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The transition toward more sustainable plant protection with reduced pesticide use is difficult, because there is no “silver bullet” available among nonchemical tools. Integrating several plant protection approaches may thus be needed for efficient pest management. Recently, increasing the genetic diversity of plantations via cultivar mixing has been proposed as a possible method to reduce pest damage. However, previous studies have not addressed either the relative efficiency of exploiting cultivar mixing and intrinsic plant herbivore resistance or the potential utility of combining these approaches to increase cropping security. Here, using a full factorial experiment with 60 woodland strawberry plots, we tested for the relative and combined effect of cultivar mixing and intrinsic plant resistance on herbivore damage and yield. The experiment comprised two levels of diversity (“high” with 10 varieties and “low” with two varieties) and three levels of resistance (“resistant” comprising only varieties intrinsically resistant against strawberry leaf beetle Galerucella tenella; “susceptible” with susceptible varieties only; and “resistance mixtures” with 50:50 mixtures of resistant and susceptible varieties). The experiment was carried out over two growing seasons. Use of resistant varieties either alone or intermixed with susceptible varieties in “resistance mixtures” reduced insect herbivory. Interestingly, resistant varieties not only reduced the mean damage in “resistance mixtures” by themselves being less damaged, but also protected intermixed susceptible varieties via associational resistance. The effect of higher genetic diversity was less evident, reducing herbivory only at the highest level of herbivore damage. In general, herbivory was lowest in plots with high diversity that included at least some resistant varieties and highest in low diversity plots consisting only of susceptible varieties. Despite this, no significant difference in yield (fruit biomass) was found, indicating that strawberry may be relatively tolerant. Our results demonstrate that combined use of high genetic diversity and resistant varieties can help reduce pest damage and provide a useful tool for sustainable food production. “Resistance mixtures” may be particularly useful for sensitive food crops where susceptible varieties are high yielding that could not be completely replaced by resistant ones.

Planar particle image velocimetry was conducted upstream and in the near-wake of a lab-scale free-rotating wind turbine model and compared to several actuator disks with the same dimensions. The Reynolds number of the incoming flow is order 104. Actuator disks with different designs and solidities were tested, and the process of actuator disk selection is explicitly shown. The drag, mean velocity and mean vorticity in the wake of the disks were compared to that of the rotating model. For the disk that was the best match, the Reynolds stresses and swirling strength are also presented. The instantaneous swirling strength illustrated that despite similar mean fields, the instantaneous phenomena were significantly different. Distinct tip vortices were present in the wake of the rotating model but were absent from the wake of the actuator disk. Proper orthogonal decomposition was used to further investigate the underlying phenomena in the two flows, again demonstrating the importance of tip vortices when studying the rotating model and the lack of such distinct vortices when using the actuator disk. Hence, despite well-matched mean characteristics, the instantaneous structures in the two flows remain distinct. © 2020 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Planar particle image velocimetry ble gjennomført oppstrøms og i den nærliggende vaken til en roterende vindturbinmodell i laboratorieskala og aktuatordisker av samme dimensjon i en vindtunell. Den innkommende strømningen hadde et Reynolds tall i størrelsesorden 10^4. Aktuatordisker med ulike design og soliditeter ble testet, og prosessen med å velge aktuatordisk er vist. Den resulterende luftmotstanden, gjennomsnittlig hastighet og gjennomsnittlig vorticity i vaken til diskene ble sammenlignet med tilsvarende størrelser for den roterende modellen. Den disken med vake som mest nøyaktig gjenskapte vaken til den roterende modellen ble så studert i mer detalj. Reynolds stresses ble sett på for å fastslå at de gjennomsnittlige karakteristikkene i strømningene sammenfalt. På tross av sammenlignbare gjennomsnittsfelt viste en analyse av instantaneous swirling strength at det var betydelige forskjeller mellom de momentane fenomenene i strømningene. Distinkte tip vortices var til stede i vaken til den roterende modellen, men var fraværende i vaken til aktuatordisken. I tillegg var swirl av høy intensitet til stede direkte nedstrøms for aktuatordisken, forårsaket av turbulent miksing av strømningsstråler som passerer gjennom disken. Tilsvarende fenomen var ikke til stede bak de roterende turbinbladene. Proper orthogonal decomposition ble brukt for å videre studere de underliggende fenomenene i de to strømningene. Også denne analysen viste viktigheten av tip vortices når man studerer den roterende modellen og mangelen på slike distinkte vortices når man bruker aktuatordisken. Dermed, på tross av lignende gjennomsnittlige karakteristikker, forblir de momentane strukturene i de to strømningene ulike. Planar particle image velocimetry was conducted upstream and in the near-wake of a lab-scale rotating wind turbine model and actuator disks of the same dimensions in a wind tunnel, at an incoming flow Reynolds number of the order 10^4. Actuator disks with different designs and solidities were tested, and the process of actuator disk selection is shown. The produced drag, mean velocity and mean vorticity in the wake of the disks were compared to that of the rotating model. The disk whose wake most closely replicated the wake of the rotating model was then studied in more detail, analyzing mean Reynolds stresses to determine that the mean characteristics of the flows were similar. However, the instantaneous swirling strength illustrated that despite similar mean fields, the instantaneous phenomena were significantly different. Distinct tip vortices were present in the wake of the rotating model, but were absent from the wake of the actuator disk. Furthermore, high intensity swirl was present directly downstream of the actuator disk, caused by turbulent mixing of jets passing through the disk, which was not present behind the rotating turbine blades. Proper orthogonal decomposition was used to further study the underlying phenomena in the two flows, again demonstrating the importance of tip vortices when studying the rotating model and the lack of such distinct vortices when using the actuator disk. Hence, despite similar mean characteristics, the instantaneous structures in the two flows remain distinct.

