Unexpected changes in community size structure in a natural warming experiment

Natural ecosystems typically consist of many small and few large organisms. The scaling of this negative relationship between body mass and abundance has important implications for resource partitioning and energy usage. Global warming over the next century is predicted to favour smaller organisms, producing steeper mass-abundance scaling and a less efficient transfer of biomass through the food web. Here, we show that the opposite effect occurs in a natural warming experiment involving 13 whole-stream ecosystems within the same catchment, which span a temperature gradient of 5-25 °C. We introduce a mechanistic model that shows how the temperature dependence of basal resource carrying capacity can account for these previously unexpected results. If nutrient supply increases with temperature to offset the rising metabolic demand of primary producers, there will be sufficient resources to sustain larger consumers at higher trophic levels. These new data and the model that explains them highlight important exceptions to some commonly assumed 'rules' about responses to warming in natural ecosystems

COVID-19: Rapid antigen detection for SARS-CoV-2 by lateral flow assay: A national systematic evaluation of sensitivity and specificity for mass-testing

Background Lateral flow device (LFD) viral antigen immunoassays have been developed around the world as diagnostic tests for SARS-CoV-2 infection. They have been proposed to deliver an infrastructure-light, cost-economical solution giving results within half an hour. Methods LFDs were initially reviewed by a Department of Health and Social Care team, part of the UK government, from which 64 were selected for further evaluation from 1st August to 15th December 2020. Standardised laboratory evaluations, and for those that met the published criteria, field testing in the Falcon-C19 research study and UK pilots were performed (UK COVID-19 testing centres, hospital, schools, armed forces). Findings 4/64 LFDs so far have desirable performance characteristics (orient Gene, Deepblue, Abbott and Innova SARS-CoV-2 Antigen Rapid Qualitative Test). All these LFDs have a viral antigen detection of >90% at 100,000 RNA copies/ml. 8951 Innova LFD tests were performed with a kit failure rate of 5.6% (502/8951, 95% CI: 5.1–6.1), false positive rate of 0.32% (22/6954, 95% CI: 0.20–0.48). Viral antigen detection/sensitivity across the sampling cohort when performed by laboratory scientists was 78.8% (156/198, 95% CI 72.4–84.3). Interpretation Our results suggest LFDs have promising performance characteristics for mass population testing and can be used to identify infectious positive individuals. The Innova LFD shows good viral antigen detection/sensitivity with excellent specificity, although kit failure rates and the impact of training are potential issues. These results support the expanded evaluation of LFDs, and assessment of greater access to testing on COVID-19 transmission. Funding Department of Health and Social Care. University of Oxford. Public Health England Porton Down, Manchester University NHS Foundation Trust, National Institute of Health Research

Disease-modifying and susceptibility genes in copd

Chronic obstructive pulmonary disease (COPD), the 3rd leading cause of disease burden in Australia, involves cigarette smoke-induced airway inflammation. Elucidating its molecular pattiophysiology is important for advancing the treatment of this disease. Critical inflammatory and defence mediators have now been identified, together with the discovery of natural genetic variation in their encoding genes. Aim: To examine how variations in ( 1 ) pro-inflammatory (TNFa, IL-6, TGFβf), (2) anti-inflammatory (IL-IRa) and (3) host defence (myelopemxidase IMPO). mamose-binding lectin (MBL), P450 CYPIA1, glutathione-S-tramferases IGST)) genes affect the COPD phenotype. Methods: Genotypes of these variants were determined by PCR in an Australian cohort of 237 COPD subjects (mean age 69y, FEVj 43 pred) and compared to 2 control groups: 76 smokers with normal lung function and 207 healthy blood donors. Detailed lung function was measured, together with TNFa levels and HRCT in a subset. Results: Susceptibility to COPD was associated with the CYPIAI variant (OR 2.7, p=0.017). Furthermore, susceptibility to chronic bronchitis was predicted by variant TGF] and TNFa genes (OR 4.0 and 1.6 respectively, p0.05). Moreover, COPD subjects with the MBL variant were more likely to be chronic bronchitics (OR 1.8, p=0.05). Lower KCO (55% vs. 62% pred.) was associated with the null GSTMl genotype (p=0.026). We also found that TNFa gene variation resulted in differences in the level of peripheral blood monocyte TNFa levels (364 vs 207 pg/ml. p=0.02). Conclusions: This is the first report in COPD of (1) novel associations between variations in key genes with susceptibility and disease phenotype, and (2) significant differences in TNFa levels due to interindividual TNFa gene variation. The identification of genes relevant to COPD should lead to biologically-based, targeted prevention and intervention strategies for at-risk individuals.</p

Disease-modifying and susceptibility genes in copd

Chronic obstructive pulmonary disease (COPD), the 3rd leading cause of disease burden in Australia, involves cigarette smoke-induced airway inflammation. Elucidating its molecular pattiophysiology is important for advancing the treatment of this disease. Critical inflammatory and defence mediators have now been identified, together with the discovery of natural genetic variation in their encoding genes. Aim: To examine how variations in ( 1 ) pro-inflammatory (TNFa, IL-6, TGFβf), (2) anti-inflammatory (IL-IRa) and (3) host defence (myelopemxidase IMPO). mamose-binding lectin (MBL), P450 CYPIA1, glutathione-S-tramferases IGST)) genes affect the COPD phenotype. Methods: Genotypes of these variants were determined by PCR in an Australian cohort of 237 COPD subjects (mean age 69y, FEVj 43 pred) and compared to 2 control groups: 76 smokers with normal lung function and 207 healthy blood donors. Detailed lung function was measured, together with TNFa levels and HRCT in a subset. Results: Susceptibility to COPD was associated with the CYPIAI variant (OR 2.7, p=0.017). Furthermore, susceptibility to chronic bronchitis was predicted by variant TGF] and TNFa genes (OR 4.0 and 1.6 respectively, p0.05). Moreover, COPD subjects with the MBL variant were more likely to be chronic bronchitics (OR 1.8, p=0.05). Lower KCO (55% vs. 62% pred.) was associated with the null GSTMl genotype (p=0.026). We also found that TNFa gene variation resulted in differences in the level of peripheral blood monocyte TNFa levels (364 vs 207 pg/ml. p=0.02). Conclusions: This is the first report in COPD of (1) novel associations between variations in key genes with susceptibility and disease phenotype, and (2) significant differences in TNFa levels due to interindividual TNFa gene variation. The identification of genes relevant to COPD should lead to biologically-based, targeted prevention and intervention strategies for at-risk individuals

Magnetic nanoparticles as mediators of ligand-free activation of EGFR signaling.

Magnetic nanoparticles (NPs) are of particular interest in biomedical research, and have been exploited for molecular separation, gene/drug delivery, magnetic resonance imaging, and hyperthermic cancer therapy. In the case of cultured cells, magnetic manipulation of NPs provides the means for studying processes induced by mechanotransduction or by local clustering of targeted macromolecules, e.g. cell surface receptors. The latter are normally activated by binding of their natural ligands mediating key signaling pathways such as those associated with the epidermal growth factor (EGFR). However, it has been reported that EGFR may be dimerized and activated even in the absence of ligands. The present study assessed whether receptor clustering induced by physical means alone suffices for activating EGFR in quiescent cells