Cities around the world are facing an ever-increasing variety of challenges that seem to make more sustainable urban futures elusive. Many of these challenges are being driven by, and exacerbated by, increases in urban populations and climate change. Novel solutions are needed today if our cities are to have any hope of more sustainable and resilient futures. Because most of the environmental impacts of any project are manifest at the point of design, we posit that this is where a real difference in urban development can be made. To this end, we present a transformative model that merges urban design and ecology into an inclusive, creative, knowledge-to-action process. This design-ecology nexus—an ecology for cities—will redefine both the process and its products. In this paper we: (1) summarize the relationships among design, infrastructure, and urban development, emphasizing the importance of joining the three to achieve urban climate resilience and enhance sustainability; (2) discuss how urban ecology can move from an ecology of cities to an ecology for cities based on a knowledge-to-action agenda; (3) detail our model for a transformational urban design-ecology nexus, and; (4) demonstrate the efficacy of our model with several case studies.

The purpose of applying social-ecological resilience thinking to food systems is twofold: First, to define those factors that help achieve a state in which food security for all and at all scales is possible. Second, to provide insights into how to maintain the system in this desirable regime. However, the resilience of food systems is distinct from the broader conceptualizations of resilience in social-ecological systems because of the fundamentally normative nature of food systems: humans need food to survive, and thus system stability is typically a primary policy objective for food system management. With that being said, society also needs food systems that can intensify sustainably i.e., feed everybody equitably, provide livelihoods and avoid environmental degradation while responding flexibly to shocks and uncertainty. Today’s failure in meeting food security objectives can be interpreted as the lack of current governance arrangements to consider the full and differential dimensions of food system functions – economic, ecological and social – at appropriate scales: in other words, the multifunctionality of food.

We focus on functional and response diversity as two key attributes of resilient, multifunctional food systems; respectively, the number of different functional groups and the diversity of types of responses to disturbances within a functional group. Achieving food security will require functional redundancy and enhanced response diversity, creating multiple avenues to fulfill all food system objectives. We use the 2013-15 drought in California to unpack the potential differences between managing for a single function – economic profit – and multiple functions. Our analysis emphasizes how the evolution of the Californian food system has reduced functional and response diversity and created vulnerabilities. Managing for the resilience of food systems will require a shift in priorities from profit maximization to the management for all functions that create full food security at multiple scales.

This article identifies equity outcomes associated with three biofuel systems in Brazil, Ethiopia and Guatemala. Acknowledging that winners and losers are socially and politically generated, the article identifies some of the factors behind the distribution of winners and losers along different stages of three sugarcane-ethanol supply chains. Analysing the outcomes for equity within each case study reveals an uneven distribution that we argue is related to the procedure and structure of the given sugarcane-ethanol system, and the recognition of the impacts on different actors within those structures. Increasing equity in sugarcane-ethanol systems will require greater openness in decision making processes, in order that multiple voices are taken into account in the promotion, production and consumption of biofuels – particularly those of smaller and less powerful actors.

Studies in both terrestrial and aquatic ecosystems have documented the potential importance of consumers on ecosystem-level nutrient dynamics. This is especially true when aggregations of organisms create biogeochemical hotspots through nutrient consumption, assimilation, and remineralization via excretion and egestion. Here, we focused on aggregations of humans in cities to examine how diet and waste management interact to drive nitrogen- (N) and phosphorus- (P) fluxes into nutrient pollution, inert forms, and nutrient recycling. We constructed six diet patterns (five US-based and one developing nation) to examine N- and P-consumption and excretion, and explored their implications for human health. Next, we constructed six waste-management patterns (three US and three for developing nations) to model how decisions at household and city scales determine the eventual fates of N and P. When compared to the US Recommended Daily Intake, all US diet patterns exceeded N and P requirements. Other than the “enriched CO₂ environment scenario” diet, the typical US omnivore had the greatest excess (37% N and 62% P). Notably, P from food additives could account for all of the excess P found in US omnivore and vegetarian diets. Across all waste-management approaches, a greater proportion of P was stored or recycled (0 to > 100% more P than N) and a greater proportion of N was released as effluent (20 to > 100% more N than P) resulting in pollution enriched with N and a recycling stream enriched with P. In developing nations, 60% of N and 50% of P from excreta entered the environment as pollution because of a lack of sanitation infrastructure. Our study demonstrates a novel addition to modeling sustainable scenarios for urban N- and P-budgets by linking human diets and waste management through socio-ecological systems.

