Social sustainability has three components. ‘Development’ social sustainability, is concerned with meeting basic needs, inter- and intra-generational equity, and so on. ‘Bridge sustainability’ ...focuses on changing behaviour so as to achieve bio-physical environmental goals. ‘Maintenance sustainability’ refers to social acceptance or what can be sustained in social terms.
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► Social sustainability has three components. ► The ‘development’ aspect is about meeting basic needs, inter- and intra-generational equity, etc. ► ‘Bridge sustainability’ focuses on changing behaviour to meet bio-physical environmental goals. ► ‘Maintenance sustainability’ refers to what can be sustained in social terms.
Though the concept of sustainable development originally included a clear social mandate, for two decades this human dimension has been neglected amidst abbreviated references to sustainability that have focused on bio-physical environmental issues, or been subsumed within a discourse that conflated ‘development’ and ‘economic growth’. The widespread failure of this approach to generate meaningful change has led to renewed interest in the concept of ‘social sustainability’ and aspects thereof. A review of the literature suggests, however, that it is a concept in chaos, and we argue that this severely compromises its importance and utility. The purpose of this paper is to examine this diverse literature so as to clarify what might be meant by the term social sustainability and highlight different ways in which it contributes to sustainable development more generally. We present a threefold schema comprising: (a) ‘development sustainability’ addressing basic needs, the creation of social capital, justice and so on; (b) ‘bridge sustainability’ concerning changes in behaviour so as to achieve bio-physical environmental goals and; (c) ‘maintenance sustainability’ referring to the preservation – or what can be sustained – of socio-cultural characteristics in the face of change, and the ways in which people actively embrace or resist those changes. We use this tripartite of social sustainabilities to explore ways in which contradictions and complements between them impede or promote sustainable development, and draw upon housing in urban areas as a means of explicating these ideas.
Catalytic C-H oxyfunctionalization reactions have garnered significant attention in recent years with their ability to streamline synthetic routes toward complex molecules. Consequently, there have ...been significant strides in the design and development of catalysts that enable diversification through C-H functionalization reactions. Enzymatic C-H oxygenation reactions are often complementary to small molecule based synthetic approaches, providing a powerful tool when deployable on preparative-scale. This review highlights key advances in scalable biocatalytic C-H oxyfunctionalization reactions developed within the past decade.
Biocatalytic methods for selective C-H oxyfunctionalization reactions are rapidly emerging and hold significant potential to streamline complex molecule synthesis. This review highlights key advances in this area developed within the past decade.
Achieving adequate bioscience learning and assessment in pre registration nursing programs has been problematic for many decades. This has been discussed extensively in national and international ...health care literature. Despite this, the quantity and quality of bioscience content appears currently in many UK registered nursing programs, to be in a period of decline.
Sub optimal bioscience knowledge of registered nurses has been consistently correlated with avoidable morbidity and mortality. An increasing evidence base indicates that a higher level of educated registered nurse, leads to improved health outcomes. It is therefore clear that continuing to fail to address the bioscience problem in nursing education has the potential to incur considerable adverse impact on the UK populations’ health.
The recent publication of new Nursing and Midwifery Council (NMC) standards of proficiency for registered nurses, and standards for pre-registration nursing programs require nurse education providers across the UK, to write new curriculum. The purpose of this discussion paper is to present the case for enhanced bioscience content within these.
•Enhanced bioscience curriculum content is required to improve health outcomes.•New proficiency and education standards give opportunity for the bioscience problem to be addressed.•Inadequate bioscience knowledge causes avoidable health harm, and dissatisfaction in nurses.•Increased bioscience knowledge is urgently required for the modern registered nursing role.
To better understand and quantify soiling rates on solar panels, we are investigating the adhesion mechanisms between dust particles and solar glass. In this work, we report on two of the fundamental ...adhesion mechanisms: van der Waals and capillary adhesion forces. The adhesion was determined using force versus distance (F-z) measurements performed with an atomic force microscope (AFM). To emulate dust interacting with the front surface of a solar panel, we measured how oxidized AFM tips, SiO2 glass spheres, and real dust particles adhered to actual solar glass. The van der Waals forces were evaluated by measurements performed with zero relative humidity in a glove box, and the capillary forces were measured in a stable environment created inside the AFM enclosure with relative humidity values ranging from 18% to 80%. To simulate topographic features of the solar panels caused by factors such as cleaning and abrasion, we induced different degrees of surface roughness in the solar glass. We were able to 1) identify and quantify both the van der Waals and capillary forces, 2) establish the effects of surface roughness, relative humidity, and particle size on the adhesion mechanisms, and 3) compare adhesion forces between well-controlled particles (AFM tips and glass spheres) and real dust particles.
