A high-precision pressure probe is described which allows non-invasive online-monitoring of the water relations of intact leaves. Real-time recording of the leaf water status occurred by data transfer to an Internet server. The leaf patch clamp pressure probe measures the attenuated pressure, Pp, of a leaf patch in response to a constant clamp pressure, Pclamp. Pp is sensed by a miniaturized silicone pressure sensor integrated into the device. The magnitude of Pp is dictated by the transfer function of the leaf, Tf, which is a function of leaf patch volume and ultimately of cell turgor pressure, Pc, as shown theoretically. The power function Tf=f(Pc) theoretically derived was experimentally confirmed by concomitant Pp and Pc measurements on intact leaflets of the liana Tetrastigma voinierianum under greenhouse conditions. Simultaneous Pp recordings on leaflets up to 10 m height above ground demonstrated that changes in Tf induced by Pc changes due to changes of microclimate and/or of the irrigation regime were sensitively reflected in corresponding changes of Pp. Analysis of the data show that transpirational water loss during the morning hours was associated with a transient rise in turgor pressure gradients within the leaflets. Subsequent recovery of turgescence during the afternoon was much faster than the preceding transpiration-induced water loss if the plants were well irrigated. Our data show the enormous potential of the leaf patch clamp pressure probe for leaf water studies including unravelling of the hydraulic communication between neighbouring leaves and over long distances within tall plants (trees).
Measurement of myocardial perfusion is important for the functional assessment of heart in vivo. Our approach is based on the modification of the longitudinal relaxation time T1 induced by magnetic spin labeling of endogenous water protons. Labeling is performed by selectively inverting the magnetization within the detection slice, and longitudinal relaxation is measured using a fast gradient echo MRI technique. As a result of blood flow, nonexcited spins enter the detection slice, which leads to an acceleration of the relaxation rate. Incorporating this phenomenon in a mathematical model that describes tissue as two compartments yields a simple expression that allows the quantification of perfusion from a slice-selective and a global inversion recovery experiment. This model takes into account the difference between T1 in blood and T1 in tissue. Our purpose was to evaluate the feasibility and reproducibility of this technique to map quantitatively myocardial perfusion in vivo in rats. Quantitative maps of myocardial blood flow were obtained from nine rats, and the reproducibility of the technique was evaluated by repeating the whole perfusion experiment four times. Evaluation of regions of interest within the myocardium yielded a mean perfusion value of 3.6 +/- .5 ml x min(-1) x g(-1) over all animals, which is in good agreement with previously reported literature values.
Background-Identification of key molecular players in myocardial healing could lead to improved therapies, reduction of scar formation, and heart failure after myocardial infarction (MI). We hypothesized that clotting factor XIII (FXIII), a transglutaminase involved in wound healing, may play an important role in MI given prior clinical and mouse model data. Methods and Results-To determine whether a truly causative relationship existed between FXIII activity and myocardial healing, we prospectively studied myocardial repair in FXIII-deficient mice. All FXIII Ϫ/Ϫ and FXIII Ϫ/ϩ (FXIII activity Ͻ5% and 70%) mice died within 5 days after MI from left ventricular rupture. In contradistinction, FXIII Ϫ/Ϫ mice that received 5 days of intravenous FXIII replacement therapy had normal survival rates; however, cardiac MRI demonstrated worse left ventricular remodeling in these reconstituted FXIII Ϫ/Ϫ mice. Using a FXIII-sensitive molecular imaging agent, we found significantly greater FXIII activity in wild-type mice and FXIII Ϫ/Ϫ mice receiving supplemental FXIII than in FXIII Ϫ/Ϫ mice (PϽ0.05). In FXIII Ϫ/Ϫ but not in reconstituted FXIII Ϫ/Ϫ mice, histology revealed diminished neutrophil migration into the MI. Reverse transcriptase-polymerase chain reaction studies suggested that the impaired inflammatory response in FXIII Ϫ/Ϫ mice was independent of intercellular adhesion molecule and lipopolysaccharideinduced CXC chemokine, both important for cell migration. After MI, expression of matrix metalloproteinase-9 was 650% higher and collagen-1 was 53% lower in FXIII Ϫ/Ϫ mice, establishing an imbalance in extracellular matrix turnover and providing a possible mechanism for the observed cardiac rupture in the FXIII Ϫ/Ϫ mice. Conclusions-These data suggest that FXIII has an important role in murine myocardial healing after infarction.
The purpose of this work was to develop high-resolution cardiac magnetic resonance imaging techniques for the in vivo mouse model for quantification of myocardial function and mass. Eight male mice were investigated on a 7-Tesla MRI scanner. High-quality images in multiple short axis slices (in-plane resolution 117 microm2, slice thickness 1 mm) were acquired with an ECG-gated cine sequence. Left ventricular end-diastolic and end-systolic volumes and mass were calculated from segmented slice volumes. There was precise agreement of left ventricular mass determined ex vivo and by MRI. Intraobserver (5%) and interobserver (5%) variability of in vivo MR measurements were low.
The purpose of this study was to assess the distribution of RF-induced E-fields inside a gel-filled phantom of the human head and torso and compare the results with the RF-induced temperature rise at the tip of a straight conductive implant, specifically examining the dependence of the temperature rise on the position of the implant inside the gel. MRI experiments were performed in two different 1.5T MR systems of the same manufacturer. E-field distribution inside the liquid was assessed using a custom measurement system. The temperature rise at the implant tip was measured in various implant positions and orientations using fluoroptic thermometry. The results show that local E-field strength in the direction of the implant is a critical factor in RF-related tissue heating. The actual E-field distribution, which is dependent on phantom/ body properties and the MR-system employed, must be considered when assessing the effects of RF power deposition in implant safety investigations. Magn Reson Med 60:312-319, 2008.
The study results show that quantitative mapping of perfusion and RBV may be performed noninvasively by means of MR imaging in the intact animal. The presented method allows determination of vasodilative and perfusion reserve, which reflects the in vivo regulation of coronary microcirculation for a given stimulus.
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