A multi basin analysis of runoff and erosion in the Blue Nile Basin, Ethiopia was conducted to elucidate sources of runoff and sediment. Erosion is arguably the most critical problem in the Blue Nile ...Basin, as it limits agricultural productivity in Ethiopia, degrades benthos in the Nile, and results in sedimentation of dams in downstream countries. A modified version of the Soil and Water Assessment Tool (SWAT) model was developed to predict runoff and sediment losses from the Ethiopian Blue Nile Basin. The model simulates saturation excess runoff from the landscape using a simple daily water balance coupled to a topographic wetness index in ways that are consistent with observed runoff processes in the basin. The spatial distribution of landscape erosion is thus simulated more correctly. The model was parameterized in a nested design for flow at eight and sediment at three locations in the basin. Subbasins ranged in size from 1.3 to 174 000 km2, and interestingly, the partitioning of runoff and infiltrating flow could be predicted by topographic information. Model predictions showed reasonable accuracy (Nash Sutcliffe Efficiencies ranged from 0.53–0.92) with measured data across all sites except Kessie, where the water budget could not be closed; however, the timing of flow was well captured. Runoff losses increased with rainfall during the monsoonal season and were greatest from areas with shallow soils and large contributing areas. Analysis of model results indicate that upland landscape erosion dominated sediment delivery to the main stem of the Blue Nile in the early part of the growing season when tillage occurs and before the soil was wetted up and plant cover was established. Once plant cover was established in mid August landscape erosion was negligible and sediment export was dominated by channel processes and re-suspension of landscape sediment deposited early in the growing season. These results imply that targeting small areas of the landscape where runoff is produced can be the most effective at controlling erosion and protecting water resources. However, it is not clear what can be done to manage channel erosion, particularly in first order streams in the basin.
Summary
Passive properties of the myocardium influence diastolic filling and cardiac output. In heart failure, changes in contributors to the passive properties of the ventricle, such as titin and ...collagen, and loss of the metabolic enzyme creatine kinase, increase resistance to filling resulting in diastolic dysfunction. Pulmonary artery hypertension (PAH) arises from interactions between the pulmonary vasculature and the right ventricle (RV) which ultimately leads to RV failure. Beta1‐adrenergic receptor blockers (BB) act on the myocardium and are beneficial in left heart failure but are not used in PAH. We investigated whether BB improved survival and RV function in a rat model of PAH. Rats were injected with monocrotaline (60 mg/kg) to induce PAH and RV failure, or saline as controls (CON). When PAH was established, rats were treated with metoprolol (10 mg/kg per day) (MCT+BB) or vehicle (sucrose) (MCT); CON were treated with vehicle. In vivo measurement of RV compliance using pressure–volume catheter, indicated diastolic dysfunction in the RV of MCT rats was improved with BB treatment. Expression of creatine kinase protein and mRNA was lower in MCT rats compared to CON, with a trend for reversion by BB treatment. Isolated CON RV myocytes had a positive contraction response to faster pacing, whereas it was negative in MCT. MCT+BB cells had an intermediate response, indicating improved ability to respond to increased demand. BB improved diastolic function, partially restored metabolic enzymes and augmented contractility in PAH. These data support the hypothesis that BB may be beneficial in PAH by supporting RV function.
Abstract Microtubules are components of the cardiac cytoskeleton that can proliferate in response to pressure-overload in animal and human heart failure. We wished to test whether there was a ...proliferation of the microtubule cytoskeleton in the right ventricle of rats with pulmonary hypertension induced by monocrotaline (MCT) and whether this contributed to contractile dysfunction. Male Wistar rats were injected with 60 mg/kg of MCT in saline or an equivalent volume of saline (CON). MCT produced clinical signs of heart failure within 4 weeks of injection. Expression of right ventricular mRNA for α-tubulin was measured by real-time reverse transcription polymerase chain reaction. Free and polymerised fractions of β-tubulin protein were assessed using Western blot analysis and immunofluorescence microscopy was used to assess tyrosinated and acetylated (stabilized) microtubules. Right ventricular myocyte contraction was measured in response to the microtubule de-polymeriser colchicine (10 μmol/l for at least 1 h). Compared to CON, in MCT right ventricles there was a small but statistically significant increase in the expression of mRNA for α-tubulin (P < 0.001); total (P < 0.05) and polymerised fraction (P < 0.01) of β-tubulin protein and level of acetylated tubulin (P < 0.01). However colchicine treatment did not increase the contraction of MCT myocytes (P > 0.05) or affect their response to increased stimulation frequency. Our observations support the hypothesis that microtubule proliferation is a common response to pulmonary hypertension in failing right ventricles but suggest that the effect this has on contraction depends upon the specific experimental or clinical conditions that prevail and the subsequent level of microtubule proliferation.
