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Here, we describe a model of C3, C3–C4 intermediate, and C4 photosynthesis that is designed to facilitate quantitative analysis of physiological measurements. The model relates the factors limiting electron transport and carbon metabolism, the regulatory processes that coordinate these metabolic domains, and the responses to light, carbon dioxide, and temperature. It has three unique features. First, mechanistic expressions describe how the cytochrome b6f complex controls electron transport in mesophyll and bundle sheath chloroplasts. Second, the coupling between the mesophyll and bundle sheath expressions represents how feedback regulation of Cyt b6f coordinates electron transport and carbon metabolism. Third, the temperature sensitivity of Cyt b6f is differentiated from that of the coupling between NADPH, Fd, and ATP production. Using this model, we present simulations demonstrating that the light dependence of the carbon dioxide compensation point in C3–C4 leaves can be explained by co-occurrence of light saturation in the mesophyll and light limitation in the bundle sheath. We also present inversions demonstrating that population-level variation in the carbon dioxide compensation point in a Type I C3–C4 plant, Flaveriachloraefolia, can be explained by variable allocation of photosynthetic capacity to the bundle sheath. These results suggest that Type I C3–C4 intermediate plants adjust pigment and protein distributions to optimize the glycine shuttle under different light and temperature regimes, and that the malate and aspartate shuttles may have originally functioned to smooth out the energy supply and demand associated with the glycine shuttle. This model has a wide range of potential applications to physiological, ecological, and evolutionary questions.

Here, we present a conceptual and quantitative model to describe the role of the Cytochrome $$\hbox {b}_{6}\hbox {f}$$ b 6 f complex in controlling steady-state electron transport in $$\hbox {C}_{3}$$ C 3 leaves. The model is based on new experimental methods to diagnose the maximum activity of Cyt $$\hbox {b}_{6}\hbox {f}$$ b 6 f in vivo, and to identify conditions under which photosynthetic control of Cyt $$\hbox {b}_{6}\hbox {f}$$ b 6 f is active or relaxed. With these approaches, we demonstrate that Cyt $$\hbox {b}_{6}\hbox {f}$$ b 6 f controls the trade-off between the speed and efficiency of electron transport under limiting light, and functions as a metabolic switch that transfers control to carbon metabolism under saturating light. We also present evidence that the onset of photosynthetic control of Cyt $$\hbox {b}_{6}\hbox {f}$$ b 6 f occurs within milliseconds of exposure to saturating light, much more quickly than the induction of non-photochemical quenching. We propose that photosynthetic control is the primary means of photoprotection and functions to manage excitation pressure, whereas non-photochemical quenching functions to manage excitation balance. We use these findings to extend the Farquhar et al. (Planta 149:78–90, 1980) model of $$\hbox {C}_{3}$$ C 3 photosynthesis to include a mechanistic description of the electron transport system. This framework relates the light captured by PS I and PS II to the energy and mass fluxes linking the photoacts with Cyt $$\hbox {b}_{6}\hbox {f}$$ b 6 f , the ATP synthase, and Rubisco. It enables quantitative interpretation of pulse-amplitude modulated fluorometry and gas-exchange measurements, providing a new basis for analyzing how the electron transport system coordinates the supply of Fd, NADPH, and ATP with the dynamic demands of carbon metabolism, how efficient use of light is achieved under limiting light, and how photoprotection is achieved under saturating light. The model is designed to support forward as well as inverse applications. It can either be used in a stand-alone mode at the leaf-level or coupled to other models that resolve finer-scale or coarser-scale phenomena.

Here, we present a conceptual and quantitative model to describe the role of the Cytochrome \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {b}_{6}\hbox {f}$$\end{document}b6f complex in controlling steady-state electron transport in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {C}_{3}$$\end{document}C3 leaves. The model is based on new experimental methods to diagnose the maximum activity of Cyt \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {b}_{6}\hbox {f}$$\end{document}b6f in vivo, and to identify conditions under which photosynthetic control of Cyt \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {b}_{6}\hbox {f}$$\end{document}b6f is active or relaxed. With these approaches, we demonstrate that Cyt \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {b}_{6}\hbox {f}$$\end{document}b6f controls the trade-off between the speed and efficiency of electron transport under limiting light, and functions as a metabolic switch that transfers control to carbon metabolism under saturating light. We also present evidence that the onset of photosynthetic control of Cyt \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {b}_{6}\hbox {f}$$\end{document}b6f occurs within milliseconds of exposure to saturating light, much more quickly than the induction of non-photochemical quenching. We propose that photosynthetic control is the primary means of photoprotection and functions to manage excitation pressure, whereas non-photochemical quenching functions to manage excitation balance. We use these findings to extend the Farquhar et al. (Planta 149:78–90, 1980) model of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {C}_{3}$$\end{document}C3 photosynthesis to include a mechanistic description of the electron transport system. This framework relates the light captured by PS I and PS II to the energy and mass fluxes linking the photoacts with Cyt \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\hbox {b}_{6}\hbox {f}$$\end{document}b6f, the ATP synthase, and Rubisco. It enables quantitative interpretation of pulse-amplitude modulated fluorometry and gas-exchange measurements, providing a new basis for analyzing how the electron transport system coordinates the supply of Fd, NADPH, and ATP with the dynamic demands of carbon metabolism, how efficient use of light is achieved under limiting light, and how photoprotection is achieved under saturating light. The model is designed to support forward as well as inverse applications. It can either be used in a stand-alone mode at the leaf-level or coupled to other models that resolve finer-scale or coarser-scale phenomena.

