Implementing academic detailing for breast cancer screening in underserved communities

Background

Canadian funding agencies are no longer content to support research that solely advances scientific knowledge, and key directives are now in place to promote research transfer to policy- and decision-makers. Therefore, it is necessary to improve our understanding of how researchers are trained and supported to facilitate knowledge translation activities. In this study, we investigated differences in health researcher characteristics and knowledge translation activities.

Methods

Our sample consisted of 240 health researchers from three Alberta universities. Respondents were classified by research domain [basic (n = 72) or applied (n = 168)] and faculty [medical school (n = 128) or other health science (n = 112)]. We examined our findings using Mode I and Mode II archetypes of knowledge production, which allowed us to consider the scholarly and social contexts of knowledge production and translation.

Results

Differences among health researcher professional characteristics were not statistically significant. There was a significant gender difference in the applied researcher faculty group, which was predominantly female (p <.05). Research domain was linked to translation activities. Applied researchers reported engaging in significantly more Mode II activities than basic researchers (p <.001), and scored higher than basic researchers regarding the perceived importance of translation activities (Mode I, p =.01; Mode II, p <.001). Main effects of faculty were limited to engaged dissemination (medical school < other faculties; p =.025) and number of publications (medical school > other faculties; p =.004). There was an interaction effect for research domain and faculty group for number of publications (p =.01), in that applied researchers in medical faculties published more than their peers in other faculty groups.

Conclusion

Our findings illustrate important differences between health researchers and provide beginning insights into their professional characteristics and engagement in Mode I and Mode II activities. A future study designed to examine these dimensions in greater detail, including potential covariates across more varied institutions, would yield richer insights and enable an examination of relative influences, needs and costs of each mode of activity.     

Novel transcriptional responses to heat revealed by turning up the heat at night

Plant Molecular Biology - Genome-wide association study of maize plant architecture using F1 populations can better dissect various genetic effects that can provide precise guidance for genetic...     

A versatile enrichment of functionalized calixarene as a facile sensor for amino acids

Amino acids are the most important part of the human biological system due to their role in living processes. The role of amino acids stretches beyond their traditional role as a building block for proteins, and deficiency of amino acids could lead to decreased immunity, digestive problems, depression, fertility issues, lower mental alertness, slowed growth in children, and many other health issues. The acute detection of amino acids is necessary to determine the human health domain. Here, in this review, we summarize and study the calixarenes as complexes that are of immeasurable value and their utilization for amino acid detection. Key factors such as noncovalent forces, limit of detection, and the supramolecular chemistry of calixarenes with amino acids have been well described. This study presents the most recent efforts made towards the development of potential and highly efficient calixarene-based sensors for the detection of amino acids.     

Effects of 1,4-phenylenebis(methylene)selenocyanate on mutagenesis and p53 protein expression in the tongue of lacI rats treated with 4-nitroquinoline-N-oxide

Previously we showed that the organoselenium compound, 1,4-phenylenebis(methylene)selenocyanate (p-XSC)(1) inhibits 4-nitroquinoline-N-oxide (4-NQO)-induced tongue tumorigenesis in Fisher rats. Here we investigate possible mechanisms of this inhibition by monitoring mutagenesis and p53 protein levels in lacI and conventional Fisher rats treated with: (1) a carcinogenic dose of 4-NQO for 10 weeks in drinking water, (2) 4-NQO+p-XSC (15 ppm as selenium), and (3) 4-NQO followed by p-XSC. For mutagenesis studies, rats were euthanized at 7, 12 or 23 weeks after the start of 4-NQO. For studies on p53 levels, rats were euthanized at 11, 15 and 23 weeks. Appropriate controls were also monitored. In the 4-NQO-alone groups, the mutant fraction (MF) in the cII gene in tongue increased at least 50x background level. The MF (in units of mutants/10(5) plaque forming units) for the 7, 12, and 23 weeks 4-NQO groups were respectively, 184 +/- 88, 237 +/- 105, and 329 +/- 110. Thus, mutagenesis increased with length of exposure and post-treatment time. p-XSC modestly (ca. 15-30%) inhibited mutagenesis under all conditions. The inhibition reached significance at the last time point. When p-XSC was administered after 4-NQO, the MF was also modestly reduced. In 4-NQO-alone animals, levels of p53 in tongue (determined by Western blotting) were 1, 1.5 and 2.4 control levels at 10, 15 and 23 weeks, respectively. In the p-XSC+4-NQO group, the enhancement in p53 levels by 4-NQO treatment was decreased about 90% at 15 weeks and 45% (P<0.05) at 23 weeks, and by slightly smaller percentages in corresponding post-treatment groups. p-XSC alone did not alter p53 levels. As p53 levels generally increase in response to DNA damage, these results suggest that p-XSC reduces 4-NQO-induced DNA damage, resulting in reduced 4-NQO-induced mutagenesis and carcinogenesis. However, the fact that p-XSC is also effective when administered after 4-NQO, suggests additional mechanisms of inhibition exist.     