Degradation of organic matter (OM) is generally considered to be primarily governed by biotic factors in aquatic environments. However, a number of abiotic processes also play key roles in mediating OM-degradation. Sunlight can act as a principal abiotic driver of the degradation of terrestrial organic matter, but its importance for freshwater ecosystems and possible interactions with biotic drivers remains poorly understood. We carried out two microcosm experiments which focused on the role of sunlight on microbial and invertebrate-mediated OM degradation using two species of plant leaves and the aquatic invertebrate Asellus aquaticus. Results indicated that sunlight was the primary driver of leaf mass loss during the early stages of decomposition, whereas microbial communities had a negligible effect. Sunlight was observed to strongly affect invertebrate behavior as invertebrates avoided direct illumination. This alteration of behavior resulted in a reduction in the consumption of a leaf surrogate (DECOTAB) by A. aquaticus. Together, these results indicate that sunlight has the potential to strongly influence structural and functional attributes of shallow freshwater systems, and hence serve as an appraisal to consider sunlight as a significant direct and indirect physical driver governing OM degradation in shallow aquatic systems.

PURPOSE: Recently, it was shown that a significantly higher T1ρ is found in compact myocardial fibrosis after chronic myocardial infarction. In this study, we investigated the feasibility of native T1ρ -mapping for the detection of diffuse myocardial fibrosis in patients with dilated cardiomyopathy (DCM). MATERIALS AND METHODS: T1ρ -mapping was performed on three explanted hearts from DCM patients at 3 Tesla (T). Histological fibrosis quantification was performed, and compared with the T1ρ -relaxation times in the heart. Furthermore, twenty DCM patients underwent an MRI at 1.5T. Native T1ρ -maps, native T1 -maps, and extracellular volume (ECV)-maps were acquired. Additionally, eight healthy volunteers were scanned for reference values. RESULTS: A significant correlation (Pearson r = 0.49; P = 0.005) was found between ex vivo T1ρ -values and fibrosis fraction from histology. Additionally, a significantly higher T1ρ -relaxation time (55.2 ± 2.7 ms) was found in DCM patients compared with healthy control subjects (51.5 ± 1.2 ms) (P = 0.0024). The relation between in vivo T1ρ -values and ECV-values was significant (Pearson r = 0.66). No significant relation was found between native T1 - and ECV-values in this study (P = 0.89). CONCLUSION: This study showed proof of principle for the endogenous detection of diffuse myocardial fibrosis with T1ρ -MRI. Ex vivo and in vivo experiments showed promising results that T1ρ -MRI can be used to measure the extent of diffuse myocardial fibrosis in the myocardium.

