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Träfflista för sökning "WFRF:(Jing Xu) srt2:(2005-2009)"

Sökning: WFRF:(Jing Xu) > (2005-2009)

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1.
  • Dominguez, Cecilia A, et al. (författare)
  • Genetic analysis of neuropathic pain-like behavior following peripheral nerve injury suggests a role of the major histocompatibility complex in development of allodynia
  • 2008
  • Ingår i: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 1872-6623 .- 0304-3959. ; 136:3, s. 313-319
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuropathic pain is a common consequence of damage to the nervous system. We here report a genetic analysis of development of neuropathic pain-like behaviors after unilateral photochemically-induced ischemic sciatic nerve injury in a panel of inbred rat strains known to display different susceptibility to autoimmune neuroinflammation. Pain behavior was initially characterized in Dark-Agouti (DA; RT1(avl)), Piebald Virol Glaxo (PVG; RT1(c)), and in the major histocompatibility complex (MHC)-congenic strain PVG-RT1(avl). All strains developed mechanical hypersensitivity (allodynia) following nerve injury. However, the extent and duration of allodynia varied significantly among the strains, with PVG displaying more severe allodynia compared to DA rats. Interestingly, the response of PVG-RT1(avR1) was similar to that of DA, suggesting regulation by the MHC locus. This notion was subsequently confirmed in an F2 cohort derived from crossing of the PVG and PVG-RT1(avl) strains, where allodynia was reduced in homozygous or heterozygous carriers of the RT1(avl) allele in comparison to rats homozygous for the RT1(c) allele. These results indicate that certain allelic variants of the MHC could influence susceptibility to develop and maintain neuropathic pain-like behavior following peripheral nerve injury in rats.
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2.
  • Hua, Dong, et al. (författare)
  • Small interfering RNA-directed targeting of toll-like receptor 4 inhibits human prostate cancer cell invasion, survival, and tumorigenicity
  • 2009
  • Ingår i: Molecular Immunology. - : Elsevier BV. - 0161-5890 .- 1872-9142. ; 46:15, s. 2876-2884
  • Tidskriftsartikel (refereegranskat)abstract
    • A major cause of tumor treatment failure is cancer cell metastasis. Toll-like receptor 4 (TLR4)-mediated signaling has been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers. In this study, we investigated the biological roles of TLR4 in prostate metastatic cell invasion and survival, and the potential of gene silencing of TLR4 using small interfering RNA (siRNA) for treatment of cancer. In cultured human prostate cancer cell lines, TLR4 were higher PC3 and DU145 as compared with the poorly metastatic LNCaP indicating that up-regulation of TLR4 was positively correlated with metastasis of tumor cell. In the highly metastatic cancer cell PC3, gene silencing of TLR4 using siRNA significantly inhibited TLR4 mRNA expression and protein level. Knockdown of TLR4 in PC3 cells resulted in a dramatic reduction of tumor cell migration and invasion as indicated by a Matrigel invasion assay. Furthermore, TLR4 siRNA suppressed cell viability and ultimately caused the induction of apoptotic cell death. The effects were associated with abrogating TLR4-mediated signaling to downstream target molecules such as myeloid differentiation factor 88 (MyD88), adaptor-inducing IFN-beta (TRIF), and interferon regulatory factor-1 (IRF-1). In a mouse prostate cancer model, administration with the plasmid construct expressing siRNA for TLR4 obviously inhibited established tumor growth and survival. These studies revealed evidence of a multifaceted signaling network operating downstream of TLR4-mediated tumor cell invasion, proliferation, and survival. Thus, RNA interference-directed targeting of TLR4 may raise the potential of its application for cancer therapy.
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3.
