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PubMed2005

Accelerated degradation models for failure based on geometric Brownian motion and gamma processes.

Based on a generalized cumulative damage approach with a stochastic process describing degradation, new accelerated life test models are presented in which both observed failures and degradation measures can be considered for parametric inference of system lifetime. Incorporating an accelerated test variable, we provide several new accelerated degradation models for failure based on the geometric Brownian motion or gamma process. It is shown that in most cases, our models for failure can be approximated closely by accelerated test versions of Birnbaum-Saunders and inverse Gaussian distributions. Estimation of model parameters and a model selection procedure are discussed, and two illustrative examples using real data for carbon-film resistors and fatigue crack size are presented.

Equipment Failure Analysis↗

PubMed1993

Cine magnetic resonance imaging and color Doppler flow mapping displays of flow velocity, spatial acceleration, and jet formation: a comparative in vitro study.

To study the effects of flow acceleration and high-velocity jets on the display characteristics of cine magnetic resonance imaging compared with color Doppler flow mapping, a custom-designed in vitro flow model was developed. This model consisted of a funnel segment tapering to an orifice (0.78 cm2) that leads into a confined receiving chamber with a second, discrete orifice (0.78 cm2) at its distal end. Cine magnetic resonance images obtained at varying flow rates (1.5 to 27.2 L/min) demonstrated loss of signal intensity throughout the tapering zone of spatial acceleration and a small zone of more marked signal loss immediately proximal to the second orifice (always < 50% of the signal intensity within the tapering funnel zone) associated with more rapid spatial acceleration. A formed jet was imaged distal to the first orifice, and the turbulence area surrounding the laminar central jet core correlated well with flow rate (r = 0.98), as did the distance from the orifice to the subsequent onset of flow relaminarization (r = 0.96). A turbulent spray area was always seen distal to the second, discrete orifice. Comparative observations with color Doppler flow mapping and continuous wave Doppler demonstrated that signal intensity on cine magnetic resonance imaging is reduced by both spatial acceleration, and the high-velocity and turbulent jets associated with obstructive and regurgitant lesions. In vitro evaluation of cine magnetic resonance imaging allows comparative observations to be made about the flow characteristics of cine magnetic resonance imaging and color Doppler flow mapping and provides a more rational basis for the interpretation of cine magnetic resonance imaging in the clinical setting.

Blood Flow Velocity↗

PubMed1986

Impaired left ventricular function in acute myocardial infarction assessed by Doppler measurement of ascending aortic blood velocity and maximum acceleration.

The Doppler-derived ejection variables systolic velocity integral, maximum acceleration and heart rate were recorded in 92 patients with acute myocardial infarction (AMI) and 73 age-matched normal subjects. Systolic velocity integral was validated as an index of stroke volume against a thermodilution technique in acutely ill patients. Patients with AMI were separated into clinically defined Forrester subsets and into survivors and nonsurvivors of the acute infarction period. Systolic velocity integral correlates significantly with stroke volume determined by thermodilution (r = 0.07) in patients with aortic root areas within the normal range. Patients had a 37% lower maximum acceleration (p less than or equal to 0.001), a 48% lower systolic velocity integral (p less than or equal to 0.001) and a 13% higher heart rate than the age-matched normal subjects (p less than or equal to 0.01). Systolic velocity integral and maximum acceleration both showed a systematic significant decrease through the Forrester subsets (p less than or equal to 0.01, p less than or equal to 0.001, respectively), and were also significantly different between the survivor and nonsurvivor groups (p less than or equal to 0.05, p less than or equal to 0.01, respectively.) Thus, noninvasive measurement of ascending aortic blood velocity and acceleration allows rapid assessment of left ventricular function and provides indexes closely related to the patients' clinical status and subsequent risk of mortality, indicating the potential of the Doppler technique in the prognosis and subsequent management of patients with myocardial infarction.

Aorta, Thoracic↗

PubMed1988

Evaluation of age, gender, heart rate and blood pressure changes and exercise conditioning on Doppler measured aortic blood flow acceleration and velocity during upright treadmill testing.

