A bioeconomic model for determining the optimal response to a new weed incursion in Australian cropping systems

Invasions by non-indigenous plant species pose serious economic threats to Australian agricultural industries. When an invasion is discovered a decision has to be made as to whether to attempt to eradicate it, contain it or do nothing. These decisions should be based on long term benefits and costs. This paper describes a bioeconomic simulation framework with a mathematical model representing weed spread linked to a dynamic programming model to provide a means of determining the economically optimal weed management strategies over time. The modelling framework is used to evaluate case study invasive weed control problems in the Australian grains industry.weeds, incursion, bioeconomic model, Crop Production/Industries, Research Methods/ Statistical Methods,

A cohort study of dietary iron and heme iron intake and risk of colorectal cancer in women

In a cohort study of 49 654 Canadian women, we assessed the association of colorectal cancer with total iron and heme iron intake, excluding iron supplements. Among women aged 40–59 years, followed for an average of 16.4 years, we identified 617 incident colorectal cancer cases. Data from a food frequency questionnaire administered at baseline were used to calculate red meat intake and intake of total dietary iron, iron from meat, and heme iron. Analyses were carried out for all cases and for the proximal colon, distal colon, and rectum, using Cox proportional hazards models. We found no association of intake of iron, heme iron, or iron from meat with risk of colorectal cancer overall or with any of the subsites, nor was there effect modification by alcohol consumption or hormonal replacement therapy

Alcohol, tobacco and breast cancer - collaborative reanalysis of individual data from 53 epidemiological studies, including 58 515 women with breast cancer and 95 067 women without the disease

Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58 515 women with invasive breast cancer and 95 067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19-1.45, P<0.00001) for an intake of 35-44 g per day alcohol, and 1.46 (1.33-1.61, P<0.00001) for 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1% per 10 g per day, P<0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers=1.03, 95% CI 0.98-1.07, and for current smokers=0.99, 0.92-1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver

Sex hormone associations with breast cancer risk and the mediation of randomized trial postmenopausal hormone therapy effects

Introduction: Paradoxically, a breast cancer risk reduction with conjugated equine estrogens (CEE) and a risk elevation with CEE plus medroxyprogesterone acetate (CEE + MPA) were observed in the Women’s Health Initiative (WHI) randomized controlled trials. The effects of hormone therapy on serum sex hormone levels, and on the association between baseline sex hormones and disease risk, may help explain these divergent breast cancer findings. Methods: Serum sex hormone concentrations were measured for 348 breast cancer cases in the CEE + MPA trial and for 235 cases in the CEE trial along with corresponding pair-matched controls, nested within the WHI trials of healthy postmenopausal women. Association and mediation analyses, to examine the extent to which sex hormone levels and changes can explain the breast cancer findings, were conducted using logistic regression. Results: Following CEE treatment, breast cancer risk was associated with higher concentrations of baseline serum estrogens, and with lower concentrations of sex hormone binding globulin. However, following CEE + MPA, there was no association of breast cancer risk with baseline sex hormone levels. The sex hormone changes from baseline to year 1 provided an explanation for much of the reduced breast cancer risk with CEE. Specifically, the treatment odds ratio (95% confidence interval) increased from 0.71 (0.43, 1.15) to 0.92 (0.41, 2.09) when the year 1 measures were included in the logistic regression analysis. In comparison, the CEE + MPA odds ratio was essentially unchanged when these year 1 measures were included. Conclusions: Breast cancer risk remains low following CEE use among women having favorable baseline sex hormone profiles, but CEE + MPA evidently produces a breast cancer risk for all women similar to that for women having an unfavorable baseline sex hormone profile. These patterns could reflect breast ductal epithelial cell stimulation by CEE + MPA that is substantially avoided with CEE, in conjunction with relatively more favorable effects of either regimen following a sustained period of estrogen deprivation. These findings may have implications for other hormone therapy formulations and routes of delivery. Trial registration clinicaltrials.gov identifier: NCT00000611

Advection-Dominated Accretion Model of Sagittarius A*: Evidence for a Black Hole at the Galactic Center

Sgr A* at the Galactic Center is a puzzling source. It has a mass M=(2.5+/-0.4) x 10^6 solar masses which makes it an excellent black hole candidate. Observations of stellar winds and other gas flows in its vicinity suggest a mass accretion rate approximately few x 10^{-6} solar masses per year. However, such an accretion rate would imply a luminosity > 10^{40} erg/s if the radiative efficiency is the usual 10 percent, whereas observations indicate a bolometric luminosity <10^{37} erg/s. The spectrum of Sgr A* is unusual, with emission extending over many decades of wavelength. We present a model of Sgr A* which is based on a two-temperature optically-thin advection-dominated accretion flow. The model is consistent with the estimated mass and accretion rate, and fits the observed fluxes in the cm/mm and X-ray bands as well as upper limits in the sub-mm and infrared bands; the fit is less good in the radio below 86 GHz and in gamma-rays above 100 MeV. The very low luminosity of Sgr A* is explained naturally in the model by means of advection. Most of the viscously dissipated energy is advected into the central mass by the accreting gas, and therefore the radiative efficiency is extremely low, approximately 5 x 10^{-6}. A critical element of the model is the presence of an event horizon at the center which swallows the advected energy. The success of the model could thus be viewed as confirmation that Sgr A* is a black hole.Comment: 41 pages (Latex) including 6 Figures and 2 Tables. Final Revised Version changes to text, tables and figures. ApJ, 492, in pres

Nicotinamide is an Endogenous Agonist for a C. elegans TRPV OSM-9 and OCR-4 Channel

TRPV ion channels are directly activated by sensory stimuli and participate in thermo-, mechano- and chemo-sensation. They are also hypothesized to respond to endogenous agonists that would modulate sensory responses. Here, we show that the nicotinamide (NAM) form of vitamin B3 is an agonist of a Caenorhabditis elegans TRPV channel. Using heterologous expression in Xenopus oocytes, we demonstrate that NAM is a soluble agonist for a channel consisting of the well-studied OSM-9 TRPV subunit and relatively uncharacterized OCR-4 TRPV subunit as well as the orthologous Drosophila Nan-Iav TRPV channel, and we examine stoichiometry of subunit assembly. Finally, we show that behaviours mediated by these C. elegans and Drosophila channels are responsive to NAM, suggesting conservation of activity of this soluble endogenous metabolite on TRPV activity. Our results in combination with the role of NAM in NAD+ metabolism suggest an intriguing link between metabolic regulation and TRPV channel activity