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Articles by F Liu
Total Records ( 13 ) for F Liu
  Y Peng , H Li , M Wu , X Wang , S Fan , F Liu , B Xiang , Q Guo , X Tang and S. Shen
 

Colorectal cancer (CRC) is a common malignant tumor that is associated with an increased incidence of morbidity and mortality. Nasopharyngeal carcinoma-associated gene 6 (NGX6) is a novel candidate suppressor gene of tumor metastasis, which is down-regulated in CRC. In the present study, we constructed a colorectal tissue microarray to examine the expression profiles of NGX6, phospho-c-Jun N-terminal kinase (p-JNK), and phospho-extracellular signal-regulated kinase (p-ERK ) in CRC tissues. We found that the NGX6 expression was lower in CRC tissues and metastatic lymph nodes, whereas the expressions of p-JNK and p-ERK were higher in CRC tissues, than in normal intestinal mucosa. The expressions of NGX6, p-JNK, and p-ERK were associated with the clinical pathological features of colorectal tissues. NGX6 overexpression inhibited the activation and nuclear translocation of JNK1, which led to an accumulation of p-JNK in the cytoplasm, but did not inhibit the activation and nuclear translocation of ERK1/2. NGX6 also inhibited the expression of the transcription factors AP-1 (c-jun and c-fos) and Ets-1. In addition, NGX6 overexpression decreased the expression of cyclin D1 and dramatically suppressed the transcriptional efficiency of the cyclin D1 promoter. We propose that NGX6 expression is lost in the multi-step process of human colorectal carcinogenesis. Its overexpression can inhibit the expression of transcription factors AP-1 and Ets-1, and down-regulate the transcriptional activity of the cyclin D1 promoter in human CRC.

  Z Zhang , Q Li , F Liu , Y Sun and J. Zhang
 

The aim of this study was to investigate the prevention of diet-induced obesity by a high safflower oil diet and adipocytic gene expression in mice. Forty 3-week-old C57BL/6 mice were randomly divided into three groups: control group (CON, 5% lard + 5% safflower oil), high lard group (LAR, 45% lard + 5% safflower oil), and high safflower oil group (SAF, 45% safflower oil + 5% lard). After 10 weeks, 10 mice of the LAR group were switched to high safflower oil diet (LAR–SAF). Ten weeks later, glucose tolerance tests were performed by intraperitoneal injection of glucose. Circulating levels of lipid and insulin were measured and white adipose tissues were taken for gene chip and reverse transcriptase–polymerase chain reaction analysis. The LAR group showed higher body weight, adiposity index, insulin, and lipids than the CON group (P < 0.05). The body weight in the LAR–SAF group decreased after dietary reversal. The plasma biochemical profiles decreased in the LAR–SAF and SAF groups (P < 0.05) compared with those of the LAR group. The blood glucose level of the LAR–SAF group was reduced during intraperitoneal glucose tolerance test compared with that of the LAR group. The LAR–SAF group had lower levels of Orexin and Ghrelin gene expression, whereas the level of PPAR gene expression was significantly enhanced compared with that of the LAR group. So, the SAF diet can alter adipocytic adiposity-related gene expression and result in effective amelioration of diet-induced obesity.

  D Martinez , K Greene , A Broft , D Kumar , F Liu , R Narendran , M Slifstein , R Van Heertum and H. D. Kleber
 

OBJECTIVE: Previous positron emission tomography (PET) imaging studies have demonstrated that cocaine dependence is associated with a decrease in dopamine type 2 and 3 (D2/D3) receptor binding in cocaine-dependent individuals relative to healthy comparison subjects. However, given the nature of PET imaging, it is possible that the measured decrease in radiotracer binding results from an increase in baseline dopamine levels. The purpose of this study was to measure D2/D3 receptors following acute dopamine depletion in cocaine-dependent volunteers relative to healthy comparison subjects. METHOD: Cocaine-dependent volunteers (N=15) and healthy matched comparison subjects (N=15) were scanned using PET, with the dopamine receptor radiotracer [11C]raclopride, at baseline and again following acute depletion of endogenous dopamine via alpha-methyl-para-tyrosine (AMPT) administration. Changes in radiotracer binding were measured in the subdivisions of the striatum (caudate, putamen, and ventral striatum) in addition to the striatum as a whole. RESULTS: Findings revealed that cocaine-dependent volunteers exhibited lower levels of endogenous dopamine relative to comparison subjects, which was measured as an increase in [11C]raclopride binding following AMPT administration. The increase in [11C]raclopride binding in the striatum was 11.1% (SD=4.4%) in healthy comparison subjects and 5.7% (SD=5.9%) in cocaine-dependent volunteers. Similar differences were seen in the subdivisions of the striatum. CONCLUSIONS: The decrease in striatal D2/D3 receptors associated with cocaine dependence cannot be attributed to higher levels of endogenous dopamine.

