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Träfflista för sökning "WFRF:(Luo Guanghua) "

Sökning: WFRF:(Luo Guanghua)

  • Resultat 1-10 av 42
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1.
  • Chen, Lujun, et al. (författare)
  • Immunochemical Staining of MT2-MMP Correlates Positively to Angiogenesis of Human Esophageal Cancer
  • 2010
  • Ingår i: Anticancer research. - 1791-7530. ; 30:10, s. 4363-4368
  • Tidskriftsartikel (refereegranskat)abstract
    • Matrix metalloproteinases (MMPs) play an important role in the pathological processes of degradation of extracellular matrix and destruction of basement membrane, which leads to tumor invasion and metastasis. In the present study, we investigated membrane-type 2 MMP (MT2-MMP) expression pattern in esophageal cancer tissues collected from 103 patients, and explored MT2-MMP expression pattern in correlation to patients' clinicopathological features, intratumoral angiogenesis and postoperative prognoses. The intensity of immunochemical staining of MT2-MMP was significantly positively correlated to the intratumoral angiogenesis of esophageal cancer tissues. Positive MT2-MMP immunoreactions were found in 85.4% of total tumor sections, whereas none or very weak MT2-MMP staining occurred in normal esophageal tissues. In addition, MT2-MMP immunochemical intensities were significantly correlated to tumor size, but not to patient's gender, age, invasion depth, lymph node metastasis and distant metastasis. Moreover, MT2-MMP levels could not be applied for predicting patients' survival rate although the H-score cut-off value showed the overall survival rate of patients with low MT2-MMP protein level to be better than those with high MT2-MMP protein level.
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2.
  • Chen, Lujun, et al. (författare)
  • Immunolocalisation of tissue factor in esophageal cancer is correlated with intratumoral angiogenesis and prognosis of the patient
  • 2010
  • Ingår i: Acta Histochemica. - : Elsevier BV. - 0065-1281. ; 112:3, s. 233-239
  • Tidskriftsartikel (refereegranskat)abstract
    • It has been demonstrated that tissue factor (TF) may be involved in the tumor-derived procoagulatory status and angiogenic modulation in certain solid tumors. In the present study, we examined immunohistochemical localisation of TF in esophageal squamous cell carcinomas (ESCC) from 103 patients. TF immunopositivity was found in 91.3% of all tumor sections, while normal esophageal tissues were immunonegative. Patients were divided into a low TF immunoreactivity group (9 cases of negative and 48 cases of weak positive) and a high TF immunoreactivity group (35 cases of moderate positive and 11 cases of strong positive). TF immunoreactivity was significantly correlated to the presence of distant metastasis (P = 0.0014), while it was not correlated to patient's gender, age, tumor size, depth of tumor invasion or lymph node metastasis. Survival analysis revealed that the overall survival rate in the patients that had high TF immunoreactivity was significantly poorer than those with low TF immunoreactivity (P = 0.0094). Univariate analysis demonstrated that tumor size (P = 0.0095), depth of tumor invasion (P = 0.0050), lymph node metastasis (P = 0.0045) and distant metastasis (P < 0.0001) were effective predictors of prognosis in patients. However, only distant metastasis could independently predict patients' outcomes by the analysis of multivariate proportional hazards regression (P = 0.0043). Furthermore, the intratumoral microvessel density (MVD), evaluated by CD34 immunolabeling, indicated that MVD was positively correlated to the TF immunoreactivity (P = 0.0056). It is concluded that TF immunopositivity in ESCC tissues is strongly correlated to the intratumoral angiogenesis and to poor patient prognosis. (C) 2009 Elsevier GmbH. All rights reserved.
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3.
  • Di, Dongmei, et al. (författare)
  • ABCA1 upregulating apolipoproein M expression mediates via the RXR/LXR pathway in HepG2 cells
  • 2012
  • Ingår i: Biochemical and Biophysical Research Communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 421:1, s. 152-156
  • Tidskriftsartikel (refereegranskat)abstract
    • We have previously reported that liver X receptor (LXR) agonist, TO901317, could significantly inhibit hepatic apolipoprotein M (apoM) expression. It has been reported that TO901317 could activate the ATP-binding cassette transporter A1 (ABCA1) that mediates cholesterol efflux to the lipid-poor apoA1, which is an essential step for the high-density lipoprotein (HDL) formation. It is unknown if ABCA1 may regulate hepatic apoM expression. In the present study, HepG2 cells were cultured with the synthetic LXR agonists, TO901317 or GW3965 in the presence or absence of ABCA1 antagonist, disodium 4,4'-diisothiocyanatostilbene-2,2'-disulfonate (DIDS). The mRNA levels of ABCA1, apoM and liver receptor homolog-1 (LRH-1) determined by the real-time RT-PCR. It demonstrated that both TO901317 and GW3965 could significantly enhance ABCA1 expression, and simultaneously, inhibit LRH1 expression. However, TO901317 alone could significantly inhibit apoM expression, while GW3965 alone did not influence apoM expression. ABCA1 antagonist, DIDS, have no effects on GW3965 induced upregulation of ABCA1 and downregulation of LRH1. However, apoM mRNA level was significantly decreased when the cells cultured with GW3965 together with DIDS. The present study demonstrated that apoM expression could be elevated by ABCA1 via the RXR/LXR pathway and LRH1 does not involve in the regulation of apoM by the activation of ABCA1, although the direct regulative pathway(s) between ABCA1 and apoM gene is still unknown yet. The detailed mechanism needs further investigation. (C) 2012 Elsevier Inc. All rights reserved.
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4.
