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Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Medicinska och farmaceutiska grundvetenskaper) hsv:(Läkemedelskemi) ;pers:(Xu Ning)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Medicinska och farmaceutiska grundvetenskaper) hsv:(Läkemedelskemi) > Xu Ning

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1.
  • Wei, Jiang, et al. (författare)
  • 17β-estradiol regulates the expression of apolipoprotein M through estrogen receptor α-specific binding motif in its promoter
  • 2017
  • Ingår i: Lipids in Health and Disease. - : Springer Science and Business Media LLC. - 1476-511X. ; 16:1, s. 1-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression. Results: Our results demonstrated either free 17β-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells. Moreover, experiments with the luciferase activity analysis of truncated apoM promoters could demonstrate that a regulatory region (from-1580 to −1575 bp (−GGTCA-)) upstream of the transcriptional start site of apoM gene was essential for the basal transcriptional activity that regulated by the ER-α. With the applications of an electrophoresis mobility shift assay and a chromatin immunoprecipitation assay, we could successfully identify a specific ER-α binding element in the apoM promoter region. Conculsion: In summary, the present study indicates that 17β-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-α-dependent pathway involving ER-α binding element in the promoter of the apoM gene.
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3.
  • Jiang, Jingting, et al. (författare)
  • Clinical Evaluation of Serum Alpha-Fetoprotein-IgM Immune Complexes on the Diagnosis of Primary Hepatocellular Carcinoma
  • 2009
  • Ingår i: Journal of Clinical Laboratory Analysis. - : Wiley. - 1098-2825 .- 0887-8013. ; 23:4, s. 213-218
  • Tidskriftsartikel (refereegranskat)abstract
    • We evaluated clinical significance of serum alpha-fetoprotein (AFP)-IgM immune complexes, in comparison with free AFP, on the diagnosis of primary hepatocellular carcinoma (HCC). Serum levels of AFP-IgM immune complexes and free AFP were determined by the ELISA method and electrochemiluminescence, respectively, in 103 healthy controls, 74 patients suffering from primary HCC, 27 patients suffering from liver cirrhosis, and 63 patients suffering from chronic hepatitis. The best cut-off value of AFP-IgM and free AFP for diagnosis of primary HCC were 300 AU/mL and 10 mu g/L respectively, according to the area under the curve (AUC) in this study. The sensitivity of AFP-IgM and free AFP were 64.9 and 79.7%, and the specificity were 75.6 and 80.3%, respectively, when all cases of primary HCC were analyzed, and the AUC of free AFP was larger than that of AFP-IgM (0.85 vs. 0.72, Z = 3.21). However, in case of primary HCC at early stages (stages I and II) were analyzed, the AUC of AFP-IgM was larger than that of free AFP (0.91 vs. 0.82, Z = 1.73), which demonstrated that the sensitivity of AFP-IgM and free AFP were 94.4 and 72.2%, and the specificity were 81.9 and 79.9%, respectively. When both AFP-IgM and free AFP were positive, the specificity of diagnosis of primary HCC was 89.1%, and the efficacy was 79.0%. It is concluded that either sensitivity or specificity of serum level of AFP-IgM immune complexes was higher than that of free AFP in the diagnosis of primary HCC at early stages. As there was false positive AFP-IgM existed in the patients suffering from cirrhosis and chronic hepatitis, the combination of free AFP and AFP-IgM could significantly increase specificity and decrease false negative and/or false positive in the primary HCC at early stages. J. Clin. Lab. Anal. 23:213-218, 2009. (C) 2009 Wiley-Liss, Inc.
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4.