  F Liu , J Li , D. M Wang , J. C Liu and Y. N. Huang
 

We investigated serial changes of circulation platelet activation markers in 40 patients undergoing carotid artery stenting under the protection of dual antiplatelet therapy and filter devices. Monocyte-platelet aggregates and PAC-1 (a marker specific for activated glycoprotein IIb/IIIa) analyzed by flow cytometry were determined in patients with symptomatic stenosis undergoing elective carotid artery stenting. Blood samples were obtained immediately before stent implantation and 0.5 hours, 18 hours, and 6 days after the procedure, respectively. All patients were already on dual antiplatelet therapy of aspirin and clopidogrel before carotid artery stenting, and all were stented with embolic protection devices. Both circulation monocyte-platelet aggregates and PAC-1 did not change significantly at the various time points after the procedure. Serial changes of monocyte-platelet aggregates and PAC-1 analyzed by flow cytometry fail to indicate the occurrence of platelet activation after carotid artery stenting under the treatment with dual antiplatelet therapy before carotid artery stenting and the application of embolic protection devices during the procedure.

  F Liu , J Shi , H Tanimukai , J Gu , I Grundke Iqbal , K Iqbal and C. X. Gong
 

It has been established for a long time that brain glucose metabolism is impaired in Alzheimer's disease. Recent studies have demonstrated that impaired brain glucose metabolism precedes the appearance of clinical symptoms, implying its active role in the development of Alzheimer's disease. However, the molecular mechanism by which this impairment contributes to the disease is not known. In this study, we demonstrated that protein O-GlcNAcylation, a common post-translational modification of nucleocytoplasmic proteins with β-N-acetyl-glucosamine and a process regulated by glucose metabolism, was markedly decreased in Alzheimer's disease cerebrum. More importantly, the decrease in O-GlcNAc correlated negatively with phosphorylation at most phosphorylation sites of tau protein, which is known to play a crucial role in the neurofibrillary degeneration of Alzheimer's disease. We also found that hyperphosphorylated tau contained 4-fold less O-GlcNAc than non-hyperphosphorylated tau, demonstrating for the first time an inverse relationship between O-GlcNAcylation and phosphorylation of tau in the human brain. Downregulation of O-GlcNAcylation by knockdown of O-GlcNAc transferase with small hairpin RNA led to increased phosphorylation of tau in HEK-293 cells. Inhibition of the hexosamine biosynthesis pathway in rat brain resulted in decreased O-GlcNAcylation and increased phosphorylation of tau, which resembled changes of O-GlcNAcylation and phosphorylation of tau in rodent brains with decreased glucose metabolism induced by fasting, but not those in rat brains when protein phosphatase 2A was inhibited. Comparison of tau phosphorylation patterns under various conditions suggests that abnormal tau hyperphosphorylation in Alzheimer's disease brain may result from downregulation of both O-GlcNAcylation and protein phosphatase 2A. These findings suggest that impaired brain glucose metabolism leads to abnormal hyperphosphorylation of tau and neurofibrillary degeneration via downregulation of tau O-GlcNAcylation in Alzheimer's disease. Thus, restoration of brain tau O-GlcNAcylation and protein phosphatase 2A activity may offer promising therapeutic targets for treating Alzheimer's disease.

  Y Wu , X Feng , Y Jin , Z Wu , W Hankey , C Paisie , L Li , F Liu , S. H Barsky , W Zhang , R Ganju and X. Zou
 

The natural compound indole-3-carbinol (I3C; found in vegetables of the genus Brassica) is a promising cancer prevention or therapy agent. The cell division cycle 25A (Cdc25A) phosphatase is overexpressed in a variety of human cancers and other diseases. In the present study, I3C induced degradation of Cdc25A, arrest of the G1 cell cycle, and inhibition of the growth of breast cancer cells. We also showed that the Ser124 site of Cdc25A, which is related to cyclin-dependent kinase 2, is required for I3C-induced degradation of Cdc25A in breast cancer cells, and that interruption of the ATM-Chk2 pathway suppressed I3C-induced destruction of Cdc25A. Our in vivo studies of different mutated forms of Cdc25A found that the mutation Cdc25AS124A (Ser124 to Ala124), which confers resistance to I3C-induced degradation of Cdc25A, attenuated I3C inhibition of breast tumorigenesis in a mouse xenograft model. The present in vitro and in vivo studies together show that I3C-induced activation of the ATM-Chk2 pathway and degradation of Cdc25A represent a novel molecular mechanism of I3C in arresting the G1 cell cycle and inhibiting the growth of breast cancer cells. The finding that I3C induces Cdc25A degradation underscores the potential use of this agent for preventing and treating cancers and other human diseases with Cdc25A overexpression. Cancer Prev Res; 3(7); 818–28. ©2010 AACR.