As a way of concluding this thematic issue, we have created a space for our contributors to read each other’s articles and to reflect on the main theme, i.e. translating culture in global times. We invited their response to four questions that we believe are not only central to the aims of the special issue, but also encourage further dialogues on the role of translation in applied linguistics and translation as mission and practice. • How does the distinction between cultural difference and cultural diversity help us understand the way culture and translation are conceptualized and operationalized? • How does the translanguaging perspective help to understand cultural translation and what are the limitations or issues for future exploration? • What are the ethical challenges in cultural translation and how do we as applied linguists address ethical issues in cultural translation? • What implications do the new ways of understanding cultural translation debated in the special issue have for the field of applied linguistics?

International audience; Disentangling the individual contributions from vegetation and soil in measured canopy reflectance is a grand challenge to the remote sensing and ecophysiology communities. Since Solar Induced chlorophyll Fluorescence (SIF) is uniquely emitted from vegetation, it can be used to evaluate how well reflectance-based vegetation indices (VIs) can separate the vegetation and soil components. Due to the residual soil background contributions, Near-infrared (NIR) reflectance of vegetation (NIRv) and Difference Vegetation index (DVI) present offsets when compared to SIF (i.e., the value of NIRv or DVI is non-zero when SIF is zero). In this study, we proposed a simple framework for estimating the true NIR reflectance of vegetation from Hyperspectral measurements (NIRvH) with minimal soil impacts. NIRvH takes advantage of the spectral shape variations in the red-edge region to minimize the soil effects. We evaluated the capability of NIRvH, NIRv and DVI in isolating the true NIR reflectance of vegetation using the data from both the model-based simulations and Hyperspectral Plant imaging spectrometer (HyPlant) measurements. Benchmarked by simultaneously measured SIF, NIRvH has the smallest offset (0–0.037), as compared to an intermediate offset of 0.047–0.062 from NIRv, and the largest offset of 0.089–0.112 from DVI. The magnitude of the offset can vary with different soil reflectance spectra across spatio-temporal scales, which may lead to bias in the downstream NIRv-based photosynthesis estimates. NIRvH and SIF measurements from the same sensor platform avoided complications due to different geometry, footprint and time of observation across sensors when studying the radiative transfer of reflected photons and SIF. In addition, NIRvH was primarily determined by canopy structure rather than chlorophyll content and soil brightness. Our work showcases that NIRvH is promising for retrieving canopy structure parameters such as leaf area index and leaf inclination angle, and for estimating fluorescence yield with current and forthcoming hyperspectral satellite measurements.

RATIONALE Induction module cavity ring-down spectroscopy (IM-CRDS) has been proposed as a rapid and cost-effective alternative to cryogenic vacuum distillation (CVD) and isotope ratio mass spectrometry (IRMS) for the measurement of δ18 O and δ2 H values in matrix-bound waters. In the current study, we characterized the performance of IM-CRDS relative to CVD and IRMS and investigated the mechanisms responsible for differences between the methods. METHODS We collected a set of 75 soil, stem, and leaf water samples, and measured the δ18 O and δ2 H values of each sample with four techniques: CVD and IRMS, CVD and CRDS, CVD and IM-CRDS, and IM-CRDS alone. We then calculated the isotopic errors for each of the three CRDS methods relative to CVD and IRMS, and analyzed the relationships among these errors and suites of diagnostic spectral parameters that are indicative of organic contamination. RESULTS The IM-CRDS technique accurately assessed the δ18 O and δ2 H values of pure waters, but exhibited progressively increasing errors for soil waters, stem waters, and leaf waters. For soils, the errors were attributable to subsampling of isotopically heterogeneous source material, whereas for stems and leaves, they were attributable to spectral interference. Unexpectedly, the magnitude of spectral interference was higher for the solid samples analyzed directly via IM-CRDS than for those originally extracted via CVD and then analyzed by IM-CRDS. CONCLUSIONS There are many types of matrix-bound water samples for which IM-CRDS measurements include significant errors from spectral interference. As a result, spectral analysis and validation should be incorporated into IM-CRDS post-processing procedures. In the future, IM-CRDS performance could be improved through: (i) identification of the compounds that cause spectral interference, and either (ii) modification of the combustion step to completely oxidize these compounds to CO2 , and/or (iii) incorporation of corrections for these compounds into the spectral fitting models used by the CRDS analyzers. Copyright © 2016 John Wiley & Sons, Ltd.