To evaluate the effect of upright exercise on aortic peak flow acceleration and velocity, 60 normal subjects between 15 and 74 years of age were evaluated by continuous wave Doppler during treadmill stress testing using the Bruce protocol. Subjects were divided into 3 age groups, each with 20 subjects: group 1, 21 +/- 4 years of age (mean +/- standard deviation), group 2, 36 +/- 5 years and group 3, 58 +/- 7 years. Periodic measurements of heart rate, blood pressure and Doppler blood flow velocity and acceleration were made before, during and after exercise. Continuous wave Doppler measurements were recorded from the suprasternal notch. The relation between Doppler aortic measurements and age, gender, normal heart rate and blood pressure responses during exercise, and exercise preconditioning, was evaluated. Age alone was significantly related (inversely) to immediate postexercise Doppler aortic peak blood flow peak acceleration (group 1, 55 +/- 15, group 2, 46 +/- 11 and group 3, 36 +/- 9 m/s2, p less than 0.05) and peak velocity (1.1 +/- 0.2, 1.0 +/- 0.2 and 0.8 +/- 0.2 m/s, respectively, p less than 0.01). Gender, heart rate and blood pressure changes during exercise, as well as preconditioning, had no significant effect on these flow characteristics. Consequently, the effects of normal aging must be considered when using Doppler measurements of peak aortic acceleration and velocity in the evaluation of left ventricular function, e.g., to detect or exclude the presence of coronary artery disease.

Adolescent↗

PubMed1989

Effects of left ventricular preload and afterload on ascending aortic blood velocity and acceleration in coronary artery disease.

Doppler measurements of the velocity and acceleration of ascending aortic blood flow have been used as indexes of left ventricular (LV) contractility. Conflicting data exist, however, on the influence of LV loading conditions on these measurements. Therefore, simultaneous LV micromanometer pressure measurements, 2-dimensional echocardiography and continuous-wave Doppler studies were performed before and after preload or afterload manipulation in 16 patients with coronary artery disease. Nitroprusside (n = 9) was administered in combination with saline to maintain preload and achieve a 10 to 20% reduction in mean aortic pressure. Saline (n = 7) was administered (850 +/- 240 ml) to increase LV end-diastolic pressure 25 to 50%. All measurements were obtained during atrial pacing at a heart rate 10 to 15 beats/min above resting sinus rate. The administration of nitroprusside plus saline decreased LV end-systolic wall stress (94 +/- 27 to 67 +/- 14 g/cm2 X 10(3), p = 0.011) without changing LV end-diastolic pressure and end-diastolic dimension. Peak velocity (0.8 +/- 0.2 to 0.9 +/- 0.3, p = 0.044), velocity time integral (11 +/- 4 to 13 +/- 5 cm, p = 0.049) and mean acceleration (12 +/- 4 to 17 +/- 7 m/s2, p = 0.0014) increased significantly. The administration of saline alone significantly increased LV end-diastolic pressure (10 +/- 4 to 22 +/- 4 mm Hg, p = 0.0006), LV end-diastolic dimension (4.8 +/- 0.5 to 5.1 +/- 0.5 cm, p = 0.0001), peak velocity (0.9 +/- 0.3 to 1.0 +/- 0.4 m/s, p = 0.008), velocity-time integral (14 +/- 5 to 18 +/- 7 cm, p = 0.005), and mean acceleration (14 +/- 6 to 17 +/- 7 m/s2, p = 0.041). Thus, even a modest change in either preload or afterload altered peak velocity, the velocity time integral and mean acceleration. These data have important clinical implications regarding the application of Doppler aortic flow indexes in the assessment of LV function.

Adult↗

PubMed1991

Pronounced reduction of aortic flow velocity and acceleration during heavy isometric exercise in coronary artery disease.

