Early mapping of industrial tomato in Central and Southern Italy with Sentinel 2, aerial and RapidEye additional data

Timely crop information, i.e. well before harvesting time and at first stages of crop development, can benefit farmers and producer organizations. The current case study documents the procedure to deliver early data on planted tomato to users, showing the potential of Sentinel 2 to map tomato at the very beginning of the crop season, which is a challenging task. Using satellite data, integrated with ground and aerial data, an initial estimate of area planted with tomato and early tomato maps were generated in seven main production areas in Italy. Estimates of the amount of area planted with tomato provided similar results either when derived from field surveys or from remote sensing-based classification. Tomato early maps showed a producer accuracy > 80% in seven cases out of nine, and a user accuracy > 80% in five cases out of nine, with differences attributed to the varying agricultural characteristics and environmental heterogeneity of the study areas. The additional use of aerial data improved producer accuracy moderately. The ability to identify abrupt growth changes, such as those caused by natural hazards, was also analysed: Sentinel 2 detected significant changes in tomato growth between a hailstorm-affected area and a control area. The study suggests that Sentinel 2, with enhanced spectral capabilities and open data policy, represents very valuable data, allowing crop monitoring at an early development stage

Role of cardiac troponin I phosphorylation in cardiac function: From molecule to mouse

Abstract only availableThe regulation of cardiac muscle contraction involves the interplay between a variety of molecules on the thick and thin filaments. One important regulatory molecule is troponin, which consists of three subunits, troponin C (TnC) that binds calcium, troponin T (TnT) that binds tropomyosin, and troponin I (TnI) that binds actin and tends to inhibit contraction. Following muscle excitation, cytoplasmic calcium rises and binds TnC, which causes a conformational change in TnI that reduces its affinity for actin; this, in turn, allows TnT and tropomyosin to shift positions revealing myosin binding sites on actin, leading to muscle contraction. Interestingly, cardiac troponin I (cTnI) has several phosphorylation sites, which are known to modulate this regulatory process. For example, phosphorylation of serines 23 and 24 on cTnI by protein kinase A (PKA) is known to decrease the calcium binding affinity of cardiac TnC and, thus, thought to speed muscle relaxation. On the other hand, phosphorylation of cTnI on serines 43 and 45 and threonine 144 by protein kinase C (PKC) decreases both force production and calcium sensitivity of force and is thought to contribute to depressed ventricular function in failing hearts. In this study we investigated the effects of chronic cTnI phosphorylation on cardiac function from transgenic animals in which either PKA phosphorylation sites (Ser-23/Ser-24) (PP) or both the PKA and PKC phosphorylation sites (Ser-23/Ser-24/Ser-43/Ser-45/T-144) (All-P) were replaced with aspartic acid to mimic phosphorylation. Left ventricular cardiac myocytes from PP transgenic mice exhibited less calcium sensitivity of force while myocytes from All-P transgenic mice exhibited decreased maximal force, decreased calcium sensitivity of force, and decreased power output, implicating a dominate role of PKC phosphorylation sites on myofilament function. Consistent with these single myocyte studies, left ventricular power output also was depressed in All-P mice compared to both WT and PP transgenic ventricles. We next tested the hypothesis that PP transgenic mice would engage in greater voluntary running compared to WT and All-P transgenic animals. In contrast to this idea, WT and All-P mice ran ~3- and ~4-fold more than the PP transgenic mouse, respectively. Overall, these results indicate that PKC phosphorylation of cTnI plays a dominant role in depressing contractility and may contribute to the maladaptive behavior.NIH grant to K.S. McDonal

Regulation of Myofilament Contractile Function in Human Donor and Failing Hearts

Heart failure (HF) often includes changes in myocardial contractile function. This study addressed the myofibrillar basis for contractile dysfunction in failing human myocardium. Regulation of contractile properties was measured in cardiac myocyte preparations isolated from frozen, left ventricular mid-wall biopsies of donor (n = 7) and failing human hearts (n = 8). Permeabilized cardiac myocyte preparations were attached between a force transducer and a position motor, and both the Ca2+ dependence and sarcomere length (SL) dependence of force, rate of force, loaded shortening, and power output were measured at 15 ± 1°C. The myocyte preparation size was similar between groups (donor: length 148 ± 10 μm, width 21 ± 2 μm, n = 13; HF: length 131 ± 9 μm, width 23 ± 1 μm, n = 16). The maximal Ca2+-activated isometric force was also similar between groups (donor: 47 ± 4 kN⋅m–2; HF: 44 ± 5 kN⋅m–2), which implicates that previously reported force declines in multi-cellular preparations reflect, at least in part, tissue remodeling. Maximal force development rates were also similar between groups (donor: ktr = 0.60 ± 0.05 s–1; HF: ktr = 0.55 ± 0.04 s–1), and both groups exhibited similar Ca2+ activation dependence of ktr values. Human cardiac myocyte preparations exhibited a Ca2+ activation dependence of loaded shortening and power output. The peak power output normalized to isometric force (PNPO) decreased by ∼12% from maximal Ca2+ to half-maximal Ca2+ activations in both groups. Interestingly, the SL dependence of PNPO was diminished in failing myocyte preparations. During sub-maximal Ca2+ activation, a reduction in SL from ∼2.25 to ∼1.95 μm caused a ∼26% decline in PNPO in donor myocytes but only an ∼11% change in failing myocytes. These results suggest that altered length-dependent regulation of myofilament function impairs ventricular performance in failing human hearts

Seismic imaging and petrology explain highly explosive eruptions of Merapi Volcano, Indonesia

Our seismic tomographic images characterize, for the first time, spatial and volumetric details of the subvertical magma plumbing system of Merapi Volcano. We present P-and S-wave arrival time data, which were collected in a dense seismic network, known as DOMERAPI, installed around the volcano for 18 months. The P-and S-wave arrival time data with similar path coverage reveal a high Vp/Vs structure extending from a depth of >= 20 km below mean sea level (MSL) up to the summit of the volcano. Combined with results of petrological studies, our seismic tomography data allow us to propose: (1) the existence of a shallow zone of intense fluid percolation, directly below the summit of the volcano; (2) a main, pre-eruptive magma reservoir at >= 10 to 20 km below MSL that is orders of magnitude larger than erupted magma volumes; (3) a deep magma reservoir at MOHO depth which supplies the main reservoir; and (4) an extensive, subvertical fluid-magma-transfer zone from the mantle to the surface. Such high-resolution spatial constraints on the volcano plumbing system as shown are an important advance in our ability to forecast and to mitigate the hazard potential of Merapi's future eruptions.We gratefully acknowledge the French Agence Nationale pour la Recherche for funding the DOMERAPI ANR project (ANR- 12-BS06-0012) and BMKG for providing data used in this stud