Evolution of the effect of sulfur confinement in graphene-based porous carbons for use in Li-S batteries

Jia, Xiangling,Zhang, Chen,Liu, Juanjuan,Lv, Wei,Wang, Da-Wei,Tao, Ying,Li, Zhengjie,Zheng, Xiaoyu,Yu, Jong-Sung,Yang, Quan-Hong The Royal Society of Chemistry 2016 Nanoscale Vol.8 No.8

<P>A controllable drying strategy is proposed for the precise and non-destructive control over the structure of a 3D graphene assembly. Such an assembly is used as a model carbon material to investigate the pore structure-dependent shuttle effect and cycling performance of the cathode of a Li-S battery.</P>

NEDD8-activating enzyme inhibitor, MLN4924 (Pevonedistat) induces NOXA-dependent apoptosis through up-regulation of ATF-4

Liu, Xiaojun,Jiang, Yanan,Wu, Jianfu,Zhang, Wenjuan,Liang, Yupei,Jia, Lijun,Yu, Jinha,Jeong, L.S.,Li, Lihui Elsevier 2017 Biochemical and biophysical research communication Vol. No.

<P><B>Abstract</B></P> <P>It has been reported that MLN4924 can inhibit cell growth and metastasis in various kinds of cancer. We have reported that MLN4924 is able to inhibit angiogenesis through the induction of cell apoptosis both in vitro and in vivo models. Moreover, Neddylation inhibition using MLN4924 triggered the accumulation of pro-apoptotic protein NOXA in Human umbilical vein endothelial cells (HUVECs). However, the mechanism of MLN4924-induced NOXA up-regulation has not been addressed in HUVECs yet. In this study, we investigated how MLN4924 induced NOXA expression and cellular apoptosis in HUVECs treated with MLN4924 at indicated concentrations. MLN4924-induced apoptosis was evaluated by Annexin V-FITC/PI analysis and expression of genes associated with apoptosis was assessed by Quantitative RT-PCR and western blotting. As a result, MLN4924 triggered NOXA-dependent apoptosis in a dose-dependent manner in HUVECs. Mechanistically, inactivation of Neddylation pathway caused up-regulation of activating transcription factor 4 (ATF-4), a substrate of Cullin-Ring E3 ubiquitin ligases (CRL). NOXA was subsequently transactivated by ATF-4 and further induced apoptosis. More importantly, knockdown of ATF-4 by siRNA significantly decreased NOXA expression and apoptotic induction in HUVECs. In summary, our study reveals a new mechanism underlying MLN4924-induced NOXA accumulation in HUVECs, which may help extend further study of MLN4924 for angiogenesis inhibition treatment.</P> <P><B>Highlights</B></P> <P> <UL> <LI> MLN4924 triggered NOXA-dependent apoptosis in a dose-dependent manner in HUVECs. </LI> <LI> Inactivation of neddylation caused up-regulation of ATF4, a substrate of CRL. </LI> <LI> NOXA was transactivated by ATF4 and further induced apoptosis. </LI> <LI> Knockdown of ATF-4 significantly decreased NOXA expression and apoptotic induction. </LI> <LI> We revealed a new mechanism underlying MLN4924-induced NOXA accumulation in HUVECs. </LI> </UL> </P>

Investigations on the Influence of Pedestrians on the Buffeting of a Long-Span Suspension Footbridge

Yu Li,Jia-Xin Xiao,Chen Li,Jia-Wu Li 한국강구조학회 2023 International Journal of Steel Structures Vol.23 No.3

According to a suspension footbridge, the pedestrian-bridge section models with different pedestrian densities (μ) were proposed. The wind tunnel tests were performed to study the influence of pedestrians on aerostatic force coefficients and flutter derivatives, and it is found that: with the increase of μ, the drag force coefficient increases, and the lift force coefficient decreases, while the effect of μ on the pitching moment coefficient can be ignored; moreover, there is a significant influence of μ on the flutter derivatives. Then, the static wind forces, buffeting forces, and self-excited forces considering the influence of pedestrians were calculated by using the measured aerostatic force coefficients, the measured flutter derivatives, and the simulated fluctuating wind field. By applying these forces to the finite element model of the suspension footbridge, a buffeting analysis was conducted by using the ANSYS Parametric Design Language, and it is found that: with the increase of pedestrians on the long-span suspension footbridge, the buffeting increases, while the effect of wind attack angles (θ) on the buffeting decreases; Especially, when μ > 1.0 P/m2, the effect of θ on the buffeting can be ignored.

