Surface heat flux estimates from NCAR electra data over the pacific warm pool during TOGA COARE

The warm pool region of the western tropical Pacific is of particular interest to atmospheric dynamics because it represents a significant source of energy to the atmosphere. A better understanding of heat transfer driven by mesoscale and turbulent circulations within this region could lead to improved global circulation models, and therefore to improved prediction of global weather patterns. A first step to this understanding is to evaluate empirical data as well as the methods used to estimate heat transfer, or heat flux, at the surface. Of specific interest here are latent heat flux, the heat transfer associated with evaporation, and sensible heat flux, the heat transfer associated with convection and conduction. In this paper, two different methods of turbulent flux calculation, eddy correlation and the bulk aerodynamic method are compared. Eddy correlation directly uses turbulence measurements to estimate heat flux whereas the bulk aerodynamic method relies on similarity theory to relate heat flux to mean flow quantities. A brief discussion of selection of averaging length based on flight altitude is included, as well as a comparison of errors introduced in averaging velocity as a scalar or as a vector. Errors introduced by averaging, including mesoscale flux enhancement, are evaluated for strong and weak wind cases during relatively light convection in the region. Finally, month to month variability in heat flux is evaluated in an effort to further understand the accuracy of various approximations used in flux calculation

Right and left ventricle native T1 mapping in systolic phase in patients with congenital heart disease

Background T1 mapping is emerging as a powerful tool in cardiac magnetic resonance (CMR) to evaluate diffuse fibrosis. However, right ventricular (RV) T1 mapping proves difficult due to the limited wall thickness in diastolic phase. Several studies focused on systolic T1 mapping, albeit only on the left ventricle (LV). Purpose To estimate intra- and inter-observer variability of native T1 (nT1) mapping of the RV, and its correlations with biventricular and pulmonary function in patients with congenital heart disease (CHD). Material and Methods In this retrospective, observational, cross-sectional study we evaluated 36 patients with CHD, having undergone CMR on a 1.5-T scanner. LV and RV functional evaluations were performed. A native modified look-locker inversion recovery short-axis sequence was acquired in the systolic phase. Intra- and inter-reader reproducibility were reported as complement to 100% of the ratio between coefficient of reproducibility and mean. Spearman rho and Mann-Whitney U-test were used to compare distributions. Results Intra- and inter-reader reproducibility was 84% and 82%, respectively. Median nT1 was 1022 ms (interquartile range [IQR] 1108-972) for the RV and 947 ms (IQR 986-914) for the LV. Median RV-nT1 was 1016 ms (IQR 1090-1016) in patients with EDVI <= 100 mL/m(2) and 1100 ms (IQR 1113-1100) in patients with EDVI >100 mL/m(2) (P = 0.049). A significant negative correlation was found between RV ejection fraction and RV-nT1 (rho = -0.284, P = 0.046). Conclusion Systolic RV-nT1 showed a high reproducibility and a negative correlation with RV ejection fraction, potentially reflecting an adaptation of the RV myocardium to pulmonary valve/conduit (dys)-function

Variability and homogeneity of cardiovascular magnetic resonance myocardial T2-mapping in volunteers compared to patients with edema