  G Fan , Y Fan , N Gupta , I Matsuura , F Liu , X. Z Zhou , K. P Lu and C. Gelinas
 

The peptidyl-prolyl isomerase Pin1 is frequently up-regulated in human cancers in which Rel/nuclear factor-B (NF-B) is constitutively activated, but its role in these cancers remains to be determined, and evidence is still lacking to show that Pin1 contributes to cell transformation by Rel/NF-B. Rel/NF-B transcriptional and oncogenic activities are modulated by several posttranslational modifications and coregulatory proteins, and previous studies showed that cytokine treatment induces binding of Pin1 to the RelA subunit of NF-B, thereby enhancing RelA nuclear localization and stability. Here we show that Pin1 associates with the Rel subunits of NF-B that are implicated in leukemia/lymphomagenesis and modulates their transcriptional and oncogenic activities. Pin1 markedly enhanced transformation of primary lymphocytes by the human c-Rel protein and also increased cell transformation by the potent viral Rel/NF-B oncoprotein v-Rel, in contrast to a Pin1 mutant in the WW domain involved in interaction with NF-B. Pin1 promoted nuclear accumulation of Rel proteins in the absence of activating stimuli. Importantly, inhibition of Pin1 function with the pharmacologic inhibitor juglone or with Pin1-specific shRNA led to cytoplasmic relocalization of endogenous c-Rel in human lymphoma-derived cell lines, markedly interfered with lymphoma cell proliferation, and suppressed endogenous Rel/NF-B–dependent gene expression. Together, these results show that Pin1 is an important regulator of Rel/NF-B transforming activity and suggest that Pin1 may be a potential therapeutic target in Rel/NF-B–dependent leukemia/lymphomas. [Cancer Res 2009;69(11):4589–97]

  F Liu , C Wu and X. Lin
 

Droste [CRYPTO’96] proposed a construction of threshold visual cryptography scheme (TVCS) under the visual cryptography model of Naor and Shamir, i.e. the visual cryptography model with the underlying operation OR. In this article, we give three extensions of TVCS. First, we prove that the TVCS proposed by Droste which was based on the OR operation is still a valid TVCS under the XOR operation, and then we propose a method to further reduce its pixel expansion. We then propose an interesting construction of TVCS with all shares being concolorous. Finally, we give a construction of threshold extended visual cryptography scheme (TEVCS) with the underlying operation OR or XOR. All of our schemes can be applied to the visual cryptography model introduced by Tuyls et al. (First Int. Conf. Security in Pervasive Computing 2004, International Patent with Application No.: PCT/IB2003/000261).

  L. J Su , P. K Auluck , T. F Outeiro , E Yeger Lotem , J. A Kritzer , D. F Tardiff , K. E Strathearn , F Liu , S Cao , S Hamamichi , K. J Hill , K. A Caldwell , G. W Bell , E Fraenkel , A. A Cooper , G. A Caldwell , J. M McCaffery , J. C Rochet and S. Lindquist
  Linhui Julie Su, Pavan K. Auluck, Tiago Fleming Outeiro, Esti Yeger-Lotem, Joshua A. Kritzer, Daniel F. Tardiff, Katherine E. Strathearn, Fang Liu, Songsong Cao, Shusei Hamamichi, Kathryn J. Hill, Kim A. Caldwell, George W. Bell, Ernest Fraenkel, Antony A. Cooper, Guy A. Caldwell, J. Michael McCaffery, Jean-Christophe Rochet, and Susan Lindquist

-Synuclein (-syn) is a small lipid-binding protein involved in vesicle trafficking whose function is poorly characterized. It is of great interest to human biology and medicine because -syn dysfunction is associated with several neurodegenerative disorders, including Parkinson’s disease (PD). We previously created a yeast model of -syn pathobiology, which established vesicle trafficking as a process that is particularly sensitive to -syn expression. We also uncovered a core group of proteins with diverse activities related to -syn toxicity that is conserved from yeast to mammalian neurons. Here, we report that a yeast strain expressing a somewhat higher level of -syn also exhibits strong defects in mitochondrial function. Unlike our previous strain, genetic suppression of endoplasmic reticulum (ER)-to-Golgi trafficking alone does not suppress -syn toxicity in this strain. In an effort to identify individual compounds that could simultaneously rescue these apparently disparate pathological effects of -syn, we screened a library of 115,000 compounds. We identified a class of small molecules that reduced -syn toxicity at micromolar concentrations in this higher toxicity strain. These compounds reduced the formation of -syn foci, re-established ER-to-Golgi trafficking and ameliorated -syn-mediated damage to mitochondria. They also corrected the toxicity of -syn in nematode neurons and in primary rat neuronal midbrain cultures. Remarkably, the compounds also protected neurons against rotenone-induced toxicity, which has been used to model the mitochondrial defects associated with PD in humans. That single compounds are capable of rescuing the diverse toxicities of -syn in yeast and neurons suggests that they are acting on deeply rooted biological processes that connect these toxicities and have been conserved for a billion years of eukaryotic evolution. Thus, it seems possible to develop novel therapeutic strategies to simultaneously target the multiple pathological features of PD.