Liposomal honokiol, a potent anti-angiogenesis agent, in combination with radiotherapy produces a synergistic antitumor efficacy without increasing toxicity

Jia Hu,Li Liu,Xiang Chen,Ping Chen,Guang-li Yang,Wen-li Hou,Ming-hai Tang,Fan Zhang,Xian-huo Wang,Xia Zhao,Yu-quan Wei,Li-juan Chen 생화학분자생물학회 2008 Experimental and molecular medicine Vol.40 No.6

Honokiol is an active compound purified from magnolia that has been shown to induce cell differentiation, apoptosis, and anti-angiogenesis effects, as well as an enhancement in tumor growth delay in combination with chemotherapeutic agents in several mouse xenograft models. Our goal was to investigate the radiosensitization effect of honokiol on lung carcinoma. The radiosensitization effect of liposomal honokiol in Lewis lung carcinoma cells (LL/2) was analyzed using an in vitro clonogenic survival assay. For an in vivo study, Lewis lung carcinoma-bearing C57BL/6 mice were treated with either liposomal honokiol at 25 mg/kg or 5 Gy of single tumor radiation, or a combination of both over 12 days of treatment. The tumor growth delay and the survival time were evaluated. In addition, histological analysis of tumor sections was performed to examine changes by detecting the microvessel density and apoptosis in tumor tissues. In the clonogenic survival assay, LL/2 cells treated with IC50 Lipo-HNK for 24 h showed a radiation enhancement ratio of 1.9. After 12 days of combination treatment, the tumor volume decreased 78% and produced an anti-tumor activity 1.3-fold greater than a predicted additive effect of honokiol and radiation alone. This combination treatment also caused an 8.7 day delay in tumor growth. The cell cycle distribution and histological analysis demonstrated that liposomal honokiol has an anti-tumor effect via inducing apoptosis and inhibiting angiogenesis. Liposomal honokiol can enhance tumor cell radiosensitivity in vitro and in vivo, indicating that radiotherapy combined with liposomal honokiol can lead to greater anti-tumor efficacy. Honokiol is an active compound purified from magnolia that has been shown to induce cell differentiation, apoptosis, and anti-angiogenesis effects, as well as an enhancement in tumor growth delay in combination with chemotherapeutic agents in several mouse xenograft models. Our goal was to investigate the radiosensitization effect of honokiol on lung carcinoma. The radiosensitization effect of liposomal honokiol in Lewis lung carcinoma cells (LL/2) was analyzed using an in vitro clonogenic survival assay. For an in vivo study, Lewis lung carcinoma-bearing C57BL/6 mice were treated with either liposomal honokiol at 25 mg/kg or 5 Gy of single tumor radiation, or a combination of both over 12 days of treatment. The tumor growth delay and the survival time were evaluated. In addition, histological analysis of tumor sections was performed to examine changes by detecting the microvessel density and apoptosis in tumor tissues. In the clonogenic survival assay, LL/2 cells treated with IC50 Lipo-HNK for 24 h showed a radiation enhancement ratio of 1.9. After 12 days of combination treatment, the tumor volume decreased 78% and produced an anti-tumor activity 1.3-fold greater than a predicted additive effect of honokiol and radiation alone. This combination treatment also caused an 8.7 day delay in tumor growth. The cell cycle distribution and histological analysis demonstrated that liposomal honokiol has an anti-tumor effect via inducing apoptosis and inhibiting angiogenesis. Liposomal honokiol can enhance tumor cell radiosensitivity in vitro and in vivo, indicating that radiotherapy combined with liposomal honokiol can lead to greater anti-tumor efficacy.

Study on the mechanism of the vortex-induced vibration of a bluff double-side box section

Yu Li,Chen Li,Feng Wang,Jia-Wu Li 국제구조공학회 2021 Steel and Composite Structures, An International J Vol.41 No.2

