Corn Growing in Ohio

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The importance of stakeholders in scoping risk assessments—Lessons from low-carbon transitions

Identifying the risks that could impact a low-carbon transition is a prerequisite to assessing and managing these risks. We systematically characterise risks associated with decarbonisation pathways in fifteen case studies conducted in twelve countries around the world. We find that stakeholders from business, government, NGOs, and others supplied some 40 % of these risk inputs, significantly widening the scope of risks considered by academics and experts. Overall, experts and academics consider more economic risks and assess these with quantitative methods and models, while other stakeholders consider political risks more. To avoid losing sight of risks that cannot be easily quantified and modelled, including some economic risks, impact assessment modelling should be complemented with qualitative research and active stakeholder engagement. A systematic risk elicitation facilitates communication with stakeholders, enables better risk mitigation, and increases the chance of a sustainable transition

IIASA/EQU Justice Framework: A descriptive guideline for science and policy

The consideration of justice has become a critical area of focus for researchers, as awareness is increasing that (perceived) injustices are a main barrier for effectively tackling the interconnected global grand challenges, such as the climate and the biodiversity crises. Insufficient attention to perceptions of justice is a major issue slowing progress on climate change and other major policy issues. Justice, however, is difficult to grasp as it is a multi-dimensional and culturally diverse term and is in many instances of global socio-environmental issues not formally institutionalized. This working paper introduces the first version of the IIASA/EQU justice framework, which comprehensively outlines justice in its multiple aspects with the aim to facilitate justice assessment across diverse research and policy contexts. It is thus a descriptive framework with no normative objectives. The framework is grounded in philosophy and is applied and tested in a variety of applications, to be useful for research and decision-making. It is meant to be accessible across disciplines, powerful in terms of capacity to express a variety of justice ideas, and modular so researchers can select and deploy the aspects that are most appropriate or useful. The framework as presented here serves as a baseline for further refinement, expansion, applications, and evaluation across disciplines, subject areas, and cultural backgrounds

Bioenergy production and sustainable development: science base for policymaking remains limited

The possibility of using bioenergy as a climate change mitigation measure has sparked a discussion of whether and how bioenergy production contributes to sustainable development. We undertook a systematic review of the scientific literature to illuminate this relationship and found a limited scientific basis for policymaking. Our results indicate that knowledge on the sustainable development impacts of bioenergy production is concentrated in a few well-studied countries, focuses on environmental and economic impacts, and mostly relates to dedicated agricultural biomass plantations. The scope and methodological approaches in studies differ widely and only a small share of the studies sufficiently reports on context and/or baseline conditions, which makes it difficult to get a general understanding of the attribution of impacts. Nevertheless, we identified regional patterns of positive or negative impacts for all categories – environmental, economic, institutional, social and technological. In general, economic and technological impacts were more frequently reported as positive, while social and environmental impacts were more frequently reported as negative (with the exception of impacts on direct substitution of GHG emission from fossil fuel). More focused and transparent research is needed to validate these patterns and develop a strong science underpinning for establishing policies and governance agreements that prevent/mitigate negative and promote positive impacts from bioenergy production

Information Needs of Hong Kong Chinese Patients Undergoing Surgery

BACKGROUND: The provision of information to patients is an important aspect of contemporary health care. Limitations in health resources necessitates that the provision of information is carefully planned and culturally specific to maximize the benefits to patients from the resources available. AIM AND OBJECTIVES: The purposes of the study were to recognize Chinese surgical patients' information needs on admission and ascertain why the information is important to assist in understanding how it is used and, therefore, its potential impact. METHODS: A descriptive study design was used. A convenience sample of 83 surgical patients took part comprising 51 men and 32 women. An eight-item questionnaire based on the right of patients to information as listed in the Patients' Charter in Hong Kong using a 5-point Likert scale and one open-ended question to comment on why the information was important to them was completed by patients on the day of admission. RESULTS: Patients rated highly the need for all types of information. They rated most highly the need for information about the signs and symptoms indicating postoperative complications and when to seek medical help. Patients did not rate as highly, information regarding why the doctor believes the surgery is important, treatment alternatives and explanation of the procedure. CONCLUSIONS: These findings indicate that Chinese patients are desirous of a range of relevant information. RELEVANCE TO PRACTICE: Nursing staff, in particular, need to consider the 'timeliness' of information and the cultural appropriateness of how information is delivered

Rab-GTPase binding effector protein 2 (RABEP2) is a primed substrate for Glycogen Synthase kinase-3 (GSK3)

Glycogen synthase kinase-3 (GSK3) regulates many physiological processes through phosphorylation of a diverse array of substrates. Inhibitors of GSK3 have been generated as potential therapies in several diseases, however the vital role GSK3 plays in cell biology makes the clinical use of GSK3 inhibitors potentially problematic. A clearer understanding of true physiological and pathophysiological substrates of GSK3 should provide opportunities for more selective, disease specific, manipulation of GSK3. To identify kinetically favourable substrates we performed a GSK3 substrate screen in heart tissue. Rab-GTPase binding effector protein 2 (RABEP2) was identified as a novel GSK3 substrate and GSK3 phosphorylation of RABEP2 at Ser200 was enhanced by prior phosphorylation at Ser204, fitting the known consensus sequence for GSK3 substrates. Both residues are phosphorylated in cells while only Ser200 phosphorylation is reduced following inhibition of GSK3. RABEP2 function was originally identified as a Rab5 binding protein. We did not observe co-localisation of RABEP2 and Rab5 in cells, while ectopic expression of RABEP2 had no effect on endosomal recycling. The work presented identifies RABEP2 as a novel primed substrate of GSK3, and thus a potential biomarker for GSK3 activity, but understanding how phosphorylation regulates RABEP2 function requires more information on physiological roles of RABEP2