The Alaska blackfish (Dallia pectoralis) is the only air-breathing fish in the Arctic. In the summer, a modified esophagus allows the fish to extract oxygen from the air, but this behavior is not ...possible in the winter because of ice and snow cover. The lack of oxygen (hypoxia) and near freezing temperatures in winter is expected to severely compromise metabolism, and yet remarkably, overwintering Alaska blackfish remain active. To maintain energy balance in the brain and limit the accumulation of reactive oxygen species (ROS), we hypothesized that cold hypoxic conditions would trigger brain mitochondrial remodeling in the Alaska blackfish. To address this hypothesis, fish were acclimated to warm (15 °C) normoxia, cold (5 °C) normoxia or cold hypoxia (5 °C, 2.1–4.2 kPa; no air access) for 5–8 weeks. Mitochondrial respiration, ADP affinity and H202 production were measured at 10 °C in isolated brain homogenates with an Oroboros respirometer. Cold acclimation and chronic hypoxia had no effects on mitochondrial aerobic capacity or ADP affinity. However, cold acclimation in normoxia led to a suppression of brain mitochondrial H202 production, which persisted and became more pronounced in the cold hypoxic fish. Overall, our study suggests cold acclimation supresses ROS production in Alaska blackfish, which may protect the fish from oxidative stress when oxygen becomes limited during winter.
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•Alaska blackfish overwinter under ice-covered lakes in severely hypoxic conditions•We hypothesized survival of these winter conditions would require metabolic readjustments•Cold acclimation and chronic hypoxia suppressed brain reactive oxygen species (ROS) production•Suppression of ROS production may protect the fish from oxidative stress during winter
Nanodomains are intracellular foci which transduce signals between major cellular compartments. One of the most ubiquitous signal transducers, the ryanodine receptor (RyR) calcium channel, is tightly ...clustered within these nanodomains. Super-resolution microscopy has previously been used to visualize RyR clusters near the cell surface. A majority of nanodomains located deeper within cells have remained unresolved due to limited imaging depths and axial resolution of these modalities. A series of enhancements made to expansion microscopy allowed individual RyRs to be resolved within planar nanodomains at the cell periphery and the curved nanodomains located deeper within the interiors of cardiomyocytes. With a resolution of ∼ 15 nm, we localized both the position of RyRs and their individual phosphorylation for the residue Ser2808. With a three-dimensional imaging protocol, we observed disturbances to the RyR arrays in the nanometer scale which accompanied right-heart failure caused by pulmonary hypertension. The disease coincided with a distinct gradient of RyR hyperphosphorylation from the edge of the nanodomain toward the center, not seen in healthy cells. This spatial profile appeared to contrast distinctly from that sustained by the cells during acute, physiological hyperphosphorylation when they were stimulated with a β-adrenergic agonist. Simulations of RyR arrays based on the experimentally determined channel positions and phosphorylation signatures showed how the nanoscale dispersal of the RyRs during pathology diminishes its intrinsic likelihood to ignite a calcium signal. It also revealed that the natural topography of RyR phosphorylation could offset potential heterogeneity in nanodomain excitability which may arise from such RyR reorganization.
Right heart failure is the major cause of death in Pulmonary Artery Hypertension (PAH) patients but is not a current, specific therapeutic target. Pre-clinical studies have shown that adrenoceptor ...blockade can improve cardiac function but the mechanisms of action within right ventricular (RV) myocytes are unknown. We tested whether the β1–adrenoceptor blocker metoprolol could improve RV myocyte function in an animal model of PAH, by attenuating adverse excitation-contraction coupling remodeling. PAH with RV failure was induced in rats by monocrotaline injection. When PAH was established, animals were given 10 mg/kg/day metoprolol (MCT + BB) or vehicle (MCT). The median time to the onset of heart failure signs was delayed from 23 days (MCT), to 31 days (MCT + BB). At 23 ± 1 days post-injection, MCT + BB showed improved in vivo cardiac function, measured by echocardiography. RV hypertrophy was reduced despite persistent elevated afterload. RV myocyte contractility during field stimulation was improved at higher pacing frequencies in MCT + BB. Preserved t-tubule structure, more uniform evoked Ca2+ release, increased SERCA2a expression and faster ventricular repolarization (measured in vivo by telemetry) may account for the improved contractile function. Sarcoplasmic reticulum Ca2+ overload was prevented in MCT + BB myocytes resulting in fewer spontaneous Ca2+ waves, with a lower pro-arrhythmic potential. Our novel finding of attenuation of defects in excitation contraction coupling by β1–adrenoceptor blockade with delays in the onset of HF, identifies the RV as a promising therapeutic target in PAH. Moreover, our data suggest existing therapies for left ventricular failure may also be beneficial in PAH induced RV failure.
•β1–adrenoceptor blocker metoprolol delayed the onset of right heart failure in PAH rats.•Metoprolol attenuated repolarisation remodelling, measured in vivo by telemetry.•Metoprolol attenuated t-tubule remodeling in single right ventricular myocytes.•Metoprolol attenuating adverse Ca2+ handling remodeling in right ventricular myocytes.•β–adrenoceptor blockade may be a useful additional treatment for PAH.
For the study of negative thermal expansion (NTE) compounds, it is critical to effectively control the thermal expansion. In this letter, a chemical approach has been taken to control the thermal ...expansion behavior in ScF
3
which has a strong NTE. Owing to the difference of radius of substituting ions, local distortion inevitably emerges in the lattice matrix, which is verified by pair distribution function analysis of high‐resolution synchrotron X‐ray scattering. It is a valuable clue that the thermal expansion behaviors in the ScF
3
based systems and other trifluorides are correlated closely to structural distortion of metal‐F‐metal linkages. In addition, the introduction of 3
d
transition‐metal enables its semiconductor and ferromagnetic characteristics. This study provides important reference opinion for the control of thermal expansion and introduction of multifunctionalization for those NTE compounds with open framework structure.