At present, researchers mainly focused on the vortex-induced vibration (VIV) of the double-side I-shaped girder, while there are only a few literatures focused on the VIV of the bluff double-side box girder, especially the study on the synchronous pressure- and vibration- measured test for the bluff double-side box girder has not been reported. Therefore, in this study, the vibration-measured test, the Numerical Wind Tunnel Simulation, and the synchronous pressure- and vibration- measured test were conducted to study the VIV mechanism of the bluff double-side box girder. Firstly, a section model of the bluff double-side box girder was designed, and the vibration-measured test was conducted to study the influence of mass ratio, damping ratio, and aerodynamic countermeasures on the VIV of the bluff double-side box girder. Secondly, the Numerical Wind Tunnel Simulation was conducted to simulate the vorticity evolution of the bluff double-side box girder, which was used to help analyze the results of the synchronous pressure- and vibration- measured test. Finally, the synchronous pressure- and vibration- measured test was conducted to investigate the wind pressure distribution and aerodynamic forces on the surface of the double-side box girder, which was then used to study the VIV mechanism of the bluff double-side box girder by combining the simulated vorticity evolutions. So, when the VIV of the double-side box girder occurs, it is found that: there is a significant difference in the mean and fluctuating wind pressure between the upper and lower surfaces; moreover, at the leading and trailing edges, the aerodynamic forces contribute greatly to the VIV, the correlation between the aerodynamic forces and the vortex-induced aerodynamic forces is positive, and with the increase of this coefficient, it will lead to the more significant VIV.

A (n, t, n) Verifiable Multi-secret Sharing Scheme with Secure Secret Reconstruction

Li Meng,Qu Shaoyun,Xun Tiantian,Yu Jia 보안공학연구지원센터 2015 International Journal of Security and Its Applicat Vol.9 No.1

Study on the Effects of Pedestrians on the Aerostatic Response of a Long-Span Pedestrian Suspension Bridge

Yu Li,Zhe Chen,Shi-Jie Dong,Jia-Wu Li 대한토목학회 2021 KSCE Journal of Civil Engineering Vol.25 No.10

According to a long-span pedestrian suspension bridge, the sectional models of the human-footbridge system were proposed, and then the force measurement tests were performed to study the effects of the pedestrian density (ρ), pedestrian permutation, and wind attack angle (α) on the drag force coefficient (CH), lift force coefficient (CV), and pitching moment coefficient (CM), respectively. So, it is found that: (1) with the increase of ρ, both CH and CV with α < -2o increase, while both CV with α ≥ -2o and CM with ρ ≠ 0.0 P/m2 decrease. (2) when ρ> 0.2 P/m2, there is a significant effect of the pedestrian permutations on CH and CM, while the effect of the pedestrian permutations on CV is small. Then, the static wind forces were calculated and applied to the pedestrian suspension bridge, and the effects of ρ and pedestrian permutations on the aerostatic response were studied. So, it is found that: 1) with the increase of ρ, the aerostatic response increases; 2) the effects of the pedestrian permutations with ρ ≤ 0.5 P/m2 on the aerostatic response can be ignored, while there are disadvantageous effects of the pedestrian permutations with ρ > 0.5 P/m2 and larger wind-blocking area on the aerostatic response.

Staged Improvement in Awareness of Disease for Elderly Cancer Patients in Southern China

Li, Xing,Dong, Min,Wen, Jing-Yun,Wei, Li,Ma, Xiao-Kun,Xing, Yan-Fang,Deng, Yun,Chen, Zhan-Hong,Chen, Jie,Ruan, Dan-Yun,Lin, Ze-Xiao,Wang, Tian-Tian,Wu, Dong-Hao,Liu, Xu,Hu, Hai-Tao,Lin, Jia-Yu,Li, Zhu Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15

Background: In mainland China, awareness of disease of elderly cancer patients largely relies on the patients' families. We developed a staged procedure to improve their awareness of disease. Materials and Methods: Participants were 224 elderly cancer patients from 9 leading hospitals across Southern China. A questionnaire was given to the oncologists in charge of each patient to evaluate the interaction between family and patients, patient awareness of their disease and participation in medical decision-making. After first cycles of treatment, increased information of disease was given to patients with cooperation of the family. Then patient awareness of their disease and participation in medical decision-making was documented. Results: Among the 224 cancer elderly patients, 26 (11.6%) made decisions by themselves and 125 (55.8%) delegated their rights of decision-making to their family. Subordinate family members tended to play a passive role in decision-making significantly. Patients participating more in medical decision-making tended to know more about their disease. However, in contrast to the awareness of disease, patient awareness of violation of medical recommendations was reversely associated with their participation in medical decision-making. Improvement in awareness of diagnosis, stages and prognosis was achieved in about 20% elderly cancer patients. About 5% participated more actively in medical decision-making. Conclusions: Chinese elderly cancer patient awareness of disease and participation in medical decision-making is limited and relies on their family status. The staged procedure we developed to improve patient awareness of disease proved effective.