The aim of the current study was to determine whether plate augmentation was a successful treatment algorithm for selected femoral nonunions initially managed with intramedullary nailing. A total of 30 femoral nonunion cases were managed using the plate augmentation strategy with 13 primary cases and 17 multi-operated femurs (avg 2.8 ineffective procedures). Adjunctive strategies included autologous bone grafting and/or BMP for atrophic/oligotrophic and bone defect cases. Deformity correction was performed when required. Osseous union occurred in 29 of 30 cases. One multi-operated case with bone defect and prior infection required repeat autologous grafting prior to union. Plate augmentation should be added to the armamentarium for management of selected femoral nonunion that have failed initial intramedullary nailing.

Methane seepage from the upper continental slopes of Western Svalbard has previously been attributed to gas hydrate dissociation induced by anthropogenic warming of ambient bottom waters. Here we show that sediment cores drilled off Prins Karls Foreland contain freshwater from dissociating hydrates. However, our modeling indicates that the observed pore water freshening began around 8 ka BP when the rate of isostatic uplift outpaced eustatic sea-level rise. The resultant local shallowing and lowering of hydrostatic pressure forced gas hydrate dissociation and dissolved chloride depletions consistent with our geochemical analysis. Hence, we propose that hydrate dissociation was triggered by postglacial isostatic rebound rather than anthropogenic warming. Furthermore, we show that methane fluxes from dissociating hydrates were considerably smaller than present methane seepage rates implying that gas hydrates were not a major source of methane to the oceans, but rather acted as a dynamic seal, regulating methane release from deep geological reservoirs., Methane seepage from continental slopes has been attributed to gas hydrate dissociation induced by anthropogenic bottom water warming. Here, the authors show that hydrates dissociated before the Anthropocene when the isostatic rebound induced by deglaciation of the Arctic ice sheet outpaced eustatic sea-level rise.

The distribution of nitrogen isotopes in the biosphere has the potential to offer insights into the past, present and future of the nitrogen cycle, but it is challenging to unravel the processes controlling patterns of mixing and fractionation. We present a mathematical model describing a previously overlooked process: nitrogen isotope fractionation during leaf-atmosphere NH3(g) exchange. The model predicts that when leaf-atmosphere exchange of NH3(g) occurs in a closed system, the atmospheric reservoir of NH3(g) equilibrates at a concentration equal to the ammonia compensation point and an isotopic composition 8.1‰ lighter than nitrogen in protein. In an open system, when atmospheric concentrations of NH3(g) fall below or rise above the compensation point, protein can be isotopically enriched by net efflux of NH3(g) or depleted by net uptake. Comparison of model output with existing measurements in the literature suggests that this process contributes to variation in the isotopic composition of nitrogen in plants as well as NH3(g) in the atmosphere, and should be considered in future analyses of nitrogen isotope circulation. The matrix-based modelling approach that is introduced may be useful for quantifying isotope dynamics in other complex systems that can be described by first-order kinetics.

The novel rhomboid-like protein RHBDD2 is distantly related to rhomboid proteins, a group of highly specialized membrane-bound proteases that catalyze regulated intramembrane proteolysis. In retina, RHBDD2 is expressed from embryonic stages to adulthood, and its levels show age-dependent changes. RHBDD2 is distinctly abundant in the perinuclear region of cells, and it localizes to their Golgi. A glycine zipper motif present in one of the transmembrane domains of RHBDD2 is important for its packing into the Golgi membranes. Its deletion causes dislodgment of RHBDD2 from the Golgi. A specific antibody against RHBDD2 recognizes two forms of the protein, one with low (39 kDa; RHBDD2(L)) and the other with high (117 kDa; RHBDD2H) molecular masses in mouse retinal extracts. RHBDD2(L) seems to be ubiquitously expressed in all retinal cells. In contrast, RHBDD2H seems to be present only in the outer segments of cone photoreceptors and may correspond to a homotrimer of RHBDD2(L). This protein consistently co-localizes with S- and M-types of cone opsins. We identified a homozygous mutation in the human RHBDD2 gene, R85H, that co-segregates with disease in affected members of a family with autosomal recessive retinitis pigmentosa. Our findings suggest that the RHBDD2 protein plays important roles in the development and normal function of the retina.