Doppler-derived parameters of aortic flow were examined during heavy isometric exercise in 48 men with coronary artery disease (CAD) and in 48 gender- and age-matched healthy controls. The aim was to determine which parameters best separated the groups and to look for a possible relation between exercise-induced Doppler patterns and the extent of CAD. Isometric exercise was performed with a 2-hand bar dynamometer, and the subjects were required to perform 50% of maximal voluntary contraction for 2 minutes. Examination was performed with a pulsed Doppler transducer positioned at the suprasternal notch. Resting peak flow velocity, acceleration time, stroke volume index and cardiac index did not show significant differences between the groups. However, mean acceleration and stroke work were significantly lower in patients with CAD. In this group, exercise peak flow velocity decreased from 98 +/- 13 to 55 +/- 12 cm/s, flow velocity integral from 14 +/- 3 to 7 +/- 3 cm, mean acceleration from 11 +/- 0.9 to 4.7 +/- 1 m/s/s, and stroke volume index from 41 +/- 6 to 23 +/- 4 ml/m2 (p less than 0.001 for all). Cardiac index decreased from 2.7 +/- 0.4 to 2 +/- 0.2 liters/min/m2 (p less than 0.05). Acceleration time increased from 82 +/- 6 to 116 +/- 7 ms. In most of the indexes, the directional changes induced by isometric exercise were similar in patients with CAD and in normal control subjects. The differences compared with the rest values were significantly greater in the CAD group, and especially in patients presenting with 3-vessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1982

Fetal heart rate accelerations and late decelerations during the course of intrauterine death in chronically catheterized rhesus monkeys.

The appearance of late decelerations and the disappearance of accelerations in the fetal heart rate were observed during the days that preceded intrauterine fetal death in nine chronically instrumented rhesus monkeys. All nine animals had recovered satisfactorily from the initial surgical procedure, as evidenced by normal biophysical and biochemical parameters. After recovery, all the fetuses had shown accelerations and no late decelerations with spontaneous uterine contractions. The mean duration of the preparations was 16.1 days. The duration of the preterminal observation period varied from 3 to 13 days, during which time no experiments were performed. The fetuses died during labor at a mean gestational age of 143 days. Late decelerations were the first sign of fetal deterioration and occurred with a slight but significant decrease in fetal PaO2 without changes in pH, whereas accelerations in fetal heart rate were still present. The loss of accelerations in fetal heart rate was a later phenomenon and was associated with significant reductions in fetal pH and PaO2.

Animals↗

PubMed1985

The distribution of accelerations of the human fetal heart rate at 38 to 40 weeks' gestational age.

In order to further understand the use of antepartum fetal heart rate monitoring we measured the distribution, in time, of two, three, or five fetal heart rate accelerations of greater than or equal to 15 bpm for greater than or equal to 15 seconds and of greater than or equal to 10 bpm for greater than or equal to 6 seconds in 12 healthy pregnant women at 38 to 40 weeks' gestation. The length of time necessary to measure 50% or 95% of intervals containing five accelerations would be substantially reduced by changing to a definition of two or three accelerations. However, an observation interval of at least 80 minutes is required to include the longest time interval of two, three, or five accelerations. These data may suggest new strategies for decreasing time and expense of fetal heart rate testing.

Female↗

PubMed1995

Accelerated induction therapy and resection for poor prognosis stage III non-small cell lung cancer.

BACKGROUND: Induction therapy and resection may improve the survival of patients with poor prognosis stage III non-small cell lung cancer, at the cost of significant treatment prolongation. The purpose of this study was to assess toxicity, response, and survival of an accelerated induction regimen and resection in poor prognosis stage III non-small cell lung cancer. METHODS: Forty-two surgically staged patients with poor prognosis stage III non-small cell lung cancer received 11 days of induction treatment consisting of 96 hours of continuous chemotherapy infusions of cisplatin (20 mg.m-2.day-2), 5 fluorouracil (1,000 mg.m-2.day-2), and etoposide (75 mg.m-2.day-2) concurrent with accelerated fractionation radiation therapy (1.5 Gy twice a day, to a dose of 27 Gy). Induction was followed in 4 weeks by resection. Postoperatively, a second course of continuous chemotherapy and concurrent accelerated fractionation radiation therapy (postoperative dose 13 to 36 Gy) was given. RESULTS: Despite some degree of induction toxicity in all patients there was only one induction death (2.4%). A clinical partial response was seen in 24 patients (57%). Thirty-six patients (86%) underwent thoracotomy, and resection was possible in 33 (79%). Pathologic downstaging was seen in 17 patients (40%), and 2 patients (5%) had no residual carcinoma at operation. There were 11 postoperative complications (31%) and 4 postoperative deaths (11%). Thirteen patients (31%) are alive and disease-free, 24 (57%) have persistent disease or have recurred (15 distant, 5 locoregional, 4 both), and 9 patients are alive with disease. The median survival is 21 months and the 2-year Kaplan-Meier survival is 43%, with no differences identified between stages IIIA and IIIB patients (p = 0.63). CONCLUSIONS: We conclude that accelerated induction therapy and resection in poor prognosis stage III non-small cell lung cancer (1) is toxic, with a 12% treatment mortality; (2) is effective with a 79% resection rate and 40% pathologic downstaging rate; (3) provides excellent local control; (4) may prolong survival; and (5) is of value in stage IIIB as well as stage IIIA patients.

