Bulges In Regions Research Articles

How Does Regional Hypertrophy Affect Strain Measurements With Different Speckle-Tracking Methods?

In this study, we evaluate the impact of abnormal myocardial shapes, such as regional hypertrophy, on longitudinal strain measurements with different tracking approaches. We selected 40 patients with normal ejection fraction and prominent septal bulge. We assessed longitudinal strain with full wall (FW) tracking, (GE EchoPAC) as well as endo-, mid-, and epicardial (EME) tracking (Tomtec ImageArena), on the same image acquired with a GE machine (using raw data and full frame rate DICOM data, respectively). We used a region of interest (ROI) which follows precisely the endo- and epicardial contours (true contour ROI) and one where the bulging region was excluded (straight ROI). In segments with bulge, absolute segmental longitudinal strain values were in all myocardial layers significantly higher with a straight ROI compared to a true contour ROI, both with FW tracking and EME tracking. The highest difference was found in the endocardial layer (3.4 ± 2.5% and 7.7 ± 7.1%, respectively, both P < 0.001). In the bulged segments, the effect of ROI shape was more pronounced in EME tracking software compared to FW tracking software. Bulged segments also influenced global longitudinal strain measurements, mostly in the endocardial layer (P < 0.001). Global longitudinal strain values obtained with the straight ROI correlated better with longitudinal fractional shortening of the LV. Regional bulging has a significant effect on both global and segmental strain measurements. Endocardial strain values obtained with EME tracking and a true contour ROI were most sensitive to bulging. Midwall strain values derived from FW tracking using a straight ROI were most robust.

Chirality provides a direct fitness advantage and facilitates intermixing in cellular aggregates.

Chirality in shape and motility can evolve rapidly in microbes and cancer cells. To determine how chirality affects cell fitness, we developed a model of chiral growth in compact aggregates such as microbial colonies and solid tumors. Our model recapitulates previous experimental findings and shows that mutant cells can invade by increasing their chirality or switching their handedness. The invasion results either in a takeover or stable coexistence between the mutant and the ancestor depending on their relative chirality. For large chiralities, the coexistence is accompanied by strong intermixing between the cells, while spatial segregation occurs otherwise. We show that the competition within the aggregate is mediated by bulges in regions where the cells with different chiralities meet. The two-way coupling between aggregate shape and natural selection is described by the chiral Kardar-Parisi-Zhang equation coupled to the Burgers’ equation with multiplicative noise. We solve for the key features of this theory to explain the origin of selection on chirality. Overall, our work suggests that chirality could be an important ecological trait that mediates competition, invasion, and spatial structure in cellular populations.

Reddening and metallicity maps of the Milky Way bulge from VVV and 2MASS

We investigate the large scale metallicity distribution in the Galactic bulge, using a large spatial coverage, in order to constrain the bulge formation scenario. We use the VISTA variables in the Via Lactea (VVV) survey data and 2MASS photometry, covering 320 sqdeg of the Galactic bulge, to derive photometric metallicities by interpolating of the (J-Ks)0 colors of individual Red Giant Branch stars based on a set of globular cluster ridge lines. We then use this information to construct the first global metallicity map of the bulge with a resolution of 30'x45'. The metallicity map of the bulge revealed a clear vertical metallicity gradient of ~0.04 dex/deg (~0.28 dex/kpc), with metal-rich stars ([Fe/H]~0) dominating the inner bulge in regions closer to the galactic plane (|b|<5). At larger scale heights, the mean metallicity of the bulge population becomes significantly more metal-poor. This fits in the scenario of a boxy-bulge originated from the vertical inestability of the Galactic bar, formed early via secular evolution of a two component stellar disk. Older, metal-poor stars dominate at higher scale heights due to the non-mixed orbits from the originally hotter thick disk stars.