There is a growing evidence that members of animal groups synchronize their vigilance behavior to minimize predation risk. Because synchronized vigilance deviates from the classical vigilance models, which assume independent scanning, it is important to understand when and why it occurs. We explored vigilance behavior of wild boar (Sus scrofa) in a population subject to spatial variation in human hunting risk and seasonal variation in food availability. Group members synchronized their vigilance behavior. We hypothesized that vigilance synchronization would be context dependent and the trade-off between energy gain and safety would shape the relationship between the degree of vigilance synchronization and group size. We predicted weaker synchronization in large groups under heavy predation risk, due to benefits of numerical dilution, and stronger synchronization in large groups when food is limiting, due to intense food competition. The degree of synchronization decreased with increasing group size in the area where human hunting added another risk factor to the natural predation, pointing at the safety benefits of vigilance synchrony for members of small groups and the role of human-induced risk in shaping vigilance synchrony. We found no relation between vigilance synchrony and group size in a food scarce, winter season. However, low levels of vigilance and its synchronization observed in winter indicated that energy gain was prioritized over safety. Thus, members of wild boar groups can adjust levels of vigilance and its synchronization depending on the forage-risk trade-off set by the ecological context.

Heart failure after myocardial infarction (MI) depends on infarct size and adverse left ventricular (LV) remodelling, both influenced by the inflammatory response. Leukocyte-associated immunoglobulin-like receptor 1 (LAIR-1) is an inhibitory receptor of ITAM-dependent cell activation, present on almost all immune cells. We investigated regulation of LAIR-1 leukocyte expression after MI in patients and hypothesized that its absence in a mouse model of MI would increase infarct size and adverse remodelling. In patients, LAIR-1 expression was increased 3 days compared to 6 weeks after MI on circulating monocytes (24.8 ± 5.3 vs. 21.2 ± 5.1 MFI, p = 0.008) and neutrophils (12.9 ± 4.7 vs. 10.6 ± 3.1 MFI, p = 0.046). In WT and LAIR-1−/− mice, infarct size after ischemia-reperfusion injury was comparable (37.0 ± 14.5 in WT vs. 39.4 ± 12.2% of the area at risk in LAIR-1−/−, p = 0.63). Remodelling after permanent left coronary artery ligation did not differ between WT and LAIR-1−/− mice (end-diastolic volume 133.3 ± 19.3 vs. 132.1 ± 27.9 μL, p = 0.91 and end-systolic volume 112.1 ± 22.2 vs. 106.9 ± 33.5 μL, p = 0.68). Similarly, no differences were observed in inflammatory cell influx or fibrosis. In conclusion, LAIR-1 expression on monocytes and neutrophils is increased in the acute phase after MI in patients, but the absence of LAIR-1 in mice does not influence infarct size, inflammation, fibrosis or adverse cardiac remodelling.

Recently, it was shown that a significantly higher TTA significant correlation (Pearson r = 0.49; P = 0.005) was found between ex vivo TThis study showed proof of principle for the endogenous detection of diffuse myocardial fibrosis with T2 J. Magn. Reson. Imaging 2017;45:132-138.

