Fungal biotransformation of 6-nitrochrysene

The fungus Cunninghamella elegans was used to biotransform 6-nitrochrysene, a mutagen that is a widespread environmental contaminant. After 6 days, 74% of the 3H-labeled 6-nitrochrysene added had been metabolized to two isomeric sulfate conjugates. These conjugates were separated by high-performance liquid chromatography and identified by UV-visible, 1H nuclear magnetic resonance, and mass spectral techniques as 6-nitrochrysene 1-sulfate and 6-nitrochrysene 2-sulfate.     

The deficiency of the ‘economic optimum’ application for evaluating models which predict crop yield response to nitrogen fertiliser

Much effort is devoted to testing N-fertiliser models against measurements of yield in N-fertiliser experiments. We show that the economic optimum application of N-fertiliser can often only be determined very imprecisely from such measurements, even when they are accurate. Hence any attempt to evaluate a simulation model by comparing simulated with experimentally determined optima, or to relate these experimental optima to other factors thought to influence yield, will be uninformative. Big differences between simulated and measured optima will occur even with good models, which may explain the apparent poor performance of some simulation models in the literature.We suggest, instead, the systematic inspection of the differences between simulated and observed yields at the levels of N-fertiliser applied in an experiment. A study of the relationship of these differences to the applied level of N-fertiliser and to other factors of interest will be a more informative method of evaluating a model, and of suggesting other factors for inclusion in it. An example of the use of the method is given.     

Enhancement and suppression of self-stimulation after ventromedial hypothalamic lesions.

Investigated the effects of lesions in the ventromedial hypothalamus (VMH) upon self-stimulation in 25 male hooded Long-Evans rats. Ss trained to press a bar for lateral hypothalamic (LH) stimulation showed an enhancement of responding during the 1st 24 hrs after VMH lesioning, followed by a suppression of responding for several days. The degree of response suppression, but not enhancement, was correlated with an increase in food intake. In Ss trained to shuttle for LH stimulation, only the suppression effect was observed after VMH lesions. Barpressing for dorsal tegmental stimulation was not affected by the lesions. Results suggest that LH stimulation activates at least 2 groups of neurons: one group is specifically involved in barpressing and the other is involved equally in barpressing and shuttling. (French summary) (36 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Response of winter wheat to N-fertiliser: Dynamic model

A concise computer simulation model is described for calculating the growth and N-content of winter-wheat. The validity of the model was tested by means of a new application of statistical theory against the results of nationwide fertiliser experiments having different designs. There was agreement within the limits of experimental error between the measured and simulated values of both total plant and of grain dry weight over the entire range of N-fertiliser treatments in the different experiments. The model also gave good estimates of the %N in the grain provided N-fertilizer levels were not high. Response curves, calculated from the model for grain yield, grain %N, are given for different combinations of potential yield, mineralisation rate and the distribution of inorganic-N down the soil profile.     

The influence of SiC particulates on fatigue crack propagation in a rapidly solidified Al-Fe-V-Si alloy

The fatigue crack propagation properties of a rapidly solidified aluminum alloy are compared with those of a metal matrix composite (MMC) made of the same base alloy with the addition of 11.5 vol pct SiC particulate. The high-temperature base material, alloy 8009 produced by Allied-Signal, Inc. (Morristown, NJ), is solidified and processed using powder metallurgy techniques; these techniques yield a fine-grained, nonequilibrium microstructure. A direct comparison between the fatigue crack propagation properties of the reinforced and unreinforced materials is possible, because alloy 8009 requires no postprocessing heat treatment. As a consequence, this comparison reflects the influence of the SiC particulate and not differences in microstructure that could arise during processing and aging. The experimental data demonstrate that the SiC-reinforced material exhibits modestly superior fatigue crack propagation properties: slower crack growth rates for a given ΔK, at near-threshold crack growth rates. Even when the data are corrected for crack closure using an effective stress intensity factor, ΔK_eff, the composite exhibits lower crack propagation rates than the unreinforced matrix alloy. Microscopic evidence shows a rougher fracture surface and a more tortuous crack path in the composite than in the base alloy. It is argued that the lower crack growth rates and higher intrinsic threshold stress intensity factor observed in the composite are associated with crack deflection around SiC particles. Formerly Graduate Research Assistant, University of California-Davis     