  • Fang, Qi, et al. (författare)
  • Increased CXCL8 expression is negatively correlated with the overall survival of patients with ER-negative breast cancer
  • 2017
  • Ingår i: Anticancer research. - : Anticancer Research USA Inc.. - 0250-7005 .- 1791-7530. ; 37:9, s. 4845-4852
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: C-X-C motif chemokine ligand 8 (CXCL8) is a multi-functional chemokine and has important roles during tumor formation and development. It was previously reported that increased CXCL8 protein levels occurred in certain patients. Materials and Methods: In the present study, we examined levels of CXCL8 mRNA in breast cancer tissues and analyzed its levels in correlation to patients' clinical data and 10-year overall survival (OS). Results: Our results clearly demonstrated that the level of CXCL8 mRNA was significantly higher in patients without estrogen receptor expression. The receiver operating characteristic curve indicated that the best cut-off value for CXCL8 expression was 3.095 for predicting patient's OS. Conclusion: The present study demonstrated that higher CXCL8 mRNA levels in breast cancer tissues together with estrogen receptor negativity was associated with significantly shorter OS, and could be applied as a negative risk factor for 10-year OS.
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5.
  • Hua, Sha, et al. (författare)
  • Influence of APOA5 locus on the treatment efficacy of three statins : Evidence from a randomized pilot study in Chinese subjects
  • 2018
  • Ingår i: Frontiers in Pharmacology. - : Frontiers Media SA. - 1663-9812. ; 9:APR
  • Tidskriftsartikel (refereegranskat)abstract
    • Pharmacogenetics or pharmacogenomics approaches are important for addressing the individual variabilities of drug efficacy especially in the era of precision medicine. One particular interesting gene to investigate is APOA5, which has been repeatedly linked with the inter-individual variations of serum triglycerides. Here, we explored APOA5-statin interactions in 195 Chinese subjects randomized to rosuvastatin (5-10 mg/day), atorvastatin (10-20 mg/day), or simvastatin (40 mg/day) for 12 weeks by performing a targeted genotyping analysis of the APOA5 promoter SNP rs662799 (-1131T > C). There were no significant differences between the treatment arms for any of the statin-induced changes in clinical biomarkers. Reductions in LDL cholesterol were influenced by the APOA5 genotype in all three treatment groups. By contrast, changes in HDL cholesterol, and triglycerides were only affected by the APOA5 genotype in the atorvastatin and simvastatin groups and not in the rosuvastatin group. Our results suggest that future studies may need to consider stratifying subjects not only by genetic background but also by prescribed statin type.
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7.
  • Jiang, Jingting, et al. (författare)
  • Expression of apolipoprotein M in human hepatocellular carcinoma tissues
  • 2011
  • Ingår i: Acta Histochemica. - : Elsevier BV. - 0065-1281. ; 113:1, s. 53-57
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study examined mRNA levels and protein mass of apolipoprotein M (apoM) in human hepatocellular carcinoma (HCC) tissues and in the adjacent tissues. Plasma apoM levels in these HCC patients were also determined and compared to the normal subjects. The mean level of plasma apoM in the HCC patients was 0.61 +/- 0.30 OD mm(-2), which was significantly higher than that in the normal subjects 0.37 +/- 0.07 OD mm(-2) (P < 0.01). However, both apoM mRNA levels and apoM protein mass in the HCC tissues were significantly lower than in the adjacent tissues (P < 0.05). It is concluded that human hepatocellular carcinoma tissues had a reduced capacity to produce apoM than the adjacent non-tumor tissues. However, the plasma apoM levels were higher in the HCC patients than in normal subjects, which suggested that tissues adjacent to the tumors or extra-hepatic apoM production in the HCC patients may contribute to the higher plasma apoM levels in these patients. The clinical significance of apoM in relation to HCC still needs further investigation. (C) 2009 Published by Elsevier GmbH.
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8.
  • 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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9.
  • 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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10.
  • Luo, Guanghua, et al. (författare)
  • Apolipoprotein M : Research Progress and Clinical Perspective
  • 2020
  • Ingår i: Advances in Experimental Medicine and Biology. - Singapore : Springer Singapore. - 0065-2598. ; 1276, s. 85-103
  • Tidskriftsartikel (refereegranskat)abstract
    • Apolipoprotein M (apoM) was first identified and characterized to the apolipoprotein family in 1999. Human apoM gene is located in a highly conserved segment in the major histocompatibility complex (MHC) class III locus on chromosome 6 and codes for an about 23 kDa protein that structurally belongs to the lipocalin superfamily. ApoM is selectively expressed in hepatocytes and in the tubular epithelium of kidney. In human plasma, apoM is mainly confined to the high-density lipoprotein (HDL) particles, but it may also occur in other lipoprotein classes, such as in the triglyceride-rich particles after fat intake. It has been demonstrated that apoM is critical for the formation of HDL, notably pre-beta HDL1. The antiatherogenic function of HDL is well established, and its ability to promote cholesterol efflux from foam cells in the atherosclerotic lesions is generally regarded as one of the key mechanisms behind this protective function. However, HDL could also display a variety of properties that may affect the complex atherosclerotic processes by other mechanisms, thus being involved in processes related to antioxidant defense, immune system, and systemic effects in septicemia, which may be partly contributed via its apolipoproteins and/or phospholipids. Moreover, it has been demonstrated that apoM functions as a natural carrier of sphingosin-1-phosphate (S1P) in vivo which may be related to its antiatherosclerotic and protective effects on endothelial cell barrier and anti-inflammatory properties. These may also provide a link between the diverse effects of HDL.
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