Induction module cavity ring-down spectroscopy (IM-CRDS) has been proposed as a rapid and cost-effective alternative to cryogenic vacuum distillation (CVD) and isotope ratio mass spectrometry (IRMS) for the measurement of δWe collected a set of 75 soil, stem, and leaf water samples, and measured the δThe IM-CRDS technique accurately assessed the δThere are many types of matrix-bound water samples for which IM-CRDS measurements include significant errors from spectral interference. As a result, spectral analysis and validation should be incorporated into IM-CRDS post-processing procedures. In the future, IM-CRDS performance could be improved through: (i) identification of the compounds that cause spectral interference, and either (ii) modification of the combustion step to completely oxidize these compounds to CO

The C-terminal catalytic domain (residues 704-1047) of the human ras GTPase-activating protein (GAP) has been engineered so as to incorporate the tripeptide, Glu-Glu-Phe, at its C terminus. This motif is recognized by the commercially available YL1/2 monoclonal antibody to alpha-tubulin and has previously been used for the immunoaffinity purification of HIV enzymes engineered to contain this epitope (Stammers, D. K., Tisdale, M., Court, S., Parmar, V., Bradley, C., and Ross, C. K. (1991) FEBS Lett. 283, 298-302). The engineered GAP catalytic domain (GAP-344) was obtained in high yield and purity from Escherichia coli extracts by means of a single affinity column of immobilized YL1/2, eluted under mild conditions with the dipeptide, Asp-Phe. The protein had similar activity to that previously described for full-length GAP, suggesting that the addition of the epitope did not grossly affect the activity. R903K and L902I mutants of GAP-344 were constructed, and the immunoaffinity purification procedure allowed their rapid characterization. The R903K mutant had less than 3% the activity of the normal protein, whereas the L902I substitution had less than 0.5% of normal activity, suggesting an important role for Leu-902 and Arg-903, residues absolutely conserved among GAP-related proteins. This work exemplifies the general utility of the C-terminal Glu-Glu-Phe motif for the rapid purification of proteins whose function is not altered by C-terminal modification.

Soil pH regulates the capacity of soils to store and supply nutrients, and thus contributes substantially to controlling productivity in terrestrial ecosystems. However, soil pH is not an independent regulator of soil fertility-rather, it is ultimately controlled by environmental forcing. In particular, small changes in water balance cause a steep transition from alkaline to acid soils across natural climate gradients. Although the processes governing this threshold in soil pH are well understood, the threshold has not been quantified at the global scale, where the influence of climate may be confounded by the effects of topography and mineralogy. Here we evaluate the global relationship between water balance and soil pH by extracting a spatially random sample (n = 20,000) from an extensive compilation of 60,291 soil pH measurements. We show that there is an abrupt transition from alkaline to acid soil pH that occurs at the point where mean annual precipitation begins to exceed mean annual potential evapotranspiration. We evaluate deviations from this global pattern, showing that they may result from seasonality, climate history, erosion and mineralogy. These results demonstrate that climate creates a nonlinear pattern in soil solution chemistry at the global scale; they also reveal conditions under which soils maintain pH out of equilibrium with modern climate.

It is often recognized, but seldom addressed, that a quantitative assessment of the cumulative effects, both additive and non-additive, of multiple stressors on fish survival would provide a more realistic representation of the factors that influence fish migration. This review presents a compilation of analytical methods applied to a well-studied fish migration, a more general review of quantitative multivariable methods, and a synthesis on how to apply new analytical techniques in fish migration studies. A compilation of adult migration papers from Fraser River sockeye salmon Oncorhynchus nerka revealed a limited number of multivariable methods being applied and the sub-optimal reliance on univariable methods for multivariable problems. The literature review of fisheries science, general biology and medicine identified a large number of alternative methods for dealing with cumulative effects, with a limited number of techniques being used in fish migration studies. An evaluation of the different methods revealed that certain classes of multivariable analyses will probably prove useful in future assessments of cumulative effects on fish migration. This overview and evaluation of quantitative methods gathered from the disparate fields should serve as a primer for anyone seeking to quantify cumulative effects on fish migration survival.

