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  • Article
    Mazza D, Assifi AR, Hussainy SY, Bateson D, Johnston S, Tomnay J, Kasza J, Church J, Grzeskowiak LE, Nissen L, Cameron ST.
    BMJ Open. 2023 08 31;13(8):e073154.
    INTRODUCTION: Improving access to effective contraception has the potential to reduce unintended pregnancy and abortion rates. Community pharmacists could play an expanded role in contraceptive counselling and referral to contraceptive prescribers particularly when women are already attending community pharmacy to obtain emergency contraceptive pills (ECPs) or to have medical abortion (MA) medicines dispensed. The ALLIANCE trial aims to compare the subsequent uptake of effective contraception (hormonal or intrauterine) in women seeking ECP or MA medicines, who receive the ALLIANCE community pharmacy-based intervention with those who do not receive the intervention.
    METHODS AND ANALYSIS: ALLIANCE is a stepped-wedge pragmatic cluster randomised trial in Australian community pharmacies. The ALLIANCE intervention involves community pharmacists delivering structured, patient-centred, effectiveness-based contraceptive counselling (and a referral to a contraceptive prescriber where appropriate) to women seeking either ECPs or to have MA medicines dispensed. Women participants will be recruited by participating pharmacists. A total of 37 pharmacies and 1554 participants will be recruited. Pharmacies commence in the control phase and are randomised to transition to the intervention phase at different time points (steps). The primary outcome is the self-reported use of effective contraception at 4 months; secondary outcomes include use of effective contraception and the rate of pregnancies or induced abortions at 12 months. A process and economic evaluation of the trial will also be undertaken.
    ETHICS AND DISSEMINATION: Ethical approval has been obtained from the Monash University Human Research Ethics Committee (#34563). An explanatory statement will be provided and written consent will be obtained from all participants (pharmacy owner, pharmacist and women) before their commencement in the trial. Dissemination will occur through a knowledge exchange workshop, peer-reviewed journal publications, presentations, social media and conferences.
    TRIAL REGISTRATION NUMBER: ACTRN12622001024730.
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  • Article
    Lee CH, Hsieh SY, Chang CC, Wang IK, Huang WH, Weng CH, Hsu CW, Yen TH.
    Oncotarget. 2017 Sep 22;8(42):___73154:::-73161.
    We investigated the rates and predictors of mortality in hepatocellular carcinoma (HCC) patients who were or were not undergoing long-term hemodialysis. The participants in this retrospective observational study were 1298 HCC patients (60.0 ± 12.1 years old, 72% male), of whom 172 were undergoing hemodialysis and 1126 were not. HCC patients on hemodialysis exhibited a higher hepatitis C virus carrier rate (49.4% versus 39.3%, P = 0.012), lower hepatitis B virus carrier rate (37.2% versus 58.3%, P < 0.001) and lower hepatitis B or C virus carrier rate (77.9% versus 89.3%, P < 0.001) than those not on hemodialysis. Serum alkaline phosphatase levels were higher in the hemodialysis than non-hemodialysis group (162.8 ± 141.1 u/l versus 124.6 ± 102.5 u/l, P < 0.001). By the end of the analysis, 32.0% of HCC patients on hemodialysis and 28.0% of those not on hemodialysis had died. Kaplan-Meier analysis confirmed that cumulative survival was poorer in HCC patients on hemodialysis (P = 0.004). In a multivariate Cox regression model, hemodialysis (P < 0.001), older age (P < 0.001) and advanced tumor stages (P < 0.001) were found to be risk factors for mortality. HCC patients on hemodialysis had a 2.036-fold greater chance of death than HCC patients not on hemodialysis. Prospective studies with longer follow-ups and larger samples are warranted.
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  • Article
    Mari A, Bagger JI, Ferrannini E, Holst JJ, Knop FK, Vilsbøll T.
    PLoS One. 2013;8(9):e___73154:::.
    The incretin effect on insulin secretion was investigated in 8 subjects with type 2 diabetes (T2D) and 8 with normal glucose tolerance (NGT), using 25, 75, and 125 g oral glucose tolerance tests (OGTT) and isoglycemic intravenous glucose infusions (IIGI). The ß-cell response was evaluated using a model embedding a dose-response (slope=glucose sensitivity), an early response (rate sensitivity), and potentiation (time-related secretion increase). The incretin effect, as OGTT/IIGI ratio, was calculated for each parameter. In NGT, the incretin effect on total secretion increased with dose (1.3 ± 0.1, 1.7 ± 0.2, 2.2 ± 0.2 fold of IIGI, P<0.0001), mediated by a dose-dependent increase of the incretin effect on glucose sensitivity (1.9 ± 0.4, 2.4 ± 0.4, 3.1 ± 0.4, P=0.005), and a dose-independent enhancement of the incretin effect on rate sensitivity (894 [1145], 454 [516], 783 [1259] pmol m(-2) L mmol(-1) above IIGI; median [interquartile range], P<0.0001). The incretin effect on potentiation also increased (0.97 ± 0.06, 1.45 ± 0.20, 1.24 ± 0.16, P<0.0001). In T2D, the incretin effect on total secretion (1.0 ± 0.1, 1.1 ± 0.1, 1.3 ± 0.1, P=0.004) and glucose sensitivity (1.2 ± 0.2, 1.3 ± 0.2, 2.0 ± 0.2, P=0.005) were impaired vs NGT; however, the incretin effect on rate sensitivity increased already at 25 g (269 [169], 284 [301], 193 [465] pmol m(-2) L mmol(-1) above IIGI; negligible IIGI rate sensitivity in T2D prevented the calculation of the fold increment). OGTT did not stimulate potentiation above IIGI (0.94 ± 0.04, 0.89 ± 0.06, 1.06 ± 0.09; P<0.01 vs NGT). In the whole group, the incretin effect was inversely associated with total secretion during IIGI, although systematically lower in T2D. In conclusion, 1) In NGT, glucose sensitivity and potentiation mediate the dose-dependent incretin effect increase; 2) In T2D, the incretin effect is blunted vs NGT, but rate sensitivity is enhanced at all loads; 3) Relatively lower incretin effect in NGT is associated with higher secretion during IIGI, suggesting that the reduced incretin effect does not result from ß-cell dysfunction.
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