The inner Galactic bar traced by the VVV survey

We use the VVV survey observations in bulge regions close to the Galactic plane to trace the bar inclination at the Galactic latitude b\sim\pm1{\deg} and to investigate a distinct structure in the inner regions of the bar that was previously detected at positive latitude (b=+1{\deg}). We use the (J-Ks) colors of the red clump stars to obtain reddening values on 6 x 6 arcmin scale, minimizing the problems arising from differential extinction. Dereddened magnitudes are then used to build the luminosity function of the bulge in regions of ~0.4 sq deg to obtain the mean red clump magnitudes. These are used as distance indicators to trace the bar structure. The luminosity function clearly shows the red clump mean magnitude variation with longitude, as expected from a large scale bar oriented towards us at positive Galactic longitude, with a dereddened magnitude varying from Ks_0=13.4 at l=-10{\deg} to Ks_0=12.4 at l=+10{\deg}. We detect a change in the orientation of the bar in the central regions with |l|<4{\deg} at b=\pm1{\deg}, in agreement with results obtained at positive latitudes by other authors. Our results are based on a different dataset and at different latitude, which shows that this change in the bar orientation is real. This suggests that there is an inner structure distinct to the large-scale Galactic bar, with a different orientation angle. This inner structure could be a secondary, inner bar, with a semi-major axis of ~500 pc that is symmetric with respect to the Galactic plane.

Cardiac MRI assessed left ventricular hypertrophy in differentiating hypertensive heart disease from hypertrophic cardiomyopathy attributable to a sarcomeric gene mutation

To evaluate the value of cardiac magnetic resonance imaging (CMRI)-assessed left ventricular hypertrophy (LVH) in differentiating between hypertensive heart disease and hypertrophic cardiomyopathy (HCM). 95 unselected subjects with mild-to-moderate hypertension, 24 patients with HCM attributable to the D175N mutation of the α-tropomyosin gene and 17 control subjects were studied by cine CMRI. Left ventricular (LV) quantitative and qualitative characteristics were evaluated. LV maximal end-diastolic wall thickness, wall thickness-to-LV volume ratio, end-diastolic septum thickness and septum-to-lateral wall thickness ratio were useful measures for differentiating between LVH due to hypertension and HCM. The most accurate measure for identifying patients with HCM was the LV maximal wall thickness ≥ 17 mm, with a sensitivity, specificity, negative predictive value, positive predictive value, and accuracy of 90%, 93%, 86%, 95% and 91%, respectively. LV maximal wall thickness in the anterior wall, or regional bulging in left ventricular wall was found only in patients with HCM. LV mass index was not discriminant between patients with HCM and those with LVH due to hypertension. LV maximal thickness measured by CMRI is the best anatomical parameter in differentiating between LVH due to mild-to-moderate hypertension and HCM attributable to a sarcomeric mutation. CMRI assessment of location and quality of LVH is also of value in differential diagnosis.

Bulging of the Inner and Outer Annulus During In Vivo Axial Loading of Normal and Degenerated Discs

Comparison of in vivo biomechanical outcomes between experimental and control group animals. To quantify the in vivo bulging response of the inner and outer annulus in animals with and without disc degeneration. Prior attempts to quantify the load-deformation response of the inner annulus have most often relied on in vitro preparations. Unfortunately, to visualize the inner annulus, these in vitro approaches rely on disc modifications that may result in nonphysiologic behaviors. In response to this problem, in vivo techniques were developed to quantify regional bulging of the inner and outer annulus during applied axial loading. Two groups of pigs were tested: a normal group and a group having disc degeneration that was induced surgically 3 months earlier. Eight adolescent pigs were evaluated and for each animal, a miniature servohydraulic actuator was attached to the third and fourth lumbar vertebrae to deliver a cyclic axial loading protocol (300 N, 1 Hz, 10 cycles) whereas regional deformations of the annulus were visualized ultrasonically via retroperitoneal access. For the normal animals, image analysis demonstrated a significantly greater bulging of the inner annular region when compared with the outer annular region. In animals with disc degeneration, the inner and outer annular regions were equal in their bulging response, which ranged from 0 bulging to 37% greater than the average response of the normal animals. This work supports prior in vitro studies that observed maximal disc bulging in the inner annulus and minimal bulging in the external annulus. Results for this in vivo study suggest that this normal bulging gradient is lost with degenerative disc disease. Compared with in vitro approaches, this new in vivo technique has the potential to demonstrate disc behavior in a variety of loading conditions and/or with a variety of induced disc pathologies.

Uplift and active tectonics of southern Albania inferred from incision of alluvial terraces

In Albania, the Osum and Vjoje rivers cross the active graben system and the active frontal thrust system of the Albanides. The effects of climatic and geodynamic forcing on the development of these two rivers were investigated by the means of field mapping, topographic surveying and absolute exposure-age dating. We established the chronology of terraces abandonment from the compilation of new dating ( 14C and in situ produced 10Be) and previously published data. We identified nine fluvial terraces units developed since Marine Isotope Stage 6 up to historic times. From this reconstituted history, we quantified the vertical uplift on a time scale shorter than the glacial climatic cycle. Regional bulging produces an overall increase of the incision rate from the west to the east that reaches a maximum value of 2.8 m/ka in the hinterland. Local pulses of incision are generated by activation of normal faults. The most active faults have a SW–NE trend and a vertical slip rate ranging from 1.8 to 2.2 m/ka. This study outlines the geodynamic control in the development of rivers flowing through the Albanides on the scale of 10 3–10 5ka.