The field of cyanobacterial biofuel production is advancing rapidly, yet we know little of the basic biology of these organisms outside of their photosynthetic pathways. We aimed to gain a greater understanding of how the cyanobacterium Synechocystis PCC 6803 (Synechocystis, hereafter) modulates its cell surface. Such understanding will allow for the creation of mutants that autoflocculate in a regulated way, thus avoiding energy intensive centrifugation in the creation of biofuels. We constructed mutant strains lacking genes predicted to function in carbohydrate transport or synthesis. Strains with gene deletions of slr0977 (predicted to encode a permease component of an ABC transporter), slr0982 (predicted to encode an ATP binding component of an ABC transporter) and slr1610 (predicted to encode a methyltransferase) demonstrated flocculent phenotypes and increased adherence to glass. Upon bioinformatic inspection, the gene products of slr0977, slr0982, and slr1610 appear to function in O-antigen (OAg) transport and synthesis. However, the analysis provided here demonstrated no differences between OAg purified from wild-type and mutants. However, exopolysaccharides (EPS) purified from mutants were altered in composition when compared to wild-type. Our data suggest that there are multiple means to modulate the cell surface of Synechocystis by disrupting different combinations of ABC transporters and/or glycosyl transferases. Further understanding of these mechanisms may allow for the development of industrially and ecologically useful strains of cyanobacteria. Additionally, these data imply that many cyanobacterial gene products may possess as-yet undiscovered functions, and are meritorious of further study.

Avian pathogenic Escherichia coli (APEC) strains cause systemic and localized infections in poultry, jointly termed colibacillosis. Avian colibacillosis is responsible for significant economic losses to the poultry industry due to disease treatment, decrease in growth rate and egg production, and mortality. APEC are also considered a potential zoonotic risk for humans. Fully elucidating the virulence and zoonotic potential of APEC is key for designing successful strategies against their infections and their transmission. Herein, we investigated the prevalence of a newly discovered E. coli common pilus (ECP) for the subunit protein of the ECP pilus (ecpA) and ECP expression amongst APEC strains as well as the role of ECP in virulence. A PCR-based ecpA survey of a collection of 167 APEC strains has shown that 76% (127/167) were ecpA+. An immunofluorescence assay using anti-EcpA antibodies, revealed that among the ecpA+ strains, 37.8% (48/127) expressed ECP when grown in DMEM +0.5% Mannose in contact with HeLa cells at 37°C and/or in biofilm at 28°C; 35.4% (17/48) expressed ECP in both conditions and 64.6% (31/48) expressed ECP in biofilm only. We determined that the ecp operon in the APEC strain χ7122 (ecpA+, ECP-) was not truncated; the failure to detect ECP in some strains possessing non-truncated ecp genes might be attributed to differential regulatory mechanisms between strains that respond to specific environmental signals. To evaluate the role of ECP in the virulence of APEC, we generated ecpA and/or ecpD-deficient mutants from the strain χ7503 (ecpA+, ECP+). Deletion of ecpA and/or ecpD abolished ECP synthesis and expression, and reduced biofilm formation and motility in vitro and virulence in vivo. All together our data show that ecpA is highly prevalent among APEC isolates and its expression could be differentially regulated in these strains, and that ECP plays a role in the virulence of APEC.