  Y Zhang , S Li , L Yuan , Y Tian , J Weidenfeld , J Yang , F Liu , A. L Chokas and E. E. Morrisey
 

Cardiomyocyte proliferation is high in early development and decreases progressively with gestation, resulting in the lack of a robust cardiomyocyte proliferative response in the adult heart after injury. Little is understood about how both cell-autonomous and nonautonomous signals are integrated to regulate the balance of cardiomyocyte proliferation during development. In this study, we show that a single transcription factor, Foxp1, can control the balance of cardiomyocyte proliferation during development by targeting different pathways in the endocardium and myocardium. Endocardial loss of Foxp1 results in decreased Fgf3/Fgf16/Fgf17/Fgf20 expression in the heart, leading to reduced cardiomyocyte proliferation. This loss of myocardial proliferation can be rescued by exogenous Fgf20, and is mediated, in part, by Foxp1 repression of Sox17. In contrast, myocardial-specific loss of Foxp1 results in increased cardiomyocyte proliferation and decreased differentiation, leading to increased myocardial mass and neonatal demise. We show that Nkx2.5 is a direct target of Foxp1 repression, and Nkx2.5 expression is increased in Foxp1-deficient myocardium. Moreover, transgenic overexpression of Nkx2.5 leads to increased cardiomyocyte proliferation and increased ventricular mass, similar to the myocardial-specific loss of Foxp1. These data show that Foxp1 coordinates the balance of cardiomyocyte proliferation and differentiation through cell lineage-specific regulation of Fgf ligand and Nkx2.5 expression.

  F Liu , N Madden , M Stynes and A. Zhou
 

The linear reaction–diffusion problem – 2u + bu = f is considered on the unit square with homogeneous Dirichlet boundary conditions. Here is a small positive parameter and the problem is in general singularly perturbed. The numerical solution of this problem is analysed on a Shishkin mesh that has N intervals in each coordinate direction, using the Galerkin finite-element method with bilinear trial functions. The accuracy of this method, measured in the associated energy norm, is shown to be O(N–2 + 1/2N–1 ln N). It is proved that a two-scale sparse grid method achieves the same order of accuracy while reducing the number of degrees of freedom from O(N2) to O(N3/2). These results are then generalized to systems of reaction–diffusion equations.

  M Majewski , P. E Ochsner , F Liu , R Fluckiger and C. H. Evans
  Background

Despite advances in the treatment of ruptured Achilles tendon, imperfections of endogenous repair often leave patients symptomatic. Local administration of autologous conditioned serum (ACS) in patients with inflammatory, degenerative conditions has shown beneficial effects.

Purpose

Because ACS also contains growth factors that should accelerate tendon healing, we studied the effect of ACS on the healing of transected rat Achilles tendon.

Study Design

Controlled laboratory study.

Methods

In preliminary in vitro experiments, rat tendons were incubated with ACS and the effect on the expression of Col1A1 and Col3A1 was assessed by real-time quantitative polymerase chain reaction. To test its effect in vivo, the Achilles tendons of 80 Sprague Dawley rats were transected and sutured back together. Ten rats from each group (ACS group, n = 40; control group, n = 40) were euthanized at 1, 2, 4, and 8 weeks postoperatively for biomechanical (n = 7) and histologic (n = 3) testing. Lysyl oxidase activity was assayed by a flurometric assay. The organization of repair tissue was assessed histologically with hematoxylin and eosin- and with Sirius red-stained sections, and with immunohistochemistry.

Results

Tendons exposed to ACS in vitro showed a greatly enhanced expression of the Col1A1 gene. The ACS-treated tendons were thicker, had more type I collagen, and an accelerated recovery of tendon stiffness and histologic maturity of the repair tissue. However, there were no differences in the maximum load to failure between groups up to week 8, perhaps because lysyl oxidase activities were unchanged.

Conclusion and Clinical Relevance

Overall, our study demonstrates that treatment with ACS has the potential to improve Achilles tendon healing and should be considered as a treatment modality in man. However, as strength was not shown to be increased within the parameters of this study, the clinical importance of the observed changes in humans still needs to be defined.

  F Liu , J. D Mih , B. S Shea , A. T Kho , A. S Sharif , A. M Tager and D. J. Tschumperlin
 

In response to tissue stiffening, fibroblasts increase production of extracellular matrix while decreasing production of matrix-degrading enzymes and the fibrosis inhibitor prostaglandin E2.

 
 
 
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