Time resolved sulphur and nutrient distribution in Norway spruce drill cores using ICP-OES

Methods were developed for detailed dendrochemical studies of low sulphur contents in Norway spruce (Picea abies L. Karst.). This tree species is the dominant conifer species in Northern and Central Europe and therefore predestined for a possible use as an environmental archive. Two independent digestion procedures were investigated with respect to their suitability for element determination and optimised for analysis of the low sulphur content in wood. A modified oxygen bomb combustion procedure and a microwave acid digestion procedure were evaluated with the goal to obtain sufficient detection limits in order to access low concentrated non-metals with an appropriate time resolution. Method development included evaluation of strategies preventing losses of volatile sulphur species. Digestion efficiency was demonstrated by recovery rates for various certified plant standard reference materials (NIST 1572, NIST 1547, RM 8436, BCR 101, NIST 1515, RM 8436, NIST 1573, NIST 1575) as well as self prepared standards with defined low sulphur content of 20 to 200mg kg−1, which are typical for Norway spruce wood samples. Ultra sonic nebulisation (USN) was evaluated with respect to signal enhancement for sample introduction to inductively coupled plasma optical emission spectrometry (ICP-OES). The optimised procedure was applied to Norway spruce drill cores from locations with different environmental conditions in Switzerland, in order to investigate the anthropogenic impact of sulphur and the suitability of Norway spruce as an environmental archive for sulphu

Effect of glucose on assimilatory sulphate reduction in Arabidopsis thaliana roots

With the aim of analysing the relative importance of sugar supply and nitrogen nutrition for the regulation of sulphate assimilation, the regulation of adenosine 5′‐phosphosulphate reductase (APR), a key enzyme of sulphate reduction in plants, was studied. Glucose feeding experiments with Arabidopsis thaliana cultivated with and without a nitrogen source were performed. After a 38 h dark period, APR mRNA, protein, and enzymatic activity levels decreased dramatically in roots. The addition of 0.5% (w/v) glucose to the culture medium resulted in an increase of APR levels in roots (mRNA, protein and activity), comparable to those of plants kept under normal light conditions. Treatment of roots with d‐sorbitol or d‐mannitol did not increase APR activity, indicating that osmotic stress was not involved in APR regulation. The addition of O‐acetyl‐l‐serine (OAS) also quickly and transiently increased APR levels (mRNA, protein, and activity). Feeding plants with a combination of glucose and OAS resulted in a more than additive induction of APR activity. Contrary to nitrate reductase, APR was also increased by glucose in N‐deficient plants, indicating that this effect was independent of nitrate assimilation. [35S]‐sulphate feeding experiments showed that the addition of glucose to dark‐treated roots resulted in an increased incorporation of [35S] into thiols and proteins, which corresponded to the increased levels of APR activity. Under N‐deficient conditions, glucose also increased thiol labelling, but did not increase the incorporation of label into proteins. These results demonstrate that (i) exogenously supplied glucose can replace the function of photoassimilates in roots; (ii) APR is subject to co‐ordinated metabolic control by carbon metabolism; (iii) positive sugar signalling overrides negative signalling from nitrate assimilation in APR regulation. Furthermore, signals originating from nitrogen and carbon metabolism regulate APR synergisticall

Chronicle of a death foretold: Plasmodium liver stage parasites decide on the fate of the host cell

Protozoan parasites of the genus Plasmodium are the causative agents of malaria. Despite more than 100years of research, the complex life cycle of the parasite still bears many surprises and it is safe to say that understanding the biology of the pathogen will keep scientists busy for many years to come. Malaria research has mainly concentrated on the pathological blood stage of Plasmodium parasites, leaving us with many questions concerning parasite development within the mosquito and during the exo-erythrocytic stage in the vertebrate host. After the discovery of the Plasmodium liver stage in the middle of the last century, it remained understudied for many years but the realization that it represents a promising target for vaccination approaches has brought it back into focus. The last decade saw many new and exciting discoveries concerning the exo-erythrocytic stage and in this review we will discuss the highlights of the latest developments in the field. During the last decade many surprising facts about exoerythrocytic development of Plasmodium parasites have been revealed and will be discusse

