Time sequence of the damage to the acceptor and donor sides of photosystem II by UV-B radiation as evaluated by chlorophyll a fluorescence

The effects of ultraviolet-B (UV-B) radiation on photosystem II (PS II) were studied in leaves of Chenopodium album. After the treatment with UV-B the damage was estimated using chlorophyll a fluorescence techniques. Measurements of modulated fluorescence using a pulse amplitude modulated fluorometer revealed that the efficiency of photosystem II decreased both with increasing time of UV-B radiation and with increasing intensity of the UV-B. Fluorescence induction rise curves were analyzed using a mechanistic model of energy trapping. It appears that the damage by UV-B radiation occurs first at the acceptor side of photosystem II, and only later at the donor side

Surface and Temporal Biosignatures

Recent discoveries of potentially habitable exoplanets have ignited the prospect of spectroscopic investigations of exoplanet surfaces and atmospheres for signs of life. This chapter provides an overview of potential surface and temporal exoplanet biosignatures, reviewing Earth analogues and proposed applications based on observations and models. The vegetation red-edge (VRE) remains the most well-studied surface biosignature. Extensions of the VRE, spectral "edges" produced in part by photosynthetic or nonphotosynthetic pigments, may likewise present potential evidence of life. Polarization signatures have the capacity to discriminate between biotic and abiotic "edge" features in the face of false positives from band-gap generating material. Temporal biosignatures -- modulations in measurable quantities such as gas abundances (e.g., CO2), surface features, or emission of light (e.g., fluorescence, bioluminescence) that can be directly linked to the actions of a biosphere -- are in general less well studied than surface or gaseous biosignatures. However, remote observations of Earth's biosphere nonetheless provide proofs of concept for these techniques and are reviewed here. Surface and temporal biosignatures provide complementary information to gaseous biosignatures, and while likely more challenging to observe, would contribute information inaccessible from study of the time-averaged atmospheric composition alone.Comment: 26 pages, 9 figures, review to appear in Handbook of Exoplanets. Fixed figure conversion error

Leucocyte subset-specific type 1 interferon signatures in SLE and other immune-mediated diseases.

OBJECTIVES: Type 1 interferons (IFN-1) are implicated in the pathogenesis of systemic lupus erythematosus (SLE), but most studies have only reported the effect of IFN-1 on mixed cell populations. We aimed to define modules of IFN-1-associated genes in purified leucocyte populations and use these as a basis for a detailed comparative analysis. METHODS: CD4+ and CD8+ T cells, monocytes and neutrophils were purified from patients with SLE, other immune-mediated diseases and healthy volunteers and gene expression then determined by microarray. Modules of IFN-1-associated genes were defined using weighted gene coexpression network analysis. The composition and expression of these modules was analysed. RESULTS: 1150 of 1288 IFN-1-associated genes were specific to myeloid subsets, compared with 11 genes unique to T cells. IFN-1 genes were more highly expressed in myeloid subsets compared with T cells. A subset of neutrophil samples from healthy volunteers (HV) and conditions not classically associated with IFN-1 signatures displayed increased IFN-1 gene expression, whereas upregulation of IFN-1-associated genes in T cells was restricted to SLE. CONCLUSIONS: Given the broad upregulation of IFN-1 genes in neutrophils including in some HV, investigators reporting IFN-1 signatures on the basis of whole blood samples should be cautious about interpreting this as evidence of bona fide IFN-1-mediated pathology. Instead, specific upregulation of IFN-1-associated genes in T cells may be a useful biomarker and a further mechanism by which elevated IFN-1 contributes to autoimmunity in SLE.SMF holds a Translational Medicine and Therapeutics PhD studentship from the Wellcome Trust and GlaxoSmithKline and has also received funding for this work from the Addenbrooke’s Charitable Trust. KGCS is the Khoo Oon Teik Professor of Nephrology, National University of Singapore. Singapore recruitment was supported by the Khoo Investigator Grant from the Duke-NUS Graduate Medical School, Singapore, and by National Medical Research Council of Singapore grants (NMRC/1164/2008 and IRG07nov089). This work was also supported by UK National Institute of Health Research Cambridge Biomedical Research Centre, the Lupus Research Institute (Distinguished Innovator Award, KGCS), the Medical Research Council UK (programme grant MR/L019027/1) and the Wellcome Trust (programme grant 083650/Z/07/Z and project grant 094227/Z/10/Z). The Cambridge Institute for Medical Research is in receipt of Wellcome Trust Strategic Award 079895.This is the final version of the article. It first appeared from BMJ Group via https://doi.org/10.1136/rmdopen-2015-00018

Frequency of D222G and Q223R Hemagglutinin Mutants of Pandemic (H1N1) 2009 Influenza Virus in Japan between 2009 and 2010

BACKGROUND: In April 2009, a novel swine-derived influenza A virus (H1N1pdm) emerged and rapidly spread around the world, including Japan. It has been suggested that the virus can bind to both 2,3- and 2,6-linked sialic acid receptors in infected mammals, in contrast to contemporary seasonal H1N1 viruses, which have a predilection for 2,6-linked sialic acid. METHODS/RESULTS: To elucidate the existence and transmissibility of α2,3 sialic acid-specific viruses in H1N1pdm, amino acid substitutions within viral hemagglutinin molecules were investigated, especially D187E, D222G, and Q223R, which are related to a shift from human to avian receptor specificity. Samples from individuals infected during the first and second waves of the outbreak in Japan were examined using a high-throughput sequencing approach. In May 2009, three specimens from mild cases showed D222G and/or Q223R substitutions in a minor subpopulation of viruses infecting these individuals. However, the substitutions almost disappeared in the samples from five mild cases in December 2010. The D187E substitution was not widespread in specimens, even in May 2009. CONCLUSIONS: These results suggest that α2,3 sialic acid-specific viruses, including G222 and R223, existed in humans as a minor population in the early phase of the pandemic, and that D222 and Q223 became more dominant through human-to-human transmission during the first and second waves of the epidemic. These results are consistent with the low substitution rates identified in seasonal H1N1 viruses in 2008