Morphactin influences guggulsterone production in callus cultures of <Emphasis Type="Italic">Commiphora wightii</Emphasis>

Guggulsterone, a hypolipidemic natural agent, is produced in resin canals of the plant Commiphora wightii. In this study, the efficacy of different plant growth regulators was evaluated for optimizing its production. Morphactin was found to be effective in enhancing the accumulation of guggulsterones in callus cultures. Maximum callus growth was recorded on medium containing morphactin (0.1 mg l⁻¹) and 2iP (2.5 mg l⁻¹), whereas maximum guggulsterone production occurred when the calluses were cultured on medium containing 0.1 mg l⁻¹ morphactin and 1.0 mg l⁻¹ 2iP. Morphactin and 2iP interacted significantly to enhance the callus growth and guggulsterone production by about 8-folds in one-year-old cultures. However, the effect of morphactin on callus growth and guggulsterone production was not uniform over the levels of 2iP tested. Such an effect of morphactin has never been reported on the production of secondary metabolites.     

Zinc lowers amyloid-beta toxicity by selectively precipitating aggregation intermediates

Soluble amyloid-beta (Abeta) aggregates are suspected to play a major role in Alzheimer's disease. Zn2+ at a concentration of a few micromolar, which is too dilute to affect the precipitation equilibrium of Abeta, can destabilize these aggregates [Garai, K., Sengupta, P., Sahoo, B., and Maiti, S. (2006) Biochem. Biophys. Res. Commun. 345, 210-215]. Here we investigate the nature of these aggregates in the context of the precipitation pathway, the mechanism underlying their destabilization, and the biological consequences of this destabilization. We show that the larger soluble aggregates (size >10 nm) form only in supersaturated Abeta solutions, implying that they are intermediates in the pathway toward fibril formation. We also show that Zn2+ destabilizes these intermediates by accelerating their aggregation kinetics. The resulting change in the size distribution of the Abeta solution is sufficient to eliminate its toxicity to cultured mammalian neurons. Our results provide an explanation for the existing observations that Zn2+ at a concentration of a few micromolar significantly reduces Abeta toxicity.     

Maternal undernutrition inhibits angiogenesis in the offspring: a potential mechanism of programmed hypertension

The underlying etiology of many chronic diseases such as hypertension and diabetes has been traced to the in utero environment. Our interest has focused on determining the mechanism of programmed hypertension. In our rodent model of 50% maternal food restriction (MFR) from day 10 of gestation to term, the offspring develop hypertension as adults. We hypothesized that maternal undernutrition inhibits angiogenesis such that the neonate is endowed with fewer microvessels, increasing their susceptibility to develop hypertension as adults. We found significantly reduced number of mesenteric branching and renal medullary microvessels in the 1-day-old MFR newborns. Endothelial cells from MFR offspring generated shorter neovessels in culture compared with controls. The inhibition of angiogenesis was associated with a significant decrease in VEGF protein expression in mesenteric microvessels and aortas in 1-day-old offspring. However, in adulthood there was a marked increase in VEGF expression in both vessel types. The expression of endothelial nitric oxide synthase protein was also found to be increased in both renal and mesenteric microvessels and in aortas in the 1-day-old MFR offspring. These results suggest that MFR results in inhibition of VEGF expression in microvascular and aortic endothelial cells early in life, resulting in decreased angiogenesis and increased peripheral vascular resistance, both of which may contribute to offspring hypertension.     

Biodegradation and decolourization of anaerobically treated distillery spent wash by a novel bacterial consortium

The aim of this study was to isolate microorganisms capable of decolourizing and degrading anaerobically treated distillery spent wash. A bacterial consortium DMC comprising of three bacterial cultures was selected on the basis of rapid effluent decolourization and degradation, which exhibited 67 +/- 2% decolourization within 24 h and 51 +/- 2% chemical oxygen demand reduction within 72 h when incubated at 37 degrees C under static condition in effluent supplemented with 0.5% glucose, 0.1% KH(2)PO(4), 0.05% KCl and 0.05% MgSO(4) x 7H(2)O. Addition of organic or inorganic nitrogen sources did not support decolourization. The cultures were identified as Pseudomonas aeruginosa PAO1, Stenotrophomonas maltophila and Proteus mirabilis by the 16S rDNA analysis.     

Kinetochore-localized BUB-1/BUB-3 complex promotes anaphase onset in C. elegans

The conserved Bub1/Bub3 complex is recruited to the kinetochore region of mitotic chromosomes, where it initiates spindle checkpoint signaling and promotes chromosome alignment. Here we show that, in contrast to the expectation for a checkpoint pathway component, the BUB-1/BUB-3 complex promotes timely anaphase onset in Caenorhabditis elegans embryos. This activity of BUB-1/BUB-3 was independent of spindle checkpoint signaling but required kinetochore localization. BUB-1/BUB-3 inhibition equivalently delayed separase activation and other events occurring during mitotic exit. The anaphase promotion function required BUB-1’s kinase domain, but not its kinase activity, and this function was independent of the role of BUB-1/BUB-3 in chromosome alignment. These results reveal an unexpected role for the BUB-1/BUB-3 complex in promoting anaphase onset that is distinct from its well-studied functions in checkpoint signaling and chromosome alignment, and suggest a new mechanism contributing to the coordination of the metaphase-to-anaphase transition.