Enhanced ozone strongly reduces carbon sink strength of adult beech (Fagus sylvatica) – Resume from the free-air fumigation study at Kranzberg Forest

Ground-level ozone (O3) has gained awareness as an agent of climate change. In this respect, key results are comprehended from a unique 8-year free-air O3-fumigation experiment, conducted on adult beech (Fagus sylvatica) at Kranzberg Forest (Germany). A novel canopy O3 exposure methodology was employed that allowed whole-tree assessment in situ under twice-ambient O3 levels. Elevated O3 significantly weakened the C sink strength of the tree–soil system as evidenced by lowered photosynthesis and 44% reduction in whole-stem growth, but increased soil respiration. Associated effects in leaves and roots at the gene, cell and organ level varied from year to year, with drought being a crucial determinant of O3 responsiveness. Regarding adult individuals of a late-successional tree species, empirical proof is provided first time in relation to recent modelling predictions that enhanced ground-level O3 can substantially mitigate the C sequestration of forests in view of climate change

Cardiac Troponin T and severity of cerebral white matter lesions in acute ischemic stroke

In the literature, there is evidence of an association between cardiac diseases and clinical cognitive impairment as well as subclinical brain injury. We examined whether there is a link between elevated cardiac troponin levels (hs-cTnT) as a marker of subclinical myocardial injury and severity of white matter lesions (WML) as a marker of subclinical brain injury in stroke patients since those patients are a high-risk population in terms of both cognitive decline and cardiac comorbidity. We conducted a retrospective analysis of consecutive acute ischemic stroke patients admitted to Charité-University Hospital, Berlin from 2011-2013. All included participants underwent 3T-cMRI and serial hs-cTnT measurements as part of the clinical routine. Severity of WML was graded using the age- related white matter severity score (ARWMS). Patients with hs-cTnT >52ng/l or dynamic change of hs- cTnT >50%, which may indicate acute myocardial damage, were excluded. We performed unadjusted and adjusted quantile regression models to determine whether there is an association between hs- cTnT (dichotomized at the 99th percentile of a healthy reference population, 14ng/l) and WML. The data of 860 patients were examined (median age 73 years, 44.8% female, median ARWMS 6). In patients with elevated hs-cTnT, WML were more severe than in patients with normal hs-cTnT (median ARWMS 8 vs. 5, adjusted beta for the 50th percentile 1.12, 95% CI 0.41-1.84). There was a more pronounced association between WML and elevated hs-cTnT in patients with moderate to severe WML (beta 1.77, 95% CI 0.26-3.27 for 80th percentile). Further division of patients with elevated hs- cTnT values showed that the association was independent of the severity of hs-cTnT elevation. Our data indicate an association between subclinical myocardial injury and severity of white matter lesions. Longitudinal studies are needed to assess the impact of risk-modifying therapy on the prevention of cognitive impairment and the value of hs-cTnT as a parameter for therapy monitoring.In der Literatur finden sich Hinweise auf einen Zusammenhang zwischen kardialen Erkrankungen und sowohl kognitiver Beeinträchtigung als auch subklinischer Schädigung des Gehirns. In dieser Arbeit wurde untersucht, ob ein Zusammenhang zwischen einer Erhöhung des kardialen Troponins (hs-cTnT) als Marker einer subklinischen Myokardschädigung und dem Schweregrad zerebraler „white matter lesions“ (WML) als Marker einer subklinischen Hirnschädigung bei Schlaganfallpatienten besteht. Es handelt sich um eine retrospektive Auswertung von Patienten mit akutem ischämischem Schlaganfall, die von 2011-2013 am Campus Benjamin Franklin stationär behandelt worden sind. Bei allen eingeschlossenen Patienten wurden im Rahmen der klinischen Routine ein 3T-cMRT und serielle Bestimmungen der Troponinwerte durchgeführt. Der Schweregrad der zerebraler WML wurde anhand des „age-related white matter severity scores“ (ARWMS) bestimmt. Patienten mit einem hs-cTnT > 52 ng/l oder einer Änderung des hs-cTnT > 50% in seriellen Kontrollen wurden ausgeschlossen, da diese Konstellationen auf einen akuten Myokardschaden hindeuten. Es wurden unadjustierte und adjustierte Quantilsregressionsanalysen durchgeführt, um festzustellen, ob ein Zusammenhang zwischen erhöhtem hs-cTnT (cut-off 14 ng/l, entsprechend der 99. Perzentile einer gesunden Kontrollpopulation) und WML besteht. Insgesamt wurden die Daten von 860 Patienten untersucht (medianes Alter 73 Jahre, 44.8% weibliches Geschlecht, medianer ARWMS 6). Patienten mit erhöhtem hs-cTnT hatten ein größeres Ausmaß an WML als Patienten mit normwertigem hs-cTnT (medianer ARWMS 8 vs. 5, adjustiertes beta für die 50. Perzentile 1.12, 95% CI 0.41-1.84). Der Zusammenhang zwischen WML und erhöhtem hs-cTnT war stärker bei Patienten mit höherem Schweregrad an WML (beta 1.77, 95% CI 0.26-3.27 für die 80. Perzentile). Eine weitere Aufteilung der Studienpopulation nach hs-cTnT-Werten zeigte, dass der Zusammenhang unabhängig vom Ausmaß der hs-cTnT-Erhöhung war. Die Ergebnisse weisen auf einen Zusammenhang zwischen subklinischem Myokardschaden und zerebralen WML hin. Es braucht longitudinale Studien, um den Einfluss einer risikomodifizierenden Therapie zur Vorbeugung einer kognitiven Einschränkung und den möglichen Stellenwert von Troponin als Marker eines Therapieerfolgs zu untersuchen