ANESTHETIC PRECONDITIONING CONFERS ACUTE CARDIOPROTECTION VIA UP-REGULATION OF MANGANESE SUPEROXIDE DISMUTASE AND PRESERVATION OF MITOCHONDRIAL RESPIRATORY ENZYME ACTIVITY

The cellular and molecular mechanisms that underlie cardioprotection against I/R by anesthetic-induced preconditioning (APC) require further elucidation. Using isoflurane as a representative anesthetic, we evaluated the hypothesis that APC induces myocardial protection against I/R by attenuation of excessive reactive oxygen species and restoration of mitochondrial bioenergetics through postischemic up-regulation of manganese superoxide dismutase (MnSOD) expression and preservation of respiratory enzyme activity. Pentobarbital anesthetized open-chest Sprague-Dawley rats were subject to 30-min left coronary artery occlusion, followed by 120-min reperfusion. Before ischemia, rats were randomly assigned to receive 0.9% saline, two cycles of brief coronary artery occlusion and reperfusion, or a 30-min exposure to 1.0 minimum alveolar concentration isoflurane in the absence or presence of a specific mitochondrial adenosine triphosphate-sensitive potassium (KATP) channel blocker, 5-hydroxydecanoate; a membrane-permeable superoxide scavenger, 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl; or a NOS inhibitor, N(G)-nitro-L-arginine methyl ester. Isoflurane exposure induced an initial increase in myocardial superoxide (O2-), but not NO level. It also significantly decreased infarct size and restored mitochondrial respiratory enzyme activity or ATP production in I/R rat hearts, along with suppression of the O2- surge at reperfusion and increase in MnSOD expression or enzyme activity. These protective effects were abrogated by 5-hydroxydecanoate or 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl, but not by N(G)-nitro-L-arginine methyl ester pretreatment. These results suggest that opening of mitochondrial KATP channel, followed by O2- signaling, induces postischemic augmentation of MnSOD and preservation of mitochondrial respiratory enzyme activities, leading to attenuated cardiac O2- surge and restored ATP production during reperfusion, and underlie APC-induced cardioprotection.

On the angular momentum transfer on to compact stars in binary systems

Results of three-dimensional numerical simulations of the gas transfer in close binary systems show that, in addition to the formation of a tidally induced spiral shock wave, it is also possible for accretion streams to be produced, having low specific angular momentum in a region close to the accreting star. These streams are mainly placed above the orbital disc but are also unevenly present in the equatorial plane. The relevance of such flows is related to formation of hot coronae or bulges in regions very close to the accretor centre. The eventual formation of such bulges and shock-heated flows is interesting in the context of advection-dominated solutions and for the explanation of spectral properties of the black hole candidates in binary systems.

Combined captopril and isosorbide dinitrate during healing after myocardial infarction: Effect on ventricular remodeling, function, mass and collagen

We sought to compare the effects of captopril plus isosorbide dinitrate versus monotherapy on infarct collagen content and left ventricular remodeling and function during healing after myocardial infarction. Captopril or isosorbide dinitrate monotherapy can limit postinfarction dilation. Whether captopril inhibits infarct collagen content, or whether captopril plus isosorbide dinitrate might be more beneficial, is not known. In vivo remodeling variables and function (echocardiography), hemodynamic variables, postmortem topography (planimetry) and collagen content (hydroxyproline) were measured in 48 chronically instrumented dogs that were randomized 2 days after left anterior descending coronary artery ligation to 6 weeks of therapy with captopril, isosorbide dinitrate, captopril plus isosorbide dinitrate or placebo. Compared with placebo, the three active therapies decreased blood pressure and left atrial pressure; limited infarct expansion, infarct thinning, noninfarct wall stretching and thickening; limited left ventricular dilation and increase in left ventricular mass; and decreased regional bulging, aneurysm frequency and left ventricular dysfunction. However, the decrease in asynergy and increase in volume ejection fraction were less with captopril or captopril plus isosorbide dinitrate than with isosorbide dinitrate. Infarct thinning and bulging at 6 weeks was also less with isosorbide dinitrate than with captopril. Although initial left ventricular asynergy, final scar sizes and noninfarct collagen content at 6 weeks were similar among the groups, collagen in the center of the infarct scar was less with captopril or captopril plus isosorbide dinitrate than with placebo or isosorbide dinitrate. Monotherapy with captopril or isosorbide dinitrate, or their combination, improved all remodeling variables, but isosorbide dinitrate improved function more than captopril or captopril plus isosorbide dinitrate. Inhibition of infarct collagen content by captopril suggests that benefits with captopril represent a balance between positive and negative effects, and its combination with isosorbide dinitrate might be advantageous.