Gestational lead exposure (GLE) produces supernormal scotopic electroretinograms (ERG) in children, monkeys and rats, and a novel retinal phenotype characterized by an increased number of rod photoreceptors and bipolar cells in adult mice and rats. Since the loss of dopaminergic amacrine cells (DA ACs) in GLE monkeys and rats contributes to supernormal ERGs, the retinal DA system was analyzed in mice following GLE. C57BL/6 female mice were exposed to low (27 ppm), moderate (55 ppm) or high (109 ppm) lead throughout gestation and until postnatal day 10 (PN10). Blood [Pb] in control, low-, moderate- and high-dose GLE was ≤ 1, ≤ 10, ~25 and ~40 μg/dL, respectively, on PN10 and by PN30 all were ≤ 1 μg/dL. At PN60, confocal-stereology studies used vertical sections and wholemounts to characterize tyrosine hydroxylase (TH) expression and the number of DA and other ACs. GLE dose-dependently and selectively decreased the number of TH-immunoreactive (IR) DA ACs and their synaptic plexus without affecting GABAergic, glycinergic or cholinergic ACs. Immunoblots and confocal revealed dose-dependent decreases in retinal TH protein expression and content, although monoamine oxidase-A protein and gene expression were unchanged. High-pressure liquid chromatography showed that GLE dose-dependently decreased retinal DA content, its metabolites and DA utilization/release. The mechanism of DA selective vulnerability is unknown. However, a GLE-induced loss/dysfunction of DA ACs during development could increase the number of rods and bipolar cells since DA helps regulate neuronal proliferation, whereas during adulthood it could produce ERG supernormality as well as altered circadian rhythms, dark/light adaptation and spatial contrast sensitivity.

Global climate change is expected to affect terrestrial ecosystems in a variety of ways. Some of the more well-studied effects include the biogeochemical feedbacks to the climate system that can either increase or decrease the atmospheric load of greenhouse gases such as carbon dioxide and nitrous oxide. Less well-studied are the effects of climate change on the linkages between soil and plant processes. Here, we report the effects of soil warming on these linkages observed in a large field manipulation of a deciduous forest in southern New England, USA, where soil was continuously warmed 5°C above ambient for 7 years. Over this period, we have observed significant changes to the nitrogen cycle that have the potential to affect tree species composition in the long term. Since the start of the experiment, we have documented a 45% average annual increase in net nitrogen mineralization and a three-fold increase in nitrification such that in years 5 through 7, 25% of the nitrogen mineralized is then nitrified. The warming-induced increase of available nitrogen resulted in increases in the foliar nitrogen content and the relative growth rate of trees in the warmed area. Acer rubrum (red maple) trees have responded the most after 7 years of warming, with the greatest increases in both foliar nitrogen content and relative growth rates. Our study suggests that considering species-specific responses to increases in nitrogen availability and changes in nitrogen form is important in predicting future forest composition and feedbacks to the climate system. Electronic supplementary material The online version of this article (doi:10.1007/s00442-011-2133-7) contains supplementary material, which is available to authorized users.

Background Gestational lead exposure (GLE) produces novel and persistent rod-mediated electroretinographic (ERG) supernormality in children and adult animals. Objectives We used our murine GLE model to test the hypothesis that GLE increases the number of neurons in the rod signaling pathway and to determine the cellular mechanisms underlying the phenotype. Results Blood lead concentrations ([BPb]) in controls and after low-, moderate-, and high-dose GLE were ≤ 1, ≤ 10, approximately 25, and approximately 40 μg/dL, respectively, at the end of exposure [postnatal day 10 (PND10)]; by PND30 all [BPb] measures were ≤ 1 μg/dL. Epifluorescent, light, and confocal microscopy studies and Western blots demonstrated that late-born rod photoreceptors and rod and cone bipolar cells (BCs), but not Müller glial cells, increased in a nonmonotonic manner by 16–30% in PND60 GLE offspring. Retinal lamination and the rod:cone BC ratio were not altered. In vivo BrdU (5-bromo-2-deoxyuridine) pulse-labeling and Ki67 labeling of isolated cells from developing mice showed that GLE increased and prolonged retinal progenitor cell proliferation. TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) and confocal studies revealed that GLE did not alter developmental apoptosis or produce retinal injury. BrdU birth-dating and confocal studies confirmed the selective rod and BC increases and showed that the patterns of neurogenesis and gliogenesis were unaltered by GLE. Conclusions Our findings suggest two spatiotemporal components mediated by dysregulation of different extrinsic/intrinsic factors: increased and prolonged cell proliferation and increased neuronal (but not glial) cell fate. These findings have relevance for neurotoxicology, pediatrics, public health, risk assessment, and retinal cell biology because they occurred at clinically relevant [BPb] and correspond with the ERG phenotype.

Summary This article describes a horse that sustained burn injury wounds over the back extending from the withers to the tail head as a result of a fire in a trailer. The extensive nature of the burn prompted investigation into treatment options which may stimulate healing. Based on current applications in human medicine, shockwave therapy was administered. This horse recovered from a substantial burn injury. Shockwave therapy may be a viable supplemental option for treating burn injuries in the horse, with no noted adverse effects.