BACKGROUND: The aim of the study was to test the reproducibility and variability of myocardial T2 mapping in relation to sequence type and spatial orientation in a large group of healthy volunteers. For control T2 mapping was also applied in patients with true edema. Cardiovascular magnetic resonance (CMR) T2-mapping has potential for the detection and quantification of myocardial edema. Clinical experience is limited so far. The variability and potential pitfalls in broad application are unknown. METHODS: Healthy volunteers (n = 73, 35 +/- 13 years) and patients with edema (n = 28, 55 +/- 17 years) underwent CMR at 1.5 T. Steady state free precession (SSFP) cine loops and T2-weighted spin echo images were obtained. In patients, additionally late gadolinium enhancement images were acquired. We obtained T2 maps in midventricular short axis (SAX) and four-chamber view (4CV) based on images with T2 preparation times of 0, 24, 55 ms and compared fast low angle shot (FLASH) and SSFP readout. 10 volunteers were scanned twice on separate days. Two observers analysed segmental and global T2 per slice. RESULTS: In volunteers global myocardial T2 systematically differed depending on image orientation and sequence (FLASH 52 +/- 5 vs. SSFP 55 +/- 5 ms in SAX and 57 +/- 6 vs. 59 +/- 6 ms in 4CV; p /= 70 ms. Mean intraobserver variability was 1.07 +/- 1.03 ms (r = 0.94); interobserver variability was 1.6 +/- 1.5 ms (r = 0.87). The coefficient of variation for repeated scans was 7.6% for SAX and 6.6% for 4CV. Mapping revealed focally increased T2 (73 +/- 9 vs. 51 +/- 3 ms in remote myocardium; p < 0.0001) in all patients with edema. CONCLUSIONS: Myocardial T2 mapping is technically feasible and highly reproducible. It can detect focal edema und differentiate it from normal myocardium. Increased T2 was found in some volunteers most likely due to partial volume and residual motion

Сложность алгоритмов криптографической системы Эль–Гамаля и ихэффективность

Objective. - Electrical remodeling as well as atrial contractile dysfunction after the conversion of atrial fibrillation (AF) to sinus rhythm (SR) are mainly caused by a reduction of the inward L-type Ca2+ current (ICaL). We investigated whether the expression of L-type Ca2+-channel subunits was reduced in atrial myocardium of AF patients. Methods. - Right atrial appendages were obtained from patients undergoing coronary artery bypass graft surgery (CAD, n = 35) or mitral valve surgery (MVD, n = 37). Seventeen of the CAD patients and 18 of the MVD patients were in chronic (>3 months) AF, whereas the others were in SR. The protein expression of the L-type Ca2+-channel subunits {alpha}1C and {beta}2 was quantified by western blot analysis. Furthermore, we measured the density of dihydropyridine (DHP)-binding sites of the L-type Ca2+ channel using 3H-PN220-100 as radioligand. Results. - Surprisingly, the {alpha}1C and the {beta}2-subunit expression was not altered in atrial myocardium of AF patients. Also, the DHP-binding site density was unchanged. Conclusion. - The protein expression of the L-type Ca2+-channel subunits {alpha}1C or {beta}2 is not reduced in atrial myocardium of AF patients. Therefore, the reduced ICaL might be due to downregulation of other accessory subunits ({alpha}2{delta}), expression of aberrant subunits, changes in channel trafficking or alterations in channel function

Myocardial T(1) and T(2) mapping at 3 T: reference values, influencing factors and implications

BACKGROUND: Myocardial T1 and T2 mapping using cardiovascular magnetic resonance (CMR) are promising to improve tissue characterization and early disease detection. This study aimed at analyzing the feasibility of T1 and T2 mapping at 3 T and providing reference values. METHODS: Sixty healthy volunteers (30 males/females, each 20 from 20--39 years, 40--59 years, 60--80 years) underwent left-ventricular T1 and T2 mapping in 3 short-axis slices at 3 T. For T2 mapping, 3 single-shot steady-state free precession (SSFP) images with different T2 preparation times were acquired. For T1 mapping, modified Look-Locker inversion recovery technique with 11 single shot SSFP images was used before and after injection of gadolinium contrast. T1 and T2 relaxation times were quantified for each slice and each myocardial segment. RESULTS: Mean T2 and T1 (pre-/post-contrast) times were: 44.1 ms/1157.1 ms/427.3 ms (base), 45.1 ms/1158.7 ms/411.2 ms (middle), 46.9 ms/1180.6 ms/399.7 ms (apex). T2 and pre-contrast T1 increased from base to apex, post-contrast T1 decreased. Relevant inter-subject variability was apparent (scatter factor 1.08/1.05/1.11 for T2/pre-contrast T1/post-contrast T1). T2 and post-contrast T1 were influenced by heart rate (p < 0.0001, p = 0.0020), pre-contrast T1 by age (p < 0.0001). Inter- and intra-observer agreement of T2 (r = 0.95; r = 0.95) and T1 (r = 0.91; r = 0.93) were high. T2 maps: 97.7% of all segments were diagnostic and 2.3% were excluded (susceptibility artifact). T1 maps (pre-/post-contrast): 91.6%/93.9% were diagnostic, 8.4%/6.1% were excluded (predominantly susceptibility artifact 7.7%/3.2%). CONCLUSIONS: Myocardial T2 and T1 reference values for the specific CMR setting are provided. The diagnostic impact of the high inter-subject variability of T2 and T1 relaxation times requires further investigation

