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Involvement of nitric oxide (NO) in plant metabolism and its connection with phytohormones has not been fully described, thus information about the role of this molecule in signalling pathways remains fragmented. In this study, the effects of NO on calmodulin (CAM), calcium protein kinase (CPK), content of phytohormones and secondary metabolites in canola plants under salinity stress were investigated.We applied 100 μM sodium nitroprusside as an NO source to canola plants grown under saline (100 mM NaCl) and non‐saline conditions at the vegetative stage.Plant growth was negatively affected by salinity, but exogenous NO treatment improved growth. NO caused a significant increase in activity of CAT, SOD and POX through their enhanced gene expression in stressed canola. Salinity‐responsive genes, namely CAM and CPK, were induced by NO in plants grown under salinity. NO application enhanced phenolic compounds, such as gallic acid and coumaric acid and flavonoid compound,s catechin, diadzein and kaempferol, in plants subjected to salinity. NO treatment enhanced abscisic acid and brassinosteroids but decreased auxin and gibberellin in stressed canola plants.The impacts of NO in improving stress tolerance in canola required CAM and CPK. Also, NO signalling re‐established the phytohormone balance and resulted in enhanced tolerance to salt stress. Furthermore, NO improved salinity tolerance in canola by increasing enzymatic and non‐enzymatic antioxidant content. [ABSTRACT FROM AUTHOR]

Lentils provide a rich plant‐based protein source and staple food in many parts of the world. Despite numerous nutritional benefits, lentil seeds also possess undesirable elements, such as anti‐nutritional factors. Understanding the genetic networks of seed metabolism is of great importance for improving the seed nutritional profile.We applied RNA sequencing analysis to survey the transcriptome of developing lentil seeds and compared this with that of the pod shells and leaves. In total, we identified 2622 genes differentially expressed among the tissues examined. Genes preferentially expressed in seeds were enriched in the Gene Ontology (GO) terms associated with development, nitrogen and carbon (N/C) metabolism and lipid synthesis.We further categorized seed preferentially expressed genes based on their involvement in storage protein production, starch accumulation, lipid and suberin metabolism, phytate, saponin and phenylpropanoid biosynthesis.The availability of transcript profile datasets on lentil seed metabolism and a roadmap of candidate genes presented here will be of great value for breeding strategies towards further improvement of lentil seed quality traits. [ABSTRACT FROM AUTHOR]

Pattern reconfigurable antennas implemented in small adaptive arrays can serve as practical solutions in applications, which are limited by available platform space while providing additional degrees of pattern control. This communication integrates the concept of pattern variability directly into an adaptive array optimization routine with a unique pattern reconfigurable antenna element equivalent model, allowing the algorithm to fully leverage the available reconfigurability—which may include individual pattern beam tilts and pattern nulls. Examples showcase the model’s impact on adaptive array performance via the signal-to-interference plus noise ratio metric. The results establish a pathway specifying the design requirements for pattern reconfigurable antennas to improve small adaptive array performance, demonstrating that designers should focus on the null steering capability of the antenna element in many cases. [ABSTRACT FROM PUBLISHER]

