Surfactant-Assisted Synthesis of Fe₂O₃ Nanoparticles and F-Doped Carbon Modification toward an Improved Fe₃O₄@CF_<i>x</i>/LiNi_0.5Mn_1.5O₄ Battery

Ming, Hai,Ming, Jun,Oh, Seung-Min,Tian, Shu,Zhou, Qun,Huang, Hui,Sun, Yang-Kook,Zheng, Junwei American Chemical Society 2014 ACS APPLIED MATERIALS & INTERFACES Vol.6 No.17

<P>A simple surfactant-assisted reflux method was used in this study for the synthesis of cocklebur-shaped Fe<SUB>2</SUB>O<SUB>3</SUB> nanoparticles (NPs). With this strategy, a series of nanostructured Fe<SUB>2</SUB>O<SUB>3</SUB> NPs with a size distribution ranging from 20 to 120 nm and a tunable surface area were readily controlled by varying reflux temperature and the type of surfactant. Surfactants such as cetyltrimethylammonium bromide (CTAB), polyvinylpyrrolidone (PVP), poly(ethylene glycol)-<I>block</I>-poly(propylene glycol)-<I>block</I>-poly(ethylene glycol) (F127) and sodium dodecyl benzenesulfonate (SDBS) were used to achieve large-scale synthesis of uniform Fe<SUB>2</SUB>O<SUB>3</SUB> NPs with a relatively low cost. A new composite of Fe<SUB>3</SUB>O<SUB>4</SUB>@CF<SUB><I>x</I></SUB> was prepared by coating the primary Fe<SUB>2</SUB>O<SUB>3</SUB> NPs with a layer of F-doped carbon (CF<SUB><I>x</I></SUB>) with a one-step carbonization process. The Fe<SUB>3</SUB>O<SUB>4</SUB>@CF<SUB><I>x</I></SUB> composite was utilized as the anode in a lithium ion battery and exhibited a high reversible capacity of 900 mAh g<SUP>–1</SUP> at a current density of 100 mA g<SUP>–1</SUP> over 100 cycles with 95% capacity retention. In addition, a new Fe<SUB>3</SUB>O<SUB>4</SUB>@CF<SUB><I>x</I></SUB>/LiNi<SUB>0.5</SUB>Mn<SUB>1.5</SUB>O<SUB>4</SUB> battery with a high energy density of 371 Wh kg<SUP>–1</SUP> (vs cathode) was successfully assembled, and more than 300 cycles were easily completed with 66.8% capacity retention at 100 mA g<SUP>–1</SUP>. Even cycled at the high temperature of 45 °C, this full cell also exhibited a relatively high capacity of 91.6 mAh g<SUP>–1</SUP> (vs cathode) at 100 mA g<SUP>–1</SUP> and retained 54.6% of its reversible capacity over 50 cycles. Introducing CF<SUB><I>x</I></SUB> chemicals to modify metal oxide anodes and/or any other cathode is of great interest for advanced energy storage and conversion devices.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/aamick/2014/aamick.2014.6.issue-17/am504144d/production/images/medium/am-2014-04144d_0009.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/am504144d'>ACS Electronic Supporting Info</A></P>

MiR-130a Overcomes Gefitinib Resistance by Targeting Met in Non-Small Cell Lung Cancer Cell Lines

Zhou, Yong-Ming,Liu, Juan,Sun, Wei Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.3

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and the most common cause of lung cancer death. Currently, the epidermal growth factor receptor inhibitor gefitinib is used for its treatment; however, drug resistance is a major obstacle. Expression of Met has been associated with both primary and acquired resistance to gefitinib, but the mechanisms regulating its expression are not fully understood. Recently, miRNAs such as miR-130a have been shown to play a role in gefitinib resistance, but importance in NSCLC and relationships with Met have not been fully explored. Here we show that miR-130a is over-expressed in gefitinibsensitive NSCLC cell lines, but is low in gefitinib-resistant NSCLC cell lines. Moreover, miR-130a expression was negatively correlated with that of Met. Further analysis revealed that over-expression of miR-130a increased cell apoptosis and inhibited proliferation of NSCLC cells treated with gefitinib, whereas lowering the expression of miR-130a decreased cell apoptosis and promoted cell proliferation after treatment with gefitinib in both gefitinib-sensitive and -resistant NSCLC cell lines, suggesting that miR-130a overcomes gefitinib resistance. We also demonstrated that miR-130a binds to the 3'-UTR of Met and significantly suppresses its expression. Finally, our results showed that over-expressing Met could "rescue" the functions of miR-130a regarding cell apoptosis and proliferation after cells are treated with gefitinib. These findings indicate that the miR-130a/Met axis plays an important role in gefitinib resistance in NSCLC. Thus, the miR-130a/Met axis may be an effective therapeutic target in gefitinib-resistant lung cancer patients.