Insect haptoelectrical stimulation of Venus flytrap triggers exocytosis in gland cells

The Venus flytrap Dionaea muscipula captures insects and consumes their flesh. Prey contacting touch-sensitive hairs trigger traveling electrical waves. These action potentials (APs) cause rapid closure of the trap and activate secretory functions of glands, which cover its inner surface. Such prey-induced haptoelectric stimulation activates the touch hormone jasmonate (JA) signaling pathway, which initiates secretion of an acidic hydrolase mixture to decompose the victim and acquire the animal nutrients. Although postulated since Darwin’s pioneering studies, these secretory events have not been recorded so far. Using advanced analytical and imaging techniques, such as vibrating ion-selective electrodes, carbon fiber amperometry, and magnetic resonance imaging, we monitored stimulus-coupled glandular secretion into the flytrap. Trigger-hair bending or direct application of JA caused a quantal release of oxidizable material from gland cells monitored as distinct amperometric spikes. Spikes reminiscent of exocytotic events in secretory animal cells progressively increased in frequency, reaching steady state 1 d after stimulation. Our data indicate that trigger-hair mechanical stimulation evokes APs. Gland cells translate APs into touch-inducible JA signaling that promotes the formation of secretory vesicles. Early vesicles loaded with H⁺ and Cl⁻ fuse with the plasma membrane, hyperacidifying the “green stomach”-like digestive organ, whereas subsequent ones carry hydrolases and nutrient transporters, together with a glutathione redox moiety, which is likely to act as the major detected compound in amperometry. Hence, when glands perceive the haptoelectrical stimulation, secretory vesicles are tailored to be released in a sequence that optimizes digestion of the captured animal

Compared to conventional, ecological intensive management promotes beneficial proteolytic soil microbial communities for agro-ecosystem functioning under climate change-induced rain regimes

Projected climate change and rainfall variability will affect soil microbial communities, biogeochemical cycling and agriculture. Nitrogen (N) is the most limiting nutrient in agroecosystems and its cycling and availability is highly dependent on microbial driven processes. In agroecosystems, hydrolysis of organic nitrogen (N) is an important step in controlling soil N availability. We analyzed the effect of management (ecological intensive vs. conventional intensive) on N-cycling processes and involved microbial communities under climate change-induced rain regimes. Terrestrial model ecosystems originating from agroecosystems across Europe were subjected to four different rain regimes for 263 days. Using structural equation modelling we identified direct impacts of rain regimes on N-cycling processes, whereas N-related microbial communities were more resistant. In addition to rain regimes, management indirectly affected N-cycling processes via modifications of N-related microbial community composition. Ecological intensive management promoted a beneficial N-related microbial community composition involved in N-cycling processes under climate change-induced rain regimes. Exploratory analyses identified phosphorus-associated litter properties as possible drivers for the observed management effects on N-related microbial community composition. This work provides novel insights into mechanisms controlling agro-ecosystem functioning under climate change