Tumor-Derived Transforming Growth Factor-β is Critical for Tumor Progression and Evasion from Immune Surveillance

Li, Zheng,Zhang, Li-Juan,Zhang, Hong-Ru,Tian, Gao-Fei,Tian, Jun,Mao, Xiao-Li,Jia, Zheng-Hu,Meng, Zi-Yu,Zhao, Li-Qing,Yin, Zhi-Nan,Wu, Zhen-Zhou Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.13

Tumors have evolved numerous mechanisms by which they can escape from immune surveillance. One of these is to produce immunosuppressive cytokines. Transforming growth factor-${\beta}$(TGF-${\beta}$) is a pleiotropic cytokine with a crucial function in mediating immune suppression, especially in the tumor microenvironment. TGF-${\beta}$ produced by T cells has been demonstrated as an important factor for suppressing antitumor immune responses, but the role of tumor-derived TGF-${\beta}$ in this process is poorly understood. In this study, we demonstrated that knockdown of tumor-derived TGF-${\beta}$ using shRNA resulted in dramatically reduced tumor size, slowing tumor formation, prolonging survival rate of tumor-bearing mice and inhibiting metastasis. We revealed possible underlying mechanisms as reducing the number of myeloid-derived suppressor cells (MDSC) and $CD4^+Foxp3^+$ Treg cells, and consequently enhanced IFN-${\gamma}$ production by CTLs. Knockdown of tumor-derived TGF-${\beta}$ also significantly reduced the conversion of na$\ddot{i}$ve $CD4^+$ T cells into Treg cells in vitro. Finally, we found that knockdown of TGF-${\beta}$ suppressed cell migration, but did not change the proliferation and apoptosis of tumor cells in vitro. In summary, our study provided evidence that tumor-derived TGF-${\beta}$ is a critical factor for tumor progression and evasion of immune surveillance, and blocking tumor-derived TGF-${\beta}$ may serve as a potential therapeutic approach for cancer.

JCAD deficiency attenuates activation of hepatic stellate cells and cholestatic fibrosis

Li Xie,Hui Chen,Li Zhang,Yue Ma,Yuan Zhou,Yong-Yu Yang,Chang Liu,Yu-Li Wang,Ya-Jun Yan,Jia Ding,Xiao Teng,Qiang Yang,Xiu-Ping Liu,Jian Wu 대한간학회 2024 Clinical and Molecular Hepatology(대한간학회지) Vol.30 No.2

Background/Aims: Cholestatic liver diseases including primary biliary cholangitis (PBC) are associated with active hepatic fibrogenesis, which ultimately progresses to cirrhosis. Activated hepatic stellate cells (HSCs) are the main fibrogenic effectors in response to cholangiocyte damage. JCAD regulates cell proliferation and malignant transformation in nonalcoholic steatoheaptitis-associated hepatocellular carcinoma (NASH-HCC). However, its participation in cholestatic fibrosis has not been explored yet. Methods: Serial sections of liver tissue of PBC patients were stained with immunofluorescence. Hepatic fibrosis was induced by bile duct ligation (BDL) in wild-type (WT), global JCAD knockout mice (JCAD-KO) and HSC-specific JCAD knockout mice (HSC-JCAD-KO), and evaluated by histopathology and biochemical tests. In situ-activated HSCs isolated from BDL mice were used to determine effects of JCAD on HSC activation. Results: In consistence with staining of liver sections from PBC patients, immunofluorescent staining revealed that JCAD expression was identified in smooth muscle α-actin (α-SMA)-positive fibroblast-like cells and was significantly up-regulated in WT mice with BDL. JCAD deficiency remarkably ameliorated BDL-induced hepatic injury and fibrosis, as documented by liver hydroxyproline content, when compared to WT mice with BDL. Histopathologically, collagen deposition was dramatically reduced in both JCAD-KO and HSC-JCAD-KO mice compared to WT mice, as visualized by Trichrome staining and semi-quantitative scores. Moreover, JCAD deprivation significantly attenuated in situ HSC activation and reduced expression of fibrotic genes after BDL. Conclusions: JCAD deficiency effectively suppressed hepatic fibrosis induced by BDL in mice, and the underlying mechanisms are largely through suppressed Hippo-YAP signaling activity in HSCs.