Determination of the wind response of Saturn 5 by statistical methods, volume 1

Statistical analysis of Saturn 5 launch vehicle wind response - Vol.

Evaluation of registration, compression and classification algorithms. Volume 1: Results

The registration, compression, and classification algorithms were selected on the basis that such a group would include most of the different and commonly used approaches. The results of the investigation indicate clearcut, cost effective choices for registering, compressing, and classifying multispectral imagery

Evaluation of registration, compression, and classification algorithms. Volume 2: Documentation

There are no author-identified significant results in this report

Role of cellular senescence and NOX4-mediated oxidative stress in systemic sclerosis pathogenesis.

Systemic sclerosis (SSc) is a systemic autoimmune disease characterized by progressive fibrosis of skin and numerous internal organs and a severe fibroproliferative vasculopathy resulting frequently in severe disability and high mortality. Although the etiology of SSc is unknown and the detailed mechanisms responsible for the fibrotic process have not been fully elucidated, one important observation from a large US population study was the demonstration of a late onset of SSc with a peak incidence between 45 and 54 years of age in African-American females and between 65 and 74 years of age in white females. Although it is not appropriate to consider SSc as a disease of aging, the possibility that senescence changes in the cellular elements involved in its pathogenesis may play a role has not been thoroughly examined. The process of cellular senescence is extremely complex, and the mechanisms, molecular events, and signaling pathways involved have not been fully elucidated; however, there is strong evidence to support the concept that oxidative stress caused by the excessive generation of reactive oxygen species may be one important mechanism involved. On the other hand, numerous studies have implicated oxidative stress in SSc pathogenesis, thus, suggesting a plausible mechanism in which excessive oxidative stress induces cellular senescence and that the molecular events associated with this complex process play an important role in the fibrotic and fibroproliferative vasculopathy characteristic of SSc. Here, recent studies examining the role of cellular senescence and of oxidative stress in SSc pathogenesis will be reviewed

Ageing, adipose tissue, fatty acids and inflammation

A common feature of ageing is the alteration in tissue distribution and composition, with a shift in fat away from lower body and subcutaneous depots to visceral and ectopic sites. Redistribution of adipose tissue towards an ectopic site can have dramatic effects on metabolic function. In skeletal muscle, increased ectopic adiposity is linked to insulin resistance through lipid mediators such as ceramide or DAG, inhibiting the insulin receptor signalling pathway. Additionally, the risk of developing cardiovascular disease is increased with elevated visceral adipose distribution. In ageing, adipose tissue becomes dysfunctional, with the pathway of differentiation of preadipocytes to mature adipocytes becoming impaired; this results in dysfunctional adipocytes less able to store fat and subsequent fat redistribution to ectopic sites. Low grade systemic inflammation is commonly observed in ageing, and may drive the adipose tissue dysfunction, as proinflammatory cytokines are capable of inhibiting adipocyte differentiation. Beyond increased ectopic adiposity, the effect of impaired adipose tissue function is an elevation in systemic free fatty acids (FFA), a common feature of many metabolic disorders. Saturated fatty acids can be regarded as the most detrimental of FFA, being capable of inducing insulin resistance and inflammation through lipid mediators such as ceramide, which can increase risk of developing atherosclerosis. Elevated FFA, in particular saturated fatty acids, maybe a driving factor for both the increased insulin resistance, cardiovascular disease risk and inflammation in older adults

Operator independent left ventricular function monitoring during pharmacological stress echo with the new peak transcutaneous acceleration signal

BACKGROUND—As the myocardium contracts isometrically, it generates vibrations that can be measured with an accelerometer. The vibration peak, peak endocardial acceleration (PEA), is an index of contractility.
OBJECTIVE—To evaluate the feasibility of PEA measured by the cutaneous precordial application of the accelerometer sensor; and to assess the usefulness of PEA monitoring during pharmacological stress echocardiography.
DESIGN—Feasibility study.
SETTING—Stress echo laboratory.
PATIENTS—34 consecutive patients underwent pharmacological stress (26 with dipyridamole; 8 with dobutamine) and PEA monitoring simultaneously.
INTERVENTIONS—A microaccelerometer was positioned in the precordial region and PEA was recorded. Dipyridamole was infused up to 0.84 mg/kg in 10 minutes, and dobutamine up to 40 µg/kg/min in 15( )minutes.
RESULTS—A consistent PEA signal was obtained in all patients. Overall mean (SD) baseline PEA was 0.26 (0.15) g (g = 9.8 m/s(2)), increasing to 0.5 (0.36) g at peak stress (+0.24 g, 95% confidence interval (CI) 0.14 to 0.34 g; p < 0.01). PEA increased from 0.26( )(0.16) to 0.37 (0.25) g in the dipyridamole group (+0.11 g, 95% CI 0.08 to 0.16 g; p < 0.01), and from 0.29 (0.1) to 0.93 (0.37) g in the dobutamine group (+0.64 g, 95% CI 0.37 to 0.91 g; p < 0.01).
CONCLUSIONS—Using precordial leads this method offers potential for diagnostic application in the short term monitoring of myocardial function. PEA monitoring is feasible during pharmacological stress and documents left ventricular inotropic response quantitatively in a non-invasive and operator independent fashion.


Keywords: ventricular function; contractility; peak endocardial acceleration; stress ech