The adverse effects of low-level developmental lead exposure [blood lead (BPb) ≤ 10 μg/dL] on cognitive, auditory, and visual-motor function are well documented (Canfield et al. 2003; Osman et al. 1999; Rothenberg et al. 2000; Wasserman et al. 2000), but only two studies have examined the impact of low-level developmental Pb exposure on retinal and visual function in children (Altmann et al. 1998; Rothenberg et al. 2002). This lack of research is despite findings that retinal and visual cortical structural–functional abnormalities occur in animals after moderate-level (BPb 11–39 μg/dL) and high-level (BPb ≥ 40 μg/dL) developmental Pb exposure (reviewed by Fox and Boyes 2007; Otto and Fox 1993). Persistent rod photoreceptor-mediated (scotopic) electroretinographic (ERG) and behavioral deficits occur in monkeys, rats, and mice after moderate-level and high-level post-natal Pb exposure (PLE) (Fox and Boyes 2007). The scotopic ERG alterations are characterized by decreases in a-wave and b-wave ERG amplitude (subnormality), sensitivity, and temporal resolution. Similar ERG changes occurred in Pb-exposed workers and isolated retinas exposed to Pb2+ (Otto and Fox 1993). In contrast, adult monkeys with high-level lifetime Pb exposure exhibited increased ERG b-wave amplitudes (supernormality) (Lilienthal et al. 1994). Moreover, our prospective epidemiologic study of children with lifetime low-level and moderate-level Pb exposure revealed that only gestational Pb exposure (GLE) showed a significant dose-dependent relationship with supernormal ERG a-waves and b-waves and increased b-wave sensitivity with no change in implicit times (Rothenberg et al. 2002). In experimental animals, supernormal scotopic ERGs are observed after the loss of retinal dopamine (DA) or zinc. For example, the destruction of dopaminergic amacrine cells by the neurotoxin 6-hydroxydopamine produced supernormal scotopic ERGs with normal implicit times (Olivier et al. 1986; Skrandies and Wassle 1988). Similarly, animals administered nonselective dopamine receptor antagonists had supernormal scotopic b-waves with normal implicit times (Jagadeesh et al. 1980; Schneider and Zrenner 1991). A persistent decrease in retinal tyrosine hydroxylase immunoreactivity after lifetime Pb exposure in monkeys suggests that a loss of DA produced supernormal ERGs (Kohler et al. 1997; Lilienthal et al. 1994). Chelation of retinal Zn produced supernormal scotopic ERGs and increased b-wave sensitivity (Redenti and Chappell 2003). Although no published reports have shown that scotopic ERG supernormality results from an increased number of rods, the log scotopic b-wave threshold and amplitude are linearly related to the number of rod photoreceptors and their rhodopsin content per eye (Dowling 1960). Therefore, we hypothesized that GLE produced supernormal scotopic ERGs by one of these three relatively independent mechanisms: an increased number of rod photoreceptors, decreased retinal DA metabolism, and/or decreased retinal Zn concentrations. To determine the sites and mechanisms of the GLE-induced supernormal scotopic ERGs, we developed a new dose–response model of GLE. Then, we conducted scotopic ERG studies and retinal histologic, morphometric, and neurochemical experiments in adult offspring. Low-level and moderate-level GLE produced supernormal scotopic ERGs, an increased neurogenesis of rods and rod bipolar cells (BCs), and decreased DA synthesis and utilization/release in the absence of retinal injury. GLE produced inverted U-shaped dose–response curves as the high-level GLE dose produced rod cell loss and thus ERG subnormality.

Bovine heart mitochondrial NADH-ubiquinone oxidoreductase (complex I) catalyzed NADH- and ubiquinone-1-dependent oxygen (O2) turnover to hydrogen peroxide that was stimulated by piericidin A and superoxide dismutase (SOD), but was insensitive to antimycin A, myxothiazol, and potassium cyanide. The extent of O2 consumption as a function of ubiquinone-1 did not correlate with piericidin A-sensitive rates of ubiquinone reduction. Decylubiquinone did not stimulate O2 consumption, but did initiate an SOD-sensitive cytochrome c reduction when complex I was isolated away from ubiquinol-cytochrome c oxidoreductase. Rates and extent of O2 turnover (ROS production) and ubiquinone reduction were higher than previously reported for submitochondrial particles (SMP) and isolated complex I. This ROS production was shown to co-isolate with complex I flavin.