Simultaneous treatment with sorafenib and glucose restriction inhibits hepatocellular carcinoma in vitro and in vivo by impairing SIAH1-mediated mitophagy

Zhou Jing,Feng Ji,Wu Yong,Dai Hui-Qi,Zhu Guang-Zhi,Chen Pan-Hong,Wang Li-Ming,Lu Guang,Liao Xi-Wen,Lu Pei-Zhi,Su Wen-Jing,Hooi Shing Chuan,Ye Xin-Pin,Shen Han-Ming,Peng Tao,Lu Guo-Dong 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-

Transarterial chemoembolization (TACE) is the first-line treatment for unresectable intermediate-stage hepatocellular carcinoma (HCC). It is of high clinical significance to explore the synergistic effect of TACE with antiangiogenic inhibitors and the molecular mechanisms involved. This study determined that glucose, but not other analyzed nutrients, offered significant protection against cell death induced by sorafenib, as indicated by glucose deprivation sensitizing cells to sorafenib-induced cell death. Next, this synergistic effect was found to be specific to sorafenib, not to lenvatinib or the chemotherapeutic drugs cisplatin and doxorubicin. Mechanistically, sorafenib-induced mitophagy, as indicated by PINK1 accumulation, increased the phospho-poly-ubiquitination modification, accelerated mitochondrial membrane protein and mitochondrial DNA degradation, and increased the amount of mitochondrion-localized mKeima-Red engulfed by lysosomes. Among several E3 ubiquitin ligases tested, SIAH1 was found to be essential for inducing mitophagy; that is, SIAH1 silencing markedly repressed mitophagy and sensitized cells to sorafenib-induced death. Notably, the combined treatment of glucose restriction and sorafenib abolished ATP generation and mitophagy, which led to a high cell death rate. Oligomycin and antimycin, inhibitors of electron transport chain complexes, mimicked the synergistic effect of sorafenib with glucose restriction to promote cell death mediated via mitophagy inhibition. Finally, inhibition of the glucose transporter by canagliflozin (a clinically available drug used for type-II diabetes) effectively synergized with sorafenib to induce HCC cell death in vitro and to inhibit xenograft tumor growth in vivo. This study demonstrates that simultaneous treatment with sorafenib and glucose restriction is an effective approach to treat HCC, suggesting a promising combination strategy such as transarterial sorafenib-embolization (TASE) for the treatment of unresectable HCC.

HMGB1 regulates autophagy through increasing transcriptional activities of JNK and ERK in human myeloid Leukemia cells

( Ming Yi Zhao ),( Ming Hua Yang ),( Liang Chun Yang ),( Yan Yu ),( Min Xie ),( Shan Zhu ),( Rui Kang ),( Dao Lin Tang ),( Zhi Gang Jiang ),( Wu Zhou Yuan ),( Xiu Shan Wu ),( Li Zhi Cao ) 생화학분자생물학회 2011 BMB Reports Vol.44 No.9

HMGB1 is associated with human cancers and is an activator of autophagy which mediates chemotherapy resistance. We here show that the mRNA levels of HMGB1 are high in leukemia cells and it is involved in the progression of childhood chronic myeloid leukemia (CML). HMGB1 decreases the sensitivity of human myeloid leukemia cells K562 to anti-cancer drug induced death through up-regulating the autophagy pathway, which is confirmed by the observation with an increase in fusion of autophagosomes and autophagolysosomes. When overexpressing HMGB1, both mRNA levels of Beclin-1, VSP34 and UVRAG which are key genes involved in mammalian autophagy and protein levels of p-Bcl-2 and LC3-II are increased. Luciferase assays document that over-expression of HMGB1 increases the transcriptional activity of JNK and ERK, which may be silenced by siRNA. The results suggest that HMGB1 regulates JNK and ERK required for autophagy, which provides a potential drug target for therapeutic interventions in childhood CML. [BMB reports 2011; 44(9): 601-606]