Current T(1) and T(2) mapping techniques applied with simple thresholds cannot discriminate acute from chronic myocadial infarction on an individual patient basis: a pilot study

BACKGROUND: Studying T1- and T2-mapping for discrimination of acute from chronic myocardial infarction (AMI, CMI). METHODS: Eight patients with AMI underwent CMR at 3 T acutely and after >3 months. Imaging techniques included: T2-weighted imaging, late enhancement (LGE), T2-mapping, native and post-contrast T1-mapping. Myocardial T2- and T1-relaxation times were determined for every voxel. Abnormal voxels as defined by having T2- and T1-values beyond a predefined threshold (T2 > 50 ms, native T1 > 1250 ms and post-contrast T1 delete acute infarction; unfortunately this is not possible in your web interface) acute infarction only in half of the subjects. Abnormal T2-values were also present in subjects with CMI, thereby matching the chronically infarcted territory in some. Abnormal native T1 times were present in voxels with AMI in 5/8 subjects, but also remote from the infarcted territory in four. In CMI, abnormal native T1 values corresponded with infarcted voxels, but were also abnormal remote from the infarcted territory. Voxels with abnormal post-contrast T1-relaxation times agreed well with LGE in AMI and CMI. CONCLUSIONS: In this pilot-study, T2- and T1-mapping with simple thresholds did not facilitate the discrimination of AMI and CMI

Multiple Potential Molecular Contributors to Atrial Hypocontractility Caused by Atrial Tachycardia Remodeling in Dogs

Background-Atrial fibrillation impairs atrial contractility, inducing atrial stunning that promotes thromboembolic stroke. Action potential (AP)-prolonging drugs are reported to normalize atrial hypocontractility caused by atrial tachycardia remodeling (ATR). Here, we addressed the role of AP duration (APD) changes in ATR-induced hypocontractility. Methods and Results-ATR (7-day tachypacing) decreased APD (perforated patch recording) by approximate to 50%, atrial contractility (echocardiography, cardiomyocyte video edge detection), and [Ca2+](i) transients. ATR AP waveforms suppressed [Ca2+](i) transients and cell shortening of control cardiomyocytes; whereas control AP waveforms improved [Ca2+](i) transients and cell shortening in ATR cells. However, ATR cardiomyocytes clamped with the same control AP waveform had approximate to 60% smaller [Ca2+](i) transients and cell shortening than control cells. We therefore sought additional mechanisms of contractile impairment. Whole-cell voltage clamp revealed reduced I-CaL; I-CaL inhibition superimposed on ATR APs further suppressed [Ca2+](i) transients in control cells. Confocal microscopy indicated ATR-impaired propagation of the Ca2+ release signal to the cell center in association with loss of t-tubular structures. Myofilament function studies in skinned permeabilized cardiomyocytes showed altered Ca2+ sensitivity and force redevelopment in ATR, possibly due to hypophosphorylation of myosin-binding protein C and myosin light-chain protein 2a (immunoblot). Hypophosphorylation was related to multiple phosphorylation system abnormalities where protein kinase A regulatory subunits were downregulated, whereas autophosphorylation and expression of Ca2+-calmodulin-dependent protein kinase II delta and protein phosphatase 1 activity were enhanced. Recovery of [Ca2+](i) transients and cell shortening occurred in parallel after ATR cessation. Conclusions-Shortening of APD contributes to hypocontractility induced by 1-week ATR but accounts for it only partially. Additional contractility-suppressing mechanisms include I-CaL current reduction, impaired subcellular Ca2+ signal transmission, and altered myofilament function associated with abnormal myosin and myosin-associated protein phosphorylation. The complex mechanistic basis of the atrial hypocontractility associated with AF argues for upstream therapeutic targeting rather than interventions directed toward specific downstream pathophysiological derangements. (Circ Arrhythm Electrophysiol. 2010;3:530-541.