Background— Arrhythmogenic ventricular remodeling is hallmarked by both reduced gap junction expression and increased collagen deposition. We hypothesized that reduced connexin43 (Cx43) expression is responsible for enhanced fibrosis in the remodeled heart, resulting in an arrhythmogenic substrate. Therefore, we investigated the effect of normal or reduced Cx43 expression on the formation of fibrosis in a physiological (aging) and pathophysiological (transverse aortic constriction [TAC]) mouse model. Methods and Results— The Cx43 fl/fl and Cx43 CreER(T)/fl mice were aged 18 to 21 months or, at the age of 3 months, either TAC or sham operated and euthanized after 16 weeks. Epicardial activation mapping of the right and left ventricles was performed on Langendorff perfused hearts. Sustained ventricular arrhythmias were induced in 0 of 11 aged Cx43 fl/fl and 10 of 15 Cx43 Cre-ER(T)/fl mice ( P CreER(T)/fl compared with aged Cx43 fl/fl mice, whereas collagen deposition was significantly increased from 1.1±0.2% to 7.4±1.3%. Aged Cx43 CreER(T)/fl mice with arrhythmias had significantly higher levels of fibrosis and conduction heterogeneity than aged Cx43 CreER(T)/fl mice without arrhythmias. The TAC operation significantly increased fibrosis in control compared with sham (4.0±1.2% versus 0.4±0.06%), but this increase was significantly higher in Cx43 CreER(T)/fl mice (10.8±1.4%). Discoidin domain receptor 2 expression was unchanged, but procollagen peptide I and III expression and collagen type 1α2 mRNA levels were higher in TAC–operated Cx43HZ mice. Conclusions— Reduced cellular coupling results in more excessive collagen deposition during aging or pressure overload in mice due to enhanced fibroblast activity, leading to increased conduction in homogeneity and proarrhythmia.

Background: Renal failure is associated with adverse cardiac remodeling and sudden cardiac death. The mechanism leading to enhanced arrhythmogenicity in the cardiorenal syndrome is unclear. The aim of this study was to characterize electrophysiological and tissue alterations correlated with enhanced arrhythmogenicity in two distinct mouse models of renal failure. Methods: Thirty-week-old 129Sv mice received a high-salt diet and deoxycorticosterone acetate (DOCA) for 8 weeks, followed by an additional period of high-salt diet for 27 weeks (DOCA-salt aged model). Adult CD-1 mice were submitted to 5/6-subtotal nephrectomy (SNx) and treated for 11 weeks with a high-salt diet (SNx-salt adult model). Vulnerability to arrhythmia as well as conduction velocities (CVs) of the hearts were determined ex vivo with epicardial mapping. Subsequently, the hearts were characterized for connexin 43 (Cx43) and fibrosis. Results: DOCA-salt and SNx-salt mice developed renal dysfunction characterized by albuminuria. Heart, lung and kidney weights were increased in DOCA-salt mice. Both DOCA-salt and SNx-salt mice were highly susceptible to ventricular arrhythmias. DOCA-salt mice had a significant decrease in both longitudinal and transversal CV in the left ventricle. Histological analysis revealed a significant reduction in Cx43 expression as well as an increase in interstitial fibrosis in both DOCA-salt and SNx-salt mice. Conclusion: DOCA-salt and SNx-salt treatment induced renal dysfunction, which resulted in structural and electrical cardiac remodeling and enhanced arrhythmogenicity. The reduced Cx43 expression and increased fibrosis levels in these hearts are likely candidates for the formation of the arrhythmogenic substrate.

Cardiac fibrosis is a major hallmark of cardiac diseases. For evaluation of cardiac fibrosis, the development of highly specific and preferably noninvasive methods is desired. Our aim was to evaluate CNA35, a protein known to specifically bind to collagen, as a specific marker of cardiac fibrosis. Fluorescently labeled CNA35 was applied ex vivo on tissue sections of fibrotic rat, mouse, and canine myocardium. After quantification of CNA35, sections were examined with picrosirius red (PSR) and compared to CNA35. Furthermore, fluorescently labeled CNA35 was administered in vivo in mice. Hearts were isolated, and CNA35 labeling was examined in tissue sections. Serial sections were histologically examined with PSR. Ex vivo application of CNA35 showed specific binding to collagen and a high correlation with PSR (Pearson r = .86 for mice/rats and r = .98 for canine; both p < .001). After in vivo administration, CNA35 labeling was observed around individual cardiomyocytes, indicating its ability to penetrate cardiac endothelium. High correlation was observed between CNA35 and PSR ( r = .91, p < .001). CNA35 specifically binds to cardiac collagen and can cross the endothelial barrier. Therefore, labeled CNA35 is useful to specifically detect collagen both ex vivo and in vivo and potentially can be converted to a noninvasive method to detect cardiac fibrosis.

