Two aspects of decadal ENSO variability modulating the long-term global carbon cycle

The El Niño–Southern Oscillation (ENSO) drives variations in terrestrial carbon fluxes by affecting the terrestrial ecosystem via atmospheric teleconnections and thus plays an important role in interannual variability of the global carbon cycle. However, we lack such knowledge on decadal time scales, that is, how the carbon cycle can be affected by decadal variations of ENSO characteristics. Here we examine how, and by how much, decadal ENSO variability affects decadal variability of the global carbon cycle by analyzing a 1,801‐year preindustrial control simulation. We identify two different aspects, together explaining ~36% of the decadal variations in the global carbon cycle. First, climate variations induced by decadal ENSO‐like variability regulate terrestrial carbon flux and hence atmospheric CO2 on decadal time scales. Second, decadal changes in the asymmetrical response of the terrestrial ecosystem, resulting from decadal modulation of ENSO amplitude and asymmetry, rectify the background mean state, thereby generating decadal variability of land carbon fluxes

What is an intelligent building? Analysis of recent interpretations from an international perspective

In recent years, the notion of intelligent buildings (IBs) has become increasingly popular due to their potentials for deploying design initiatives and emerging technologies towards maximized occupants’ comfort and well-being with sustainable design. However, various definitions, interpretations, and implications regarding the essence of IBs exist. Various key performance indicators of IBs have been proposed in different contexts. This study explores the notion of IBs and presents an analysis of their main constituents. Through a comparison of these constituents in different contexts, this study aims to extract the common features of IBs leading to an evolved definition which could be useful as a reference framework for design, evaluation, and development of future IBs. Findings also scrutinize the long run benefits of IBs, while demonstrating the constraints and challenges of the current international interpretations

Resistant Starch: Promise for Improving Human Health

Ongoing research to develop digestion-resistant starch for human health promotion integrates the disciplines of starch chemistry, agronomy, analytical chemistry, food science, nutrition, pathology, and microbiology. The objectives of this research include identifying components of starch structure that confer digestion resistance, developing novel plants and starches, and modifying foods to incorporate these starches. Furthermore, recent and ongoing studies address the impact of digestion-resistant starches on the prevention and control of chronic human diseases, including diabetes, colon cancer, and obesity. This review provides a transdisciplinary overview of this field, including a description of types of resistant starches; factors in plants that affect digestion resistance; methods for starch analysis; challenges in developing food products with resistant starches; mammalian intestinal and gut bacterial metabolism; potential effects on gut microbiota; and impacts and mechanisms for the prevention and control of colon cancer, diabetes, and obesity. Although this has been an active area of research and considerable progress has been made, many questions regarding how to best use digestion-resistant starches in human diets for disease prevention must be answered before the full potential of resistant starches can be realized

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)

Lack of increased availability of root-derived C may explain the low N₂O emission from low N-urine patches

Urine deposition on grassland causes significant N2O losses, which in some cases may result from increased denitrification stimulated by labile compounds released from scorched plant roots. Two 12-day experiments were conducted in 13Clabelled grassland monoliths to investigate the link between N2O production and carbon mineralization following application of low rates of urine-N. Measurements of N2O and CO2 emissions from the monoliths as well as d13C signal of evolved CO2 were done on day )4, )1, 0, 1, 2, 4, 5, 6 and 7 after application of urine corresponding to 3.1 and 5.5 g N m)2 in the first and second experiment, respectively. The d13C signal was also determined for soil organic matter, dissolved organic C and CO2 evolved by microbial respiration. In addition, denitrifying enzyme activity (DEA) and nitrifying enzyme activity (NEA) were measured on day )1, 2 and 7 after the first urine application event. Urine did not affect DEA, whereas NEA was enhanced 2 days after urine application. In the first experiment, urine had no significant effect on the N2O flux, which was generally low ()8 to 14lg N2O-N m)2 h)1). After the second application event, the N2O emission increased significantly to 87 lg N2O-N m)2 h)1 and the N2O emission factor for the added urine-N was 0.18%. However, the associated 13C signal of soil respiration was unaffected by urine. Consequently, the increased N2O emission from the simulated low N-urine patches was not caused by enhanced denitrification stimulated by labile compounds released from scorched plant roots