The northwest shelf of Australia is a region with known petroleum reserves. Recent geological investigations have revealed carbonate knolls postulated to be of biological origin. Sediment microbial populations at three sites on the northwest shelf, Pee Shoal, Mermaid Reef, and Scott Reef, were investigated for the presence of hydrocarbon-degrading bacteria. From two sampling trips, 246 bacterial strains were purified, and 182 of these strains displayed preferential growth on hydrocarbon-selective media. Strains were tested for nutrient specificity using single hydrocarbon fermentations. Metabolic profiles were constructed using biochemical testing, fatty acid analysis, and metabolic rate experiments. 16S rRNA gene sequence analysis of four strains identified these strains as members of the genera Sphingomonas, Bacillus, and Microbacterium, and one strain as a member of the alpha-Proteobacteria. The potential of these strains as bioindicators of hydrocarbon pollutants or for bioremediation in marine environments is discussed.

Rho transcription termination factor mutant, F355W, showed tryptophan fluorescence intensity approximately twice that of wild-type Rho at equivalent protein concentrations and underwent a decrease in relative fluorescence intensity at 350 nm when 100 μm ATP was added in the presence or absence of RNA. Titration of this fluorescence quenching with varying concentrations of ATP (0–600 μm), where Rho is shown to exist as a hexamer (400 nm Rho), revealed tight and loose ATP-binding sites. Bicyclomycin, a specific inhibitor of Rho, increased the tight ATP binding and was used to calibrate ATP-induced fluorescence quenching by using [γ-32P]ATP filter binding. For the Rho mutant F355W, three tight (K d 1 = 3 ± 0.3 μm) and three loose (K d 2 = 58 ± 3 μm) ATP-binding sites per hexamer were seen on Scatchard analysis in the absence of bicyclomycin and poly(C). In the presence of bicyclomycin, the K d 1 changed from 3.0 to 1.4 μm, but K d 2underwent a lesser change. The non-hydrolyzable ATP analogue, γ-S-ATP, gave a similar profile with three tight (K d 1 = 0.2 μm) and three loose (K d 2 = 70 μm) ATP-binding sites per hexamer. Adding poly(C) to F355W did not alter the K d 1 orK d 2 for ATP or for γ-S-ATP. ADP-induced quenching produced 5.5 loose (K d = 92 μm) binding sites in the absence of poly(C), and the binding became weaker (K d = 175 μm) in the presence of poly(C). The data suggest that in the presence of ADP Rho has six equivalent nucleotide-binding sites. When ATP was added these sites converted to three tight and three loose binding loci. We propose an alternating ATP site mechanism where ATP binding creates heterogeneity in the ATP binding in adjacent subunits, and we suggest that ATP binding to a neighboring loose site stimulates hydrolysis at a neighboring tight binding site such that all six subunits can be potential “active” sites for ATP hydrolysis. The dynamic nature of the ATP binding to Rho is discussed in the terms of the mechanism of RNA tracking driven by ATP hydrolysis.

BACKGROUND Transforming growth factor (TGF)-beta2 can produce effective pleurodesis in animals, but its efficacy has not been compared with commonly used pleurodesing agents in sheep, which have a thick pleura resembling that of humans. The acute physiological effects and the level of systemic TGF-beta absorption after its intrapleural administration have not been studied. The aims of the present study were to compare: (i) the effectiveness of TGF-beta2, talc and bleomycin in producing pleurodesis in sheep; (ii) the acute side-effects and systemic TGF-beta levels following the intrapleural administration of these agents; and (iii) histological changes after intrapleural injections of these agents. METHODOLOGY Twelve sheep were divided into three groups and were given a single intrapleural dose of TGF-beta2 (0.25 microg/kg), talc slurry (5 g) or bleomycin (60 IU) via a chest tube. Saline or buffer was injected into the contralateral side, which served as the control. Arterial blood gases and respiratory and heart rates were monitored for the first 24 h. Plasma levels of TGF-beta1 and TGF-beta2 were measured. Pleurodesis was graded macroscopically from 1 (none) to 8 (symphysis > 50% of hemithorax) at day 14. RESULTS At day 14, the pleurodesis score of the TGF-beta2 group (7.7+/-0.6) was similar to that of the talc (7.0+/-1.7) group and significantly higher than that of the bleomycin group (3.3+/-2.3; P < 0.05). No significant differences were seen in arterial blood gas analysis, vital signs and plasma TGF-beta1 and TGF-beta2 concentrations among the three groups. CONCLUSIONS Transforming growth factor-beta2 was as effective as talc and more so than bleomycin in inducing pleurodesis in sheep. Intrapleural administration of TGF-beta2 appeared safe. No acute changes in gaseous exchange or macroscopic abnormalities were seen following intrapleural TGF-beta2. Importantly, there was no evidence of an increase in systemic TGF-beta levels following its intrapleural administration.