Physical review letters 108, 267403 (2012). doi:10.1103/PhysRevLett.108.267403, Published by APS, College Park, Md.

While biofuels have currently been regarded as a good alternative for fossil fuels, there remain many debates on their impacts on human and environment. This paper tried to shed light on bio-ethanol in Brazil as one of the main producers and exporters in the world. The main question was to understand “how sustainable is bio-ethanol production in Brazil?” To answer, the political motives of producing bio-ethanol followed by its ecological and socio-economic impacts were discussed. The paper concluded that although bio-ethanol production in Brazil seems environmentally friendly, it might socio-economically be hazardous.

Item does not contain fulltext BACKGROUND: Reduced expression of connexin43 (Cx43) and sodium channel (Nav1.5) and increased expression of collagen (fibrosis) are important determinants of impulse conduction in the heart. OBJECTIVE: To study the importance and interaction of these factors at very low Cx43 expression, inducible Cx43 knockout mice with and without inducible ventricular tachycardia (VT) were compared through electrophysiology and immunohistochemistry. METHODS: Cx43(CreER(T)/fl) mice were induced with tamoxifen and killed after 2 weeks. Epicardial activation mapping was performed on Langendorff-perfused hearts, and arrhythmia vulnerability was tested. Mice were divided into arrhythmogenic (VT+; n = 13) and nonarrhythmogenic (VT-; n = 10) animals, and heart tissue was analyzed for Cx43, Nav1.5, and fibrosis. RESULTS: VT+ mice had decreased Cx43 expression with increased global, but not local, heterogeneity of Cx43 than did VT- mice. Nav1.5-immunoreactive protein expression was lower in VT+ than in VT- mice, specifically at sites devoid of Cx43. Levels of fibrosis were similar between VT- and VT+ mice. QRS duration was increased and epicardial activation was more dispersed in VT+ mice than in VT- mice. The effective refractory period was similar between the 2 groups. Premature stimulation resulted in a more severe conduction slowing in VT+ than in VT- hearts in the right ventricle. Separate patch-clamp experiments in isolated rat ventricular myocytes confirmed that the loss of Cx43 expression correlated with the decreased sodium current amplitude. CONCLUSIONS: Global heterogeneity in Cx43 expression and concomitant heterogeneous downregulation of sodium-channel protein expression and sodium current leads to slowed and dispersed conduction, which sensitizes the heart for ventricular arrhythmias. 01 april 2012

Excessive collagen deposition is a major hallmark of cardiac disease. Fibrosis reduces cardiac function and plays a major role in cardiac arrhythmogeneity. Despite the clinical importance, there is no non-invasive technique for direct detection of myocardial fibrosis yet. Ultra short echo time (UTE) MRI has been shown to detect tissues with a fast T 2 * signal decay. Collagen has a fast T 2 * signal decay compared to myocardium and should therefore be detectable with UTE MRI. This study aims to investigate the use of UTE MRI to detect fibrosis after myocardial infarction without using exogenous contrast. In 7 male Lewis rats either myocardial infarction was created (n = 5) or sham surgery was performed (n = 2). Six weeks after surgery, hearts were isolated and visualized by MRI. Images were acquired with UTE (TE 0.15 ms), to detect tissue with a fast T 2 * decay. Acquired conventional images (TE = 6.0 ms) were subtracted from UTE images to maintain only ‘short living signal’ (SLS): tissue with a fast decay. In infarcted hearts, SLS was observed in subtracted images, whereas in control hearts hardly any SLS was detected. Subtracted images were cross-referenced with histology and showed that the SLS area observed with UTE MRI corresponded to the collagen-rich areas observed in histology. Normalized SLS areas correlated well with the normalized collagen-rich areas; r = 0.7, p = 0.002. We show for the first time that UTE MRI technology can be used for direct detection of post-infarcted fibrosis without the use of contrast agents.