* Background and Aims Loss of seed viability has been associated with deteriorative processes that are partly caused by oxidative damage. The breaking of dormancy, a seed trait that prevents germination in unfavourable seasons, has also been associated with oxidative processes. It is neither clear how much overlap exists between these mechanisms nor is the specific roles played by oxygen and reactive oxygen species. * Methods Antioxidant profiles were studied in fresh (dormant) or after-ripened (non-dormant) sunflower (Helianthus annuus) embryos subjected to controlled deterioration at 40 °C and 75% relative humidity under ambient (21%) or high O2 (75%). Changes in seed vigour and viability, dormancy, protein carbonylation and fatty acid composition were also studied. * Key Results After-ripening of embryonic axes was accompanied by a shift in the thiol-based cellular redox environment towards more oxidizing conditions. Controlled deterioration under high O2 led to a faster loss of seed dormancy and significant decreases in glutathione reductase and glutathione peroxidase activities, but viability was lost at the same rate as under ambient O2. Irrespective of O2 concentration, the overall thiol-based cellular redox state increased significantly over 21 d of controlled deterioration to strongly oxidizing conditions and then plateaued, while viability continued to decrease. Viability loss was accompanied by a rapid decrease in glucose-6-phosphatede-hydrogenase, which provides NADPH for reductive processes such as required by glutathione reductase. Protein carbonylation, a marker of protein oxidation, increased strongly in deteriorating seeds. The lipid-soluble tocochromanols, dominated by α-tocopherol, and fatty acid profiles remained stable. * Conclusions After-ripening, dormancy-breaking during ageing and viability loss appeared to be associated with oxidative changes of the cytosolic environment and proteins in the embryonic axis rather than the lipid environment. High O2 concentrations accelerated dormancy alleviation but, surprisingly, did not accelerate the rate of viability loss. [ABSTRACT FROM AUTHOR]

This letter estimates the long-run impacts of shocks to real disposable personal income on the environment in the United States through the use of a structural vector autoregression model. Coal use in the electricity sector and vehicle use data are considered specifically as these are major contributors to carbon dioxide emissions and capture demand from both firms and households. [ABSTRACT FROM AUTHOR]

This study investigates the performance of planar fixed and/or pattern reconfigurable antennas on a model laptop in terms of diversity gain and spatial coverage. The reconfigurable antenna used in this work has the ability to change its radiation pattern from endfire to broadside while operating over a common impedance bandwidth. The research combines diversity gain and spatial coverage into a single parameter that takes into account the effects of both simultaneously. Experimental data, including the resulting diversity gain and spatial coverage calculations, are presented. This work reveals the possibilities and importance of using reconfigurable radiation antennas and weighs their potential impact on high performance wireless systems. © 2007 Wiley Periodicals, Inc. Microwave Opt Technol Lett 49: 535–539, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.22181 [ABSTRACT FROM AUTHOR]

Objective Few data exist on the efficacy of antiretroviral therapy in individuals infected with HIV in the Caribbean. We evaluated the virological and immunological responses of HIV-infected adults starting highly active antiretroviral therapy (HAART). Design This was a prospective observational cohort study. Methods A total of 158 antiretroviral-naive patients who initiated HAART between January 2002 and March 2003, and completed at least 6 months of treatment and follow up, were included in the analysis. The response to therapy was assessed by changes in CD4 cell counts and viral loads from baseline. The mean increase in CD4 cell count, the rate of virological success (a viral load of <50 HIV-1 RNA copies/mL) and the rate of immunological success (an increase in CD4 cell count of≥50 cells/μL over the baseline value) after commencing HAART were measured. Results In total, 82% of patients (123 of 150) achieved viral loads of <50 copies/mL after 6 months of therapy. Viral success rate after 6 months of HAART was similar irrespective of gender, pre-HAART CD4 cell count and pre-HAART viral load. However, patients older than 40 years were significantly more likely to achieve virorological success than those younger than 40 years. At 6 months after starting HAART, 79.5% of patients were estimated to have achieved immunological success and 17.9% had an increase in CD4 cell count of ≥200 cells/μL over the baseline value. The median increase in CD4 cell count for the 156 patients who had CD4 cell counts at baseline and at 6 months of therapy was 122 cells/μL. Conclusion In this cohort of antiretroviral-naive HIV-infected adults, there was a high rate of virological and immunological success after 6 months of HAART, irrespective of the pre-HAART viral load and CD4 cell count. [ABSTRACT FROM AUTHOR]