  • Jiang, Jingting, et al. (författare)
  • Increased plasma apoM levels in the patients suffered from hepatocellular carcinoma and other chronic liver diseases
  • 2008
  • Ingår i: Lipids in Health and Disease. - 1476-511X. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: To determine plasma apolipoprotein M ( apoM) levels and other lipid profiles in hepatocellular carcinoma ( HCC) patients compared to other chronic liver diseases and normal subjects. Materials and methods: 36 HCC, 68 chronic hepatitis, 29 liver cirrhosis patients and 64 normal controls were subjected in the present study. Serum lipids, lipoproteins, apolipoprotein AI ( apoAI) and apoB were determined by the conventional methods. Plasma apoM levels were semiquantitatively determined by both dot- blotting and western blotting analysis. Results: Serum levels of triglycerides ( TG), HDL- cholesterol, apoAI and lipoprotein ( a) ( Lp( a)) were significantly lower in the HCC patients than in the normal subjects, whereas there were no obvious differences on serum total cholesterol, LDL- cholesterol and apoB between HCC patients and normal subjects. However, plasma apoM levels in HCC patients were significantly increased than those in the normal subjects, but lower than those in the chronic hepatitis and cirrhosis patients. Conclusion: It is concluded that serum TG, apoAI, HDL- C and Lp( a) were significantly decreased in HCC patients than in controls, whereas plasma apoM levels were significantly increased in the HCC patients. Decreased serum TG, apoAI, HDL- C and Lp( a) may reflect the liver damage in HCC patients, whereas the clinical significance of increased plasma apoM levels in relation to HCC is not clear.
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5.
  • Jiang, Jingting, et al. (författare)
  • Influence of liver cancer on lipid and lipoprotein metabolism
  • 2006
  • Ingår i: Lipids in Health and Disease. - 1476-511X. ; 5
  • Forskningsöversikt (refereegranskat)abstract
    • Liver plays a key role in the metabolism of plasma apolipoproteins, endogenous lipids and lipoproteins. Hepatocellular carcinoma (HCC) is one of the most common fatal malignant tumors in China and in other Southeast Asian countries. This has been attributed to the high incidence of hepatitis B infection. Hepatitis B proteins, such as the hepatitis B X protein (HBx) that is large hepatitis B surface protein could regulate transcription of many candidate genes for liver carcinogenesis. It has known that patients who suffered from acute hepatitis B could have lipid disorders such as decreased plasma level of high-density lipoproteins (HDL). Furthermore, aberrations of lipid metabolism are often seen in the chronic hepatitis B infection. Plasma lipid profiles could be changed under HCC. In majority of the reports in HCC, plasma levels of triglycerides (TG), cholesterol, free fatty acids (FFA), HDL, low-density lipoproteins (LDL), lipoprotein (a) (Lp(a)), apolipoprotein AI (apoAI) and apoB were slight to significantly decreased, however, in some cases plasma levels of TG and Lp(a) might be increased. It has been suggested that analysis of plasma levels of lipids, lipoproteins and apolipoproteins in the patients suffered from HCC reflects on the hepatic cellular impairment status. Studies revealed that alterations seen in the plasma levels of lipids, lipoproteins and apolipoproteins reflecting patients' pathologic conditions. Decreased serum levels of cholesterol and apoAI may indicate a poor prognosis. Human leukaemic cells and certain tumor tissues have a higher receptor-mediated uptake of HDL and LDL than the corresponding normal cells or tissues. LDL and HDL have therefore been proposed as a carrier for the water-insoluble anti-cancer agents.
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6.
  • 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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7.
  • 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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8.
  • Luo, Guanghua, et al. (författare)
  • Apolipoprotein M
  • 2004
  • Ingår i: Lipids in Health and Disease. - 1476-511X. ; 3
  • Forskningsöversikt (refereegranskat)abstract
    • Apolipoprotein M (apoM) is a 26-kDa protein that is mainly associated with high-density lipoprotein (HDL) in human plasma, with a small proportion present in triglyceride-rich lipoproteins (TGRLP) and low-density lipoproteins (LDL). Human apoM gene is located in p21.31 on chromosome 6 (chromosome 17, in mouse). Human apoM cDNA (734 base pairs) encodes 188-amino acid residue-long protein. It belongs to lipocalin protein superfamily. Human tissue expression array study indicates that apoM is only expressed in liver and in kidney and small amounts are found in fetal liver and kidney. In situ apoM mRNA hybridization demonstrates that apoM is exclusively expressed in the hepatocytes and in the tubule epithelial cells in kidney. Expression of apoM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF) and leptin in vivo and/or in vitro. It has been demonstrated that apoM expression is dramatically decreased in apoA-I deficient mouse. Hepatocyte nuclear factor-1alpha (HNF-1alpha) is an activator of apoM gene promoter. Deficiency of HNF-1alpha mouse shows lack of apoM expression. Mutations in HNF-1alpha (MODY3) have reduced serum apoM levels. Expression of apoM is significantly decreased in leptin deficient (ob/ob) mouse or leptin receptor deficient (db/db) mouse. ApoM concentration in plasma is positively correlated to leptin level in obese subjects. These may suggest that apoM is related to the initiation and progression of MODY3 and/or obesity.