Increased cardiac collagen deposition is observed in almost every cardiac disease and plays an important role in the deteriorating function of the diseased heart. Propeptides of procollagen types I and III, the 2 major collagen types in the heart, can be detected in circulation. Although these propeptides reflect collagen synthesis, also breakdown products of collagen and the matrix metalloproteinases, responsible for the breakdown of the extracellular matrix, can be detected in blood and are used for investigating the turnover of collagen. Clinical trials are performed in recent years to examine the usage of these biomarkers in a diagnostic or prognostic way in heart failure patients. This review aims to discuss the formation of fibrosis, and studies investigating these biomarkers in heart failure are reviewed in this article. In addition, it is conferred what the flaws are of translating these biomarker levels to cardiac fibrosis formation and where we stand in using these biomarkers in clinics.

Clinical immunotherapy trials like dendritic cell-based vaccinations are hampered by the tumor's offensive repertoire that suppresses the incoming effector cells. Regulatory T cells are instrumental in suppressing the function of cytotoxic T cells. We studied the effect of low-dose cyclophosphamide on the suppressive function of regulatory T cells and investigated if the success rate of dendritic cell immunotherapy could be improved. For this, mesothelioma tumor-bearing mice were treated with dendritic cell-based immunotherapy alone or in combination with low-dose of cyclophosphamide. Proportions of regulatory T cells and the cytotoxic T cell functions at different stages of disease were analyzed. We found that low-dose cyclophosphamide induced beneficial immunomodulatory effects by preventing the induction of Tregs, and as a consequence, cytotoxic T cell function was no longer affected. Addition of cyclophosphamide improved immunotherapy leading to an increased median and overall survival. Future studies are needed to address the usefulness of this combination treatment for mesothelioma patients.

The electronic structure of YBa2Cu3O6+x and La2−xSrxCuO4 for various values of x has been investigated using hard x-ray photoemission spectroscopy. The experimental results establish that the cleaving of YBa2Cu3O6+x compounds occurs predominantly in the BaCuO3 complex, leading to charged surfaces at higher x and to uncharged surfaces at lower x values. The bulk component of the core-level spectra exhibits a shift in binding energy as a function of x, from which a shift of the chemical potential as a function of hole concentration in the CuO2 layers could be derived. The doping dependence of the chemical potential across the transition from a Mott-Hubbard insulator to a Fermi-liquid-like metal is very different in these two series of compounds. In agreement with previous studies in the literature the chemical-potential shift in La2−xSrxCuO4 is close to zero for small hole concentrations. In YBa2Cu3O6+x, similar to all other doped cuprates studied so far, a strong shift of the chemical potential at low hole doping is detected. However, the results for the inverse charge susceptibility at small x shows a large variation between different doped cuprates. The results are discussed in view of various theoretical models. None of these models turns out to be satisfactory

Infection with parasitic helminths of the genus Schistosoma results in a wide range of immunopathology. Studies in murine schistosomiasis suggest that Th17 cells play a major role in the development of severe pathology; conversely, regulatory T (Treg) cells represent a mechanism to curtail excessive inflammation. We assessed by flow cytometry the profile of peripheral blood (PB) CD4 T cells in a cohort of children with urinary schistosomiasis from the village of Pakh, Department of Richard Toll, Senegal. S. hematobium-infected children with bladder pathology had a significantly higher percentage of PB IL-17+ cells with higher RORγt+/ Foxp3+ and IL-17+/ IL-10+ cell ratios than infected children without pathology. To investigate the relationship between PB values and target organs, we also examined the PB T cell response in murine S. mansoni infection (S. hematobium is non-permissive in mice) and, similar to humans, found a significantly higher percentage of CD4+ IL-17+ cells in high-pathology CBA mice than in low-pathology BL/6 mice. Moreover, a significant increase in IL-17+ cells in spleen and liver granulomas together with lower Foxp3+ cells in the spleen of CBA mice denoted a good correlation between PB and target organs. Our findings for the first time demonstrate an association between pathology and PB Th17 cells in human schistosomiasis and suggest human PB T cell subsets to faithfully reflect those mediating lesions in organs affected by the disease.