391 research outputs found

    Tachycardia Related Cardiomyopathy: Response to Control of the Arrhythmia

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75609/1/j.1540-8183.1989.tb00780.x.pd

    Yearling bulls have reduced sperm concentration and increased seminal plasma interleukin-8 after a 28-day breeding season

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    We hypothesized that yearling bulls selected for a 28-d breeding season would have reduced sperm concentrations and morphology, and have increased seminal plasma concentrations of pro-inflammatory cytokine interleukin-8 (IL-8). Yearling bulls were selected based on a breeding soundness examination (BSE) at approximately 415 d of age and contained at least 750 million sperm in the ejaculate, with 12 bulls randomly selected for breeding (BREEDERS) and 12 bulls not selected for breeding (NON-BREEDERS). After a 28-d breeding period, all bulls underwent a BSE. Plasma and seminal plasma were collected at each time point for analysis. Data were analysed utilizing either the MIXED or GLIMMIX procedures with repeated measures in SAS with breeding group, age and the interaction as fixed effects. Sperm concentration per ml of ejaculate was reduced (p \u3c .05) in yearling bulls used for breeding compared with those not used for breeding at the end of the breeding season. Seminal plasma IL-8 concentrations in yearling bulls used for breeding were increased (p \u3c .05) after the breeding season compared with bulls not used for breeding. Taken together, yearling bulls selected for a 28-d breeding season have reduced sperm production per ml of an ejaculate and increased inflammatory response in the seminal plasma that can lead to impaired breeding response if they are to be used for more than 30 d of breeding

    Congenital aortic arch thrombosis diagnosed by echocardiography

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26803/1/0000359.pd

    Pulsed Doppler assessment of left ventricular diastolic filling in coronary artery disease before and immediately after coronary angioplasty

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    To determine if left ventricular (LV) diastolic filling abnormalities are detectable by Doppler echocardiography in patients with coronary artery disease (CAD), 34 patients with CAD and 24 normal, agematched control subjects underwent mitral valve pulsed Doppler examination. At catheterization, all CAD patients had typical angina, at least 70% diameter narrowing of 1 major coronary artery, ejection fraction of 50% or more and no valvular heart disease. Seventeen CAD patients underwent coronary angioplasty and had a Doppler examination 1 day before and 1 day after the procedure. Doppler diastolic time intervals, peak velocities at rapid filling (E velocity), atrial contraction (A velocity) and the ratio peak E/peak A velocities were measured. The following areas under the Doppler velocity envelope and their percentage of the total area were calculated: first third of diastole (0.33 area), triangular area under the peak E velocity (E area), and triangular area under the peak A velocity (A area). Patients with CAD and normal subjects were significantly different (p < 0.01) in peak E velocity (CAD 0.60 +/- 0.12 m/s, normal 0.68 +/- 0.12 m/s), peak A velocity (CAD 0.59 +/- 0.12 m/s, normal 0.48 +/- 0.11 m/s), ratio peak E/peak A velocities (CAD 1.0 +/- 0.27, normal 1.5 +/- 0.32), A area (CAD 0.052 +/- 0.015 m, normal 0.036 +/- 0.010 m), ratio E area/A area (CAD 1.7 +/- 0.53, normal 2.5 +/- 0.69), and all area fractions. In the CAD patients who had undergone coronary angioplasty, no differences were found in any Doppler index before and immediately after the procedure. Thus, abnormal patterns of LV diastolic filling occur in patients with CAD and normal global systolic function. The decreased percentage of the Doppler area occurring during rapid filling and the increased percentage of the Doppler area occurring in late diastole suggest that CAD patients have impaired early diastolic filling. These diastolic filling abnormalities are unimproved 24 hours after successful coronary angioplasty. Doppler echocardiography provides a useful, noninvasive technique for assessment of LV diastolic filling in patients with CAD.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26727/1/0000277.pd

    Comparison of Pittsburgh compound B and florbetapir in cross-sectional and longitudinal studies.

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    IntroductionQuantitative in vivo measurement of brain amyloid burden is important for both research and clinical purposes. However, the existence of multiple imaging tracers presents challenges to the interpretation of such measurements. This study presents a direct comparison of Pittsburgh compound B-based and florbetapir-based amyloid imaging in the same participants from two independent cohorts using a crossover design.MethodsPittsburgh compound B and florbetapir amyloid PET imaging data from three different cohorts were analyzed using previously established pipelines to obtain global amyloid burden measurements. These measurements were converted to the Centiloid scale to allow fair comparison between the two tracers. The mean and inter-individual variability of the two tracers were compared using multivariate linear models both cross-sectionally and longitudinally.ResultsGlobal amyloid burden measured using the two tracers were strongly correlated in both cohorts. However, higher variability was observed when florbetapir was used as the imaging tracer. The variability may be partially caused by white matter signal as partial volume correction reduces the variability and improves the correlations between the two tracers. Amyloid burden measured using both tracers was found to be in association with clinical and psychometric measurements. Longitudinal comparison of the two tracers was also performed in similar but separate cohorts whose baseline amyloid load was considered elevated (i.e., amyloid positive). No significant difference was detected in the average annualized rate of change measurements made with these two tracers.DiscussionAlthough the amyloid burden measurements were quite similar using these two tracers as expected, difference was observable even after conversion into the Centiloid scale. Further investigation is warranted to identify optimal strategies to harmonize amyloid imaging data acquired using different tracers

    Melanoma cells break down LPA to establish local gradients that drive chemotactic dispersal.

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    The high mortality of melanoma is caused by rapid spread of cancer cells, which occurs unusually early in tumour evolution. Unlike most solid tumours, thickness rather than cytological markers or differentiation is the best guide to metastatic potential. Multiple stimuli that drive melanoma cell migration have been described, but it is not clear which are responsible for invasion, nor if chemotactic gradients exist in real tumours. In a chamber-based assay for melanoma dispersal, we find that cells migrate efficiently away from one another, even in initially homogeneous medium. This dispersal is driven by positive chemotaxis rather than chemorepulsion or contact inhibition. The principal chemoattractant, unexpectedly active across all tumour stages, is the lipid agonist lysophosphatidic acid (LPA) acting through the LPA receptor LPAR1. LPA induces chemotaxis of remarkable accuracy, and is both necessary and sufficient for chemotaxis and invasion in 2-D and 3-D assays. Growth factors, often described as tumour attractants, cause negligible chemotaxis themselves, but potentiate chemotaxis to LPA. Cells rapidly break down LPA present at substantial levels in culture medium and normal skin to generate outward-facing gradients. We measure LPA gradients across the margins of melanomas in vivo, confirming the physiological importance of our results. We conclude that LPA chemotaxis provides a strong drive for melanoma cells to invade outwards. Cells create their own gradients by acting as a sink, breaking down locally present LPA, and thus forming a gradient that is low in the tumour and high in the surrounding areas. The key step is not acquisition of sensitivity to the chemoattractant, but rather the tumour growing to break down enough LPA to form a gradient. Thus the stimulus that drives cell dispersal is not the presence of LPA itself, but the self-generated, outward-directed gradient
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