•Determination of the initial soiling mechanisms on solar glass: van der Waals, capillary forces.•Measurements using simulated dust particles, AFM tips and glass spheres, and real dust particles.•Study of the influence of surface roughness, humidity, particle size on the soiling mechanisms.•Results explain report that hurricane-speed wind is not able to remove small particles from glass.•Theoretical model provides good agreement with the van der Waals interaction.
The endothelial cell adhesion molecule E-selectin is a key component of the bone marrow hematopoietic stem cell (HSC) vascular niche regulating balance between HSC self-renewal and commitment. We now ...report in contrast, E-selectin directly triggers signaling pathways that promote malignant cell survival and regeneration. Using acute myeloid leukemia (AML) mouse models, we show AML blasts release inflammatory mediators that upregulate endothelial niche E-selectin expression. Alterations in cell-surface glycosylation associated with oncogenesis enhances AML blast binding to E-selectin and enable promotion of pro-survival signaling through AKT/NF-κB pathways. In vivo AML blasts with highest E-selectin binding potential are 12-fold more likely to survive chemotherapy and main contributors to disease relapse. Absence (in Sele
hosts) or therapeutic blockade of E-selectin using small molecule mimetic GMI-1271/Uproleselan effectively inhibits this niche-mediated pro-survival signaling, dampens AML blast regeneration, and strongly synergizes with chemotherapy, doubling the duration of mouse survival over chemotherapy alone, whilst protecting endogenous HSC.
Summary
Background CRTH2 is a G‐protein‐coupled receptor that mediates the activation of Th2 lymphocytes, eosinophils and basophils in response to prostaglandin D2 and may be involved in the ...pathogenesis of airway inflammation and dysfunction in asthma.
Objective To evaluate the effects of a potent and selective CRTH2 antagonist, OC000459, on the lung function, symptoms and eosinophilic airway inflammation in a double‐blind, parallel group trial in steroid‐free subjects with moderate persistent asthma.
Methods Adult subjects were randomized to oral OC000459 200 mg twice daily (N=65) or a placebo (N=67) for 28 days. The primary end‐point was the change from baseline in pre‐bronchodilator forced expiratory volume in 1 s (FEV1); eosinophilic airway inflammation was assessed by induced sputum differential eosinophil count. The trial was registered on the clinicaltrials.gov database (Identifier NCT01057927).
Results Data were analysed for both the Full Analysis (FA) population and the Per Protocol (PP) population (55 treated with OC000459 and 52 with placebo), which excluded non‐compliant subjects. In the FA population, the mean change in FEV1 was 7.1% on OC000459 compared with 4.3% on placebo (not significant); in the PP population, the mean changes were 9.2% and 1.8%, respectively (P=0.037). Improvement in quality of life was apparent in both FA and PP populations difference from the placebo in AQLQ(S) total score of 0.29, P=0.0113 and 0.37, P=0.0022, respectively. OC000459 also improved the night‐time symptom scores (mean reduction of 0.36 vs. 0.11, P=0.008, FA population; 0.37 vs. 0.12, P=0.022, PP population). The geometric mean sputum eosinophil count reduced from 2.1% to 0.7% (P=0.03) after OC000459, but this effect was not significant when compared with the change on placebo (P=0.37). Adverse events on OC000459 were comparable to those on placebo; respiratory infections were notably less common during OC000459 than the placebo treatment.
Conclusion and Clinical Relevance This study provides the first clinical evidence that CRTH2 receptors contribute to airflow limitation, symptoms and eosinophilic airway inflammation in asthma. OC000459 shows promise as a novel oral treatment for asthma and related disorders.
Cite this as: N. Barnes, I. Pavord, A. Chuchalin, J. Bell, M. Hunter, T. Lewis, D. Parker, M. Payton, L. Pearce Collins, R. Pettipher, J. Steiner and C. M. Perkins, Clinical & Experimental Allergy, 2012 (42) 38–48.