Adult↗

PubMed1977

Optimization of vehicle accelerator-brake pedal foot travel time.

This study was directed towards reducing the lag time between stimulus and incidence of braking. The effect of the relative vertical heights of the brake and accelerator pedals on foot travel time was the subject of the first part of the investigation. In the second part, two new pedal designs in which the accelerator was mounted directly on the brake pedal were evaluated. A significant reduction in foot travel time of approximately 12.5% was realised by locating the accelerator pedal 25-50 mm (1-2 in) higher than the brake pedal. Mounting of the accelerator pedal adjacent to or directly on the brake pedal allowed reductions in braking lag time of 46% to 74%.

Journal Article↗

PubMed1985

Solute-induced acceleration of transbilayer movement and its implications on models of blood-brain barrier.

Hexylglycerol accelerates the transbilayer (flip-flop) movement of phospholipids, lysophospholipids and peptides. For example, lysophosphatidylcholine added to dimyristoylphosphatidylcholine vesicles activates the action of pig pancreatic phospholipase A2 (Jain and DeHaas (1983) Biochim. Biophys. Acta 736, 157-162) This activating effect is dissipated slowly after mixing, and no activation is observed when the lysophospholipid molecules are equally distributed on both sides of the bilayer. The half time for transbilayer movement of lysophosphatidylcholine is about 7 h, and it is accelerated over 100-fold in the presence of n-hexylglycerol, as well as by a variety of other amphipathic solutes including n-alkanols, ketamine, and flufenamic acid. Hexylglycerol also accelerates the rate of transbilayer movement of an amphipathic hexapeptide bocLALALW, as well as of the phosphatidylcholine molecules in erythrocyte membrane. These effects are observed without any change in the gross bilayer organization as judged by 31P-NMR. Biophysical significance of such solute induced acceleration of transbilayer movement of amphipathic solutes is discussed to account for the effect of alkylglycerols on blood brain barrier.

Animals↗

PubMed1996

Accelerated recovery following polyamines and aminoguanidine treatment after facial nerve injury in rats.

Accelerated axon regeneration is of paramount importance for improved functional recovery after motor nerve injuries. Following injury of their axon neurones undergo a series of changes, termed the axon reaction, aimed at survival and regeneration of a new axon. We and others have found that early treatment with exogenous polyamines can enhance neuronal survival and accelerate the rate of axon regeneration and functional recovery after sympathetic and motor (sciatic) nerve injuries. Results of the present study corroborate the previous findings and demonstrate that after facial nerve injury in adult rats, polyamine treatment can accelerate the early phases of motor function recovery (vibrissae movement). Treatment with aminoguanidine, an inhibitor of several oxidation reactions, produced a further improvement at the early phase of functional recovery. In the facial nucleus, the injury-induced transient reduction in the activity of the acetylcholine synthesizing enzyme choline acetyltransferase was not affected by the treatment. After nerve injury in 5-day-old male rats, polyamines and aminoguanidine treatment exerted a minor neuroprotective effect (127.6% surviving neurones compared to control). We conclude that polyamines and aminoguanidine may have therapeutic potential in the acceleration of recovery after nerve injuries.

Animals↗

PubMed1978

alpha- and beta-receptor blockade of isoproterenol- and norepinephrine-induced effects on regional blood flow and blood flow acceleration.