Dual modification of Alzheimer’s disease PHF-tau protein by lysine methylation and ubiquitylation: a mass spectrometry approach

In sporadic Alzheimer’s disease (AD), neurofibrillary lesion formation is preceded by extensive post-translational modification of the microtubule associated protein tau. To identify the modification signature associated with tau lesion formation at single amino acid resolution, immunopurified paired helical filaments were isolated from AD brain and subjected to nanoflow liquid chromatography–tandem mass spectrometry analysis. The resulting spectra identified monomethylation of lysine residues as a new tau modification. The methyl-lysine was distributed among seven residues located in the projection and microtubule binding repeat regions of tau protein, with one site, K254, being a substrate for a competing lysine modification, ubiquitylation. To characterize methyl lysine content in intact tissue, hippocampal sections prepared from post mortem late-stage AD cases were subjected to double-label confocal fluorescence microscopy using anti-tau and anti-methyl lysine antibodies. Anti-methyl lysine immunoreactivity colocalized with 78 ± 13% of neurofibrillary tangles in these specimens. Together these data provide the first evidence that tau in neurofibrillary lesions is post-translationally modified by lysine methylation

Hypothermia-induced hyperphosphorylation: a new model to study tau kinase inhibitors

Tau hyperphosphorylation is one hallmark of Alzheimer's disease (AD) pathology. Pharmaceutical companies have thus developed kinase inhibitors aiming to reduce tau hyperphosphorylation. One obstacle in screening for tau kinase inhibitors is the low phosphorylation levels of AD-related phospho-epitopes in normal adult mice and cultured cells. We have shown that hypothermia induces tau hyperphosphorylation in vitro and in vivo. Here, we hypothesized that hypothermia could be used to assess tau kinase inhibitors efficacy. Hypothermia applied to models of biological gradual complexity such as neuronal-like cells, ex vivo brain slices and adult non-transgenic mice leads to tau hyperphosphorylation at multiple AD-related phospho-epitopes. We show that Glycogen Synthase Kinase-3 inhibitors LiCl and AR-A014418, as well as roscovitine, a cyclin-dependent kinase 5 inhibitor, decrease hypothermia-induced tau hyperphosphorylation, leading to different tau phosphorylation profiles. Therefore, we propose hypothermia-induced hyperphosphorylation as a reliable, fast, convenient and inexpensive tool to screen for tau kinase inhibitors

Phosphorylation of a splice variant of collapsin response mediator protein 2 in the nucleus of tumour cells links cyclin dependent kinase-5 to oncogenesis

Background Cyclin-dependent protein kinase-5 (CDK5) is an unusual member of the CDK family as it is not cell cycle regulated. However many of its substrates have roles in cell growth and oncogenesis, raising the possibility that CDK5 modulation could have therapeutic benefit. In order to establish whether changes in CDK5 activity are associated with oncogenesis one could quantify phosphorylation of CDK5 targets in disease tissue in comparison to appropriate controls. However the identity of physiological and pathophysiological CDK5 substrates remains the subject of debate, making the choice of CDK5 activity biomarkers difficult. Methods Here we use in vitro and in cell phosphorylation assays to identify novel features of CDK5 target sequence determinants that confer enhanced CDK5 selectivity, providing means to select substrate biomarkers of CDK5 activity with more confidence. We then characterize tools for the best CDK5 substrate we identified to monitor its phosphorylation in human tissue and use these to interrogate human tumour arrays. Results The close proximity of Arg/Lys amino acids and a proline two residues N-terminal to the phosphorylated residue both improve recognition of the substrate by CDK5. In contrast the presence of a proline two residues C-terminal to the target residue dramatically reduces phosphorylation rate. Serine-522 of Collapsin Response Mediator-2 (CRMP2) is a validated CDK5 substrate with many of these structural criteria. We generate and characterise phosphospecific antibodies to Ser522 and show that phosphorylation appears in human tumours (lung, breast, and lymphoma) in stark contrast to surrounding non-neoplastic tissue. In lung cancer the anti-phospho-Ser522 signal is positive in squamous cell carcinoma more frequently than adenocarcinoma. Finally we demonstrate that it is a specific and unusual splice variant of CRMP2 (CRMP2A) that is phosphorylated in tumour cells. Conclusions For the first time this data associates altered CDK5 substrate phosphorylation with oncogenesis in some but not all tumour types, implicating altered CDK5 activity in aspects of pathogenesis. These data identify a novel oncogenic mechanism where CDK5 activation induces CRMP2A phosphorylation in the nuclei of tumour cells