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9.
  • Luo, Guanghua, et al. (författare)
  • Expression and localization of apolipoprotein M in human colorectal tissues
  • 2010
  • Ingår i: Lipids in Health and Disease. - 1476-511X. ; 9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: It has been well documented that apolipoprotein M (apoM) is principally expressed in the liver and kidney. However we found that there was weak apoM expression in other tissues or organs too, which could not be ignored. In the present study, we therefore examined apoM expression in human colorectal tissues including cancer tissues, cancer adjacent normal tissues, polyp tissues and normal mucosa as well as inflammatory mucosa. Methods: Tissue samples were collected from patients who underwent surgical resection or endoscopic examination. ApoM mRNA levels were determined by the real-time RT-PCR and apoM protein mass were examined by the immunohistochemistry. Results: ApoM protein can be detected in all colorectal tissues. However, apoM protein mass were significantly lower in the cancer tissues than its matched adjacent normal tissues, polyp tissues, normal mucosa and inflammatory mucosa. In parallel, apoM mRNA levels in the colorectal cancer tissues (0.0536 +/- 0.0131) were also significantly lower than those in their adjacent normal tissues (0.1907 +/- 0.0563) (P = 0.033). Interestingly, apoM mRNA levels in colorectal cancer tissues were statistic significant higher in the patients with lymph node metastasis than the patients without lymph node metastasis (P = 0.008). Patients under Dukes' C and D stages had much higher apoM mRNA levels than patients under Dukes' A and B stages (P = 0.034). Conclusion: It is concluded that apoM could also be expressed in human colorectal tissues besides liver and kidney. ApoM mRNA levels in the colorectal cancer tissues were significantly increased in the patients with lymph node metastasis. Whether increased apoM expression in the patients with lymph node metastasis being related to patients' prognosis and the physiopathological importance of apoM expression in colorectal tissues need further investigation.
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10.
  • Luo, Guanghua, et al. (författare)
  • Genotyping of single nucleotide polymorphisms using base-quenched probe: A method does not invariably depend on the deoxyguanosine nucleotide
  • 2009
  • Ingår i: Analytical Biochemistry. - : Elsevier BV. - 1096-0309 .- 0003-2697. ; 386:2, s. 161-166
  • Tidskriftsartikel (refereegranskat)abstract
    • Most available methods for detecting single nucleotide polymorphisms (SNPs) are based principally on the system that can produce an increased fluorescence signal during hybridization. In the current study, we demonstrate a method of base-quenched probe for polymerase chain reaction (PCR) genotyping that requires only a pair of primers and one fluorescent probe and does not invariably depend on the deoxyguanosine nucleotide. This method further exploits the phenomenon of fluorescence quenching of fluorescent-labeled probe during hybridization to its complementary target gene's sequence. 6-Carboxyfluorescein (FAM) can be directly conjugated to a base of either adenine (A), thymine (T), cytosine (C), or guanine (G), referred to as A-, T-, C-, or G-quenched probe, respectively, at either the 5' or 3' end. For describing the method in detail, we chose apolipoprotein M (apoM) as a target gene in the current study. DNA sequencing analyses validated that all four types of base-quenched probes could provide unbiased genotyping results (K = 1, P = 0.000), although the maximum speed of fluorescence increase, max(dF/dT), when using the G-quenched probe method, was approximately twofold lower than the others (P < 0.0001). Moreover, we applied this method to detect another seven SNPs in the genomes of phospholipase A2, monocyte chemoattractant protein I (MCP1), and L-ficolin, further confirming our method. It is concluded that this method is precise, simple, and economic as well as suitable for large-scale genotyping Studies. (C) 2008 Elsevier Inc. All rights reserved.
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