The unicellular green microalga Desmodesmus sp. S1 can produce more than 50% total lipid of cell dry weight under high light and nitrogen-limitation conditions. After irradiation by heavy ¹²C⁶⁺ ion beam of 10, 30, 60, 90 or 120 Gy, followed by screening of resulting mutants on 24-well microplates, more than 500 mutants were obtained. One of those, named D90G-19, exhibited lipid productivity of 0.298 g L^-1⋅d^-1, 20.6% higher than wild type, likely owing to an improved maximum quantum efficiency (Fv/Fm) of photosynthesis under stress. This work demonstrated that heavy-ion irradiation combined with high-throughput screening is an effective means for trait improvement. The resulting mutant D90G-19 may be used for enhanced lipid production.

Urban areas consume more than 66% of the world’s energy and generate more than 70% of global greenhouse gas emissions. With the world’s population expected to reach 10 billion by 2100, nearly 90% of whom will live in urban areas, a critical question for planetary sustainability is how the size of cities affects energy use and carbon dioxide (CO₂) emissions. Are larger cities more energy and emissions efficient than smaller ones? Do larger cities exhibit gains from economies of scale with regard to emissions? Here we examine the relationship between city size and CO₂ emissions for U.S. metropolitan areas using a production accounting allocation of emissions. We find that for the time period of 1999–2008, CO₂ emissions scale proportionally with urban population size. Contrary to theoretical expectations, larger cities are not more emissions efficient than smaller ones.

Introduction: The ketogenic diet (KD) is a high-fat, low-carbohydrate diet that alters metabolism by increasing the level of ketone bodies in the blood. KetoCal® (KC) is a nutritionally complete, commercially available 4∶1 (fat∶ carbohydrate+protein) ketogenic formula that is an effective non-pharmacologic treatment for the management of refractory pediatric epilepsy. Diet-induced ketosis causes changes to brain homeostasis that have potential for the treatment of other neurological diseases such as malignant gliomas.

Methods: We used an intracranial bioluminescent mouse model of malignant glioma. Following implantation animals were maintained on standard diet (SD) or KC. The mice received 2×4 Gy of whole brain radiation and tumor growth was followed by in vivo imaging.

Results: Animals fed KC had elevated levels of β-hydroxybutyrate (p = 0.0173) and an increased median survival of approximately 5 days relative to animals maintained on SD. KC plus radiation treatment were more than additive, and in 9 of 11 irradiated animals maintained on KC the bioluminescent signal from the tumor cells diminished below the level of detection (p<0.0001). Animals were switched to SD 101 days after implantation and no signs of tumor recurrence were seen for over 200 days.

Conclusions: KC significantly enhances the anti-tumor effect of radiation. This suggests that cellular metabolic alterations induced through KC may be useful as an adjuvant to the current standard of care for the treatment of human malignant gliomas.

Background: The successful treatment of malignant gliomas remains a challenge despite the current standard of care, which consists of surgery, radiation and temozolomide. Advances in the survival of brain cancer patients require the design of new therapeutic approaches that take advantage of common phenotypes such as the altered metabolism found in cancer cells. It has therefore been postulated that the high-fat, low-carbohydrate, adequate protein ketogenic diet (KD) may be useful in the treatment of brain tumors. We have demonstrated that the KD enhances survival and potentiates standard therapy in a mouse model of malignant glioma, yet the mechanisms are not fully understood.

Methods: To explore the effects of the KD on various aspects of tumor growth and progression, we used the immunocompetent, syngeneic GL261-Luc2 mouse model of malignant glioma.

Results: Tumors from animals maintained on KD showed reduced expression of the hypoxia marker carbonic anhydrase 9, hypoxia inducible factor 1-alpha, and decreased activation of nuclear factor kappa B. Additionally, tumors from animals maintained on KD had reduced tumor microvasculature and decreased expression of vascular endothelial growth factor receptor 2, matrix metalloproteinase-2 and vimentin. Peritumoral edema was significantly reduced in animals fed the KD and protein analyses showed altered expression of zona occludens-1 and aquaporin-4.

Conclusions: The KD directly or indirectly alters the expression of several proteins involved in malignant progression and may be a useful tool for the treatment of gliomas.