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Breast Cancer Survival at a Leading Cancer Centre in Malaysia
Abdullah, Matin Mellor,Mohamed, Ahmad Kamal,Foo, Yoke Ching,Lee, Catherine May Ling,Chua, Chin Teong,Wu, Chin Huei,Hoo, LP,Lim, Teck Onn,Yen, Sze Whey Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.18
Background: GLOBOCAN12 recently reported high cancer mortality in Malaysia suggesting its cancer health services are under-performing. Cancer survival is a key index of the overall effectiveness of health services in the management of patients. This report focuses on Subang Jaya Medical Centre (SJMC) care performance as measured by patient survival outcome for up to 5 years. Materials and Methods: All women with breast cancer treated at SJMC between 2008 and 2012 were enrolled for this observational cohort study. Mortality outcome was ascertained through record linkage with national death register, linkage with hospital registration system and finally through direct contact by phone or home visits. Results: A total of 675 patients treated between 2008 and 2012 were included in the present survival analysis, 65% with early breast cancer, 20% with locally advanced breast cancer (LABC) and 4% with metastatic breast cancer (MBC). The overall relative survival (RS) at 5 years was 88%. RS for stage I was 100% and for stage II, III and IV disease was 95%, 69% and 36% respectively. Conclusions: SJMC is among the first hospitals in Malaysia to embark on routine measurement of the performance of its cancer care services and its results are comparable to any leading centers in developed countries.
The Forbidden Number of a Knot
CRANS, ALISSA S.,MELLOR, BLAKE,GANZELL, SANDY Department of Mathematics 2015 Kyungpook mathematical journal Vol.55 No.2
Every classical or virtual knot is equivalent to the unknot via a sequence of extended Reidemeister moves and the so-called forbidden moves. The minimum number of forbidden moves necessary to unknot a given knot is an invariant we call the forbidden number. We relate the forbidden number to several known invariants, and calculate bounds for some classes of virtual knots.
In Silico Prediction of Organ Level Toxicity: Linking Chemistry to Adverse Effects
Cronin, Mark T.D.,Enoch, Steven J.,Mellor, Claire L.,Przybylak, Katarzyna R.,Richarz, Andrea-Nicole,Madden, Judith C. Korean Society of ToxicologyKorea Environmental Mu 2017 Toxicological Research Vol.33 No.3
In silico methods to predict toxicity include the use of (Quantitative) Structure-Activity Relationships ((Q)SARs) as well as grouping (category formation) allowing for read-across. A challenging area for in silico modelling is the prediction of chronic toxicity and the No Observed (Adverse) Effect Level (NO(A)EL) in particular. A proposed solution to the prediction of chronic toxicity is to consider organ level effects, as opposed to modelling the NO(A)EL itself. This review has focussed on the use of structural alerts to identify potential liver toxicants. In silico profilers, or groups of structural alerts, have been developed based on mechanisms of action and informed by current knowledge of Adverse Outcome Pathways. These profilers are robust and can be coded computationally to allow for prediction. However, they do not cover all mechanisms or modes of liver toxicity and recommendations for the improvement of these approaches are given.
In Silico Prediction of Organ Level Toxicity
Mark T.D. Cronin,Steven J. Enoch,Claire L. Mellor,Katarzyna R. Przybylak,Andrea-Nicole Richarz,Judith C. Madden 한국독성학회 2017 Toxicological Research Vol.33 No.3
In silico methods to predict toxicity include the use of (Quantitative) Structure-Activity Relationships ((Q)SARs) as well as grouping (category formation) allowing for read-across. A challenging area for in silico modelling is the prediction of chronic toxicity and the No Observed (Adverse) Effect Level (NO(A)EL) in particular. A proposed solution to the prediction of chronic toxicity is to consider organ level effects, as opposed to modelling the NO(A)EL itself. This review has focussed on the use of structural alerts to identify potential liver toxicants. In silico profilers, or groups of structural alerts, have been developed based on mechanisms of action and informed by current knowledge of Adverse Outcome Pathways. These profilers are robust and can be coded computationally to allow for prediction. However, they do not cover all mechanisms or modes of liver toxicity and recommendations for the improvement of these approaches are given.
Reconstitution of human RNA interference in budding yeast
Suk, Kyoungho,Choi, Jihye,Suzuki, Yo,Ozturk, Sedide B.,Mellor, Joseph C.,Wong, Koon Ho,MacKay, Joanna L.,Gregory, Richard I.,Roth, Frederick P. Oxford University Press 2011 Nucleic acids research Vol.39 No.7
<P>Although RNA-mediated interference (RNAi) is a widely conserved process among eukaryotes, including many fungi, it is absent from the budding yeast <I>Saccharomyces cerevisiae</I>. Three human proteins, Ago2, Dicer and TRBP, are sufficient for reconstituting the RISC complex <I>in vitro</I>. To examine whether the introduction of human RNAi genes can reconstitute RNAi in <I>S. cerevisiae</I>, genes encoding these three human proteins were introduced into <I>S. cerevisiae</I>. We observed both siRNA and siRNA- and RISC-dependent silencing of the target gene <I>GFP</I>. Thus, human Ago2, Dicer and TRBP can functionally reconstitute human RNAi in <I>S. cerevisiae</I>, <I>in vivo</I>, enabling the study and use of the human RNAi pathway in a facile genetic model organism.</P>
Kim, Young H.,Choi, Beom K.,Kang, Woo J.,Kim, Kwang H.,Kang, Sang W.,Mellor, Andrew L.,Munn, David H.,Kwon, Byoung S. Wiley (John WileySons) 2009 Journal of leukocyte biology Vol.85 No.5
<P>It has been reported that 4-1BB triggering in vivo selectively suppressed the recall response of staphylococcal enterotoxin A (SEA)-specific CD4(+) T cells, in which CD8(+) T-derived TGF-beta was involved. Here, we have examined an alternative mechanism for the 4-1BB-mediated CD4(+) T suppression, as the neutralization of TGF-beta is only effective in rescuing the SEA-specific recall response at high cellular concentrations. We show that this selective suppression of CD4(+) T cells by 4-1BB triggering in vivo is mediated mainly by induction of indoleamine 2,3-dioxygenase (IDO) in an IFN-gamma-dependent manner. SEA-specific CD4(+) T responses were suppressed partly by TGF-beta-expressing CD8(+) T cells, particularly CD11c(+)CD8(+) T cells, but strongly inhibited by dendritic cells (DCs) expressing IDO. IFN-gamma that increased IDO in DCs was produced primarily from CD11c(+)CD8(+) T cells, which were expanded selectively by 4-1BB stimulation. CD4(+), CD8(+), and plasmacytoid DCs exerted a similar suppressive activity toward the SEA-specific CD4(+) T cells. Neutralization of IFN-gamma or IDO activity in vivo largely reversed the 4-1BB-mediated CD4(+) T suppression. Collectively, these data indicate that 4-1BB-dependent suppression of SEA-specific CD4(+) T responses was mediated mainly by IFN-gamma-dependent IDO induction and partially by TGF-beta.</P>