Within-patient HIV evolution reflects the strong selection pressure driving viral escape from cytotoxic T-lymphocyte (CTL) recognition. Whether this intrapatient accumulation of escape mutations translates into HIV evolution at the population level has not been evaluated. We studied over 300 patients drawn from the B- and C-clade epidemics, focusing on human leukocyte antigen (HLA) alleles HLA-B57 and HLA-B5801, which are associated with long-term HIV control and are therefore likely to exert strong selection pressure on the virus. The CTL response dominating acute infection in HLA-B57/5801-positive subjects drove positive selection of an escape mutation that reverted to wild-type after transmission to HLA-B57/5801-negative individuals. A second escape mutation within the epitope, by contrast, was maintained after transmission. These data show that the process of accumulation of escape mutations within HIV is not inevitable. Complex epitope- and residue-specific selection forces, including CTL-mediated positive selection pressure and virus-mediated purifying selection, operate in tandem to shape HIV evolution at the population level. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that, like bacterial lipopolysaccharide (LPS), arabinofuranosyl-terminated lipoarabinomannan (AraLAM) from an attenuated strain of Mycobacterium induces potent early gene (c-fos, KC, JE and TNF-α) responses in murine macrophages, whereas extensively α-Manp capped LAM (ManLAM) from virulent M. tuberculosis do not. In this study we have extended analysis of the influence of mycobacterial LAM on macrophage function by demonstrating that AraLAM (but not ManLAM), like bacterial LPS, is a potent stimulator of inducible nitric oxide synthase (iNOS) expression independent of the autocrine activity of co-stimulated tumour necrosis factor-α (TNF-α) release. The inability of ManLAM to induce iNOS expression was not due to induction of the 'deactivating' cytokine interleukin-10 (IL-10). Indeed, like LPS, AraLAM was also a potent inducer of IL-10 expression. However, analysis of AraLAM- or LPS-induced responses in the presence of interferon-γ (IFN-γ) showed that, whereas IFN-γ acts as a potent co-stimulus for iNOS, it completely inhibits the IL-10 response. Hence, the presence of IFN-γ early in infection will have an important immunomodulatory role in determining the macrophage response. These results have important implications for the pathogenesis of virulent and avirulent mycobacteria in vivo. [ABSTRACT FROM AUTHOR]

The murine resistance gene Lsh/Ity/Bcg regulates activation of macrophages for turnout necrosis factor-α (TNF-α)-dependent production of nitric oxide mediating antimicrobial activity against Leishmania, Salmonella and Mycobacterium. As Lsh is differentially expressed in macrophages from different tissue sites, experiments were performed to determine whether interaction with extracellular matrix (ECM) proteins would influence the macrophage TNF-α response. Plating of bone marrow-derived macrophages onto purified fibrinogen or fibronectin-rich L929 cell-derived matrices, but not onto mannan, was itself sufficient to stimulate TNF-α release, with significantly higher levels released from congenic B10.L-Lshr compared to C57BL/10ScSn (Lsh8) macrophages. Only macrophages plated onto fibrinogen also released measurable levels of nitrites, again higher in Lshr compared to Lsh8 macrophages. Addition of interferon-γ (IFN-γ), but not bacterial lipopolysaccharide or mycobacterial lipoarabinomannan, as a second signal enhanced the TNF-α and nitrite responses of macrophages plated onto fibrinogen, particularly in the Lshr macrophages. Interaction with fibrinogen and fibronectin also primed macrophages for an enhanced TNF-α response to leishmanial parasites, but this was only translated into enhanced nitrite responses in the presence of IFN-γ. In these experiments, Lshr macrophages remained superior in their TNF-α responses throughout, but to a degree which reflected the magnitude of the difference observed on ECM alone. Hence, the specificity for the enhanced TNF-α responses of Lshr macrophages lay in their interaction with fibrinogen and fibronectin ECM, while a differential nitrite response was only observed with fibrinogen and/or IFN-α. The results are discussed in relation to the possible function of the recently cloned candidate gene Nramp, which has structural identity to eukaryote transporters and an N-terminal cytoplasmic proline/serine-rich putative SH3 binding domain. [ABSTRACT FROM AUTHOR]

