When Research and Practice Collide: The Role of Action Research When There Is a Conflict of Interest with Stakeholders

This article discusses problematic aspects of the role of the action researcher when working with multiple stakeholders on a complex research project concerning regional development. The case presented here deals with the improvement of the regional innovation system in a small region in the south of Norway. The project resulted in a conflict between stakeholders and the action research (AR) team. We claim that when working in a regional context, the role of the action researcher is set to be a collaborator in a context of power play; the ultimate stakeholders must be defined as the citizens in that region. Therefore, in some situations the action researcher must have a legitimatised right to abandon collaboration and present a critical voice in the public deliberation. Strategic power play and strategic action by stakeholders represent a clear threat to the soft approach of collaboration, reflectivity, and democratic dialogue that AR represents. The ultimate challenge and obligation of the action researcher is to improve democracy in society in a long-term perspective through representing a critical capacity in the public deliberation.     

Interannual variability in the oxygen isotopes of atmospheric CO2 driven by El Niño

The stable isotope ratios of atmospheric CO(2) ((18)O/(16)O and (13)C/(12)C) have been monitored since 1977 to improve our understanding of the global carbon cycle, because biosphere-atmosphere exchange fluxes affect the different atomic masses in a measurable way. Interpreting the (18)O/(16)O variability has proved difficult, however, because oxygen isotopes in CO(2) are influenced by both the carbon cycle and the water cycle. Previous attention focused on the decreasing (18)O/(16)O ratio in the 1990s, observed by the global Cooperative Air Sampling Network of the US National Oceanic and Atmospheric Administration Earth System Research Laboratory. This decrease was attributed variously to a number of processes including an increase in Northern Hemisphere soil respiration; a global increase in C(4) crops at the expense of C(3) forests; and environmental conditions, such as atmospheric turbulence and solar radiation, that affect CO(2) exchange between leaves and the atmosphere. Here we present 30 years' worth of data on (18)O/(16)O in CO(2) from the Scripps Institution of Oceanography global flask network and show that the interannual variability is strongly related to the El Ni?o/Southern Oscillation. We suggest that the redistribution of moisture and rainfall in the tropics during an El Ni?o increases the (18)O/(16)O ratio of precipitation and plant water, and that this signal is then passed on to atmospheric CO(2) by biosphere-atmosphere gas exchange. We show how the decay time of the El Ni?o anomaly in this data set can be useful in constraining global gross primary production. Our analysis shows a rapid recovery from El Ni?o events, implying a shorter cycling time of CO(2) with respect to the terrestrial biosphere and oceans than previously estimated. Our analysis suggests that current estimates of global gross primary production, of 120 petagrams of carbon per year, may be too low, and that a best guess of 150-175 petagrams of carbon per year better reflects the observed rapid cycling of CO(2). Although still tentative, such a revision would present a new benchmark by which to evaluate global biospheric carbon cycling models.     

Compositional maps of Saturn's moon Phoebe from imaging spectroscopy

The origin of Phoebe, which is the outermost large satellite of Saturn, is of particular interest because its inclined, retrograde orbit suggests that it was gravitationally captured by Saturn, having accreted outside the region of the solar nebula in which Saturn formed. By contrast, Saturn's regular satellites (with prograde, low-inclination, circular orbits) probably accreted within the sub-nebula in which Saturn itself formed. Here we report imaging spectroscopy of Phoebe resulting from the Cassini-Huygens spacecraft encounter on 11 June 2004. We mapped ferrous-iron-bearing minerals, bound water, trapped CO2, probable phyllosilicates, organics, nitriles and cyanide compounds. Detection of these compounds on Phoebe makes it one of the most compositionally diverse objects yet observed in our Solar System. It is likely that Phoebe's surface contains primitive materials from the outer Solar System, indicating a surface of cometary origin.     

Glioma stem cells promote radioresistance by preferential activation of the DNA damage response

Ionizing radiation represents the most effective therapy for glioblastoma (World Health Organization grade IV glioma), one of the most lethal human malignancies, but radiotherapy remains only palliative because of radioresistance. The mechanisms underlying tumour radioresistance have remained elusive. Here we show that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity. The fraction of tumour cells expressing CD133 (Prominin-1), a marker for both neural stem cells and brain cancer stem cells, is enriched after radiation in gliomas. In both cell culture and the brains of immunocompromised mice, CD133-expressing glioma cells survive ionizing radiation in increased proportions relative to most tumour cells, which lack CD133. CD133-expressing tumour cells isolated from both human glioma xenografts and primary patient glioblastoma specimens preferentially activate the DNA damage checkpoint in response to radiation, and repair radiation-induced DNA damage more effectively than CD133-negative tumour cells. In addition, the radioresistance of CD133-positive glioma stem cells can be reversed with a specific inhibitor of the Chk1 and Chk2 checkpoint kinases. Our results suggest that CD133-positive tumour cells represent the cellular population that confers glioma radioresistance and could be the source of tumour recurrence after radiation. Targeting DNA damage checkpoint response in cancer stem cells may overcome this radioresistance and provide a therapeutic model for malignant brain cancers.