The effects of the beta-receptor blocking agent propranolol (100 microgram/kg i.v.) and of the alpha-receptor blocking agent dihydroergotamine (50 microgram/kg i.v.) on hemodynamic responses to isoproterenol and norepinephrine (both 1--1024 ng/kg) were investigated in anesthetized dogs. The effects studied were: (1) flow in the ascending aorta and the coronary, common hepatic, gastroduodenal, splenic, cranial mesenteric, renal and femoral arteries: (2) maximal flow acceleration in the splenic, cranial mesenteric and femoral arteries; (3) maximal rate of change of left ventricular pressure (LV dP/dt max). Propranolol shifted the dose-response curves for the isoproterenol-induced flow increases in the common hepatic, gastro-duodenal, and cranial mesenteric arteries to the right. It did not influence the flow responses to isoproterenol in the ascending aorta or the coronary, splenic, renal and femoral arteries. Propranolol prevented the decrease of arterial pressure evoked by isoproterenol. Propranolol shifted the isoproterenol-induced increase of LV dP/dt max and maximal blood flow to the same extent. Propranolol blocked the flow to the liver and gastrointestinal tract to a greater extent than the LV dP/dt max and maximal flow acceleration. Propranolol had no effect on the norepinephrine-induced increases in flow in the splenic, femoral and coronary arteries, but blocked the norepinephrine-evoked increases of flow accelerations and LV dP/dt max to the same extent. Dihydroergotamine inhibited the norepinephrine-induced increase in flow in the femoral artery and the decreases in flow in the hepatic, splenic, cranial mesenteric and renal arteries, and reversed the reduction of flow in the gastroduodenal artery. It is argued that dihydroergotamine may inhibit the increase in femoral flow through two mechanisms: (1) blocking the flow reduction to norepinephrine in the abdomen, and thereby passively shunting blood from the abdomen in preference to the femoral bed; (2) attenuating the norepinephrine-evoked reflexogenic femoral vasodilatation. It is concluded that: (1) propranolol is a beta-receptor blocking agent with a preference for blockade of isoproterenol-induced vascular effects; (2) norepinephrine-induced flow increases are not direct actions on vascular beta-receptors; (3) the increase of maximal blood flow accelerations after isoproterenol and norepinephrine is mediated by stimulation of cardiac beta-receptors; (4) dihydroergotamine is an alpha-receptor blocking agent particularly in the splanchnic vascular region.

Adrenergic alpha-Antagonists↗

PubMed1985

Nerve growth factor accelerates the early cellular events associated with wound healing.

The effects of injecting nerve growth factor (NGF) into subdermal air sacs on the backs of mice was studied. Sequential infiltration of cells into the lining of the sacs was observed. The initial cell type to infiltrate was the polymorphonuclear leukocyte, followed by highly vacuolated mononuclear cells, and then by fibroblast-like cells. This resembles the classical pattern of cellular responses during the normal process of wound healing. The kinetics for the peak accumulation of each cell type were dependent upon the concentration of NGF injected, and significant acceleration of infiltration of each cell type was observed with as little as 1 nM NGF. A similar acceleration of cellular infiltration was observed when mice were injected with the synthetic chemotactic peptide n-formyl-methionyl-leucyl-phenylalanine. This finding suggests that application of any chemotactic factor to wound sites may lead to accelerated tissue repair and an enhanced rate of wound contraction. The observation that NGF can act as a chemotactic factor in vivo may explain its ability to accelerate the healing of experimentally induced wounds in mice.

Animals↗

PubMed1986

Early polyamine treatment accelerates regeneration of rat sympathetic neurons.

After injury of their axons, damaged neurons shift their metabolic activity into a reparative mode aimed at survival and regeneration or, alternatively, they undergo degeneration and die. Previous reports have shown that at the initial stages of the response to axonal injury, polyamines are essential for neuronal survival and can accelerate functional recovery. In this study we examined the ability of exogenous polyamines to accelerate regeneration following crush of the pre- or postganglionic sympathetic nerves of the superior cervical ganglion in adult rats. We found that early treatment with polyamines after pre- or postganglionic nerve crush, accelerated the reappearance of choline acetyltransferase activity in the superior cervical ganglion, and of [3H]norepinephrine uptake in the iris, respectively. Functional recovery from eyelid ptosis was also accelerated. We conclude that treatment with polyamines can enhance regeneration of peripheral sympathetic neurons.

Animals↗

PubMed1995

Substrate-induced acceleration of N-ethylmaleimide reaction with the Cys-65 mutant of the transposon Tn10-encoded metal-tetracycline/H+ antiporter depends on the interaction of Asp-66 with the substrate.