MUC1 is associated with cellular transformation and tumorigenicity and is considered as an important tumor-associated antigen (TAA) for cancer therapy. We previously reported that anti-MUC1 ...monoclonal antibody C595 (MAb C595) plus docetaxel (DTX) increased efficacy of DTX alone and caused cultured human epithelial ovarian cancer (EOC) cells to undergo apoptosis. To further study the mechanisms of this combination-mediated apoptosis, we investigated the effectiveness of this combination therapy in vivo in an intraperitoneal (i.p.) EOC mouse model. OVCAR-3 cells were implanted intraperitoneally in female athymic nude mice and allowed to grow tumor and ascites. Mice were then treated with single MAb C595, DTX, combination test (MAb C595 and DTX), combination control (negative MAb IgG(3) and DTX) or vehicle control i.p. for 3 weeks. Treated mice were killed 4 weeks post-treatment. Ascites volume, tumor weight, CA125 levels from ascites and survival of animals were assessed. The expression of MUC1, CD31, Ki-67, TUNEL and apoptotic proteins in tumor xenografts was evaluated by immunohistochemistry. MAb C595 alone inhibited i.p. tumor growth and ascites production in a dose-dependent manner but did not obviously prevent tumor development. However, combination test significantly reduced ascites volume, tumor growth and metastases, CA125 levels in ascites and improved survival of treated mice compared with single agent-treated mice, combination control or vehicle control-treated mice (P<0.05). The data was in a good agreement with that from cultured cells in vitro. The mechanisms behind the observed effects could be through targeting MUC1 antigens, inhibition of tumor angiogenesis, and induction of apoptosis. Our results suggest that this combination approach can effectively reduce tumor burden and ascites, prolong survival of animals through induction of tumor apoptosis and necrosis, and may provide a potential therapy for advanced metastatic EOC.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Autosomal recessive polycystic kidney disease (ARPKD), usually considered to be a genetically homogeneous disease caused by mutations in PKHD1, has been associated with ciliary dysfunction. Here, we ...describe mutations in DZIP1L, which encodes DAZ interacting protein 1-like, in patients with ARPKD. We further validated these findings through loss-of-function studies in mice and zebrafish. DZIP1L localizes to centrioles and to the distal ends of basal bodies, and interacts with septin2, a protein implicated in maintenance of the periciliary diffusion barrier at the ciliary transition zone. In agreement with a defect in the diffusion barrier, we found that the ciliary-membrane translocation of the PKD proteins polycystin-1 and polycystin-2 is compromised in DZIP1L-mutant cells. Together, these data provide what is, to our knowledge, the first conclusive evidence that ARPKD is not a homogeneous disorder and further establish DZIP1L as a second gene involved in ARPKD pathogenesis.
ACE (adverse childhood experience) studies typically examine the links between childhood stressors and adult health harming behaviours. Using an enhanced ACE survey methodology, we examine impacts of ...ACEs on non-communicable diseases and incorporate a proxy measure of premature mortality in England.
A nationally representative survey was undertaken (n = 3885, aged 18-69, April-July 2013). Socio-demographically controlled proportional hazards analyses examined the associations between the number of ACE categories (<18 years; e.g. child abuse and family dysfunction such as domestic violence) and cancer, diabetes, stroke, respiratory, liver/digestive and cardiovascular disease. Sibling (n = 6983) mortality was similarly analysed as a measure of premature mortality.
Of the total, 46.4% of respondents reported ≥1 and 8.3% ≥4 ACEs. Disease development was strongly associated with increased ACEs (e.g. hazard ratios, HR, 0 versus ≥4 ACEs; cancer, 2.38 (1.48-3.83); diabetes, 2.99 (1.90-4.72); stroke, 5.79 (2.43-13.80, all P < 0.001). Individuals with ≥4 ACEs (versus no ACEs) had a 2.76 times higher rate of developing any disease before age 70 years. Adjusted HR for mortality was strongly linked to ACEs (≥4 versus 0 ACEs; HR, 1.97 (1.39-2.79), P < 0.001).
Radically different life-course trajectories are associated with exposure to increased ACEs. Interventions to prevent ACEs are available but rarely implemented at scale. Treating the resulting health costs across the life course is unsustainable.
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