Adaptation of photosystem II to high and low light in wild-type and triazine-resistant Canola plants: analysis by a fluorescence induction algorithm

Plants of wild-type and triazine-resistant Canola (Brassica napus L.) were exposed to very high light intensities and after 1 day placed on a laboratory table at low light to recover, to study the kinetics of variable fluorescence after light, and after dark-adaptation. This cycle was repeated several times. The fast OJIP fluorescence rise curve was measured immediately after light exposure and after recovery during 1 day in laboratory room light. A fluorescence induction algorithm has been used for resolution and analysis of these curves. This algorithm includes photochemical and photo-electrochemical quenching release components and a photo-electrical dependent IP-component. The analysis revealed a substantial suppression of the photo-electrochemical component (even complete in the resistant biotype), a partial suppression of the photochemical component and a decrease in the fluorescence parameter Fo after high light. These effects were recovered after 1 day in the indoor light

Analysis of Combinatorial Regulation: Scaling of Partnerships between Regulators with the Number of Governed Targets

Through combinatorial regulation, regulators partner with each other to control common targets and this allows a small number of regulators to govern many targets. One interesting question is that given this combinatorial regulation, how does the number of regulators scale with the number of targets? Here, we address this question by building and analyzing co-regulation (co-transcription and co-phosphorylation) networks that describe partnerships between regulators controlling common genes. We carry out analyses across five diverse species: Escherichia coli to human. These reveal many properties of partnership networks, such as the absence of a classical power-law degree distribution despite the existence of nodes with many partners. We also find that the number of co-regulatory partnerships follows an exponential saturation curve in relation to the number of targets. (For E. coli and Bacillus subtilis, only the beginning linear part of this curve is evident due to arrangement of genes into operons.) To gain intuition into the saturation process, we relate the biological regulation to more commonplace social contexts where a small number of individuals can form an intricate web of connections on the internet. Indeed, we find that the size of partnership networks saturates even as the complexity of their output increases. We also present a variety of models to account for the saturation phenomenon. In particular, we develop a simple analytical model to show how new partnerships are acquired with an increasing number of target genes; with certain assumptions, it reproduces the observed saturation. Then, we build a more general simulation of network growth and find agreement with a wide range of real networks. Finally, we perform various down-sampling calculations on the observed data to illustrate the robustness of our conclusions

High precision branching ratio measurement for the superallowed beta decay of Rb-74: A prerequisite for exacting tests of the standard model

Journals published by the American Physical Society can be found at http://publish.aps.org/Nonanalog Fermi and Gamow-Teller branches in the superallowed beta decay of Rb-74 have been investigated using gamma-ray and conversion-electron spectroscopy. Nine observed transitions, in conjunction with a recent shell model calculation, determine the branching ratio of the analog transition to be 99.5(1)%. The experimental upper limits for the Fermi decay to the 0(2)(+) and (0(3)(+)) levels are in agreement with recent theoretical predictions. The Q(EC) value for the Rb-74 beta decay is predicted to be 10405(9) keV

Estimating Infection Attack Rates and Severity in Real Time during an Influenza Pandemic: Analysis of Serial Cross-Sectional Serologic Surveillance Data

This study reports that using serological data coupled with clinical surveillance data can provide real-time estimates of the infection attack rates and severity in an emerging influenza pandemic

Prevalence of 2009 Pandemic Influenza A (H1N1) Virus Antibodies, Tampa Bay Florida — November–December, 2009

BACKGROUND: In 2009, a novel influenza virus (2009 pandemic influenza A (H1N1) virus (pH1N1)) caused significant disease in the United States. Most states, including Florida, experienced a large fall wave of disease from September through November, after which disease activity decreased substantially. We determined the prevalence of antibodies due to the pH1N1 virus in Florida after influenza activity had peaked and estimated the proportion of the population infected with pH1N1 virus during the pandemic. METHODS: During November-December 2009, we collected leftover serum from a blood bank, a pediatric children's hospital and a pediatric outpatient clinic in Tampa Bay Florida. Serum was tested for pH1N1 virus antibodies using the hemagglutination-inhibition (HI) assay. HI titers ≥40 were considered seropositive. We adjusted seroprevalence results to account for previously established HI assay specificity and sensitivity and employed a simple statistical model to estimate the proportion of seropositivity due to pH1N1 virus infection and vaccination. RESULTS: During the study time period, the overall seroprevalence in Tampa Bay, Florida was 25%, increasing to 30% after adjusting for HI assay sensitivity and specificity. We estimated that 5.9% of the population had vaccine-induced seropositivity while 25% had seropositivity secondary to pH1N1 virus infection. The highest cumulative incidence of pH1N1 virus infection was among children aged 5-17 years (53%) and young adults aged 18-24 years (47%), while adults aged ≥50 years had the lowest cumulative incidence (11-13%) of pH1N1 virus infection. CONCLUSIONS: After the peak of the fall wave of the pandemic, an estimated one quarter of the Tampa Bay population had been infected with the pH1N1 virus. Consistent with epidemiologic trends observed during the pandemic, the highest burdens of disease were among school-aged children and young adults