We previously reported that the reaction of [14C]N-ethylmaleimide (NEM) with the S65C mutant of the transposon Tn10-encoded metal-tetracycline/H+ antiporter (TetA(B)) is competitively inhibited by tetracycline [Yamaguchi, A. et al., FEBS Lett. 322 (1993) 201-204]. However, this observation has been revealed to be a mistake. The reaction of [14C]NEM with S65C TetA(B) was significantly and reproducibly accelerated by tetracycline, i.e. not inhibited. When Asp-66 was replaced by Ala, the reaction of NEM with the Cys-65 residue was no longer affected by tetracycline. In contrast, when Arg-70 was replaced by Ala, the acceleration of the reaction was unaltered. The tetracycline acceleration of the reaction to the Cys-65 residue was further stimulated with energization of the membrane on the addition of NADH. On the other hand, the tetracycline-induced acceleration was not observed in the absence of a divalent cation. These observations indicated that the Cys-65 locus is exposed to the medium according to the interaction of a divalent cation-tetracycline chelation complex with Asp-66.

Amino Acid Sequence↗

PubMed1992

Scintigraphic demonstration of lactulose-induced accelerated proximal colon transit.

Although lactulose, a widely used cathartic, is known to increase stool frequency, details of its site of action in the colon are obscure. In the present study a noninvasive scintigraphic technique was used to closely follow the movements of proximal colonic contents. Lactulose, 10-20 mL three times daily, significantly accelerated mean transit through the ascending colon from 12.9 +/- 3.7 to 7.0 +/- 2.5 hours (n = 11; P less than 0.01). This was associated with the occurrence of mass movements, with six such events seen during lactulose treatment whereas only one was seen during the control study (P less than 0.05). Lactulose also accelerated movement through the rest of the colon so that at 24 hours after dosing the geometric center of the isotope bolus was distal to that seen during the control study (6.6 +/- 1.2 vs. 4.7 +/- 1.3; n = 11, P less than 0.001). This model of diarrhea in otherwise normal subjects was subsequently used to study the effects of viscous gels in diarrhea. The viscous and relatively poorly fermented gel ispaghula, 3.5 g three times daily, abolished mass movements and was associated with a small but significant increase in proximal colonic transit time, which increased from 6.1 +/- 2.1 to 7.7 +/- 1.5 hours (n = 8; P less than 0.05). By contrast, the viscous but readily fermentable gelling agent guar gum, 5 g three times daily, further accelerated the cathartic effect of lactulose, with the mean transit time decreasing from 6.4 +/- 2.3 to 4.7 +/- 1.7 hours (n = 8; P less than 0.05). The acceleration of proximal colonic transit by lactulose may be a useful model to study diarrhea and its modification by therapy.

Adolescent↗

PubMed1995

A nitric oxide-releasing nonsteroidal anti-inflammatory drug accelerates gastric ulcer healing in rats.

BACKGROUND & AIMS: Nonsteroidal anti-inflammatory drugs (NSAIDs) have well-characterized inhibitory effects on gastric ulcer healing. A new class of gastrointestinal-sparing, nitric oxide-releasing NSAID derivatives has been recently described. This study was performed to determine if one of these compounds (nitrofenac) would influence healing of a preexisting ulcer. METHODS: Seven days after induction of gastric ulcer with serosal acetic acid, daily oral treatment with antiinflammatory doses of diclofenac, nitrofenac, or vehicle was started. After 7 days of treatment, the ulcer area was measured. The effects of misoprostol and two drugs that show in vitro selectivity for inhibiting cyclooxygenase 2 (nabumetone and L745,337) were also assessed. RESULTS: Diclofenac, nabumetone, and L745,337 had no effect on ulcer healing when compared with vehicle. Only diclofenac significantly decreased hematocrit and weight gain. On the other hand, nitrofenac significantly accelerated healing. Glyceryl trinitrate also significantly and dose dependently accelerated healing. Nitrofenac suppressed cyclooxygenase 1 activity to a similar extent as diclofenac. CONCLUSIONS: These results show that an NO-releasing NSAID derivative and an NO donor could accelerate ulcer healing, whereas a standard NSAID, misoprostol, and two inhibitors of cyclooxygenase 2 had no effect. In addition to sparing the gastrointestinal tract, NO-releasing NSAIDs, despite suppressing cyclooxygenase activity, are capable of accelerating tissue repair.

Animals↗