Effect of enalapril on ventricular remodeling and function during healing after anterior myocardial infarction in the dog.

Ventricular remodeling after myocardial infarction involves changes in ventricular size, shape, structure, and matrix that impact on function. Prolonged angiotensin-converting enzyme inhibition after infarction with captopril reduces ventricular enlargement and improves clinical outcome, but whether enalapril produces similar benefits is controversial. The effect of enalapril during healing between 1 day and 6 weeks after myocardial infarction on in vivo changes in ventricular size, shape, mass, and function (asynergy, or akinesis and dyskinesis, and ejection fraction), as determined by serial two-dimensional echocardiography, hemodynamics, postmortem topography (planimetered short- and long-axis ventricular contours), and collagen content (determined by levels of hydroxyproline, a marker for collagen), was measured in 25 instrumented dogs. The dogs were randomized 1 day after left anterior descending coronary artery ligation to a control group (no treatment) and a group receiving oral enalapril (2.5 mg BID). Compared with no treatment, enalapril produced a sustained lowering of left atrial pressure but no difference in heart rate and mean blood pressure over the 6 weeks. Also compared with no treatment, enalapril modified in vivo remodeling parameters between 1 day and 6 weeks, with less elongation of the asynergy-containing segment, a lower expansion index (ratio of endocardial lengths of infarct to non-infarct-containing segments demarcated by papillary muscle landmarks), less scar wall thinning, a lower thinning ratio (ratio of average thickness of infarcted wall to average thickness of the normal wall), smaller ventricular volume, less regional bulging and aneurysm frequency, prevention of the increase in ventricular mass, less total extent of asynergy, and higher volume ejection fraction. At postmortem examination, scar mass was similar in the two groups, but topographic maps with enalapril revealed less infarct bulging, flatter infarct scars, and less noninfarct wall thickness. In addition, postmortem collagen content was similar in noninfarct zones of the two groups but lower in infarct zones of the dogs given enalapril. Prolonged enalapril therapy, in a dose that did not lower blood pressure, during healing after anterior infarction produced prolonged reduction of left ventricular preload in dogs. This diastolic unloading was associated with limitation of remodeling parameters (infarct expansion and thinning, progressive ventricular dilation and hypertrophy, and regional bulging), less total asynergy, and improved left ventricular ejection fraction. Although angiotensin-converting enzyme inhibition was associated with lower collagen content in the infarct area and altered scar topography, these effects did not impact negatively on overall remodeling and function.

Impact of increased infarct transmurality on remodeling and function during healing after anterior myocardial infarction in the dog.

To determine the impact of greater infarct transmurality on changes in left ventricular remodeling and function after acute anterior myocardial infarction, serial topographic and functional parameters (two-dimensional echocardiograms) and hemodynamics over 6 weeks, and postmortem topography (planimetry) at 6 weeks, were measured in chronically instrumented dogs randomized to standard coronary artery ligation (group 1) or a modified lower ligation plus collateral obliteration to decrease collateral inflow and increase transmurality (group 2). At 6 weeks, postmortem scar size and collagen were similar in the two groups, but group 2 had greater transmurality associated with more necrosis relative to area at risk, Q waves, infarct expansion, thinning, regional bulging, and cavity dilatation. Over the 6 weeks, group 2 showed more early expansion, late thinning and regional bulging in the short axis, larger diastolic and systolic volumes, and more apical aneurysmal bulging in the long-axis, reflecting more topographic deterioration. More important, group 2 showed greater regional and global left ventricular dysfunction over 6 weeks, lower ejection fraction at 2 days with further decrease over 6 weeks, and more left ventricular thrombus, ventricular arrhythmias, and deaths. In addition, transmurality correlated with the severity of remodeling and dysfunction. The findings indicate that transmurality is a major determinant of remodeling and left ventricular dysfunction during healing after anterior infarction.