  • Jiang, Jing-Ting, et al. (författare)
  • Lipids changes in liver cancer
  • 2007
  • Ingår i: Journal of Zhejiang University-Science B. - 1862-1783. ; 8:6, s. 398-409
  • Forskningsöversikt (refereegranskat)abstract
    • Liver is one of the most important organs in energy metabolism. Most plasma apolipoproteins and endogenous lipids and lipoproteins are synthesized in the liver. It depends on the integrity of liver cellular function, which ensures homeostasis of lipid and lipoprotein metabolism. When liver cancer occurs, these processes are impaired and the plasma lipid and lipoprotein patterns may be changed. Liver cancer is the fifth common malignant tumor worldwide, and is closely related to the infections of hepatitis B virus (HBV) and hepatitis C virus (HCV). HBV and HCV infections are quite common in China and other Southeast Asian countries. In addition, liver cancer is often followed by a procession of chronic hepatitis or cirrhosis, so that hepatic function is damaged obviously on these bases, which may significantly influence lipid and lipoprotein metabolism in vivo. In this review we summarize the clinical significance of lipid and lipoprotein metabolism under liver cancer.
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4.
  • Jiang, Jing-Ting, et al. (författare)
  • Mechanisms and significance of lipoprotein(a) in hepatocellular carcinoma
  • 2009
  • Ingår i: Hepatobiliary and Pancreatic Diseases International. - 1499-3872. ; 8:1, s. 25-28
  • Forskningsöversikt (refereegranskat)abstract
    • BACKGROUND: The liver plays a key role in the metabolism of plasma apolipoproteins, endogenous lipids and lipoproteins. Hepatocellular carcinoma is one of the most common fatal malignant tumors in China and in other Southeast Asian countries. It has been demonstrated that plasma lipid profiles are changed in liver cancer. DATA SOURCES: A MEDLINE database search was performed to identify relevant articles using the keywords "hepatocellular carcinoma" and "lipoprotein(a)". The search was conducted and research articles were reviewed from 1960 to 2008. RESULTS: Production and homeostasis of lipids, apolipoproteins and lipoproteins depend on the integrity of hepatocellular functions, which ensures normal lipid and lipoprotein metabolism in vivo. When hepatocellular injury or liver cancer occurs these processes can be impaired. It has been suggested that plasma levels of apolipoprotein(a) (apo(a)) and/or lipoprotein (a) (Lp(a)) may be considered as sensitive markers of hepatic impairment. CONCLUSIONS: Plasma levels of apo(a) and Lp(a) display significant correlations with hepatic status. Most studies demonstrated that the plasma levels of apo(a) and Lp(a) can be considered as an additional clinical index of liver function.
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5.
  • Jiang, Jing-Ting, et al. (författare)
  • Metabolism of high density lipoproteins in liver cancer
  • 2007
  • Ingår i: World Journal of Gastroenterology. - 1007-9327. ; 13:23, s. 3159-3163
  • Forskningsöversikt (refereegranskat)abstract
    • Liver plays a vital role in the production and catabolism of plasma lipoproteins. It depends on the integrity of cellular function of liver, which ensures homeostasis of lipid and lipoprotein metabolism. When liver cancer occurs these processes are impaired and high-density lipoproteins are changed. (C) 2007 The WJG Press. All rights reserved.
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6.
  • Zhang, Hongxia, et al. (författare)
  • Effects of angular misalignment in interferometric detection of distributed polarization coupling
  • 2009
  • Ingår i: Measurement science and technology. - : IOP Publishing. - 0957-0233 .- 1361-6501. ; 20:9, s. 095112-
  • Tidskriftsartikel (refereegranskat)abstract
    • White light interferometry is used to measure the distributed polarization coupling (DPC) in polarization-maintaining fibers (PMFs). By using a scanning Michelson interferometer to compensate the optical path difference (OPD) induced by the modal birefringence of PMFs, both the coupling strength and positions of the coupling points can be acquired. In ideal DPC measurement, the two reflective mirrors on the fixed and scanning arms of the Michelson interferometer are normal to each other. But in practice, the movable reflective mirror cannot be aligned normally to the fixed mirror exactly, which leads to an angular misalignment. The angular misalignment causes a variation of the OPD, which will reduce the fringe visibility. The theoretical simulation is investigated correspondingly. Consequently, the angular error leads to the miscalculation of the polarization coupling intensity. Based on the experimental results, a revised coupling strength calculation equation is proposed to minimize the influence of angular misalignment.
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