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Articles by A Liu
Total Records ( 5 ) for A Liu
  A Liu , T Bui , H Van Nguyen , B Ong , Q Shen and D. Kamalasena
 

Background: although C-reactive protein (CRP) is widely used in younger populations, its value for diagnosing bacterial infection in older population is not well established. This study examined the usefulness of serum CRP level in the early detection of bacterial infection in older patients.

Methods: in a prospective cohort study, consecutive patients aged 70 years or over admitted to Aged Care wards were recruited. CRP levels were measured within 24 h of presentation, and their significance in predicting bacterial infections was analysed. The relationship between CRP and other clinical features of diagnosing bacterial infections (e.g. temperature, white cell count, neutrophil count, oxygen saturation, blood pressure and heart rate) was also examined.

Results: a total of 232 patients were recruited over a period of 3 months. CRP levels were 21.3 ± 36.0 and 150.5 ± 114.1 mg/l (mean ± SD) in the non-infection and infection groups, respectively (P < 0.001). We found that the CRP cut-off value of 60 mg/l had the best combination of sensitivity and specificity. At this level, the sensitivity of diagnosing bacterial infection was 80.7%, specificity 96.0%, positive predictive value 91.9% and negative predictive value 89.8%. CRP and temperature had higher sensitivity and specificity than white cell count and neutrophil count in the diagnosis of infection. For every 1-mg/l increment in CRP, the risk of bacterial infection increases by 2.9%.

Conclusion: CRP is a convenient and useful biomarker to predict early bacterial infection in older patients especially when other markers are atypical or not present.

  G Lu , H Xiao , G. X Li , S. C Picinich , Y. K Chen , A Liu , M. J Lee , S Loy and C. S. Yang
 

The present study investigated the effects of a preparation of a -tocopherol-rich mixture of tocopherols (-TmT) on chemically induced lung tumorigenesis in female A/J mice and the growth of H1299 human lung cancer cell xenograft tumors. In the A/J mouse model, the lung tumors were induced by either 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; intraperitoneal injections with 100 and 75 mg/kg on Week 1 and 2, respectively) or NNK plus benzo[a]pyrene (B[a]P) (8 weekly gavages of 2 µmole each from Week 1 to 8). The NNK plus B[a]P treatment induced 21 tumors per lung on Week 19; dietary 0.3% -TmT treatment during the entire experimental period significantly lowered tumor multiplicity, tumor volume and tumor burden (by 30, 50 and 55%, respectively; P < 0.05). For three groups of mice treated with NNK alone, the -TmT diet was given during the initiation stage (Week 0 to 3), post-initiation stage (Week 3 to 19) or the entire experimental period, and the tumor multiplicity was reduced by 17.8, 19.7 or 29.3%, respectively (P < 0.05). -TmT treatment during the tumor initiation stage or throughout the entire period of the experiment also significantly reduced tumor burden (by 36 or 43%, respectively). In the xenograft tumor model of human lung cancer H1299 cells in NCr-nu/nu mice, 0.3% dietary -TmT treatment significantly reduced tumor volume and tumor weight by 56 and 47%, respectively (P < 0.05). In both the carcinogenesis and tumor growth models, the inhibitory action of -TmT was associated with enhanced apoptosis and lowered levels of 8-hydroxydeoxyguanine, -H2AX and nitrotyrosine in the tumors of the -TmT-treated mice. In cell culture, the growth of H1299 cells was inhibited by tocopherols with their effectiveness following the order of -T > -TmT > -T, whereas -T was not effective. These results demonstrate the inhibitory effect of -TmT against lung tumorigenesis and the growth of xenograft tumors of human lung cancer cells. The inhibitory activity may be due mainly to the actions of -T and -T.

  S Mangos , P. y Lam , A Zhao , Y Liu , S Mudumana , A Vasilyev , A Liu and I. A. Drummond
  Steve Mangos, Pui-ying Lam, Angela Zhao, Yan Liu, Sudha Mudumana, Aleksandr Vasilyev, Aiping Liu, and Iain A. Drummond