Effect of postextrasystolic potentiation on systolic bulging of ischemic myocardium

Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined.By 5 min after the left anterior descending coronary artery was occluded, there was regional bulging. Postextrasystolic potentiation diminished the extent of bulging by increasing both isovolumic and ejection percent systolic shortening (isovolumic −9.1 ± 2.0% to −5.9 ± 1.7%, p < 0.008; ejection 2.2 ± 0.7% to 4.3 ± 2.0%, p < 0.008). The tension-length loops after coronary occlusion showed an exponential upstroke and almost superimposed downstroke consistent with passive movement. The loops were unchanged by postextrasystolic potentiation. Wall tension data showed that bulging was reduced because of a shift down the tension-length curve as end-systolic wall tension was reduced by augmented nonischemic contraction. Similar results were seen at 60 min of coronary occlusion.This study demonstrates that the decrease in bulging seen with postextrasystolic potentiation is due to changes in loading conditions and not to contractile reserve.

Stellar and gas kinematics in disk galaxies

view Abstract Citations (34) References (45) Co-Reads Similar Papers Volume Content Graphics Metrics Export Citation NASA/ADS Stellar and gas kinematics in disk galaxies. Whitmore, B. C. ; Rubin, V. C. ; Ford, W. K., Jr. Abstract Extended absorption- and emission-line rotation curves and stellar velocity dispersion curves have been obtained for NGC 3898 (Sab), NGC 2841 (Sb), NGC 4062 (Sc), and NGC 2998 (Sc), along with a few observations of NGC 3200 (Sab) and M82 (I). These have been combined with additional observations by Kormendy and Illingworth (1982) to establish the following results. In the disk, the rotation of the gas and stellar components are similar. In the bulge, stellar rotational velocities are only about half of the rotation of the disk. The velocity dispersion curves exhibit a decline with radius, with the small bulge systems showing the steepest decline. A reevaluation of the V(bulge)/sigma(0)-versus-ellipticity diagram for spiral bulges shows that models of rotationally flattened oblate spheroids do not fully explain the observations. As part of this analysis, numerical experiments have been performed to determine values of the intrinsic rotation of the bulge in regions where significant fractions of the light come from both the bulge and the disk. These mixing experiments show that differences in both line strengths and velocity dispersions play major roles in producing the observed velocities. Publication: The Astrophysical Journal Pub Date: December 1984 DOI: 10.1086/162663 Bibcode: 1984ApJ...287...66W Keywords: Angular Velocity; Disk Galaxies; Gas Dynamics; Stellar Motions; Stellar Rotation; Absorption Spectra; Astronomical Catalogs; Galactic Structure; Oblate Spheroids; Spiral Galaxies; Astrophysics full text sources ADS | data products NED (11) SIMBAD (10)

The relationship of transmural myocardial blood flow to midwall function

The relationship of transmural myocardial blood flow to midwall function was evaluated in seven adult mongrel dogs anesthetized with morphine SO 4 (3 mg/kg) and a-chloralose (80 mg/kg) and instrumented with catheters for measuring aortic and left ventricular end-diastolic pressures and dp/dt. Three pairs of miniature ultrasonic transducers (3 mm diameter) were positioned at midwall level of the left ventricle along the minor axis within each of the three regions: anterior, lateral, and posterior segments. Transmural blood flow in the epicardium and endocardium was measured utilizing 8- to 10-μm tracer microspheres before and after a 60-sec circumflex occlusion. Functional data for extent (ΔL) and rate ( dl/dt) of systolic shortening were determined and systolic excursion was normalized to an initial end-diastolic length of 10 mm. Total circumflex occlusion for 1 min was associated with a severe flow imbalance to the posterior endocardium (endocardium/epicardium 0.2 ± 0.1) resulting in marked functional impairment ( ΔL = -0.5 ± 0.2 mm, dl/dt = -1.6 ± 1.1 mm/sec) and holosystolic bulging. Flow within the lateral region was not as severely impaired (endocardium/epicardium 0.5 ± 0.1, P < 0.05), and was associated with less dysfunction ( P < 0.01) without regional bulging. Function and flow in the anterior region were augmented. These data suggest that midwall regional function is dependent on flow, especially endocardium. Holosystolic bulging represents marked flow reduction (97%) while flow may be decreased by 79% without holosystolic bulging.