DNA markers for genes conditioning resistance to soybean [Glycine max (L.) Merr.] root infection by [Fusarium solani (Mart.) Sacc. f. sp. glycine (Burk.)] (Rfsl ), sudden death syndrome (SDS), and soybean cyst nematode (SCN; Heterodera glycines Ichinohe; Rhg4 and rhg1) were previously identified in 'Essex' X 'Forrest'. This study tests the effectiveness of those markers in selecting for disease resistance among recombinant inbred lines from 'Flyer' × 'Hartwig'. A total of 535 among 739 lines were scored by two markers, providing four genotypes. A stratified random sample of 50 lines was evaluated for SDS by F. solani root infection severity at two locations and SCN race 3 index of parasitism in the greenhouse. Selection with BLT65 identified 281 among 671 lines with the genomic region that underlies Rhg4-derived SCN resistance. Selection with Satt038 identified 230 among 613 lines containing the genomic region that underlies resistance to SDS (rfs1) and rhg1-derived SCN resistance. A total of 93 out of 535 lines had genomic regions that underlie resistance to both SDS and SCN in Essex × Forrest. Segregation of both markers was not random (P ≤ 0.05). Infection severity means for genotypes with the Hartwig allele at Satt038 (28-29%) were lower (P = 0.0001, R 2 = 28%) than with the Flyer allele (31-42%); irrespective of maturity group. BLT65 was not associated with infection severity. Mean SCN index of parasitism was lower (P ≤ 0.05) only for genotypes carrying the Hartwig allele at both Satt038 and BLT65. Therefore, alleles conferring resistance to SDS and SCN in Essex × Forrest are transferable to other populations.

Summary: A synthetic peptide (peptide 10) representing a surface-exposed, linear B cell epitope from outer-membrane (OM) protein F of Pseudomonas aeruginosa was shown previously to afford protection in mice from P. aeruginosa infection. This peptide was expressed in tandem with the protein F peptide 18 on each of the two coat proteins of cowpea mosaic virus (CPMV). The chimaeric virus particles (CVPs) expressing the peptides on the S (small) coat protein (CPMV-PAE4) and L (large) coat protein (CPMV-PAE5) were used to immunize mice. Following subcutaneous immunization in Freund's and QuilA adjuvants, CPMV-PAE4 induced antibodies predominantly against peptide 18, whereas CPMV-PAE5 produced antibodies exclusively against peptide 10, indicating that the site of peptide expression on CPMV influences its immune recognition. The anti-peptide antibodies elicited by CPMV-PAE5 were predominantly of the IgG2a isotype, indicating a highly polarized TH1-type response. The peptide-specific IgG2a strongly recognized the whole F protein, but more importantly, recognized protein F in all seven Fisher-Devlin immunotypes of P. aeruginosa. Furthermore, the peptide-specific IgG2a in CVP/QS-21 adjuvant-immunized mice was shown to bind complement and to augment phagocytosis of P. aeruginosa by human neutrophils in vitro. The ability of CPMV-PAE5 to induce P. aeruginosa-specific opsonic IgG2a gives it potential for further development as a protective vaccine against P. aeruginosa.

Landsat Thematic Mapper data were acquired for four flyby dates that coincided with field data collection of chlorophyll a and Secchi disc depth for Bull Shoals Reservoir, Arkansas, USA. Predictive models were developed for chlorophyll a from July 1994 ( R2= 0.80) and December 1994 ( R=2 0.84) data and for Secchi disc depth ( R2= 0.96) from February 1995 data. These models were then tested using historic chlorophyll a data compiled from the previous ten years. The July 1994 model satisfactorily predicted chlorophyll a levels in six of the ten years and this improved to five out of five years when only summer seasons were considered. Phytoplankton analyses suggested an influence on algorithm development with respect to species composition at the time of satellite flyby.

Previous studies showed that the HIV-1 envelope (Env) protein was not incorporated into vesicular stomatitis virus (VSV) virions unless its cytoplasmic tail was replaced with that of the VSV glycoprotein (G). To determine whether the G tail provided a positive incorporation signal for Env, or if sequences in the Env tail prevented incorporation, we generated mutants of Env with its 150-amino-acid tail shortened to 29, 10, or 3 amino acids (Envtr mutants). Cells infected with VSV recombinants expressing these proteins or an Env-G tail hybrid showed similar amounts of Env protein at the surface. The Env-G tail hybrid or the Envtr3 mutant were incorporated at the highest levels into budding VSV virions. In contrast, the Envtr29 or Envtr10 mutants were incorporated poorly. These results defined a signal preventing incorporation within the 10 membrane-proximal amino acids of the Env tail. Confocal microscopy revealed that this signal functioned by causing localization of human immunodeficiency virus type 1 Env to plasma membrane domains distinct from the VSV budding sites, where VSV proteins were concentrated.