A Power Allocation Algorithm Based on Variational Inequality Problem for Cognitive Radio Networks

Zhou, Ming-Yue,Zhao, Xiao-Hui Korea Information Processing Society 2017 Journal of information processing systems Vol.13 No.2

Power allocation is an important factor for cognitive radio networks to achieve higher communication capacity and faster equilibrium. This paper considers power allocation problem to each cognitive user to maximize capacity of the cognitive systems subject to the constraints on the total power of each cognitive user and the interference levels of the primary user. Since this power control problem can be formulated as a mixed-integer nonlinear programming (NP) equivalent to variational inequality (VI) problem in convex polyhedron which can be transformed into complementary problem (CP), we utilize modified projection method to solve this CP problem instead of finding NP solution and give a power control allocation algorithm with a subcarrier allocation scheme. Simulation results show that the proposed algorithm performs well and effectively reduces the system power consumption with almost maximum capacity while achieve Nash equilibrium.

P008 Inhibition of collagen synthesis by a small molecule tankyrase inhibitor IWR in fibroblasts

( Ming-wei Zhou ),( Cho-ah Lim ),( Hae-eul Lee ),( Myung Im ),( Young Lee ),( Chang Deok Kim ),( Young-joon Seo ),( Jeung-hoon Lee ) 대한피부과학회 2016 대한피부과학회 학술발표대회집 Vol.68 No.2

<div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div> Background: Keloid is a benign tumor that is characterized by the hyperproliferation of dermal fibroblasts and excessive deposition of extracellular matrix (ECM) especially the collagen. Aberrant activation of Wnt/β-catenin signaling is implicated in the pathogenesis of keloid. Objectives: We investigated the effects of IWR-1, a small molecule inhibitor for Wnt/β-catenin signaling via the inhibition of tankyrase, on production of collagen and matrix metalloproteinase (MMP) in dermal fibroblasts. Methods: We cultured human normal skin- and keloid-derived fibroblasts, then treated with IWR-1. The effects of IWR-1 on collagen and MMP production were determined by Western blot, ELISA and zymography. Results: IWR-1 significantly suppressed the proliferation and migration of both the normal and keloid fibroblasts. IWR-1 also inhibited the production and secretion of type I collagen from the fibroblasts. In addition, IWR-1 significantly increased the expression of MMPs, such as MMP-1, MMP-3 and MMP-13, along with the increase of gelatinase activity. These results suggest that inhibitory effect of IWR-1 on collagen production may be related with the increased MMP activity. Conclusion: These results provide evidence that IWR-1 can be a possible candidate to be developed as a therapeutics for keloid.

Clinical Significance of Expression and Amplification of the DcR3 Gene in Pancreatic Carcinomas

Zhou, Jian,Song, Shi-Duo,Li, De-Chun,Zhou, Jin,Zhu, Dong-Ming,Zheng, Shi-Ying Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.2

This study aimed to investigate the clinical significance of expression and amplification of decoy receptor 3 (DcR3) in pancreatic carcinomas (PC). mRNA expression was detected by PQ-PCR, and amplification was determined. DcR3 protein expression was detected by immunohistochemistry and ELISA. Correlations between DcR3 expression and clinical pathological factors were analyzed. The relative amount of DcR3 in PC tissues and non-cancerous tissues showed a statistically significant difference, 21 cases displaying more than two fold DcR3 amplification, while no such amplification was found in normal pancreatic tissues. DcR3 positive cell staining was located in the cytoplasm. The positive rate of DcR3 in PC and non-cancerous tissues showed a significant difference. DcR3 mRNA expression was correlated with clinical staging, size of the tumor, lymph node metastasis and histological staging, while protein expression was correlated with clinical data like tumor size. DcR3 gene amplification only correlated with tumor size. The level of DcR3 in serum of the PC resectable group before operation was $72.2{\pm}10.2$ pg/ml, showing a significant difference compared to gallbladder carcinoma group (GC) or pancreatic benign tumor (PBT) group (P < 0.01). In conclusion, DcR3 amplification is correlated with DcR3 expression in PC tissues, especially those clinical pathological factors which reflect tumor progression. Assessment of DcR3 level in sera of PC patients may be helpful for the early diagnosis and prognostic judgement.