Mutations in polycystin1 (PKD1) account for the majority of autosomal dominant polycystic kidney disease (ADPKD). PKD1 mutations are also associated with vascular aneurysm and abdominal wall hernia, suggesting a role for polycystin1 in extracellular matrix (ECM) integrity. In zebrafish, combined knockdown of the PKD1 paralogs pkd1a and pkd1b resulted in dorsal axis curvature, hydrocephalus, cartilage and craniofacial defects, and pronephric cyst formation at low frequency (10–15%). Dorsal axis curvature was identical to the axis defects observed in pkd2 knockdown embryos. Combined pkd1a/b, pkd2 knockdown demonstrated that these genes interact in axial morphogenesis. Dorsal axis curvature was linked to notochord collagen overexpression and could be reversed by knockdown of col2a1 mRNA or chemical inhibition of collagen crosslinking. pkd1a/b- and pkd2-deficient embryos exhibited ectopic, persistent expression of multiple collagen mRNAs, suggesting a loss of negative feedback signaling that normally limits collagen gene expression. Knockdown of pkd1a/b also dramatically sensitized embryos to low doses of collagen-crosslinking inhibitors, implicating polycystins directly in the modulation of collagen expression or assembly. Embryos treated with wortmannin or LY-29400 also exhibited dysregulation of col2a1 expression, implicating phosphoinositide 3-kinase (PI3K) in the negative feedback signaling pathway controlling matrix gene expression. Our results suggest that pkd1a/b and pkd2 interact to regulate ECM secretion or assembly, and that altered matrix integrity may be a primary defect underlying ADPKD tissue pathologies.

  A Liu , A. D Patterson , Z Yang , X Zhang , W Liu , F Qiu , H Sun , K. W Krausz , J. R Idle , F. J Gonzalez and R. Dai
 

Fenofibrate, widely used for the treatment of dyslipidemia, activates the nuclear receptor, peroxisome proliferator-activated receptor . However, liver toxicity, including liver cancer, occurs in rodents treated with fibrate drugs. Marked species differences occur in response to fibrate drugs, especially between rodents and humans, the latter of which are resistant to fibrate-induced cancer. Fenofibrate metabolism, which also shows species differences, has not been fully determined in humans and surrogate primates. In the present study, the metabolism of fenofibrate was investigated in cynomolgus monkeys by ultraperformance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOFMS)-based metabolomics. Urine samples were collected before and after oral doses of fenofibrate. The samples were analyzed in both positive-ion and negative-ion modes by UPLC-QTOFMS, and after data deconvolution, the resulting data matrices were subjected to multivariate data analysis. Pattern recognition was performed on the retention time, mass/charge ratio, and other metabolite-related variables. Synthesized or purchased authentic compounds were used for metabolite identification and structure elucidation by liquid chromatographytandem mass spectrometry. Several metabolites were identified, including fenofibric acid, reduced fenofibric acid, fenofibric acid ester glucuronide, reduced fenofibric acid ester glucuronide, and compound X. Another two metabolites (compound B and compound AR), not previously reported in other species, were characterized in cynomolgus monkeys. More importantly, previously unknown metabolites, fenofibric acid taurine conjugate and reduced fenofibric acid taurine conjugate were identified, revealing a previously unrecognized conjugation pathway for fenofibrate.

  A Liu , A. D Patterson , Z Yang , X Zhang , W Liu , F Qiu , H Sun , K. W Krausz , J. R Idle , F. J Gonzalez and R. Dai
 

Fenofibrate, widely used for the treatment of dyslipidemia, activates the nuclear receptor, peroxisome proliferator-activated receptor . However, liver toxicity, including liver cancer, occurs in rodents treated with fibrate drugs. Marked species differences occur in response to fibrate drugs, especially between rodents and humans, the latter of which are resistant to fibrate-induced cancer. Fenofibrate metabolism, which also shows species differences, has not been fully determined in humans and surrogate primates. In the present study, the metabolism of fenofibrate was investigated in cynomolgus monkeys by ultraperformance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOFMS)-based metabolomics. Urine samples were collected before and after oral doses of fenofibrate. The samples were analyzed in both positive-ion and negative-ion modes by UPLC-QTOFMS, and after data deconvolution, the resulting data matrices were subjected to multivariate data analysis. Pattern recognition was performed on the retention time, mass/charge ratio, and other metabolite-related variables. Synthesized or purchased authentic compounds were used for metabolite identification and structure elucidation by liquid chromatographytandem mass spectrometry. Several metabolites were identified, including fenofibric acid, reduced fenofibric acid, fenofibric acid ester glucuronide, reduced fenofibric acid ester glucuronide, and compound X. Another two metabolites (compound B and compound AR), not previously reported in other species, were characterized in cynomolgus monkeys. More importantly, previously unknown metabolites, fenofibric acid taurine conjugate and reduced fenofibric acid taurine conjugate were identified, revealing a previously unrecognized conjugation pathway for fenofibrate.

 
 
 
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