus, it is impossible to realize visualization measurement of the permanent magnet temperature distribution. In this case, temperature sensors attached to the PM cam be used. However, the cost and robustness need to be considered. Therefore, in this paper, by solving a magnetic–thermal coupling finite element model, the temperature field distribution of a high power density PMSM is obtained. Then, an experimental platform is built to verify the model. Finally, the model is used to verify the reliability of the modified estimation method.