How much heat can we grow in our cities? Modelling UK urban biofuel production potential

Biofuel provides a globally significant opportunity to reduce fossil fuel dependence; however, its sustainability can only be meaningfully explored for individual cases. It depends on multiple considerations including: life cycle greenhouse gas emissions, air quality impacts, food versus fuel trade‐offs, biodiversity impacts of land use change and socio‐economic impacts of energy transitions. One solution that may address many of these issues is local production of biofuel on non‐agricultural land. Urban areas drive global change, for example, they are responsible for 70% of global energy use, but are largely ignored in their resource production potential; however, underused urban greenspaces could be utilized for biofuel production near the point of consumption. This could avoid food versus fuel land conflicts in agricultural land and long‐distance transport costs, provide ecosystem service benefits to urban dwellers and increase the sustainability and resilience of cities and towns. Here, we use a Geographic Information System to identify urban greenspaces suitable for biofuel production, using exclusion criteria, in 10 UK cities. We then model production potential of three different biofuels: Miscanthus grass, short rotation coppice (SRC) willow and SRC poplar, within the greenspaces identified and extrapolate up to a UK‐scale. We demonstrate that approximately 10% of urban greenspace (3% of built‐up land) is potentially suitable for biofuel production. We estimate the potential of this to meet energy demand through heat generation, electricity and combined heat and power (CHP) operations. Our findings show that, if fully utilized, urban biofuel production could meet nearly a fifth of demand for biomass in CHP systems in the United Kingdom's climate compatible energy scenarios by 2030, with potentially similar implications for other comparable countries and regions.     

Climate change decreases the cooling effect from postfire albedo in boreal North America

Fire is a primary disturbance in boreal forests and generates both positive and negative climate forcings. The influence of fire on surface albedo is a predominantly negative forcing in boreal forests, and one of the strongest overall, due to increased snow exposure in the winter and spring months. Albedo forcings are spatially and temporally heterogeneous and depend on a variety of factors related to soils, topography, climate, land cover/vegetation type, successional dynamics, time since fire, season, and fire severity. However, how these variables interact to influence albedo is not well understood, and quantifying these relationships and predicting postfire albedo becomes increasingly important as the climate changes and management frameworks evolve to consider climate impacts. Here we developed a MODIS‐derived ‘blue sky’ albedo product and a novel machine learning modeling framework to predict fire‐driven changes in albedo under historical and future climate scenarios across boreal North America. Converted to radiative forcing (RF), we estimated that fires generate an annual mean cooling of ?1.77 ± 1.35 W/m² from albedo under historical climate conditions (1971–2000) integrated over 70 years postfire. Increasing postfire albedo along a south–north climatic gradient was offset by a nearly opposite gradient in solar insolation, such that large‐scale spatial patterns in RF were minimal. Our models suggest that climate change will lead to decreases in mean annual postfire albedo, and hence a decreasing strength of the negative RF, a trend dominated by decreased snow cover in spring months. Considering the range of future climate scenarios and model uncertainties, we estimate that for fires burning in the current era (2016) the cooling effect from long‐term postfire albedo will be reduced by 15%–28% due to climate change.     

The C0C1 fragment of human cardiac myosin binding protein C has common binding determinants for both actin and myosin

The N-terminal domains of cardiac myosin binding protein C (MyBP-C) play a regulatory role in modulating interactions between myosin and actin during heart muscle contraction. Using NMR spectroscopy and small-angle neutron scattering, we have determined specific details of the interaction between the two-module human C0C1 cMyBP-C fragment and F-actin. The small-angle neutron scattering data show that C0C1 spontaneously polymerizes monomeric actin (G-actin) to form regular assemblies composed of filamentous actin (F-actin) cores decorated by C0C1, similar to what was reported in our earlier four-module mouse cMyBP-C actin study. In addition, NMR titration analyses show large intensity changes for a subset of C0C1 peaks upon addition of G-actin, indicating that human C0C1 interacts specifically with actin and promotes its assembly into filaments. During the NMR titration, peaks corresponding to cardiac-specific C0 domain are the first to be affected, followed by those from the C1 domain. No peak intensity or position changes were detected for peaks arising from the disordered proline/alanine-rich (P/A) linker connecting C0 with C1, despite previous suggestions of its involvement in binding actin. Of considerable interest is the observation that the actin-interaction “hot-spots” within the C0 and C1 domains, revealed in our NMR study, overlap with regions previously identified as binding to the regulatory light chain of myosin and to myosin ΔS2. Our results suggest that C0 and C1 interact with myosin and actin using a common set of binding determinants and therefore support a cMyBP-C switching mechanism between myosin and actin.     

Analyzing proteomes and protein function using graphical comparative analysis of tandem mass spectrometry results

Although generating large amounts of proteomic data using tandem mass spectrometry has become routine, there is currently no single set of comprehensive tools for the rigorous analysis of tandem mass spectrometry results given the large variety of possible experimental aims. Currently available applications are typically designed for displaying proteins and posttranslational modifications from the point of view of the mass spectrometrist and are not versatile enough to allow investigators to develop biological models of protein function, protein structure, or cell state. In addition, storage and dissemination of mass spectrometry-based proteomic data are problems facing the scientific community. To address these issues, we have developed a relational database model that efficiently stores and manages large amounts of tandem mass spectrometry results. We have developed an integrated suite of multifunctional analysis software for interpreting, comparing, and displaying these results. Our system, Bioinformatic Graphical Comparative Analysis Tools (BIGCAT), allows sophisticated analysis of tandem mass spectrometry results in a biologically intuitive format and provides a solution to many data storage and dissemination issues.     