Ucma/GRP inhibits phosphate-induced vascular smooth muscle cell calcification via SMAD-dependent BMP signalling

Vascular calcification (VC) is the process of deposition of calcium phosphate crystals in the blood vessel wall, with a central role for vascular smooth muscle cells (VSMCs). VC is highly prevalent in chronic kidney disease (CKD) patients and thought, in part, to be induced by phosphate imbalance. The molecular mechanisms that regulate VC are not fully known. Here we propose a novel role for the mineralisation regulator Ucma/GRP (Upper zone of growth plate and Cartilage Matrix Associated protein/Gla Rich Protein) in phosphate-induced VSMC calcification. We show that Ucma/GRP is present in calcified atherosclerotic plaques and highly expressed in calcifying VSMCs in vitro. VSMCs from Ucma/GRP(-/-) mice showed increased mineralisation and expression of osteo/chondrogenic markers (BMP-2, Runx2, beta-catenin, p-SMAD1/5/8, ALP, OCN), and decreased expression of mineralisation inhibitor MGP, suggesting that Ucma/GRP is an inhibitor of mineralisation. Using BMP signalling inhibitor noggin and SMAD1/5/8 signalling inhibitor dorsomorphin we showed that Ucma/GRP is involved in inhibiting the BMP-2-SMAD1/5/8 osteo/chondrogenic signalling pathway in VSMCs treated with elevated phosphate concentrations. Additionally, we showed for the first time evidence of a direct interaction between Ucma/GRP and BMP-2. These results demonstrate an important role of Ucma/GRP in regulating osteo/chondrogenic differentiation and phosphate-induced mineralisation of VSMCs.NWO ZonMw [MKMD 40-42600-98-13007]; FCT [SFRH/BPD/70277/2010]info:eu-repo/semantics/publishedVersio

Regulation of vascular smooth muscle cell calcification by syndecan-4/FGF-2/PKCα signaling and cross-talk with TGFβ

Aims: Vascular calcification is a major cause of morbidity and mortality. Fibroblast growth factor-2 (FGF-2) plays an instructive role in osteogenesis and bone development, but its role in vascular calcification was unknown. Therefore, we investigated the involvement of FGF-2 in vascular calcification and determined the mechanism by which it regulates this process. Methods and Results: We demonstrate that FGF-2 expression is increased in vascular smooth muscle cells (VSMCs) induced to deposit a mineralized matrix by incubation with β-glycerophosphate. FGF-2 is also localized to sites of calcification within human atherosclerotic plaques. The expression of syndecan-4, a heparan sulfate proteoglycan which regulates FGF-2 signaling, is also increased in mineralizing VSMCs and co-localizes with FGF-2 in human calcified atherosclerotic plaques. Exogenous FGF-2 inhibits VSMC mineralization, and this inhibition is reduced when syndecan-4 expression is knocked-down using siRNA. Biochemical inhibition of FGFR signaling using a pan FGFR inhibitor (BGJ398) or knocking-down syndecan-4 expression in VSMCs using siRNA increases VSMC mineralization. These increases are prevented by inhibiting transforming growth factor-β (TGFβ) signaling with SB431542, suggesting cross-talk between FGF-2 and TGFβ signaling is crucial for the regulation of VSMC mineralization. Syndecan-4 can also regulate FGF-2 signaling directly via protein kinase Cα (PKCα) activation. Biochemical inhibition of PKCα activity using Gö6976, or siRNA-mediated suppression of PKCα expression increases VSMC mineralization; this increase is also prevented with SB431542. Finally, the ability of FGF-2 to inhibit VSMC mineralization is reduced when PKCα expression is knocked-down. Conclusion: This is the first demonstration that syndecan-4 promotes FGF-2 signaling, and in turn, suppresses VSMC mineralization by down-regulating TGFβ signaling. Our discoveries that FGF-2 and syndecan-4 expression is increased in mineralizing VSMCs and that PKCα regulates FGF-2 and TGFβ signaling in VSMCs suggests that the syndecan-4/FGF-2/TGFβ signaling axis could represent a new therapeutic target for vascular calcification