Descriptions of primary HIV-1 infection have so far been based on Caucasians living in industrialized nations. Due to studies of leptospirosis in the predominantly black population of Barbados, serum was available for patients admitted with acute febrile illnesses to the Queen Elizabeth Hospital (QEH). By searching the medical records of 510 adult patients with known HIV-1 infection we identified 10 patients who had stored serum from an admission for an acute febrile illness that predated or coincided with their first HIV-1-positive test. Serological testing confirmed primary HIV-1 infection in 9 and was suggestive in the 10th patient. The clinical features of these 10 patients were in keeping with previous descriptions of primary HIV-1 infection but differed from leptospirosis cases seen at the QEH. One patient died during his seroconversion illness and another died 3 months after seroconversion. The findings suggest that severe primary HIV-1 infection could be a relatively uncommon occurrence, that the condition may be misdiagnosed, and that cases may not occur until the AIDS epidemic is established. [ABSTRACT FROM AUTHOR]

Functional studies have shown that the murine macrophage resistance gene Lsh/Ity/Bcg (candidate Nramp) regulates macrophage priming/activation for antimicrobial activity via the tumour necrosis factor-alpha (TNF-α)-dependent production of reactive nitrogen intermediates. Since Toxoplasma gondii also parasitizes macrophages. is a stimulator of endogenous TNF-α release, and is sensitive to nitric oxide-mediated killing in activated macrophages. studies were carried out using chromosome I congenic mouse Strains to determine whether Lsh influences I gondu infection. Two interesting observations were made: (i) contrary to expectation, mice carrying the Lsh-resistant allele died earlier over the acute phase of infection than Lsh-susceptible mice: and (ii) Lsh-resistant mice which survived this acute phase of infection showed lower brain cyst numbers than the Lsh-susceptible mice. Whilst the latter occurred independently of route of inoculation (oral. intraperitoneal, or subcutaneous). the former was influenced both by the route of inoculation and the genetic background on which the Lxh- resistant allele had been isolated. Hence. following oral administration of 21) brain cysts of the RRA strain of T. gondii. mice currying the Is/s-resistant allele on a 1310 genetic background showed a significantly enhanced rate of mortality over the acute first 8 12 days) phase of infection than 810 tx/i-susceptible mice. Although this acute phase of infection in B10 background mice was accompanied by an increase in serum TNF-α levels in both Lsh-resistant and -susceptible mouse strains. early mortality preceded the TN F-α peak. and administration of neutralzing rabbit anti-TN F-n did not significantly enhance survival. hence, inflammatory mediators other than TNF-n appear to be responsible for the increased rate of acute mortality observed in resistant mice. Infection intraperutoneally led to delayed mortality in 810 mice. with the mean time to 50% mortality now being significantly longer in tsh-resistant than in Ish-susceptible mice. On a BALB genetic background. it was the i.p. route of infection which led to acute mortality and more rapid death in the Lilt-resistant strain. When a less virulent inoculum was used and mortality delayed. Lilt-susceptible mice died more rapidly, and i.p. administration of rabbit anti-TNF-α led to 100% mortality between days 8 and 10 of infection in both susceptible and resistant mouse strains, consistent with a crucial protective rote for during this phase of infection. Overall the results show that the Lsh gene plays different modulating roles over the course of 11 gondii infection depending on the potency of the parasite inoculum the route and kinetics of infection, and the genetic background of the congenic mouse strains upon which the resistant allele has been isolated. These results probably reflect pleiotropic effects of macrophage products stimulated by differential priming activation rather than the direct effect of macrophage toxoplasmacudal activity. [ABSTRACT FROM AUTHOR]

Multiple pleural biopsies (up to 10) were taken with the Abrams needle through a single aspiration site in 55 patients with pleural effusions. A definite positive or suggestive pleural biopsy diagnosis was made in 33 patients (60%). In 32 of the 33 patients the pathological abnormality was confined to only a proportion of the biopsies. Pleural biopsies were positive or suggestive in 26 out of 36 patients (72%) eventually shown to have tumour and seven out of eight patients (88%) with tuberculosis. Small pneumothoraces occurred in four patients and surgical emphysema in two. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented concerning Pneumocystis jiroveci pneumonia occurring in HIV-infected patients.