Intraperitoneal Incubation of Bladder Acellular Matrix Grafts Improves Bladder Smooth Muscle Regeneration via Neovascularization

Zhou Zhe,Zhang Ming,Xu Mingxi,Zhang Ke,Zhao Yang,Zhou Juan,Zhu Yingjian,Wang Zhong,Lu Mujun 한국생물공학회 2015 Biotechnology and Bioprocess Engineering Vol.20 No.3

The objective of this study was to investigate whether intraperitoneal incubation improves the regenerative capacity of bladder acellular matrix grafts (BAMGs) in a rat model of bladder augmentation. After 2 weeks of incubation in the peritoneum of male rats, BAMG flaps with vascular pedicles were harvested for autologous bladder augmentation. As the control, BAMGs were directly used for bladder augmentation without intraperitoneal incubation. Histological analyses of the incubated BAMGs demonstrated extensive cell growth and vasculature in homogeneous collagen bundles. The cells were positive for vimentin and negative for α-smooth muscle actin and pan-cytokeratin AE1/AE3. Cystography revealed smoother contours of the augmented bladders in the incubated group at 4 and 12 weeks postoperatively. However, the bladder capacity was not significantly different between the two groups. In both groups, the entire urothelium regenerated well without obvious differences. At both time points, compared with the control group, increased numbers of smooth muscle cells (SMCs) and blood vessels were found in the incubated group. At 12 weeks, the SMCs in the incubated group were more similar to those in the native smooth muscle fiber bundles of the bladder. Taken together, our results demonstrated that BAMGs preincubated in the peritoneum promote the regeneration of bladder smooth muscle via neovascularization in a rat bladder augmentation model.

Comparison of two recycle dilated banyan network with output buffers

Ming Zhou,Zeng Ji Liu 한국통신학회 1998 한국통신학회 기타 간행물 Vol.- No.-

Preparation and property evaluation of a temperature-resistant Zr-crosslinked fracturing fluid

Ming Zhou,Jinfeng Zhang,Zhonghua Zuo,Mao Liao,Peng’ao Peng 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.96 No.-

Compared with the traditional water-based fracturingfluid thickener guanidine gum, the price ofsynthetic polymer is relatively low, and the temperature resistance, shear resistance and viscoelasticityof the formed fracturingfluid are better. Therefore, the fracturingfluid formed by the crosslinking ofHPAM and organic metal crosslinker will become one of the hot spots in the research of water-basedfracturingfluid. In this paper, zirconium oxychloride, acetic acid and triethanolamine were used as rawmaterials to prepare organic Zr-crosslinked agent. The polymer gel was formed by crosslinking theorganic Zr-crosslinked agent with the acrylamide copolymer KY-5S solution, and the viscosity of the gelwith different concentrations was investigated. The performance of the fracturingfluid was evaluatedthrough laboratory experiments. The results showed that the viscosity of the fracturingfluid remainedabove 100 mPa s at the shear rate of 170 s 1 and after 2 h of shear at 140 C. When the temperature was20 C, the shear stress was 0.1 Pa, and the frequency f varied from 0.1 to 10 Hz, the elastic modulus offracturingfluid was at least 11.6 Pa, and the viscous modulus was at least 8.54 Pa. At the temperature of90 C, when the addition of glue breaker was 0.01 wt%, the longest breaking time was 3 h, and themaximum viscosity of breaking liquid was 4.05 mPa s. The damage rate of core permeability of gluebreaker was about 13%. When the temperature was 25 C and the shear rate was 0–170 s-1, the viscosity offracturingfluid remained above 200 mPa s.