• Title/Summary/Keyword: Min Jiang

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REMARKS ON FIXED POINT THEOREMS

  • Jiang, Guo-Jing;Kang, Shin-Min
    • East Asian mathematical journal
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    • v.16 no.2
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    • pp.175-181
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    • 2000
  • In this paper we show fixed point theorems related with the diameter of orbit on metric spaces. The results presented in this paper extend, improve and unify the results of $Heged\"{u}s$ [1], Kim, Kim, Leem and Ume [2], Kim and Leem [3], Ohta and Nikaido [4] and $Taskovi\'{c}$ [5].

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Dexmedetomidine alleviates blood-brain barrier disruption in rats after cerebral ischemia-reperfusion by suppressing JNK and p38 MAPK signaling

  • Canmin Zhu;Dili Wang;Chang Chang;Aofei Liu;Ji Zhou;Ting Yang;Yuanfeng Jiang;Xia Li;Weijian Jiang
    • The Korean Journal of Physiology and Pharmacology
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    • v.28 no.3
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    • pp.239-252
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    • 2024
  • Dexmedetomidine displays multiple mechanisms of neuroprotection in ameliorating ischemic brain injury. In this study, we explored the beneficial effects of dexmedetomidine on blood-brain barrier (BBB) integrity and neuroinflammation in cerebral ischemia/reperfusion injury. Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 1.5 h and reperfusion for 24 h to establish a rat model of cerebral ischemia/reperfusion injury. Dexmedetomidine (9 ㎍/kg) was administered to rats 30 min after MCAO through intravenous injection, and SB203580 (a p38 MAPK inhibitor, 200 ㎍/kg) was injected intraperitoneally 30 min before MCAO. Brain damages were evaluated by 2,3,5-triphenyltetrazolium chloride staining, hematoxylin-eosin staining, Nissl staining, and brain water content assessment. BBB permeability was examined by Evans blue staining. Expression levels of claudin-5, zonula occludens-1, occludin, and matrix metalloproteinase-9 (MMP-9) as well as M1/M2 phenotypes-associated markers were assessed using immunofluorescence, RT-qPCR, Western blotting, and gelatin zymography. Enzyme-linked immunosorbent assay was used to examine inflammatory cytokine levels. We found that dexmedetomidine or SB203580 attenuated infarct volume, brain edema, BBB permeability, and neuroinflammation, and promoted M2 microglial polarization after cerebral ischemia/reperfusion injury. Increased MMP-9 activity by ischemia/reperfusion injury was inhibited by dexmedetomidine or SB203580. Dexmedetomidine inhibited the activation of the ERK, JNK, and p38 MAPK pathways. Moreover, activation of JNK or p38 MAPK reversed the protective effects of dexmedetomidine against ischemic brain injury. Overall, dexmedetomidine ameliorated brain injury by alleviating BBB permeability and promoting M2 polarization in experimental cerebral ischemia/reperfusion injury model by inhibiting the activation of JNK and p38 MAPK pathways.

COMMON FIXED POINT THEOREMS FOR COMPATIBLE MAPPINGS OF TYPE (A) AND (P) WITH APPLICATIONS IN DYNAMIC PROGRAMMING

  • Jiang, Guojing;Liu, Min;Lee, Suk-Jin;Kang, Shin-Min
    • East Asian mathematical journal
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    • v.25 no.1
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    • pp.11-26
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    • 2009
  • In this paper, the concepts of compatible mappings of types (A) and (P) are introduced in an induced metric space, two common xed point theorems for two pairs of compatible mappings of types (A) and (P) in an induced complete metric space are established. As their applications, the existence and uniqueness results of common solution for a system of functional equations arising in dynamic programming are discussed.

The Effect of MOCVD Growth Parameters on the Photolumenescence Intensity of InN/GaN Multi-layers (MOCVD 성장조건이 InN/GaN 다층박막의 발광세기에 미치는 영향)

  • Kim, Hyeon-Su;Lee, Jeong-Ju;Jeong, Sun-Yeong;Lee, Jeong-Yong;Lin, J.Y.;Jiang, H.X.
    • Korean Journal of Materials Research
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    • v.12 no.3
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    • pp.190-194
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    • 2002
  • InN/GaN multi-layers were grown by metalorganic chemical vapor deposition(MOCVD) in order to get the appropriate structure for an high power blue-green light emitting diode(LED), and effects of growth conditions (growth temperature, pressure, and $trimethylindium(TMIn)-NH_3-N_2\; flow\; rare)$ on the integrated photoluminescence (PL) intensity and PL peak energy in InN/GaN multi-layers were investigated. The optimized growth conditions with the highest integrated PL intensity for InN/GaN multi-layers were obtained: the growth temperature at $780^{\circ}C$, the growth pressure at 325 Torr, the TMIn flow rate with 150 $m\ell$/min, the $NH_3$flow rate with 3.2 ι/min, and $N_2$ flow rate with 2 ι/min.

Radix Tetrastigma Hemsleyani Flavone Induces Apoptosis in Human Lung Carcinoma A549 Cells by Modulating the MAPK Pathway

  • Zhong, Liang-Rui;Chen, Xian;Wei, Ke-Min
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.10
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    • pp.5983-5987
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    • 2013
  • Radix Tetrastigma Hemsleyani Flavone (RTHF) is widely used as a traditional herb for its detoxification and anti-inflammation activity. Recently, several studies have shown that RTHF can inhibit growth and induce apoptosis in human cancer cell lines. However, the mechanisms are not completely understood yet. In this study we investigated the potential effects of RTHF on growth and apoptosis in human lung adenocarcinoma A549 cells as well as its mechanisms. A549 cells were treated with RTHF at various concentrations for different times. In vitro the MTT assay showed that RTHF had obvious anti-proliferation effects on A549 cells in a dose- and time-dependent manner. Cell morphological changes observed by inverted microscope and Hoechst33258 methods were compared with apoptotic changes observed by fluorescence microscope. Cell apoptosis inspected by flow cytometry showed significant increase in the treatment group over the control group (P<0.01). Expression of apoptosis related Bax/Bcl-2, caspases and MAPK pathway proteins were detected by Western blotting. The results showed that RTHF up-regulated the Bax/Bcl-2 ratio and cle-caspase3/9, cle-PARP expression in a dose-dependent manner. Expression of p-p38 increased, p-ERK decreased significantly and that of p-JNK was little changed in the RTHF group when compared with the control group. These results suggest that RTHF might exert anti-growth and apoptosis activity against lung cancer A549 cells through activation of caspases and Bcl-2 family proteins and the MAPK pathway, therefore presenting as a promising therapeutic agent for the treatment of lung cancer.