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Articles by A Long
Total Records ( 5 ) for A Long
  C. L Shields , M Furuta , A Thangappan , S Nagori , A Mashayekhi , D. R Lally , C. C Kelly , D. S Rudich , A. V Nagori , O. A Wakade , S Mehta , L Forte , A Long , E. F Dellacava , B Kaplan and J. A. Shields
 

Objective  To determine the rate of metastasis of uveal melanoma on the basis of tumor thickness in millimeters.

Methods  Retrospective medical record review.

Results  The mean (median) patient age was 58 (59) years. A total of 8033 eyes were examined. Of the 285 eyes with iris melanoma, the mean tumor thickness was 2.7 mm and metastasis occurred in 0.5%, 4%, and 7% at 3, 5, and 10 years, respectively. Of the 492 eyes with ciliary body melanoma, the mean tumor thickness was 6.6 mm and metastasis occurred in 12%, 19%, and 33% at 3, 5, and 10 years, respectively. Of the 7256 eyes with choroidal melanoma, the mean tumor thickness was 5.5 mm and metastasis occurred in 8%, 15%, and 25% at 3, 5, and 10 years, respectively. For all uveal melanoma, metastasis at 5, 10, and 20 years was 6%, 12%, and 20% for small melanoma (0-3.0 mm thickness), 14%, 26%, and 37% for medium melanoma (3.1-8.0 mm), and 35%, 49%, and 67% for large melanoma (>8.0 mm). More specifically, metastasis per millimeter increment at 10 years was 6% (0-1.0 mm thickness), 12% (1.1-2.0 mm), 12% (2.1-3.0 mm), 16% (3.1-4.0 mm), 27% (4.1-5.0 mm), 28% (5.1-6.0 mm), 29% (6.1-7.0 mm), 41% (7.1-8.0 mm), 50% (8.1-9.0 mm), 44% (9.1-10.0 mm), and 51% (>10.0 mm). Clinical factors predictive of metastasis by multivariate analysis included increasing patient age, ciliary body location, increasing tumor diameter, increasing tumor thickness, having a brown tumor, and the presence of subretinal fluid, intraocular hemorrhage, or extraocular extension.

Conclusion  Increasing millimeter thickness of uveal melanoma is associated with increasing risk for metastasis.

  T Guiraud , L Leger , A Long , N Thebault , J Tremblay and P. Passelergue
  Background and aims

The validity of five brands of cycle ergometers was evaluated by the comparison of the Vo2 requirements at different displayed power.

Methods and results

Five physically active men performed a continuous incremental exercise test on five ergometers (Ergomeca, Lifecycle, Monark, Polar S710 and CompuTrainer). The latter was also compared with a standard dynamometer in order to associate Vo2 values with the real power. Every test started with a 5-min warm-up on the same cycle ergometer (Ergomeca) at 100 W to make sure that the Vo2 differences do not come from Vo2 measurement error. Only last minute steady-state Vo2 values of each 2-min stage were used for the Vo2–watt curve. Large differences (5– 10 ml kg–1 min–1) at the same displayed power indicate inaccuracy of displayed power output (PO). Using corrected power values from the dynamometer revealed that for the same Vo2 the CompuTrainer underestimates PO by ~30 W between 100 and 300 W, whereas the Lifecycle overestimate it by 3–53 W from 100 to 300 W. The Monark and Polar S710 underestimate PO by 15 W and the Ergomeca by ~5 W.

Conclusion

Inaccuracies between –10% and 18% in displayed PO of various cycle ergometers question their interchangeability.

  S. P Duggan , F. M Behan , M Kirca , S Smith , J. V Reynolds , A Long and D. Kelleher
 

Reflux of gastroduodenal contents and consequent inflammatory responses are associated with the development of Barrett's oesophagus (BO) and the promotion of oesophageal adenocarcinoma (OAC). Deregulation of inflammatory processes is a hallmark of oesophageal cancer. In this study, we aimed to investigate (i) the transcriptional responses to deoxycholic acid (DCA) in cell lines representative of either end of the oesophageal cancer sequence, (ii) the expression of DCA-regulated genes in data charting oesophageal carcinogenesis and (iii) the impact of these genes on oesophageal inflammatory signalling. Gene expression microarrays were utilized to demonstrate differential transcriptional responses between squamous (HET-1A) and adenomatous (SKGT4) cell lines exposed to DCA. Differential basal and DCA-inducible expression of cytokines such as interleukin (IL) 8 was observed between both cell types. A cohort of DCA-regulated genes specific to each cell type was identified in microarray experimentation and subsequently validated. Cell type-specific genes included TRB3, CXCL14, GDF15 and LIF in HET-1A cells, with COX2-, ESM1-, URHF1- and IL1-and IL1β-specific expression in SKGT4 cells. Over 30% of the genes altered in BO and OAC were shown to be regulated by DCA utilizing an integrative genomic approach. One such gene, tribbles-homology-3 (TRB3) was induced specifically in HET-1A cells, absent in SKGT4 cells and decreased in BO samples in silico and in vivo. Inhibition and re-introduction of TRB3 in HET-1A and SKGT4 cells, respectively, demonstrated the ability of TRB3 to regulate inflammatory signalling through nuclear factor-kappaB. This study identifies mechanisms through which bile acids such as DCA, in conjunction with the loss of key signalling molecules, could regulate oesophageal metaplasticity.

 
 
 
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