In situ Forming Hyperbranched PEG—Thiolated Hyaluronic Acid Hydrogels With Honey-Mimetic Antibacterial Properties

The rapidly increasing resistance of bacteria to currently approved antibiotic drugs makes surgical interventions and the treatment of bacterial infections increasingly difficult. In recent years, complementary strategies to classical antibiotic therapy have, therefore, gained importance. One of these strategies is the use of medicinal honey in the treatment of bacterially colonized wounds. One of the several bactericidal effects of honey is based on the in situ generation of hydrogen peroxide through the activity of the enzyme glucose oxidase. The strategy underlying this work is to mimic this antibacterial redox effect of honey in an injectable, biocompatible, and rapidly forming hydrogel. The hydrogel was obtained by thiol–ene click reaction between hyperbranched polyethylene glycol diacrylate (HB PEGDA), synthesized using reversible addition-fragmentation chain transfer (RAFT) polymerization, and thiolated hyaluronic acid (HA-SH). After mixing 500 µL HB PEGDA (10%, w/w) and 500 µL HA-SH (1%, w/w) solutions, hydrogels formed in ∼60 s (HB PEGDA/HA-SH 10.0–1.0), as assessed by the tube inverting test. The HB PEGDA/HA-SH 10.0–1.0 hydrogel (200 µL) was resistant to in vitro dissolution in water for at least 64 days, absorbing up to 130 wt% of water. Varying glucose oxidase (GO) amounts (0–500 U/L) and constant glucose content (2.5 wt%) were loaded into HB PEGDA and HA-SH solutions, respectively, before hydrogel formation. Then, the release of H2O2 was evaluated through a colorimetric pertitanic acid assay. The GO content of 250 U/L was selected, allowing the formation of 10.8 ± 1.4 mmol H2O2/L hydrogel in 24 h, under static conditions. The cytocompatibility of HB PEGDA/HA-SH 10.0–1.0 hydrogels loaded with different GO activities (≤ 500 U/L) at a constant glucose amount (2.5 wt%) was investigated by in vitro assays at 24 h with L929 and HaCaT cell lines, according to DIN EN ISO 10993-5. The tests showed cytocompatibility for GO enzyme activity up to 250 U/L for both cell lines. The antibacterial activity of HB PEGDA/HA-SH 10.0–1.0 hydrogels loaded with increasing amounts of GO was demonstrated against various gram-positive bacteria (S. aureus and S. epidermidis), antibiotic-resistant gram-positive bacteria (MRSA and MRSE), gram-negative bacteria (P. aeruginosa, E. coli, and A. baumanii), and antibiotic-resistant gram-negative strains (P. aeruginosa and E. coli) using agar diffusion tests. For all gram-positive bacterial strains, increasing efficacy was measured with increasing GO activity. For the two P. aeruginosa strains, efficacy was shown only from an enzyme activity of 125 U/L and for E. coli and A. baumanii, efficacy was shown only from 250 U/L enzyme activity. HB PEGDA/HA-SH 10.0–1.0 hydrogels loaded with ≤250 U/L GO and 2.5 wt% glucose are promising formulations due to their fast-forming properties, cytocompatibility, and ability to produce antibacterial H2O2, warranting future investigations for bacterial infection treatment, such as wound care