MDA-MB-453, an androgen-responsive human breast carcinoma cell line with high level androgen receptor expression

The role of androgens and the androgen receptor (AR) in the development and progression of breast cancer is poorly understood. To further define a potential model for androgen action in breast cancer, MDA-MB-453 cells, which express AR in the absence of oestrogen receptors and progesterone receptors, were further characterised in terms of AR expression and androgen responsiveness. High level expression of AR was confirmed by northern blot analysis, radioligand binding and immunocytochemistry, and could not be accounted for by AR gene amplification. Three endogenous androgen-responsive genes (fatty acid synthetase, gross cystic disease fluid protein of 15 kDa and prolactin receptor) and a transfected reporter gene, containing an androgen-responsive element, were induced following androgen administration. A synthetic androgen, mibolerone, induced moderate (27% above control) stimulation of MDA-MB-453 cell proliferation, which was abrogated by the simultaneous administration of the synthetic androgen antagonist, anandron, demonstrating that the effect was AR-mediated. In summary, MDA-MB-453 cells express high levels of functional AR, and thus provide a valuable in vitro model for further studies on androgen regulation of gene expression, and perhaps cell proliferation in breast cancer.     

Estradiol induction of retinoic acid receptors in human breast cancer cells

Retinoic acid inhibits proliferation and steroid receptor gene expression in human breast cancer cell lines. Retinoic acid receptors (RAR)alpha, -beta, and -gamma are expressed in these cells and the expression of RAR alpha is significantly greater in estrogen receptor (ER)-positive cells. This study was undertaken to determine whether the same relationship between RAR alpha and ER gene expression was present in human breast cancers and to explore the possibility that the higher level of RAR alpha in ER-positive cells was due to estrogen regulation of RAR alpha gene expression. RAR alpha and ER mRNA expression were determined by Northern blot analysis in 116 primary breast tumors; 94 (81%) tumors were ER-positive and of these 87 (93%) were also RAR alpha-positive. The coexpression of ER and RAR alpha was statistically significant (P = 0.0052 by chi 2 contingency analysis). There was also a positive correlation (by linear regression analysis) between the levels of expression of ER and RAR alpha mRNA (r2 = 0.251, P = 0.0001), which confirmed the relationship previously documented in breast cancer cell lines and suggested that RAR alpha expression may be modulated in breast cancer in vivo by estrogens acting via the ER. The ability of estradiol to regulate RAR alpha gene expression was examined in vitro using T-47D cells which had been rendered sensitive to estrogen by repeated passage in steroid-depleted medium. Estradiol increased RAR alpha gene expression, but not that of RAR beta or RAR gamma, in a concentration-dependent manner, with the effect being maximal at 10(-10) M and less marked at higher concentrations. The effect was rapid, being detectable 1 h after and maximal 6 h after treatment with 10(-10) M estradiol. Co-treatment of cells with estradiol and antiestrogens (tamoxifen or ICI 164384, 4 x 10(-7) M for 6 h) inhibited the estradiol induction of RAR alpha gene expression, demonstrating that the effect was ER mediated. The estradiol sensitivity of the effect was underscored by the demonstration that addition of untreated serum to cells growing under steroid-depleted conditions was sufficient to induce maximal RAR alpha gene expression. This effect was totally abolished by addition of ICI 164384. In summary, the demonstration that estradiol increased RAR alpha mRNA levels in breast cancer cells supports the hypothesis that the correlation between RAR alpha and ER gene expression in breast tumors and breast cancer cell lines is due to estradiol augmentation of RAR alpha gene expression.