Savanna chimpanzees, Pan troglodytes verus, hunt with tools

Although tool use is known to occur in species ranging from naked mole rats [1] to owls [2], chimpanzees are the most accomplished tool users [3-5]. The modification and use of tools during hunting, however, is still considered to be a uniquely human trait among primates. Here, we report the first account of habitual tool use during vertebrate hunting by nonhumans. At the Fongoli site in Senegal, we observed ten different chimpanzees use tools to hunt prosimian prey in 22 bouts. This includes immature chimpanzees and females, members of age-sex classes not normally characterized by extensive hunting behavior. Chimpanzees made 26 different tools, and we were able to recover and analyze 12 of these. Tool construction entailed up to five steps, including trimming the tool tip to a point. Tools were used in the manner of a spear, rather than a probe or rousing tool. This new information on chimpanzee tool use has important implications for the evolution of tool use and construction for hunting in the earliest hominids, especially given our observations that females and immature chimpanzees exhibited this behavior more frequently than adult males.     

Childhood cancer survival: A report from the United Kingdom Childhood Cancer Study

Background: Improvements in diagnostic approaches and refinements to treatment protocols have resulted in 5-year survival levels above 70% for children diagnosed with cancer in economically developed parts of the world. For some cancers, including leukaemia and tumours of the central nervous system, age and sex have been identified as important prognostic indicators. Methods: We examined long-term survival, and affects of age and sex, in a population-based case–control study. Children (0–14 years) newly diagnosed with cancer were ascertained between 1991 and 1996 (n = 4433). Follow-up information was obtained from the National Health Service (NHS) Information Centre for Health and Social Care which records all exits from the NHS including deaths. Results: For all cancer diagnoses combined, 5-year survival was 72.7% dropping to 67.9% at 15 years. As expected, survival differed between diagnostic subtypes ranging from 38.1% for intracranial embryonal tumours to 96.2% for Hodgkin lymphoma. Compared to girls, boys diagnosed with acute lymphoblastic leukaemia were at a higher risk of dying (RR = 1.26, 95% CI 1.03–1.53), whereas boys diagnosed with an intracranial embryonal tumour were at a lower risk of death (RR = 0.63, 95% CI 0.43–0.91). Conclusion: Our initial findings are consistent with previous reports, and highlight the importance of considering differences by age and sex. The completeness and population-based nature of the original case–control study is an important feature which will provide the basis for future more detailed investigations linking disease determinants to outcome.     

Cardioprotective effects of ingliforib, a novel glycogen phosphorylase inhibitor

Interventions such as glycogen depletion, which limit myocardial anaerobic glycolysis and the associated proton production, can reduce myocardial ischemic injury; thus it follows that inhibition of glycogenolysis should also be cardioprotective. Therefore, we examined whether the novel glycogen phosphorylase inhibitor 5-Chloro-N-[(1S,2R)-3-[(3R,4S)-3,4-dihydroxy-1-pyrrolidinyl)]-2-hydroxy-3-oxo-1-(phenylmethyl)propyl]-1H-indole-2-carboxamide (ingliforib; CP-368,296) could reduce infarct size in both in vitro and in vivo rabbit models of ischemia-reperfusion injury (30 min of regional ischemia, followed by 120 min of reperfusion). In Langendorff-perfused hearts, constant perfusion of ingliforib started 30 min before regional ischemia and elicited a concentration-dependent reduction in infarct size; infarct size was reduced by 69% with 10 microM ingliforib. No significant drug-induced changes were observed in either cardiac function (heart rate, left ventricular developed pressure) or coronary flow. In open-chest anesthetized rabbits, a dose of ingliforib (15 mg/kg loading dose; 23 mg.kg(-1).h(-1) infusion) selected to achieve a free plasma concentration equivalent to an estimated EC(50) in the isolated hearts (1.2 microM, 0.55 microg/ml) significantly reduced infarct size by 52%, and reduced plasma glucose and lactate concentrations. Furthermore, myocardial glycogen phosphorylase a and total glycogen phosphorylase activity were reduced by 65% and 40%, respectively, and glycogen stores were preserved in ingliforib-treated hearts. No significant change was observed in mean arterial pressure or rate-pressure product in the ingliforib group, although heart rate was modestly decreased postischemia. In conclusion, glycogen phosphorylase inhibition with ingliforib markedly reduces myocardial ischemic injury in vitro and in vivo; this may represent a viable approach for both achieving clinical cardioprotection and treating diabetic patients at increased risk of cardiovascular disease.     

Emerging views of integrin signaling: implications for prostate cancer

Integrins are heterodimeric transmembrane cellular receptors that link the cell to its underlying substratum. Alterations in integrin expression and signaling have been implicated in many aspects of tumorigenesis and metastasis including cell survival, migration, and invasion. In prostate cancer, the progression from normal to metastatic cells is accompanied by changes in the repertoire of integrins expressed and up-regulation of key adhesion-dependent signaling pathways. Recent work from several laboratories indicates the emergence of new mechanisms for the regulation of growth and migratory pathways by integrin engagement. These pathways are likely to provide novel sites of therapeutic intervention for the treatment of prostate cancer.