Centrifuge modelling of building response to tunnel excavation

Understanding the building response to tunnelling-induced settlements is an important aspect of urban tunnelling in soft ground. Previous centrifuge modelling research demonstrated significant potential to study this tunnel–soil–structure interaction problem. However, these recent studies were limited by simplified building models, which might result in uncertainties when interpreting the building performance to tunnelling subsidence. This paper presents an experimental modelling procedure and the results of a series of centrifuge tests, involving relatively complex surface structures subjected to tunnelling in sand. Powder-based three-dimensional (3D) printing was adopted to fabricate building models with realistic layouts, facade openings and foundations. The 3D printed material had a Young's modulus and a brittle response similar to historic masonry. Modelling effects and boundary conditions are quantified. The good agreement between the experimentally obtained results and previous research demonstrates that the soil–structure interaction during tunnel excavation is well replicated. The experimental procedure provides a framework to quantify how building features affect the response of buildings to tunnelling subsidence.The authors are grateful to EPSRC grant EP/K018221/1 and Crossrail for the financial support

Stepped wedge cluster randomized controlled trial designs: a review of reporting quality and design features

Background The stepped wedge (SW) cluster randomized controlled trial (CRCT) design is being used with increasing frequency. However, there is limited published research on the quality of reporting of SW-CRCTs. We address this issue by conducting a literature review. Methods Medline, Ovid, Web of Knowledge, the Cochrane Library, PsycINFO, the ISRCTN registry, and ClinicalTrials.gov were searched to identify investigations employing the SW-CRCT design up to February 2015. For each included completed study, information was extracted on a selection of criteria, based on the CONSORT extension to CRCTs, to assess the quality of reporting. Results A total of 123 studies were included in our review, of which 39 were completed trial reports. The standard of reporting of SW-CRCTs varied in quality. The percentage of trials reporting each criterion varied to as low as 15.4%, with a median of 66.7%. Conclusions There is much room for improvement in the quality of reporting of SW-CRCTs. This is consistent with recent findings for CRCTs. A CONSORT extension for SW-CRCTs is warranted to standardize the reporting of SW-CRCTs.This work was supported by the Wellcome Trust (grant number 099770/Z/12/Z to MJG); the Medical Research Council (grant number MC_UP_1302/2 to APM) and the National Institute for Health Research Cambridge Biomedical Research Centre (MC_UP_1302/4 to JMSW)

Nitric Oxide Deficiency Accelerates Chlorophyll Breakdown and Stability Loss of Thylakoid Membranes during Dark-Induced Leaf Senescence in Arabidopsis

<div><p>Nitric oxide (NO) has been known to preserve the level of chlorophyll (Chl) during leaf senescence. However, the mechanism by which NO regulates Chl breakdown remains unknown. Here we report that NO negatively regulates the activities of Chl catabolic enzymes during dark-induced leaf senescence. The transcriptional levels of the major enzyme genes involving Chl breakdown pathway except for <em>RED CHL CATABOLITE REDUCTASE</em> (<em>RCCR</em>) were dramatically up-regulated during dark-induced Chl degradation in the leaves of Arabidopsis NO-deficient mutant <em>nos1/noa1</em> that exhibited an early-senescence phenotype. The activity of pheide <em>a</em> oxygenase (PAO) was higher in the dark-induced senescent leaves of <em>nos1/noa1</em> compared with wild type. Furthermore, the knockout of <em>PAO</em> in <em>nos1/noa1</em> background led to pheide <em>a</em> accumulation in the double mutant <em>pao1 nos1/noa1</em>, which retained the level of Chl during dark-induced leaf senescence. The accumulated pheide <em>a</em> in darkened leaves of <em>pao1 nos1/noa1</em> was likely to inhibit the senescence-activated transcriptional levels of Chl catabolic genes as a feed-back inhibitory effect. We also found that NO deficiency led to decrease in the stability of photosynthetic complexes in thylakoid membranes. Importantly, the accumulation of pheide <em>a</em> caused by <em>PAO</em> mutations in combination with NO deficiency had a synergistic effect on the stability loss of thylakoid membrane complexes in the double mutant <em>pao1 nos1/noa1</em> during dark-induced leaf senescence. Taken together, our findings have demonstrated that NO is a novel negative regulator of Chl catabolic pathway and positively functions in maintaining the stability of thylakoid membranes during leaf senescence.</p> </div

Transcript levels of chlorophyll breakdown pathway genes in wild type and <i>nos1/noa1</i> mutant leaves during dark-induced senescence.

<p>(A) A suggestive model for chlorophyll breakdown pathway with integrating the recent findings in Arabidopsis. Thickness of arrows reflects relative activities of respective enzymes (Hörtensteiner, 2009). (B–F) qRT-PCR analysis of mRNA abundance of enzyme genes (<i>SGR</i>, <i>NYC1</i>, <i>PPH</i>, <i>PAO</i> and <i>RCCR</i>) involved in chlorophyll degradation in wild type and <i>nos1/noa1</i> mutant leaves during dark-induced senescence. <i>ACTIN2</i> was used as the internal standard. Error bars indicate standard deviations of three technical replicates, and the results were consistent in three biological replicates.</p

Dark-induced leaf senescence phenotypes of wild type, <i>nos1/noa1</i>, <i>pao1</i> and the double mutant <i>pao1 nos1/noa1</i>.

<p>(A) 3-week-old seedling phenotypes of wild type, <i>nos1/noa1</i>, <i>pao1</i> and the double mutant <i>pao1 nos1/noa1</i>. (B) Senescing phenotypes of the detached leaves in dark. The fully-expanded leaves were detached from the plants of the different genotypes shown in (A).</p

Activities of PAO in wild type and <i>nos1/noa1</i> leaves during dark-induced leaf senescence.

<p>HPLC analysis of pFCC-1 generated by PAO-RCCR coupled assay with crude extracts of PAO and RCCR from wild type and <i>nos1/noa1</i> leaves during a 4-d dark treatment. pFCC-1 was eluted after 9 min, as indicated by arrows. The experiment was repeated once with qualitatively identical results.</p

The file contains more information about the data and privacy compliance, the code, and the list of HEIs included in this study.

The file contains more information about the data and privacy compliance, the code, and the list of HEIs included in this study.</p

Percentage of negative sentiment distribution for all schools in each year (blue and red line represents median and mean, respectively).

Percentage of negative sentiment distribution for all schools in each year (blue and red line represents median and mean, respectively).</p

Abundance analysis of thylakoid membrane protein complexes from leaves incubated in dark.

<p>(A) Blue native-PAGE analysis of thylakoid membrane protein complexes from the detached leaves of wild type and the indicated mutants after a 4-d-dark treatment. (B) Western blotting analysis of thylakoid membrane protein degradation from the detached leaves of wild type and the indicated mutants after a 4-d-dark treatment.</p

Histograms of number of messages across schools by year (blue and red lines represent median and mean, respectively).

Histograms of number of messages across schools by year (blue and red lines represent median and mean, respectively).</p